Microbiological Aspect of

Traveler Medicine

dr. Tri Wibawa, PhD

Dept. of Microbiology
Gadjah Mada Univ. Sch. of Med.
 Traveler medicine
Microbiology
Infectious diseases
Tropical medicine
Epidemiology
Public health
Travel risk, Risk-Benefit, and Cost-Benefit
(Traveler clinics Immunization)
The death rate of Americans traveling overseas :
< 5 per 100,000
Most of the infection-related deaths are preventable
All travel vaccines are probably cost-ineffective (in
society level)

Individual risk-benefit
No vaccine is 100% effective
No vaccine is completely safe
Not all trips or all travelers are the same
Various Modes and Routes of Infectious
Diseases Transmission
 Vaccine/Chemoprophylaxis
Prevented diseases
Diseases associated with Contaminated
Water and Food
Hepatitis A
Cholera
Typhoid Fever
Polio

Diseases associated with Insect Vectors

Malaria
Japanese encephalitis virus infection
Yellow fever
Tick-borne encephalitis virus infection
Diseases associated with Environmental or
Animal Contacts
Tetanus
Diphtheria
Rabies

Diseases associated with Person-to-Person

Transmission
Hepatitis B
Influenza
Measles, mumps, and rubella
Meningococcal disease
Pertussis
Pneumococcal disease
Varicella

(Blair, 1997, CMR 10,650-673)

 Vaccine/Chemoprophylaxis
un-prevented diseases
Diseases associated with Contaminated
Water and Food
Travelers diarrhea
Hepatitis E
Transmissible spongiform encephalopathy mad cow
Parasitic diseases

Diseases associated with Insect Vectors

Dengue
Venezuelan equine ecephalitis
Chagas disease Trypanosoma cruzi
Ebola fever
Diseases associated with Environmental

Schistosomiasis
Plague Yersinia pestis
Rabies

Sexually transmitted diseases

HIV
Urethritis Gonorhoeae
Syphilis
etc
 Etiology of Travelers Diarrhea
Invasive Bacteria
Aeromonas hydrophila Viruses
Campylobacter jejuni HAV
Clostridium perfringens type A HEV
Escherichia coli, entero invasive Norwalk agent
Escherichia coli O157-H7 Rotavirus
Plesiomonas shigelloides
Salmonella sp.
Shigella sp.
Vibrio vulnificus
Yersinia enterocolitica
Parasites
Entamoeba histolytica
Non Invasive Bacteria Dientamoeba fragilis
Clostridium botulinum Giardia lamblia
Clostridium difficile etc
E. coli enterotoxigenic
Vibrio cholerae (O1, O139)
Vibrio fluvialis
Vibrio parahaemolyticus
 Pathogenesis
of Rotavirus
Primarily localize in duodenum
and proximal jejunum.
Destruction of villous epithelial
cells with blunting/shortening
of villi.
Mononuclear and PMN
infiltration in the villi.
Decrease in absorptive
surface in the small intestine.
Decrease of brush border
enzymes production.
Transient mal-absorptive
state.
Typhoid Fever
Caused by Salmonella typhi
Less severe and similar disease is caused by
Salmonella paratyphi A
Human is the only natural host and reservoir
Transmit by ingestion of food or water
contaminated with feces.
Water borne (less inocula) vs food borne
Ingest 105 28% - 55% develop
disease
Ingest 103 none
Laboratory Diagnosis

Culture
Blood culture (Ox bile medium)
Bone marow aspirate culture (gold standard)
Duodenal aspirate culture
Stool or rectal swab culture (typhoid carriers)
Serology
Serological identification of Salmonella
Felix- Widal test
New diagnostic test (e.g. IDL Tubex test,
Typhidot, Typhidot-M)
 GEOGRAPHIC DISTRIBUTION OF
HEPATITIS A VIRUS INFECTION

Anti HAV prevalence

high
High/intermediate
intermediate
low
Very low
 ACUTE HEPATITIS A CASE
DEFINITION FOR SURVEILLANCE

Clinical criteria
An acute illness with:
discrete onset of symptoms (e.g. fatigue, abdominal pain,
loss of appetite, intermittent nausea, vomiting), and
jaundice or elevated serum aminotransferase levels

Source : CDC, USA

Laboratory criteria
IgM antibody to hepatitis A virus (anti-HAV) positive
IgM antibody to the virus are present in > 99%
of individual at the time of their initial presentation

Source : Lemon SM, Clin. Chem 43, 1997

 HEPATITIS A VIRUS

RNA Picornavirus
Positive sense
Single serotype worldwide
Acute disease and asymptomatic
infection
No chronic infection
Protective antibodies develop in
response to infection - confers lifelong
immunity
 CONCENTRATION OF HEPATITIS A VIRUS
IN VARIOUS BODY FLUIDS
Feces
Body Fluids

Serum

Saliva

Urine

100 102 104 106 108 1010

Infectious Doses per mL
Source: Viral Hepatitis and Liver Disease 1984;9-22
J Infect Dis 1989;160:887-890
HEPATITIS A VIRUS TRANSMISSION
Close personal contact (e.g. household contact, sex
contact, child day-care centers)
Contaminated food, water (e.g. infected food
handlers)
Blood exposure (rare)( e.g. injection drug use, rarely
by transfusion)

PREVENTING HEPATITIS A
Hygiene (e.g., hand washing)
Sanitation (e.g., clean water sources)
Hepatitis A vaccine (pre-exposure)
Immune globulin (pre- and post-exposure)
 RISK FACTORS ASSOCIATED WITH
REPORTED HEPATITIS A,
1990-2000, UNITED STATES
Sexual or
Household
Contact 14% International
travel 5%
Unknown
46% Men who have
sex with men
10%

Injection drug use

6%

Child/employee in
Other Contact day-care 2%
8% Food- or
Contact of day-
waterborne
care
outbreak 4%
child/employee
Source: NNDSS/VHSP 6%
 Poliomyelitis

First described by Michael Underwood in

1789.
Outbreak in Europe and US in 19th cent.
Spreading to developing country.
Polio incidence fell rapidly following
introduction of effective vaccine.
Polio virus

RNA virus
Member of enterovirus subgroup, family
picornaviridae
Three serotypes (P1, P2, P3)
Minimal heterotypic immunity between
serotypes
Rapidly inactivated by heat, formaldehyde,
chlorine, ultraviolet light
Poliomyelitis pathogenesis

Entry into mouth

Replication in pharynx, GI tract, local lymphatics
Virus invades local lymphoid tissue, enters the
blood stream, and cells of CNS
Virus replicates in motor neurons of the anterior
horn and brain stem
Destruction of motor neurons
Incubation period: range from 3-35 days
(common: 6-20 days)
Laboratory diagnosis

Viral isolation: Stool, pharynx,

CSF (rare but diagnostic).
Wild type vs vaccine type
Serology
CSF analysis
 Inactivated Polio Vaccine

Contains 3 serotypes of vaccine virus

Grown on monkey kidney (vero) cells
Inactivated with formaldehyde.

Oral Polio Vaccine

Contains 3 serotypes of vaccine virus

Grown on monkey kidney (vero) cells
Shed in stool for up to 6 weeks following
vaccination
Japanese Encephalitis

CLINICAL FEATURES
Acute encephalitis; can progress to paralysis, seizures, coma and
death
The majority of infections are sub-clinical

ETIOLOGIC AGENT
Japanese encephalitis (JE) virus: flavivirus antigenically related to St.
Louis encephalitis virus

INCIDENCE
Leading cause of viral encephalitis in Asia with 30-50,000 cases
reported annually
Fewer than 1 case/year in U.S. civilians and military personnel
traveling to and living in Asia
SEQUELAE
Case-fatality ratio: 30%
Serious neurologic sequela: 30%

TRANSMISSION
Mosquito-borne Culex tritaeniorhynchus group

RISK GROUPS
Residents of rural areas in endemic locations
Active duty military deployed to endemic areas
Expatriates in rural areas
Disease risk extremely low in travelers
Where is Japanese
Enchepalitis
Endemic?

Rice field breeding mosquitoes

(primarily the Culex
tritaeniorhynchus group)
 Diphtheria

Early stage of diphtheritic membrane

On the right tonsil Diphtheritic membrane extending from
Uvula to the pharyngeal wall
Diphtheria
Acute communicable disease
Caused by exotoxin-producing
Corynebacterium diphtheriae.
Gram positive rod
Exotoxin: Arrest the protein synthesis of host cells
C.diphtheriae usually localizes in the upper
respiratory tract and ulcerates the mucosa
Induces inflammatory pseudomembrane
Usually transmitted by direct contact or by
sneezing or coughing
Algorithm for laboratory diagnosis of diphtheria
RABIES
Cause acute encephalitis in all warm blooded hosts
Outcome is almost always fatal.
Infected saliva pass to the uninfected host.
contamination of mucous membrane, aerosol, corneal
transplantation (documented)

High risk animal:

Bats, Raccoons,
Skunks, Cats,
Dogs, Foxes,
Coyotes.
 Rabies Virion

(Single stranded RNA virus)

Laborary tests
Microbiology: Virus isolation from saliva
Serum rapid fluorescent focus inhibition test (RFFIT) : positive in
50% of cases.
Results of the CSF RFFIT are antibody-positive (2-25% of serum
titer) after the first week of illness
Others: CSF analysis, IHC, Hematology, urinalysis

Future tests

The nucleic acid sequence-based amplification (NASBA)

technique on urine samples may be used in the future.
The NASBA technique on saliva and CSF can be used for rapid
diagnosis as early as 2 days after symptom onset.