Guidelines for the Control of

Infectious Diseases

THE
BLUE
BOOK
 Acknowledgements
Editorial Committee
Dr John Carnie
Dr Kath Taylor
Dr Rosemary Lester
Dr Sally Ng
Ms Sheila Beaton
Ms Pam Norris
Sr Anne Murphy
Dr Graham Rouch

The editorial committee is grateful to:

• the staff of the Microbiological Diagnostic Unit,
especially:
Dr G. Hogg, Director
Dr J. Forsyth
Dr D. Lightfoot
Dr M. Veitch
• other contributors:
Dr Andrew Fuller, Alfred Hospital, Melbourne
Dr Graeme Brown, Royal Melbourne Hospital
Dr Noel Bennett, Department of Human Services
Standing Committee on Infection Control
Dr John Harrison, Department of Human Services
Ms Gabrielle Keeshan. Department of Human Services.
for their assistance to the preparation of these guide-
lines.

This manual has been prepared to provide guidelines for

Human Services and local government staff, general
practitioners and infection control officers involved in
preventing and controlling infectious diseases.

Published by the Infectious Diseases Unit, Public Health

Division, Victorian Government of Human Services.

Design and production by Human Services Promotions

Unit.

This publication is available at Internet address:

http://hna.ffh.vic.gov.au/phb/

(040AP96)

ii
 Disclaimer

These guidelines have been prepared following consul-

tation with experts in the field of infectious diseases and
are based on information available at the time of their
preparation.

Practitioners should have regard to any information on

these matters which may become available subsequent
to the preparation of these guidelines.

Neither the Department of Human Services, Victoria, nor

any person associated with the preparation of these
guidelines accept any contractual, tortious or other
liability whatsoever in respect of their contents or any
consequences arising from their use.

While all advice and recommendations are made in

good faith, neither the Department of Human Services,
Victoria, nor any other person associated with the
preparation of these guidelines accepts legal liability or
responsibility for such advice or recommendations.

iii
 Contents

Introduction 1 Food - or Water-Borne Illness 53

Abbreviations Used 5 Giardiasis 59

Acquired Immunodeficiency Haemophilus influenzae

Syndrome 7 Infections 61
Information Sheets 64
Acute Bacterial Conjunctivitis 11
Hand, Foot and Mouth Disease 67
Amoebiasis 13 Information Sheet 69

Anthrax 15 Hepatitis A 71

Arbovirus Infections 17 Hepatitis B 75

Ross River Virus Disease 17
Australian Arboencephalitis (AE) 19 Hepatitis C 81
Dengue 21
Kunjin 22 Hepatitis D 85

Botulism 23 Hepatitis E 87

Brucellosis 27 Herpes Simplex 89

Campylobacter Infection 29 Hydatid Disease 91

Chicken Pox/Herpes Zoster 31 Impetigo 93

Cholera 35 Influenza 95

Cryptococcal Infection 39 Infectious Mononucleosis 97

Cryptosporidiosis 41 Legionellosis 99

Cytomegalovirus (CMV) Infection 43 Leprosy 103

Diphtheria 45 Leptospirosis 105

Erythema Infectiosum 49 Listeriosis 109

Information Sheet 51

v
 Malaria 113 Rubella 173
Information Sheet 117
Salmonellosis 177
Measles 119
Scabies 181
Meningococcal Infections 123 Information Sheets 183
Information Sheet 127
Shigellosis 185
Meningoencephalitis 129
Streptococcal Disease Caused by
Mumps 131 Group A Beta-Haemolytic
Streptococcus 187
Mycobacterial Infections 133
Tuberculosis 133 Ta e n i a s i s 189
Atypical (Non-Tuberculosis) 139

Te t a n u s 191
Pediculosis/Headlice 141 NH&MRC Recommendations 192
Information Sheet 143

To x o p l a s m o s i s 193
Pertussis 145
Typhoid/Paratyphoid 195
Plague 149
Ty p h u s 199
Pneumonia due to Chlamydia
pneumoniae 153 Verotoxin Producing E. coli 201

Poliomyelitis 155 Viral Gastroenteritis Caused

by Agents Other than Rotavirus 203
Psittacosis 157
Viral Haemorrhagic Fevers 205
Q Fever 159
Information Sheet 162
Yellow Fever 209
Vaccination Outlets 211
Rabies 163
Ye r s i n i o s i s 215
R ingw o rm/Tin ea 167
Information Sheet 170
Appendix 1: Telephone Numbers 217
Rotaviral Gastroenteritis 171 Appendix 2: Glossary 219

vi
Appendix 3: Outbreak
Investigation 221

Appendix 4: Standard Precautions 223

Appendix 5: Procedure for

Dealing with Spills of Blood and
Body Fluids 225

Appendix 6: Management of
Needlestick Injury and Exposure
to Blood or Body Fluids 227

Appendix 7: Specimen Collection

and Transport Guidelines 231

Appendix 8: Infections in
Children’s Services Centres 237

Appendix 9: School Exclusion

Table 239

vii
 Introduction

Infectious diseases still occur frequently throughout the
world and constant vigilance is required to prevent the
reappearance of diseases thought to have been con-
quered. Changes in lifestyle have also led to the emer-
gence of new threats to public health from infections.
Health authorities depend on medical practitioners for
information on the incidence of infectious diseases and
notification is vital in efforts to prevent or control the
A case of any of these diseases should be notified to
Human Services, Victoria, by telephone or facsimile upon
initial diagnosis (presumptive or confirmed) and written
notification should follow within seven days. Notification
forms are available from the Department:
Telephone (03) 9616 7777.
The telephone numbers for notification of diseases are:
Infectious Diseases Unit (03) 9616 7777 or 1800 034 280.

spread of infection. Fax: (03) 9616 8329 (Attention: Chief Health Officer).
After hours, contact the duty medical officer.
Telephone the paging service on (03) 9625 5000 and
The Health (Infectious Diseases) Regulations 1990
give pager number 46870.
replaced the outdated legislative provisions relating to
such diseases.
Group B Diseases
Notifiable infectious diseases are to be found in schedule
Amoebiasis.
2 of the Regulations and are divided into four groups on
Arbovirus infections (except for Australian
the basis of the method of notification and the information
Arboencephalitis and Yellow Fever).
required.
Brucellosis.
Campylobacter infection.
Group A Diseases Giardiasis.

Australian Arboencephalitis. Hepatitis A.

Anthrax. Hepatitis B.

Botulism. Hepatitis C.
Hepatitis non-A non-B.
Cholera.
Hepatitis (viral, unspecified).
Diphtheria.
Hydatid disease.
Food-borne and water-borne illness (two or more related
Leprosy.
cases).
Leptospirosis.
Legionellosis.
Listeriosis.
Measles.
Malaria.
Meningitis or epiglottitis due to Haemophilus influenzae.
Mumps.
Meningococcal infection.
Pertussis.
Plague.
Psittacosis (Ornithosis).
Poliomyelitis.
Q Fever.
Primary amoebic meningo-encephalitis.
Rubella (including congenital Rubella).
Rabies.
Salmonellosis.
Typhoid and Paratyphoid fevers.
Shigellosis.
Typhus.
Taeniasis (tape worm infections).
Viral haemorrhagic fevers.
Tetanus.
Yellow Fever.
Tuberculosis.
Yersiniosis.

1
Note Laboratory Notification
For these, written notification only is sufficient, within
Around Australia and overseas, it has been recognised
seven days of confirmation of diagnosis.
that laboratory notification of infectious diseases should
be an integral part of any disease surveillance system.
Group C Diseases
Chancroid. The Health (Infectious Diseases) Regulations 1990
Donovanosis. require notification from laboratories under the
Gonorrhoea (all forms). circumstanceslisted below.
Lymphogranuloma venereum.
Other Chlamydial infections. A. Food and Water Supplies
Syphilis (all forms).
Isolate the following pathogens from food for human
consumption or from water supplies:
Note
• Campylobacter jejuni.
These sexually transmissible diseases should be notified
• Listeria monocytogenes.
using the same notification form but, to preclude identifi-
• Salmonella species.
cation of the patient, only the first two letters of the given
name and surname of the patient are required.
Isolate the following pathogens from water supplies:
• Campylobacter coli.
Not all chlamydial diseases are STDs.
• Campylobacter lari.
• Vibrio cholerae.
Group D Diseases • Giardia cysts.
Acquired lmmunodeficiency Syndrome. • Cryptosporidium oocysts.
HIV was made notifiable in September 1996.
Detection of any of the above organisms should be
Note notified in writing to Human Services within seven days,
Written notification is required within seven days of stating the pathogen isolated, the source, the date of
confirmation of diagnosis. isolation, and any batch identification (if appropriate).

A separate form is used for this purpose due to the need

to have national uniformity in collection of data.
To preclude identification of the patient, only the first two
letters of the given name and surname of the patient are
required.
B. Material of Human Origin
A laboratory test that indicates the probable presence of
a human pathogenic organism associated with an
infectious disease listed in Groups A, B or C should be
notified to Human Services.

Send all notifications to: If the disease is in Group A, the notification should be
Freepost 547 made by telephone or other rapid transmission.
Infectious Diseases Unit
Public Health Branch If the disease is in Groups B or C, Human Services
GPO Box 4057 should be notified in writing within seven days.
Melbourne 3001
and mark them Confidential.

2
The notification from the laboratory should state the
laboratory finding, the family name and given name of
the patient (except for Group C diseases); the age, sex
and postcode of the patient; and the name, address and
telephone number of the doctor requesting the test.

This manual has been published by the Infectious

Diseases Unit, Public Health Division, Victorian Govern-
ment Department of Human Services, Victoria, to assist
all public health practitioners in the control and preven-
tion of infectious diseases.

Any comments and suggestions regarding the format of

the manual, as well as on the information provided, are
welcome and should be directed to:
Dr John Carnie
Manager
Infectious Diseases Unit
Public Health Branch
Department of Human Services
PO Box 4057
Melbourne 3001

3
 Abbreviations Used

ADT adult diphtheria tetanus vaccine

ALT alanine aminotransferase
anti-HBc hepatitis B core antibody
anti HBs hepatitis B surface antibody
AST aspartate aminotransferase
CDT combined diphtheria tetanus vaccine
CF/CFT complement fixation test
CNS central nervous system
CSF cerebro-spinal fluid
CT Scan computerised tomography
DFA direct fluorescent antibody
DTP diphtheria tetanus pertussis vaccine
EBV Epstein-Barr virus
EIA enzyme immunoassay
ELISA enzyme-linked immunosorbent assay
EM electron microscopy
FA direct fluorescent or immunofluorescent
antibody test
HAI haemagglutination inhibition test
HAV hepatitis A virus
HBIG hepatitis B immune globulin
HbsAg hepatitis B surface antigen
HbeAg hepatitis B e antigen
HBV hepatitis B virus
HCV hepatitis C virus
HDV hepatitis D virus
Hib Haemophilus influenzae type b
HIV human immunodeficiency virus
IFA indirect immunofluorescent antibody test
IG immune globulin
IHA indirect haemagglutination
IM intramuscular
IV intravenous
MDU Microbiological Diagnostic Unit
MIF micro immunofluorescent test
MMR measles-mumps-rubella vaccine
NH&MRC National Health and Medical Research
Council
PCR polymerase chain reaction
VIDRL Victorian Infectious Diseases Reference
Laboratory
WHO World Health Organisation

5
 Acquired Immunodeficiency Syndrome

Victorian Statutory Public Health Significance and

Re quirem en t O c c u r re n c e
AIDS Group D notification. Occurrence is worldwide.
HIV infection was made notifiable in September 1996.
According to the World Health Organisation (WHO)
estimation, close to 6.8 million cases of AIDS and 22
Infectious Agent million cases of HIV occurred by 1994.
Human Immunodeficiency virus (HIV), types 1 and 2
(retrovirus). Of HIV infected persons, approximately 15–20 per cent
will develop AIDS within five years, and about 50 per
cent within 10 years.
Clinical Features
AIDS is a severe, life-threatening disease that represents
With modern antiviral therapy, these incubation periods
the late clinical stage of infection with HIV.
have lengthened.

Within several weeks after infection with HIV, many

By 1995, there were 1,234 cases of AIDS diagnosed in
people will develop a self-limited mononucleosis-like
Victoria, and 926 notified deaths.
illness lasting for a week or two.

In 1994, 217 new diagnoses of HIV were made, bringing

Infected persons may then be free of clinical signs or
the total HIV infections in Victoria to 3372.
symptoms for months or years, before developing
specific opportunistic infections and cancers and a
range of other indicative diseases. Method of Diagnosis
Careful history and physical examination looking for risk
Major diseases that may be indicative of AIDS include: factors and clinical manifestations of immunodeficiency.
• Pneumocystis carinii pneumonia.
• Candidiasis. Laboratory confirmation of diagnosis by:
• Kaposi sarcoma. • Detecting HIV antibodies with ELISA test (confirmed by
• Herpes simplex infection. Western blot analysis).
• Cryptococcosis. • Diagnosing opportunistic infection or secondary
• Cryptosporidiosis. cancer.
• Toxoplasmosis.
• Cytomegalovirus infection.
• Mycobacteriosis.
Reservoir
• Lymphoma. Human.
• HIV encephalopathy.
• HIV wasting disease.

7
Mode of Transmission Presence of other sexually transmitted diseases, espe-
cially those causing genital ulceration, increases suscep-
HIV can be transmitted by:
tibility for sexual transmission.
• Unprotected sexual intercourse with an infected
person.
• Inoculation with infected blood, blood products and Control of Case
through transplantation of infected organs, bone graft,
Standard fluid precautions apply to all patients.
tissue or semen.
• From infected woman to the foetus during pregnancy
Additional precautions apply for specific infections that
or breastfeeding. Approximately 15 to 30 per cent of
occur in AIDS patients.
infants from HIV positive mothers are infected, but
treatment during pregnancy can result in a marked
Concurrent disinfection of equipment, contaminated with
reduction in infections.
blood or body fluids.
• Needle-stick injuries or other exposure to blood and
body fluids by health care or emergency workers. The
Patients and their sexual partners should not donate:
rate of seroconversion following a needle stick injury
• Blood.
involving HIV infected blood is said to be less than 0.5
• Plasma.
per cent.
• Organs for transplantation.
• Tissues.
Note
• Cells.
Social contact with HIV infected person carries no risk of
• Semen for artificial insemination.
transmission.
• Breast milk for human breast banks.

Incubation Period All HIV positive persons should be evaluated for the
presence of tuberculosis.
From infection to primary illness, three weeks to three
months.
Tre a t m e n t
The time from HIV infection to the diagnosis of AIDS
Zidovudine (AZT), dideoxycytidine (DDC) and
ranges from about two months to 20 years or longer, with
dideoxyinosine (DDI) are the current anti-retroviral drugs
a median of 10 years.
available in Australia specifically indicated for HIV
infection.
Treatment lengthens the incubation period.

Other treatment includes specific treatment or prophy-

Period of Communicability
All antibody positive persons carry HIV.
Infectivity must be presumed to be lifelong.
Susceptibility and Resistance
Susceptibility seems to be general.
laxis for the opportunistic infectious diseases that result
from HIV infection.
For further information, see Antibiotic Guidelines pub-
lished by the Victorian Medical Postgraduate Foundation
Inc.

8
Control of Contacts Epidemic Measures
If a person is diagnosed as having HIV infection, the HIV infection is usually pandemic.
diagnosing practitioner has a responsibility to ensure that
sexual and needle-sharing contacts are followed up.
Assistance with partner notification may be provided by
International Measures
Human Services through its partner notification officers: A global prevention and control program coordinated by
telephone (03) 9482 5700. WHO was initiated in 1987.

Pre- and post-test counselling should be provided for all Currently all countries have developed AIDS prevention
contacts who seek HIV testing. and control programs.

Preventive Measures
Personal:
• Public education on the use of condoms and safer sex
practices.
• Public education should stress that having unprotected
sex with multiple sexual partners and sharing needles
(drug users) increases the risk of infection with HIV.
• Sexual intercourse with persons with known or sus-
pected HIV should be avoided.
• HIV-infected persons should be offered confidential
counselling.
• Care sould be taken when handling, using and dispos-
ing of needles or other sharp instruments.
• Use of needle exchange programs by injecting drug
users.

Institutional:
• Use of appropriate infection control measures by all
health care and emergency workers.
• Use of appropriate infection control measures in all
premises where skin penetration is carried out; for
example, by tattooists or beauty therapists carrying out
electrolysis.
• Blood and blood products for transfusion and tissues
for donation should be tested for HIV infection.
• Needle-stick/sharps injuries and parenteral exposure
to laboratory specimens containing high titre of virus
should be dealt with according to the Australian
National Council on AIDS guidelines.

9
 Acute Bacterial Conjunctivitis

Victorian Statutory Mode of Transmission

Re quirem en t
Statutory notification not required except for gonococcal
disease (ophthalmia neonatorum).
School and child care exclusion.
It can be transmitted by ontact with:
• Discharge from the conjunctivae or upper respiratory
tract of infected persons.
• Contaminated fingers or fomites (contaminated ob-
jects).
• Infected mothers during vaginal delivery.

Infectious Agent
Haemophilus influenzae, Streptococcus pneumoniae. Incubation Period
Usually 24–72 hours.
Other organisms include:
• Staphylococcus aureus, Pseudomonas aeruginosa.
Period of Communicability
• Neisseria gonorrhoeae in neonates.
It is infectious while there is discharge.

Clinical Features
Susceptibility and Resistance
Excessive tears, irritation and redness of eyes, followed
Children under five years are most often affected.
by oedema of lids, photophobia and mucopurulent
Incidence decreases with age.
discharge which usually lasts from two days to two to
Immunity after attack is low-grade.
three weeks.

Viral conjunctivitis can cause a similar clinical picture. A Control of Case

blocked tear duct predisposes to recurrent infection. Children should not attend school and child care settings
until discharge from eyes has ceased. Soiled articles

Public Health Significance and should be disinfected.

Oc c u r re n c e
A common communicable disease, frequently epidemic, Tre a t m e n t
affecting children under five years of age. Local application of antibiotic ointment or drops.

Occurrence is worldwide.
Control of Contacts
Investigation of contacts and source of infection not
Method of Diagnosis practicable.
Microscopic examination of a smear or bacteriologic
culture of the discharge.
Preventive Measures
Personal hygiene and proper treatment of infected eyes.
Reservoir
Human.
Epidemic Measures
Not applicable.

11
 Amoebiasis
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agent
Entamoeba histolytica.
Clinical Features
An infection with a protozoan parasite that exists in two
forms: an infective cyst and a potentially pathogenic
trophozoite. Further, the difficulty of distinguishing
infection with the non-pathogenic Entamoeba dispar
must be noted.
Clinically, it may present as intestinal or extra-intestinal
disease. Most infections are asymptomatic. Intestinal
disease includes diarrhoea which may be bloody, fever
and abdominal discomfort.
Intestinal amoebiasis may be complicated by:
• Granuloma of the large intestine.
• Colonic perforation and haemorrhage.
• Perianal ulceration.
• Extra-intestinal amoebiasis with abscess formation that
occurs as a result of bloodstream spread to the liver,
brain or lungs.
Public Health Significance and
Oc c u r re n c e
Occurrence is worldwide.
High-risk groups include:
• Patients in institutions for the intellectually disabled.
• Male homosexuals.
• People living in areas with poor sanitation.
• Travellers returning from developing countries.
This active disease occurs mostly in young adults and is
rare below the age of five years.
Method of Diagnosis
Microscopic examination for trophozoites or cysts in:
• Fresh or suitably preserved faecal specimens.
• Smears of aspirates or scrapings obtained by
proctoscopy.
• Aspirates of abscesses or sections of tissue.
As cysts are shed intermittently in asymptomatic and
mild infections, repeated stool specimens may be
needed to establish a diagnosis.
The presence of trophozoites containing red blood cells
is indicative of invasive amoebiasis.
Serology, raised titre of specific antibodies is valuable in
diagnosis of amoebiasis.
X-ray, ultrasound and CT scan are used in diagnosis and
location of an amoebic liver abscess.
Reservoir
Human.
Mode of Transmission
Amoebiasis can be transmitted by:
• Ingestion of faecally contaminated water containing
amoebic cysts.
• Hand-to-mouth transfer of faecal contamination.
• Contaminated raw vegetables.
• Sexually, by unprotected oral-anal contact.
Incubation Period
Average incubation period is two to four weeks.
Patients may present months after the initial infection.
13
 Period of Communicability • Educate the public about the possibility of transmitting
the disease via sexual contact.
Cases are infectious as long as cysts are present in the
• Protect public water supplies from faecal contamina-
faeces.
tion.

In some instances, cyst excretion may persist for years.

Epidemic Measures
Susceptibility and Resistance • Ensure proper laboratory confirmation of diagnosis.
• Undertake epidemiological investigation to determine
Recurrent infections can occur.
source of infection and to look for a common vehicle
such as food or water.
Control of Case
Amoebiasis can be controlled by:
• Standard Precautions.
• Exclusion of infected person from food handling until
asymptomatic.
• Sanitary disposal of faeces.

Tre a t m e n t
For acute amoebic dysentery, use metronidazole. After
initial treatment of invasive amoebiasis with metronida-
zole, cyst eradication with furamide may be indicated.

For extra-intestinal amoebiasis, use metronidazole.

Surgical aspiration of abscesses may be necessary.

Control of Contacts
Routine investigation of contacts is not indicated. How-
ever, in residential institutions or in the case of fellow
travellers, microscopic examination of faeces is advis-
able.

Preventive Measures
• Educate the public in personal hygiene.
• Provide information to intending travellers about the
risk involved in eating uncooked vegetables and fruits
and drinking contaminated water.

14
 Anthrax
Victorian Statutory
Re quirem ent
Group A notification.
Infectious Agent
Bacillus anthracis, a Gram-positive, encapsulated spore-
forming, non-motile aerobic rod.
Clinical Features
Anthrax is an acute bacterial disease usually affecting
the skin.
It may rarely involve the intestinal tract.
Cutaneous Anthrax
Lesions are usually painless.
Itchiness is common followed by a skin lesion that
progresses from a papule to a vesicle (which may be
haemorrhagic), and in two to six days develops into a
depressed black eschar (malignant pustule).
Untreated lesions can progress to involve the regional
lymph nodes. In severe cases, an overwhelming septi-
caemia can occur.
Untreated cutaneous anthrax has a case fatality rate of
between 5–20 per cent.
Pulmonary Anthrax
This is very rare and often presents with mild and non-
specific symptoms resembling common URTI.
This is followed three to five days later by acute respira-
tory distress and changes on X-ray.
Untreated, the mortality rate is 70–80 per cent.
Intestinal Anthrax
It is rare in developed countries, but may occur in
explosive outbreaks.
Gastro-intestinal symptoms may be followed by fever,
septicaemia and death (mortality rate is 25–75 per cent).
Public Health Significance and
O c c u r re n c e
Anthrax is primarily an occupational hazard for handlers
of:
• Processed hides.
• Goat hair.
• Bone and bone products.
• Wool.
• Infected wildlife.
It can also be contracted by contact with infected meat;
for example, knackery workers.
New areas of infection in livestock may develop through
introducing animal feed containing bone meal.
Cutaneous outbreaks sometimes occur in knackery
workers and those handling pet meat.
Known infectious land can remain contaminated for
years.
Method of Diagnosis
Demonstrate the presence of Gram-positive Bacillus
anthracis in blood, lesions or discharges by:
• Direct staining of smears using Gram or special stains.
• Isolation or animal inoculation in the laboratory.
Reservoir
Dried or otherwise processed skins and hides of infected
animals may harbour spores for years.
Spores remain viable in contaminated soil for many
years.
15
 Mode of Transmission
Usually two to seven days. Most cases occur within 48
hours of exposure.
Period of Communicability
There is no evidence of direct spread from person to
person.
Articles and soil contaminated with spores may remain
infective for years.
Susceptibility and Resistance
Recovery is usually followed by prolonged immunity.
Control of Case
To control anthrax, it is important to:
• Seek laboratory confirmation.
• Find out the occupation of patient.
• Seek the source of infection.
• Arrange isolation of patient in hospital. Soiled articles
require pressure steam sterilisation or incineration.
• Use penicillin as the drug of choice. Tetracyclines,
erythromycin, chloramphenicol or ciprofloxacin could
be used if penicillin is contraindicated.
Control of Contacts
History of exposure to infected animals/products should
be examined.
Control of Environment
To control the environment:
• Seize suspected animal products.
• Incinerate infected animal products.
• Use formaldehyde for disinfection of contaminated
premises.
• Inform the Department of Natural Resources and
Energy of the case.
16
• Sterilise imported bone meal before use as animal
feed.
• Sterilise wool, hair, hides and other infected products
by ethylene oxide gas or ionising (gamma) radiation.
Note
Soiled articles require pressure steam sterilisation or
incineration.
Preventive Measures
• Educate employees who are handlers of potentially
infected articles in the proper care of skin abrasions.
• Ensure proper ventilation in hazardous industries and
use of protective clothing.
• Sterilise hair, wool or hides, bone meal or other feed of
animal origin prior to processing.
• Use vaporised formaldehyde for terminal disinfection of
textile mills contaminated with B. anthracis.
• Collect a jugular blood sample from the animal for
culture if anthrax is suspected in an animal.
• Deeply bury carcasses with quicklime at site of death if
possible. Do not necropsy or burn on open field.
• Decontaminate soil or discharges with quicklime, or
preferably bury deeply with carcass.
• Promptly vaccinate all animals at risk and revaccinate
annually.
• Control effluent and trade wastes from factories that
manufacture products from hair, wool or hides likely to
be contaminated.
• Decontaminate soil on infected farms with 5 per cent
formalin.
Treatment of Animals
Symptomatic animals can be treated with penicillin or
tetracyclines.
Epidemic Measures
Trace the source of infection.
 Arbovirus Infections
Victorian Statutory
Re q u i re m e n t s
Group A for Australian arboencephalitis.
Group B for other arbovirus infections.
Prevention of mosquito breeding (section 29 of the
Health (Infectious Diseases) Regulations 1990).
Infectious Agents
Flaviviruses: Murray Valley Encephalitis (the cause of
Australian arboencephalitis), Kunjin, Dengue.
Alphaviruses: Ross River virus, Barmah Forest virus,
Sindbis.
Ross River Virus Disease
(Epidemic Polyarthritis)
Infectious Agent
Ross River virus (alphavirus).
Sindbis and particularly Barmah Forest viruses (both
alphaviruses) can cause similar illnesses.
Clinical Features
A self-limited disease characterised by arthritis or
arthralgia lasting from days to months and primarily
affecting the wrist, knee, ankle and small joints of the
extremities. Prolonged symptoms are common.
In some cases, there may be remissions and
exacerbations of decreasing intensity for years.
In many patients, the onset of arthritis is followed in one
to 10 days by a maculopapular rash (usually non-pruritic)
mainly affecting the trunk and limbs.
Buccal and palatal enanthema may occur.
The rash resolves within seven to 10 days, followed by a
fine desquamation.
Cervical lymphadenopathy occurs frequently, and
parasthesiae and tenderness of palms and soles are
present in a small percentage of cases.
Fever is commonly absent.
Public Health Significance and
O c c u r re n c e
Major outbreaks have occurred in Australia in the Murray
Valley, Gippsland, coastal New South Wales, Northern
Territory, Queensland and Western Australia, chiefly from
January to May.
Sporadic cases occur in other coastal regions of Aus-
tralia and Papua New Guinea.
In 1979, a major outbreak occurred in Fiji and spread to
other Pacific islands, including Tonga and the Cook
Islands. There were 15,000 cases in American Samoa in
1979–80.
Morbidity: 30 per cent of the population will develop
symptoms of the disease if infected.
Infection is rare in prepubertal children and increases
with age.
In those affected, the disease can cause incapacity to
work for two to three months and sometimes longer.
Method of Diagnosis
Serology can show a rise in antibody titre to Ross River
virus. The virus may be isolated from the blood of acutely
ill patients.
Tests are usually necessary to distinguish it from other
causes of arthritis. However, in the event of a local
outbreak clinical diagnosis may be sufficient.
17
 Reservoir
Probably macropods (for example, kangaroos); possibly
other marsupials and wild rodents.
Transovarian transmission in the mosquito Aedes vigilax
has been demonstrated in the laboratory, making an
insect reservoir a possibility.
Mode of Transmission
It is transmitted by mosquitoes Culex annulirostris, Ae.
camptorhynchus. Ae. vigilax, Ae. polynesiensis and other
Aedes spp. of mosquitoes.
Incubation Period
Usually three to 11 days.
Period of Communicability
There is no evidence of transmission from person to
person.
Susceptibility and Resistance
Recovery is universal and is followed by lasting immu-
nity. Second attacks are unknown.
Inapparent infections are common, especially in children,
among whom the clinical disease is rare.
Arthritis occurs more frequently among adult females
and in persons with a particular HLA DR7 phenotype.
Control of Case
Not applicable.
Symptomatic treatment.
Control of Contacts
Unreported or undiagnosed cases should be searched
for in the region where the patient had been during the
incubation period of their illness.
18
All family members should be questioned about symp-
toms and evaluate serologically if appropriate.
Preventive Measures
Ross River virus can be prevented by:
• Mosquito control measures (see local municipality).
• Personal protection measures (long sleeves and
mosquito repellents).
• Avoidance of mosquito-prone areas. Vectors usually
bite at dusk and dawn.
Epidemic Measures
• Conduct a community survey to determine species of
vector mosquitoes. Identify their breeding places and
promote their elimination.
• Use mosquito repellents for persons exposed because
of occupation or otherwise to mosquito bites.
• Identify the infection among animal reservoirs; for
example, kangaroos, small marsupials, farm and
domestic animals.
Note
See the Victorian Arbovirus Task Force Contingency Plan
for Outbreaks of Ross River Virus Disease.
International Measures
Airport vector control in Australia and Papua New
Guinea.
These measures may be necessary to prevent the
spread from endemic areas in Australia and Papua New
Guinea to avert epidemics in countries where local
vectors (for example, Ae polynesiensis) carry the dis-
ease.
Australian Arboencephalitis (AE)
Infectious Agent
Murray Valley Encephalitis (MVE) virus. Kunjin virus may
also cause an encephalitic illness indistinguishable from
AE.
Clinical Features
Fever, headache and sometimes nausea and vomiting,
followed by the features of encephalitis.
A diagnosis of AE should be considered in any patient
who presents with encephalitis and who has been in the
Murray Valley area within the incubation period of the
disease, especially in the period between November and
March.
The disease may also be acquired at any time in the
northern parts of Australia.
Public Health Significance and
O c c u r re n c e
AE is endemic in Northern Australia and Papua New
Guinea.
Outbreaks of the disease occur approximately once
every 20 years in South Eastern Australia when weather
patterns promote large increases in water bird and
vector mosquito populations.
This results in amplification of arboviruses in the mosqui-
toes that infect the non-immune human populations in the
Murray-Darling catchment.
Morbidity during an epidemic year is related to exposure.
Cases of AE seem to occur in people who receive large
numbers of mosquito bites during a single exposure.
Serological studies show that only one person in every
800 who has seroconversion develops the disease.
During the 1974 epidemic, of those affected, one-third
died, one-third were left with residual brain damage, and
one-third recovered completely.
Method of Diagnosis
Serology: Two blood specimens are required seven to10
days apart. Sera for diagnosis should be sent to the
Director of Virology, VIDRL, preceded by telephone
contact via the Royal Melbourne Hospital on (03) 9342
7000.
Reservoir
The primary hosts of AE during years of high virus
activity are waterbirds. Ardeiformes (herons), particularly
the Rufous Night-heron and the Pelicaniformes (cormo-
rants/darters) show the strongest evidence of infection.
Modes of Transmission
The primary mosquito vector during epidemics is Culex
annulirostris. Other mosquitoes such as Culex australicus
and some Aedes species may be involved in other
aspects of MVE virus ecology.
Incubation Period
Usually seven to 28 days.
Period of Communicability
There is no evidence of person-to-person transmission.
Susceptibility and Resistance
One in every 800 people infected is said to show signs of
the disease.
Control of Case
Patients can be managed at any hospital, but facilities for
providing artificial respiration must be available.
19
 Investigate the source of infection. Search for unreported
or undiagnosed cases of encephalitis from the
Murray-Darling drainage basin.

Control of Contacts
Not applicable.

Preventive Measures
• Apply mosquito control measures (local municipalities).
• Use personal protection measures (long sleeves, long
trousers, mosquito repellents and so on).
• Avoid mosquito-prone areas; vectors usually bite at
dusk and dawn.

Epidemic Measures
See the Victorian Arbovirus Task Force Contingency Plan
for outbreaks of AE for details.

20
Dengue
Infectious Agent
Dengue virus 1, 2, 3 and 4 (flavivirus).
Clinical Features
Dengue Fever (Break Bone Fever)
Classically, dengue fever presents as an acute febrile
illness of sudden onset.
It is characterised by fever (three to five days), myalgia,
arthralgia, retro-orbital pain, anorexia, gastrointestinal
disturbance, rash and increased vascular permeability
(see below).
Dengue Haemorrhagic Fever (Dengue
Shock Syndrome)
In contrast to classic dengue, myalgia and bone pains
are unusual in dengue haemorrhagic fever which is a
disease of abrupt onset characterised by fever, palpable
lymph nodes and liver, scattered petechiae and rapid
deterioration.
Other haemorrhagic phenomena such as melaena,
haematemesis and shock are poor prognostic signs.
Death usually occurs on the fourth or fifth day.
Public Health Significance and
O c c u r re n c e
Outbreaks of this disease have occurred throughout the
tropics and over the past 40 years.
A complication, dengue shock syndrome, is believed to
be caused by immune enhancement of infection, in
which dengue antibodies from prior infections appear to
promote the infection of other serotypes.
Outbreaks of dengue have occurred in Northern Australia
but have been limited by the distribution of Aedes aegypti.
The detection of larvae of Aedes albopictus (a potential
vector overseas) on one occasion in South Australia in
imported car tyres is cause for concern.
Method of Diagnosis
Serology: Rising titre to Dengue virus antibodies.
Reservoir
Humans and monkeys (in most cases monkeys play no
role).
Mode of Transmission
It is transmitted by the bite of an infected mosquito
usually Ae. aegypti and Ae. albopictus. (Other Aedes
species are involved in the enzootic monkey complex).
Incubation Period
Usually three to 14 days; commonly seven to 10 days.
Susceptibility and Resistance
There is universal susceptibility but children usually have
a milder primary disease than adults.
Recovery from infection with one serotype provides
homologous immunity, but does not provide protection
against another serotype.
A previous infection may exacerbate a second infection.
Dengue antibodies from earlier infections appear to
promote infection by other serotypes.
Control of Case
• Isolate patient and prevent mosquito access until fever
subsides.
• Investigate source of infection.
Preventive Measures
• Search for and eliminate breeding sites of Aedes aegypti.
• Use mosquito repellents, mosquito nets and other
methods of personal protection.
• Control Aedes aegypti near airports.
• Prevent importation of new vectors; for example, Aedes
albopictus.
21
 Kunjin Incubation Period
Infectious Agent Uncertain, probably weeks.

Kunjin virus (flavivirus).

Period of Communicability
Clinical Features There is no evidence of person-to-person transmission.

Most infections are subclinical.

Susceptibility
When symptoms occur, the syndrome varies from a mild The ratio of subclinical to clinical infections appears to
febrile illness with nausea, lethargy, lymphadenopathy be large but the precise ratio is unknown.
and a rash to encephalitis.
Cross-reaction between MVE virus and Kunjin virus has
Public Health Significance and complicated the assessment of the prevalence of Kunjin
O c c u r re n c e infection in the general population.

Kunjin virus has been found in Australia and Sarawak.

Control of Case
Unlike the Murray Valley Encephalitis virus (MVE), Kunjin No specific treatment is required.
virus has been detected in Victoria on several occasions
since the last outbreak of AE in 1974. Investigate the source of infection and search for unre-
ported or undiagnosed cases from the Murray-Darling
Further study is needed to define the morbidity rate of drainage basin.
infections with Kunjin virus.
Control of Contacts
Method of Diagnosis Not applicable.
Serology: Two specimens, seven to 10 days apart. Sera
should be sent to VIDRL. Preventive Measures
Intensify mosquito surveillance and control in areas
Reservoir where cases are identified.
Kunjin virus can infect a wide range of mammals includ-
ing cattle, sheep, horses and so on. Epidemic Measures
See the Victorian Arbovirus Task Force Contingency Plan
Birds, particularly waterbirds, are thought to be the major on AE.
vertebral hosts during epidemics of AE caused by MVE
virus. Their role in the transmission of Kunjin is unknown.

Mode of Transmission
Culex annulirostris is the major vector of the Kunjin virus.

22
 Botulism
Victorian Statutory
Re quirem ent
Group A notification.
Infectious Agent
Clostridium botulinum, a spore-forming obligate anaero-
bic bacillus. Different types are recognised, for example,
types A, B, E, F and G.
Clinical Features
There are three forms of botulism: the classical form,
infant botulism and wound botulism.
Classical botulism is a severe and often fatal intoxication
resulting from ingestion of toxin in contaminated food.
Symptoms include double vision, dysphagia and dry
mouth. This may be followed by descending flaccid
paralysis in an alert person. Fever is absent unless a
complicating infection occurs.
Infant botulism is the most common form, and usually
affects infants under one year of age, but can affect
adults who have altered gastrointestinal anatomy and
microflora. The illness typically begins with constipation,
followedby lethargy, listlessness, poor feeding, ptosis,
difficulty in swallowing, and generalised muscle weak-
ness (floppy baby).
Wound botulism is rare, but has been seen after contami-
nation of wounds in which anaerobic conditions devel-
oped.
Public Health Significance and
Oc c u r re n c e
Rare but serious intoxication can occur from improperly
cooked, canned or preserved food. Infant and wound
botulism are due to colonisation by the causative organ-
ism.
Most human outbreaks are due to types A, B and E.
Outbreaks of type E are usually related to consumption
of fish, seafood and meat from marine mammals. The
toxin is destroyed by boiling.
Method of Diagnosis
Botulism can be diagnosed by demonstration of specific
toxin in serum, faeces and incriminated food, or by
culture of C. botulinum from stool in a clinical case.
Wound botulism is diagnosed by serum toxin or positive
wound culture.
Electro-myography may be useful in corroborating the
clinical diagnosis in infant botulism.
Reservoir
Spores are ubiquitous in soil and are frequently recov-
ered from agricultural products. They are also found in
marine sediments and the intestinal tract of animals,
including fish.
Mode of Transmission
Classical botulism is acquired by ingestion of food in
which toxin has been formed without subsequent ad-
equate cooking. Suitable conditions for the formation of
toxin in foods have included inadequate heating during
canning (especially home canning of alkaline foods) and
contamination of cans post-processing.
Most cases of wound botulism are secondary to contami-
nation of the wounds by ground-in soil or gravel. Several
cases have been reported among chronic drug abusers.
Infant botulism arises from ingestion of spores rather
than preformed toxin. Sources of spores include foods
(for example, honey) and dust. Honey has been de-
scribed in the US literature as a source of infection but
never implicated in Australia, nor have surveys of Aus-
tralian honey shown C. botulinum.
23
 Incubation Period
Within 12–36 hours (sometimes several days) after eating
contaminated food.
In general, the shorter the incubation period, the more
severe the disease and the higher the case fatality rate.
Period of Communicability
There are no instances of secondary person-to-person
transmission have been documented.
Control of Case
Suspected botulism is a medical emergency. Suspected
cases should immediately be referred for specialist care.
Isolation or quarantine is not needed, but hand washing
is indicated after handling soiled nappies. Usual sanitary
disposal of faeces from infant cases is acceptable.
Any implicated food should be retained for collection and
investigation by public health authorities.
Contaminated utensils should be cleaned by boiling or
by using household bleach.
Control of Contacts
Those who have eaten incriminated food should be
purged, for example, cathartics, gastric lavage, high
enemas.
Administration of polyvalent antitoxin to asymptomatic
individuals should be considered carefully; that is,
potential protection versus risk of sensitisation and
reactions to horse serum.
24
Investigation of contacts and source of toxin and search
for other cases of botulism to rule out food-borne botu-
lism.
Specific Treatment
Intravenous and intramuscular administration as soon as
possible of trivalent botulinum antitoxin (types A,B,E).
This is available from Centers for Disease Control,
Atlanta. Limited supply is available from Commonwealth
Serum Laboratories for use in hospitalised patients.
Blood should be collected and antitoxin administered.
This should occur in an intensive care facility.
For wound botulism, in addition to antitoxin, the wound
should be debrided and/or drained, and appropriate
antibiotics (for example, penicillin) administered.
In infant botulism, meticulous supportive care is essen-
tial, and assisted respiration may be required. Antitoxin is
not used because of sensitisation and anaphylaxis.
Antibiotics have not been shown to affect the course of
the disease.
Preventive Measures
• Ensure effective control of processing and preparation
of commercially canned and preserved foods.
• Educate people undertaking home canning and other
food preservation techniques about cooking time,
pressure, temperature, adequate refrigeration, storage
and so on.
• Be aware that C. botulinum may or may not cause
container lids to bulge and the contents to have
unpleasant odours.
• Recall any implicated food product immediately.
Epidemic Measures
• Investigate home-preserved foods as prime source of
single case or suspect group outbreak (for example,
family).
• Recall any food implicated by epidemiologic or labora-
tory findings immediately.
• Submit food for laboratory examination.
• Take sera and faeces from cases (and exposed but not
ill persons) for reference laboratory examination,
before administration of antitoxin.
• Undertake international efforts, if necessary, to recover
and test implicated foods.
• This should be coordinated through the:
Australia New Zealand Food Authority
PO Box 7186
Canberra MC
ACT 2610
Tel: (06) 271 2222

25
 B r u c ello sis
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agents
B. abortus, B. melitensis, B. suis and B. canis.
Clinical Features
This is a systemic bacterial disease with acute or insidi-
ous onset.
Localised suppurative infections may occur.
Subclinical and unrecognised infections are frequent.
Fever is the most common symptom and may be associ-
ated with a variety of other complaints.
Osteoarticular complications are common.
Less common are orchitis, epididymitis, osteomyelitis
and endocarditis.
Public Health Significance and
Oc c u r re n c e
Since the success of the national eradication campaign
for B. abortus in cattle herds in 1989, only an occasional
case of brucellosis is now seen which is usually acquired
overseas. In 1992, 29 cases were reported in Australia.
The majority of these (25) were due to B. suis, contracted
in Queensland, often by people hunting or butchering
feral pigs.
In Victoria in 1991, two cases of B. abortus were re-
ported, and both were believed to be long-standing
infections. One case notified in 1992 was an imported
case due to B. melitensis.
Brucellosis occurs worldwide. The sources of infection
and responsible organism vary according to geographic
area. Regions of concern are West Africa, Iran and India
and Central America.
Brucellosis used to be an occupational hazard in Aus-
tralia for:
• Farm workers.
• Veterinarians.
• Abattoir workers.
Currently, the major risk factor for brucellosis is exposure
to B. suis infection in feral pigs.
Method of Diagnosis
Laboratory diagnosis is made by either isolating the
infectious agent from blood, bone marrow or other
tissues or discharges of the patient, or by a specific
antibody response.
The interpretation of serological results can be difficult.
Reservoir
Infection in humans can be transmitted from cattle,
swine, goats, sheep and dogs.
Incubation Period
Variable and difficult to ascertain.
Usually five to 60 days; can be several months.
Mode of Transmission
Brucellosis can be transmitted by contact with infected
tissues, blood, urine, vaginal discharges, aborted animal
foetuses and especially placentae; also by ingestion of
raw milk and dairy products from infected animals.
27
 Epidemics are generally attributed to inhalation of Epidemic Measures
aerosols.
Trace source of infection.

A small number of cases used to occur from accidental

self-inoculation of strain 19 Brucella vaccine.

Period of Communicability
There is no evidence of communicability from person to
person.

Susceptibility and Resistance

Severity and duration of clinical illness are subject to
wide variation.

Duration of acquired immunity is uncertain.

Control of Case
• Treat with rifampicin and doxycycline for at least six
weeks.
• Inform the Department of Agriculture.

Control of Infected Source

Enquire into source of infection and trace infection to
common source.

Recall incriminated products. Stop distribution of milk

and milk products unless pasteurisation is instituted.

Preventive Measures
• Educate the public against drinking untreated/unpas-
teurised milk or eating dairy products produced from
such milk. Boiling milk is effective when pasteurisation
is not available.
• Educate farmers and handlers of potentially infected
animals (for example, feral pigs) to reduce exposure
and exercise care in handling placentae, discharges
and foetuses.
• Search for and investigate livestock at risk of infection.

28
 Campylobacter Infection
Victorian Statutory
Re quirem ent
Group B notification.
Note
Also notifiable if isolation of C. jejuni, C. coli or C. lari
from water supplies or C. jejuni from food.
Infectious Agents
C. jejuni (commonest), C. coli, C. lari, C. upsaliensis and,
rarely, other Campylobacter spp.
Clinical Features
Gastrointestinal infection due to Campylobacter spp
varies in severity from asymptomatic to severe. Typical
cases of C. jejuni infection experience diarrhoea (which
may be mucopurulent and/or bloody), abdominal pain
and fever.
Symptoms usually last two to five days. Campylobacter
infection has been associated with rare sequelae includ-
ing reactive arthritis and Guillain-Barre syndrome.
Human infection with C. fetus is rare, but may cause
localised abscesses or generalised sepsis, particularly in
immunosuppressed persons.
Public Health Significance
Campylobacter infections are now the most commonly
notified cause of bacterial diarrhoea in Victoria. They
occur worldwide and are common in the developing
world.
Most cases in Australia appear sporadic, but food- and
water-borne outbreaks may occur.
All age groups are affected, most commonly children
less than five years of age and young adults. In devel-
oped countries, asymptomatic carriage is probably rare.
Method of Diagnosis
Isolation of common types requires selective media and
microaerophilic conditions at 42˚C.
Other types may require more specialised techniques.
Subspeciation methods are available in specialist
centres to assist in epidemiologic investigation.
Reservoir
Many animals, including cattle, sheep, birds and poultry
may be chronic carriers of Campylobacter spp. House-
hold pets, including puppies and kittens, are another
possible source of infection.
Mode of Transmission
It is transmitted when organisms are ingested via con-
taminated food (particularly undercooked chicken) or
water, or by contact with infected pets or infants.
The organism does not multiply in food or water, but the
infectious dose required to cause illness is very low.
Person-to-person transmission is a particular risk from
infected infants to nappy changers (where there is poor
personal hygiene).
Incubation Period
Usually three to five days, with a range of one to 10
days.
29
 Period of Communicability Control of Contacts
Cases are infectious throughout their illness. The diagnosis should be considered in symptomatic
contacts.
Excretion of organisms may continue for some weeks
after symptoms resolve.
Preventive Measures
• Ensure scrupulous hand washing and hygiene, espe-
Susceptibility and Resistance cially in food handlers.
Most persons in the developed world are susceptible. • Thoroughly cook all meat and, particularly, poultry and
avoid recontamination after cooking.
Immunity to serologically related strains may follow • Thoroughly wash utensils used to prepare raw meats
infection. and poultry before using them to prepare non-cooked
food such as salads.
• Pasteurise milk and chlorinate water.
Control of Case • Recognise pets as sources of infection and encourage
• Report case to Department of Human Services. hand washing after handling animals.
• Immediately report clusters of cases by telephone or • Minimise contact with poultry and their faeces.
fax.
• Investigate related cases or outbreaks to identify a
common source.
• Use Standard Precautions for hospitalised patients.
• Exclude infected children from child care centres until
diarrhoea has ceased.
• Exclude symptomatic persons from food handling, care
of patients in hospitals, or care of infants in child care
centres.
• Exclude asymptomatic convalescent stool-positive
individuals if strict attention to personal hygiene cannot
be assured.
• Stress hand washing/personal hygiene education.
• Do not share towels, washers or personal items such
as toys that may be contaminated.

Tre a t m e n t
Antibiotics (for example, erythromycin) are indicated for
severe illness or where prompt termination of faecal
excretion of organisms is desired.

Treatment given early in the illness may reduce the

severity and duration of symptoms.

30
 Chicken Pox/Herpes Zoster
Victorian Statutory
Re quirem ent
Statutory notification not required.
School exclusion.
Infectious Agent
Human (alpha) herpesvirus 3 (Varicella-zoster or V-Z
virus).
Clinical Features
Chicken pox presents with a low-grade fever, malaise
and a rash that is maculopapular then vesicular for three
to four days, becoming crusted. Lesions appear in crops
on the trunk, face, scalp and mucous membranes of the
mouth.
Herpes zoster or shingles is characterised by a unilateral
vesicular eruption within a dermatome, often associated
with severe pain that may precede lesions by 48–72
hours. The rash lasts up to several weeks depending on
severity.
A common complication in children with chicken pox is
bacterial superinfection of the skin. Other complications
include aseptic meningitis, encephalitis and Reye’s
syndrome. Varicella pneumonia may be a complication in
adults. Those at risk of a more severe form of infection
are children who have acute leukaemia and those in
remission following chemotherapy.
Herpes zoster in the immunosuppressed host is more
severe and prolonged than in the normal individual; for
example, those who have received a bone marrow
transplant, those with Hodgkins disease, non-Hodgkins
lymphoma or HIV infection.
A most debilitating complication of herpes zoster in all
patients is pain associated with acute neuritis and post-
herpetic neuralgia and hyperaesthesia; the latter persists
for months after resolution of the disease.
V-Z Virus in Pregnancy
Varicella infection during the first trimester of pregnancy
can cause spontaneous abortion but, overall, the risk is
not significantly increased.
In the third trimester, maternal varicella may precipitate
the onset of premature labour.
Severe maternal varicella and pneumonia at any stage of
pregnancy can cause foetal death.
Perinatal varicella is associated with a high mortality rate
when maternal disease develops within five days prior to
delivery and up to 48 hours postpartum. The neonatal
fatality rate is reported as being up to 30 per cent.
A foetal varicella zoster syndrome has been reported in a
small number of cases.
Clinical manifestations include growth retardation,
cutaneous scarring, limb hypoplasia and cortical atro-
phy.
Public Health Significance and
O c c u r re n c e
Chicken pox is a highly contagious but generally mild
disease and is endemic in the population. It becomes
epidemic among susceptible individuals mainly during
winter and early spring. More than 90 per cent of cases
are children aged one to 14 years.
Herpes zoster, a sporadic disease, is the consequence
of reactivation of a latent virus from the dorsal root
ganglia. It is most commonly seen in the elderly.
Method of Diagnosis
Clinical: Isolation of the virus in cell cultures or visualisa-
tion by electron microscopy (EM) is not routinely re-
quired.
31
 Serological:
• Complement fixation tests showing detectable IgM
antibody.
• Immunofluorescence on lesion swab/fluid.
• ELISA (kit) now more commonly used.
Reservoir
Humans.
Mode of Transmission
It can be transmitted from person to person by direct
contact, or by droplet or airborne spread of secretions
from the respiratory tract of chicken pox cases, or of the
vesicle fluid of patients with herpes zoster. Indirect
contact occurs through articles freshly soiled by dis-
charges from vesicles of infected persons. Scabs are not
infective.
Chicken pox is highly contagious, and zoster has a much
lower rate of transmission (the non-immune contact
develops chicken pox).
Incubation Period
From two to three weeks; usually 13–17 days.
May be prolonged in the immunosuppressed, or follow-
ing immune globulin.
Period of Communicability
It is usually communicable for one to two days (up to five
days) before onset of rash, and for five days after the
appearance of the first crop of vesicles, but prolonged in
patients with altered immunity.
Those with zoster may be infectious for a week after
lesions appear.
32
Susceptibility
Universal among those not previously infected but the
disease is more severe in adults. Infection remains latent
and may occur years later as shingles in some older
adults.
Neonates whose mothers are not immune and leukaemia
patients may suffer severe, prolonged or fatal chicken-
pox.
Adults with cancer, especially of lymphoid tissue,
immunodeficient patients and those on immunosuppres-
sive therapy may have increased frequency of severe
zoster.
Control of Case
Chicken Pox:
• Exclude from school until fully recovered, or at least
one week after eruption first appears.
• Avoid contact with immunosuppressed persons.
• Exclude adults from work for the same time.
Herpes Zoster: Acyclovir is effective for treatment of
varicella zoster infections in patients with a rash less than
72 hours old. It gives some pain relief, but is of no benefit
on the incidence of post-herpetic neuralgia.
Control of Contacts
Contacts are not excluded from school.
The risk of spread to immunosuppressed patients means
that if a susceptible child with known exposure is in
hospital, quarantine of these patients should be consid-
ered for days 10–21 after exposure (up to 28 days if
immune globulin given).
Preventive Measures
Immunosuppressed individuals should be protected from
exposure.

If exposure has occurred in these persons, varicella

zoster immune globulin (VZIG) (prepared from the
plasma of blood donors with high antibody titre to the V-Z
virus) is effective in modifying or preventing the disease
if given within 96 hours of exposure. VZIG is available
from Australian Red Cross.

VZIG may be given within 96 hours of exposure to

newborns of mothers who develop chickenpox within five
days prior to, or within 48 hours after, delivery.

A live attenuated varicella virus vaccine protects children

with leukaemia exposed to siblings with chickenpox (not
yet available in Australia).

Epidemic Measures
Not applicable aside from protection of
immunosuppressed.

33
 Cholera
Victorian Statutory
Re quirem ent
Group A notification.
Infectious Agent
Vibrio cholerae serogroup O1 or O139.
V. cholerae occurs in two major biovars: the classical
and the El Tor type. These two differ in biological and
biochemical characteristics and both include organisms
of the Inaba and Ogawa serotypes. Both biotypes can
also be classified into various phage types.
Note
Non-O1 vibrios, formerly known as non-agglutinable
vibrios (NAG) or non-cholera vibrios (NCV) are now
included in the species Vibrio cholerae, but the reporting
of Non-O1 infections as ‘cholera’ is inaccurate.
Most Non-O1 strains do not secrete enterotoxin but these
strains can cause sporadic cases, and outbreaks of
diarrhoeal illness due to them have occurred in Venice
(1981 and 1984) and in Lima, Peru (1984).
Large-scale epidemics of cholera caused by V.cholerae
O139 have been seen in India and Bangladesh.
Another confusing term (sometimes used but better
avoided) is non-vibrio cholera (NVC) which refers to
cases of cholera-like illness caused by organisms other
than vibrios.
Clinical Features
Asymptomatic illness is much more frequent than clinical
illness, and mild cases with diarrhoea are common,
especially among children.
In the severe case, however, there is sudden onset of
symptoms with profuse watery stools not associated with
pain, occasional vomiting, rapid dehydration, acidosis
and circulatory collapse. In untreated cases, death may
occur in a few hours and the case fatality rate may
exceed 50 per cent.
Public Health Significance and
O c c u r re n c e
Cholera can occur in epidemics or pandemics and, in
any single epidemic, one particular biovar (that is,
classical or El Tor) tends to predominate.
Endemic cholera occurs in parts of Africa, Central
Europe and Asia.
The seventh cholera (EI Tor) pandemic that began in
Asia in 1961 spread to Africa in 1970 and to South
America in 1990–91.
Over 300,000 cholera cases around the world were
reported to WHO in 1994.
In Victoria, only sporadic imported cases in returned
travellers occur.
V. cholerae O1 is established in the riverine environment
in some parts of Queensland and NSW.
Method of Diagnosis
Culture of V. cholerae serogroup O1 or O139 from
faeces.
Faecal samples to be stored at 4˚C or added to transport
media, and forwarded to MDU.
Visualisation by dark field or phase microscopy of
characteristic motility, specifically inhibited by preserva-
tive-free serotype-specific antiserum.
35
 Reservoir
Water and humans.
Marine waters where they may be associated with
copepods or other zooplankton.
Mode of Transmission
Cholera can be transmitted by:
• Contaminated water.
• Ingestion of food contaminated by dirty water, soiled
hands or flies; for example, vegetables fertilised with
sewage or night soil or washed in contaminated water.
• Fish or shellfish obtained from contaminated waters.
The organism can survive for long periods in water and
ice.
Incubation Period
From a few hours to five days; usually two to three days.
Period of Communicability
Cholera is communicable during the acute stage and for
a few days after recovery.
By the end of the first week, 70 per cent of patients are
non-infectious, and by the end of the third week 98 per
cent are non-infectious.
Occasionally the carrier state may persist for months,
and exceptionally chronic biliary infection with intermit-
tent shedding of organisms may last for years.
Susceptibility and Resistance
Even in severe epidemics, attack rates of overt disease
rarely exceed 2 per cent.
Gastric achlorhydria increases risk of disease. Breastfed
infants are protected.
36
Infection results in a rise in agglutinating, vibriocidal and
antitoxic antibodies with increased resistance to reinfec-
tion.
Control of Case
Severely ill patients should be isolated in hospital, with
Standard Precautions.
Less severe cases can be managed at home.
Concurrent disinfection is required of linen and articles
used by the patient.
Faeces and vomitus can be disposed of into the toilet
without preliminary disinfection, except in areas without
an adequate sewage disposal system.
Terminal cleaning of the room and articles used by the
patient is required.
Specific Treatment
Prompt fluid therapy with adequate volumes of electro-
lyte solution (Gastrolyte) should be undertaken.
Patients with severe dehydration require urgent intrave-
nous fluid therapy with Hartmann’s solution or WHO
solution (NaCl 4.0 g/l, KCl 1.0 g/l, Sod acetate 6.5 g/l and
glucose 8.0 g/l), or other similar fluid.
Antimicrobial agents (to which the strain is sensitive)
shorten the duration of diarrhoea and the duration of
vibrio excretion:
• Adults: Tetracycline drugs (if strain sensitive).
• Children: Co-trimoxazole (if strain sensitive).
Control of Contacts
Contacts should be observed for five days from the date
of last exposure.
This may include, for example, all air travellers on a flight
from overseas.
Stool culture of any contacts with symptoms of diarrhoea
and stool culture of all household contacts, even if
asymptomatic, should be underaken.
Cases should also be looked for among those possibly
exposed to a common source.
Immunisation of contacts is not indicated.
Epidemic Measures
• Immediately notify Communicable Diseases Network,
Australia and New Zealand (CDN-ANZ) and WHO.
• Initiate thorough investigation to determine the vehicle
and circumstances of transmission and plan control
measures accordingly.
• Educate the population at risk about the need to seek
appropriate treatment without delay.
• Adopt emergency measures to assure a safe water
supply.
• Assure careful supervision of food and drink prepara-
tion.
Note
Immunisation of contacts is not indicated, even in the
epidemic situation.

Investigate Possible Sources of

Infection
For example, in a non-traveller, look for sources of
contaminated food or water.

Preventive Measures
Cholera vaccine is a heat-killed suspension of the Inaba
and Ogawa serotypes of the classical biotype of V.
cholerae O1.

It provides partial protection (approximately 50 per cent)

for three to six months.

It is not routinely recommended and advice to overseas

travellers should emphasise careful selection of food and
water rather than immunisation. Officially, cholera vacci-
nation certificates are no longer required by any country
or territory. Unofficially, some countries may still require
such a certificate, in which case a single dose of cholera
vaccine would satisfy this requirement.

37
 Cryptococcal Infection

Victorian Statutory CSF and serum should be tested for cryptococcal

Re quirem ent antigen.

Notification not required.

Pulmonary cryptococcosis in non-HIV infected persons
usually manifests as a nodule, which must be distin-
Infectious Agent guished from a malignancy (which may coexist).

Cryptococcus neoformans, an encapsulated yeast-like

fungus. Reservoir
C. neoformans var. neoformans occurs worldwide,
C. neoformans var. neoformans (serotypes A & D).
frequently in association with pigeon or other bird
droppings.
C. neoformans var. gattii (serotypes B & C).

C. neoformans var. gattii occurs in endemic foci in the

Clinical Features tropical and sub-tropical world where certain eucalypts

Cryptococcal infection usually presents as a sub-acute provide an ecological niche.

or chronic meningo-encephalitis with headache and

altered mental state. Mode of Transmission
It is transmitted by inhalation.
Lung involvement may cause symptoms of lower respira-
tory tract infection or may be asymptomatic.
Communicability
The skin, bone and other organs are less frequently Cryptococcal infection is not spread from person-to-
infected. person or animal-to-person.

Public Health Significance and Susceptibility

Oc c u r re n c e Persons with impaired immunity due to corticosteroid
Sporadic cryptococcal infections occur worldwide. therapy, lymphoma and sarcoidosis are at increased risk
of crytococcal infection.

Method of Diagnosis
Persons with AIDS are particularly prone and now
HIV-infected persons may have cryptococcal meningitis, constitute a majority of cryptococcal infection cases.
even in the absence of inflammatory cells in the cerebro-
spinal fluid (CSF).

CSF should be stained with an India ink stain.

CSF, blood, sputum and urine should be cultured for

cryptococci.

39
 Control of Case
The diagnosis should be established.

The possibility of underlying HIV infection should be

considered.

Referral to a specialist centre should occur.

Therapy for cryptococcal meningitis usually involves at

least six weeks of antifungal medications: Amphotericin
B in combination with 5-flucytosine.

Persons with AIDS then require lifelong suppressive

therapy, usually with an imidazole antifungal agent.

Discrete lung lesions may need diagnosis by biopsy and

the need for antifungal therapy depends upon the
underlying health of the host.

Immunosuppressed persons are usually treated to

prevent dissemination.

Control of Contacts
Contacts of cases need no specific follow-up.

Preventive Measures
Remove large accumulations of bird droppings.

Epidemic Measures
Clusters have not been reported.

40
 Cryptosporidiosis
Victorian Statutory
Re quirem ent
Statutory notification is not required.
Note
Notification if Cryptosporidium spp are isolated from
water supplies, or are associated with a food or water-
borne illness outbreak.
Infectious Agents
Cryptosporidium spp. (coccidian protozoa).
Clinical Features
Cryptosporidiosis is a parasitic protozoan infection that
affects the gastrointestinal tract.
The major symptoms are watery diarrhoea associated
with cramping abdominal pain.
The disease may sometimes be mild, but in persons with
impaired immunity, particularly those with AIDS, it may
be a life-threatening illness.
Public Health Significance and
Oc c u r re n c e
Cryptosporidiosis occurs worldwide. Young children, the
families of infected persons, homosexual men, travellers,
health care workers and people in close contact with
animals comprise most reported cases.
Small outbreaks may occur related to child care centres.
Substantial water-borne outbreaks have been reported in
the United States in 1993.
Method of Diagnosis
The laboratory should be informed of clinical suspicion of
cryptosporidiosis.
Oocysts may be identified by microscopy of faecal
smears treated with a modified acid fast stain. A
monoclonal antibody test is useful for detecting oocysts
in faecal and environmental samples. Oocyst excretion is
most intense during the first days of illness. Oocysts are
rarely recovered from solid faeces.
ELISA assays have been developed for the detection of
antibodies, but these are not in routine use.
Reservoir
Humans, domestic and wild animals.
Modes of Transmission
Cryptosporidium spp. are spread by the faecal-oral route
directly from person-to-person and animal-to-person,
and via contaminated food and water.
Incubation Period
From one to 12 days, with an average of about seven
days.
Period of Communicability
Cases may be infectious for as long as oocysts are
excreted in the stool: from the onset of symptoms until
several weeks after symptoms resolve.
Under suitable conditions, oocysts may survive in soil
and be infective for up to six months.
Susceptibility and Resistance
People with normal immune systems usually have
asymptomatic or self-limited symptomatic disease.
People with impaired immunity may experience pro-
longed illness, depending on the course of their altered
immune function.
41
 Control of Case
• Exclude symptomatic persons from food handling and
direct care of hospitalised and institutionalised patients
until asymptomatic.
• Stress the importance of hand washing.
• Disinfect soiled articles.
• Exclude symptomatic persons from direct care of
children in child care centres.
• Exclude children with diarrhoea from child care centres
until their diarrhoea has ceased.

Tre a t m e n t
Symptomatic. Supportive care with fluid and electrolyte
replacement and anti-diarrhoeal agents may be needed
by severely affected cases, particularly those with
underlying immune deficiency.

Control of Contacts
The diagnosis should be considered in symptomatic
contacts.

Preventive Measures
• Educate the public in personal hygiene.
• Dispose of faeces in a sanitary manner.
• Insist on careful hand washing by persons in contact
with animals.
• Filter or boil contaminated drinking water (chemical
disinfectants such as chlorine are not effective against
oocysts at the concentrations used in water treatment).

Epidemic Measures
Investigate clustered cases. Look for sources of infection
such as water or raw milk supplies.

42
 Cytomegalovirus (CMV) Infection

Victorian Statutory Public Health Significance and

Re quirem ent
Notification is not required.
Infectious Agent
Cytomegalovirus, a human herpesvirus.
Clinical Features
Primary CMV infection of children and adults may cause
a mononucleosis syndrome very similar to that caused by
the Epstein-Barr virus (‘glandular fever’).
Features include fever, lymphadenopathy, mild hepatitis
and, more rarely, anaemia, thrombocytopenia, pneumo-
nitis, meningoencephalitis and Guillain-Barre syndrome.
Many cases, particularly young children, have few
symptoms.
O c c u r re n c e
Serosurveys of adult populations have shown wide-
spread evidence of previous CMV infection, particularly
in developing countries where crowding and poor
hygiene facilitate the spread of infection. In Australia,
approximately 50 per cent of young adults have been
infected.
CMV is not readily spread by casual contact but requires
prolonged, intimate exposure for transmission. This can
occur in settings such as child care centres where
toddlers shed the virus in saliva and urine and thereby
spread the infection among themselves.
Method of Diagnosis
CMV may be detected in urine, saliva and other body
fluids (including breast milk, semen and cervical secre-
tions) during primary and reactivated infection.

Congenital infection occurs when a non-immune preg-

Isolation of CMV from urine and saliva does not neces-
nant woman experiences primary or reactivated CMV
sarily imply acute infection, as CMV may be excreted for
infection.
months to years following infection. The clinician should
consider diagnostic tests for CMV in conjunction with the
Congenital infection may cause severe generalised
clinical presentation.
sepsis of the foetus, with death in utero or in the neonatal
period.
CMV causes typical ‘cytomegalic’ cells in tissue culture
and characteristic histologic features in affected tissues.
Sequelae in survivors include deafness, mental retarda-
tion, psychomotor disability and neurological problems.
Rapid diagnostic tests using monoclonal antibodies to
early CMV antigens are available in specialist centres.
Immunosuppressed persons (for example, with ad-
vanced HIV/AIDS or organ transplants), are at risk of
False-positive and false-negative serological tests may
serious illness due to CMV infection. In such persons,
occur, but a fourfold or greater rise in serum antibody
disease is usually due to reactivation of previous infec-
titres to CMV suggests acute infection.
tion.

Manifestations include sight-threatening retinitis, pneu- Reservoir

monitis, gastrointestinal ulceration and inflammation, and Humans.
neurological disease, particularly affecting the brain and
spinal cord.

43
 Modes of Transmission
CMV may be transmitted by:
• Transplacental infection of the foetus of a mother with
primary or reactivated infection.
• Perinatal infection of neonates via infective maternal
cervical secretions or breast milk or infective secre-
tions of attendants or siblings.
• Blood transfusion or organ transplantation.
• Close personal contact with infective secretions of
infected persons:
– Children: peers and siblings.
– Adults: peers, sexual partners and young children.
Incubation Period
The incubation period of cases of sporadic cases of CMV
usually cannot be determined.
Perinatal infection develops three to 12 weeks after
delivery. In adults, illness usually occurs three to eight
weeks after blood transfusion, and between four weeks
and four months after organ transplantation.
Period of Communicability
CMV is excreted in urine and saliva for months to years
after primary infection.
Neonatal infection in particular is associated with pro-
longed excretion.
The period of excretion seems to be shorter in adults.
Susceptibility and Resistance
Immunosuppressed persons are at increased risk of
severe disease due to CMV infection.
44
Control of Case
• Use standard precautions for hospitalised and acute
cases.
• Do not need exclude cases from school or child care.
• Seek specialist advice if CMV infection is suspected
during pregnancy.
Tre a t m e n t
There is no specific treatment for primary CMV infection
of normal hosts.
Immunosuppressed persons with severe CMV infection
are treated in specialist centres with ganciclovir and/or
foscarnet.
Preventive Measures
• Wash hands after handling nappies or exposure to the
secretions of young children.
• Educate persons working in hospitals, child care
centres and centres for the disabled to adhere to
infection control precautions and to regard all body
fluids as potentially infectious.
• Advise women of childbearing age of the risk which
CMV infection may pose.
• Avoid transfusing neonates with CMV seropositive
blood or transplanting organs from CMV seropositive
donors to seronegative recipients.
 Diphtheria
Victorian Statutory
Re quirem ent
Group A notification.
School exclusion.
Infectious Agent
Corynebacterium diphtheriae.
Clinical Features
Acute bacterial disease of tonsils, pharynx, larynx, nose
and occasionally other mucous membranes, skin,
conjunctivae and genitalia. The throat is sore in faucial or
pharyngotonsillar diphtheria with cervical lymph nodes
enlarged and tender. In severe cases, there is marked
swelling and oedema of the neck.
Cutaneous diphtheria also occurs, generally without
systemic symptoms.
Laryngeal disease is serious in infants and young
children.
Case fatality rate is 5–10 per cent for non-cutaneous
diphtheria.
Public Health Significance
Cases are now rare since widespread immunisation.
They occur mainly in winter, generally in unimmunised
children under 15 years, but also in unimmunised adults.
Case fatality rate is high, especially if there is delay in
diagnosis and treatment with antitoxin.
Outbreaks have occurred in Europe among non-immu-
nised populations.
Method of Diagnosis
Culture of C. diphtheriae from the infected site.
Presumptive Diagnosis
Whitish membrane on tonsils, especially if extending to
uvula and soft palate with cervical lymphadenopathy or a
serosanguinous nasal discharge. If strong suspicion of
diphtheria, give antitoxin immediately and commence
antibiotic treatment after bacteriological specimens are
taken without waiting for results.
Bacteriological Investigations
• Verify diagnosis.
• Determine toxigenicity of C. diphtheriae. Non-toxigenic
strains can sometimes be associated with disease: skin
lesions, pharyngitis, bacteraemia, arthritis and endo-
carditis.
Collection of Specimens
For cases:
• Nasopharyngeal cultures should be obtained with a
flexible alginate swab that reaches deep into the
posterior nares.
• Throat cultures should be taken with a cotton swab that
is firmly applied to any area with a membrane or
inflammation.
• Any chronic crusting lesion should also be swabbed.
Before cultures of wounds are taken, lesions should be
cleansed with sterile normal saline and crusted mate-
rial removed. A cotton-tipped applicator is then firmly
applied to the base of the wound.
For contacts:
• Ideally the nasopharynx, the tonsillar fossae, posterior
pharynx and retrouvular areas should be sampled as
well as any crusting lesion.
• Where large-scale screening is to be carried out, nose
and throat swabs should suffice.
45
 For transport: Control of Case
• If no extended delays in culture setup are anticipated,
• Isolate until two cultures taken more than 24–48 hours
ordinary semi-solid transport medium, such as Amies
apart are clear (the first to be taken more than 24
or Stuarts, is adequate.
• When longer transit times (greater than 24 hours) are hours after the cessation of antibiotics).

unavoidable, swabs should be shipped in silica gel. • Isolate for l4 days, if no culture available. Disinfect
contact articles.

Reservoir
Specific Treatment
Humans only.
If strong suspicion of diphtheria:
• Make bacteriological diagnosis, take cultures.
Mode of Transmission • Give Antitoxin without delay:
Transmission occurs by droplet spread through contact – First test for hypersensitivity.
with a patient or carrier, or articles soiled with discharges – Dose (Equine) Antitoxin (20,000–100,000 units) IM.
from infected lesions. Dose depends on assessed clinical severity.
– May need IV antitoxin in addition if very severe
infection (diluted and given as IV infusion).
Incubation Period
Usually two to five days. Administration of antitoxin is the most important facet of
treatment and must not be delayed until bacteriological
confirmation.
Period of Communicability
It is variable, until virulent bacilli disappear from dis-
Antibiotics are commonly used. These are used to
charges (usually more than two weeks; seldom more
eradicate C. diphtheriae from disease sites:
than four weeks).
• Oral erythromycin (preferred to penicillins).
• IM procaine penicillin.
Rarely chronic carriage.
• Benzathine penicillin (single dose).

Susceptibility and Resistance Control of Contacts

Infants born of immune mothers are relatively immune.
Swabs should be taken for culture from throat and nose.
Contacts should be kept under surveillance for seven
Passive immunity is usually lost by six months.
days (regardless of immunisation status).

Clinical attack does not always lead to lasting immunity.

lf cultures are positive, carriers should be treated with
erythromycin. Those who handle food or work with
Immunity may be acquired through inapparent infection.
school children should be excluded from work or school
until cultures are negative.
Prolonged active immunity is induced by immunisation
with diphtheria toxoid.

Antitoxic immunity protects against systemic disease but

not against local infection in the nasopharynx.

46
Household contacts should be excluded from schools
and children’s services centres until investigated by the
Medical Officer of Health or a health officer of Human
Services and shown to be clear of infection.

Previously immunised contacts should be given a

booster dose of a diphtheria vaccine according to age as
diphtheria toxoid, CDT (under eight years of age), or
diphtheria toxoid diluted for adult use, ADT (more than
eight years of age).

For previously unimmunised or incompletely immunised

contacts:
• Start primary immunisation.
• Give oral erythromycin for seven days.
• Keep under daily medical surveillance.

Preventive Measures
Diphtheria toxoid is recommended for all persons at two,
four, six, 18 months and five years (given as DTP (Triple
Antigen)) and at 15 years and every 10 years thereafter
(given as ADT).

Health workers and those at high risk of patient exposure

should be fully immunised and receive 10-year boosters.

Epidemic Measures
• Define population groups at special risk.
• Immunise the largest possible proportion of the popula-
tion group involved, especially infants and
preschoolers.
• Repeat immunisation efforts one month later to provide
at least two doses to recipients.

47
 Erythema Infectiosum
(also known as ‘Slapped Cheek Disease’
and ‘Fifth Disease’)

Victorian Statutory Public Health Significance and

Re quirem ent
Notification is not required.
School exclusion is not required.
Infectious Agent
Human parvovirus B19.
Clinical Features
Human parvovirus B19 infection causes a mild illness,
with little or no fever but a striking redness of the cheeks
(hence ‘slapped cheek disease’). This is followed one to
four days later by a lacy pink rash on the trunk and limbs
that fades but may recur over several weeks on exposure
to heat. The illness may also cause headache, itch and
upper respiratory tract symptoms.
O c c u r re n c e
Human parvovirus infection occurs worldwide and is a
common childhood disease. Outbreaks occur during
winter and spring. Up to 50 per cent of susceptible
household contacts and 10–60 per cent of child care or
school contacts may be infected during outbreaks.
Method of Diagnosis
The diagnosis can usually be made on clinical grounds.
Serological tests for IgG and IgM antibodies can be
performed on serum and amniotic fluid.
PCR can be used for confirmation of the above.
Electron microscopy can also be performed on foetal
tissue.

In adults, the rash is often atypical or absent but pain, Other diagnostic techniques may be available in some
inflammation and swelling of joints may occur and, rarely, specialised centres.
persist for months.

Asymptomatic infection is common. Reservoir

Humans.
Several groups of people are at particular risk from the
effects of parvovirus infection on developing red blood
cells. Persons with chronic haemolytic diseases (for
example, sickle cell disease) may develop transient
aplastic crises after parvovirus infection, and
immunosuppressed persons may develop severe
chronic anaemia.

Adverse effects from parvovirus infection during preg-

nancy are uncommon, but infection of the foetus may
cause foetal anaemia, hydrops foetalis and foetal death
(in fewer than 10 per cent of cases of maternal infection).
Parvovirus infection has been associated with spontane-
ous abortion, but does not appear to cause congenital
abnormalities.

49
 Mode of Transmission Pregnant Women
The infection is transmitted by contact with infected A pregnant woman who believes she has been in
respiratory secretions. It may be spread vertically from contact with a case of parvovirus infection should
mother to foetus and, rarely, by transfusion of blood or consult the doctor supervising her pregnancy.
blood products.
Antibody testing is available at VIDRL and this may
assist doctors advising women who are pregnant or
Incubation Period
contemplating pregnancy of the risk, if any, which
Usually one to two weeks. parvovirus infection poses.

Period of Communicability There is no risk to women who have antibodies due to

previous infection.
Children with erythema infectiosum are most infectious
before the onset of the rash, and are probably not
infectious after the rash appears. Preventive and Outbreak
Me a s u re s
Persons with aplastic crises are infectious for a week
Non-immune persons who are immunosuppressed (due
after the onset of symptoms.
to illness and/or treatment), have chronic haemolytic
disorders, or who are pregnant are at risk of potentially
Immunosuppressed persons with chronic infection and
serious outcomes from parvovirus infection.
anaemia may excrete virus for years.

All ‘at risk’ persons in close contact with children in

Susceptibility and Resistance
Generally 5–10 per cent of preschool children and more
than 50 per cent of adults have serological evidence of
infection. Infection confers immunity.
settings where parvovirus infection may occur (schools,
child care centres, health care facilities and so on)
should be advised of the risk that parvovirus infection
may pose, and warned of school and child care centre
outbreaks.

Control of Case
Persons with parvovirus infection need not be excluded
from child care or schools.

There is no specific treatment for erythema infectiosum.

Specialist advice should be sought if a person with

immunodeficiency or a blood disorder suffers parvovirus
infection. The risk of transmission to staff should be
considered when immunosuppressed persons are
hospitalised with anaemia associated with parvovirus
infection.

50
 Information Sheet
Erythema Infectiosum
(also known as ‘Slapped Cheek Disease’ and ‘Fifth Disease’)

Erythema infectiosum, also known as ‘slapped cheek Control Measures

disease’ or ‘fifth disease’ is a common childhood viral
infection caused by human parvovirus B19.
Clinical Features
Human parvovirus B19 infection generally causes a mild
illness with little or no fever but a striking redness of the
cheeks (hence ‘slapped cheek disease’). This is followed
• Non-immune persons who are immunosuppressed
(due to illness and/or treatment), have chronic haemo-
lytic disorders, or are pregnant are at risk of potentially
serious outcomes from parvovirus infection.
• Such ‘at risk’ persons should, if possible, avoid contact
with infectious cases of parvovirus infection.
• A pregnant woman who believes she has been in

one to four days later by a lace-like rash on the trunk and contact with a case of parvovirus infection should
limbs that fades but may recur over several weeks on consult the doctor supervising her pregnancy.
exposure to heat. There is no specific treatment for the • School/child care exclusion is not required.
infection. Adults often have little rash, but may experi-
ence joint pains and swelling that are sometimes pro- If you require further information, telephone the
longed. Many cases experience no symptoms at all. Infectious Diseases Unit, Human Services, Victoria on
(03) 9616 7777.
The diagnosis can usually be made on clinical grounds,
but blood tests to confirm current or past infection are For specific advice relating to infection and pregnancy,
available. consult the Genetic Clinic, Royal Women’s Hospital or
the Foetal Diagnostic Unit, Monash Medical Centre.
Several groups of people are at particular risk from the
effects of parvovirus infection on developing red blood
cells. People with impaired immunity and/or chronic
blood disorders may develop severe anaemia after
parvovirus infection.

Infection during pregnancy can rarely cause a fatal form

of anaemia in the unborn child. Parvovirus infection does
not cause congenital abnormalities.

Spread of Infection
Parvovirus infection is spread by contact with infected
respiratory secretions and can spread rapidly in child
care centres and schools.

Spread from mother to foetus occurs by blood.

The incubation period of the infection is one to two

weeks and cases are most infectious before the onset of
the rash but are probably not infectious after the rash
appears. Persons with impaired immunity may be
infectious for much longer.

51
 Food- or Water-Borne Illness

Victorian Statutory Viruses:

• Hepatitis A virus.
Re quirem ent
• Norwalk and Norwalk-like viruses (small round struc-
Group A notification.
tured viruses—SRSV).
• Rotavirus.
Food handling exclusion.

Parasites:
School exclusion.
• Cryptosporidium spp.
• Entamoeba histolytica.
Infectious Agent • Giardia lamblia.

The more common infectious agents of food- or water-

Note
borne illnesses are bacteria, viruses and certain para-
Refer to specific sections for more details.
sites. The illness may also be caused by:
• Heavy metals that can produce acute gastrointestinal
symptoms. Some of these are antimony, cadmium, Clinical Symptoms
copper, lead, tin and zinc.
Symptoms vary with the infectious agent and range from
• Fish toxicants that may be present in shellfish or fish
slight abdominal pain and nausea to retching, vomiting,
from Queensland resulting in conditions such as
abdominal cramps and diarrhoea—all of varying severity.
paralytic shellfish poisoning or ciguatera.
• Plant toxicants naturally occurring in some foods such
Vomiting, with or without diarrhoea, abdominal cramps
as toxic fungi and potatoes.
and fever are common symptoms of viral disease or
• Toxic cyanobacteria (blue green algae) in water.
staphylococcal intoxication.

Some of the infectious agents are bacteria and their

Symptoms may be severe enough to result in hospitalisa-
enterotoxins, viruses and parasites.
tion.

Bacteria and their enterotoxins:

The gastrointestinal symptoms may be accompanied by
• Toxin in food:
fever, chills, malaise and muscular pains.
– Staphylococcus aureus.
– Clostridium botulinum.
The duration of illness varies: short-lived (lasting 24–48
– Bacillus cereus.
hours in viral and staphylococcal infections), to days,
• Toxin in gut:
even weeks, in salmonellosis and campylobacteriosis.
– Clostridium perfringens.
– Campylobacter spp, E. coli.
Certain food-borne illnesses can present with meningitis
– Listeria monocytogenes.
or septicaemia (listeriosis) or with neurological symptoms
– Salmonella serovars.
(paralytic shellfish poisoning, botulism).
– Shigella spp.
– S. Typhi/Paratyphi.
– Vibro cholerae/V. parahaemolyticus.
– Yersinia enterocolitica.

53
 Public Health Significance and
Oc c u r re n c e
Occurrence is worldwide with sporadic cases and
common source outbreaks reported. Incidence varies
from country to country.
In Victoria, outbreaks where food and water have been
implicated have occurred in association with hospitals,
school camps, nursing homes and restaurants.
In recent years, there has been an increasing number of
documented outbreaks of viral origin, especially SRSV.
Method of Diagnosis
Bacteria:
• Isolation from faeces or implicated food.
• Detection of toxin.
Parasites: Microscopy of fresh or appropriately pre-
served faeces.
Viruses:
• Electron microscopy (EM) of stools.
• Immune EM.
• Paired sera from patients to detect seroconversion.
• Seek advice from VIDRL or from MDU regarding other
specific tests.
Reservoir
Soil, dust, cereals.
Fish, birds, reptiles, wild and domestic animals for most
bacteria and parasites.
Humans for viruses.
Mode of Transmission
The mode of transmission is mainly faecal-oral, but
sometimes person to person or airborne.
54
Water is rendered unsafe by human or animal faecal
contamination.
Food may be contaminated by contact with raw materi-
als, including animal products, environmental pathogens
or carrier humans or animals.
Incubation Period
Typically short for toxin-producing bacteria and longer
for the others (see chart).
Period of Communicability
Viruses: Generally during the acute phase and up to two
days after recovery.
Bacteria: Generally during the acute diarrhoeal stage.
Parasites: Refer to relevant sections.
Susceptibility
With most infections, susceptibility is general.
Rotavirus and E. coli occurs typically in infants and
young children.
SRSV is found in older children and adults.
Investigation Procedures
• Verify diagnosis.
• Obtain case histories to determine if outbreak has
occurred.
• Estimate incubation period, duration of illness (if
possible) to indicate likely infectious agent (see chart).
• Obtain food history for the 72 hours before onset of
illness (from other exposed, but asymptomatic, per-
sons as well).
• Inform MDU and Virology Laboratory of impending
samples.
• Obtain clinical specimens of:
– Faeces. Forward to MDU.
– Blood (if collected). Forward to VIDRL.
– Suspected food/water. Forward to MDU.
• Investigate place where foods are produced or pre-
pared.
• Trace source of contamination.
Control of Case
As appropriate, ranging from supportive treatment and
rehydration, to hospitalisation.
Exclusion from food handling and schools and children’s
services centres.
Exclusion from nursing duties if employed in an area with
high-risk patients such as special care nurseries or
nursing homes.
Note
Cases are excluded until diarrhoea has ceased.
Control of Contacts/
En v i ro n m e n t
Contacts who are food handlers may require surveil-
lance.
Implicated food (if in retail outlets) to be withdrawn from
sale.
Investigation of place of manufacture/preparation of
incriminated food and institute corrective action.
Preventive Measures
Prevention of the contamination of potable water. Con-
taminated water should be treated by adequate filtration
and disinfection, or by boiling.
Avoidance of contamination of food. This can be
achieved by:
• Providing raw materials of better microbiological
quality.
• Educating food handlers about proper food processing,
preparation, storage and in personal hygiene.
• Adopting the following ‘Ten Golden Rules for Safe Food
Preparation’ developed by WHO:
– Choose food processed for safety.
– Cook food thoroughly.
– Eat cooked food immediately.
– Store cooked food carefully.
– Reheat cooked food thoroughly.
– Avoid contact between raw foods and cooked
foods.
– Wash hands repeatedly.
– Keep all kitchen surfaces meticulously clean.
– Protect food from insects, rodents, and other
animals.
– Use pure water.
Incorporation of HACCP (Hazard Analysis Critical Control
Point) system into good manufacturing practices for food
industries.
Epidemic Measures
• Withdraw implicated food from sale.
• Close implicated source of water or issue boiling order
on water supplies.
• Issue closing order on food establishments if neces-
sary.
• Issue public warning if necessary.
55
 Common Food- or Water-Borne Pathogens
Incubation Duration of Predominant Foods
Causative Agent Period Illness Symptoms Commonly Implicated

Bacteria

Campylobacter jejuni 3–5 days 2–5 days occ. Sudden onset of Raw or undercooked
>10 days diarrhoea, abdominal poultry, raw milk,
pain, nausea, vomit- meat, untreated
ing. water.

E. coli enteropatho- 12–72 hrs 3–14 days Severe colic, watery Many raw foods,
genic, enterotoxigenic, (enterotoxigenic) to profuse diarrhoea, unpasteurised milk,
enteroinvasive, longer in others sometimes bloody. contaminated water,
enterohaemorrhagic See also Haemolytic minced beef.
Uraemic Syndrome.

Salmonella serovars 6–72 hrs 3–5 days Abdominal pain, Meat, chicken, eggs
diarrhoea, chills, and egg products.
fever, malaise.

S. Typhi/Paratyphi Typhoid 1–3 weeks Days–weeks (chronic Sustained fever, Raw shellfish, salads,
Paratyphoid 1–10 carriers occur) headache, constipa- contaminated water,
days tion rather than foods from unsafe
diarrhoea—systemic sources.
illness.

Shigella spp. 12–96 hrs 4–7 days Malaise, fever, Any contaminated
vomiting, diarrhoea food or water.
(blood and mucus).

Yersinia enterocolitica 3–7 days 1–21 days Acute diarrhoea Raw meat and
sometimes bloody, poultry, milk and milk
fever, vomiting. products.

V. cholerae Few hours to 5 days 3–4 days Asymptomatic to Raw seafood, con-
profuse dehydrating taminated water.
diarrhoea.

V. parahaemolyticus 12–24 hrs 1–7 days Abdominal pain Raw and cooked fish,
diarrhoea/vomiting of shellfish, other
moderate severity. seafoods.

L. monocytogenes 1–90 days Days Gastrointestinal Unpasteurised milk,

symptoms rare; flu- soft cheese, pate,
like symptoms to coleslaw.
meningitis/septicae-
mia; infection in
pregnancy can
result in abortions,
neonatal infection.

56
Common Food- or Water-Borne Pathogens (continued)
Incubation Duration of Predominant Foods
Causative Agent Period Illness Symptoms Commonly Implicated

Viruses

Norwalk and other 24–48 hrs 12–48 hrs Severe vomiting, Oysters, clams, other
SRSV diarrhoea. food contaminated by
human excreta.

Rotaviruses 24–72 hrs 3–7 days Malaise, headache, Contaminated water.

fever, vomiting,
diarrhoea.

Hepatitis A 15–50 days Usually 1–2 Fever, nausea, Contaminated water,

weeks abdominal discomfort, shellfish, salads.
possibly jaundice.

Parasites

Cryptosporidium 1–12 days 4–21 days Profuse watery Contaminated water

diarrhoea. and food.

G. lamblia 1–3 weeks 1–2 weeks to months Loose pale greasy Contaminated water,
stools, abdominal food contaminated by
pain. infected food han-
dlers.
E. histolytica 2–4 weeks Weeks-months Colic, mucous or Contaminated water
bloody diarrhoea. and food.

Toxin Producing Bacteria

B. cereus 1–6 hours < 24 hours Nausea, vomiting, Cereals, rice, meat
(toxin in food) diarrhoea, cramps. products, soups,
vegetables.

C. botulinum 12–36 hours Variable (Neurotoxin) hence Canned food, often

blurred or double home canned food
vision, difficulty (low acid).
swallowing, respira-
tory paralysis.

C. perfringens 8–20 hours 24 hours Sudden onset colic, Meats poultry, stews,
(toxin in gut) diarrhoea. gravies, (often
reheated).

Staphylococcus 30 mins–8 hours 24 hours Acute vomiting, Cold foods (much

aureus (toxin in food) purging, may lead to handled during
collapse. preparation) milk
products, salted
meats.

57
 Giardiasis

Victorian Statutory Reservoir

Re quirem ent Humans.
Group B notification.
The possible contribution of domestic (dogs, cats) and
School exclusion. wild animals is unknown.

Infectious Agent Modes of Transmission

Giardia lamblia. Person-to-person by hand to mouth transfer of cysts from
infected faeces or faecally contaminated surfaces.

Clinical Features Water-borne outbreaks due to faecal contamination of

A protozoan infection that is usually asymptomatic but public water supplies.
may present as an acute or chronic diarrhoea, malnutri-
tion, fatigue and abdominal cramps. Direct transmission of infection from animals to people,
and vice versa.
Fat malabsorption may lead to steatorrhoea.

Incubation Period
Public Health Significance and Usually one to three weeks or longer; on average seven
Oc c u r re n c e to 10 days.
Giardiasis is a common infection that affects children
more frequently than adults.
Period of Communicability
It is communicable for the entire period of cyst excretion.
It spreads very easily in institutions such as day care
centres among children who are not toilet trained.
Susceptibility and Resistance
The rate of asymptomatic carriage may be high.
Susceptibility is general.
Asymptomatic carrier rate is high.
Occurrence is worldwide.

Infection is frequently self-limited.

Method of Diagnosis
The identification of cysts or trophozoites in:
• Faeces.
• Duodenal secretion.
• Mucosa obtained by small intestinal biopsy (rarely
indicated).
• Repeated examination of stool may be necessary.
However, in the presence of strong clinical suspicion,
examination of duodenal aspirate would be indicated.

59
 Control of Case
• Dispose of faeces in a sanitary manner.
• Disinfect Soiled clothing and other articles concur-
rently.

Tre a t m e n t
Metronidazole for seven days or tinidazole.

Relapses may occur.

Control of Contacts
Microscopic examination of faeces of household mem-
bers and other suspected contacts only if they are
symptomatic.

There is rarely an indication for case finding or treatment

of asymptomatic carriers.

Preventive Measures
• Educate families, and adult personnel of day care
centres in personal hygiene such as the need for hand
washing before meals, after toilet use and changing
nappies.
• Protect public water supplies against faecal contami-
nation.
• Exclude a child from attending school or a day care
centre until diarrhoea has ceased.

Epidemic Measures
Epidemic investigation of outbreaks of disease, espe-
cially in day care centres and institutions, must be based
upon documented microbiological diagnosis and consid-
eration of the phenomenon of asymptomatic carriage.

60
 Haemophilus influenzae Infections

Victorian Statutory Since the introduction of Hib vaccines, there has been a
dramatic fall in the number of invasive cases in children
Re quirem ent
under five years.
Group A notification for meningitis or epiglottitis.

Epiglottitis also occurs in adults and this diagnosis

Infectious Agent should be considered when an adult presents with fever
and signs of upper respiratory obstruction.
H. influenzae is a Gram-negative cocco-bacillus. Inva-
sive infections are commonly caused by serotype b.
Immune-suppressed individuals of any age are also at
risk of Hib infection.
Clinical Features
Meningitis: The onset can be subacute or sudden with
Method of Diagnosis
fever, vomiting, lethargy and meningeal irritation with a
Presumptive diagnosis based on Gram strain of CSF:
bulging fontanelle in infants and stiff neck and back in
• CSF culture (meningitis).
older children.
• Blood culture (meningitis or epiglottitis).
• Throat or epiglottis swabs (epiglottitis). Epiglottal
Epiglottitis: The patient, usually a child, presents with
swabbing should not be attempted unless facilities for
signs of upper respiratory obstruction and a characteris-
ensuring a clear airway are immediately available.
tic expiratory snore, difficulty in swallowing with drooling
• Detection of Hib antigen in CSF and/or urine (meningi-
of saliva, irritability, restlessness and fever. Complete
tis or epiglottitis).
respiratory obstruction may occur.

Note Reservoir
H. influenzae type b (Hib) may cause other conditions,
Humans. It is estimated that approximately 5 per cent of
such as pneumonia, septic arthritis, cellulitis, osteomyeli-
children under six years are colonised with Hib. It is
tis and so on. These are not notifiable, but the Depart-
generally carried in the nasopharynx without causing
ment of Human Services would appreciate information
symptoms for a period of months before it disappears.
on cases to increase its knowledge of the epidemiology
of these infections.
Carriage rates decline with age, though they are higher
in household and other contacts of children with estab-
Public Health Significance lished Hib infections.

Prior to the introduction of vaccine, Hib infections were

the most common serious invasive bacterial infections in Mode of Transmission
children.
It is transmitted by droplet infection and discharges from
nose and throat during the infectious period.
The mean age in patients with epiglottitis tended to be
older than that of patients with meningitis.
The portal of entry is most commonly nasopharyngeal.

Aboriginal children are at a five to six times greater risk

of developing Hib disease, and they acquire it at a much Incubation Period
younger age than do other children. Unknown. Probably short: two to four days.

61
 Period of Communicability
It is communicable for as long as the organisms are
present in the nasopharynx.
It is non-communicable within 24–48 hours after starting
effective antibiotic therapy.
Susceptibility and Resistance
Prior to the introduction of vaccine, the risk of secondary
cases in household contacts within 30 days of the index
case has been estimated to be 3.3 per cent for children
under two years, 1.4 per cent for children two to three
years, 0.06 per cent for children four to five years, and nil
over the age of six years.
Most secondary cases among close contacts occur
within the first week after exposure, though late second-
ary cases are reported.
Control of Case
Cefotaxime, ceftriaxone, or chloramphenicol are used for
treatment.
The patient should be given a course of rifampicin prior
to discharge from hospital to ensure elimination of the
organism from the nasopharynx (for dosage see below).
If the treated patient is less than two years of age and
has not been immunised, a course of Hib vaccine should
be given after discharge from hospital.
Respiratory isolation is recommended for 24 hours after
the start of treatment. Concurrent or terminal disinfection
is not required.
62
Control of Contacts
All contacts under the age of six years should be placed
under surveillance for the earliest signs of illness so that
prompt medical attention can be sought.
A surveillance letter should be provided as soon as
possible to the parents of contacts in a kindergarten or
day care centre.
Antibiotic Prophylaxis
Rifampicin is the drug of choice. It is given in a dose of
20 mg/kg/day once daily for four days (up to a maximum
of 600 mg daily). Note that the dose used is different
from that used in meningococcal infections. (For adverse
effects and contraindications to rifampicin, see section
on meningococcal infections.) For infants less than one
month old, reduce the dose to 10 mg/kg once daily for
four days.
All household members, irrespective of age, should be
offered prophylaxis where there are children in the
household under four years of age (apart from the index
case), even if immunised.
Chemoprophylaxis for household contacts is useful up to
one month after the index case has been diagnosed,
though ideally it should be commenced as soon as
possible after diagnosis.
In day care centres, kindergartens and so on, all room
contacts, teachers and children should be offered
prophylaxis if two or more cases of Hib disease have
occurred within a period of 120 days.
Note
Chemoprophylaxis does not eliminate the need for
surveillance, and parents of contacts should be advised
of the risk of late secondary cases despite prophylaxis.
Investigative Procedures
In households with siblings under four years of age,
determine if household contacts have been offered
chemoprophylaxis and ensure that this is done by
treating doctor. Any missed immunisations should be
brought up to date.

If the child attends a kindergarten, day care centre, baby

sitter and so on, determine the last date of attendance,
and ensure that surveillance letters are distributed to
parents. If more than two cases have occurred in the
same day care centre, arrange for chemoprophylaxis for
all contacts.

Determine if the patient has been immunised against Hib

disease.

Note
Nose and throat swabs are not routinely recommended.

Preventive Measures
All children should receive Hib immunisation, usually at
two, four and six months of age, and a booster dose at
18 months.

Children at high risk of early disease such as Aboriginal/

Torres Strait Islander (ATSI) children should receive a
vaccine that has been demonstrated to give early
protection, such as PedvaxHIB.

Note
Vaccination may be recommended for older persons
who are immune suppressed.

Epidemic Measures
Increased surveillance and chemoprophylaxis for all
household and day care centre contacts as detailed
above. Throat swabs may be indicated in the epidemic
situation to assess carriage rates.

63
 Information Sheet
Haemophilus influenzae type b Infection
(Epiglottitis)

A case of epiglottitis (swelling of the throat causing

difficulty in breathing) has occurred in a child, at this
school/creche/child minding centre/kindergarten.

This disease is spread through droplets, which may be

produced when coughing and sneezing, and may
spread to intimate and household contacts.

The indications of this illness to look for are fever, sore

throat and noisy and difficult breathing. Another serious
type of infection by the same bacteria is meningitis,
indications of which include intense headache, nausea
and often vomiting. Serious signs include drowsiness,
neck stiffness, delirium, coma and sudden collapse.
Even the earliest sign (that is, fever) in such contacts
warrants immediate attention from your local doctor or
nearest hospital. Please take this letter with you.

If you need any further information, please telephone:

Public Health Nurse or Medical Officer, Infectious
Disease Unit: (03) 9616 7777.

64
 Information Sheet
Haemophilus influenzae type b Infection
(Meningitis)

A case of haemophilus meningitis has occurred in a

child, at this school/creche/child minding centre/kinder-
garten.

This disease is spread through droplets, which may be

produced when coughing and sneezing, and may spread
to intimate and household contacts.

The indications of this illness to look for are fever, intense

headache, nausea and often vomiting. Serious signs
include drowsiness, neck stiffness, delirium, coma and
sudden collapse. Even the earliest sign (that is, fever) in
close contacts warrants immediate medical attention
from your local doctor or the nearest hospital. Please take
this letter with you.

If you need any further information, please telephone:

Public Health Nurse or Medical Officer, Infectious Dis-
ease Unit: (03) 9616 7777.

65
 Information Sheet
Rifadin (Rifampicin)

Warning
• Should not be taken in cases of impaired liver function.
• Should not be taken in pregnancy.
• Can interrupt the effectiveness of oral contraception.
• May produce a reddish colour of the urine, sputum and
tears and so discolour contact lenses.
• May increase the requirement for anticoagulant drugs.
• This medication will usually eliminate the bacterium
from the nose/throat.

However, if in spite of taking this medication you or your

child develop any of the symptoms of fever, nausea,
vomiting, headache, lethargy or neck stiffness, we
recommend that you seek immediate medical attention
from your local doctor or the nearest hospital. Please
take this letter with you.

If you need any further information, please telephone:

Public Health Nurse or Medical Officer, Infectious
Disease Unit: (03) 9616 7777.

66
 Hand, Foot and Mouth Disease
(Enteroviral Vesicular Stomatitis with
Exanthem)

Victorian Statutory Reservoir

Re quirem ent Humans.
Statutory notification not required.
Note
School exclusion not required. This disease is not related to foot and mouth disease of
animals.

Infectious Agent
Coxsackievirus group A, mainly type 16.
Mode of Transmission
It is transmitted by:
• Direct contact with fluid from the vesicular lesions.
Clinical Features • Direct contact with nose and throat discharges and
This viral infection occurs mainly in children under 10 faeces of an infected person.
years of age and in young adults. It lasts seven to 10 • Aerosol droplet spread.
days.

Incubation Period
The clinical picture consists of sore throat, fever and
Usually three to seven days.
vesicular lesions on the buccal surfaces of the cheeks,
gums and sides of the tongue.
Period of Communicability
Papulovesicular lesions of the palms, fingers and soles
It is communicable during the acute stage of disease
commonly occur; occasionally maculopapular lesions
from nose and throat secretions, and as long as there is
appear on the buttocks.
fluid in the lesions. Viruses persist in the stools for
several weeks.
Public Health Significance and
Oc c u r re n c e Susceptibility and Resistance
Hand, foot and mouth disease occurs worldwide sporadi- Immunity to the specific virus may be acquired due to
cally and in epidemics; the greatest incidence is in previous infection.
summer and early autumn.
Second attacks may occur with group A coxsackievirus
Outbreaks occur frequently among groups of children in of a different serotype.
child care centres and schools.

Control of Case
Method of Diagnosis • Do not exclude children with hand, foot and mouth
Usually clinical (viral isolation from nasopharyngeal or disease as the virus is present in the faeces for many
stool specimens is rarely indicated). weeks.
• Cover lesions on hands and feet if possible and allow
to dry naturally.
• Avoid piercing lesions.
• Take care with hand washing and disposing of soiled
articles.

67
 Tre a t m e n t
Usually none required. Paracetamol may be used for
fever and discomfort.

Control of Contacts
Of no practical value.

Preventive Measures
Use of hand washing and other hygienic measures at
home and at child care centres.

Epidemic Measures
General practitioners should be informed about periods
of increased incidence of the disease.

68
 Information Sheet
Hand, Foot and Mouth Disease

This is a viral disease that usually lasts seven to 10 days. • Exclusion from school and child care centres is not
usually recommended because the virus may be
The incubation period is between three to seven days. present in the faeces for many weeks.

This disease is spread by direct contact with fluid from Note

the blisters, nose and throat discharges, droplets (sneez- This disease is not to be confused with foot and mouth
ing, coughing) and faeces (stools). disease in cattle.

Symptoms
• Fever.
• Sore throat.
• Small, blister-like lesions that may occur on the inside of
the mouth, sides of the tongue, palms of the hands,
fingers and soles of the feet and nappy area.

To Avoid the Spread of This

Disease
• Wash hands carefully after handling nose and throat
discharges.
• Wash hands carefully after handling faeces (nappy
changing).
• Wash hands carefully after contact with the blister-like
lesions.
• Allow blisters to dry naturally.
• Do not pierce blisters as the fluid within is infectious.
• Use separate eating and drinking utensils for each
child.

Infectious Period
• As long as there is fluid in the blisters.
• The faeces can remain infectious for several weeks.

Tre a t m e n t
• Usually none is required.
• Use paracetamol for fever and any discomfort. Do not
use aspirin where there is fever.
• The disease itself is not serious. If the child complains
of severe headache and fever persists, consult your
local doctor immediately.

69
 Hepatitis A
Victorian Statutory
Re quirem ent
Group B notification.
School and child care exclusion (see below).
Infectious Agent
Hepatitis A virus (HAV) (RNA picornavirus).
Clinical Features
Illness due to hepatitis A typically causes acute fever,
malaise, anorexia, nausea and abdominal discomfort,
followed a few days later by dark urine and jaundice.
Symptoms usually last several weeks, although convales-
cence may sometimes be prolonged.
Severe illness may rarely occur when hepatitis A compli-
cates pre-existing liver disease.
Infants and young children infected with hepatitis A may
have few or no recognised symptoms, and are often
anicteric (without jaundice).
Public Health Significance
Hepatitis A occurs worldwide.
In developing countries, most people are infected during
childhood. In the developed world, with good sanitation
and hygiene, most people now reach adulthood without
experiencing infection. They are, therefore, at risk of
infection from sporadic low-level transmission that occurs
in the community. A large outbreak affecting homosexual
men occurred in Australia and overseas during the early
1990s.
Common source outbreaks due to contaminated food are
rare.
Method of Diagnosis
A blood test showing IgM anti-HAV antibodies confirms
recent infection. These antibodies are present for two to
four months after infection. IgG antibodies alone are
evidence of past infection.
Blood biochemical testing shows elevated transaminase
levels during the acute phase of hepatitis. Later in the
illness, the pattern of liver function tests may be non-
specific.
Adults usually experience a distinct illness with acute
onset of symptoms and jaundice, but a high index of
suspicion is needed to diagnose young children with few
symptoms. Related adult cases are a clue.
Reservoir
Humans.
Mode of Transmission
The highly infectious hepatitis A virus is spread by the
faecal-oral route from person to person directly or via
fomites (contaminated objects). It may also be spread
via food or water.
Non-cooked foods, such as salads, may be contami-
nated by infectious food handlers, and filter-feeding
shellfish raised in contaminated waters may harbour the
virus.
The precise timing and mode of transmission are often
difficult to define.
Incubation Period
Usually 15 to 50 days; the average 28 to 30 days.
71
 Period of Communicability
Cases are most infectious from the latter half of the
incubation period until a few days after the onset of
jaundice (corresponding to a peak in transaminase levels
in anicteric cases).
Most cases are not infectious after the first week of
jaundice.
Long-term carriage or excretion does not occur.
Susceptibility and Resistance
Most persons born in Australia after 1945 are suscepti-
ble. Immunity after infection is probably lifelong.
Control of Case
• Determine the occupation of the case.
• Exclude the case from child care, school or work for
one week after the onset of illness or jaundice.
• Educate the case and family on the need for strict
hygiene practices.
• Do not prepare family meals while infectious, nor share
eating utensils, toothbrushes, towels and face washers.
• Dispose of or thoughly wash nappies of infants with
hepatitis A.
Control of Contacts
Normal immunoglobulin (IG), 0.02 ml/kg body weight,
intramuscularly, is recommended for:
• Household and sexual contacts of the case.
• Staff and children in close contact with a case in a
child care centre.
IG is not recommended for usual office, school or factory
contacts.
IG must be given within seven to 10 days of exposure to
be effective.
72
IG is rarely given to persons exposed to a potential
common source of hepatitis A (such as food or water)
because cases related to such a source are usually
recognised too long after the exposure for IG to be
effective for the co-exposed persons.
Timely administration of IG will prevent or modify clinical
illness for approximately six weeks after the dose.
However, people exposed and infected before the
administration of IG may still experience a mild infection,
and may have the potential to infect others if their per-
sonal hygiene is not exemplary.
Surveillance of contacts in a household or workplace
should be maintained.
Live vaccines (for example, Mumps-Measles-Rubella)
should not be administered for three months after a dose
of IG, and may also be ineffective if given in the 14 days
prior to IG. Reschedule such routine vaccinations.
When the case is a food handler:
• Consider serological testing of co-workers to determine
whether they have been infected or are susceptible.
• Place uninfected susceptible co-workers under surveil-
lance and give them immunoglobulin prophylaxis.
These persons remain at a risk of developing mild
illness (modified by immunoglobulin) but can generally
continue to work provided their personal hygiene and
food handling practices are exemplary.
• Undertake surveillance for hepatitis A in patrons by
seeking a history of exposure to the food premises
from cases notified over the next two to three months.
• Carefully consider the role of the infected food handler.
If transmission to patrons appears likely, consider
urgent follow-up of exposed patrons to offer them
immunoglobulin prophylaxis. Note that when the index
case is a patron, it is usually too late to offer immu-
noglobulin prophylaxis to other diners, although
personal contacts of the patron case/s should be
offered immunoglobulin according to the usual proto-
col.
Control of Environment The dose is one ml (720 ELISA units) administered
intramuscularly into the deltoid. A second dose must be
A source of infection should always be sought. For
given two to four weeks after the first dose, and a third
apparently sporadic cases, consider contact with an-
dose should be given six to 12 months after the first
other known case and recent travel to an area where the
dose.
disease is endemic. If these do not provide an answer,
acquisition from young children, particularly those in
Protective immunity is acquired approximately two weeks
child care, should be considered.
after the second dose, and long-term immunity (up to 10
years) is expected to follow the third dose.
A number of cases occurring at the one time should
prompt a search for a common source, particularly food
Alternatively, if ‘Havrix 1440’ is used (one ml contains
or water.
1440 ELISA units), then a single dose followed by a
booster dose at six to 12 months provides long-term
Special attention should be given to toilet hygiene in
immunity.
schools and child care centres. Ensure soap and water
are available and are used.
Travellers to countries where hepatitis A is common (for
example, Asia, Africa, Central and South America), have
Clusters of cases, possibly related to a single source,
previously been offered short-term protection with
may require epidemiologic investigation, including case
immunoglobulin, but should now be offered active
finding and surveillance, and public health measures to
vaccination with inactivated hepatitis A vaccine, particu-
prevent further cases.
larly if their stay is long or ‘rough’.

Preventive Measures Further indications for vaccine are being considered by

Good hygiene is very important, particularly hand
washing before eating or handling food and after using
the toilet.
Inadequate sanitation and housing may contribute to
endemic illness.
the NH&MRC. These may include such persons at
increased risk of hepatitis A infection as staff in child
care centres, residents and staff in institutions for intel-
lectually disabled persons, some health care workers
exposed to the faeces of potentially infected persons,
homosexual men, injecting drug users and others.

Use IG for contacts. The role of active immunisation in managing outbreaks

has not yet been determined.

Active Immunisation
Inactivated hepatitis A vaccine (‘Havrix’, SmithKline
Beecham) is licensed for use for persons aged more
than five years.

73
 Passive Immunisation When cases occur in three or more staff, attendees or
families with members at the centre, or new cases occur
In most instances where prophylactic immunisation is
more than three weeks after the onset of the first case,
undertaken, vaccine should be used.
consider giving IG to all family contacts of all children
aged two years or less at the centre, and all attendees,
However, when immunoglobulin is used to provide
staff and family contacts of cases.
passive protection, the following dosages are recom-
mended:
Food- and Water-Borne Outbreaks
Dosage of Immunoglobulin The source of such outbreaks is usually recognised too
late for IG to be usefully given to persons exposed to the
Dosage source.
Person’s Short-Term Long-Term
Weight (Kg) Prophylaxis Prophylaxis
Contacts of acutely ill cases should be given IG accord-
(six weeks) (ml) (5 months) (ml)
ing to the usual guidelines.
Under 25 0.5 1.0
25 to 50 1.0 2.5
Over 50 2.0 5.0

Epidemic Measures
Outbreaks Associated with Child
Care Centres
Clusters of cases of hepatitis A associated with child
care centres are not uncommon. When centre staff and/
or family of attendees develop hepatitis A, it usually
reflects an outbreak of hepatitis among young children at
the centre.

When one nappy-wearing attendee of a child care centre

has hepatitis A diagnosed, IG should be administered to
family contacts of the case, to all centre attendees, and
to all staff at the centre.

When the index case is an older, toilet-trained child, the

use of IG within the centre may be restricted to staff in
contact with the case, and attendees in the same room
as the case.

Where several cases of hepatitis A occur in association

with a child care centre, it may be necessary to adminis-
ter IG to a wider circle of contacts of potential cases.

74
 Hepatitis B

Victorian Statutory Public Health Significance

Re quirem ent Hepatitis B is carried by an estimated 300 million people
worldwide.
Group B notification.

HBV is a major cause of chronic hepatitis, cirrhosis and

School exclusion of acute cases.
hepatocellular carcinoma.

Infectious Agent The prevalence of the carrier state varies widely between
Hepatitis B virus (HBV) ( a DNA hepadnavirus). populations with parts of Africa, Oceania and Asia having
carrier rates of approximately 10 per cent.

Clinical Features
The onset is usually insidious with anorexia, abdominal
Method of Diagnosis
discomfort, nausea, vomiting, dark urine and jaundice. The diagnosis is established by a blood test and clinical
features. (See Case Definition.)
Rarely, arthralgia, rashes and renal disease may occur.
Reservoir
The severity ranges from inapparent cases to fatal cases
Humans.
of acute hepatic necrosis.

Case Definitions for Hepatitis B Mode of Transmission

Although HBsAg has been found in virtually all body
The screening definition for hepatitis B infection is the
secretions and excretions, only blood, semen and vaginal
presence of HBV surface antigen (HBsAg) in serum.
fluids have been shown to be infectious.

For acute hepatitis B:

• IgM core antibody (anti-HBc IgM) detected in serum Transmission occurs by three main routes:
usually indicates recent infection. • Percutaneous exposure (when infected body fluids
• Clinical illness consistent with acute viral hepatitis gain entry via inoculation, breaks in skin or by contact
(jaundice, elevated serum transaminase levels). with mucous membrane).
• Sexual.
• Perinatal.
For chronic carriers and chronic hepatitis B:
• Negative anti-HBc IgM.
• Positive anti-HBc IgG or positive anti-HBc total. Note
• No clinical illness consistent with acute viral hepatitis. Most cases in Africa and many in Asia are acquired in
• Presence of HBe antigen (HBeAg) indicates high childhood but not perinatally.
infectivity of blood and body fluids.
Incubation Period
Note
The presence of HBV surface antibody (anti-HBs) Usually 60 to 90 days. The range is 45 to 180 days.

indicates immunity to HBV.

75
 Period of Communicability
Blood from infected persons is infective many weeks
before the onset of symptoms and remains infective
through the acute clinical course of the disease and
during the chronic carrier state, which may persist for
life.

The proportion of infected individuals who become

carriers is inversely related to the age at infection.
Persons who are HBeAg positive are highly infectious.

Susceptibility and Resistance

Usually, the disease is milder and often anicteric in
children; in infants it is usually asymptomatic.

Protective immunity follows infection if anti-HBs develops

and HBsAg is absent.

More data are needed on the duration of immunity after

immunisation.

76
Serology of Hepatitis B Infection

Acute
Hepatits Resolution
Titre
HBsAg Anti-HBcIgM Anti-HBs Anti-HBcIgG
HBeAg Anti-HBe

INFECTION 6 months 12 months 10 years

Source: Australian Gastroenterology Institue

Chronic Hepatitis B and Failure to Clear Virus

Acute Chronic Hepatocellular

Cirrhosis
Hepatits Hepatits Carcinoma
Titre
Anti-HBcIgM Anti-HBclgG

HBsAg HBeAg Anti-HBe

6 months 12 months 10 years 20 years

INFECTION INTEGRATION
Source: Australian Gastroenterology Institue
Hepatitis B: An information Booklet for Health Care Providers

77
 Recommendations for Hepatitis B Prophylaxis Following
Percutaneous or Permucosal Exposure

Treatment When Source Found To Be:

Source not Tested
HBsAg-positive HBsAg-negative or Unknown
Exposed Person
Unvaccinated HBIG x 1* and initiate HB Initiate HB vaccine. If known high-risk source,
vaccine. may treat as if source
were HBsAg-positive.
Previously Vaccinated
Known sero-conversion Test exposed for anti-HBs No treatment. No treatment.
1. If adequate**, no
treatment.
2. If inadequate, HB
vaccine booster dose.

Known non HBIG x 2 or HBIG x 1 plus No treatment. If known high-risk source,

sero-conversion 1 dose HB vaccine. may treat as if source
were HBsAg-positive.

Unknown sero-conversion Test exposed for anti-HBs. No treatment. Test exposed for anti-HBs.

1. IG inadequate, 1. If inadequate, HB
HBIG x1 plus HB vaccine vaccine booster dose
booster dose. plus HBIG x1.

2. If adequate, no 2. If adequate, no
treatment. treatment.

* Hepatitis B Immunoglobulin (HBIG). Adult dose 400 Units.

** An adequate antibody level is greater than 10 milli International Units per ml, approximately equivalent to 10 sample ratio units (SRU) by radio-
immune-assay (RIA) or positive by enzyme-immuno-assay (EIA).

78
Control of Case
Exclusion from school and work until the diagnosis is
confirmed. Blood and body fluid precautions should be
observed until the disappearance of HBsAg and the
appearance of anti-HBs.
Control of Contacts
Household contacts should be tested for anti-HBc and
HBsAg and offered vaccination if susceptible.
Paediatric hepatitis B vaccine is given for:
• Infants of HBsAg positive mothers (as discussed
above).
• Infants in ethnic groups of high HBsAg endemicity,
whether the mother is a carrier or not.
• Children up to 10 years of age in both of the above
groups.
WHO recommends that hepatitis B vaccine should be
included in all childhood immunisation protocols.

Sexual contacts should:

• Be offered HBIG (400 IU IM) within 14 days of sexual
contact.
• Commence active immunisation at the same time.

Infants born to HBsAg positive mothers should:

• Be given HBIG (100 IU IM) within 12 hours of birth.
• Commence active immunisation within seven days.
This can be given at the same time as HBIG but at a
separate site.

Preventive Measures
Pre-exposure vaccination is recommended for:
• Health care workers. Individual risk depends on HBsAg
carrier rate in the population served, degree of blood
(not patient) exposure, and thoroughness of hygiene
measures in dealing with blood.
• Haemodialysis patients and recipients of blood prod-
ucts such as factors VIII and IX.
• Residents and staff in institutions for the intellectually
disabled.
• Those with multiple sexual contacts.
• Injecting drug users.
• Household and sexual contacts of hepatitis B virus
carriers.
• Inmates of long-term correctional facilities.

79
 Hepatitis C

Victorian Statutory Approximately 20 to 30 per cent of chronic carriers may

progress to liver cirrhosis within a period of about 20
Re quirem ent
years, and a proportion of those with cirrhosis will de-
Group B notification.
velop primary liver cancer within a further five to 10 years.

Infectious Agent
Hepatitis C virus (HCV), a small RNA virus, is closely
related to the flaviviruses and animal pestiviruses.
There are at least six major genotypes of HCV and it is
thought that some are more pathogenic than others. It is
also believed that repeat infection of a HCV carrier with a
different strain may exacerbate underlying liver disease.

Clinical Features At present, the main genotypes found in the Australian

Most patients with HCV are asymptomatic.
In the acute stage, patients develop elevated serum
alanine aminotransferase (ALT) levels.
Up to 25 per cent of patients may develop jaundice.
Symptoms and signs, when they occur, are similar to
other forms of hepatitis, but are usually milder than those
seen in hepatitis B.
The majority of patients progress to the chronic carrier
state that is also, in most cases, asymptomatic. Symp-
toms, when they occur, may be non-specific and include
fatigue, headaches and nausea.
Public Health Significance and
O c c u r re n c e
population are 1 (52 per cent), 3 (41 per cent) and 2 (7
per cent).
Method of Diagnosis
Laboratory diagnosis is based on detection of antibodies
directed against the products of expressed clones or
peptides of the hepatitis C virus and/or demonstration of
HCV RNA by polymerase chain reaction (PCR).
First generation enzyme immunoassay (EIA) became
available in Australia in 1990 and since then the second
and third generation EIAs have improved sensitivity and
specificity.
Supplemental tests are also available in the form of
recombinant immunoblot assays (RIBA). Equivocal
reactivity by EIA tests and indeterminate reactivity by
RIBA testing remains problematic in low-risk groups.

Hepatitis C occurs worldwide.

A positive PCR test is a marker for viraemia and infectiv-
ity, but a negative PCR does not rule out infection as
The estimated prevalence in the Australian community
viraemia may be intermittent.
based on blood donor screening is 0.14 to 0.45 per cent,
but the percentage of HCV positive individuals is higher
Current EIA tests cannot distinguish between patients
in certain groups, such as injecting drug users. In
who are currently infectious and those who have recov-
injecting drug users, seropositivity approaches 100
ered from infection and developed immunity.
percent in those injecting for more than eight years.

Infection with HCV results in the chronic carrier state in Reservoir

over 70 per cent of cases.
Humans.

81
 Mode of Transmission
It is primarily transmitted by blood-to-blood contact.
In Australia and other Western countries, sharing inject-
ing equipment by drug users is the most common mode
of transmission.
Tattooing, earpiercing and body piercing using unsterile
equipment are other potential sources.
Health care and laboratory staff handling blood and
blood products are at increased risk. The risk of con-
tracting hepatitis C from a needle-stick injury from a
seropositive source has been estimated at 3 per cent,
compared to 0.3 per cent for HIV infection and 30 per
cent for hepatitis B infection.
Sexual transmission rates of HCV are very low, but the
risk is increased if the HCV positive partner is immuno-
compromised as the virus titre may be increased.
Mother-to-baby transmission is also very low but may be
increased if the mother is also infected with HIV or has a
high titre of HCV in the blood. The risk of transmission
through breast milk is considered minimal.
Community or household transmission of HCV is consid-
ered rare.
A proportion of HCV individuals do not fall into any
known subgroup. It is thought that some may have had
exposure to injecting drugs many years ago that they
have forgotten or are unwilling to discuss.
Poorly cleaned needles used by medical practitioners in
some countries, and cultural practices that involve skin
piercing, are other potential sources of infection.
82
Incubation Period
Ranges from two weeks to six months—most commonly
six to nine weeks after which serum ALT levels rise.
Current HCV antibody tests become positive two to three
months after exposure.
Period of Communicability
Communicability occurs during the acute clinical stage
and indefinitely in the chronic carrier stage.
All HCV positive individuals need to be considered
potentially infectious.
Susceptibility and Resistance
Susceptibility is general. The degree of immunity follow-
ing infection is unknown.
Control of Case
The patient needs to be considered for possible Inter-
feron therapy that is available, for selected patients,
under the Highly Specialised Drugs Program of the
Commonwealth at certain liver clinics in Melbourne.
Assessment would include examination for signs of liver
disease, monitoring of the ALT levels and a PCR test.
Advice should be sought from a liver clinic when neces-
sary.
About 50 per cent of patients treated with Interferon
respond initially, but about 50 per cent of these relapse
after treatment ceases.
Counselling of the patient is a very important part of the Preventive Measures
management. This counselling should include:
• Use standard precautions by all health care providers
• Likely source of the infection.
with potential contact with blood or body fluids.
• Current knowledge of the natural history.
• Use disposable equipment for all skin penetration
• Possible symptoms.
procedures, or use adequate sterilisation methods
• Advice on prevention of further transmission of infec-
when reusable needles are used for any procedure.
tion.
• Lifestyle issues, such as immunisation against hepatitis
B, minimisation of alcohol intake, cessation of smoking,
healthy diet.

The patient should be advised not to:

• Donate blood or body organs.
• Share injecting equipment.
• Share personal items such as toothbrushes or razors.

They should also be advised to:

• Advise any health care providers of their HCV status
when undergoing any dental or medical procedure.
• Wipe up any blood spills with household bleach and
disposable paper towels.
• Cover any cuts or wounds with a dressing.
• Place blood-stained paper tissues, sanitary towels or
dressings in a plastic bag before disposal.
• Use ‘safer sex’ practices. People in long-term stable
relationships will need to discuss condom use with
their health care provider.

Control of Contacts
There is no vaccine available for hepatitis C.

The role of prophylactic immunoglobulin for contacts has

not been established.

83
 Hepatitis D

Victorian Statutory Incubation Period

Re quirem ent Not firmly established.
Group B notification (as hepatitis non-A, non-B, or
associated with hepatitis B).
Period of Communicability
Blood is potentially infectious during all stages of active
Infectious Agent HDV infection.
Hepatitis D virus (HDV) is a virus-like particle consisting
of a coat of HBsAg and a unique internal antigen (delta
Control of Case
antigen). (Replication can only occur in the presence of
As for hepatitis B.
hepatitis B virus.)

Clinical Features Control of Contacts

As for hepatitis B.
Two types of infection with hepatitis D occur:
• Co-infection: simultaneous acute infection with HBV
and HDV. This usually causes a self-limited hepatitis. Susceptibility and Resistance
• Superinfection: HDV infection in a HBV carrier. This
All persons who are susceptible to hepatitis B or who are
often causes a fulminant acute hepatitis that
HBV carriers can be infected with HDV.
progresses to chronic active hepatitis.

Among HBV carriers, avoiding exposure to any potential

Public Health Significance and source of HDV is the only effective measure.

Oc c u r re n c e
Two general epidemiological patterns are recognised:
• Endemic infection occurs in Italy, the Middle East,
some areas of Africa and South America, although the
ratio of the two infections varies widely with location.
Transmission occurs primarily within the household
setting.
• Non-endemic infection occurs in Australia, North
America and Western Europe, where HDV occurs
sporadically in the HBsAg population and is largely
confined to the risk group of injecting drug users.

Method of Diagnosis
Identification of HDV antigen or anti-HDV in the serum.

Mode of Transmission
The mode of transmission is similar to hepatitis B (see
Public Health Significance).
85
 Hepatitis E

Victorian Statutory Incubation Period

Re quirem ent Two weeks to two months; the mean has varied from 26
Group B notification (as hepatitis non-A non-B). to 42 days in different epidemics.

Infectious Agent Period of Communicability

Hepatitis E virus (RNA virus). Unknown.

Clinical Features Susceptibility and Resistance

Clinical course is similar to that of hepatitis A. Susceptibility unknown.

A high mortality rate (up to 40 per cent) has been de-

scribed in pregnant women affected in their third trimes-
ter of pregnancy.
Public Health Significance and
O c c u r re n c e
Sporadic and epidemic cases have occurred in India,
areas of the former Soviet Union, some African countries,
Mexico and parts of Asia.
Imported cases have been identified in Australians, and
one case in the Northern Territory in a patient who had
not been overseas.
Control of Case
• Determine occupation of the patient.
• Exclude the patient from food handling until at least
one week after the onset of jaundice.
• Educate the patient on the need for strict hygiene
practices such as hand washing after toilet and before
eating.
Control of Contacts
No specific measures.
The efficacy of immunoglobulin has not been estab-
lished.

Method of Diagnosis
Immune electron microscopy of faeces.

Serological tests, including fluorescent antibody assay

and EIR, are available through VIDRL.

Reservoir
Humans, transmissible to some other primates.

Mode of Transmission
Hepatitis D can be transmitted:
• From contaminated water.
• Person-to-person by the faecal-oral route.
87
 Herpes Simplex
Victorian Statutory
Re quirem ent
Statutory notification not required.
Infectious Agent
Human herpes virus 1 and 2 (HSV).
Clinical Features
This viral infection is characterised by a localised primary
lesion, latency and a tendency to local recurrence.
The two causal agents, HSV types 1 and 2, generally
produce distinct clinical syndromes, depending on the
portal of entry.
HSV type 1:
• The primary infection may be mild and generally
occurs in early childhood before the fifth year of life.
• About 10 per cent of primary infections cause a more
severe form of disease manifested by fever and
malaise.
• This may last a week or more, and is associated with
vesicular lesions in the mouth, eye infection or a
generalised skin eruption complicating chronic ec-
zema.
• Reactivation of latent infection results in cold sores
appearing as clear vesicles on an erythematous base,
usually on the face and lips, which crust and heal in a
few days.
• This reactivation may be precipitated by trauma, fever
or intercurrent disease.
HSV type 2:
• This virus is the usual cause of genital herpes, al-
though this can also be caused by type 1 virus.
• Genital herpes occurs mainly in adults and is sexually
transmitted.
• Primary and recurrent infections occur, with or without
symptoms.
Public Health Significance and
O c c u r re n c e
Asymptomatic infections with HSV type 1 virus are
common. Seventy to 90 per cent of adults have circulat-
ing antibodies to HSV type 1 virus, indicating previous
infection.
HSV type 1 is a common cause of meningoencephalitis.
Vaginal delivery in pregnant women with active genital
infection carries a high risk to the newborn. It can cause
disseminated visceral infection, encephalitis and death.
HSV type 2 has been associated with aseptic meningitis.
Method of Diagnosis
Cytologic changes in tissue scrapings or biopsy.
Confirmation by direct FA tests or isolation of the virus
from oral or genital lesions.
Techniques are available differentiate type 1 from type 2
antibody.
Reservoir
Humans.
Mode of Transmission
Contact with type 1 in the saliva of carriers is the most
important mode of spread.
Infection on the hands of health care personnel from
patients shedding HSV results in an infection of the tip of
the finger. It begins with intense itching and pain, and is
followed by deep vesicle formation and tissue destruc-
tion.
89
 Transmission of HSV type 2 to non-immune adults is
usually by sexual contact.
Incubation Period
Usually two to 12 days.
Period of Communicability
Secretion of virus in the saliva may occur up to seven
weeks after recovery from stomatitis.
Patients with primary genital lesions are infective for
seven to 10 days. Those with recurrent disease are
infective for four to seven days.
Susceptibility and Resistance
Severe extensive disease may occur in
immunosuppressed individuals.
Preventive Measures
• Emphasise personal hygiene to minimise the transfer of
infectious material.
• Avoid contamination of the skin of patients with ec-
zema.
• Wear gloves when in direct contact with infectious
lesions and wash hands with soap and water after-
ward.
• Advise cesarean section before membranes rupture
when primary or recurrent genital infections occur in
late pregnancy because of the risk of neonatal infec-
tion.
Epidemic Measures
Not applicable.

Control of Case
The patient should be kept away from newborns, children
with burns or eczema, and immunosuppressed patients.

Tre a t m e n t
Treatment includes:
• Idoxuridine (Stoxil) for cutaneous lesions.
• Povidone-iodine ointment and paint (Betadine).
• Acyclovir (Zovirax tablets) for initial and recurrent
genital herpes.
• Acyclovir intravenous infusion for H. simplex encephali-
tis and immunosuppressed patients.

Control of Contacts
Contact isolation is necessary only for neonatal or severe
primary lesions.

No immunisation is available.

90
 Hydatid Disease

Victorian Statutory As result of the success of the Tasmanian hydatid control

campaign, no new cases of human hydatid disease has
Re quirem ent
been reported from Tasmania for the past decade.
Group B notification.

Cases notified in Victoria are usually those who have a

Infectious Agent
Echinococcus granulosus (dog tapeworm).
Clinical Features
Hydatid disease is produced by cysts that are the larval
stages of the tapeworm Echinococcus.
long standing history of infection that was acquired from
areas such as Greece, Cyprus or the former Yugoslavia,
or from areas in rural Victoria. A few cases of recently
acquired hydatid infection occur in visitors to rural areas
where there are infected sheep or dingoes. The mode of
transmission is the urban dog that accompanies the
traveller. People who trap wild dogs are similarly at risk.

Symptoms depend on the location of the cyst, and

Method of Diagnosis
develop as a result of pressure, leakage or rupture.
Dignosis can occur by plain X-ray, ultrasound or CT.

The most common site for the cysts is the liver; less
If a cyst ruptures, examine for protoscolices, brood
commonly brain, lungs, kidneys, and uncommonly the
capsules and cyst wall in sputum, vomitus, faeces and
heart, thyroid and bone.
urine.

Cysts remain viable or die and calcify. They may be

detected on routine X-ray. Serological Tests
Screening, ELISA and IHA.
Prognosis is generally good and depends on the site and
potential for rupture and spread.
Diagnosis, Immune electrophoresis (IEP), IHA and
ELISA.
Sudden rupture of the brood capsules and liberation of
the daughter cysts may cause fatal anaphylaxis.
IEP is used as a follow-up after surgery or chemotherapy
(negative within two years of surgical cure).
Persons who have a calcified cyst detected on X-ray may
have active infection.
There is no longer a place for the Casoni skin test.

Public Health Significance and Reservoir

Oc c u r re n c e Dogs, foxes and dingoes.
Occurrence is worldwide.
Sheep are the major intermediate hosts. Pigs, goats and
It is mainly associated with sheep farming. some species of wallaby and kangaroo can act as
intermediate hosts.
In Australia, most human cases are notified from New
South Wales, followed by Western Australia, the Austral-
ian Capital Territory, Victoria and Queensland.

91
 Mode of Transmission
Infection occurs by hand-to-mouth transfer of tapeworm
eggs from dog faeces. The larvae penetrate the intestinal
mucosa, enter the portal system and are carried to
various organs where they produce cysts in which
infectious protoscolices develop.
The important life cycle is dog-sheep-dog. A
dingo-wallaby-dingo (or wild dog) sylvatic cycle also
occurs. A dog-wild pig-dog cycle has recently been
recognised with risks for hunters from urban areas.
Incubation Period
Variable: from months to years.
Period of Communicability
It is not communicable through person-to-person trans-
mission.
Dogs pass eggs approximately seven weeks after
infection.
In the absence of reinfection, this ends in about one
year.
Susceptibility and Resistance
Children are more often infected than adults.
Control of Case
No need for isolation, or concurrent disinfection.
No vaccine is available.
92
Tre a t m e n t
Surgery is the treatment of choice.
Mebendazole (Vermox) is used when surgery is contrain-
dicated.
Albendazole (special access scheme) has been used
successfully.
Control of Contacts
Household contacts should be examined for evidence of
infection.
Dogs in contact with the patient should be investigated
(obtain advice from the Department of Natural Resources
and Energy).
Preventive Measures
• Educate the public on the danger of close association
with dogs and on the need to wash hands after contact
with dogs.
• Treat infected dogs and destroy unwanted dogs.
• Control the slaughter of animals, particularly sheep.
The area should be enclosed to prevent access by
dogs and have adequate drainage, an incinerator and/
or disposal pit.
• Do not allow children to play with strange dogs,
especially in rural areas.
• Dispose of animal carcasses as soon as possible.
• Report all stray dogs to the local council.
• Destroy wild and stray dogs in highly endemic areas.
• Control dogs on farms at all times and do not allow
them to have access to vegetable gardens.
• Treat all dogs for E. granulosus regularly (every six
weeks) in rural or endemic areas with praziquantel
(Droncit).
• Do not feed offal to dogs.
 Impetigo

Victorian Statutory Mode of Transmission

Re quirem ent Impetigo can be transmitted by direct or intimate contact
Statutory notification not required. with patients or asymptomatic carriers.

School exclusion. It is rarely transmitted through indirect contact with

objects or hands.

Infectious Agent
Streptococcus pyogenes (Group A streptococci).
Period of Communicability
It is communicable while active lesions persist.
Staphylococcus aureus.

Susceptibility and Resistance

Clinical Features Susceptibility to streptococcal and staphylococcal skin
It is a superficial vesiculo-pustular skin infection seen infection is general.
mainly in children.

Control of Case
It begins as a papule that vesiculates and then breaks
Local treatment-crusts should be bathed with cetrimide
leaving a denuded area covered by a honey-coloured
0.1 per cent lotion or saline or water.
crust.

General bathing with antibacterial soap such as

Local lymph nodes may be enlarged and the affected
Sapoderm or Gamophen should occur.
child may be acutely ill.

The lesions should be covered with a watertight dress-

Public Health Significance and ing.
Oc c u r re n c e
Treatment should continue until lesions have healed.
Occurrence is worldwide.

In outbreak situations, lesions should be swabbed and

Impetigo is a rapidly spreading, highly infectious skin
systemic antibiotic given for severe cases.
rash that frequently occurs in children’s settings such as
day care centres, kindergartens and schools.
Flucloxacillin is usually used for staphylococal impetigo.

Method of Diagnosis The child should be excluded from child care settings
Culture taken from active skin lesions. until sores have fully healed.

The child may be allowed to return earlier provided that

Reservoir appropriate treatment has begun and sores on exposed
Humans. surfaces such as scalp, face, hands or legs are properly
covered with moisture-proof dressings.

93
 Preventive Measures
Personal hygiene.

Public education in modes of transmission and possible

complications. The necessity for completing a full course
of antibiotic therapy when prescribed should be rein-
forced within the community.

Epidemic Measures
• Investigate if a cluster of two or more concurrent cases
occur in a hospital nursery or maternity ward.
• Take swabs from all patients, care personnel and
search for active lesions.
• Investigate if a a large number of cases occur in
schools and community settings.
• See attached sheet of investigative procedures for
protocol.

Epidemic Investigative
Procedures for Impetigo
Case:
• Obtain swab of discharging lesion.
• Obtain nasal swab.
• Instruct patient to cover active lesion with dressings.
• Dispose of soiled dressings appropriately.
• Educate regarding personal hygiene. Emphasise hand
washing, especially after changing dressings, and the
importance of avoiding sharing toilet articles, towels or
clothing.
• Instruct on the use of anti-bacterial soap for bathing for
two to three weeks (Gamophen soap).

Contacts:
• Obtain nasal swabs.
• Educate about modes of transmission.

Environment:
• Trace source of infection.
• Swab communal laundry facilities if applicable.
• Educate public in modes of infection and personal
hygiene.

94
 I n fl u en z a
Victorian Statutory
Re quirem ent
Statutory notification not required.
Infectious Agent
Influenza virus (A, B, C). Influenza A virus subtypes are
classified by the antigenic uniqueness of the surface
glycoproteins haemagglutinin (H) and neuraminidase
(N).
Clinical Features
It is an acute respiratory tract illness characterised by
fever, headache, myalgia, prostration, coryza, sore throat
and cough.
Recovery is usual in two to seven days; however, cough
may be longer lasting.
Public Health Significance and
Oc c u r re n c e
Influenza occurs as pandemics, epidemics and as
sporadic cases.
Type A viruses cause most epidemics. Mixed A and B
epidemics also occur.
The emergence of completely new subtypes of A virus
(antigenic shift) occurs at irregular intervals and is
responsible for pandemics.
Minor antigenic changes (antigenic drift) are responsible
for annual epidemics and regional outbreaks.
During major epidemics, severe disease and complica-
tions (especially viral and bacterial pneumonia) occur
primarily among the elderly and those debilitated by a
chronic disease.
In temperate zones, outbreaks tend to occur in winter.
Method of Diagnosis
Inluenza can be diagnosed by isolation of influenza virus
from nasopharyngeal aspirate or throat washing by the
FA test (send specimens to VIDRL).
It can be confirmed by virus culture.
Serology
In outbreak situations, special arrangements can be
made with the WHO Collaborating Centre for Influenza
References and Research and the Commonwealth
Serum Laboratories for the isolation of influenza virus.
(Contact Mr Alan Hampson, Deputy Director.)
Reservoir
Humans. Animal reservoirs are suspected as sources of
new human subtypes (perhaps by reassortment with
human strains) and may occur particularly when people
and livestock (for example, pigs, ducks) live closely
together.
Mode of Transmission
It is predominately transmitted by airborne spread.
Transmission also occurs by direct contact through
droplet spread.
Direct contact may be important as the virus will survive
some hours in dried mucus.
Incubation Period
Usually one to five days.
Period of Communicability
It is probably communicable for three to five days from
clinical onset in adults; up to seven days in young
children.
95
 Susceptibility and Resistance • Aboriginal and Torres Strait Islander adults over 50
years of age, partly because of the greatly increased
When a new subtype appears, all are susceptible except
risk of premature death from respiratory disease.
those who have lived through earlier epidemics caused
• Children with cyanotic congenital heart disease.
by a related subtype.
• Staff caring for immunosuppressed patients.
• Staff and residents of nursing homes and other chronic
Infection produces immunity to the specific infecting
care facilities.
virus, but the duration and breadth of immunity depends
• Adults and children receiving immuosuppressive
on the degree of antigenic drift and the number of
therapy.
previous infections.

Control of Case Epidemic Measures

Surveillance of the extent and progress of the epidemic
Symptomatic treatment only.
and reporting of findings to the community are important.

Amantadine given early in the course of influenza A is

said to reduce symptoms and virus titre in respiratory
secretions but is not routinely used.

Control of Contacts
No routine measures.

Chemoprophylaxis with amantadine may be considered,

in special circumstances, against influenza A strains.

Preventive Measures
Inactivated influenza vaccine is formulated annually so
that changes in composition can be made to counter
antigenic shifts and antigenic drift.

The vaccine confers about 70 per cent protection against

infection for approximately 12 months.

Annual immunisation is recommended for individuals in

the following categories:
• Persons over 65 years of age.
• Adults and children with chronic debilitating disease,
especially those with chronic cardiac, pulmonary, renal
and metabolic disorders.

96
 Infectious Mononucleosis
(Glandular Fever)

Victorian Statutory Method of Diagnosis

Re quirem ent A full blood examination shows mononucleosis and
Statutory notification not required. lymphocytes of 50 per cent or more, including 10 per
cent or more atypical cells.

Infectious Agent Paul Bunnell Test.

Epstein-Barr virus (EBV).
Liver Function Tests (AST, ALT) abnormal.

Clinical Features
Serological
It is an acute viral infection affecting mainly young adults.
ELISA IgG and IgM for viral capsid antigen.

Clinical features include fever, sore throat (usually with

ELISA IgG for nuclear antigen, takes two to three months
exudative pharyngotonsillitis) and lymphadenopathy.
to become positive.

Splenomegaly occurs in 50 per cent of cases; jaundice

in 4 per cent. Reservoir
Humans.
In young children the disease is mild or asymptomatic.
Duration is from one to several weeks.
Mode of Transmission
The disease is rarely fatal. It is transmitted by person-to-person spread by the
oropharyngeal route via saliva.
A chronic form is suggested as one of the causes of
Chronic Fatigue Syndrome. Young children may be infected by saliva on the hands
of attendants or on toys.
A syndrome resembling infectious mononucleosis
clinically and haematologically may be caused by
herpesvirus 6, cytomegalovirus or toxoplasmosis.
Incubation Period
From four to six weeks.

Public Health Significance and

Oc c u r re n c e Period of Communicability
Glandular fever is most commonly seen in high school The period of communicability is prolonged.

and university students.

Pharyngeal excretion may persist for a year or more after

About 50 per cent of those infected will develop the infection.

disease that is spread by close, personal contact.

Healthy adults may be long-term oropharyngeal carriers.

Occurrence is worldwide and widespread in early

childhood in developing countries.

97
 Susceptibility and Resistance
Infection confers a high degree of resistance.

Reactivation of EBV may occur in immunosuppressed

individuals.

Control of Case
Isolation is not necessary.

Tre a t m e n t
None. Steroids may be of some value in severe, toxic
cases.

Control of Contacts
Investigation of contacts is not necessary. No immunisa-
tion is available.

Preventive Measures
• Use hygienic measures including hand washing to help
prevent spread.
• Disinfect articles soiled with nose and throat dis-
charges.

Epidemic Measures
None.

98
 Legionellosis

Victorian Statutory • There is usually multi-system involvement with diar-

rhoea, vomiting, mental confusion, delirium and renal
Re quirem ent
failure.
Group A notification, Prevention of Legionellosis Health
• In epidemics, it has an attack rate of up to 5 per cent
(Infectious Diseases) Regulations 1990, Division 3.
and a case fatality rate of around 15 per cent.
• Legionnaires’ disease was made notifiable in Victoria in
Infectious Agent 1979.

The infectious agent is Gram negative bacilli belonging

Pontiac fever:
to the genus Legionella.
• The non-pneumonic form, presents mainly as a flu-like
illness with spontaneous recovery and no reported
There are currently more than 30 species, but L.
deaths.
pneumophila (with 14 recognised serogroups) is respon-
• It has a high attack rate (95 per cent) and outbreaks
sible for at least 75 per cent of cases in Australia and
have been reported overseas.
overseas.
• Pontiac fever has not been reported in Australia.
• It was made notifiable in Victoria in May 1990.
Variations in the species/serogroups implicated have
been noted in a number of countries at different times. In
1988, L. micdadei accounted for the majority of cases Public Health Significance and
reported in Victoria. In 1993, 20 of the 37 reports of
O c c u r re n c e
Legionellosis in Victoria were caused by L. longbeachae.
Sporadic and epidemic forms of Legionnaires’ disease
have occurred overseas and in Australia. Major out-
Another species, L. bozemanii, has been implicated in
breaks have been reported in South Australia and New
Victorian cases.
South Wales, but not in Victoria.

Though commonly found in aquatic habitats, Legionella

Most of the overseas outbreaks have been associated
spp. are fastidious organisms requiring specific condi-
with cooling towers and warm water systems.
tions for culture in the laboratory.

Some outbreaks have occurred in hospitals where the

The bacteria will not grow on conventional culture media.
Clinical Features
Legionellosis (infection by any Legionella species) is an
acute bacterial infection with two recognised presenta-
tions:
Legionnaires’ disease:
• This is the pneumonic form of the illness where the
patient typically presents with severe pneumonia that
frequently culminates in respiratory failure.
• Early symptoms are anorexia, malaise, myalgia and
fever (flu-like).
case fatality rate has been high (for example, in 1985 at
Stafford District Hospital in the UK, the case fatality rate
was 28 per cent).
The largest outbreak in Australia occurred at
Wollongong, NSW, in 1987 where there were at least 44
cases and 10 deaths. The implicated cooling tower was
situated 50 m to 70 m from the Gateway Shopping
Centre that was visited by most of the cases.

99
 In 1988–1989, an outbreak, where L. longbeachae SG1
was implicated, occurred in South Australia. Epidemio-
logical investigations found an association with the use of
potting mix. Further work by the Institute of Medical and
Veterinary Science, Adelaide (IMVS) found L.
longbeachae to be present in approximately 70 per cent
of samples of commercial potting mix tested.
Case fatality in the Victorian cases is around 20 per cent.
Reservoir
The bacterium is water-associated and ubiquitous.
It is often isolated from natural habitats (rivers, creeks,
hot springs) and from artificial equipment such as
cooling towers associated with airconditioning and
industrial processes, and in warm water systems where
the temperature is maintained around 43˚C favouring
proliferation of the bacteria.

Since the disease was made notifiable in 1979, the

L. longbeachae has been found in potting mixes.
number of cases has been slowly increasing over the
years, possibly due to increased awareness on the part
of the clinician. Mode of Transmission
Legionellosis is transmitted through inhalation of con-
taminated aerosols. Aerosols of less than five microns
Case Definition and Method of are particularly effective in reaching the lower depths of
Diagnosis the lungs.
It is diagnosed by a clinically compatible illness (pneu-
monia) and at least one of the following: The mode of transmission with potting mix is less clear
• Isolation of Legionella species from lung tissues, and is under further study.
respiratory secretions, pleural fluid, blood, or other
tissues.
Incubation Period
or
Legionnaires’ disease: usually five to six days but can
• A fourfold or greater rise in (IFA) titre against
range from two to 10 days.
Legionella species, to at least 128, between acute and
convalescent phase sera (four to six weeks apart).
Pontiac fever: four to 66 hours.
or
• A stable high Legionella titre (at least 512) in convales-
cent phase serum. Susceptibility
or Legionnaires’ disease has a low attack rate and males
• Demonstration of Legionella species antigens in urine, are more frequently affected than females.
lung tissue, respiratory secretions or pleural fluid.

In Victoria, the mean age of patients affected is now in

Note
the low 60s.
Most cases are diagnosed by serological tests; hence,
the diagnosis is usually a retrospective one.
Though the disease can affect any age group, it is rarely
reported in children.
Antigen to L. longbeachae was included in the Indirect
Fluorescent Antibody (IFA) tests in 1992. This has led to
Other groups at risk include the immunosuppressed,
an increase in the number of cases reported due to L.
diabetics, those perhaps who smoke and/or consume
longbeachae.
alcohol excessively, and those with chronic respiratory
disease.
Cultures can take up to 10 days.
100
Period of Communicability
There have been no reports of person-to-person trans-
mission.
Control of Case
Specific antibiotic treatment includes erythromycin and
rifampicin.
Supportive treatment is needed if there is respiratory
failure.
Dialysis may be required if there is renal failure.
Investigation
After estimating the onset of illness, the patient’s move-
ments during the incubation period should be estab-
lished.
Inspection should be underatken of places where the
following aerosol generating equipment may be present:
• Cooling towers.
• Fountains or sprinklers.
• Spas.
• Humidifiers.
• Showers, especially associated with warm water
systems (temperature especially ranging from 35˚C to
43˚C).
• Oxygen nebulizers.
• Others (be suspicious).
Places inspected may include workplaces, hospitals,
homes and others.
The temperature of water should be checked.
Maintenance records, where appropriate, should be
checked to ensure compliance with the Health (Infec-
tious Diseases) Regulations 1990 (Division 3).
The possibility of undetected, associated case/s (mainly
through the personnel manager, sickness records and
work doctor/nurse, hospital medical records) should be
investigated.
Where necessary, meetings should take place with staff,
occupational health and safety representatives, union
representatives to:
• Discuss the presentation of disease.
• Allay fears.
To help identify a common source, serology should be
considered for work colleagues. Tests are generally
offered to those who have been away four or more
consecutive days with a respiratory illness.
These tests are, however, of limited value as 13 to 35 per
cent of the normal population (WA) and 30 per cent (SA)
have been found to have antibodies to L. pneumophila
serogroup 1.
Clotted blood, 10 ml should be sent to Legionella Refer-
ence Laboratory, VIDRL. Ample warning should be given
of expected numbers of specimens.
Potential sources should be sampled, and the tempera-
ture of water recorded.
Water sample (100 ml) should be collected in containers
(available from MDU) and sent to MDU.
En v i ro n m e n t
As indicated from inspection and/or results of samples.
Immediate recommendations may include dosing the
cooling tower with a chlorine-releasing compound,
followed by:
• Decontaminating cooling towers as per Guidelines*.
(See 5.14 of these guidelines.)
• Decontaminating the reticulated water system as per
Guidelines*. (See 6.9 of these guidelines.) Shutting
down the system (there should not be any need for
evacuation).
101
 Long-term measures may include advice on: Epidemic Measures
• The maintenance procedures of cooling towers.
An outbreak is defined as more than one case associ-
• Elevation of temperature of hot and warm water sys-
ated in time and place.
tems.
• Engineering modifications.
When an epidemic occurs, activate Displan which allows
• Relocation of cooling towers.
for investigation for common source of infection and
• Relocation of air intakes.
resultant action as indicated.
• Replacement of cooling towers by air-cooled systems.

* Guidelines refers to Guidelines for the Control of

Pre ve n t i o n Legionnaires’ Disease, 1989.

As eradication of Legionella spp. in artificial systems is

impractical, preventing or controlling Legionellosis is
based on appropriately maintaining aerosol-generating
equipment.

The folowing recommended measures aim to minimise

the proliferation of the bacteria:
• Ensure compliance with Health (Infectious Diseases)
Regulations 1990.
• Improve future design of aerosol-generating equipment
to facilitate maintenance and to reduce aerosols.
• Ensure appropriate siting of cooling towers; that is,
away from air intakes, areas of public access, and so
on.
• Promote ongoing education of building owners and
managers regarding preventive measures as outlined
in the Guidelines*.

Potting Mix
To minimise the risk of infection, gardeners should:
• Open the bag with care to avoid inhalation of airborne
potting mix.
• Moisten the contents to avoid creating dust.
• Wear gloves to avoid transferring the potting mix from
hand to mouth.
• Wash hands after handling potting mix, even if gloves
have been worn.
• Adopt the same measures when handling other gar-
dening material such as compost.

102
 Leprosy (Hansen’s Disease)

Victorian Statutory Public Health Significance and

Re quirem ent O c c u r re n c e
Group B notification. It is occasionally seen on routine refugee screening.

The world prevalence is estimated to be between 10 to

Infectious Agent 12 million cases.
Mycobacterium leprae.
The disease is endemic in tropical and subtropical Asia,

Clinical Features Africa, Central and South America, Pacific regions and
the USA (Hawaii, Texas, California, Louisiana, Puerto
It is a chronic bacterial infection involving the cooler
Rico).
body tissues, skin, superficial nerves, nose, pharynx,
larynx, eyes and testicles.
Method of Diagnosis
Skin lesions may occur as pale, anaesthetic macular Clinical examination.
lesions or erythematous infiltrated nodules.
Laboratory tests which show:
Neurologic disturbances are manifested by nerve • The demonstration of acid-fast bacilli in scrapings from
infiltration and thickening with anaesthesia, neuritis, skin or the nasal septum.
paraesthesia and trophic ulcers. • A typical histologic picture in a biopsy of skin or of a
thickened involved nerve.
The disease is divided clinically and by laboratory tests
into two overlapping types: lepromatous and tuberculoid.
Reservoir
The lepromatous type is progressive with nodular skin Humans.
lesions, slow symmetric nerve involvement, numerous
acid-fast bacilli in the skin lesions and a negative lep-
romin skin test.
Mode of Transmission
The mode of transmission is not clearly established. The

The tuberculoid type is benign and non-progressive with disease is probably transmitted by aerosol with a high

localised skin lesions, asymmetric nerve involvement, subclinical rate of infection.

few bacilli present in the lesions and a positive lepromin

skin test. Household and prolonged close contact seem to be
important.

Leprosy should always be suspected in any patient with

an undiagnosed peripheral neuropathy or chronic skin In cases of children under one year of age, transmission
lesions. is probably transplacental.

103
 Incubation Period For tuberculoid leprosy, the recommended regimen is
rifampicin and dapsone for a period of six months (for
The incubation period is difficult to determine.
detailed treatment see Control of Communicable Dis-
eases in Man by Benenson).
It probably ranges from nine months to 20 years; on
average four years, for tuberculoid leprosy and eight
years for lepromatous leprosy. Control of Contacts
Investigation of contacts and source of infection.
Period of Communicability
Early detection and treatment of new cases.
Leprosy is not infectious after three months of continuous
treatment with dapsone or clofazimine, or after two to
Prophylactic BCG has resulted in a considerable reduc-
three weeks of treatment with rifampicin.
tion in the incidence of tuberculoid leprosy among
contacts in some trials.
Susceptibility and Resistance
Infection among close contacts of leprosy patients is
Epidemic Measures
frequent, but clinical disease occurs only in a small
Not applicable.
proportion.

Control of Case
No isolation is required for cases of tuberculoid leprosy;
contact isolation is required for cases of lepromatous
leprosy.

Nasal discharges of infectious patients should be

concurrently disinfected.

Tre a t m e n t
The minimal regimen recommended by WHO for lepro-
matous leprosy is rifampicin, dapsone and clofazimine
and, recently, ofloxacin.

The treatment should be continued until skin smears

become negative for at least two years.

104
 Leptospirosis
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agent
Leptospira species (many serovars). In Victoria, the most
common serovar is Leptospira borgpetersenii var hardjo.
Clinical Features
Clinical features include fever, headache, chills, myalgia
and red eyes.
Other manifestations are diphasic fever, rash, meningitis,
haemolytic anaemia, haemorrhage into skin and mucous
membranes, hepato-renal failure, jaundice, mental
confusion/depression, pulmonary involvement and
haemoptysis.
Clinical illness lasts a few days to three weeks or more.
Recovery, if untreated, may take months.
Public Health Significance and
Oc c u r re n c e
It is a zoonotic disease that needs exposure to water
contaminated by animal urine, or contact with tissues or
urine of infected animals.
It is an occupational hazard for farmers, sewer workers,
miners, dairy and abattoir workers and fish workers, and
a recreational hazard to bathers, campers and sports-
men.
Many cases have arisen in herringbone-style milking
sheds.
Method of Diagnosis
See checklist at the end of this section.
Laboratory diagnosis:
• Rising titres on repeated serology.
• Take blood during acute illness and two to three weeks
later.
• Isolate leptospires:
– Blood (days 0 to 7).
– CSF (days 4 to 10) lumbar puncture.
– Urine (after 10 days).
Repeated blood cultures, into specific media during the
first week of disease are usually successful.
Preferably take blood cultures before antibiotic therapy is
commenced.
Reservoir
Many animal hosts. In Victoria, cows, rats and pigs.
Mode of Transmission
It can be transmitted by:
• Contact of skin, especially if abraded, or of mucous
membranes with water, moist soil or vegetation con-
taminated with urine of infected animals.
• Direct contact with urine or tissues of infected animals.
• Ingestion of foods contaminated with urine of infected
rats.
• Inhalation of droplet-aerosols of contaminated fluids.
Incubation Period
Usually 10 to 12 days (the range is four to 19 days).
Period of Communicability
Leptospires may be excreted in the urine of animals for
one month usually (but up to 11 months has been
reported).
105
 Susceptibility and Resistance • Consult the Department of Natural Resources and
Energy on herd immunisation.
Immunity to the specific serovar follows infection, but
• Prevent the contamination of accommodation, working
may not protect against infection with a different serovar.
and recreational areas.

Control of Case
Epidemic Measures
• Isolate the case with blood/body fluid precautions.
• Seek source of infections and eliminate contamination
• Disinfect articles soiled with urine.
or prohibit use of infected waters.
• Use antibiotic treatment: penicillin, doxycycline or
• Search for industrial and occupational source.
amoxycillin.

Investigation
• Ascertain occupational exposure.
• Seek the source of the infection; for example, contact
with contaminated water, farm or domestic animals,
rodent infestations.
• Inform the Department of Natural Resources and
Energy.

Control of Contacts
No human vaccine is available.

Search for exposure to infected animals and potentially

contaminated waters.

Control of Environment
Recognise potentially contaminated waters and soil, and
drain such waters when possible.

Preventive Measures
• Educate the public on modes of transmission to avoid
swimming or wading in potentially contaminated
waters, and to use proper protection when work
requires such exposure.
• Protect workers in hazardous occupations with boots
and gloves.
• Control rodents.
• Segregate infected domestic animals.

106
Diagnosis of Leptospirosis in Humans
This checklist is designed for those who deal directly with the patient. To use the list, note the main clinical features
listed, mark Yes or No, and write the appropriate score in the right-hand column.
A presumptive diagnosis of leptospirosis may be made if:
• Part A, or Parts A and B score: 26 or more.
• Parts A, B and C total: 25 or more.

A score between 20 and 25 suggests leptospirosis as a possible, but unconfirmed, diagnosis.

Question Answer Score

A. Has the patient:

• Headache of sudden onset? Yes = 2 No = 0 ____
• Fever? Yes = 2 No = 0 ____
• If yes, is the temperature 39˚C or more? Yes = 2 No = 0 ____
• Red eyes (bilateral)? Yes = 4 No = 0 ____
• Meningism? Yes = 4 No = 0 ____
• Muscle pains (especially calf muscles)? Yes = 4 No = 0 ____
• Are all three features (red eyes, muscle pains and meningism)
present together? Yes = 10 No = 0 ____
• Jaundice? Yes = 1 No = 0 ____
• Albuminuria or nitrogen retention? Yes = 2 No = 0 ____
Total Score for Part A _____

B. Epidemiological factors:
• Has there been contact with animals at home, work, leisure, or
in travel, or contact with known (or possibly) contaminated water? Yes = 10 No = 0 ____

C. Bacteriological laboratory findings:

• Isolation of leptospires in culture—diagnosis certain.

• Positive serology—leptospirosis endemic:

Single positive, low titre (that is, < 200). Yes = 2 No = 0 ____
Single positive, high titre (that is, > 400). Yes = 10 No = 0 ____
Paired sera, rising titre ( ≥ 4 fold). Yes = 25 No = 0 ____

• Positive serology—leptospirosis not endemic:

Single positive, low titre (that is, < 200). Yes = 5 No = 0 ____
Single positive, high titre (tha is, > 400). Yes = 15 No = 0 ____
Paired sera, rising titre ( ≥ 4 fold). Yes = 25 No = 0 ____

Total ______________

Source: Courtesy of Dr Ben Adler, Microbiology Dept, Monash University

107
 L i s t e rio sis

Victorian Statutory • The immunosuppressed, alcoholics, diabetics, debili-

Re quirem en t tated and the elderly.

Group B notification.
Infection of healthy adults is usually transient with mild to
moderate flu-like symptoms, but in pregnant women,
Note
foetal infection through the placenta can result in abor-
Also isolation of L. monocytogenes from food is notifiable
tion, stillbirth or premature birth of severely affected
under the Health (Infectious Diseases) Regulations 1990.
babies (early-onset neonatal listeriosis).

Infectious Agent Late-onset neonatal listeriosis generally affects full-term

babies who are usually healthy at birth.
L. monocytogenes is a Gram positive bacterium belong-
ing to the genus Listeria.
The onset of symptoms in these babies occurs several
days to weeks after birth (a mean of 14 days has been
Of the seven recognised species, it is currently the only
reported), possibly as a result of infection acquired from
one implicated in human cases. Serotypes 1/2a, 1/2b
the mother’s genital tract during delivery or postnatally
and 4b account for the majority of human isolates
through cross-infection.
serotyped in the USA.

In non-pregnant cases, listeriosis can also be subacute

L. monocytogenes grows over a wide range of tempera-
or sudden in onset. Fever, severe headache, nausea and
tures, from 1˚C to 45˚C; hence, it has the unusual ability
vomiting can lead to prostration and shock.
to multiply and survive for long periods in refrigerated
foods.
The reported case fatality rate has been around 30 per
cent in both groups.
It has been found in a variety of foods, particularly raw
meat, dairy products (especially soft cheese), and
smallgoods. Public Health Significance and
O c c u r re n c e
The bacterium is relatively heat resistant, but will not
Listeriosis is an uncommon disease in humans. An
survive pasteurisation in milk at 72˚C for 15 seconds.
incidence of around four cases per million population has
been quoted in the UK, and a study by the Centers for
Clinical Features Disease Control in 1986 estimated an overall annual
Although focal infections (such as pneumonia, endocar- incidence in the USA of 7.1 cases per million population.
ditis, infected prosthetic joints and hepatitis) have been
described, listeriosis presents usually as an acute Although most human cases appear to be sporadic,
meningoencephalitis and/or septicaemia. three large outbreaks documented in the past decade
have clearly established L. monocytogenes to be a food-
The infection predominantly affects two main groups of borne pathogen.
people:
• Pregnant women, resulting in severe infection of their
foetuses or newborn babies.

109
 These three outbreaks in the Maritime Provinces (1981),
Massachusetts (1983) and Los Angeles County (1985)
involved a total of 232 cases. The overall case fatality
rate was 36 per cent.
The implicated foods were coleslaw, pasteurised milk
and Mexican-style soft cheese.
Method of Diagnosis
Culture of the organism from blood, CSF, placenta,
meconium and other sites of infection.
Reservoir
L. monocytogenes is widespread in the environment and
is commonly isolated from sewage, silage, sludge, birds,
wild and domestic animals.
It has caused infection in many animals and resulted in
abortion in sheep and cattle. The bacteria are commonly
isolated from poultry.
Thus, it is a common contaminant of raw food.
In humans, asymptomatic vaginal carriage occurs, and
faecal carriage of up to 5 per cent in the general popula-
tion has been reported.
The significance of these carriers in the epidemiology of
listeriosis is unknown.
Mode of Transmission
The main route of transmission is oral, through ingestion
of contaminated food.
Other routes include mother to foetus via the placenta or
at birth.
The infectious dose is unknown.
110
Incubation Period
Unknown and may be up to 90 days.
In pregnancy, the foetus is infected within a few days of
the mother’s illness.
Period of Communicability
Mothers of infected newborns may shed the infectious
agent in vaginal discharges and urine for seven to 10
days.
Susceptibility
Although healthy people can be infected, the disease
generally affects vulnerable groups in the community,
such as:
• Neonates.
• Elderly, diabetics, alcoholics.
• The immunosuppressed.
• Pregnant women, with their foetuses most affected.
Control of Case
Specific treatment with penicillin or ampicillin in combina-
tion with aminoglycosides.
In penicillin-sensitive patients, co-trimoxazole, tetracy-
cline and chloramphenicol may be effective.
Investigation Procedures
• Obtain medical history from attending doctor (physi-
cian, obstetrician, paediatrician).
• Obtain food history from patient.
• Test suspect food (especially inspect refrigerator) for
isolation of Listeria (send samples to MDU).
• Arrange for faecal examination of all members of the
family (including case).
• Assess the possibility of common source outbreaks if
there is a cluster of cases.
Control of Contacts/ • Utilising a multidisciplinary approach to the investiga-
tion of cases.
En v i ro n m e n t
The significance of vaginal and faecal carriers is un-
New regulations for the control of Listeria approved by
known.
the National Food Standards Council became effective
from September 1994. These regulations require that
When implicated, food is to be withdrawn from sale.
pâté, soft cheese, smoked fish and smoked seafood
have zero Listeria at the point of wholesale distribution.
Preventive Measures
A surveillance program should be estblished to monitor: Epidemic Measures
• The epidemiological aspects of the disease.
• Epidemiological investigation of cases should be used
• The presence of Listeria in food and its public health
to detect outbreaks and to determine source.
importance.
• Molecular subtyping should be used to determine the
association between isolates from cases and food
This is achieved through notification and surveys of at-
samples.
risk foods.
• If a common source is detected, implicated food
should be withdrawn from sale.
Dairy products should be withheld from sale should
Listeria be isolated.

The Australian Manual for Control of Listeria in the Dairy

Industry issued by the Chief Dairy Officers Committee,
sets out procedures designed to:
• Prevent Listeria contamination in the processing plant,
hence in milk and milk products.
• Facilitate clearance of product for sale should Listeria
be found in either the dairy product or in the environ-
ment of the plant.

The presence of L. monocytogenes in other food is

currently being monitored.

Other procedures of importance are:

• Developing a code of hygienic practice to prevent, limit
and (where possible) eliminate the presence of the
bacteria in processed food.
• Educating pregnant women and the
immunosuppressed about the foods likely to be
contaminated, and the importance of reheating food to
a core temperature of at least 70˚C. Reheating in a
microwave oven may be inadequate for this purpose.

111
 Malaria
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agent
The malarial parasite, Plasmodium spp.
Four species can infect humans: P. vivax, P. ovale, P.
malariae and P. falciparum.
Infection is most commonly caused by P. vivax and/or P.
falciparum.
Mixed infections may occur in endemic areas.
Clinical Features
The features include indefinite malaise and slowly rising
fever of several days duration. This is followed by shak-
ing chills and rapidly rising temperature, that ends with
profuse sweating.
The fever is usually accompanied by headache and
nausea.
While, classically, fever due to malaria may occur every
second or third day, in practice, the fever may have no
specific pattern.
Falciparum malaria (malignant tertian) may present a
varied clinical picture with an atypical onset including
diarrhoea.
The above features may progress to jaundice, coagula-
tion defects, shock, renal and hepatic failure, acute
encephalopathy, pulmonary and cerebral oedema, coma
and death.
Every year, Australians die of falciparum malaria when
diagnosis or treatment has been delayed. Any person
returning from an endemic area who develops a fever
should be promptly investigated.
Individuals who are partially immune or have been taking
anti-malarial chemoprophylaxis may show an atypical
clinical picture with wide variations in incubation period.
Most antibiotics also can modify the course of malaria.
Malaria due to species other than P. falciparum is
generally not life threatening except in the very young,
very old, and those with immunodeficiency or other
concurrent disease.
Public Health Significance and
O c c u r re n c e
The malaria situation worldwide is deteriorating. There
are increasing levels of transmission, and it has returned
to areas where it had been previously eradicated. Drug
resistance has increased and there has been a spread of
resistance of the vector to insecticides.
There are said to be over 220 million new infections a
year worldwide, and the disease is endemic in areas of
Asia, Africa and Central and South America.
Australia was certified by WHO as being free of endemic
malaria in 1981, but several hundred imported cases are
recorded each year. However, the region lying north of a
line joining Townsville on the east coast and Port
Hedland on the west remains receptive and vulnerable to
the re-establishment of the disease due to the presence
of known or suspected vectors, suitable environmental
conditions, and the continual arrival of malaria-infected
travellers.
Many cases occur among migrants returning to their
native country for holidays after many years, when they
may have lost their immunity.
A large percentage of Australian cases originate in
Papua New Guinea.
113
 Method of Diagnosis reach the lumen of these glands that communicates with
the salivary ducts and are then passed into a skin wound
Malaria can be diagnosed by demonstration of malaria
in the salivary fluid when the insect next bites a human.
parasites in blood films. Blood samples should be sent to
a laboratory with experience in the diagnosis of malaria
The cycle in the mosquito takes eight to 35 days, de-
by the use of thick and thin films. Repeated examination
pending on the species and the temperature.
may be necessary due to variations in density of para-
sites.
In the human host, the period between the infective bite
and the appearance of parasites in the blood is called
Confirmation of the species should be sought from a
the pre-patent period. This period varies from six to nine
reference laboratory.
days for P. falciparum, P. vivax and P. ovale, and 12 to
16 days for P. malariae.
Reservoir
Humans are the only important reservoir of human Malaria can also be transmitted by transfusion of blood
malaria, although other Plasmodium species may natu- of infected persons, or by using contaminated needles or
rally infect non-human primates. syringes.

Congenital transmission occurs rarely.

Mode of Transmission
Malaria is transmitted by the bite of an infective female
anopheles mosquito, most species of which feed at dusk
Incubation Period
or in the early night hours. The time between the infective bite and the appearance
of symptoms is approximately 12 days for P. falciparum,
On introduction into the body, the young parasites 14 days for P. vivax and P. ovale and 30 days for P.
(sporozoites) circulate in the blood for less than one hour malariae.
and then invade liver cells where they multiply.
Occasionally there can be a protracted incubation
After this liver stage, the parasites again enter the period, especially with strains from temperate regions.
bloodstream where they invade red cells and multiply by
asexual reproduction to produce merozoites that rupture
Period of Communicability
the cell and invade further red cells.
For infection of mosquitoes, it is communicable for as
long as infective gametocytes remain in the blood.
Some merozoites do not multiply in the red cell but
become the male and female gametocytes that multiply
Gametocytes usually appear within three days of parasi-
by sexual reproduction when taken up by the insect
taemia with P. vivax and P. ovale, and after 12 to 14 days
vector.
with P. falciparum.

In the mosquito, the male and female gametes fuse to

Untreated or inadequately treated patients may be a
form an oocyst within which sporozoites develop. These
source of mosquito infection for more than three years
are set free in the insect’s haemocoele, then carried to all
with P. malariae, one to two years with P. vivax, and
parts of its body including the salivary glands. They
generally not more than one year with P. falciparum.

114
Infected mosquitoes remain infective for life.
Transmission by transfusion may occur as long as
asexual forms remain in the circulating blood; with P.
malariae, this can continue for over 40 years.
Stored blood can remain infective for 16 days.
Susceptibility and Resistance
With P. vivax and P. ovale infections, parasites can
remain dormant in liver cells and mature months later to
produce true relapses, and this can occur for up to two
and five years respectively.
With P. malariae infections, low levels of erythrocytic
forms can persist for many years to multiply at some
future time and produce disease.
Control of Case
Prompt and adequate treatment is required for the
prevention of complications and relapses.
The drugs used in treatment include chloroquine, pri-
maquine, quinine, doxycycline, Fansidar and mefloquine.
For complete details, please see the annual publication
International Travel and Health from WHO, available from
Hunter Publications, or Antibiotic Guidelines published
by the Victorian Postgraduate Medical Foundation.
Isolation of the patient is not required, but blood precau-
tions should be taken. Concurrent or terminal disinfection
is not required.
Control of Contacts
The diagnosis of malaria in travelling companions should
be considered.
In transfusion-induced malaria, all donors must be
located and their blood tested for malaria parasites and
anti-malarial antibodies.
If a history of needle sharing is obtained from a malaria
patient, all persons who shared the equipment should be
investigated and treated.
Preventive Measures
Advice to travellers intending to visit malarial areas of the
world should include both self-protection measures
against mosquito bites and the use of chemoprophylaxis.
Over-reliance on either measure, particularly chemopro-
phylactic drugs, is ill-advised (drug resistance by the
malaria parasite continues to change and travellers may
not always take the recommended drug/s as directed).
There is no drug that is completely safe and completely
effective for prophylaxis against malaria. The decision to
recommend chemoprophylaxis and the choice of drug/s
must involve an analysis of the risks and benefits based
on the following considerations:
• Prevalence and type of resistance to the available
drugs.
• Level of malaria transmission.
• Duration and place of stay, particularly in rural areas.
• Intensity of vector mosquito contact.
• Availability of adequate health care.
• Age.
• Traveller’s current health and medical history.
• Risk of traveller not complying with recommendations.
Travellers should be advised of the symptoms of malaria
and warned to seek medical attention as soon as possi-
ble if they occur.
115
 Malaria poses a serious threat to pregnant women as it International Measures
can compromise foetal development, possibly resulting
Aircraft, ships and other vehicles should be sprayed with
in premature labour or miscarriage.
insecticides on arrival if there is reason to suspect
importation of malaria vectors.
Pregnant women should be advised to avoid travel to
malarious areas if possible.
Anti-mosquito sanitation should take place within the
mosquito flight range of all ports and airports.
Similarly, malaria presents considerable risks for chil-
dren, particularly the very young, and the choice of
WHO should be notified by national health administra-
suitable drugs is limited. Mosquito avoidance measures
tions of details of cases twice yearly for the WHO Malarial
should be emphasised.
Surveillance Program.

Self-protection measures include:

• Avoiding outdoor exposure between dusk and dawn.
• Wearing long, loose clothing after dusk, preferably in
light colours.
• Avoiding perfumes and colognes.
• Using effective insect repellents; for example, products
containing up to 20 per cent DEET.
• Using knock-down sprays, mosquito coils, or plug-in
vaporising devices indoors.
• Using mosquito nets.

Chemoprophylaxis
Drugs used for this purpose include chloroquine,
mefloquine and doxycycline.

See table provided and obtain further details from the

publication Health Information for International Travel
issued by the Commonwealth Department of Health and
Family Services.

Patients should be warned that if they develop any signs

of fever or other illness while travelling or after their return
to Australia in spite of having had chemoprophylaxis,
they should seek prompt medical attention.

116
 Information Sheet
Malaria

Malaria Prophylaxis Multi-Drug Resistant Areas

• Travellers should be advised of the appropriate type of (includes resistance to
prophylaxis for the area which they wish to visit. m e fl o q u i n e )
• Many areas are now chloroquine resistant.
Forests and rural areas in Cambodia, Myanmar (Burma),
• The only drugs recommended are chloroquine (when
Thailand, Vietnam, Laos.
appropriate), doxycycline and mefloquine. Chloroquine
should be started two weeks before, mefloquine one
week before, and doxycycline two days before entering Short stay (less than 8 weeks):
the malarious area. All must be continued for up to four – Doxycycline (100 mg/day).
weeks after leaving the area.
Long stay (more than 8 weeks):
• Special precautions should be taken for pregnant
– Chloroquine (300 mg/week) and doxycycline (50 mg/day).
women and children. (see publications listed).
or
• Whatever drugs are prescribed, personal protection
– Chloroquine (300 mg/week) with mefloquine carried
measures against mosquitoes should also be advised.
for presumptive self-treatment.
• Travellers should be advised of the symptoms of
malaria and warned that they should seek medical
attention as soon as possible if they occur.
Chloroquine-Sensitive Areas
Short and long stay:
Chloroquine-Resistant Areas – Chloroquine (300 mg/week).
• A major part of Africa and the Kruger National Park.
• Papua New Guinea, Solomon Islands, Vanuatu.
Proguanil is now available in Australia, although not yet
• India, parts of Indonesia, Malaysia, Nepal, Pakistan,
recommended by the NH&MRC. It is effective against
Philippines and parts of Sri Lanka.
Pl.falciparum, can be given to children and has been
• Iran and parts of Saudi Arabia.
used by pregnant women.
• Central and South America including Bolivia, Brazil
(Amazon Basin).
Combined with chloroquine, the dose for adults is:
– Chloroquine 300 mg/week (2 tablets).
Malaria Prophylaxis
– Proguanil 200 mg/day (2 tablets).
Short stay (less than 8 weeks):
– Doxycycline (100 mg/day). For children, the dose of proguanil is 3.5 mg/kg body
or weight daily.
– Mefloquine (250 mg/week).
Chloroquine for children:
Long stay (more than 8 weeks):
– 1 to 4 years1/2 tablet per week.
– Chloroquine (300 mg/week) and Doxycycline (50 mg/day).
– 4 to 8 years1 tablet per week.
or
– > 8 years adult dose.
– Chloroquine (300 mg/week) with Mefloquine carried
for presumptive self-treatment.

117
 Further Information
• For up-to-date recorded advice, telephone the Interna-
tional Travel Health Info Line on (06) 269 7815.
• The following publications:
– Health Information for International Travel, 1995,
fourth edition, Australian Government Publishing
Service, Canberra.
– International Travel and Health, Vaccination Require-
ments and Health Advice, World Health Organisa-
tion, Geneva. (published annually).
• Any travel health clinic. The address of the nearest
clinic may be obtained by ringing Infectious Diseases
Unit (03) 9616 7777.

118
 Measles

Victorian Statutory • A fourfold or greater change in measles antibody titre

between acute and convalescent-phase sera, obtained
Re quirem ent
at least two weeks apart, with the tests preferably
Group A notification.
conducted at the same laboratory.
or
School exclusion.
• Isolation of measles virus from a clinical specimen.
or
lnfectious Agent • A clinically compatible case epidemiologically related
to another case.
Measles virus (morbillivirus).

Clinical Features Public Health Significance and

Clinical features include prodromal fever, conjunctivitis,
coryza, cough and Koplik’s spots on the buccal mucosa.
The characteristic red, blotchy rash appears on the third
to seventh day. It begins on the face before becoming
generalised. It generally lasts four to seven days.
O c c u r re n c e
It was once a common, acute highly communicable
disease with potentially serious sequelae. It is much rarer
since the introduction of widespread immunisation, but
epidemics are still occurring, especially in school-aged
children.

Complications can include otitis media, pneumonia and Death is rare but does occur.
encephalitis.

Method of Diagnosis
Subacute sclerosing panencephalitis (SSPE) develops
See Case Definition.
very rarely as a late sequel.

Persons who have been previously immunised may Reservoir

present with non-classical features.
Humans.

Case Definition Mode of Transmission

It is defined as an illness characterised by all the follow-
Its transmission is airborne by droplet spread, or it is
ing features:
transmitted by direct contact with infected nasal or throat
• A generalised maculopapular rash lasting three or
secretions.
more days.
• A fever (at least 38˚C if measured).
• Cough or coryza or conjunctivitis or Koplik’s spots. Incubation Period
or Incubation period is approximately 10 days, but varies
• Demonstration of measles-specific IgM antibody. from seven to 10 days from exposure to the onset of
or fever. It is usually 14 days until the rash appears.

119
 Period of Communicability
From slightly before the beginning of the prodromal
period to four days after the appearance of the rash.
Susceptibility and Resistance
Vaccination at 12 months produces antibody in approxi-
mately 95 per cent of recipients. It is not yet clear
whether vaccine-induced immunity is lost over time, but
the majority of evidence suggests that this is uncommon.
Control of Case
School exclusion for at least five days from the appear-
ance of the rash, or until receipt of a medical certificate
of recovery from infection.
Control of Contacts
Household and other general contacts should be
checked for documentation of measles immunisation. If
non-immune, immunisation should be given within 72
hours of contact.
Persons born before 1970 are generally regarded as
immune as they would have contracted measles in
childhood.
Children aged between six to 12 months should be given
a measles-containing vaccine, but should be
revaccinated at 12 months or three months after the last
dose, whichever is later. It is also acceptable to give
normal immunoglobulin to children in this age group in a
dose of 0.2 ml/kg then to vaccinate them at 12 months
(or three months after the administration of immuno-
globulin).
In school, immunisation status of close contacts should
be checked. This refers to classroom contacts of the
child, not the whole school.
120
Classroom contacts without a valid school entry immuni-
sation certificate must be excluded for 13 days from the
first appearance of rash in the last occurring case,
unless they are immunised within 72 hours of first con-
tact.
Preventive Measures
Live attenuated measles vaccine is recommended for all
persons born after 1970 unless specific contraindications
to live vaccines exist.
It is recommended to be given as measles-mumps-
rubella (MMR) vaccine at 12 months and at 10–16 years
(or Year 6 in Victoria).
Epidemic Measures
A measles outbreak exists whenever one case of mea-
sles is confirmed.
The diagnosis should establish that the disease is
actually measles (see clinical or laboratory case
definition).
Nasopharyngeal aspirates may be collected and rapidly
transported to Royal Childrens Hospital or VIDRL for
immunofluorescent identification of measles antigen. This
is a rapid method of virus identification. The specimen is
then cultured for virus.
Alternatively, a blood sample (10 ml in a plain tube)
should be collected immediately after the child presents
with the rash, and sent to VIDRL to look for measles-
specific IgM.
A second specimen 10 days later is useful if the IgM
result is equivocal.
For school-based outbreaks: class levels involved should
be revaccinated, for all children who do not have docu-
mented evidence of two doses of measles-containing
vaccine.

For outbreaks involving preschool-aged children:

• Children aged six to 12 months: These children can be
offered MMR vaccine, which may prevent measles
occurring if given within 72 hours of contact. If these
children are immunised, they should be given another
dose of MMR at 12 months of age or three months after
the first dose, whichever is later. These children do not
need to be excluded from the centre if the parents do
not wish them to be immunised yet.
• Children aged from birth to six months: These children
can be offered immunoglobulin (an injection of anti-
bodies from blood donors), which may prevent mea-
sles if given within six days of contact. These children
do not need to be excluded if the parents do not wish
them to have immunoglobulin.

121
 Meningococcal Infections
Victorian Statutory
Re quirem ent
Group A notification.
School exclusion of household contacts.
Infectious Agent
Neisseria meningitidis (the meningococcus) is a Gram
negative diplococcus.
Several serogroups have been recognised: Groups A, B,
C, 29E, H, I, K, L, W135, X, Y and Z.
Within these groups, certain serotypes have been
identified; for example, Group B serotypes 2b and 15.
In Victoria at present, Groups B and C organisms are the
most common.
Clinical Features
Clinical features include an acute onset of meningitis
and/or septicaemia, the typical features of which are
fever, intense headache, nausea, vomiting and neck
stiffness.
There may be a petechial or purpuric rash on the trunk
and limbs that may sometimes cover large areas of the
body.
In fulminating cases, there is sudden prostration and
shock associated with the characteristic rash and this
condition has a high fatality rate.
Chronic meningococcal septicaemia can also occur with
febrile episodes, skin rashes and fleeting joint pains.
Public Health Significance and
O c c u r re n c e
In the absence of prompt diagnosis and appropriate
treatment, acute meningococcal infections have a high
case fatality rate, especially in children.
They occur in all areas of the world with a high incidence
in certain endemic regions such as the sub-Saharan
region of mid-Africa (predominantly Group A organisms).
Epidemics of Groups A, B or C disease have occurred in
different countries and, in Australia, Group A outbreaks
have occurred among Aboriginal communities in central
Australia.
Most cases occur in winter and spring, and the infection
is more common in children under five years. In young
adults outbreaks typically occur in crowded living
conditions, such as in military barracks and institutions.
The worldwide incidence of meningococcal infections
has been rising in recent years. In Victoria 63 cases were
notified in 1993, 59 in 1994 and 75 in 1995.
Method of Diagnosis
Diagnosis is usually made on clinical grounds confirmed
by laboratory tests. These are:
• A presumptive diagnosis is made following Gram stain
of cerebro-spinal fluid or of material obtained by
needling an area of rash.
• Blood and CSF culture.
If treatment has been given before a blood or CSF
sample is taken, a throat swab should be done.
Although serogrouping may be performed in some
hospital laboratories, meningococcal isolates from all
cases of invasive disease should be sent to MDU, The
University of Melbourne, to ensure appropriate monitor-
ing of serogroups and to perform susceptibility testing.
123
 Detection of meningococcal antigen in CSF and/or serum
can be obtained by techniques such as counter-current
immuno-electrophoresis (CIE). This is particularly useful
in partially treated cases where both smear and culture
may be negative.
Reservoir
Humans. Asymptomatic naso-pharyngeal carriers of the
organism can spread infection, but there is no consistent
relationship between the carrier rate in a given commu-
nity and the incidence of disease.
Carrier rates of up to 25 per cent or more may exist
without cases of meningitis.
Mode of Transmission
Transmission can occur through direct contact including
airborne droplets from nose and throat of infected
persons.
Transmission by fomites is insignificant.
Incubation Period
It is commonly three to four days, but can vary from two
to 10 days.
Period of Communicability
It is communicable until the organisms are no longer
present in discharges from the nose and mouth.
Susceptibility and Resistance
Susceptibility to clinical disease is low as evidenced by
the usual high ratio of carriers to cases.
Susceptibility decreases with age. However, a secondary
peak of meningococcal meningitis occurs in adolescents
and young adults in the age group of 15 to 24 years.
124
Patients deficient in certain complement components in
the blood are prone to recurrent meningococcal infec-
tions.
There is an increased and prolonged risk of secondary
infections in close contacts. In one series, the incidence
of such infection was 0.5 per cent with a median interval
of seven weeks between the index and secondary cases.
Secondary cases have been reported up to five months
later. The risk in household contacts is 500 to 800 times
higher than in the general population.
Control of Case and the
En v i r o n m e n t
Prompt treatment with parenteral penicillin in adequate
doses should begin when a presumptive clinical diagno-
sis is made prior to laboratory confirmation.
In cases with a very acute onset, such treatment should
commence prior to transfer of the patient to hospital,
even though there may be some interference with
laboratory confirmation by culture. Suitable alternatives
for patients who are allergic to penicillin include
ceftriaxone, cefotaxime or chloramphenicol.
Respiratory isolation is recommended for 24 hours after
commencing treatment. There should be concurrent
disinfection of discharges from nose or throat and
articles soiled with such discharges. Articles used by the
patient should be terminally cleaned.
Since penicillin only temporarily suppresses but does not
eradicate the organisms in the nasopharynx, all patients
should be treated with a drug such as rifampicin prior to
discharge from hospital (for dosage, see below).
If ceftriaxone is used in treatment, rifampicin need not be
given.
Contacts
All household and other contacts should be placed
under close surveillance for the earliest signs of infection
(such as fever, headache, nausea/vomiting or rash), so
that prompt treatment can be instituted. A surveillance
letter should be provided as soon as possible to the
parents of all children in a class, school or day care
centre where a case has occurred.
Household contacts must be excluded from school or
child care until they have received appropriate chemo-
therapy for at least 48 hours.
Antibiotic Prophylaxis
All family and household contacts and other close
contacts should be offered antibiotic prophylaxis. Close
contacts include those who have shared sleeping
quarters or eating utensils, sexual contacts in older
patients, and those who have kissed the patient in the 10
days prior to onset of illness.
In a school class, only the patient’s close friends would
require antibiotic treatment. However in a day care
centre, because of the high risk in young children,
everybody (including staff) should be offered antibiotic
treatment unless groups of children are kept quite
separate, in which case only children in the patient’s
group need treatment.
Special circumstances may justify wider use of antibiotic
prophylaxis, such as attendance of the index case in the
10 days before onset at a party where young children
and teenagers were present.
Health care personnel do not usually require antibiotic
treatment except where intimate contact (such as mouth-
to-mouth resuscitation) has occurred.
When indicated, chemoprophylaxis should be instituted
as soon as possible, preferably within 24 to 48 hours of
diagnosis of the index case.
Note
Antibiotic prophylaxis does not eliminate the need for
close surveillance of contacts.
Selection of Antibiotic for
Pr o p h y l a x i s
Rifampicin is the drug of choice. It is given in a dose of:
• An adult: 600 mg.
• A child over one month old: 10 mg/kg.
• A child less tha one month old: 5.0 mg/kg.
This dose is given twice daily for two days in all cases.
Rifampicin may cause a red-orange colouration of urine,
faeces, saliva, sputum, sweat and tears, and may cause
permanent staining of soft contact lenses.
Itching, rashes and gastro-intestinal reactions may
occur. It should be used with caution in patients with liver
damage, and is contraindicated in pregnant or lactating
women. Patients on oral contraceptives should be
advised to use other contraceptive methods during
treatment with this drug and for the remainder of the
cycle.
Patients receiving anticoagulants may need to increase
their prescribed dose.
Alternatives to rifampicin include:
• Ceftriaxone. 5.0 mg/kg to a maximum of 250 mg IM as
a single dose (safe in pregnancy), reduce to 125 mg in
children under 15 years of age.
• Ciprofloxacin. 500 mg orally as a single dose. It should
not be prescribed to children under 12 years of age or
40 kg body weight, or to pregnant women.
125
 Note Preventive Measures
Antibiotic prophylaxis of family and household contacts
A quadrivalent vaccine is available in Australia against
is the responsibility of the treating hospital while the
Groups A, C, Y and W135. Group C vaccine does not
Department of Human Services will take responsibility for
induce a reliable antibody response under two years of
follow-up of other contacts. Rifampicin supplies are
age, but Group A vaccine can elicit a response in
available through the Public Health nurses or through the
children as young as three months.
Department. Written consent should be obtained prior to
administration of any antibiotic prophylaxis to children.
However, in children aged three months to two years,
two doses are given three months apart instead of a
Throat or Nasopharyngeal single dose as in older children and adults. The vaccine
provides effective immunity one to two weeks after
Swabs
administration which lasts for more than one year (though
Obtaining such swabs prior to chemoprophylaxis is
the duration of protection is limited in young children).
unnecessary, of no value in control and therefore not
routinely recommended. They may be of some value
It is recommended for travellers to epidemic and highly
during epidemics to estimate the prevalence of carriage
endemic areas such as Brazil, Mongolia, Vietnam, India,
of the causative strain.
Nepal and sub-Saharan Africa and is a requirement for
visits to Mecca. There is, at present, no effective vaccine
Routine post-prophylaxis swabs are also not cost-
against Group B available.
effective as rifampicin is effective in eliminating carrier
status in 90 to 95 per cent of patients.
Epidemic Measures
The major emphasis is on surveillance and early detec-
Investigative Procedures
tion of cases.
• Determine if household and other close contacts have
been offered chemoprophylaxis by the treating doctor.
Individuals should be separated and living and sleeping
Ensure that this is done.
quarters of those in crowded conditions ventilated.
• Determine if there is a school, kindergarten, child care
centre, baby sitter and so on involved, and ensure that
Rifampicin is not recommended for mass prophylaxis
all close contacts in such situations are offered chemo-
because of the danger of producing drug-resistant
prophylaxis.
strains.
• Ensure that surveillance letters are distributed to all
close contacts or their parents.
If the epidemic is due to Groups A or C, vaccination of
persons in a given area should be considered.

126
 Information Sheet
Meningococcal Septicaemia/Meningitis

A case of meningococcal infection has occurred in a

child at this school/creche/child minding centre/kinder-
garten.

This disease generally spreads to close intimate and

household contacts and can progress very quickly.

The indications of this illness to look for are fever, rash,

intense headache, nausea and often vomiting. Serious
signs include drowsiness, neck stiffness, delirium, coma
and sudden collapse. Even the earliest sign (that is,
fever), in such contacts warrants immediate medical
attention from your local doctor or the nearest hospital.

Please take this letter with you.

The most important period in which to look for these

signs is up to 10 days from the last date of contact with
the patient.

If you need any further information, please telephone:

Public Health Nurse or Medical Officer, Infectious
Disease Unit: (03) 9616 7777.

127
 Meningoencephalitis (Primary Amoebic)
Victorian Statutory
Re quirem ent
Group A notification.
Infectious Agent
Naegleria fowleri, Acanthamoeba culbertsoni and other
species of Acanthamoeba, Balamuthia mandrillaris.
Clinical Features
It is a serious disease of brain and meninges.
Naegleria spp enter the brain via the nasal mucosa and
olfactory nerve and causes a syndrome of fulminating
pyogenic meningoencephalitis with sore throat, severe
headache, neck stiffness and death within 10 days,
usually on the fifth or sixth day.
Acanthamoeba spp invade through skin lesions and
spread to the brain and meninges causing insidious and
prolonged disease. Balamuthia spp appears to behave
similarly and prolonged skin lesions may be present.
Public Health Significance and
Oc c u r re n c e
It is a rare disease with a high case fatality rate.
Infection with N. fowleri occurs mainly in young people
as opposed to infection with Acanthamoeba spp that
attacks the chronically ill or immunosuppressed.
Meningoencephalitis due to N. fowleri has been reported
from the USA, Europe, Australia, New Zealand. PNG,
Thailand, India, West Africa, Venezuela and Panama.
Cases caused by Acanthamoeba spp have been re-
ported from Africa, India, Korea, Japan, Peru, Venezuela,
Panama and the USA.
Two cases notified in Victoria in 1992 and one in 1996
were caused by a free-living amoeba hitherto regarded
as an innocuous soil organism incapable of infecting
mammals. This is the Balamuthia mandrillaris. It is a rare
cause of meningoencephalitis.
Method of Diagnosis
It can be diagnosed by:
• Microscopic examination of fresh CSF.
• Culture on non-nutrient agar plates spread with bacte-
ria (for example, E. coli).
• Culture on cell cultures of monkey kidney (Balamuthia
spp).
Reservoir
The amoebae are free-living in water, soil and vegetation.
Mode of Transmission
Naegleria fowleri: By diving, jumping into, or underwater
swimming in warm, fresh water, stagnant ponds or lakes,
or inadequately maintained public heated swimming
pools, when water is forced into the nose.
Acanthamoeba culbertsoni: Haematogenous spread
from the site of primary colonisation (for example,
damaged skin mainly in chronically ill or
immunosuppressed patients) with unknown source of
infection.
Incubation Period
Usually three to seven days for N. fowleri; longer for
Acanthamoeba spp.
Period of Communicability
There is no person-to-person transmission.
129
 Control of Case
No isolation, concurrent disinfection or quarantine is
necessary.

Tre a t m e n t
Amphotericin B, miconazole and rifampicin. Recovery
from infection is rare.

Control of Contacts
Investigation of contacts and source of infection should
take place.

Preventive Measures
• Educate the public on the danger of swimming in lakes
and ponds where the infection has been acquired.
• Maintain a residual chlorine of 1 to 2 ppm in swimming
pools.
• Chlorinate public water supplies that are naturally
warm.

Epidemic Measures
Any grouping of cases needs proper epidemiological
investigation.

130
 Mumps

Victorian Statutory Method of Diagnosis

Re quirem ent Mumps is usually diagnosed clinically.

Group B notification.
Serologic tests (CF, HAI, EIA) are useful in confirming the
School exclusion.
diagnosis.

Infectious Agent The virus can be isolated in duck embryo or cell cultures
Mumps virus (paramyxovirus). from saliva, blood, urine and CSF during the acute phase
of the disease.

Clinical Features
Reservoir
Mumps is an acute viral disease characterised by fever,
Humans.
swelling and tenderness of one or more salivary glands,
usually the parotid.
Mode of Transmission
Orchitis occurs in 20–30 per cent of postpubertal males, It is transmitted by droplet spread and by direct contact
and oophoritis in about 5 per cent of females. Involve- with saliva of an infected person.
ment of the CNS results in meningitis, encephalitis or
meningoencephalitis in up to 15 per cent of cases but
permanent sequelae are rare.
Incubation Period
Usually 12–25 days; commonly 18 days.

Nerve deafness is one of the most serious of the rare

complications (one in 500 hospitalised cases). Pancreati- Period of Communicability
tis, neuritis, arthritis, mastitis, nephritis, thyroiditis and It is communicable from six days before to nine days
pericarditis may also occur. after the onset of swelling of glands.

Public Health Significance and Maximum infectivity occurs 48 hours before onset of
illness.
Oc c u r re n c e
Occurrence is worldwide. Serologic studies show 85 per Inapparent infection can be communicable.
cent or more people have had mumps infection by adult
life.
Susceptibility and Resistance
Most infections in children less than two years of age are Immunity is lifelong and develops after inapparent and
subclinical. clinical infections.

Due to effective immunisation, the greatest risk of infec- Control of Case

tion has shifted to older children, adolescents and young
Exclusion from school, child care or workplace until nine
adults.
days after the onset of swelling.

No specific treatment.

131
 Control of Contacts
Isolation is unnecessary.
Susceptible contacts should be offered immunisation.

Preventive Measures
Live attenuated vaccine is available singly or combined
with rubella and measles.

It is recommended for all children at any age after 12

months, unless specific contraindications to live vaccines
exist.

Two doses of MMR vaccine are recommended: the first

at 12 months and the second at 10–16 years (or Year 6 in
Victoria).

Epidemic Measures
Susceptible persons should be immunised, especially
those at risk of exposure.

Those who are not certain of their immunity can be

vaccinated if no specific contraindications to live
vaccines exist.

132
 Mycobacterial Infections
Tubercu l o si s
Victorian Statutory
Re quirem en t
Group B notification.
School exclusion.
Infectious Agent
Mycobacterium tuberculosis (human tuberculosis).
Mycobacterium bovis (cattle tuberculosis).
Clinical Features
Tuberculosis (TB) is an acute or chronic infection caused
by the tubercle bacillus, Mycobacterium tuberculosis
and, rarely, by Mycobacterium bovis.
The initial infection usually goes unnoticed with lesions
healing and leaving no residual changes except pulmo-
nary or tracheo-bronchial lymph node calcifications.
The infection may, however, progress to pulmonary
tuberculosis or, through blood or lymphatic spread,
produce miliary, meningeal or other extrapulmonary
involvement.
Common symptoms include:
• A chronic cough, especially with haemoptysis.
• Fevers and night sweats.
• Loss of weight.
• Feeling generally unwell.
Public Health Significance and
Oc c u r re n c e
Tuberculosis occurs worldwide and had been decreas-
ing steadily over past decades in developed countries.
This pattern, however, has been reversed with the arrival
of HIV and increased mobility of the world’s population.
In the USA, TB is on the increase. A combination of
factors is thought to be responsible for this increase,
including the high rate of HIV infection, overcrowding,
limited health care resources and falling living standards.
In the USA, large outbreaks of TB have occurred in
institutions, particularly prisons and hospitals. These
outbreaks have predominantly affected HIV-infected
persons.
WHO estimated that a third of the world’s population is
infected and, globally, tuberculosis accounts for three
million deaths annually, with one-fifth of all deaths in
adults in developing countries related to TB. Two-thirds
of the world’s tuberculosis-infected people reside in Asia
and this will have a significant impact on the control of
TB in Australia as a result of increased immigration.
In Victoria, notified cases of TB have dropped dramati-
cally, from 1,000 cases in 1954 to 336 in 1994. However,
the incidence rate increased from 5.9 per 100,000 in
1992 to 7.5 per 100,000 in 1994. The proportion of
notified cases in the overseas-born has also increased
from 37 per cent in 1970 to 75.8 per cent in 1994. The
highest country-specific incidence rates are in the
Vietnamese, Cambodian, Filipino and Chinese-born
populations. This reflects the pattern of disease in their
countries of birth.
Of the overseas-born patients, almost 50 per cent
presented within five years and 30 per cent within two
years of their arrival in Australia.
Method of Diagnosis
TB can be diagnosed by:
• Clinical presentation.
• Tuberculin skin test, using the Mantoux procedure.
• Radiographic examination sometimes including CT
scans.
• Bacteriology, direct staining and culture of sputum or
other specimens for the presence of M. tuberculosis.
Definitive diagnosis of TB rests on isolation of M. tuber-
culosis (or M. bovis) from sputum, urine, biopsy material,
CSF or other clinical specimens. A negative sputum,
however, does not rule out a diagnosis of TB.
133
 Recovery and identification of mycobacteria from speci-
mens has been made more rapid with test procedures
such as the Bactec Systems and DNA probes. Further
information on these tests can be obtained from the
Mycobacterium Reference Laboratory, VIDRL.
Reservoir
Primarily humans; rarely diseased cattle.
Mode of Transmission
TB is transmitted mainly by inhalation of infectious
droplets produced by persons with pulmonary or laryn-
geal tuberculosis during coughing, laughing, shouting or
sneezing.
Invasion may occur through mucous membranes or
damaged skin.
Extrapulmonary tuberculosis, other than laryngeal, is
generally not communicable.
Urine is infectious in cases of renal tuberculosis.
Bovine tuberculosis results mainly from ingestion of
unpasteurised milk and dairy products.
Aerosol transmission has been reported among abattoir
workers.
Incubation Period
From infection to the primary lesion or significant tuber-
culin reaction: about four to 12 weeks.
Period of Communicability
In theory, the patient is infectious as long as viable bacilli
are being discharged from the sputum.
134
In practice, the greatest risk of transmitting infection is in
the period prior to diagnosis of an open case; a sputum
smear positive case is more infectious than a case only
positive on culture.
The risk of transmitting the infection is significantly
reduced within days to two weeks after commencing
appropriate chemotherapy.
Susceptibility and Resistance
Clinical suspicion of active disease should be high in
those who have a newly positive tuberculin reaction,
juveniles with positive tuberculin reactions, and those
with a history of inadequately treated active tuberculosis.
Positive tuberculin reactors with inactive tuberculosis on
chest X-ray without a previous diagnosis of active
tuberculosis remain at some risk.
The risk of developing the disease is highest in children
under three years of age, lowest in later childhood, but
rises again for adolescents, young adults and the very
old.
Special groups at risk:
• Recent immigrants and refugees from countries with a
high incidence of tuberculosis. These countries include
Vietnam, Cambodia, China and the Philippines.
• Aboriginal people and Torres Strait Islanders.
• Drug- and alcohol-dependent people.
• The elderly.
• Institutionalised persons including prisoners.
• The socially disadvantaged.
• Those with HIV infection and AIDS.
• Immunosuppressed patients.
• Health professionals.
• Diabetics.
• Those in close contact with a case of active TB.
Of all these groups, the highest risk of active TB is in
patients with AIDS.
Control of Case
Tre a t m e n t
Adequate anti-TB chemotherapy for an appropriate
period of time will result in almost 100 per cent cure rate.
There is, however, a potential risk of MDRTB in Victoria
as most of the patients notified each year are foreign-
born and developing countries have high rates of drug
resistance.

Short treatment regimes have been in use for some Control of Contacts
years. These involve the use initially of three or four Contact tracing and surveillance is the responsibility of
drugs (isoniazid, rifampicin, pyrazinamide and ethambu- the Department and is managed by the TB Program.
tol) for two months, and continuing with isoniazid and Anyone identified by health care workers as a contact of
rifampicin for a further four months. a case of TB should be referred to the TB Program on
(03) 9616 7777.
Where there is evidence of drug resistance to INH or
rifampicin or to both, short course anti-TB chemotherapy Contact investigation consists of:
would be inappropriate. • History taking.
• Tuberculin testing.
With the introduction of potent anti-TB drugs, hospitalisa- • Radiographic examination.
tion of tuberculous patients is no longer mandatory
unless social conditions or coexisting medical conditions The extent of investigation is governed by the character-
dictate otherwise. istics of the source case.

The success of treatment relies heavily on patient The scope of investigation is extended when the follow-
compliance and direct supervision should be the aim of ing factors in the source case are present:
any treatment program. • AFB in sputum smear.
• Cavitation on chest X-ray.
Compliance is important to prevent the development of • Laryngeal TB.
drug resistance. • Cough.
• High volume and reduced viscosity of respiratory
For drugs used in treatment of tuberculosis, see TB in secretions.
Australia and New Zealand into the 1990s, Australian • Where there is evidence of tuberculin conversion in
Government Publishing Services, Canberra. Telephone: any of the contacts.
(06) 289 7646, or fax (06) 289 6957.
Note
Multi-Drug Resistant TB (MDRTB) Tuberculosis testing should never be omitted for child

Resistance to at least isoniazid and rifampicin (whether contacts.

or not it is also resistant to other drugs) is classified as

multi-drug resistant.

MDRTB is rare in Australia. It has remained at less than 2

per cent per year in the past 15 years.

135
 Following tuberculin testing, contacts can be grouped See Management, Control and Prevention of
as: Tuberculosis,Guidelines for Health Care Providers
• Initial negative reactors: published by Human Services and available from Infor-
– Tuberculin conversion takes a few weeks and may mation Services, Human Services, telephone: (03) 9616
not have occurred yet in these contacts. 7333.
– Testing should be repeated in eight to 12 weeks after
a break of contact or in some cases, initial testing
may be delayed for eight weeks.
Preventive Measures
– Chest X-rays may be indicated. The public should be educated about the mode of
spread and methods of control and the importance of
Initial positive reactors: early diagnosis.
• Definition of a positive tuberculin reactor.
Chemoprophylaxis should be given to persons with a
Dimension of Induration
Conditions (greater than or equal to)
positive tuberculin reaction without any clinical or radio-
logical evidence of active tuberculosis including those
No BCG, adult 10 mm
Past BCG, adult 15 mm who are HIV sero-positive.
HIV-infected individual 5 mm
No BCG, child 5 mm
The only drug currently used for routine chemoprophy-
BCG <5 years ago—child 15 mm
BCG >5 years ago—child 10 mm laxis is isoniazid given for six to 12 months as a single
daily dose of 5.0 mg/kg bodyweight up to a maximum of

Initial positive reactors should be evaluated to exclude 300 mg.

active disease. The positive tuberculin test may signify

recent tuberculin conversion. People who should be considered for chemoprophylaxis
are recent convertors, particularly children and teenag-

Contacts identified by the TB Program as requiring ers, and contacts who react strongly to the tuberculin

further assessment are referred to chest physicians. test.

When X-ray and physical examination are normal, Chemoprophylaxis is not usually recommended for

contacts with positive reaction should be offered isoni- people over 35 years of age because of the hepatotoxic-

azid chemoprophylaxis given once daily at a dosage of ity of isoniazid.

5mg/kg body weight to a maximum of 300 mg daily.

However, there is a group of people who, in spite of their

Treatment should be for a minimum period of six months. age (over 35), should be considered for chemoprophy-
laxis.

Contacts, with positive reactions, who refuse isoniazid

should be kept under surveillance and followed up with This group includes all tuberculin-positive persons

chest X-rays taken at six months and 12 months. receiving corticosteroids, on immunosuppressive drugs,
insulin-dependent diabetics, persons following gastrec-
tomy and persons with silicosis.

136
Epidemic Measures
• Recognise and treat new cases.
• Search for the sources of infection.

International Measures
Individuals from high-prevalence countries should be X-
ray screened upon immigration.

137
 Mycobacterial Infections
Atypical (Non-Tuberculosis)

Victorian Statutory Cases of M. kansasii lung infection have occurred in

western Victoria in recent years.
Re quirem ent
Group B notification (under tuberculosis).
Infection with M. marinum is associated with contact with
swimming pools, aquariums and other bodies of water.
Infectious Agents
M. ulcerans infection should be considered as a possible
Mycobacteria other than Mycobacterium tuberculosis.
diagnosis of chronic skin lesions in persons exposed to
These include M. avium-intracellulare complex (MAC), M.
the eastern Victorian coastal environment.
kansasii, M. scrofulaceum, M. fortuitum, M. marinum, M.
ulcerans, M. chelonae.
Atypical mycobacteria may colonise and infect persons
without causing clinical disease. Skin tests to tuberculin
Clinical Features and other mycobacterial derivatives may be positive in
MAC and M. kansasii are rare causes of lung disease in such persons.
humans, and mainly affect middle-aged and elderly
persons with underlying chronic lung conditions.
Method of Diagnosis
Clinicians who suspect infection with atypical mycobac-
Disseminated MAC infection frequently occurs in ad-
teria should liaise with a pathology laboratory to ensure
vanced HIV infection, but is rare in immunocompetent
that clinical specimens are appropriately collected and
hosts.
transported.

Cervical and submandibular lymphadenitis due to MAC,

To establish a definite diagnosis of atypical mycobacte-
M. scrofulaceum and M. kansasii may occur in otherwise
rial infection, organisms must be cultured from a case
healthy young children.
with clinically compatible disease or identified by direct
smear on at least two occasions. Histologic examination
M. fortuitum and M. chelonae cause skin and wound
of biopsies of clinical lesions may also assist in the
infections and abscesses. They are frequently associ-
diagnosis.
ated with trauma or surgery.

M. marinum causes ‘swimming pool granuloma’, a Reservoir

nodular lesion that may ulcerate and is usually located
Mycobacteria are ubiquitous in the environment. Some
on an extremity.
pathogenic non-tuberculous mycobacteria have been
cultured from various environmental sources (such as
M. ulcerans infection causes ‘Bairnsdale’ or ‘Buruli’ ulcer,
ground waters, dust and soil), while the environmental
a chronic ulcerative skin lesion, usually of an extremity.
niches of many others remain unknown.

Public Health Significance and

Oc c u r re n c e
Disease due to atypical mycobacterial infection is
relatively rare.

139
 Mode of Transmission Disseminated and pulmonary infections are treated with
combinations of antimycobacterial drugs. The clinical
The mode of transmission can rarely be determined for
outcome is strongly influenced by the underlying health
individual cases. Atypical mycobacteria are probably
of the host.
transmitted by aerosol from soil, dust or water, by
ingestion, or by skin inoculation.
No specific measures are needed for contacts of cases.

Person-to-person spread of atypical mycobacteria is

rare. M. avium causes disease in poultry and pigs but
animal-to-human transmission is rare.

Incubation Period
The incubation periods of atypical mycobacterial infec-
tions can rarely be determined, but are probably weeks
to several months.

Period of Communicability
Communicability of human cases is usually not a practi-
cal concern. Localised foci of disease due to atypical
mycobacteria suggest that an established environmental
focus of organisms may remain the source of infections
for years.

Susceptibility and Resistance

Persons with tissue damage (skin trauma, pulmonary
disease) and immunodeficiency may be at increased risk
of atypical mycobacterial infection.

Control of Case
Cases of atypical mycobacterial infection usually require
specialist management.

Skin lesions and childhood lymphadenopathy are usually

cured by surgery, sometimes with antimycobacterial
drugs.

140
 P e d ic ulo sis/ Headlice
Victorian Statutory
Requirem en t
Statutory notification not required.
School exclusion.
Infectious Agent
Pediculus capitis:
• Lice are tiny parasitic insects, about 2 mm to 3 mm
long and coloured reddish brown to whitish brown.
• The louse is wingless, has a flat body and six legs.
Headlice remain close to the scalp and move quickly
when disturbed.
• The adult louse is capable of laying eggs (nits) after 10
days.
• Eggs are tiny specks that are firmly glued to the hair
close to the scalp.
• Eggs that are more than 12 mm from the base of the
scalp are dead or are only empty egg casings that are
pearly white and resemble dandruff.
• The life cycle of the louse is about 28–30 days.
Clinical Features
Itching occurs, generally behind the ears and at the back
of the neck.
Public Health Significance and
O c c u r re n c e
Headlice infestation is more of a social problem than a
public health problem as head lice do not transmit any
disease.
Outbreaks are common among children in schools and
child care facilities.
Lice may infest people of any socioeconomic position,
age or sex.
Method of Diagnosis
Lice may be seen on the scalp if the hair is rapidly
parted.
Eggs (nits) are detected on the hair shaft close to the
scalp, behind the ears and at the back of the neck. (Nits
further than 10–15 mm from the scalp are hatched or
dead.)
Discarded skins and black sandy excrement are seen on
pillows and collars.
Itching of the scalp causing the person to scratch may
prompt examination.
Reservoir
Humans, usually affecting most family members.
Mode of Transmission
Spread of lice is mainly by head-to-head contact.
Other modes of transmission are shared headgear and
shared combs but these are less common.
Head lice do not live in bedding, furniture or clothes.
Incubation Period
The incubation period varies slightly according to the
temperature needed for egg hatching.
Eggs usually hatch in seven to 10 days.
Sexual maturity occurs eight to 10 days after hatching.
Period of Communicability
Communicability can occur as long as lice or eggs
remain alive on the infested person.
141
 Susceptibility and Resistance Note
Pregnant women, people with sensitive skin, and parents
Lice are host-specific.
with children less than 12 months old should consult a
doctor before using pediculicides.
Those that live on animals will not infest humans, al-
though they may be present transiently.
Preventive Measures
Repeated infestations often result in dermal hypersensi-
• Exclude infested children until treated.
tivity.
• Educate children, child care workers and parents
about headlice and the importance of regular inspec-
Control of Case tion of heads, and discourage sharing of personal
items such as combs and hats.
• Exclude confirmed or suspected case from school or
• Promote grooming and general hygiene.
child care facility.
• Educate the public.
• Readmit the day after appropriate treatment has
commenced.
• Do not preclude readmission because of the presence
of a few remaining nits.
• Treat with an appropriate lotion that kills louse and
egg.
• Use products containing maldison or permethrin as the
first line of treatment.
• Apply again seven to 10 days after treatment if using a
product that does not kill the egg, such as pyrethrins.
• Take care to avoid contact with the eyes, nose and
throat.
• Wash clothes, linen and towels on a hot water cycle,
and soak combs and brushes in hot water and deter-
gent for 10 minutes.

Note
To prevent unnecessary or repeated exposure to
pediculicides, the person applying the chemical should
wear protective gloves.

Control of Contacts
All household contacts should be treated simultaneously.

Close contacts should be inspected regularly for signs of

infestation.

142
 Information Sheet
H e a d lic e/ Pedic ulosis

What are Head Lice? Transmission may occur indirectly by sharing personal
items such as combs, brushes and hats but is far less
Head lice are tiny insects that live on the human scalp
common.
and feed on blood.

Head lice are not spread by lack of cleanliness and may

The adult louse is wingless, about 2 mm long, has a flat
affect people of any social class.
body, six legs and varies in colour from whitish-brown to
reddish-brown.
They do not spread disease.

Head lice remain close to the scalp and move quickly

Lice that live on animals do not live on humans, and vice
when disturbed.
versa.

They cannot fly or jump; they only crawl.

What are the Signs of Head Lice?
The life cycle of the louse is about 28–30 days.
Nits are usually noticed first and are easier to see behind
the ears and at the back of the neck.
What are Nits?
An itchy scalp: lice bites result in generalised scratching.
Head lice lay eggs called nits that are oval-shaped
specks that firmly attach to the hair very close to the
Lice may be seen on the scalp if the hair is rapidly
scalp (within 6 mm).
parted.

Young lice usually hatch from the eggs within seven to

Finding a dry black powder, grey casts or skins on the
10 days and leave a pearly white empty case behind still
pillows in the morning, suggests the presence of lice.
cemented to the hair.

Nits found more than 12 mm out from the scalp are dead What is the Incubation Period?
or are only empty casings since human hair grows
Nits usually hatch in seven to 10 days.
approximately 1 cm/month.

Lice are capable of laying eggs eight to 10 days after

Once hatched, the lice are capable of laying eggs within
hatching.
10 days.

Large numbers of nits resemble dandruff, except that What is the Contagious Period?
nits cannot be brushed out. As long as lice or nits (eggs) remain alive on the infested
person.

How do Head Lice Spread?

Head lice outbreaks are common among children in
schools and child care facilities because children have
close head contact with one another throughout the day
in classroom and playgrounds. This enables easy
transmission from person to person.
How To Control Spread
• Exclude confirmed or suspected cases from school or
child care facility. Readmit the day after appropriate
treatment has commenced. The presence of a few
remaining nits does not preclude readmission.

143
 • Treat with an appropriate lotion that kills louse and nits.
• Use a fine metal comb or fingernails to remove nits.
• Treat all household contacts simultaneously.
• Wash clothes, bed linen and towels on a hot water
cycle.
• Wash combs and brushes in hot water and detergent.
• Never share combs, brushes or hats.
• Inspect close contacts regularly for signs of infestation.
How To Treat Head Lice
• There are a number of effective products available for
the treatment of head lice. These products can be
obtained from a chemist without prescription.
• Resistant head lice can be eradicated by switching to
a different product.
• The most effective products contain maldison or
permethrins: 0.5 per cent Malathion or Maldison Lotion
(Lice Rid or Cleensheen).
• The lotion should be applied to dry hair and left for 12
hours. Care should be taken to protect the eyes.
• The hair is then washed and combed with a fine-tooth
comb.
• Permethrins (Nix Creme Rinse, Quellada Creme Rinse,
Quellada Head Lice Treatment, Pyrifoam Shampoo).
These liquids are applied to clean, damp hair for 10
minutes, then rinsed out. An application of Nix may be
repeated in two weeks if necessary. The other applica-
tions may be repeated after one week.
• Pyrethrins (Lyban Foam, Banlice Mousse) should be
applied according to directions.
Note
The whole family should be treated if one member is
found to have head lice.
Compliance with product instructions eliminates the need
for nit removal after treatment.
For children less than 12 months of age, the recom-
mended treatment is Lyban Foam or Pyrifoam.
• Lyban Foam, Pyrifoam and Banlice Mousse are also
recommended as safe preparations in pregnancy.
If Lice Are Found Following
Tre a t m e n t
The lotion may have been inadequately applied.
The person may have been in contact with another
infected person.
Prevention
• Ordinary hair care is the best way to discourage head
lice.
• Daily brushing is likely to damage the lice.
• To obtain effective control of head lice, the whole
community should be involved.
• Parents should be encouraged to screen themselves
and their children regularly in the home, and to treat
themselves only when necessary.

Listing of Currently Available Head Lice Preparations, August 1997

Product Dose/Form Active Ingredients Concentration

Cleensheen Liquid Maldison 0.5 per cent

Lice Rid Liquid Maldison 0.5 per cent
Nix Creme Rinse Liquid Permethrin 1.0 per cent
Quellada Creme Rinse Liquid Permethrin 1.0 per cent
Quellada Head Lice Treatment Liquid Permethrin 1.0 per cent
Pyrifoam Shampoo(foam) Permethrin 10 mg/ml
Lyban Foam Liquid (foam) Pyrethrins 0.165 per cent
Piperonyl butoxide 2.0 per cent
Banlice Mousse Mousse Pyrethrins 1.65 mg
Piperonyl butoxide 16.5 mg
Quaternium-52 10 mg/g

144
 Pertussis
(Whooping Cough)

Victorian Statutory • An illness lasting two weeks or more with one of the
following:
Re quirem ent
– Paroxysms of coughing.
Group B notification.
or
– Inspiratory ‘whoop’ without other apparent causes.
School exclusion.
or
– Post-tussive vomiting.
Infectious Agent
Bordetella pertussis. Public Health Significance and
O c c u r re n c e
Clinical Features It is a distressing and often serious illness, particularly in
The catarrhal state may be indistinguishable from a viral children under one year of age.
upper respiratory tract infection.
The mortality rate is 0.5 per cent in infants under six
The infection damages respiratory epithelium, producing months.
respiratory obstruction and paroxysmal coughing, often
with a characteristic whoop. High immunisation levels reduce cases, and good
nutrition and medical care reduce case fatality.
There is little fever.

Many vaccinated adults may have asymptomatic infec-

Apnoea, seizures and encephalopathy may occur.
tion and act as a source of infection for younger children.

Infants aged less than six months and adults often do not
have the characteristic whoop.
Paroxysms frequently end with the expulsion of clear,
tenacious mucus, often followed by vomiting.
Pneumonia is the most common cause of death. Fatal
encephalopathy, probably hypoxic, and inanition from
repeated vomiting occasionally occur.
Case Definition
The case can be defined by:
• Isolation of Bordetella pertussis from a clinical speci-
men.
or
• Elevated Bordella pertussis-specific IgA in serum, or B.
pertussis antigen in a nasopharyngeal specimen using
immunofluorescence with a history of clinically compat-
ible illness.
or
Method of Diagnosis
It can be diagnosed by:
• Elevated B. pertussis-specific IgA in serum.
• DFA identification of B. pertussis in nasopharyngeal
specimens.
• Culture:
– The definitive diagnosis of B. pertussis infection relies
on the culture of the organism from nasopharyngeal
swabs.
– Unfortunately, the organism is fastidious and slow
growing and its culture is usually complicated by
contamination and overgrowth of other nasopharyn-
geal organisms.
– Nasopharyngeal (not anterior nares) specimens
should be taken with Dacron or calcium alginate
swabs rather than cotton swabs.
– Patient specimens should be directly plated on
selective transport media; for example, Charcoal
agar, Regan-Lowe, Modified Stainer-Scholte agar,
Fresh Bordet-Gengou medium.
145
 – Isolation rates are highest in the first three to four
weeks of illness. Prior antibiotic treatment will mark-
edly decrease the detection rate.
• Fluorescent antibody tests:
– Direct fluorescent antibody identification of B. pertus-
sis in nasopharyngeal specimens is a useful tech-
nique.
– This needs good reagents and experienced person-
nel.
– False negative and false positive results occur.
– These tests are particularly useful in situations later in
disease or during antimicrobial therapy when viable
organisms are no longer present.
• Other tests:
– Polymerase Chain Reaction (PCR).
– Serology, anti-B. pertussis IgA, IgG or IgM may be
utilised in diagnosis. The role of these studies in
clinical practice remains to be clarified.
Reservoir
Humans only.
Mode of Transmission
It is transmitted primarily by direct contact with dis-
charges from respiratory mucous membranes of infected
persons by the airborne route, probably droplet spread.
Adults and older siblings may be infected despite
adequate vaccination, and may transmit infection without
clinical disease.
Incubation Period
It is commonly seven to 10 days; rarely more than 14
days.
Period of Communicability
It is highly communicable in the early catarrhal stage
before the onset of paroxysmal cough.
146
Thereafter, communicability decreases and becomes
negligible in about three weeks.
When treated with erythromycin, the period of infectivity
usually lasts five days or less after commencement of
therapy.
Susceptibility and Resistance
Young infants are at risk of disease as there is poor
placental transfer of immunity.
Severity is greatest in young infants; milder and atypical
cases occur in all age groups.
Incomplete immunisation or waning immunity results in
cases occurring in older children and adults.
There may not be lifelong immunity, even after clinical
disease.
Control of Case
The suspected case should be excluded from the
presence of others outside the home (especially young
children and infants) until the patient has received more
than five days of a minimum 14-day course of antibiotics.
Antibiotics: Erythromycin shortens the period of commu-
nicability. Antibiotics do not reduce symptoms unless
they are given during the incubation period or early in the
catarrhal stage of the disease. (A 14-day course of co-
trimoxazole should be given if erythromycin is contraindi-
cated.)
Antibiotics should be given if case has been coughing
less than three weeks.
Exclusion from school should take place until a medical
certificate of recovery from infection has been received.
This certificate is issued when the case has received at
least five days of 14-day course of erythromycin.
Note
This is in accordance with NH&MRC guidelines for
school exclusion. The Infectious Diseases Regulations in
Victoria will be amended accordingly.
Control of Contacts
Vaccination:
• Protection is not afforded by passive immunisation.
• Close contacts under eight years of age who have not
received five doses of DTP should be given a DTP
dose as soon after exposure as possible.
Antibiotics: A 14-day course of erythromycin for house-
hold or other close contacts, regardless of immunisation
status, is recommended. Erythromycin should be given
as soon as possible. It should be given no later than 14
days after the recipient’s first contact with the primary
case during the infectious period (in high-risk household
Preventive Measures
• Educate the public to the dangers of whooping cough
and the advantages of initiating immunisation at two
months of age and adhering to the immunisation
schedule (DTP at two, four, six and 18 months and five
years).
• Delay immunisation only for significant intercurrent
infection or evolving neurological disorder. Minor URTI
is not a contraindication to immunisation.
Health Care Workers
When there is an outbreak, consider protection of health
workers at high risk of exposure by using a 14-day
course of erythromycin.
Epidemic Measures
• Search for unrecognised and unreported cases and

exposure settings, chemoprophylaxis may be considered ensure their exclusion from schools and child care

for up to 21 days). centres. Protect preschool children from exposure and

assure adequate preventive measures for exposed

Exclusion: Inadequately immunised household contacts children.

under eight years old should be excluded from school • Consider accelerated immunisation with the first dose

and child care centres until cases and contacts have at two weeks of age and the second and third doses at

received a minimum of five days of a 14-day course of four-week intervals. Complete immunisation for those

erythromycin. who have already commenced a course.

• Initiate antibiotic therapy for all exposed individuals.

Investigation: A search for early, missed and atypical

cases is indicated where a non-immune infant or young
child is, or might be, at risk, in school. Check immunisa-
tion status of close contacts.

Note
Close contacts may include all children in a child care
centre, or all children in the same school classroom.
Please contact the Department of Human Services for
further advice.

147
 Plague
Victorian Statutory
Re quirem ent
Group A notification.
Infectious Agent
Yersinia pestis, the plague bacillus.
Clinical Features
It is an acute, severe infection appearing in a bubonic or
pneumonic form.
Bubonic plague:
• This is the most common form.
• Onset is abrupt and associated with chills.
• Enlarged lymph nodes (buboes) appear with, or shortly
before, the fever.
• The most commonly involved lymph nodes are femoral
or inguinal followed by axillary and cervical.
• The nodes are tender, firm and fixed, and may suppu-
rate in the second week.
Primary pneumonic plague:
• Onset is abrupt with high fever, tachycardia and
headache.
• Cough develops within 24 hours. Sputum is mucoid at
first and then becomes bright red and foamy.
• Chest X-rays show a rapidly progressing pneumonia.
Secondary pneumonic plague:
• Occurrence as a complication of bubonic plague, due
to septicaemia with lung involvement.
• This clinical form may be a source of primary pneu-
monic or pharyngeal plague due to aerosolised drop-
lets of sputum.
Public Health Significance and
O c c u r re n c e
This is a highly infectious disease, which is endemic in
Indonesia, Burma and especially in Vietnam.
Plague is not present in Australia.
Wild rodent plague exists in parts of USA, South
America, Africa, Central and South East Asia. Human
plague has occurred recently in several countries in
Africa and in India.
Method of Diagnosis
It can be diagnosed by:
• Visualisation of Gram-negative organisms on direct
microscopic examination of Gram-stained smear of
clinical material. Examination by FA test is more
specific and particularly useful in sporadic cases.
• An antigen capture ELISA test (if available) may permit
an early rapid diagnosis in acute cases.
Diagnosis is confirmed by:
• Culture of the organism from blood, sputum, CSF or
lymph node aspirate.
• A fourfold rise or fall in titre in a serological test (the
passive haemagglutination test (PHA) is most com-
monly used).
Reservoir
Wild rodents.
Rabbits, hares and domestic cats may also be a source
of infection.
149
 Mode of Transmission
It is transmitted from rodent to human by the bite of an
infected flea vector.
Human-to-human transmission comes from inhalation of
infected droplets spread by coughing patients with
plague pneumonia or pharyngitis.
It can also be transmitted by handling tissues of infected
animals.
Incubation Period
Usually one to six days.
Period of Communicability
It is communicable as long as fleas remain infective.
Fleas may remain infective for months under suitable
conditions of temperature and humidity.
Bubonic plague is not usually transmitted from person to
person unless there is contact with pus from suppurating
buboes.
Pneumonic plague may be highly communicable under
appropriate climatic conditions; overcrowding facilitates
transmission.
Susceptibility and Resistance
The disease does not always confer immunity.
Control of Case
• Use a safe insecticide to rid the patient (including
clothing and baggage) of fleas.
• Hospitalise the case. For cases with bubonic plague, if
there are no respiratory symptoms, secretion precau-
tions are indicated for three days after the start of
150
effective therapy. For patients with pneumonic plague,
isolate the case to prevent airborne spread until the
completion of three days of appropriate antibiotic
therapy with clinical improvement.
• Disinfect sputum, purulent discharges and soiled
articles concurrently.
• Clean terminally.
• Handle bodies of plague victims with strict aseptic
precautions.
• Use streptomycin, tetracyclines, chloramphenicol early
when they are highly effective.
Control of Contacts
Contacts and sources of infection should be investi-
gated.
Close contacts of confirmed or suspected plague
pneumonia cases should be offered chemoprophylaxis
with tetracycline or sulphonamides and placed under
surveillance for seven days.
Preventive Measures
• Reduce the likelihood of people being bitten by in-
fected fleas, or being exposed to pneumonic plague
patients.
• Educate the public on the importance of appropriate
storing food to reduce rodent problem, and avoiding
flea bites by using insecticides and repellents.
• Control rats on ships, docks and in warehouses.
• Immunise with a vaccine of killed bacteria that gives
protection for at least several months (two to three
primary doses plus booster). This vaccine is used for
people entering high-incidence areas, and laboratory
or field workers handling plague bacilli or infected
animals. The vaccine is available from CSL.
Epidemic Measures
• Investigate all possible plague deaths by autopsy and
laboratory examination.
• Inform the public through the press and news media
(but avoid panic).
• Destroy all rodents within affected areas, after satisfac-
tory flea control has been achieved.
• Protect field workers against fleas by using insecticide
powders and insect repellents.

International Measures
Within 24 hours, government should notify WHO and
adjacent countries of the first cases of plague in any area
previously free of the disease according to the Interna-
tional Health Regulations.

Measures applicable to ships, aircraft, land transport and

international travellers arriving from plague areas are
specified in International Health Regulations 1969, third
annotated edition 1983, WHO, Geneva.

Prior to departure from an area where there is an epi-

demic of pulmonary plague, those suspected of signifi-
cant exposure should be placed in isolation for six days
after their last exposure.

On arrival of a suspected infected ship or aircraft,

travellers should be disinfected and kept under surveil-
lance for not more than six days from the date of arrival.

151
 Pneumonia Due to Chlamydia pneumoniae
Victorian Statutory
Re quirem ent
Nil.
Infectious Agent
Chlamydia pneumoniae strain TWAR. Chlamydia
pneumoniae (TWAR) was named in 1989 as a new
member of the chlamydia family with C. trachomatis and
C. psittaci.
Clinical Features
These are similar to psittacosis with headache, fever,
myalgia and the development of a dry cough on days
three to five.
Sore throat and sinusitis are occasionally seen.
A chest X-ray usually reveals lower zone changes.
Most cases of the C. pneumoniae pneumonia are consid-
ered mild to moderate in severity.
Patients who have died usually have had underlying
disease or additional bacterial infections.
Public Health Significance and
Oc c u r re n c e
C. pneumoniae is a common respiratory pathogen
causing a recognisable clinical pattern.
A carrier state is probably important in maintaining and
spreading infection in the community.
In a Melbourne study, 10 per cent of cases of commu-
nity-acquired pneumonia were due to this pathogen.
Method of Diagnosis
CFT is used but is only genus-specific and may be
positive for any chlamydial infection.
Currently, the laboratory diagnosis of C. pneumoniae
infection is made by detecting a rise in antibody titre
using MIF.
More recently, antigen detection in nasopharyngeal
aspirate, throat swabs or bronchial lavages by direct
immunofluorescence has become available.
Diagnosis by PCR methodology is under development.
Reservoir
Humans.
Mode of Transmission
The mode of transmission is not defined. Possibly, it
occurs through direct contact with secretions, via fo-
mites, and airborne spread.
Incubation Period
Usually five to 10 days.
Period of Communicability
The period of communicability is not defined, but pre-
sumed to be prolonged. Outbreaks may last for months.
Susceptibility and Resistance
There is increased likelihood of clinical disease in the
presence of pre-existing chronic disease.
Immunity usually occurs after infection, but reinfection
may occur.
153
 Control of Case
• Apply personal hygiene measures.
• Cover mouth when coughing.
• Dispose of discharges from mouth and nose in a
sanitary manner and wash hands.

Tre a t m e n t
Doxycycline for 14 days.

Erythromycin for 14 days is an alternative, although

relapses have occurred with short courses.

Roxithromycin is also effective.

Preventive Measures
• Avoid crowding in living and sleeping quarters.
• Educate the public in hygiene measures.

Epidemic Measures
Case finding and treatment.

154
 Poliomyelitis
Victorian Statutory
Re quirem en t
Group A notification.
School exclusion.
Infectious Agents
Poliovirus, types 1, 2 and 3 (enterovirus).
Clinical Features
The clinical features range from inapparent infection,
through non-specific febrile illness, aseptic meningitis,
paralytic disease and death.
When symptoms occur they include fever, malaise,
headache, nausea and vomiting, muscle pain, stiffness
of the neck and back with or without flaccid paralysis.
Case Definition
The disease is defined as an acute onset of a flaccid
paralysis of one or more limbs with decreased or absent
tendon reflexes in the affected limbs without other
apparent cause, and without sensory or cognitive loss.
Public Health Significance
Each case of indigenous poliomyelitis needs a complete
clinical, laboratory and epidemiological investigation and
should be regarded as an outbreak since each case
probably represents 100–200 infected persons (unless
the case is vaccine-associated).
Outbreaks have occurred in developed countries among
pockets of unimmunised persons.
Polio is still endemic in many developing countries.
Method of Diagnosis
It is diagnosed by isolation of virus by inoculating cell
culture systems with CSF, faecal specimens or oropha-
ryngeal secretions.
The National Polio Reference Laboratory should be
contacted.
Reservoir
Humans only. There are no long-term carriers.
Mode of Transmission
Transmission is by direct contact through close associa-
tion.
Faecal-oral route is especially important where sanitation
is poor.
Pharyngeal spread is more important where there is
good sanitation and during epidemics.
Incubation Period
Usually seven to 14 days; the range is three to 35 days
for paralytic cases.
Period of Communicability
The risk of transmission of infection is greatest for the
seven to 10 days prior to and following the onset of
symptoms.
The virus persists in the pharynx for approximately one
week and in the faeces for up to six weeks, or longer in
the immunosuppressed.
155
 Control of Case
• Obtain details of vaccine history, lot number, virus
type, severity and persistence of residual paralysis 60
days after onset (if vaccine-associated).
• Isolate patient with Standard Precautions in hospital.
Exclude from schools and children’s settings until at
least 14 days after onset of illness and until receipt of a
medical certificate of recovery from infection.
• Disinfect throat discharges, faeces and soiled articles.
• Determine whether the patient’s disease represents an
indigenous or imported case.
Control of Contacts
Vaccination of families and other close contacts contrib-
utes little to immediate control because susceptible
contacts are generally already infected by the time the
first case is recognised.
Epidemic Measures
After a single case of paralytic poliomyelitis from wild
poliovirus, a dose of OPV should be given to all persons
in the immediate neighbourhood of the case, regardless
of their previous immunisation history.
All suspected cases of polio must have appropriate
faecal specimens sent to the National Polio Reference
Laboratory.
International Measures
National health administrations are expected to promptly
inform WHO of outbreaks.
The notification should be supplemented with details of
source, nature, extent of the epidemic and virus identity
type.

A thorough search for unrecognised cases, especially

among children, ensures early detection and facilitates
control.

Preventive Measures
OPV (Sabin) is recommended at two, four and six
months, five years and 15 years.

IPV (Salk) should be substituted in those for whom the

oral vaccine is contraindicated (that is, those who are
immunosuppressed).

Persons who have a household contact who is

immunosuppressed should receive IPV.

For unimmunised or incompletely immunised adults, a

course of OPV should be commenced or completed if
there is risk of exposure; for example, travel to an en-
demic area, or a person in the household being immu-
nised with OPV.

156
 Psittacosis (Ornithosis)
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agent
Chlamydia psittaci.
Clinical Features
The onset is usually abrupt with fever, chills, malaise,
headache, myalgia and upper or lower respiratory tract
symptoms.
Cough is often a feature with little sputum.
Chest X-rays often show focal consolidation.
The illness, which usually lasts for seven to 10 days, is
mild or moderate, but may be severe in older, untreated
patients.
Complications include encephalitis, endocarditis, myo-
carditis and thrombophlebitis. Relapses may occur.
Public Health Significance and
Oc c u r re n c e
Outbreaks generally occur in individual households or
are associated with pet shops or aviaries. They can
occur occupationally in poultry workers.
Chlamydia psittaci is highly infectious, and immunity
following infection is incomplete and transitory.
Method of Diagnosis
Humans:
• Infection is also generally diagnosed by serology using
paired acute and convalescent phase sera.
• Culture of the organism from sputum, blood or biopsy
material (spleen, liver) is generally not performed
(because of danger to laboratory workers).
• For infants with pneumonia, swabs may be collected
from the posterior nasopharynx or the throat, although
aspirates collected by intubation appear to be supe-
rior.
Birds:
• Special transport medium and culture techniques are
required so it is necessary to contact the Avian Medi-
cine Section at the Victorian Institute of Animal Sci-
ence, Attwood (03) 9333 1200 to obtain further details
of specimen collection and transport requirements.
Transport:
• For transport of specimen, see appendix 7.
Reservoir
Birds of many different types, especially parakeets,
parrots, pigeons, waterfowl, seabirds, budgerigars,
turkeys and ducks. Healthy birds may be carriers. Wild
birds may be a source of infection.
Mode of Transmission
Infection is generally acquired by inhaling the agent from
desiccated droppings and secretions (ocular and nasal)
of infected birds in an enclosed space, or directly from
infected birds.
Laboratory infections and rare person-to-person trans-
mission associated with paroxysmal coughing have
occurred.
Incubation Period
Usually four to 15 days; commonly 10 days.
Period of Communicability
Infected birds may shed the agent for a prolonged
period.
157
 Susceptibility and Resistance Wearing gloves and dust masks are recommended when
cleaning areas where bird nests are found.
Immunity following infection is incomplete and transitory.

Older adults have a more severe illness. Preventive Measures

• Educate the public about the danger of household or
Control of Case occupational exposure to infected pet birds.
• Prevent or eliminate infections of birds by quarantine
Isolation is not necessary, but instruct patient to cough
and antibiotic treatment.
into disposable tissues.
• Implement appropriate surveillance of commercial
psittacine birds, pet shops and aviaries.
All discharges should be disinfected and terminal
• Destroy or treat infected birds and disinfect premises.
cleaning performed.

Tre a t m e n t Epidemic Measures

Cases should be investigated in order to recognise more
Tetracyclines should be continued for 10–14 days after
extensive outbreaks.
temperature returns to normal.

Outbreaks should be reported to Department of Human

If tetracyclines are contraindicated (pregnancy, children
Services, Victoria and the Department of Natural Re-
less than eight years) erythromycin should be used.
sources and Energy.

Control of Contacts
The diagnosis in symptomatic contacts should be
considered.

Control of Environment
The origin of suspected birds should be traced.

The Department of Natural Resources and Energy should

be informed.

Large doses of tetracycline will suppress, but not elimi-

nate, infection in poultry flocks and may complicate
investigations.

Appropriate disinfectants for infected premises are

iodophors (for cages), 5 per cent formalin (for surfaces)
and phenol (for wastes). For routine daily or weekly
disinfection of floors and cages respectively, iodophors
or formalin are used.

158
 Q Fever
Victorian Statutory
Re quirem ent
Group B notification.
Scheduled WorkCover compensable disease for certain
occupations.
Infectious Agent
Coxiella burnetii.
Clinical Features
The onset is usually acute and characterised by fever,
chills, sweats, severe headache (especially behind the
eyes), weakness, anorexia, myalgia and cough. Transient
mild rashes are an occasional feature.
Abnormal liver function tests are common.
Chronic complications include granulomatous hepatitis
and endocarditis. The latter is the most serious concern
as it usually involves the aortic valve and occurs months
to years after the acute illness.
A relapsing fatigue syndrome may occur in 20–40 per
cent of cases.
Public Health Significance
It is an acute febrile rickettsial disease of low mortality
but significant morbidity.
It is most commonly found in abattoir workers who have
recently handled contaminated stock (for example, feral
goats or sheep from interstate endemic areas). It is an
occupational hazard for tannery and knackery workers,
shearers, meat inspectors, dairy workers, farm workers,
animal transporters, wool sorters and veterinary person-
nel.
It also occurs in others handling fomites; for example,
laundering contaminated clothing.
Outbreaks are usually of short duration.
Method of Diagnosis
It can be diagnosed by a demonstrated rise in specific
antibodies by complement fixation (CF) test.
Preferably, blood samples are collected 14 days apart.
Acute Q Fever:
• Fourfold rise in CFT antibodies to phase II antigen that
can be confirmed with phase II IgM ELISA.
Chronic Q Fever:
• High CFT antibody titre to phase I and II, and low or
absent IgM antibody.
• An alternative and improved serological test for diag-
nosis is based on direct immunofluorescence (IF)
testing.
Reservoir
No endemic reservoir is known in Victoria (even though
Victorian sheep are sero-positive).
The organism is commonly introduced in stock from
interstate.
Animals include goats, cattle, sheep, other farm and
domestic animals and some wild animals (including
kangaroos, bandicoots and feral pigs).
Mode of Transmission
Q fever can be transmitted by:
• Inhaling water droplets and dust that have been
contaminated by placental tissues, birth fluids or
excreta of infected animals.
• Having direct contact with contaminated materials
such as straw, wool or hides, or during slaughtering of
infected animals.
• Drinking unpasteurised milk from an infected animal.
Incubation Period
Usually two to four weeks, commonly 19–21 days, and
occasionally up to 60 days.
159
 Period of Communicability Epidemic Measures
Person-to-person spread occurs rarely, if ever. All notified cases should be investigated to ascertain if
other associated cases are likely to have occurred.

Susceptibility and Resistance If two or more related cases are evident in the same
Infection usually confers lifelong immunity. workplace, staff should be assessed for immune status
(if not already known) with CFT levels and skin testing.

Control of Case
Non-immune staff should be offered vaccination.
The notification details required are:
• Occupation.
The Department of Natural Resources and Energy and
• Possible source of infection (for example, batch of
the Occupational Health and Safety Organisation should
stock from endemic areas).
be notified.
• Any other known recent cases (for example, at
workplace).
• Immunisation status for Q Fever. Q Fever Guidelines
Persons who wish to be vaccinated should first complete
Specific treatments are: a questionnaire to elicit the type and duration of their
• Tetracycline for two to three weeks. When endocarditis work (abattoir, shearer, farmer, veterinary surgeon),
occurs, treatment should be prolonged and rifampicin previous Q Fever infection, previous Q Fever vaccination,
may be used in combination with tetracycline. egg allergy and current medications such as cortisone.
• Isolation is not necessary.
• Articles contaminated with blood, sputum and excreta
Skin Testing
should be disinfected.
Vaccine dilution:
• Immunisation of household contacts is not necessary.
• The required dilution of vaccine for a skin-testing
solution can be achieved by diluting 0.1 ml of vaccine
Preventive Measures in 30 ml normal saline.
• Eliminate source of infection if known.
• Disinfect incriminated stock-holding facilities if practi- Skin-test procedure:
cable; for example, 0.05 per cent hypochlorite (500 • Prepare the skin with methylated spirits.
• Dry well before injecting.
ppm available chlorine) or 5 per cent peroxide.
• Inject 0.1 ml of the diluted vaccine solution
• Immunise high-risk occupational groups.
intradermally into the volar surface of the left forearm.
Choose a smooth, unblemished area of skin.
Note
• Cover with a bandaid if returning to work.
Prevaccination assessment with CFT levels and skin • Instruct the patient to remove the bandaid when
testing is essential to reduce risk of severe local reac- showering then leave uncovered.
tions in those already immune. A certain degree of
training is required to recognise positive skin tests.

160
Reading Note
Where a history of Q Fever infection or previous vaccina-
The skin test can be read between three to 10 days
tion is given, confirm results through the admitting
(optimum seven days). After 10 days, it is unreliable. A
hospital, laboratory or LMO. If the results are negative,
positive reaction is indicated by induration at the site of
vaccination is recommended. In immunosuppressed
the injection.
individuals and in pregnancy, the risk-benefit ratio should
be evaluated before use.
Serology (CF):
• Positive titre: 1:2.5 and above.
• Negative titre: <1: 2.5. Side Effects
• Doubtful: A.C. (Anti-Complementary) <1:5 or <1:10. A localised redness/soreness around the injection site for
three to four days post-vaccination occurs in approxi-
Vaccination mately 45 per cent.

Indicated if patient presents with the following:

Note
• Negative skin reaction and negative serology.
Severe local reactions, including formation of abscesses
• Negative skin reaction and doubtful A.C. serology
at the site of injection, may occur on inadvertent vaccina-
result <1:5 with no previous history of either Q Fever
tion of immune individuals.
infection or Q Fever vaccination.

Note
Approximately 10 per cent experience a general reaction

Vaccination must be given subcutaneously. such as slight fever, headache and ‘flu-like’ symptoms 14
hours post-vaccination.

Retest
Australian vaccine induces protective immunity and in-
If a person with no previous history of Q Fever infection
vitro cell mediated immune responses within two to three
or Q Fever vaccination presents with the following:
weeks in over 90 per cent of individuals. Seroconversion
• Negative skin reaction and doubtful A.C. serology
rates are lower (50–60 per cent) when measured as
<1:10.
complement fixing or immunofluorescent antibody
• Doubtful skin reaction and negative serology.
responses.

Retest in approximately three months. Seroconversion

Humoral immune responses are noted in a higher
may have occurred or the immune response may be
proportion of abattoir workers (who are at high risk of
‘boosted’ by intra-dermal skin test dose alone.
occupational exposure to C. burnetii) than in individuals
at low risk. Cell mediated immunity persists for at least
Do not vaccinate if a person has the following:
five years.
• Positive skin reaction and positive serology.
• Negative skin reaction and positive serology.
Vaccination during the incubation period does not
• Positive skin reaction and negative serology.
prevent the disease. Post-exposure prophylaxis is not
• Negative skin reaction and negative serology but
recommended.
history of laboratory confirmed Q Fever.
• Hypersensitivity to egg protein.

161
 Information Sheet
Q Fever

The Illness To detect immunity, two tests are done, a blood test and
a skin test:
Q Fever is an acute illness with fever, chills, headache
• For the blood test, 5–10 ml of blood is taken and tested
and muscle pains similar to severe influenza. Some
for Q Fever antibodies.
people become infected without any illness being
• For the skin test, a very small dose of diluted vaccine is
apparent, and a few develop a long-lasting illness with
injected into the skin. A previous history of infection
liver and heart complications. It is an infectious disease
with Q Fever or having recent Q Fever vaccine is a
caught from infected animals.
contraindication to vaccination.

The Germ The skin test is read seven days later. If both the skin test
The germ is a very small organism that is carried by and the blood test are negative and the person is not
cattle, sheep and goats and particularly by feral (wild) allergic to eggs, they are offered the vaccine which is
goats. Humans may occasionally become infected after given by injection under the skin.
drinking unpasteurised milk or, more usually, from
inhaling dust from infected premises. Animal faeces,
urine, blood and pregnancy fluids may contain large
numbers of organisms that are not killed by sunlight or
drying.

Those most at risk from contracting the disease are

abattoir workers, shearers and sometimes farmers.
Visitors to abattoirs and workers may become ill after
inhaling infected dust.

Pre ve n t i o n
The Commonwealth Serum Laboratories have prepared a
vaccine, Q-Vax, which gives a very high level of protec-
tion, except if given after a person has already been
infected. Some reddening and tenderness at the injection
site is common.

A lump or swelling is rare. Occasionally the vaccine may

cause a mild fever and muscle aches.

Q-Vax is different from other vaccines in that the recipi-

ent must first be tested for immunity, since those already
immune may have severe reactions to the vaccine.

162
 Rabies

Victorian Statutory Worldwide, there are an estimated 30,000 deaths/year,

almost all in developing countries.
Re quirem ent
Group A notification.
Method of Diagnosis
Rabies can be diagnosed by:
Infectious Agent
• Detection by direct fluorescent antibody of virus
Rabies virus (rhabdovirus).
antigen in a clinical specimen (preferably brain tissue
or the nerves surrounding hair follicles in the nape of
Clinical Features the neck).
• Isolation in cell culture (or laboratory animal) of virus
It is an acute viral disease of the central nervous system.
from saliva, CSF or CNS tissue.
• Identification of rabies-neutralising antibody titre ≥1:5
CNS symptoms are preceded by non-specific prodrome
(complete neutralisation) in serum or CSF of unvacci-
of fever, headache, malaise, anorexia, nausea and
nated persons.
vomiting lasting one to four days.

Confirmation by all the above methods is recommended.

This is followed by signs of encephalitis manifested by
periods of excitation and agitation leading to delirium,
The Australian Animal Health Laboratory at Geelong
confusion, hallucinations and convulsions.
(telephone: (03) 5226 4720) is the reference laboratory
for the diagnosis of rabies.
Signs of brain stem dysfunction begin shortly after with
excessive salivation and difficulty in swallowing. This
The State chief quarantine officer and chief veterinary
produces the traditional picture of ‘foaming at the mouth’.
officer should also be forewarned at the time of submit-
ting any specimen.
The disease is invariably fatal. Death from respiratory
paralysis generally occurs within two to six days of onset.
Reservoir
Public Health Significance and It is primarily a disease of animals, particularly wild and
domestic canine species, cats, skunks, raccoons,
Oc c u r re n c e
mongooses, monkeys, bats and other biting mammals.
There have been two rabies cases in humans in Australia
in recent years that were diagnosed following an au-
topsy. Mode of Transmission
It is transmitted by the virus-laden saliva of a rabid
The infection in each case was considered to have been animal introduced via bite or scratch.
acquired overseas some years prior the patients’ arrival
in Australia. Dogs and cats are the main urban vectors.

To date, rabies has been excluded from this country by Person-to-person transmission via saliva is theoretically
animal quarantine measures and rapid destruction and possible but has never been documented.
investigation of suspect cases of rabies in animals.

163
 The virus is comparatively fragile and does not survive
for long periods outside the host.
It is readily inactivated by heat and direct sunlight.
Incubation Period
The incubation period is variable, usually two to eight
weeks, but can occur from five days to over a year
depending on factors such as severity, site of wound and
infective dose.
Very long incubation periods of up to six years or more
have been reported.
Period of Communicability
Dogs and cats may transmit virus for three to 10 days
(rarely over three days) prior to onset of their own clinical
signs and throughout the course of the disease.
Susceptibility and Resistance
All warm-blooded mammals are susceptible.
Natural immunity in humans is unknown.
Control of Case
• Isolate patient (because of respiratory secretion) for
duration of illness.
• Institute intensive supportive therapy for all clinical
cases.
• Notify the chief veterinary officer (CVO) Agriculture,
Victoria in all cases. Telephone (03) 9651 7137 during
working hours; fax (03) 9651 7005. The duty principal
veterinary officer could also be contacted (03) 5430
4517 (24-hour contact). The CVO will take action to
identify the source and limit/eradicate the spread of
infection in animals.
164
• Implement the AUSVETPLAN rabies control proce-
dures. In designated areas, animal owners may be
required to have susceptible animals vaccinated with
rabies vaccine. Animal movements will be restricted
and stray animals destroyed.
• Take contact precautions (gloves, gown and mask)
when nursing a case of rabies in view of the potential
hazard of saliva.
Control of Contacts
Rabies immunoglobulin should be given and contacts
immunised who report possibly infectious exposure to
the case; for example, through bites, scratches, open
wounds or mucous membranes contaminated with saliva
or other infectious material.
Human Diploid Cell rabies Vaccine (HDCV) is available
from Pasteur Merieux. (See NH& MRC Immunisation
Procedures for details.)
Preventive Measures
Domestic cats and dogs in urban areas of endemic
countries should be vaccinated. Reduction of street dogs
is most important.
Prophylactic vaccination of groups at high risk should
take place. (It is not recommended for travellers unless
they are known to be particularly at occupational risk.)
Travellers should be counselled not to ignore animal
bites. Wounds should be immmediately washed and
cleaned with soap or detergent and water. The wound
should not be sutured if possible. Expert medical advice
should be sought.
Post-exposure prophylaxis should be provided via rabies
vaccine and rabies immunoglobulin for those bitten or
scratched by animals that may be carrying the disease.
The same prophylaxis should also be given to those
people with open wounds or mucous membranes that
have been contaminated with saliva or other potentially
infectious material (brain tissue) from a rabid animal.

Epidemic Measures
Control of rabies in the animal population, if relevant, will
be carried out according to the AUSVETPLAN rabies
procedures as described under Control of Case.

165
 Ringwor m/Tinea
Tinea capitis (Head), Tinea corporis (Body), Tinea pedis
(Feet), Tinea unguium (Nails)

Victorian Statutory Public Health Significance and

Re quirem en t O c c u r re n c e
Statutory notification not required. Tinea capitis:
• Mainly affects children.
School exclusion. • M.canis is usually contracted from infected kittens or
puppies.
• The highly contagious Microsporum audouinii, which
Infectious Agents spreads from person to person, does not occur in
Microsporum spp. for example, Microsporum canis is the Australia.
primary causative agent in Australia of tinea capitis and • Tinea capitis may extend to tinea corporis.
corporis. Trichophyton spp. for example, T. rubrum, T. • Occurrence is worldwide.
mentagrophytes, Epidermophyton floccosum.
Tinea corporis:

Clinical Features • Occurrence is worldwide and relatively frequent.

• Males are infected more than females.
The clinical features are superficial fungal infection of the
• Infection can occur from direct or indirect contact with
skin, nails or hair.
skin and scalp lesions of infected persons or animals.
• The infectious agents are Microsporum trichophyton
Tinea capitis:
and Epidermophyton floccosum.
• A small papule begins and spreads peripherally
leaving fine, scaly patches of temporary baldness.
Tinea pedis:
• Infected hairs become brittle and break off easily.
• Children and adults spread it by using communal
facilities such as showers at swimming pools.
Tinea corporis:
• Adults are affected more often than children; males
• A flat, red-ring-shaped lesion of the skin appears. It
more than females.
often contains fluid or pus, but may be dry and scaly or
• Infection is more frequent and severe in hot weather.
moist and crusted.
• The infectious agents are Trichophyton rubrum, T.
• The lesion tends to heal centrally.
mentagrophytes var. interdigitale, Epidermophyton
floccosum.
Tinea pedis:
• Commonly known as ‘athlete’s foot’. The features of this
Tinea unguium:
common condition are scaling or cracking of the skin,
• Occurrence is common but there are low rates of
especially between the toes, or blisters containing a
transmission, even to close family associates.
thin watery fluid.
• It is spread by direct contact with skin or nail lesions of
infected persons, or indirectly through contact with
Tinea unguium:
contaminated floors or showers.
• It is a chronic fungal disease involving one or more
• Toe and finger nails infected with T. rubrum are resist-
nails of the hands or feet.
ant to topical treatment.
• The nail gradually thickens, and becomes discoloured
and brittle.
• Caseous-looking material forms beneath the nail, or the
nail becomes chalky and disintegrates.

167
 Method of Diagnosis Incubation Period
Tinea capitis: Tinea corporis: four to 10 days.
• Microscopic examination of hair. Tinea capitis: 10–14 days.
• Examination of hair with a Wood’s lamp. Tinea pedis and Tinea unguium: unknown.
• Fungal culture.

Tinea corporis:
Period of Communicability
• Microscopic examination of skin scrapings. The fungus persists on contaminated materials as long
• Fungal culture. as lesions or animal hair harbour viable spores.

Tinea pedis: Susceptibility and Resistance

• Microscopic examination of skin scrapings.
Tinea capitis:
• Fungal culture.
• Young children are particularly susceptible to Micro-
sporum canis.
Tinea unguium:
• All ages are susceptible to infections particularly
• Microscopic examination of the nail and of detritus
caused by Trichophyton spp.
beneath the nail.
• Fungal culture.
Tinea corporis:
• Susceptibility is widespread. It is aggravated by friction
Reservoir and excessive perspiration in axillary and inguinal
Tinea capitis: Humans, animals, especially dogs, cats regions, and when environmental temperatures and
and cattle. humidity are high.

Tinea corporis: Humans, animals; for example, cattle, Tinea pedis:

kittens, puppies, guinea pigs, mice, horses, and soil. • Susceptibility is variable and infection may be inappar-
ent.
Tinea pedis: Humans. • Repeated attacks are frequent.

Tinea unguium: Humans; rarely animals or soil. Tinea unguium:

• An injury to the nail predisposes to infection. Reinfec
tion is frequent.
Mode of Transmission
Direct transmission occurs through:
• Human-to-human contact; for example, T. rubrum, T.
Control of Case
mentagrophytes. Tinea corporis:
• Animal-to-human contact, for example, M. canis, T. • Infected children should be excluded from schools and
verrucosum. swimming pools until at least 24 hours following the
commencement of appropriate treatment.

It can be transmitted indirectly through contaminated • It can be treated effectively with topical medications.

soil; for example, M. gypseum.

168
Tinea capitis:
• Oral griseofulvin is the treatment of choice for resistant
infection; for example, T. tonsurans.
• Topical antifungal medication may be used concur-
rently.
Tinea pedis:
• Gymnasiums, showers and similar sources of infection
should be thoroughly cleaned and washed.
• Shower areas should be frequently hosed and rapidly
drained.

Tinea pedis:
• Topical fungicides, oral griseofulvin may be indicated
Epidemic Measures
in severe protracted disease. Children and parents should be eduated about modes of
• Feet should be exposed to air by wearing sandals. spread, prevention, and the necessity of maintaining a
• Socks of heavily infected individuals should be boiled high standard of personal hygiene.
to prevent reinfection.

Tinea unguium:
• Oral terbinafine hydrochloride should be given until
nails grow: six months for fingernails and 18 months for
toenails.

Note
M. canis infection is self-limiting in children before
puberty and griseofulvin may not be necessary. Consult
a specialist about treatment.

Control of Contacts
• Investigate household contacts, pets and farm animals
for evidence of infection.
• Treat infected contacts, human or animal.

Preventive Measures
Tinea capitis:
• Parents should be educated about modes of spread
from infected children and animals.
• In case of epidemics, consider examination of all
children to identify cases. Disinfect contaminated
articles.

Tinea corporis:
• Shower bases, mats and floors adjacent to showers
should be disinfected.
• Infected animals should be avoided.

169
 Information Sheet
Tinea (Ringworm)

What is Ringworm? Ringworm of the Scalp and Beard

Ringworm is a fungal infection that can affect any part of This condition begins as a small pimple. It spreads
the body. outward leaving fine, scaly patches of temporary bald-
ness. Infected hairs become brittle and break off easily.

How Long is the Incubation Ringworm of the Foot (Commonly Known

Period? as Tinea or Athlete’s Foot)
The incubation period lasts from one to three weeks. It
The characteristics of this common condition are scaling
varies with the site of infection.
or cracking of the skin, especially between the toes, or
blisters containing a thin watery fluid.
How Long is the Infectious
Period? Ringworm of the Nail
This condition tends to be a long-term fungal disease
The infectious period lasts as long as the condition
and is difficult to treat. It usually affects one or more nails
persists.
of the hands or feet. The nail gradually thickens and
becomes discoloured and brittle. Cheesy-looking mate-
How do You Get Ringworm? rial forms beneath the nail, or the nail becomes chalky
Ringworm is spread by direct and indirect contact with and disintegrates.
humans, animals, and soil.

How do You Control Ringworm?

Humans: through skin and scalp lesions of infected
• Seek medical advice to confirm diagnosis and receive
persons, contaminated clothing, bath mats, towels, floors
appropriate treatment.
and showers.
• Exclude infected persons from communal swimming
and bathing facilities until appropriate treatment has
Animals: through cats, dogs, mice, guinea pigs. Cattle
commenced.
and horses may be infected.
• Maintain hygiene by regular, thorough bathing with
soap and water and special attention to drying moist
How do You Recognise areas.
R i n g w o rm ? • Do not share clothing or personal linen.
• Frequently launder clothing and linen in hot water.
Ringworm of the Skin
• Inspect close contacts regularly for signs of infection.
This appears as a flat, spreading, circular lesion. The
• Educate persons regarding the nature of the infection,
outer edge is usually reddish. It often contains fluid or
its mode of spread and the need to maintain good
pus, but may also be dry and scaly or moist and crusted.
personal hygiene.
Single or multiple rings may appear. The centre of the
• Wash pets with anti-fungal solution.
patch may appear to be healing.

170
 Rotaviral Gastroenteritis

Victorian Statutory Method of Diagnosis

Re quirem en t Rotavirus infection is diagnosed by identifying rotavirus
Notification is not required. antigen in stools by electron microscopy, ELISA, or latex
School and child care exclusion. agglutination.

Infectious Agent Reservoir

Rotavirus. Human.

Clinical Features Mode of Transmission

Rotavirus infection of children causes a syndrome of The mode of transmission is faecal-oral.
vomiting, diarrhoea and fever that may lead to dehydra-
tion.
Incubation Period
Usually 24–72 hours.
Symptoms last from four to six days.

Public Health Significance and Period of Communicability

During acute illness, viral shedding occurs before
Oc c u r re n c e
symptoms start and lasts for up to 14 days from the
Rotavirus is a major cause of childhood gastroenteritis
onset of diarrhoea.
worldwide.

Patients with a suppressed immune system may shed the

One-third of hospitalised cases of diarrhoea in young
virus for 30 days or more.
children and babies are due to rotavirus. Such cases are
most prone to develop complications such as dehydra-
Asymptomatic cases may also spread infection.
tion and electrolyte disturbances.

Nosocomial infection and outbreaks occur. Susceptibility and Resistance

Susceptibility is greatest between six and 24 months of
Children in child care are at increased risk of infection. age.

In temperate climates, outbreaks of rotavirus gastroen- Immunosuppressed infants are at increased risk of
teritis occur mostly in the cooler months. infection.

Infection in adults is usually subclinical, although out- By three years of age, most children have rotavirus
breaks have been reported among parents of children antibodies.
with rotavirus gastroenteritis, and travellers.

Immunosuppressed persons and the elderly may experi-

ence severe illness.

171
 Control of Case
Cases should be excluded from school and child care
until diarrhoea has ceased.

Lactose intolerance may follow viral gastroenteritis and

cause prolonged diarrhoea. If this occurs, a child may
return to school or child care when they can provide a
doctor’s explanatory letter.

Contact of symptomatic cases with other young family

members should be minimised.

Tre a t m e n t
Oral rehydration therapy.

Control of Contacts
The diagnosis should be considered in symptomatic
contacts.

Preventive Measures
In child care centres, hospitals and family settings,
exposure of infants and young children to persons with
acute gastroenteritis should be prevented.

Patients, families and child care staff should be edu-

cated about personal and environmental hygiene.

All dirty nappies should be assumed to be infectious and

disinfected or disposed of in a sanitary fashion.

Passive immunity may be conferred to persons at risk in

an outbreak by a specially prepared hyperimmune cows’
milk product.

Epidemic Measures
• Investigate outbreaks to determine the source of
infection and mode/s of transmission.
• Do not enrol new children at child care centres during
an outbreak.
172
 Rubella

Victorian Statutory Case Definition

Re quirem ent There is a generalised maculopapular rash and a fever,
Group B notification for both acute rubella and congeni- and one or more of:

tal rubella syndrome (CRS). • Arthralgia/arthritis.

• Lymphadenopathy.
• Conjunctivitis.
School exclusion (acute rubella).
and
• An epidemiological link to a confirmed case.
lnfectious Agent or

Rubella virus. • Demonstration of rubella-specific IgM antibody, except

following immunisation.
or
Clinical Features • A fourfold or greater change in rubella antibody titre
Rubella is a mild febrile viral illness characterised by a between acute and convalescent-phase sera obtained
diffuse punctate and maculopapular rash. at least two weeks apart.
or

Children usually experience few or no constitutional • Isolation of rubella virus from a clinical specimen.

symptoms but adults may experience a one- to five-day

prodrome of low-grade fever, headache, malaise, mild Public Health Significance and
coryza and conjunctivitis.
O c c u r re n c e
Congenital rubella syndrome was a major cause of
Postauricular, occipital and posterior cervical lymphad-
congenital abnormalities, particularly deafness, prior to
enopathy is common and precedes the rash by five to 10
commencing immunisation.
days.

This syndrome still occurs; therefore, there is a the need

Complications include arthralgia and, less commonly,
for immunisation.
arthritis, particularly among adult females.

Encephalitis is a rare complication. Method of Diagnosis

Rubella is diagnosed by a combination of clinical fea-
Congenital rubella syndrome (CRS) occurs in less than tures and laboratory tests (see Case Definition).
25 per cent of infants born to women who acquire rubella
during the first trimester of pregnancy.
Reservoir
The risk of a single congenital defect falls to approxi- Human.
mately 10–20 per cent by the 16th week. Defects are rare
when the maternal infection occurs after the 20th week of
gestation.
Mode of Transmission
It is transmitted by droplet spread or direct contact with
infectious patients.

Infants with CRS shed the virus in their pharyngeal

secretions and urine.
173
 Incubation Period
Usually 16–18 days. There is a range of 14–23 days.
Period of Communicability
It is communicable approximately one week before and
at least four days after the onset of the rash.
CRS infants may shed the virus for months after birth.
Susceptibility and Resistance
Immunity after natural disease is usually permanent.
Immunity after vaccination is long term (usually lifelong),
but reinfection during pregnancy has resulted in cases of
CRS.
Exposure of Pregnant Women to
Rubella
All women should be routinely tested for the presence of
rubella antibodies early in every pregnancy. If this result
is available and the woman is known to be immune, she
may be reassured that her foetus is at little risk.
Pregnant women, in whom immunity to rubella has not
been confirmed for the current pregnancy, and who may
have been exposed to rubella, must be investigated
serologically—irrespective of a history of vaccination,
clinical rubella or previous positive rubella antibody.
Serological testing:
• The pregnant woman should be tested for rubella
antibodies as soon as possible after exposure.
• If the woman is rubella antibody-negative and remains
asymptomatic, a second blood specimen should be
obtained 21 days after the exposure date. However, a
second blood specimen should be obtained as soon
as possible if the woman develops clinical symptoms
suggestive of rubella. A third blood specimen may be
necessary seven days after the onset of symptoms.
174
It is essential that all requests to laboratories state:
• Duration of pregnancy and last menstrual period
(LMP).
• Date of exposure to possible rubella.
• Date of blood specimen.
Ideally, a virologist should be consulted when the
diagnosis is first considered. The clinical picture and all
test results should be discussed by the virologist and the
clinician to enable accurate interpretation of serological
results prior to advising the woman about her individual
risk.
Control of Case
Contact should be avoided, as far as possible, with
pregnant women.
The case should be excluded from school for at least five
days after onset of the rash.
Adults should be excluded from work for the same time.
If the case is pregnant, the diagnosis should be con-
firmed serologically, then the patient referred to her
obstetrician for specialist advice.
Control of Contacts
School contacts should not be excluded from school
regardless of immunisation status.
Post-exposure immunisation will not necessarily be in
time to prevent infection or illness.
Immunoglobulin may be given after exposure in early
pregnancy. It may not prevent infection or viraemia, but
may modify abnormalities in the baby.
Preventive Measures
MMR vaccine is recommended for all infants at 12
months, and at 10–16 years (Year 6 in Victoria).

Women attending for antenatal care should be tested for

rubella antibodies and, if negative, the vaccine should be
recommended immediately post partum.

Women of childbearing age should be tested prior to

pregnancy, if possible. All seronegative women, if not
pregnant, should be offered rubella vaccine.

Women receiving rubella vaccine should be instructed

not to become pregnant for at least three full menstrual
cycles.

Inadvertent rubella vaccination during pregnancy has not

been associated with any CRS-like defects; hence, it is
not necessary to recommend termination.

All health workers should receive rubella vaccine if not

immune.

Epidemic Measures
All suspected outbreaks should be reported promptly to
Human Services.

An outbreak of rubella in a school may justify mass

immunisation, regardless of immune status.

175
 Salmonellosis

Victorian Statutory Method of Diagnosis

Re q u i re m e n t s Isolation of Salmonella from faeces in cases of entero-
Group B notification. colitis.

Isolation of Salmonella from blood and faeces in cases of

Infectious Agent septicaemia.
There are numerous serovars of Salmonella. Salmonella
Typhimurium and Salmonella Enteritidis are the two most
commonly reported worldwide. In 1993 in Victoria, the
Reservoir
most common infections were with Salmonella Domestic and wild animals, including poultry.
Typhimurium, Salmonella Infantis and Salmonella
Bovismorbificans. Patients, convalescent carriers and mild and unrecog-
nised cases.

Clinical Features Pets such as dogs and cats, tortoises, turtles and
It is a bacterial disease that commonly presents as an reptiles.
acute gastroenterocolitis with fever, vomiting, nausea,
abdominal pain and diarrhoea. Chronic carriers are rare among humans but common
among birds and animals.
Dehydration may occur, especially among infants and
the elderly.
Mode of Transmission
Salmonellosis may be complicated by septicaemia or It can be transmitted by:
focal infection. • Ingestion of the organisms in food derived from in-
fected food animals or contaminated by human or
animal faeces:
Public Health Significance and – Raw and undercooked eggs and egg products.
O c c u r re n c e – Raw milk and raw milk products.
Occurrence is worldwide. – Poultry and poultry products.
– Raw red meats.
The prevalence of infection is highest in infants and • Faecal-oral transmission from person to person,
young children. especially when diarrhoea is present.
• Contaminated utensils or tables used for food process-
Outbreaks occur in hospitals, institutions for children and ing and preparation.
nursing homes. • Pet turtles and chickens.

There is high morbidity, but death is uncommon except

Incubation Period
in infants and the elderly.
Usually six to 72 hours; generally about 12–36 hours.

177
 Period of Communicability Patients at high risk (for example, infants under two
months of age, the elderly and the immunosuppressed),
It is communicable through the course of infection—
may need antibiotic therapy.
usually several days to several weeks.

The recommended antibiotics for adults include co-

One per cent of infected adults and 5 per cent of chil-
trimoxazole, amoxycillin, ciprofloxacin and cefotaxime/
dren under five years excrete the organism for more than
ceftriaxone.
one year.

Specialist advice should be sought for treating infants

Antibiotics, given in the acute illness, can prolong the
under two months of age.
carrier state.

Susceptibility and Resistance Control of Contacts

Investigation of contacts and source of infection is not
Susceptibility may be increased by some medical
routinely performed in sporadic cases.
conditions, immunosuppresive therapy and malnutrition.

Severity of the disease varies with: Preventive Measures

• The serotype.
• Thoroughly cook all food derived from animals sources,
• The numbers of organisms ingested.
particularly poultry, pork, egg products and meat
• The vehicle of transmission.
dishes.
• Host factors.
• Avoid recontamination from raw food within the kitchen
after cooking is completed.
Control of Case • Emphasise the importance of refrigerating food and
maintaining a sanitary kitchen.
• Use Standard Precautions when handling faeces,
• Avoid consuming raw or incompletely cooked eggs, or
contaminated clothing and bed linen from hospitalised
using dirty or cracked eggs.
patients.
• Pasteurise all milk and egg products.
• Exclude symptomatic cases from food handling and
• Educate food handlers on the importance of hand
direct care of children, the elderly and
washing and separation of raw and cooked foods.
immunosuppressed patients.
• Exclude all individuals with diarrhoea from food han-
• Instruct asymptomatic individuals in strict personal
dling and care of hospitalised patients, the elderly and
hygiene. Stress proper hand washing.
children.
• Consider the use of quinolones in long-term carriers
• Inspect and supervise abattoirs, butcher shops, food-
who are food handlers.
processing plants and egg-grading stations.

Tre a t m e n t
Epidemic Measures
No antibiotic treatment is indicated in uncomplicated
Sources of contamination, such as use of uncooked
enterocolitis. Antibiotics, given in the acute illness, may
products and inadequate cooking should be investi-
prolong the carrier state.
gated.

Rehydration may be required.

178
Attention should be paid to environmental cleaning,
particularly in institutions, child care centres and food
premises.

In cases of salmonella outbreaks in which eggs are

implicated, look for the egg source and contact the Egg
Industry Co-operative Ltd, telephone: (03) 9789 7077.

179
 Scabies

Victorian Statutory Public Health Significance and

Re quirem ent O c c u r re n c e
Statutory notification not required. Occurrence is worldwide, regardless of age, sex, race or
standards of personal hygiene.
School exclusion.
Cyclical epidemics occur at intervals of 10 to 15 years.

Infectious Agent Outbreaks may occur in child care centres and kinder-
Sarcoptes scabiei (mite). gartens, and not infrequently are reported in nursing
homes and institutions.

Clinical Features
It is a highly contagious parasitic skin infestation, charac- Method of Diagnosis
terised by thin, slightly elevated wavy greyish-white See Clinical Features.
burrows that contain the mites and eggs. Multiple
papules and vesicles soon appear. Diagnosis is confirmed by scraping the burrows with a
needle or scalpel blade and identifying the mites or eggs
The most common sites for burrows are between the under the microscope.
fingers and toes, anterior surfaces of the wrists and
elbows, axillae, lower abdomen, beneath female breasts
and genitalia. The face, head, palms and soles are
Reservoir
seldom involved in adults, but in infants any area of skin Human. Other species of mite can also live on humans
may be infected. but do not reproduce in the skin.

Immunosuppressed patients, those with Down syndrome

Mode of Transmission
and geriatric patients may also show a pattern of infesta-
tion similar to that in infants. It is transmitted by:
• Skin contact with an infected person.

Itching varies from person to person but may be severe. • Contact with infected towels, bedclothes and under-

It tends to be more marked at night or after a hot bath. garments only if these have been contaminated by

Scratching frequently leads to secondary infection. infested persons within the last four to five days.

A particularly virulent infection, known as crusted or Incubation Period

Norwegian scabies can occur in debilitated or
Usually two to six weeks before itching occurs in a
immunosuppressed patients including those with HIV
person not previously infected.
infection. These cases are highly infective.

If a person is re-exposed, the incubation period is one to

four days.

181
 Period of Communicability
It is communicable until mites and eggs are destroyed .

Control of Case
Infested patients should be excluded from school or
workplace until the day following the first application of
appropriate treatment.

For hospitalised patients, contact isolation should be

used until appropriate treatment has commenced.

Infested personal garments, towels and bedclothes

should be laundered or dry cleaned.

For details of treatment, see scabies information sheet.

Control of Contacts
• Investigate contacts and source of infestation.
• Treat all household contacts prophylactically and
simultaneously.

Preventive Measures
• Educate the public about the mode of spread, early
diagnosis and treatment.
• Promote good personal hygiene.
• Isolate the case until appropriate treatment has com-
menced.
• Treat patients and their contacts simultaneously.

Epidemic Measures
In an institution, ensure that investigations, screening,
treatment and education are undertaken on a coordi-
nated basis.

182
 Information Sheet
Scabies

What is Scabies? Lesions of scabies are very small, wavy, threadlike,

slightly elevated, greyish-white burrows, most frequently
Scabies is a highly contagious parasitic infestation
localised around finger webs, interior surface of wrists
caused by the mite, Sarcoptes scabiei (itch mite).
and elbows, axilla, lower abdomen, genitalia and under
breasts in women.
Fertilisation of the female mite (less than .33 mm in size)
occurs on the surface of the skin. The female then
The burrow is usually from 1 mm to 10 mm long. The
excavates a burrow into the top layer of the skin where
terminal end of the burrow, where the mites reside, may
she lays her eggs.
be capped with a small blister.

The period from fertilisation to adult mite ranges from two

Bacterial infections can result from constant scratching.
to three weeks.

How Long is the Incubation Are There Any Preventive

Period?
The incubation period is usually two to six weeks. How-
ever, in persons who have been previously infested and
are re-exposed, symptoms recur within one to four days.
How Long is the Period of
Communicability?
It is communicable until mites and for eggs are de-
stroyed by treatment.
Me a s u re s ?
• Maintain good personal hygiene.
• Do not share clothes, towels or bed linen with others.
• Ensure that all household members are treated simulta-
neously.
• Exclude affected children from school and child care
until treatment has commenced.
• Isolate cases until appropriate treatment has com-
menced.

How do You Get Scabies?

Anybody can get scabies regardless of age, sex, race or
standards of personal hygiene. Scabies spreads from
person to person by direct body contact especially in
children, or by using clothes, bedclothes or towels soon
after being used by an infested person.

How Can You Recognise

Scabies?
The primary presenting complaint is intense itching that
characteristically worsens at night after the bed is
warmed by the patient’s body heat. A severe itch for
weeks or months should arouse suspicion of scabies.

183
 Information Sheet
Treatment of Scabies

• Lotions or creams used for treatment are available from

chemists. A prescription is not needed.
• All household members and sexual contacts should be
treated simultaneously.
• The lotions or creams are applied to the whole body
from the neck to the toes, but the face and head
should be avoided.
• Another person should help apply it.
• After eight to 12 hours, the application is washed off
with soap and water.
• Hot baths are not taken before treatment.
• Treatments of choice are lindane (Quellada), benzyl
benzoate (Ascabiol), pyrethrins (Lyban Foam,
Pyrifoam) and permethrin (Lyclear).
• Note that lindane should not be used during preg-
nancy, lactation, in young children or in those with
extensive dermatitis.
• Crotamiton (Eurax) is recommended for children as is
Lyclear and diluted benzyl benzoate. (For children
under 12 years, dilute the benzyl benzoate with an
equal quantity of water; for infants, dilute with three
parts water).
• The patient will be non-infectious within 24 hours, but
up to two months may be required for the skin lesions
and itch to disappear completely.
• A second application may be recommended in one
week, but repeated retreatment should be avoided
since dermatitis may develop.
• Antihistamines, calamine lotion and Eurax are useful to
counteract itchiness. Antibiotics may be needed if
there is secondary infection.
• Bed linen, clothes and towels used by the patient prior
to treatment should be machine washed in hot water.
• Blankets can be dry cleaned or placed in a tumble
dryer on a hot setting for half an hour, or sealed in a
plastic bag for one week.
• Fumigation of living areas is not necessary.

184
 Shigellosis
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agents
The genus Shigella consists of four species:
• Group A: Sh. dysenteriae.
• Group B: Sh. flexneri.
• Group C: Sh. boydii.
• Group D: Sh. sonnei.
Groups A, B and C are further divided into approximately
40 serotypes, designated by numbers.
Clinical Features
It is an acute bacterial disease characterised by diar-
rhoea, fever, nausea, vomiting and abdominal cramps.
Toxaemia may be present.
Typically the stools contain blood, mucus and pus,
although some cases will present with a watery diar-
rhoea.
Asymptomatic infections occur.
The illness is usually self-limited, and lasts from several
days to weeks with an average of four to seven days.
The severity of the infection depends on the age and
state of nutrition of the patient and the serotype of
Shigella; for example, many infections with Sh. sonnei
result in a short clinical course, and a very low case
fatality rate. In contrast, Sh. dysenteriae is often associ-
ated with serious disease and a high case fatality rate.
Public Health Significance and
O c c u r re n c e
Occurrence is worldwide.
Two-thirds of the cases and most of the deaths are in
children under 10 years. The disease is very rare in
infants under six months of age.
Secondary attack rates in households may be as high as
40 per cent.
Outbreaks commonly occur in prisons, institutions for
children, child care centres, psychiatric hospitals,
crowded camps and in homosexual groups.
Sh. boydii, Sh. dysenteriae and Sh. flexneri occur mostly
in developing countries. Sh. sonnei is the most common
and Sh. dysenteriae is uncommon in developed coun-
tries, but may be imported by travellers.
Method of Diagnosis
It can be diagnosed by isolation of Shigella spp. from
faeces or rectal swabs.
Reservoir
Humans are the only significant reservoir.
Mode of Transmission
It is transmitted by:
• The faecal-oral route from patients or carriers. Infection
may occur after the ingestion of very few organisms.
• Contaminated water or milk.
Incubation Period
From 12 hours to four days (usually one to three days);
up to one week for Sh. dysenteriae.
185
 Period of Communicability
It is communicable during acute infection and while the
infectious agent is present in faeces (usually no longer
than four weeks).

Asymptomatic carriers may transmit infection.

Cases of severe dysentery need antibiotic therapy based

on sensitivity test results.

Shigellosis imported from South and East Asia is often

drug resistant but norfloxacin remains effective.

Control of Contacts
Symptomatic contacts of shigellosis patients should be
excluded from food handling and the care of children or
patients until investigated.

Contacts and the source of infection should be investi-

gated. Stool cultures from contacts need only to be
confined to food handlers and those in situations where
the spread of infection is particularly likely (child care
centres, hospitals, institutions).

Epidemic Measures
• Investigate food, water and milk supplies.
• Stress the importance of hand washing after toilet use.
• Pay attention to cleaning, particularly in toilet areas.

186
 Streptococcal Disease Caused by Group A
Beta-Haemolytic Streptococcus
Streptococcal Sore Throat, Scarlet Fever (see also impetigo)

Victorian Statutory Method of Diagnosis

Re quirem en t Culture of S. pyogenes from a throat swab is the routine
Statutory notification not required. method of diagnosis. Serological tests are also available.

School exclusion.
Reservoir
Human.
Infectious Agent
Streptococcus pyogenes. Modes of Transmission
It is transmitted by direct contact with patient or carriers.
Clinical Features
Streptococcal sore throat in its typical form is manifested Outbreaks of streptococcal infection may also occur as a
by sore throat, fever, red pharynx and tonsillar exudate. result of ingestion of contaminated foods such as milk,
This form occurs in about 20 per cent of patients. In its milk products and eggs.
atypical form in children, convulsions may occur. Cervi-
cal and submaxillary nodes may enlarge and become
Incubation Period
tender. In children younger than four years of age,
Usually one to three days.
rhinorrhoea may be the sole manifestation of the infec-
tion.
Period of Communicability
The clinical manifestation of scarlet fever consists of
With adequate penicillin therapy, it is communicable for
streptococcal pharyngitis and a diffuse pink-red cutane-
24–48 hours; in untreated cases, for 10–21 days.
ous flush that blanches on pressure. The rash is seen
best on the abdomen, lateral chest and in cutaneous
Patients with untreated streptococcal infection with
folds. Characteristic manifestations of the disease
purulent discharges may spread the infection for weeks
include ‘strawberry tongue’ and circumoral pallor.
or months.

Public Health Significance and Susceptibility and Resistance

Oc c u r re n c e
It is a common infection with potentially serious compli-
cations such as rheumatic fever or glomerulonephritis.
Scarlet fever and streptococcal sore throat are common
infections in temperate zones. Sick children should be
excluded from children’s settings until a medical certifi-
cate of recovery from infection has been obtained.
Susceptibility to streptococcal infection and scarlet fever
is general.
Due to different types of streptococci, repeated attacks
are frequent, although many people will develop a type-
specific immunity.

187
 Control of Case
Secretion precautions may be terminated after 24–48
hours of treatment with penicillin or other effective
antibiotics.
There should be concurrent disinfection of purulent
discharges and other soiled articles.
Tre a t m e n t
Penicillin IM or oral for 10 days. For penicillin-sensitive
patients, use erythromycin. If the above antibiotics are
contraindicated, clindamycin or a cephalosporin may be
used.
Control of Contacts
Not required for sporadic cases.
Preventive Measures
The public should be educated regarding:
• Modes of transmission.
• Complications.
• The need to complete the full course of antibiotic.
Long-term antimicrobial prophylaxis. Persons with
previous rheumatic fever or chorea should receive
injections of long-acting penicillin or daily oral penicillin.
Epidemic Measures
Any outbreaks should be thoroughly investigated to
identify a possible common source. In an outbreak of
scarlet fever in a classroom or preschool, throat swabs
should be obtained from all children. This should be
followed by treatment with appropriate antibiotics of
those with streptococcal infection.
188
Necrotising Fasciitis
Necrotising fasciitis due to Streptococcus pyogenes
(Group A streptococcus) is an acute infection of the
subcutaneous fascia resulting in its necrosis and gan-
grene of the overlying skin. It is associated with severe
malaise, fever, prostration and prolonged morbidity. The
fatality rate is high in spite of prompt treatment with
penicillin and surgical excision. The speed with which
such infections develop is matched by few other infec-
tious organisms.
Between February and May 1994, a cluster of seven
people living in Gloucestershire, UK developed
necrotising fasciitis and three died. The isolates were
typed by the PHLS Streptococcus Reference Laboratory
and found to be four different M types (M1(2), M3, M5,
untypable). There was no increase in reports of systemic
infection with Group A streptococci elsewhere in Britain.
The cluster in Gloucestershire, although unusual, was
probably a chance occurrence.
Data from the Victorian Hospital Pathogen Surveillance
Scheme (VHPSS) and the Commonwealth Laboratory
Database of Organisms from normally Sterile Sites
(LabDOSS) do not show any increase in the frequency of
such cases. Both schemes receive data voluntarily from
hospital laboratories on pathogens from blood and CSF.
VHPSS data over a six-year period shows an incidence
of invasive Group A streptococcal infection, measured by
blood culture isolation, at less than 1 per cent with a
mortality rate of approximately 25 per cent. There were
no clusters and no increase in incidence.
 Ta e n i a s i s
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agent
Taenia solium (pork tapeworm).
Taenia saginata (beef tapeworm).
Clinical Features
Taeniasis is the intestinal infection with the adult stage of
either of the large tapeworms, and follows ingestion of
viable larval forms in undercooked meat.
Cysticercosis results from infection with the larval stages
of T. solium and results from the ingestion of eggs.
Taenia saginata: Usually asymptomatic, although epigas-
tric pain, diarrhoea and weight loss may be presenting
symptoms. Anal passage of segments occurs.
Taenia solium: Infection with the adult worm is usually
asymptomatic. Infection with larvae (cysticercosis) may
manifest as meningoencephalitis, epilepsy or blindness if
vital structures are affected.
Public Health Significance and
Oc c u r re n c e
Occurrence is worldwide.
Both diseases are usually imported to Australia, but
sporadic locally acquired cases of T. saginata infection
have been reported.
Tapeworm infections are commonly seen in parts of Latin
America, Africa, South East Asia and Eastern Europe.
Method of Diagnosis
It can be diagnosed by identification of segments, ova or
head of the parasite in the faeces. (Identification of eggs
can only indicate the genus, not the species).
In cases of cysticercosis, ultrasound, CT scan or X-ray
when cysticerci are calcified.
In the case of T. saginata, infection eggs can be de-
tected with perianal swabs.
Reservoir
Humans are the definitive host for both species.
Cattle are the intermediate host for T. saginata and pigs
for T. solium and certain Asian strains of T. saginata.
Mode of Transmission
T. saginata: Humans are infected with T. saginata by
ingestion of raw or undercooked infected beef. The
tapeworm develops in the intestine in two to three
months. Segments and infectious ova are passed in the
faeces, ingested by cattle and migrate to the muscle to
develop into cysts in about three months.
T. solium: As above with pigs as an intermediate host.
Person-to-person transmission may occur in T. solium
infection, but the result is cysticercosis rather than
tapeworm formation.
Incubation Period
T. saginata: eight to 10 weeks.
T. solium: eight to 12 weeks.
Symptoms of cysticercosis may appear after days, or
more than 10 years after infection.
189
 Period of Communicability Use of raw sewage for irrigation of soil should be
avoided.
It is communicable as long as infectious ova are
passed—sometimes for years.
Beef and pork, should be adequately cooked; for exam-
ple, at 56˚C for five minutes.
Eggs may remain viable in the environment for months.

Cysticerci should be killed by freezing meat below -5˚C

T. solium may be transmitted from person to person.
for more than four days.

Susceptibility and Resistance Persons harbouring adult T. solium should be immedi-

Susceptibility is general. ately identified and treated to prevent human cysticerco-
sis.
No apparent resistance follows infection.
Meat should be routinely inspected at slaughter.

Control of Case
Isolation is indicated only for persons infected with T.
Epidemic Measures
solium until treated. Not applicable.

There should be sanitary disposal of faeces.

Tre a t m e n t
Praziquantel (Biltricide) or niclosamide (Yomesan) are
used for treatment of beef and pork tapeworm.

Surgical intervention is required for cysticercosis and

Praziquantel for certain cases of cysticercosis.

Control of Contacts
• Investigate contacts and source of infection.
• Evaluate symptomatic contacts.

Preventive Measures
Proper public education should be undertaken.

Soil contamination by human excreta should be pre-

vented.

190
 Te t a n u s
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agent
Clostridium tetani.
Clinical Features
Tetanus is caused by an exotoxin (neurotoxin) secreted
by the tetanus bacillus multiplying at the site of injury.
Symptoms consist of stiffness followed by painful muscu-
lar contractions. These usually begin near the site of
injury and often become generalised. Opisthotonus
(painful spasms of the back muscle), lockjaw and
interference with respiration and laryngeal spasm can
occur.
Tetanus may occur after a trivial or inapparent injury.
Case fatality rate is 30 to 90 per cent, varying inversely
with the incubation period. It is highest in infants
(neonatal tetanus) and the elderly.
Case Definition
It is a clinically compatible illness without other apparent
cause, with or without a history of injury, and with or
without laboratory evidence of the organism or its toxin.
Public Health Significance and
Oc c u r re n c e
Tetanus is now rare in this community and usually
reflects waning immunity in the elderly.
Occurrence is worldwide.
Nosocomial cases have been described and may be a
particular risk in setting peripheral vascular disease in
the elderly.
Neonatal tetanus is common in developing countries, but
is extremely rare in Australia.
Method of Diagnosis
Attempts at laboratory confirmation are of little help.
The organism is often not recovered from the site of
infection and usually there is no detectable antibody
response.
Reservoir
C. tetani is widely distributed in cultivated soil and in the
gut of humans and animals. Spores are found on con-
taminated fomites.
Mode of Transmission
Spores may be introduced through contaminated punc-
ture wounds, lacerations, burns, trivial wounds or in-
jected contaminated street drugs.
Incubation Period
Usually three to 21 days (may range from one day to
several months). The average is 10 days.
Period of Communicability
It is not directly transmitted from person to person.
Spores may remain viable for many years in the environ-
ment.
191
 Susceptibility and Resistance Control of Contacts
Active immunity is produced by immunisation with There is no need for quarantine, disinfection or immuni-
tetanus toxoid and persists for at least 10 years after full sation of contacts.
immunisation.

Transient passive immunity follows injection of tetanus

Preventive Measures
immune globulin (TIG) or tetanus antitoxin. The public should be educated about the necessity for
complete immunisation with tetanus toxoid.

Recovery from tetanus is not necessarily associated with

immunity. Tetanus toxoid is recommended at two, four, six and 18
months and at five years (given as DTP) and every 10
years thereafter (given as ADT).
Control of Case
• Refer the patient immediately to a specialised centre Tetanus prophylaxis shold be used in wound manage-
with intensive care facilities. ment.
• Use IV Tetanus immune globulin (TIG).
• Use IV penicillin in large doses for 10 to 14 days.
• Ensure adequate debridement.
Epidemic Measures
• Pay careful attention to control of the airway and Not applicable.
muscle spasm.
• Conduct case investigation to determine the circum-
stances of injury.
• Ensure completion of course of active immunisation.

NH&MRC Recommendations for Tetanus Prophylaxis

Tetanus
History of Active Immunisation Type of Wound Tetanus Toxoid* Immunoglobulin
Uncertain or less than three doses Clean, minor wound Yes No
All other wounds Yes No

Three doses or more: – If less than five years Clean, minor wound No No
since last dose All other wounds No No

– If 5–10 years Clean, minor wound No No

since last dose All other wounds Yes No

– If more than 10 years Clean, minor wound Yes No

since last dose All other wounds Yes Yes

* If child less than eight years old, use DTP in preference to tetanus toxoid alone.

If the person is eight years of age or older, use ADT in preference to tetanus toxoid alone.

192
 To x o p l a s m o s i s

Victorian Statutory Public Health Significance and

Re quirem en t O c c u r re n c e
Statutory notification not required. Toxoplasmosis occurs worldwide in mammals and birds.
Infection in humans is common.
School exclusion not required.
No immunisation is available.

Infectious Agent
Toxoplasma gondii, an intracellular coccidian protozoan Method of Diagnosis
of cats. It is diagnosed by:
• Clinical signs and supportive laboratory results.
• Visualisation of the protozoa in body tissues or isolation
Clinical Features in animals.
Toxoplasmosis is a systemic disease that is contracted • Serology: rising antibody titres, or specific IgM anti-
by eating raw or undercooked meat, or through contact bodies in infants and rising titres in sequential sera are
with cat faeces. evidence of congenital infection.

Primary infection is frequently asymptomatic, or it may Note

present as an acute disease. When the disease occurs,
common symptoms are:
• Enlarged lymph nodes.
• Muscle pain.
• Intermittent fever.
• Generally feeling ill.
• Very rarely with cerebral signs and pneumonitis.
Cerebral toxoplasmosis is a frequent component of AIDS.
Toxoplasmosis in pregnant women can affect the unborn
child. It may cause rashes, damage to the child’s nerv-
ous system, liver or other organs, but rarely death.
In Australia, very few cases of affected newborn children
High levels of antibody titres may persist for years
without active disease.
Reservoir
The main hosts are cats and other felines that acquire
infection mainly from eating affected mammals (espe-
cially rodents) or birds.
Intermediate hosts that carry an infective stage include
sheep, goats, rodents, swine, cattle, chicken and birds.
Mode of Transmission
Children may become infected by ingesting oocysts from

have occurred. dirt, sandpits and playgrounds in which cats have

defecated.

Toxoplasmosis acquired after birth usually results in no

symptoms or mild illness. Infections may be acquired by eating raw or
undercooked infected meat containing tissue cysts.

193
 Transplacental infection occurs when a woman has a Common exposure to cat faeces, soil, raw meat or
primary infection. infected animals should be determined.

Apart from transmission from mother to unborn child, Treatment is not usually indicated except in an initial
person-to-person spread does not occur. infection during pregnancy, presence of active chorio-
retinitis, myocarditis or other organ involvement.

Incubation Period
Uncertain, but probably ranges from several days to Preventive Measures
months. Pregnant women should:
• Cook meat thoroughly.
• Avoid cleaning litter trays and contact with cats.
Period of Communicability
Oocysts spread by cats may remain infective in water or Cats should be fed with dry, canned or boiled food. Cats
moist soil for about a year. should be discouraged from hunting and scavaging.

Cysts in the flesh of infected animals remains infective as Cat faeces and litter should be disposed of daily, as it
long as the meat is uncooked. becomes infectious after 24 hours.

Susceptibility and Resistance
Susceptibility to infection is general, but immunity is
readily acquired and most infections are asymptomatic.
Hands should be washed thoroughly before eating, and
after handling raw meat or having contact with soil and
cat litter/faeces.

Stray cats should be controllled and prevented from

The duration and degree of immunity is assumed to be
gaining access to sandpits and soil used by children.
long lasting or permanent.
Sandpits should be covered when not in use.

Patients undergoing cytotoxic or immunosuppressive

• Patients with AIDS who have severe symptomatic
therapy or patients with AIDS are at high risk of develop-
toxoplasmosis should receive prophylactic treatment
ing illness from reactivated infection.
throughout life.

Control of Case
School exclusion is not required as person-to-person
spread does not occur.

Isolation of patient is not required.

The source of infection should be investigated.

194
 Typhoid and Paratyphoid Fevers

Victorian Statutory Reservoir

Re quirem ent Typhoid fever: Human, especially gallbladder carriers
Group A notification. and, rarely, urinary carriers.

Infectious Agent Paratyphoid fever: Human and, occasionally, domestic

animals.
Salmonella Typhi.

Salmonella Paratyphi—A,B,C. Mode of Transmission

Clinical Features
It is a generalised infection with non-specific onset
characterised by involvement of the lymphoid tissues
and fever, bradycardia, ‘rose spots’, splenomegaly and
abdominal symptoms.
It is transmitted by contaminated water and food; rarely
by contact.
For travellers, important sources are water or ice, raw
vegetables, salads and shellfish.

Incubation Period
Complications such as intestinal haemorrhage or perfo-
Typhoid fever: Usually one to three weeks (depending on
ration can develop in untreated patients or when treat-
the infective dose, from three days to three months).
ment is delayed.

Paratyphoid fever: Usually one to 10 days.

Paratyphoid infection presents a similar clinical picture
but is usually milder, shorter in duration and with fewer
complications. Period of Communicability
It is communicable as long as typhoid or paratyphoid
Public Health Significance and bacilli are present in excreta.
Oc c u r re n c e
Occurrence is worldwide. Some patients become permanent carriers.

Outbreaks occur in areas with poor sanitation and

Susceptibility and Resistance
inadequate sewerage systems.
Susceptibility is general.

In Victoria, approximately 30–40 cases of enteric fever

Immunity following clinical disease or immunisation is
occur each year, the majority being in returned travellers,
insufficient to protect against large infectious doses of
especially from the Indian subcontinent.
organisms.

Method of Diagnosis
It can diagnosed by the demonstration of typhoid bacilli
Control of Case
in the blood, urine and/or faeces. Repeated sampling Hospitalisation is required for an acute infection.
may be necessary. Serology (that is, the Widal test), is no
longer routinely used. Ciprofloxacin, ceftriaxone, chloramphenicol, amoxycillin
or co-trimoxazole are used in treatment.

195
 However, strains resistant to chloramphenicol,
amoxycillin and co-trimoxazole are common in south
Asia. Failure to respond to ciprofloxacin has been
reported from Vietnam.
Investigative Procedures
Establish:
• Occupation and whether the case is a food handler.
• Recent overseas travel (dates, localities).
• Contact with recent overseas traveller (dates and
places of travel).
• Food history.
• Clinical history such as:
– Date of onset and symptoms.
– Hospital admission and discharge.
– Therapy provided.
– Criteria used in diagnosis.
– Date of pre-travel immunisation (oral or injection).
Follow-Up Procedures
• Educate and counsel the patient regarding the possi-
bility of relapse, persisting excretion, the need for good
personal hygiene and precautions in food preparation.
• Obtain specimen of faeces each week for three weeks
commencing at least 48 hours after cessation of
chemotherapy.
• Keep under supervision and exclude from food han-
dling or patient care until three consecutive negative
specimens of faeces are obtained at weekly intervals.
If the patient has to prepare food in the household, this
should only continue after education, counselling and
evaluation.
• Repeat the procedure with three faecal cultures at
weekly intervals three months after diagnosis if the
three initial faecal cultures are negative.
• Refer back to treating doctor for reassessment if
positive cultures appear at any stage.
196
• Collect urine samples in addition to faeces if the
patient:
– Was initially diagnosed with a positive urine culture.
– Has a past history of urinary tract disease, especially
with stone formation.
– Has a history of schistomiasis.
Control of Contacts
Surveillance of all contacts for four weeks is advised from
the last date of contact with a case.
For household contacts of patient who has been an
overseas traveller:
• Obtain one specimen of faeces after four weeks if the
contact is a food handler. If a not a food handler, no
investigation is necessary.
• Obtain one specimen of faeces after four weeks for
children under the age of 10 years.
For household contacts of a patient who has not been
overseas (that is, the source of infection uncertain):
• Collect a specimen of faeces each week for three
weeks in order to eliminate the possibility of an asymp-
tomatic carrier as the source of infection. This should
be done for all contacts. If the faecal samples are
negative, consider urine samples for detection of an
asymptomatic urinary carrier.
For fellow travellers who have remained well (that is,
travel companions):
• Obtain a specimen of faeces each week for three
weeks to eliminate the possibility of asymptomatic
carriage.
• Exclude from food handling until three consecutive
negative samples are obtained at weekly intervals if a
food handler.
Environment:
• Document suspected overseas source, if possible.
• Trace local source. Consider any other known cases of
same type. Consider food history, play groups and so
on.
Typhoid Carrier purging with 15 grams of magnesium sulphate dis-
solved in 250 ml of water.
The following is an extract from the Health (Infectious
• Repeat the above procedure two months later.
Diseases) Regulations 1990. S.R. No. 85/1990.
• Repeat the above procedure after an interval of one
month, if any of these specimens are positive, until two
Division 2—Prevention of Typhoid.
sets of three consecutive negative specimens are
Definition obtained.
‘22. In this Division—
‘Typhoid carrier’ means any person who continues to
excrete Salmonella Typhi organisms in their excre- Specimen Collection
tion or discharges 90 days or longer after cessation See appendix 7.
of a course of antibiotics or other treatment although
presenting no signs or symptoms of typhoid fever.
Transport of Specimens
Duties of Chief General Manager See appendix 7.

‘23. The Chief General Manager:

‘(a) must investigate all cases of typhoid fever and Laboratory Destination
isolations of Salmonella Typhi notified under Part 3 of
Microbiological Diagnostic Unit
these Regulations, and
Department of Microbiology
‘(b) must keep a register of typhoid carriers, and
University of Melbourne
‘(c) may remove from the register the name of any
Parkville Vic. 3052
person if satisfied that the person is no longer a
carrier, and
(A copy of all results to be forwarded to Human Services,
‘(d) must inform a person that his or her name has been
Victoria.)
included in, or removed from, the register.

Prohibition on food handing Preventive Measures

‘24. A typhoid carrier must not engage in the prepara-
tion, manufacture or handling of food for consump-
tion by others. Penalty 20 penalty units.’
Removal from Typhoid Register
No attempt should be made to remove a patient from the
typhoid register within one month after cessation of
specific therapy.
Pr o c e d u re
• Obtain three consecutive negative cultures from
authenticated specimens of faeces at weekly intervals.
One of these specimens should be obtained by
Vaccination is not routinely recommended, except for
travellers who will be exposed for prolonged periods to
potentially contaminated food and water in countries
such as Asia, the Middle East, Africa, Latin America and
the Pacific Islands.
Vaccination should be considered for laboratory workers
in potential contact with Salmonella Typhi. Three
vaccines are currently available in Australia. The oral
vaccine and Vi antigen injectable vaccine generally
cause fewer adverse reactions than the heat-inactivated
injectable vaccine. All are about equally effective.

197
 Vaccination does not offer full protection from infection,
and travellers should be advised to exercise care in
selecting food and drink.

No vaccine is available against paratyphoid fever.

The community should be educated about personal

hygiene, especially thorough hand washing after toilet
use and before food preparation.

It is important to provide a:
• Pure water supply.
• Pasteurised milk supply.
• Proper sewerage system.

Strict supervision of the preparation, storage and distri-

bution of food in factories, shops, kitchens and canteens
should take place.

The supply of shellfish from approved sources should be

secured.

Carriers should be excluded from handling food.

Chronic carriers should be investigated and treated with

ampicillin, co-trimoxazole or ciprofloxacin. Gallbladder
function should be assessed. If gallstones are present, a
cholecystectomy may be required. A full investigation of
the urinary tract should take place in the case of urinary
carriers.

Epidemic Measures
• Look for sources of infection such as chronic carriers,
and/or contaminated water or food supplies.
• Boil or pasteurise milk.
• Chlorinate or boil drinking water before use.

198
 Typhus (Epidemic Louse-Borne Typhus)

Victorian Statutory Method of Diagnosis

Re quirem ent It can be diagnosed by:
Group A notification. • Serologic tests.
• Weil-Felix reaction with Proteus OX-19 (largely obso-
lete).
Infectious Agent • Complement fixation test with group-specific or type-
Rickettsia prowazekii, Rickettsia rickettsii, Rickettsia specific antigen.
conorii, Rickettsia australis, Rickettsia tsutsugamushi. • The IFA test (most commonly used).
• Toxin neutralisation test.
• Isolation and identification of rickettsiae by inoculation
Clinical Features of guinea pigs with infected blood.
It is an acute, severe febrile disease characterised by
prolonged high fever, headache and a maculopapular
rash. Reservoir
Humans and, in the USA, flying squirrel.
Fever may reach 40oC and remain at a high level for
about two weeks.
Mode of Transmission
On the fourth to sixth day, small pink macules appear in R. prowazekii is found in faeces of the infected human
the axillae and on the upper trunk. They rapidly cover the body louse.
body.
Infection occurs when a puncture wound on the skin is
In severe cases, the rash becomes petechial and contaminated by scratching.
haemorrhagic.
Inhalation of dry infective louse faeces may be responsi-
Splenomegaly occurs in some cases. ble for some infections.

The disease resolves after about two weeks. Incubation Period

Usually seven to 14 days; commonly 12 days.
In untreated cases, the fatality rate increases with age
and may reach 40 per cent.
Period of Communicability
Public Health Significance and The disease is not directly transmitted from person to
person.
Oc c u r re n c e
Occurrence is worldwide.
The patient is infective for lice during the febrile illness
and probably two to three days after the temperature
It is associated with overcrowding and poor hygiene
returns to normal.
favouring infestation with body lice.

The louse is infective for two to six days after the infected
blood meal.

199
 Susceptibility and Resistance
Susceptibility is general.
There is long-lasting Immunity following infection.
Control of Case
Isolation is not required after proper delousing of patient,
clothing, living quarters and household contacts.
There should be concurrent disinfection of clothing and
bedding of patient and contacts, and laundering of
clothing and bedding of patient and contacts.
Epidemic Measures
Typhus can be rapidly controlled by applying an insecti-
cide with residual effect to all contacts.
In case of a widespread infection, systematic application
of residual insecticide to all persons in the community is
indicated.
International Measures
Government should notify WHO and neighbouring
countries of the occurrence of disease in an area previ-
ously free of the disease.

Louse-borne typhus is a disease under surveillance by

Tre a t m e n t WHO that should be reported to the Communicable
It should be treated with tetracyclines or chloramphenicol Diseases Network.
orally until the patient becomes afebrile.

Doxycycline in a single dose is also curative.

Seriously ill patients should be treated without waiting for

laboratory confirmation.

Control of Contacts
• Investigate all contacts.
• Look for a source of infection.
• Keep all immediate contacts under surveillance for two
weeks.

Preventive Measures
• Apply an effective residual insecticide powder (Carba-
ryl) to population at risk.
• Improve living conditions and standard of hygiene.
• Immunise susceptible persons or groups of persons
entering typhus area (two doses of 1 ml for children
over 10 years of age and adults, with intervals of four
weeks between doses).

200
 Verotoxin-Producing E. coli
Victorian Statutory
Re quirem ent
Not notifiable at present.
Infectious Agent
Enterohaemorrhagic E. coli (EHEC).
Virulence is determined by secreted toxins, Shiga-like
toxins (SLT) also called verotoxins (Vt), are similar to
toxin produced by Shigella dysenteriae type 1.
Common strains are E. coli O157: H7, E. coli O111: H8,
E. coli O26: H11.
Clinical Features
Diarrhoea may range from mild to severe bloody diar-
rhoea with cramping abdominal pain.
EHEC strains can cause the haemolytic uraemic syn-
drome (HUS), especially in children under five years of
age, and thrombotic thrombocytopaenic purpura.
Public Health Significance and
Oc c u r re n c e
These infections are an important problem in North
America, Europe, Japan, parts of South America and
Australia.
Serious outbreaks, including deaths, have occurred in
the USA from inadequately cooked hamburgers.
A large outbreak in South Australia in 1995 was associ-
ated with the consumption of a brand of fermented
sausage.
Other outbreaks overseas have been caused by unpas-
teurised milk.
Methods of Diagnosis
It can be diagnosed by culture of the organism from
faeces, and then by:
• Demonstrating the presence of Shiga-like toxins.
• Serotyping.
• DNA probes that identify the toxic genes or the pres-
ence of the EHEC virulence plasmid.
Reservoir
Cattle are the reservoir of EHEC.
Humans may also serve as a reservoir for person-to-
person transmission.
Mode of Transmission
It is transmitted by means of contaminated food, mostly
with inadequately cooked beef (especially ground beef)
and raw milk.
Transmission also occurs directly from person to person
in families, child care centres and custodial institutions.
Waterborne transmission has occurred.
Incubation Period
The range is three to eight days; median, three to four
days.
Period of Communicability
It is communicable for the duration of excretion of the
pathogen:
• Typically one week or less in adults.
• Up to three weeks in some children.
201
 Susceptibility and Resistance • Heat beef adequately during cooking to at least 68oC.
• Chlorinate water supplies and swimming pools.
The infectious dose is very low. Little is known about
• Ensure adequate hygiene in child care centres, espe-
susceptibility and immunity.
cially hand washing.

Old age appears to be a risk factor.

Epidemic Measures
Children less than five years are at greatest risk of
Each case of HUS needs a complete laboratory and
developing haemolytic uraemic syndrome (HUS).
epidemiological investigation.

Control of Case A questionnaire should be used to determine the type of

food concerned, water supply and sickness of others in
Standard Precautions should be undertaken during acute
the household or neighbourhood.
illness. The patient should not handle food or provide
child or patient care until two successive negative faecal
Human Services should be notified of any group of cases
samples are taken more than 24 hours apart, and more
of bloody diarrhoea.
than 48 hours after ceasing treatment.

The vehicle (food or water) by which the infection was

Specific treatment includes fluid and electrolyte replace-
transmitted should be looked for, and the potential for
ment.
person-to-person transmission evaluated.

Depending on severity and complications, the patient

The source of contaminated food should be traced and
may need transfusion, dialysis, anticonvulsants or
excluded.
antihypertensives.

If outbreak is water-borne, only boiled or chlorinated

Control of Contacts
Contacts with diarrhoea should be excluded from food
handling and the care of children or patients until the
diarrhoea has ceased and two negative faeces cultures
obtained.
Hand washing and personal hygiene should be stressed.
water should be used for drinking and cooking.
If outbreak is milk-borne, milk should be pasteurised or
boiled.
The importance of hand washing after toilet should be
stressed.

Preventive Measures
• Identify source.
• Instruct family members in hand washing, disposal of
waste, and prevention of contamination of food and
beverages.
• Pasteurise milk and dairy products.
• Manage abattoir operations to minimise contamination
of meat by animal faeces.

202
 Viral Gastroenteritis Caused by Agents
Other than Rotavirus

Victorian Statutory There is probably a low background level of infection in a

community until one or several infected individuals
Re quirem ent
introduce infection and an explosive outbreak occurs.
Group A notification if food- or water-borne transmission
is suspected of causing two or more related cases.
Method of Diagnosis
In many instances, a combination of clinical and epide-
Infectious Agent
miological features will lead to a presumptive diagnosis
Small Round Structured Viruses (SRSVs) including
of viral gastroenteritis.
Norwalk virus and Norwalk-like viruses, Caliciviruses and
Astroviruses, Adenoviruses. (Rotavirus may cause
Bacterial and protozoal gastroenteritis share many
gastroenteritis in adults as well as children.)
features with viral gastroenteritis and should be consid-
ered in the differential diagnosis.
Clinical Features
If a specific diagnosis is sought, stool specimens should
Viral gastroenteritis causes acute non-bloody diarrhoea
be collected during the acute phase of the illness and
and/or vomiting that may be severe.
examined by electron microscopy (EM) at a specialist
centre.
Diarrhoea is more common among adults, vomiting
among children.
Acute and convalescent sera (three to four weeks apart)
may help associate virus particles observed by EM with
Nausea is a prominent symptom and headache, fever,
the acute illness, but routine serologic testing for enteric
chills and myalgia are common.
viruses is not available.

Secondary cases in household and other close contacts

are very common. Mode of Transmission
It is transmitted by:
Public Health Significance and • Person-to-person contact.
• Fomites.
Oc c u r re n c e
• Aerosols.
Enteric viruses are major causes of endemic (back-
• Water and food-borne contact.
ground or sporadic) gastroenteritis and epidemic gastro-
enteritis (particularly institutional outbreaks).
Note
Viral gastroenteritis is highly infectious.
More than half of all outbreaks of acute non-bacterial
gastroenteritis are associated with viruses.
Incubation Period
Outbreaks have been described in many settings includ- Approximately 24 to 48 hours.
ing banquets, cruise ships, tour buses, hospitals and
geriatric care facilities, schools, workplaces and camp-
ing grounds.

203
 Period of Communicability
It is communicable during the acute phase of the dis-
ease and up to 48 hours after the diarrhoea ceases.
Susceptibility and Resistance
Short-term immunity lasts several weeks after infection.
Epidemic Measures
• Investigate outbreaks to determine the source/s and
route/s of transmission.
• Institute control measures.
• Clean exposed environmental surfaces.
• Exclude cases from work, school and gatherings until
48 hours after symptoms cease.
• Consider cohorting exposed persons within institutions.

Control of Case
In most cases the illness is self-limited.

Good hydration should be maintained.

Most cases respond well to oral rehydration. Hospitalisa-

tion and intravenous fluids may be required if dehydra-
tion is severe.

Control of Contacts
Secondary cases should be anticipated in household
contacts and persons exposed to the faeces or vomitus
of cases.

Usually, no specific action is necessary.

Control of Environment
Environmental surfaces exposed to infectious faecal
matter or vomitus should be thoroughly cleaned.

Enteric viruses cannot multiply in food, but food exposed

to viruses may act as a fomite for transmission. There-
fore, discard exposed cooked or ready-to-eat food.

Preventive Measures
Attention should be paid to hygiene and Standard
Precautions taken to reduce transmission of enteric
viruses.

204
 Viral Haemorrhagic Fevers

Victorian Statutory plained fever who has been exposed to the infection in
an area with endemic VHF during the preceding three
Re quirem ent
weeks.
Group A notification.

Method of Diagnosis
Infectious Agents
Lassa Fever (LF):
Lassa fever virus (LF) (Arenavirus); Crimean-Congo
• Isolation of the virus from blood, urine, or throat wash-
Haemorrhagic fever (CCHF) virus (Nairovirus); Ebola
ing.
virus (EV); Marburg virus (MV) (Filoviridae).
• Presence of IgM antibodies to LF.
• Fourfold rise in IgG antibody titre, between acute and
Clinical Features convalescent sera.

Clinically apparent infection with any of these viruses has

Ebola Virus Disease and Marburg Disease (EV & MV):
similar presentations.
• Isolation of the virus from blood.
• Presence of IgM antibodies or rising IgG antibodies to
Fever is typically insidious in onset, and accompanied by
the EV or MV.
headache, significant myalgia and malaise. This is
followed in severe cases by shock and haemorrhage. A
Crimean Congo HF (CCHF):
sore throat often occurs in LF infection.
• Isolation of the virus from blood during the first week of
illness.
The recovery is slow and the overall case fatality rate
• Rising IgG antibody titre to the CCHF virus.
ranges from 2 to 88 per cent in hospitalised patients.

Public Health Significance and Reservoir

Lassa Fever: wild rodents.
Oc c u r re n c e
Lassa, Marburg and Ebola viruses are restricted to sub-
Crimean Congo HF: hares, birds, rodents and infected
Saharan Africa.
ticks.

Crimean-Congo haemorrhagic fever virus is more widely

Ebola Virus: unknown for EV.
distributed in Africa, the Mediterranean region, the
Middle East, Eastern Europe, Central Asia and China.
Marburg Virus: possibly monkeys.

The origins of the Marburg and Ebola viruses are still

unclear but most cases appear to have arisen in Africa. Mode of Transmission
Lassa Fever:
The atypical clinical symptoms and high case fatality rate • Direct or indirect contact with urine of infected rodents.
means that it is important that the diagnosis is made and • Person to person by sexual contact or inoculation with
treatment instituted as early as possible. blood.
• Laboratory-acquired infection.
Viral haemorrhagic fevers should be considered in the
differential diagnosis of every patient with an unex-

205
 Crimean Congo HF: Control of Case
• Bite of infective adult tick.
The Infectious Diseases Unit, Department of Human
• Nosocomial transmission from patients to medical
Services should be immediately contacted (03) 9616
workers by accidental inoculation of blood.
7777, or duty medical officer: (03) 9625 5000, pager
• Butchering infected animals.
number 46870.

Ebola Virus and Marburg Virus:

• Person-to-person transmission by inoculation with
infected blood, and sexual transmission.
Incubation Period
All travellers who arrive in Australia with any risk of a
quarantinable VHF should be notified to the State chief
quarantine officer: (03) 9483 4444, pager number
323757, who will make any decisions concerning pa-
tient’s assessment, transport and quarantine.

Lassa Fever: seven to 21 days.

Isolating Cases
Crimean Congo HF: two to nine days.
All patients should be cared for at the hospital where
they are first seen (if possible), or transferred to an
Ebola Virus: two to 21 days.
infectious disease unit nominated by the State for the
treatment of VHF.
Marburg Virus: three to 10 days.

The obligatory period of isolation for a proven VHF is a

Period of Communicability minimum of two days without fever and a total of 21 days
from onset of illness.
Lassa Fever:
• During the acute febrile phase when virus is present in
Convalescent patients and their contacts should be
the throat.
informed that VHF viruses may be excreted for many
• Three to nine weeks from onset of illness while virus is
weeks in semen (M&E viruses) and in urine (LF). Meticu-
excreted in the urine.
lous personal hygiene is necessary. Abstinence from
sexual intercourse is advised until genital fluids have
Crimean Congo HF:
been shown to be free of the virus.
• It is usually not directly transmitted from person to
person.
For further details of quarantine and isolation proce-
• Nosocomial infections are common.
dures, see Management of Quarantinable Diseases in
• Infected tick remains infective for life.
Australia 1992, Australian Government Publishing
Service, Canberra.
Ebola Virus and Marburg Virus:
• As long as blood and secretions contain virus.
Collecting Specimens
Susceptibility and Resistance Specimens from confirmed or suspected cases should
be regarded as potentially highly infectious. All the
Susceptibility is general.
routine precautions should be taken.

The duration of immunity following infection is unknown.

206
In addition, specimens should be collected in tightly
sealed, screw-top plastic containers labelled with the
patient’s details. The outside of each container should be
swabbed with disinfectant.
The specimens should be double-bagged in secure,
airtight and watertight bags that have been similarly
labelled.
Bags containing specimens should be sprayed with
disinfectant before they are removed from the patient’s
room.
Transporting and Packaging
Specimens
The watertight, primary container with the specimen (no
greater than 50 ml) should be wrapped in sufficient
absorbent material to soak up the contents if a breakage
occurs. It should then be placed in a secondary water-
tight container (sealed plastic bag, leak-proof plastic
bottle or box).
The outer packaging must be of sufficient strength to
protect the secondary packaging from fracture during
transmission.
The secondary container may be placed in a plastic
foam or fibreboard box for further protection.
Examining Specimens
Laboratory staff dealing with specimens from patients
who might have a VHF must wear surgical gloves,
gowns, shoe-covers and masks.
In Australia, all serological tests for the quarantinable
VHF agents are currently carried out at the VIDRL.
Tre a t m e n t
Supportive care with viral haemorrhagic fevers may save
lives.
Fluid and electrolyte balance should be maintained.
Some patients will need intensive care facilities.
Patients with LF and high-risk contacts should receive
the antiviral drug ribavirin.
Its use in patients with CCHF and their high-risk contacts
seems to be justified, although no clinical experience is
available.
Definition of Contact
A contact is a person who has been exposed to an
infected person or to an infected person’s secretions,
excretaor tissues within three weeks of the patient’s
onset of illness.
Contact may be:
• Casual.
• Close.
• High-risk.
Casual contacts are people on the same aeroplane or in
the same hotel. No special surveillance is required.
Close contacts are defined as those living with the
patient, nursing and hugging the patient, or handling the
patient’s laboratory specimens.
These persons should be identified by Human Services,
Victoria, as soon as diagnosis of VHF is considered to be
a likely diagnosis for the index case.
When the diagnosis is confirmed, they should be placed
under surveillance, (record body temperature twice daily
and report any temperature 38.3oC or above to the health
officer responsible for surveillance).
207
 Surveillance should continue for three weeks after the
person’s last contact with the patient.

High-risk contacts are those with:

• Mucous membrane contact with the patient (kissing,
sexual intercourse).
• Needle-stick or other penetrating injury.

These contacts should be placed under surveillance as

soon as VHF is considered to be a likely diagnosis in the
index patient.

Any contact who develops a temperature 38.3oC or

higher or any other symptoms of illness should be
immediately isolated and treated as a VHF patient.

Ribavirin should be prescribed as post-exposure prophy-

laxis for high-risk contacts of patients with LF or with
CCHF.

Preventive Measures
Not applicable in Australia.

Intending travellers to endemic areas of Africa, for

example, should avoid contact with ticks and rodents.

Epidemic Measures
Not determined.

International Measures
Government should notify WHO, source country and
receiving countries of possible exposures by infected
travellers.

208
 Yellow Fever
Victorian Statutory
Re quirem ent
Group A notification.
Infectious Agent
Yellow Fever Virus (flavivirus).
Clinical Features
Yellow fever is an acute viral disease of short duration
with a wide variation in intensity.
The classic triad of jaundice, haemorrhage and severe
albuminuria is present only in a small number of severe
cases.
In mild cases, the only symptoms may be headache and
fever or a ‘dengue-like’ illness with fever, chills and
myalgia.
Malignant cases have three characteristic stages of
infection, remission and intoxication.
Stage one: Fever, chills, backache, myalgia, nausea,
vomiting and epistaxis with Fagets sign (relative brady-
cardia: high temperature, slow pulse) that appear on the
second day. On the third day, the fever falls by crisis and
patient enters remission.
Stage two: Remission that may last several hours to
several days but haemorrhages, anuria and delirium may
occur without remission.
Stage three: Development of the classic symptoms of
jaundice and haemorrhagic manifestations (epistaxis,
haematemesis, melaena and uterine bleeding) followed
by albuminuria, coma and death two to three days later.
Public Health Significance and
O c c u r re n c e
Yellow fever is confined by the ecosystem and suitable
vectors.
It is endemic in Central America and Central Africa, but
outbreaks may occur in unaffected areas if mosquitoes
are infected by migrating humans or monkeys.
The case fatality is 5 per cent in indigenous populations
in endemic areas. In non-indigenous individuals or
during epidemics it may be 50 per cent.
Method of Diagnosis
It is diagnosed by:
• Serology: presence of IgM in early sera.
• Virus isolation by mice inoculation or cell culture.
Reservoir
Mainly an ecosystem in monkeys.
Mode of Transmission
Urban yellow fever is transmitted from person to person
by the Aedes aegypti mosquito.
Jungle yellow fever is a zoonosis transmitted among non-
human hosts (mainly monkeys) by various forest mosqui-
toes that may also bite and infect humans.
If these humans are subsequently bitten by Aedes
aegypti mosquitoes, they become the source of out-
breaks of the urban form of the disease.
Incubation Period
Usually two to five days.
209
 Period of Communicability Insect quarantine should be used to prevent the intro-
duction of Ae. albopictus.
Human blood is infective for mosquitoes shortly before
the onset of fever. For three to five days thereafter,
Certification of yellow fever vaccination should be
mosquitoes require nine to 12 days after a blood meal to
required for travellers over one year of age entering
become infectious and remain so for life.
Australia within six days of leaving an infected country.

Susceptibility and Resistance Unimmunised contacts who visit or stay in the northern
Mild infections are common in endemic areas. part of Australia are subject to quarantine.

Previous infection with dengue gives some degree of A yellow fever vaccination certificate is valid for 10 years
immunity, and passive immunity in infants born to im- and begins 10 days after vaccination.
mune mothers may last for six months.

Epidemic Measures
Recovery from yellow fever gives lifelong immunity.
Epidemic measures include:
• Using mass vaccination.
Control of Case • Spraying all houses with insecticide.
Access of mosquitoes should be prevented (with mos- • Controlling Ae.aegypti near airports.
quito nets and residual sprays) for at least five days after
onset of disease.
International Measures
The Commonwealth Department of Health and Family
Control of Contacts and the Services and WHO should be notiifed.
En v i ro n m e n t
• Investige contacts and source of infection.
• Investigate places visited three to six days before
onset.
• Investigate mild febrile illness.
• Immunise population at risk.
• Determine presence and source of vector mosquitoes.

Preventive Measures
All travellers to endemic areas in Africa and South
America should be immunised.

All people returning from areas with endemic yellow fever

to areas in Australia in which Aedes aegypti multiply
should be immunised.

Ae.aegypti should be controlled near airports.

210
Yellow Fever Vaccine Outlets in Victoria
Name of Vaccine Outlet Telephone Number Facsimile Number

Dr T. Ruff, Dr A. Yung (03) 9818 1594 (03) 9818 0031

Fairfield Travel Health
Allendale Private Hospital
25–27 Linda Crescent
Hawthorn 3122

Dr A. Yung, Dr T. Ruff (03) 9342 7000 (03) 9342 7277

Travellers Medical Vaccination Centre
c/- Royal Melbourne Hospital
Grattan Street
Parkville 3052

Dr D. Gras (03) 9285 8385 (03) 9285 8370

Australian Government Health Service
International Vaccination Clinic
PO Box 9848
Melbourne 3001

Dr S. Lau (03) 9602 5788 (03) 9670 8394

Traveller’s Medical & Vaccination Centre Pty Ltd
2nd Floor, 393 Little Bourke Street
Melbourne 3000

Dr J. Acheson (03) 9614 6444 (03) 9629 2009

World Trade Medical Centre
Building ‘B’ Concourse Level
PO Box 470
Melbourne 3005

Dr C. Okraglik (03) 9670 3871

Central Travel & Vaccination Clinic
3rd Floor, 114 William Street
Melbourne 3000

Dr A. Taylor (03) 5979 1605 (03) 5979 3436

Hastings Clinic
44 Victoria Street
Hastings 3915

211
 Yellow Fever Vaccine Outlets in Victoria
Name of Vaccine Outlet Telephone Number Facsimile Number

Dr R. Shields (03) 9426 (03) 9428 6503

Epworth Healthcheck
34 Erin Street
Richmond 3121

Dr J. Wright (03) 9592 0222 (03) 9592 6095

Brighton Medical Travel Clinic
26 Carpenter Street
Brighton 3186

Dr B. Gilbert (03) 9867 2366 (03) 9866 4885

St Kilda Road Medical Centre
Level 1, 391 St Kilda Road
Melbourne 3000

Dr P. Henderson (03) 5278 9288 (03) 5277 9944

Northern Medical Centre
62 Princess Hwy
Norlane 3214

Dr M. Martin (03) 5523 2322 (03) 5523 6171

Seaport Medical Centre
PO Box 284
Portland 3305

Dr N. Kimpton (03) 5333 1253

South Medical Practice
10 Drummond Street
Ballarat 3350

Dr G. Patience (03) 5762 1022 (03) 5762 6344

Benalla Church Street
Surgery 34 Church Street
Benalla 3672

Dr J. MacKellar (03) 5825 2755 (03) 5825 4235

Mooroopna Medical Centre
87 McLennan Street
Mooroopna 3629

212
Yellow Fever Vaccine Outlets in Victoria
Name of Vaccine Outlet Telephone Number Facsimile Number

Dr I. Nicolson (03) 5144 5766 (03) 5143 1609

The Cunninghame Street Clinic
49 Desailly Street
Sale 3850

Dr R. Grenfell (03 9609 3330 (03) 9609 3661

BHP Medical Centre
40/600 Bourke Street
Melbourne 3000

Dr S. Rosenbaum (03) 9335 2848 (03) 9330 3881

Melbourne Airport Medical Centre
International Terminal
Melbourne Airport
PO Box 637
Tullamarine 3043

Dr F. Bramwell (03) 9398 3711 (03) 9398 4579

Pier Street Medical Centre
125 Pier Street
Altona 3108

Dr M. Bullen (03) 9344 6905 (03) 9437 6684

Student Health Service
257 Grattan Street
Carlton 3053

Dr P. Demaio (03) 9888 8177 (03) 9888 8937

Burwood Health Care
400 Burwood Hwy
Burwood 3125

Dr A. Schmerling (03) 9561 3200 (03) 9561 3608

Wheelers Hill Clinic
847 Ferntree Gully Road
Wheelers Hill 3150

Dr R. Lee (03) 9791 1122 (03) 9679 0118

Heatherton Road N\Medical Clinic
127 Chandler Road
Noble Park 3174

213
 Yellow Fever Vaccine Outlets in Victoria
Name of Vaccine Outlet Telephone Number Facsimile Number

Dr M. Fox (03) 5975 4088

Mornington Travel Health
64 Wilsons Road
Mornington 3931

Dr J. Cohen (03) 9528 1910 (03) 9352 9555

The Travel Clinic 263 Glen Eira Rd
North Caulfield 3161

Dr J. Scally (03) 9331 1666 (03) 9337 1129

Essendon Travel Health Centre
278 Buckley Street
Essendon 3040

Dr D. Jones (03) 5243 1111

South Barwon Medical Group
66 Settlement Rd
Belmont 3216

214
 Ye r s i n i o s i s
Victorian Statutory
Re quirem ent
Group B notification.
Infectious Agents
Yersinia pseudotuberculosis.
Yersinia enterocolitica (many serovars).
Clinical Features
Yersiniosis is an acute bacterial enteric disease mani-
fested by acute watery diarrhoea (especially in young
children), enterocolitis, acute mesenteric lymphadenitis,
fever, headache, pharyngitis, anorexia, vomiting, ery-
thema nodosum, post-infectious arthritis, iritis, cutaneous
ulceration, hepatosplenic abscesses, osteomyelitis and
septicaemia.
Many cases of yersiniosis occur in children.
Public Health Significance and
Oc c u r re n c e
It is a serious acute enteric disease that is primarily a
zoonotic disease of wild and domesticated birds and
mammals. Humans are accidental hosts.
Yersinia can be transmitted by blood transfusion when
the donor is asymptomatically infected and the organism
multiplies at refrigeration temperatures.
Yersinia spp. are able to multiply at low temperatures (for
example, under refrigeration).
Method of Diagnosis
The specimen of choice in an enteric disease is a freshly
passed stool. Rectal swabs will not yield maximal
number of positive cultures and are not of value when
examining convalescent patients or surveying for carri-
ers.
Multiple specimens should be cultured. The specimens
should be collected early in the course of disease before
initiation of antimicrobial therapy.
All fluids, including pus and wound exudate, should be
collected in a sterile syringe and transported directly to
the laboratory or transferred to an anaerobic transport
vial.
Tr a n s p o r t
Swab-transport medium devices will generally maintain
aerobic and facultatively anaerobic bacteria for several
hours when stored at room or refrigerator temperature.
Urine should be processed within two hours of its collec-
tion unless refrigerated (4oC).
Reservoir
Animals are the principal reservoirs; for example, pigs for
Y. enterocolitica.
Y. pseudotuberculosis is widely spread among many
species of avian and mammalian hosts, particularly
rodents and other small mammals.
Mode of Transmission
It is transmitted faecal-orally by eating and drinking
contaminated food or water, especially through eating
raw pork or pork products.
It can also be transmitted through contact with infected
persons or animals.
Nosocomial infection and infections from blood transfu-
sion have been reported.
Incubation Period
Usually three to seven days; generally less than 10 days.
215
 Period of Communicability
Faecal shedding occurs for as long as symptoms persist
(about two to three weeks).
If untreated, shedding may occur for two to three
months.
Susceptibility and Resistance
Gastroenterocolitis is more severe in children.
Post-infectious arthritis is more severe in adolescents
and older adults, especially those who are HLA-B27
positive.
Y. pseudotuberculosis shows a predilection for male
adolescents.
Y. enterocolitica attacks both sexes equally.
Those with iron overload (for example, haemochromato-
sis) or the immunocompromised are predisposed to the
septicaemic form of disease.
Control of Case
The case should be isolated and Standard Precautions
taken for patients in hospitals.
Those with diarrhoea should be removed from food
handling, patient care, and occupations involving care of
young children.
There is no quarantine and sewerage disposal of faeces
is adequate.
Specific Treatment
Specific treatments include:
• Co-trimoxazole for Y. enterocolitica; aminoglycosides
for the septicaemic form of disease only.
• Tetracyclines.
• Quinolones; for example, ciprofloxacin.
216
Control of Contacts
Searching for unrecognised cases and convalescent
carriers among contacts is indicated only when a com-
mon source of exposure is suspected.
Control of Environment
General sanitation should be investigated and a com-
mon-source vehicle sought.
Attention should be paid to close contacts with animals,
especially pet dogs, cats and other domestic animals.
Water supplies should be chlorinated to kill Yersinia spp.
Preventive Measures
Preventive measures include:
• Education.
• Hand washing prior to food handling and eating, after
handling raw pork and after animal contact.
• Sanitary preparation of food and meats, especially of
food to be eaten raw.
• Pasteurisation of milk.
• Protection of water supplies from animal and human
faeces.
• Disposal of faeces in a sanitary manner.
• Removal of head and neck from the body of pigs after
slaughter to avoid contaminating other parts from the
heavily colonised pharynx.
Epidemic Measures
Any group of cases of acute gastroenteritis or appendici-
tis syndrome should be investigated for a common-
source vehicle.
Attention should be given to close contacts with animals,
especially pet dogs, cats and other domestic animals.
 Appendix 1: Telephone and Facsimile
Numbers

Organisation Telephone Number Facsimile Number After Hours Contact

Interstate Health Departments

Adelaide: Communicable Diseases Unit (08) 8266 6352 (08) 8226 6339 Mobile 041 981 2788
Brisbane (07) 3234 0938 (07) 3234 1480 –
ACT (06) 205 5111 (06) 205 1300 –
ACT Commonwealth (06) 289 1555 (06) 281 6946 –
Darwin (089) 228 265 (089) 228 310 (089) 228 888 Hospital
switchboard
Hobart: Public Health Branch (002) 333 775 (002) 336 620 Pager 016 010 Quote
164861
Perth: Communicable Diseases Unit (09) 388 4999 (09) 388 4955 –
Sydney (02) 391 9288 (02) 391 9209 –

Department of Human Services, Victoria

Infectious Diseases Unit (03) 9616 7777 (03) 9616 8329 Pager (03) 9625 500
Quote 46870
Melbourne Sexual Health Centre (03) 9347 0244 (03) 9347 2230 —

Tuberculosis Program (03) 9616 7777 (03) 9616 8329 –

Laboratories
Microbiological Diagnostic Unit (03) 9344 5713 (03) 9344 7833 –
Victorian Infectious Diseases Reference (03) 9280 2222 (03) 9280 2898 24-hour switchboard
Laboratory
Victorian Institute of Animal Science: Attwood (03) 9217 4200 (03) 9217 4299 Night message on
switchboard
Australian National Animal Health Laboratory: (03) 5275 5000
Geelong –

Other Government Instrumentalities

Australia New Zealand National
Food Authority (06) 271 2222 (06) 271 2278 Night switch
Chief Veterinary Officer (03) 9338 3344 (03) 9338 0844 Night switch
Food Research: Werribee (03) 9742 0111 (03) 9742 0201 Recorded message
Commonwealth Serum Laboratories (03) 9389 1911 (03) 9389 1434 Night switch
Egg Marketing Board (03) 9798 7077 (03) 9701 5729 –

217
 Appendix 2: Glossary
Blood and body substance precautions
See appendix 4.
Carrier
A person or animal that harbours a specific infectious
agent in the absence of clinical disease and serves as a
potential source of infection.
Communicable disease
A disease capable of being transmitted from an infected
person or species to a susceptible host, either directly or
indirectly.
Contact
A person or animal that has associated with an infected
person or animal that might provide an opportunity to
acquire the infection.
Disinfection
Killing of infectious agents outside the body by direct
exposure to chemical or physical agents. High level
disinfection refers to the inactivation of all microorgan-
isms except some bacterial spores.
Concurrent disinfection
Immediate disinfection and disposal of discharges and
infective matter all through the course of a disease.
Drainage/secretion precautions
Precautions used to prevent infections transmitted by
direct or indirect contact with purulent material or
drainage from an infected body site.
Endemic
The constant presence of a disease or infectious agent
within a given geographic area.
Epidemic
The occurrence of a number of cases of a disease (or
condition) in excess of a number expected in a given
time and place. In some instances a single case will
constitute such an unusual occurrence.
Fomes (plural fomites)
An object such as a book, wooden object, or an article of
clothing that is not harmful in itself, but is able to harbour
pathogenic microorganisms and thus may serve as an
agent of transmission of an infection.
Immunity
The protection against infectious disease generated by
immunisation, previous infection or by other
nonimmunologic factors.
Inapparent infection
The presence of infection in a host without recognisable
clinical signs or symptoms.
Incubation period
The time interval between initial contact with an infectious
agent and the appearance of clinical signs and symp-
toms.
Infection
Invasion and multiplication of micro-organisms in body
tissues.
Infectious agent
An organism that is capable of producing infection or
infectious disease.
Infestation
The lodgement, development and reproduction of
arthropods on the surface of the body of persons or
animals or in clothing.
Isolation
Represents separation for the period of communicability,
of infected persons or animals from others in such places
and under such conditions as to prevent or limit the
direct or indirect transmission of the infectious agent.
Categories of isolation include:
• Strict isolation: for highly contagious infections spread
by air and contact.
219
 • Contact isolation: for diseases spread primarily by School exclusion
close or direct contact. Exclusion from school under Health (Infectious Diseases)
• Respiratory isolation: to prevent transmission over short Regulations 1990.
distances through the air.
Source of infection
Drainage/secretion precautions are defined elsewhere in The person, animal or substance from which an infec-
this appendix. For blood and body substance precau- tious agent passes to a host.
tions, see appendix 4.
Surveillance
Nosocomial infection Personal surveillance is the practice of close medical or
Hospital-acquired infection. other supervision of contacts to permit prompt recogni-
tion of infection or illness but without restricting the
Notification movements of the individual.
The process of reporting a notifiable infectious disease.
Susceptibility
Outbreak Lack of resistance to a particular pathogenic agent.
See epidemic.
Transmission
Period of communicability In terms of infection, it relates to any mechanism by
The time during which an infectious agent may be which an infectious agent is spread from a source or
transferred directly or indirectly from an infected person reservoir to a person. This may be direct, indirect (that is,
or animal to a susceptible host. vehicle-borne, vector-borne, or airborne).

Personal hygiene Standard Precautions

The protective measures within the responsibility of the See appendix 4.
individual that limit the spread of infectious diseases.
Vector
Quarantine A carrier, especially the animal (usually an arthropod)
The restriction of freedom of movement of apparently that transfers an infective agent from one host to another.
healthy individuals who have been exposed to infectious
disease. Zoonosis
A disease of animals that may be transmitted to humans
Reservoir of infectious agents under natural conditions.
Any person, animal, or substance in which an infectious
agent normally lives and multiplies in such a manner that
it can be transmitted to a susceptible host.

Resistance
The natural ability of an organism to resist micro-organ-
isms or toxins produced in disease.

220
 Appendix 3: Outbreak Investigation

This section contains a brief summary of the principles of
disease outbreak investigation. Any outbreak (or sus-
pected outbreak) should be reported promptly to the
Infectious Diseases Unit. Personnel from the unit will then
conduct the investigation assisted by public health
personnel from local government.
Characterise the Data
Time: Determine date and/or hour of onset. Construct
epidemic curve of cases.
Place: Prepare spot map of cases with respect to home,
work, recreational places and special meetings.

An outbreak (or epidemic) is when the number of cases
of a disease (or condition) exceeds the number expected
in a given time and place. In some instances, a single
case will constitute such an unusual occurrence.
The following steps are a guide only and the later steps
will not necessarily be followed in sequence. Complete-
ness and accuracy of data may be less than ideal in the
situation of a field investigation.
Determine the Existence of an
Outbreak
• Check the diagnosis and compare with previous data
on the disease.
• Remember to allow for causes of spurious ‘outbreaks’,
such as new or improved laboratory tests, better
reporting, or a change in the size or structure of the
population.
Person: Determine age, sex, occupation and ethnic
groups.
Formulate a Working
Hypothesis of the Source and
Manner of Spread
Test hypothesis:
• Determine infection and/or illness rates in persons
exposed and not exposed to the putative source/s by
questionnaire, interviews or laboratory tests.
• Try to isolate the agent from the putative source/s.
Analyse data: On the basis of the data analysis, initiate
short- and long-term control measures.
Disseminate information: Inform physicians, other health
officials and departments, as appropriate, on the nature
of the outbreak and the control measures being imple-
mented.

Develop a Case Definition Below is a list of contact numbers in the event of an

• Establish an aetiological diagnosis if possible. If not, outbreak:
define the condition clinically and epidemiologically. Contact Person Telephone Numbers
Manager, Infectious Tel: (03) 9616 7777
Diseases Unit Mobile: 019 403 997
Determine the Extent of the Pager: 483 4444 Quote 323 757
Outbreak
• Conduct a quick telephone or record survey of hospi- Chief Health Officer Tel: (03) 9616 7777
tals, clinics or appropriate physicians if necessary. Pager: 625 5000 Quote 804 6518
• Conduct a random telephone survey of homes (if
indicated) for diseases in the community such as Manager, Health Tel: (03) 9616 7777
influenza. Protection Mobile: 018 583 945
• Determine absenteeism rates from school and indus- After Hours Public Health Doctor Tel: (03) 9625 5000
tries (if indicated). Pager: 46870

221
 Appendix 4: Standard Precautions

Universal blood and body fluid precautions (‘Universal Additional Precautions

Precautions’) were originally devised by the US Centers
Additional Precautions are used for patients known or
for Disease Control and Prevention (CDC) in 1985,
suspected to be infected or colonised with
largely due to the HIV/AIDS epidemic and an urgent
epidemiologically important or highly transmissible
need for strategies to protect hospital personnel from
pathogens that can cause infection:
blood borne infections.
• By air borne transmission (for example, Mycobacte-
rium tuberculosis, measles virus, chickenpox virus).
Due to confusion in the use of the term ‘Universal
or
Precautions’, the Infection Control Working Party of the
• By droplet transmission (for example mumps, rubella,
NH&MRC has recommended the adoption of the term
pertussis, influenza).
‘Standard Precautions’ as the basic risk minimisation
or
strategy with ‘Additional Precautions’ where Standard
• By direct or indirect contact with dry skin (for example
Precautions may be insufficient to prevent transmission
colonisation with MRSA), or with contaminated sur-
of infection, particularly via the air borne route. This
faces.
change in terminology is in line with changes in terminol-
or
ogy adopted by CDC.
• By any combination of these routes.

Standard Precautions are work practices required for the

Additional Precautions are designed to be interrupt
basic level of infection control. They include good
transmission of infection by these routes and should be
hygiene practices, particularly washing and drying
used in addition to Standard Precautions when transmis-
hands before and after patient contact, the use of
sion of infection might not be contained by using Stand-
protective barriers which may include gloves, gowns ,
ard Precautions alone. Additional Precautions may be
plastic aprons, masks, eye shields or goggles, appropri-
specific to the situation for which they are required, or
ate handling and disposal of sharps and other contami-
may be combined where micro-organisms have multiple
nated or infectious waste, and use of aseptic techniques.
routes of transmission.

Standard Precautions apply to all patients regardless of

Source: ‘Infection Control in the health care setting.
their diagnosis or presumed infection status, and in the
Guidelines for the prevention of transmission of infec-
handling of:
tious diseases’ NH&MRC April 1996.
• Blood.
• All other body fluids, secretions and excretions (ex-
Handwashing
cept sweat), regardless of whether they contain visible
blood. • Wash hands after touching blood, body fluids, secre-

• Non-intact skin. tions, excretions and contaminated items, regardless

• Mucous membranes. of whether gloves are worn or not.

• Wash hands immediately after gloves are removed,

Standard Precautions also apply to dried blood and between patient contacts and when otherwise indi-

other body substances, including saliva. cated to avoid transfer of micro-organisms to other
patients or environments.
• An antimicrobial agent or waterless antiseptic agent
may be used in an outbreak.

223
 Gloves
• Wear gloves (clean non sterile gloves are adequate)
when touching blood, body fluids, secretions,
excretions and contaminated items; put on clean
gloves just before touching mucous membrane and
non-intact skin.
• Change gloves between tasks and procedures on the
same patients after contact with material that may
contain a high concentration of micro-organisms.
• Remove gloves promptly after use, before touching
non-contaminated items and environmental surfaces
and before going to another patient and wash hands
immediately to avoid transfer of micro-organisms to
other patients or environments.

Gowns
• Wear a gown (a clean non sterile gown is adequate) to
protect skin and prevent soiling of clothing during
procedures and patient care activities that are likely to
generate splashing or sprays of blood, body fluids,
secretions, or excretions or cause soiling of clothing.
• Select a gown that is appropriate for the activity and
the amount of fluid likely to be encountered.
• Remove a soiled gown as promptly as possible and
wash hands to avoid transfer of micro-organisms to
other patients and environments.

Masks, Eye Protection, Faceshields

• Wear a mask and eye protection or a faceshield to
protect mucous membranes of the eyes, nose and
mouth during procedures and patient-care activities
that are likely to generate splashes or sprays of blood,
body fluids, secretions and excretions.

Environmental Control
• Ensure that the health care establishment has ad-
equate procedures for the routine care, cleaning, and
disinfection of environmental surfaces, beds, bedrails,
bedside equipment, and other frequently touched
surfaces and that these procedures are being followed.

224
 Appendix 5: Procedure for Dealing with
Spills of Blood and Body Fluids
Equipment
A spills kit should contain a large (10 litre) reusable
plastic container or bucket with fitted lid, containing:
• A 5 litre impervious container (treated cardboard or
plastic) with fitted lid for waste material.
• Two large (10 litre) zip-seal plastic bags for waste
material.
• A disposable, sturdy cardboard scraper and pan
(similar to a ‘pooper scooper’).
• Five granular disinfectant sachets containing 10,000
ppm available chlorine or equivalent. (Each sachet
should contain sufficient granules to cover a 10 cm
diameter spill.)
• Disposable rubber gloves that are suitable for clean-
ing.
• Eye protection (disposable or reusable).
• A plastic apron.
• A mask (for protection against inhalation of powder
from the disinfection granules, or aerosols from high-
risk spills that may be generated during the cleaning
process).
Pr o c e d u re s
Spot Cleaning:
• Wipe up spot immediately with a damp cloth, tissue or
paper towel. An alcohol wipe may be used.
• Discard contaminated materials (tissue, paper towel-
ling, alcohol wipe) in accordance with State/Territory
regulations.
• Wash hands.
Small Spills (up to 10 cm diameter):
• Collect cleaning materials and equipment (‘Spills kit
optional’).
• Wear disposable cleaning gloves. Eyewear and plastic
apron should be worn where there is a risk of splashing
occurring.
• Wipe up spill immediately with absorbent material (for
example, paper hand towelling). Place contaminated
absorbent material into impervious container or plastic
bag for disposal.
• Clean the area with warm water and detergent using
disposable cleaning cloth or sponge.
• Where contact with bare skin is likely, disinfect area by
wiping with sodium hypochlorite 1,000 ppm available
chlorine (or other suitable disinfectant solution) and
allow to dry.
• Discard contaminated materials (absorbent towelling,
cleaning cloths, disposable gloves and plastic apron)
in accordance with State/Territory regulations.
• Wash hands.
• Reusable eyewear should be cleaned and disinfected
before reuse.
Large Spills (greater than 10 cm diameter):
• Collect cleaning materials and equipment (‘Spills kit
optional’).
• Wear disposable cleaning gloves, eyewear, mask and
plastic apron.
• Cover area of the spill with granular chlorine releasing
agent (10,000 ppm available chlorine) or other equiva-
lent-acting granular disinfectant and leave for three to
10 minutes, depending on formulation and labelling
instructions.
• Use disposable (for example, cardboard) scraper and
pan to scoop up granular disinfectant and any
unabsorbed blood or body substances. Place all
contaminated items into impervious container or plastic
bag for disposal.
• Wipe area with absorbent paper towelling to remove
any remaining blood and place in container for dis-
posal.
• Discard contaminated materials (absorbent towelling,
cleaning cloths, disposable gloves and plastic apron)
in accordance with State/Territory regulations.
• Wash hands.
• Use ward cleaning materials to mop with warm water
and detergent.
• Where contact with bare skin is likely, disinfect area by
wiping with sodium hypochlorite 1,000 ppm available
chlorine (or other suitable disinfectant solution) and
allow to dry.
225
 • Clean and disinfect bucket and mop. Dry and store
appropriately.
• Reusable eyewear should be cleaned and disinfected
before reuse.

Notes:
1. Spill = a spill of blood or body substances.
2. * Spills kit (see above).
3. Where a spill occurs on a carpet, shampoo as soon as
possible. Do not use disinfectant.
4. Hypochlorites are corrosive to metals. Sodium
dichloroisocyanurates are less corrosive to metals, but
it may be difficult or impossible to prepare concen-
trated solutions above 1,000 ppm.
5. Wash hands thoroughly after cleaning is completed.

Reprinted from Infection Control in the Health Care

Setting, 1996, NH&MRC, page 21.

226
 Appendix 6: Management of Needlestick
Injury and Exposure to Blood or Body
Fluids
Personnel Management
If a staff member has parenteral (needlestick, cut or
other) or mucous membrane (splash to eye, nose, or
mouth) exposure to blood or other body fluids, or has
cutaneous exposure of non-intact skin (chapped,
abraded, or afflicted with dermatitis) involving blood, the
action outlined below should be taken.
Immediate Action
If skin is penetrated, wash the area with soap and water.
(Alcohol-based hand rinses or foams (60–90 per cent
alcohol by weight should be used when water is not
available).
If blood gets on the skin, irrespective of whether there
are cuts or abrasions, wash well with soap and water.
If the eyes are contaminated, rinse the area gently but
thoroughly with water or normal saline while the eyes are
open.
If blood gets in the mouth, spit it out and then rinse the
mouth with water several times.
Report to Supervisor or Occupational
Health Officer
Complete an accident report form and include:
• Date and time of exposure.
• How the incident occurred.
• Name of the source individual (if known).
Incidents that did not occur at work should be reported
to a doctor or the Accident and Emergency (Casualty)
Department at the nearest hospital.
If a needle/syringe was involved, place it in a rigid-walled
container such as a lunch box. Take it with you to the
doctor.
Note
Do not attempt to cover the needle because of the risk of
further injury.
In the event of an exposure to a source individual who
has been previously tested and confirmed as HIV, HBV
or HCV positive, the affected person should immediately
be evaluated by a physician with experience in the
management of these infections.
The source patient should be informed of the exposure,
and following appropriate explanation, should be asked
to consent to serologic testing for evidence of:
• HIV antibody (informed consent required).
• Hepatitis B surface antigen (HBsAg).
• Hepatitis C Antibody (Anti-HCV).
Blood samples should be collected as soon as possible
after the incident and processed urgently.
Human Immunodeficiency
Virus (HIV)
If the source individual is positive for HIV antibody or the
source is unknown, the affected person should be
offered counselling. They should also be informed about
the risk of transmission, which is estimated to be 0.3 per
cent if the source is HIV positive.
Informed consent should be obtained for baseline HIV
serology as soon as possible after exposure. An initial
positive result would indicate that transmission had
occurred prior to exposure.
The affected person who is initially positive should be
retested for HIV antibody at three weeks, and finally
retested three months after exposure.
When the source individual is HIV positive, post-expo-
sure prophylaxis with zidovudine, also known as
azidothymidine (AZT) (or other drugs that may become
available for this purpose), may be offered to the af-
fected person.
227
 The risk of zidovudine to mother and foetus should be Source HBV positive (HBsAg
carefully considered against the benefit of this antiviral
positive)
drug in a pregnant woman who has had a significant
The approach to investigation is modified according to
exposure. Prophylaxis should be commenced only after
whether or not the affected person has received a course
counselling the affected person and informing them of
of hepatitis B vaccine.
the absence of data regarding the efficacy, toxicity and
safety of zidovudine for this purpose.
If the affected person has been vaccinated, take blood
for estimation of hepatitis B surface antibody (Anti-HBs)
Prophylactic zidovudine should be at no cost to the
to confirm that vaccine immunity is being maintained.
affected person. Treatment should begin as soon as
Antibody titres may fall below protective levels some
possible after exposure (preferably within two hours).
years after vaccination (non-protective levels less than
10 IU/l).
The suggested dose of zidovudine is 200 mg orally five
times per day, or 250 mg four times a day for six weeks.
If the affected person has not been previously vacci-
nated for hepatitis B, take blood for estimation for hepati-
Doctors should emphasise the importance of strict
tis B core antibody (Anti-HBc), Anti-HBs or other such
compliance with the treatment regimen. They should
test such as HBsAg that is available in your local labora-
describe the potential side effects and the appropriate
tory to determine previous infection.
course of action if these are experienced.

These tests will indicate whether the affected person has

Note
previously been infected with hepatitis B. If the affected
Supplies of AZT may be obtained from the Alfred or
person has been previously infected, no further action is
Royal Melbourne Hospital pharmacy.
required.

The affected person should be followed up to ascertain

Where the affected person has not been infected with
any febrile illness that occurs within three months after
hepatitis B and is negative for Anti-HBs or has levels that
exposure. Such illness, particularly one characterised by
are non-protective (less than 10 IU/l), hepatitis B immu-
fever, rash or lymphadenopathy, may indicate primary
noglobulin (HBIG) should be given within 48 hours of
infection with HIV.
injury when:
• The source individual is HBsAg positive.
During the period of surveillance (that is, three months):
• The source individual is unknown.
• Do not donate plasma or blood, body tissue, milk or
• The results of tests on the source individual and
sperm until approved by the evaluating physician.
affected person are unavailable within 48 hours.
• Protect sexual partners from contact with blood, semen
or vaginal fluids by using condoms.
Persons eligible for HBIG should commence a vaccina-
• Avoid pregnancy until HIV status is known.
tion course at the same time. Three vaccinations at zero,
• Consider work practices for health care workers.
one and six months are required.

When the affected person is immune (Anti-HBs positive),

consider checking antibody levels or providing booster
vaccination if the previous course was completed more
than five years ago.
228
Source Anti-HCV Positive
The risks and some mechanisms of HCV transmission in
health care settings are not firmly established.

At present, apart from thorough washing (as for HIV and

HBV) at the time of injury, there is no known treatment
that can alter the likelihood of transmission.

The reasons for following up affected persons are to

ascertain whether HCV infection occurs and to provide
treatment and support.

The affected person should be tested for Anti-HCV at

zero, three and six months.

Follow-up should be undertaken by a specialist with

knowledge of HCV infection.

Source Unknown
Reasonable efforts should be made to identify source
persons or syringes. If the source remains unknown,
appropriate follow-up should be determined on an
individual basis depending on:
• Type of exposure.
• Likelihood of source being positive for a blood patho-
gen.
• Prevalence of HIV, HBV and HCV in the community
from which the instrument or needle comes.

Appropriate follow-up should also determine the risk of

tetanus. Depending on the circumstances of the expo-
sure, the following may need to be considered:
• Tetanus immunoglobulin.
• A course of adult diphtheria and tetanus (ADT).
or
• ADT booster.

229
 Appendix 7: Specimen Collection and
Transport Guidelines
Specimen Collection
General
Blood and other specimens for laboratory evaluation
should be collected with gloved hands and placed in
leak- and spill-proof containers for transport. Containers
should be checked for exterior contamination and
disinfected with hypochlorite solution if necessary.
The identity of the patient from whom the specimen is
taken is crucial. Please ensure that the correct name is
on the specimen container and the request slip.
Request slips must be legible and contain surname, first
name, date of birth, gender and clinical details of the
affected person. They should also include the requesting
person’s name, address and telephone number, the tests
requested, and addresses of all persons who are to
receive reports.
Adequate clinical and epidemiological information are
needed to ensure appropriate tests are performed on
specimens. Please provide this on the request form.
All specimens must be placed in sealed plastic bags.
The request form should not be in the same part of the
bag as the specimen container as this may cause
contamination of the request form.
If you have any questions about the appropriate speci-
men or test for a particular investigation, please contact
the laboratory to discuss the appropriate approach. This
is particularly important when less commonly performed
tests are considered (including virology and serology).
Faeces
General Instructions for Collecting Faeces
Faecal specimens should be collected during the first 48
hours of illness. The chance of identifying a pathogen
diminishes as time after acute illness passes. For exam-
ple, viral diagnosis can be made only when the excretion
of virus is approximately one million particles/g of faeces.
This occurs in the first two days of illness and, occasion-
ally, on the third.
In an outbreak, specimens should be collected from as
many ill persons as possible. Specimens should be as
fresh as possible and, ideally, reach the laboratory on
the day of collection. Specimens can be stored in the
refrigerator overnight (or for up to two days) at 4˚C. Do
not freeze faeces.
Patients should be provided with a copy of Instructions
for the Collection of Faeces (see below). This explains
how to pass faeces into a clean wide-mouthed recepta-
cle such as an ice-cream container (or onto paper or
plastic wrap) and to avoid contamination with urine.
A specimen at least the size of a golf ball is then trans-
ferred with a spatula or spoon into a specimen container
that has been labelled with the patient’s name. If viral
infection is suspected, please provide a nearly full
specimen container if possible. The specimen container
should be firmly secured and placed in a sealed plastic
bag with a completed request slip attached.
Note
Motile trophozoites of protozoal (parasitic) infections will
probably only be seen if a fresh specimen is examined
within 30 minutes of passage.
As an alternative to such an urgent process, faeces may
be preserved for later parasitological examination.
Prompt and appropriate preservation is necessary. MDU
can provide special collection kits for faecal parasitol-
ogy.
Rectal Swab
This method of sampling is less satisfactory than collect-
ing faeces. It is not appropriate for parasitology.
231
 • Moisten a charcoal swab and insert it into rectum 2 cm
to 3 cm. Gently rotate it so that faeces cover the swab.
Place it in transport medium, break off the top portion
of swab stick and discard.
• Label the specimen and place it in a plastic hazard
bag with the appropriate request slip attached.
• Explain the procedure to patient and ask them to:
– Wash, rinse and thoroughly dry hands.
– Uncap specimen jar, handling only the outside of
the jar and lid.
– Wash external genitalia with warm tap water and
discard swabs onto a tray.

Urine Specimen Collection Female:

• Part the legs and then labia.
If specimens of urine are required for culture for typhoid
• Wash the area between from front to back using a
or paratyphoid, no special preparation of the patient is
piece of cotton wool and normal saline.
necessary (that is, a midstream specimen is not neces-
• Wipe from front to back with one swab at a time.
sary).

Male:
Early morning specimens are more concentrated, and
• Draw back the foreskin.
therefore more likely to be positive for culture.
• Clean the area underneath thoroughly using cotton
wool dipped in saline.
• Instruct the patient to collect a 10 ml to 20 ml specimen
• Stand or sit over the toilet bowl.
of urine in the sterile container on the morning of the
required day.
• Collect a specimen of 10 ml to 20 ml, when urine flow
• Clearly label container. Place it in a sealed plastic
is established, then complete the flow in the toilet.
hazard bag and attach the request form.
• Take care not to touch the inside of the specimen jar or
• Send it to MDU on the day of collection.
cap. Screw cap on firmly.
• Return the specimen container and kidney dish to
Infants and Young Children
nurse.
Plastic collection bags are available for this purpose. The
• Place the specimen in a plastic hazard bag with a
adhesive bag is attached over the genitalia and 4 ml to 5
request slip, and send to the laboratory within 24 hours
ml collected in one voiding. The specimen should be
of collection.
transferred to a sterile container by removing the tab and
draining the urine into the container.
Throat Swabs
If the specimen is inadequate, a new bag must be Stuart’s transport medium kits should be used for trans-

applied and the procedure repeated. porting throat swabs to the laboratory.

The sites to be swabbed are the tonsillar surface, pillars

Midstream Urine Collection (MSU)
of the fauces and posterior pharyngeal wall. Areas of
Equipment:
exudation, membrane formation or inflammation are the
• Kidney dish.
best sites. All other areas should be avoided, including
• Small bowl.
the tongue and teeth when withdrawing the swab.
• Cotton wool swabs.
• Sterile specimen jar, labelled with name, date and
The patient should sit in a well-lit area and be asked to
identification number if required.
open their mouth and say, ‘Ahh’.
• Sachet of normal saline.

232
The tongue should be gently pressed down with the
depressor. The two tonsillar areas, pillars of the fauces
and the posterior pharyngeal wall behind the uvula
should be rapidly swabbed with slight pressure .
It is an advantage to sit a child on an adult’s knee. The
adult should hold the child’s hands with one hand. Their
other hand should firmly hold the child’s forehead
against the adult’s chest. This prevents the child from
retracting their head.
When swabbing a child, it is important to be successful
the first time. If the child refuses to open their mouth, the
spatula should be pushed gently into their mouth. When
it touches the back of the tongue, there is a reflex
opening of the mouth. This gives a short opportunity that
must not be missed.
With a baby, the moment they open their mouth to cry,
the opportunity to swab should be seized.
Swabs should be clearly labelled and placed in a sealed
plastic hazard bag. The appropriate request slip should
be attached and forwarded to the laboratory within 24
hours of collection.
Nasal Swabs
• Use a swab moistened with sterile saline for children.
• Tilt the patient’s head back. Sample each nostril from
the vestibule to a point just below the middle turbinate
and rotate the swab.
• Use the same swab to sample each nostril.
• Place the specimen in Stuart’s medium.
• Transport it to the laboratory as soon as possible,
preferably within 24 hours.
Nasopharyngeal Swabs
• Hold the patient’s head firmly because of the natural
tendency to withdraw.
• Use a swab moistened with saline.
• Pass the perinasal swab horizontally along the floor of
the nasal passage under the lower turbinate until it
reaches the posterior nasopharyngeal wall. Rotate and
gently remove it. Place it in transport medium.
• Collect material behind the soft palate through the
mouth with a swab on a bent wire stalk.
• Label specimens for identification.
• Place them in a hazard bag and attach a request slip.
• Forward them to laboratory, preferably within 24 hours
of collection.
Sputum (for Microscopy and
Culture)
Sputum should be collected in the morning before
eating, drinking or cleaning the teeth. It should be
collected in a sterile container.
The patient should cough up material from deep in the
lungs and expectorate without saliva. Saliva or mucus
from the back of the nose should not be provided as
sputum.
The specimen should be delivered to the laboratory with
minimum delay.
Sputum required for mycobacterial examination (often
several consecutive early morning specimens) should be
refrigerated at 4oC until transported to the laboratory. Do
not freeze.
Guidelines for Collecting Blood for
Serological Diagnosis
Paired samples of blood are required for serological
diagnosis of certain conditions:
• Acute: during the first week of symptoms.
• Convalescent: third to fourth week.
Serum samples may also be of value in the diagnosis of
viral gastroenteritis; please discuss this with the electron
microscopist.
233
 Quantity:
• Adults 8 ml to 10 ml.
• Children 3 ml to 4 ml.
The samples should be collected in plain tubes and
stored at 4oC.
Whole blood samples must not be frozen.
Blood specimens shuold be delivered to the laboratory
within six hours of sampling. If a delay of more than six
hours is likely, the specimens should be stored in a
refrigerator (but do not freeze whole blood samples).
Centrifuged specimens of separated serum can be
frozen and transported on dry ice. If this process is
considered, please discuss it with the laboratory.
Food and Water Samples
Specimens of food, water or ice can be submitted for
testing if they are considered to be possibly implicated
as a vehicle of the disease or outbreak.
Always consider seeking advice from the laboratory on
appropriate specimens to collect.
Food
• Collect a minimum of 100 g. Wherever possible, submit
samples in the original retail container/packaging.
• Submit any available empty cans of the implicated
product if the suspect product was sold in a can.
• Place samples in sterile containers/plastic bags to
avoid any cross-contamination.
o
• Store and transport samples chilled, ideally at 4 C.
• Label samples clearly. Information on the product/food
(source, date of purchase, date of production, useby
date and so on) should be included on the request
slip.
234
• Ensure the request slip also identifies the cases/s and/
or incident by name/s and location and circumstances
of the incident. Please also include clinical details of
illnesses attributed to the food.
Water
• Collect a minimum of 200 ml if testing water for potabil-
ity.
• Collect a minimum of one litre if samples are required
for investigation of possible contamination by Salmo-
nella or Campylobacter.
• Collect water in sterile bottles provided by laboratory.
• Label samples carefully. The request slip should
identify the cases/s and/or incident by name/s, and
location and circumstances of the incident. Please also
include clinical details of illnesses attributed to the
water. Store and transport water samples chilled,
ideally at 4˚C.
Water must be examined within 24 hours of collection.
The laboratory should be notified before samples are
collected.
Note
For suspected parasite investigation, seek advice from
the laboratory.
Laboratory
Food and water samples are routinely sent to the Micro-
biological Diagnostic Unit at The University of Melbourne
(MDU).
Microbiological Diagnostic Unit
Department of Microbiology
The University of Melbourne
Royal Parade
Parkville 3052
Telephone: (03) 9344 5713
Facsimile: (03) 9344 7833
Specimen Transport Guidelines Specimens related to investigation of outbreaks and
public health screening are routinely sent to:
Packaging
• Place specimen containers in sealed plastic bags in an
Microbiological Diagnostic Unit
insulated container (Esky) containing frozen icepacks.
Department of Microbiology
Do not use paper bags. Do not use ice cubes.
The University of Melbourne
• Keep the specimen container upright to reduce the risk
Royal Parade
of leakage and cross-contamination of other speci-
Parkville 3052
mens.
Telephone: (03) 9344 5713
• Place trays of blood tubes from mass screening
Facsimile: (03) 9344 7833
surveys in a sealed plastic bag and maintain in an
upright position.
Hours: 8.30 a.m. to 5.00 p.m., Monday to Friday.
• Keep chilled but not frozen and deliver them to the
laboratory as soon as possible. If frozen samples of
Please notify laboratory if specimens to arrive out of
separated serum are to be transported, please discuss
normal hours.
this process with the laboratory. If specimens have to
be transported by rail, ensure the insulated container
The entrance is at Gate 11, Royal Parade (approximately
has several icepacks to maintain the temperature as
100 metres from Grattan Street, traffic lights) through the
close to 4oC for as long as possible.
loading bay on ground floor; or via Gate 12 (200 metres
• Seal all containers well.
from Grattan Street). Turn right to reach the car park in
• Label the insulated container clearly with the address
front of MDU.
and telephone numbers of the laboratory and the
submitting authority.
After hours:
• Notify the laboratory of impending specimen delivery.
• An overnight box for specimens is located on northern
side of MDU adjacent to Royal Parade.
Transport • The area is well-lit and clearly signposted. Place the
The preferred method of transport is door-to-door bagged specimens with the request slips in the hatch.
delivery by courier. • Always give laboratory staff prior notification if out-of-
hours delivery of specimens is anticipated.
If specimens have to be delivered by rail, ensure that the • Saturdays and Sundays: place specimens in the
package contains sufficient icepacks to keep the con- overnight box (emergency only).
tents chilled. Seal containers well.

The laboratory should be notified of impending specimen

delivery by rail and the approximate time of arrival.

The railway station staff should advise the laboratory

when specimens arrive at the station, and a laboratory
staff member should then collect the container from the
railway station.

235
 Instructions for Collecting Faeces

• Label the specimen container clearly with your

name and date of collection. If a specimen con-
tainer is not available, a clean jar with a screw-top
lid may be used.
• Place a separate clean container with a wide
opening (for example, a plastic ice-cream con-
tainer), or plastic wrap or newspaper in the toilet
bowl. Pass faeces directly into the container or onto
the plastic wrap or newspaper.
• Do not contaminate the faeces with urine.
• Using a wooden spatula or plastic spoon, place
enough faeces to at least half fill the specimen
container (a sample about the size of a golf ball).
• Screw the lid on the specimen container firmly.
Place it in a sealed plastic bag.
• Keep specimen cool (at 4oC) but do not freeze.

236
 Appendix 8: Infections in Children’s
Services Centres

Children in day care centres and other children’s serv-

ices centres and kindergartens are particularly at risk of
developing communicable diseases because of:
• Close contact with other children and staff.
• Lack of previous exposure to common infections.
• Lack of toilet training.
• Lack of control of other body secretions.
• Mouthing behaviour.

These risk factors may be increased when staff are not

appropriately trained, group sizes are large, and mixing
of age groups occurs.

Infections with the following organisms have been shown

to be more common in these settings, or have been
reported as epidemic:
• Respiratory Syncytial virus (RSV).
• Influenza virus.
• Haemophilus influenzae type b.
• Neisseria meningitidis.
• Shigella spp.
• Rotavirus.
• Giardia lamblia.
• Cryptosporidium.
• Hepatitis A.
• E. coli.
• Campylobacter spp.
• Parvovirus B19 (erythema infectiosum).
• Coxsackievirus group A (hand, food and mouth dis-
ease).
• Streptococcus, pyogenes, Staphylococcus aureus
(impetigo).
• Cytomegalovirus.
• Scabies, head lice.

237
 Appendix 9: School Exclusion Table
School Exclusion Table
Disease or Condition
Chickenpox
Conjunctivitis (Acute infectious)
Diphtheria
Giardiasis (diarrhoea)
Hepatitis A (infectious hepatitis)
Hepatitis B
Impetigo (School sores)
Leprosy
Measles
Meningococcal infection
Mumps
Exclusion of Cases
Until fully recovered or at least one
week after the eruption first appears.
Until discharge from eyes has
ceased.
Until receipt of a medical certificate
of recovery from infection.
Until diarrhoea ceases.
Until receipt of a medical certificate
of recovery from infection or on
subsidence of symptoms.
Until recovered from acute attack.
Until sores have fully healed. The
child may be allowed to return
earlier provided that appropriate
treatment has commenced, and that
sores on exposed surfaces (such as
scalp, face, hands or legs) are
properly covered with occlusive
dressings.
Until receipt of a medical certificate
of recovery from infection.
Until at least five days from the
appearance of rash, or until receipt
of a medical certificate of recovery
from infection.
Until receipt of a medical certificate
of recovery from infection.
Until fully recovered.
Exclusion of Contacts
Not excluded.
Not excluded.
Domiciliary contacts excluded until
investigated by the medical officer
of health, or a health officer of the
Department and shown to be clear
of infection.
Not excluded.
Not excluded.
Not excluded.
Not excluded.
Not excluded.
Non-immunised contacts must be
excluded for 13 days from the first
day of appearance of rash in the last
case unless immunised within 72
hours of first contact.
Domiciliary contacts must be
excluded until they have received
appropriate chemotherapy for at
least 48 hours.
Not excluded.
239
 School Exclusion Table (continued)
Disease or Condition Exclusion of Cases Exclusion of Contacts

Pediculosis (Headlice) Until appropriate treatment has Not excluded.

commenced.

Pertussis (Whooping cough)
Until two weeks after the onset of
illness and until receipt of a medical
certificate of recovery from infec-
tion.
Domiciliary contacts must be
excluded from attending a children’s
services centre for 21 days after the
last exposure to infection if the
contacts have not previously had
whooping cough or immunisation
against whooping cough.

Poliomyelitis Until at least 14 days after onset of Not excluded.

illness, and until receipt of a medical
certificate of recovery from infection.

Ringworm Until appropriate treatment has Not excluded.

commenced.

Rotavirus (diarrhoea) Until diarrhoea ceases. Not excluded.

Rubella Until fully recovered or at least five Not excluded.

days after onset of rash.

Scabies Until appropriate treatment has Not excluded.

commenced.

Shigellosis (diarrhoea) Until diarrhoea ceases. Not excluded.

Streptococcal infection including Until receipt of a medical certificate Not excluded.

scarlet fever of recovery from infection.

Trachoma Until appropriate treatment has Not excluded.

commenced.

Tuberculosis Until receipt of medical certificate Not excluded.

from a health officer of the Depart-
ment that the child is not considered
to be infectious.

Typhoid and paratyphoid fevers Until receipt of a medical certificate Not excluded unless the medical
of recovery from infection. officer of health or a health officer of
the Department considers exclusion
to be necessary.

240