1.

COMMUNICABLE DISEASES AND SPECIAL Communicable Diseases

HEALTH ISSUES TO TOPIC OUTLINE
BE PROGRESSIVELY COVERED BY THE •
COMMUNITY NETWORK Definition of terms in Communicable
1.1 For the diseases/health issues listed Disease
below, surveillance within the EU •
network will be performed by standardised Chain of infection
collection and analysis of data in a •
way that will be determined for each Control and Management of Infectious
disease/health issue where specific EU Disease
surveillance networks are put in place. •
2. DISEASES Immunization
2.1 Diseases preventable by vaccination •
Diphtheria Protective Precautions / Isolation
Infections with haemophilus influenza •
group B Diseases acquired thru GI tract
Influenza •
Measles Diseases acquired thru the skin
Mumps •
Pertussis Diseases acquired thru the respiratory
Poliomyelitis tract
Rubella •
2.2 Sexually transmitted diseases Diseases acquired thru sexual contact
Chlamydia infections COMMUNICABLE DISEASE
Gonococcal infections •
HIV-infection It is an illness caused by an infectious
Syphilis agent or its toxic products that are
2.3 Viral hepatitis transmitted directly or indirectly to a well
Hepatitis A person through an agent, vector or
Hepatitis B inanimate object
Hepatitis C TWO TYPES
2.4 Food- and water-borne diseases and INFECTIOUS DISEASE
diseases of environmental origin •
Botulism Not easily transmitted by ordinary contact
Campylobacteriosis but
Cryptosporidiosis require a direct inoculation through a
Giardiasis break in
Infection with Enterohaemorrhagic E.coli the previously intact skin or mucous
Leptospirosis membrane
Listeriosis CONTAGIOUS DISEASE
Salmonellosis •
Shigellosis Easily transmitted from one person to
Toxoplasmosis another
Trichinosis through direct or indirect means
Yersinosis TERMINOLOGIES
2.5 Other diseases •
2.5.1. Diseases transmitted by non- DISINFECTION –destruction of pathogenic
conventional agents microorganism outside the body by directly
Transmissible spongiform applying physical or chemical means
encephalopathies variant (CJD) Concurrent – method of disinfection
2.5.2. Air-borne diseases done immediately after the infected
Legionellosis individual discharges infectious
Meningococcal disease material/secretions. This method of
Pneumococcal infections disinfection is when the patient is still
Tuberculosis the source of infection
2.5.3. Zoonoses (other than in 2.4) Terminal – applied when the patient is
Brucellosis no longer the source of infection.
Echinococcosis •
Rabies Disinfectant -chemical used on non living
2.5.4. Serious imported diseases objects
Cholera •
Malaria Antiseptic – chemical used on living things.
Plague •
Viral haemorrhagic fevers Bactericidal – kills microorganism
3. SPECIAL HEALTH ISSUES •
3.1 Nosocomial infections Sterilization – complete destruction of all
3.2 Antimicrobial resistance microorganism
General Principles
•
Pathogens move through spaces or air Some microbes have so many strains that a
current single vaccine can’t protect against all of
• them
Pathogens are transferred from one ex. Influenza
surface to •
another whenever objects touch Most viruses resist antiviral drugs
• •
Hand washing removes microorganism Opportunistic organisms can cause
• infection in
Pathogens are released into the air on immunocompromised patients
droplet •
nuclei when person speaks, breaths, Most people have not received
sneezes vaccinations
• •
Pathogens are transferred by virtue of Increased air travel can cause the spread
gravity of virulent microorganism to heavily
• populated area in hours
Pathogens move slowly on dry surface but •
very Use of immunosupressive drugs and
quickly through moisture invasive
INFECTION procedures increase the risk of infection
• •
invasion and multiplication of Problems with the body’s lines of defense
microorganisms Three Lines of Defense
on the tissues of the host resulting to signs •
and FIRST LINE OF DEFENSE
symptoms as well as immunologic response o
• MECHANICAL BARRIERS
injures the patient either by: o
o CHEMICAL BARRIERS
competing with the host’s metabolism o
o BODY’S OWN POP. OF
cellular damage produced by the MICROORGANISM - “microbial
microbes intracellular multiplication antagonism principle”
Factors of severity of infection •
o SECOND – inflammatory response
disease producing ability o
o Phagocytic cells and WBC to destroy
the number of invading microorganism invading microorganism manifesting the
o cardinal signs
The strength of the host’s defence and •
some other factors. THIRD – immune response -
Epidemiological triad: Natural/Acquired:
o active/passive
Agent RISK FACTORS
o •
Host Age, sex, and genes
o •
Environment Nutritional status, fitness, environmental
Classification accdg to incidence: factors
• •
SPORADIC - disease that occur occasionally General condition, emotional and mental
and irregularly with no specific pattern state
• •
ENDEMIC – those that are present in a Immune system
population or community at times. •
• Underlying disease ( diabetes mellitus,
EPIDEMIC – diseases that occur in a greater leukemia, transplant)
number than what is expected in a specific •
area over a specific time. Treatment with certain antimicrobials
• (prone to
PANDEMIC – is an epidemic that affects fungal infection), steroids,
several immunosuppresive
countries or continents drugs etc.
Causes of INFECTION
•
Some bacteria developres is tance to
antibiotics
•
 •
Handwashing
o
Before and after using gloves, after
hand contact with patients, patient’s
blood and other potentially infected
materials.
•
Protective Equipment shall be removed
immediately upon leaving the work area.
Like
apron, mask, gloves etc.
o
Place in designated area.
•
Used needles and sharps shall not be bent,
broken, recapped. Used needles must not
be
removed from disposable syringes.
•
Eating, drinking, smoking, applying
cosmetics
or handling contact lenses are prohibited
in
work areas.
•
Foods and drinks shall not be stored in
refrigerators, freezers where blood or
other
infectious materials are stored.
•
All procedures involving blood or other
potentially infectious materials shall be
performed in such a manner as to minimize
Mode of Transmission splashing, or spraying.
Contact transmission Control Measures
• •
Direct contact - person to person Masking – Wear mask if needed. Patient
• with
Indirect - thru contaminated object infectious respiratory diseases should wear
o mask.
Droplet spread - contact with •
respiratory secretions thru cough, Handwashing – Practice it with soap and
sneezing, talking. Microbes can travel water.
up to 3 feet. •
• Gloving – Wear gloves for all direct contact
Airborne Transmission with patients. Change gloves and wash
• hands
Vector Borne Transmission every after each patient.
• •
Vehicle Borne Transmission Gowning - Wear gown during procedures
Emerging problems in infectious diseases which
• are likely to generate splashes of blood or
Developing resistance to antibiotics eg: sprays of blood and body fluids, secretions
anti tb or
drugs, MRSA, VRE excretions.
• •
Increasing numbers of immunosuppressed Eye protection (goggles) – wear it to
patients. prevent
• splashes.
Use of indwelling lines and implanted •
foreign Environmental disinfection – Clean surfaces
bodies has increased. with disnfectant 70% alcohol,diluted
INFECTION CONTROL MEASURES bleach)
• o
UNIVERSAL PRECAUTION – All blood, blood Ex. Normal clean – clean the room post
products and secretions from patients are discharge, final clean- MRSA and
considered as infected. infectious pts.
WORK PRACTICE CONTROL ISOLATION PRECAUTIONS
• education such as
Separation of patients with communicable o
diseases from others so as to reduce or > development of materials for
prevent transmission of infectious agents. environmental sanitation
7 Categories Recommended in isolation o
• > providing group counselling,
Strict isolation – prevent spread of holding community assemblies and
infection conferences.
from patient to patient/staff.- o
handwashing, > create programs for sanitation
infectous materials must be discarded, use o
of > be a role model
single room, use of mask, gloves and Immunization – introduction of specific
gowns antibody to
and (-) pressure if possible produce immunity to certain disease
•
Contact isolation – prevent spread by close
or
direct contact
•
Respiratory isolation – prevent
transmission
thru air.
•
TB isolation – for (+) TB or CXR suggesting
active PTB.
•
Enteric Isolation – direct contact with feces
•
Drainage/secretion precaution- prevents
infection thru contact with materials or
drainage from infected person.
•
Universal Precaution – for handling blood
and
body fluids. (Bloods, pleural fluid,
peritoneal
fluid etc.)
PREVENTION Natural –pa s siv e (from placenta),
Health Education – educate the family active (thru immunization & recovery
about from diseases)
• o
Immunization Artificial–pa ss iv e (antitoxins ),
• active (vaccine, toxoid)
MOT Maintain vaccine potency by preventing:
• o
Environmental sanitation – breeding places Heat and sunlight
of o
mosquito, disposal of feces Freezing
• •
Importance of seeking medical advice for Antiseptic/ disinfectants/ detergents lessen
any the
health problem potency of vaccine. Use water only when
• cleaning fridge/ref.
Preventing contamination of food and •
water. COLD CHAIN SYSTEM – maintenance of
Environmental Sanitation correct
o temperature of vaccines, starting from the
Water Supply Sanitation Program – manufacturer, to regional store, to district
DOH thru EHS (Environmental Health hospital, to the health center to the
Services) immunizing staff and to the client.
o Diseases Acquired Thru Respiratory
Policies on Food Sanitation Program TUBERCULOSIS
o •
Policies on Hospital Waste Chronic respiratory disease affecting the
Management lungs
• characterized by formation of tubercles in
The CHNurse is in the best position to do the
health
tissues---> caseation –--> necrosis ---> o
calcification. Minimal manifestations
• o
AKA: Phthisis, Consumption, Koch’s, Lymphadenopathy
Immigrant’s dse DX
• •
Etiologic agent: – Mycobacterium Tuberculin testing
tuberculosis •
• CXR
Incubation period: 2 – 10 wks. •
• Sputum AFB
Period of communicability: all throughout Prevention
the •
life if not treated BCG
• •
MOT: Droplet Avoid overcrowding
• •
Sources of infection – sputum, blood, nasal Improve nutritional status
discharge, saliva TX
Classification •
1. Inactive – asymptomatic, sputum is (-), DOTS
no cavity on •
chest X ray 6 months of RIPE
2. Active – (+) CXR, S/S are present, •
sputum (+) smear Respiratory isolation,
Classification 0-5 •
A. Minimal – slight lesion confined to small Take medicines religiously – prevent
part of resistance
the lung •
B. Moderately advanced – one or both Stop smoking
lungs are •
involved, volume affected should not Plenty of rest
extend to one •
lobe, cavity not more than 4 cm. Nutritious and balance meals, increase
C. Far advance – more extensive than B CHON, Vit. A, C
MANIFESTATIONS MENINGITIS
• •
Primary Complex: TB in children: non Inflammation of the meninges usually
contagious, children swallow phlegm, some combination of headache, fever, stiff
fever, neck, and delirium
cough, anorexia, weight loss, easy •
fatigability Meningococcemia: cerebrospinal fever
• o
Adult TB Etiologic agent: Neisseria
o meningitidis
afternoon rise in temperature o
o Incubation: 2-10 days
night sweats o
o MOT: droplet
weight loss •
o Acute meningococcemia - with or without
cough dry to productive meningitis
o o
Hemoptysis Waterhouse Friederichsen
o Syndrome
sputum AFB (+) Diagnostic exams:
• o
Milliary TB - very ill, with exogenous TB Lumbar tap, CSF - high WBC and
like CHON, low glucose
Pott’s disease Manifestations:
• o
Primary Infection Sudden onset of fever x 24h
o o
Asymptomatic Petechiae, Purpuric rashes
o o
No manifestations even at CXR, Meningeal irritation
Sputum AFB
•
Primary Complex
 Manifestation
 PSEUDOMEMBRANE - grayish white,
smooth,
leathery and spider web like structure that
bleeds when detached
Types of Respiratory Diptheria
•
NASAL
o
serous to serosanginous purulent
discharge
o
Pseudomebrane on septum
o
Dryness/ excoriation on the upper lip
and nares
•
PHARYNGEAL
o
pharyngeal pseudomembrane
 o
Stiff neck bull neck ( cervical adenitis)
 o
Opisthotonus Difficulty swallowing
 •
Kernig’s sign LARYNGEAL
 o
Brudzinski sign Sorethroat, pseudomemb
o o
ALOC Barking, dry mettallic cough
o Complications
S/S of Increase ICP o
Nursing Mgt: Due to TOXEMIA
• 
Administer prophylactic antibiotics: Toxic endocarditis
Rifampicin - drug of choice 
• Neuritis
Aquaeous Pen 
• Toxic nephritis
Mannitol o
• Due to Intercurrent Infection
Dexamethasone 
• Bronchopneumonia
Priority: AIRWAY, SAFETY 
• Respiratory failure
Maintain seizure precaution DX
• •
Respiratory precaution Nose and throat swabs - culture of
• specimen form beneath membrane
Handwashing •
• Virulence test
Suction secretions •
DIPTHERIA SHICK’s TEST: test for susceptibility to
• diptheria
Acute contagious disease characterized by •
generalized toxemia coming from localized MOLONEY’s TEST: test for hypersensitivity
inflammatory process to
• diptheria
Etiologic agent: Corynebacterium Diptheria MANAGEMENT
(Klebs loffer bacillus) 1. Penicillin, Erythromycin
• 2. Diptheria Antitoxin – after – skin test if
Incubation period: 2-5 days (+), fractional
• dose
Period of communicability: variable, ave:2- 3. Supportive
4 •
weeks O2, if laryngeal obstruction –
• tracheostomy
MOT – Droplet, direct or intimate contact, •
fomites, discharge from nose, skin, eyes CBR for 2 weeks
•
Increase fluids, adequate nutrition-
soft food, rich in Vit C
•
Ice collar
4. Isolation till 3 NEGATIVE cultures
Prevention
 DPT
PERTUSIS (whooping cough)
•
Repeated attacks of spasmodic coughing
with
series of explosive expirations ending in
long
drawn force inspiration
•
Etiologic agent: Bordetella pertusis or
Haemiphilus pertussis
•
Incubation period: 7-14 days
•
Period of communicability: 7 days post
exposure to 3 wks post disease onset
•
MOT – Droplet
Manifestation
o
rapid cough 5-10x in one •
inspiration ending a high pitched Prone position during attack
whoop. •
• Abdominal binder
Catarrhal – slight fever in PM, colds, • Adequate ventilation, avoid dust, smoke
watery nasal discharge, teary eyes, •
nocturnal coughing, 1-2 weeks Isolation
• •
Paroxysmal – Spasmodic stage; 5-10 Gentle aspiration of secretions
successive forceful coughing ending with MEASLES
inspiratory whoop, involuntary micturition •
and defecation, choking spells, cyanosis Acute viral disease with prodromal fever,
• conjunctivitis, coryza, cough and Koplik’s
Convalescent – 4th- 6th week; diminish in spots
severity, frequency •
Complications: AKA: Rubeola, 7-day measles
• •
Otitis media Etiologic agent: Morbilli Paramyxoviridae
• virus
Acute bronchopneumonia •
• Incubation period: 10-12 days
Atelectasis or emphysema •
• Period of communicability: 3 days before
Rectal prolapse, umbilical hernia and 5 days after the appearance of rashes.
• Most communicable during the height of
Convulsions (brain damage - rash.
asphyxia, hemorrhage) •
Dx: MOT: Airborne
• •
Elevated WBC Sources of infection – secretions from eyes,
• nose and throat
Nasopharyngeal swab Pathognomonic sign:
Nursing Management •
• Koplik’s spots
Prevention: Manifestations
o •
DPT 1.Pre eruptive stage / Prodromal (10-11
• days)
Parenteral fluids o
• Coryza, Cough, Conjunctivitis
Erythromycin - drug of choice o
Koplik’s Spots, whitish spot at the
inner cheek 3rd
o to 5th day
Fever, photophobia •
• 2. Eruptive – FORSCHEIMER’S SPOTS:
2. Eruptive stage pinkish
o rash on soft palate, rash on face, spreading
Maculopapular rashes to
o the neck, arms and trunk
Rash is fully developed by 2nd day o
o lasts1-5 days with no pigmentation or
High grade fever –on and off desquamation
o o
Anorexia, throat is sore muscle pain
• •
3. Convalescence (7-10 days) Treatment
o o
Desquamation of the skin symptomatic treatment
Diagnostics• Complications
Nose and throat swab •
Treatment 1. Encephalitis, neuritis
• •
1. Antiviral drugs- Isoprenosine 2. Rubella syndrome – microcephaly,
• mental
2. Antibiotics – if with complications retardation, deaf mutism, congenital heart
• disease
3. Supportive – O2, IVF RISK for congenital malformation
• •
Complications – bronchopneumonia, 1. 100% when maternal infection happens
otitis media, encephalitis on
Nursing Management first trimester of pregnancy.
• •
Preventive – measles vaccine at 9 2. 4% - second/third trimester
months, MMR 15 months and then 11- Nursing Management
12; defer if with fever, illness 1. Isolation. Bed rest
• 2. Room darkened – photophobia
Isolation - contact/respiratory 3. Encourage fluid
• 4. Like measles tx
TSB , Skin care – daily cleansing wash PREVENTION;
• •
Oral and nasal care MMR, Pregnant women should
• avoid exposure to rubella patients
Plenty of fluids •
• Administration of Immune serum globulin
Avoid direct glare of the sun- due to one week after exposure to rubella.
photophobia CHICKEN POX
GERMAN MEASLES •
• Acute and highly contagious viral disease
Mild viral illness caused by rubella virus. characterized by vesicular eruptions on the
• skin
AKA: Rubella; 3-Day Measles •
• Infectious agent – Herpes zoster virus or
Incubation period– from exposure to rash Varicella zoster
14 •
-21d Incubation period – 10 -21 days
• •
Period of communicability – one week Period of communicability: 1 day before
before eruption up to 5 days after the appearance
and and 4 days after onset of rashes. of the
Worst last crop
when rash is at it’s peak. •
• MOT: airborne, direct, indirect
MOT: Droplet, nasal ceretions, o
transplacental in Direct contact thru shedding vesicles,
congenital o
Manifestations Indirect thru linens or fomites
• Manifestations
1. Prodromal – low grade fever, headache , •
malaise, colds, lymph node involvement on Pre eruptive: Mild fever and malaise
Eruptive: rash starts from trunk Pain and burning sensation over lesions
• of vesicles along nerve pathway
Lesions - red papules then becomes milky o
and Smear of vesicle fluid- giant cells
pus like within 4 days, o
• Viral cultures of vesicle fluid
Pruritis o
Stages of skin affectations Electron microscopy
o Macule – flat o
o Papule – elevated above the skin Giemsa-stained scraping –
diameter multinucleate giant epithelial cells
about 3 cm S/S
o Vesicle o
o Pustule Burning, itching, pain then
o Crust – scab , drying on the skin erythematous patches followed by crops of
Complications vesicles
o o
pneumonia, sepsis Eruptions are unilateral
Treatment o
• Lesions may last 1-2 weeks
Zovirax 500mg tablet 1 tab BID X 7 o
days Fever, regional lymphadenopathy
• o
Acyclovir Paralysis of cranial nerve, vesicles at
• external auditory canal
Oral antihistamine o
• Paralytic ileus, bladder paralysis,
Calamine lotion encephalitis
• Complications
Antipyretics o
NURSING MANAGEMENT Opthalmia herpes – blindness because
• of damage of gasserian ganglion
Strict isolation until all vesicles o
scabs disappear Geniculate herpes – deafness because
• of infection of 7th CN (AKA: Ramsay
Hygiene of patient Hunt Syndrome)
• Nursing Intervention
Cut finger nails short o
• Compress of NSS or alluminum acetate
Baking soda - pruritus over lesions
• o
PREVENTION: Live attenuated Analgesics, sedatives – weeks to mos
varicella vaccine o
• Steroids
VZIG - effective if given 96h post o
exposure Keep blister covered with sterile
Herpes Zoster powder esp after break
• o
Acute inflammatory disease known to be Prevent bacterial invasion
caused by herpes virus varicellae or VZ o
virus Encourage proper disposal of
• secretions and usage of gown and
Infection of the sensory nerve charac by mask
extremely painful infection along the MUMPS
sensory •
nerve pathway Acute viral disease manifested by swelling
• of
Occurs as reinfection of VZ virus one or both of the parotid glands, with
• occasional involvement of other glandular
MOTo structures,particularly testes in male.
Direct •
o Etiologic agent – filterable virus of
Indirect – airborne paramyxovirus group usually found in
• saliva of
Incubation: 1-2 weeks infected person.
Diagnostic procedure •
o AKA: Epidemic/ infectious parotitis
Hx of chickenpox •
o Incubation period: 14 -25 days.
• o Papule – elevated above the skin
Period of communicability – 6d before and diameter
9d about 3 cm
post onset of parotid gland swelling o Vesicle
o o Pustule
48 hrs immediately preceding the o Crust – scab , drying on the skin
onset of swelling is the highest Complications
communicability. o
• pneumonia, sepsis
MOT: direct, indirect - droplet, airborne Treatment
CLINICAL MANIFESTATIONS •
1. Sudden headache, earache, loss of Zovirax 500mg tablet 1 tab BID X 7
appetite days
2. Swelling of the parotid gland •
3. Pain is related to extent of the swelling Acyclovir
of •
the gland which reaches its peak in 2 days Oral antihistamine
and •
continues for 7-10 days. Calamine lotion
•
Antipyretics
NURSING MANAGEMENT
•
Strict isolation until all vesicles
scabs disappear
•
Hygiene of patient
•
Cut finger nails short
•
Baking soda - pruritus
•
PREVENTION: Live attenuated
varicella vaccine
•
VZIG - effective if given 96h post
exposure
Herpes Zoster
•
Acute inflammatory disease known to be
caused by herpes virus varicellae or VZ
virus
•
Infection of the sensory nerve charac by
extremely painful infection along the
sensory
nerve pathway
•
Occurs as reinfection of VZ virus
•
MOTo
Direct
o
Indirect – airborne
•
Incubation: 1-2 weeks
Diagnostic procedure
o
• Hx of chickenpox
Eruptive: rash starts from trunk o
• Pain and burning sensation over lesions
Lesions - red papules then becomes milky of vesicles along nerve pathway
and o
pus like within 4 days, Smear of vesicle fluid- giant cells
• o
Pruritis Viral cultures of vesicle fluid
Stages of skin affectations o
o Macule – flat Electron microscopy
o
Giemsa-stained scraping – MOT: direct, indirect - droplet, airborne
multinucleate giant epithelial cells CLINICAL MANIFESTATIONS
S/S 1. Sudden headache, earache, loss of
o appetite
Burning, itching, pain then 2. Swelling of the parotid gland
erythematous patches followed by crops of 3. Pain is related to extent of the swelling
vesicles of
o the gland which reaches its peak in 2 days
Eruptions are unilateral and
o continues for 7-10 days
Lesions may last 1-2 weeks
o
Fever, regional lymphadenopathy 4. Fever may reach 40 C during acute
o stage,
Paralysis of cranial nerve, vesicles at 5. One gland may be affected first and 2
external auditory canal days
o later the other side is involved
Paralytic ileus, bladder paralysis, COMPLICATIONS
encephalitis 1. Orchitis – testes are swollen and tender
Complications to
o palpation.
Opthalmia herpes – blindness because 2. Oophoritis- pain and tendeness of the
of damage of gasserian ganglion abdomen
o 3. Mastitis
Geniculate herpes – deafness because 4. Deafness may happen
of infection of 7th CN (AKA: Ramsay 5. Meningo-encephalitis -possible
Hunt Syndrome) DIAGNOSTIC PROCEDURES
Nursing Intervention 1. Viral culture
o 2. WBC count
Compress of NSS or alluminum acetate PREVENTION: MMR Vaccine
over lesions TREATMENT MODALITIES
o 1. Antiviral drugs
Analgesics, sedatives – weeks to mos 2. NSAIDS - Acetaminophen
o Nursing Interventions
Steroids o
o Symptomatic
Keep blister covered with sterile o
powder esp after break Application of warm/ cold compress
o o
Prevent bacterial invasion Oral care, warm salt water gargle
o o
Encourage proper disposal of Diet – semi solid, soft food easy to
secretions and usage of gown and chew•
mask Acid foods/fluids – fruit juices may
MUMPS increase discomfort
• Diseases Acquired thru GIT
Acute viral disease manifested by swelling •
of Diseases caused by Bacteria
one or both of the parotid glands, with o
occasional involvement of other glandular Typhoid Fever
structures,particularly testes in male. o
• Cholera
Etiologic agent – filterable virus of o
paramyxovirus group usually found in Dysentery
saliva of •
infected person. Diseases caused by Virus
• o
AKA: Epidemic/ infectious parotitis Poliomyelitis
• o
Incubation period: 14 -25 days. Infectious Hepatitis A
• •
Period of communicability – 6d before and Diseases caused by Parasites
9d o
post onset of parotid gland swelling Amoebiasis
o o
48 hrs immediately preceding the Ascariasis
onset of swelling is the highest TYPHOID FEVER
communicability. •
•
Infection of the GIT affecting the lymphoid 4. Widal test – blood serum agglutination
tissues(ulceration of Peyer’s patches) of test
the 
small intestine O antigen – active typhoid
• 
Etiologic Agent: Salmonella typhosa and H antigen- previously infected
typhi, or vaccinated
Typhoid bacillus 
• Vi antigen - carrier
Incubation period: 1-2 weeks TREATMENT
• 1. Chloramphenicol – drug of choice
Period of communicability: as long as the 2.Paracetamol
patient is excreting the microorganism, NURSING MANAGEMENT
• 1. Restore FE balance
MOT: fecal-oral route, contaminated water, 2. Bedrest
milk or other food 3. Enteric precaution
• 4. Prevent falls/ safety prec
Sources of Infection 5. Oral/personal hygiene
o 6. WOF intestinal bleeding-bloody
A person who recovered from the stool,sweating, pallor 7. NPO, BT
disease can be potential carrier. CHOLERA
o • An acute bacterial disease of the GIT
Ingestion of shellfish taken from waters characterized by profuse diarrhea,
contaminated by sewage disposal vomiting, loss
o of fluid
Stool and vomitus of infected person
are sources of infection. Etiologic agent: Vibrio cholerae, V. comma
CLINICAL MANIFESTATIONS • Pathognomonic sign: rice watery stool
ONSET • Incubation period: 2-3 days
• • Period of Communicability: entire
Ladderlike fever illness, 7-14d
• • MOT: fecal oral route
Nausea, vomiting and diarrhea Clinical manifestations
• o
RR is fast, skin is dry and hot, abdomen Acute, profuse, watery diarrhea.
is distended o
• Initial stool is brown and contains
Head-ache, aching all over the body fecal materialà becomes“rice
• water”
Worsening of symptoms on the 4th and o
5th day Nausea/ Vomiting
• o
Rose spots S/s of Dehydration
TYPHOID STATE o
• poor tissue trugor, eyes are sunken
Tongue protrudes- dry and brown o
• Pulse is low or difficult to obtain, BP
sordes is low and later unobtainable.
• o
(coma vigil) RR – rapid and deep
• o
(subsultus tendinus) Cyanosis – later
• o
(Carphologia) Voice becomes hoarse– speaks in
• whisper
Always slip down to the foot part of the •
bed, Oliguria or anuria
• •
Severe case - delirum sets in often Conscious, later drowsy
ending in death •
Complications Deep shock
o •
Hemorrhage, Peritonitis, Pneumonia, Death may occur as short as four hours
Heart failure, Sepsis after onset.
DIAGNOSTIC PROCEDURES •
1. WBC – elevated Usually first or 2nd day if not treated
2. Blood Culture – (+) S. typhosa Principal deficits
3. Stool Culture (+) 1. Severe dehydration - circulatory collapse
2. Metabolic acidosis – loss of large volume
of •
bicarbonate rich stool. RR rapid and deep Weight loss
3. Hypokalemia – massive loss of K. DIAGNOSTICS
abdominal •
distention – paralytic ileus Fecalysis
DIAGNOSTIC EXAMS •
Fecal microscopy Rectal Swab/culture
1. Rectal swab •
2. Stool exam Bloods – WBC elevated
Treatment •
1. IVF- rapid replacement Blood culture
2. Oral rehydration TREATMENT
3. Strict I and O •
4. Antibiotics – Tetracycline, Antibiotics- Ampicillin,
Cotrimoxazole. Cotrimoxazole, Tetracycline
NURSING MANAGEMENT •
1. Medical Asepsis IVF
2. Enteric precaution •
3. VS monitoring Anti diarrheal are
4. I and O Contraindicated
5. Good personal hygiene NURSING MANAGEMENT
6. Proper excreta disposal 1. Maintain fluid and electrolyte balance
7. Concurrent disinfection. 2. Restrict food until nausea and vomiting
8. Environmental sanitation subsides.
PREVENTION 3. Enteric precaution
1. Protection of food and water supply 4. Excreta must be disposed properly.
from 5. Prevention- food preparation, safe
fecal contamination. washing
2. Water should be boiled/ chlorinated. facilities, fly control
3. Milk should be pasteurized. POLIOMYELITIS
4. Sanitary disposal of human excreta •
5. Environmental sanitation. An acute infectious disease caused by any
DYSENTERY of the 3 types of poliomyelitis virus which
• affects mainly the anterior born cells of the
Acute bacterial infection of the intestine spinal cord and the medulla, cerebellum
characterized bydi a rrhea and fever and the midbrain
• •
Etiologic Agent: Shigella group AKA: Acute anterior poliomyelitis,
o heinmedin disease, infantile paralysis
Shigella flesneri - commmon in the •
Philippines Etiologic Agent: Poliovirus (Legio
o Debilitans)
Shigella boydii, S. connei, 3 Types of Poliovirus
o •
S. dysenteria – most infectious, Type I - most paralytogenic, most frequent
habitat exclusively in man, they •
develop resistance to antibiotics Type II - next most frequent
• •
Incubation period – 7 hrs. to 7 days Type III - least frequent associated with
• paralytic disease
Period of communicability – during acute 3 Strains
infection until the feces are (-) o
• Brunhilde
MOT – fecal-oral route, contaminated o
water/ Laasing
milk/ food. o
Clinical manifestations Leon
• •
Fever esp. in children MOT: Fecal-Oral
• •
Nausea, vomiting and headache Incubation period: 7-14 days ave (3-21
• days)
Anorexia, body weakness •
• Period of communicability:
Cramping abdominal pain (colicky) o
• 7-16 days before and few days
Diarrhea – bloody and mucoid after onset of s/s
• •
Tenesmus S/S
o •
Febrile episodes with varying Supportive, Preventive – Salk and
degrees of muscle weakness Sabin Vaccine
o •
Occasionally progressive Flaccid NO morphine
Paralysis •
3 Types of Paralysis Moist heat application for spasms
• •
Spinal Paralytic AIRWAY: tracheotomy
o •
Flaccid paralysis Footboard to prevent foot drop
o •
Autonomic involvement Fluids, NTN, Bedrest
o •
Respiratory difficulty Enteric and strict precautions
• HEPATITIS A
Bulbar Form •
o Inflammation of the liver caused by
Rapid & serious hepatitis A
o virus
Vagus and glossopharyngeal •
nerves affected AKA: infectious hepatitis
o •
Cardiac and respiratory reflexes Incubation period: 2-6weeks
altered •
o MOT: oral-fecal/ enteric transmission
Pulmo edema •
o Diagnostic test: liver function (SGOT/SGPT)
Hypertension, impaired temp Clinical manifestations
regulation Prodromal/ pre icteric
o •
Encephalitic s/s S/S of URTI
• •
Bulbospinal Weight loss
o •
Combination Anorexia
• •
Minor Polio RUQ pain
o •
Inapparent / subclinical Malaise
o Icteric
Abortive: recover within 72 hours; •
flulike; backache; vomiting Jaundice
• •
Major Polio Acholic stool
o •
Paralytic:as ym m etrical Bile-colored urine
weakness, paresthesia, urinary Diagnostic tests: HaV Ag, Ab, SGOT, SGPT
retention, constipation Nursing Interventions
o o
Non paralytic: slight involvement Provide rest periods
of the CNS; stiffness and rigidity of
the spine, spasms of hamstring
muscles, with paresis
o
Tripod position: extend his arms
behind him for support when
upright
o
Hoyne’s sign: head falls back
when he is in supine position with
the shoulder elevated
o
Meningeal irritation:(+)
Brudzinski, Kernig’s sign
Diagnostic tests:
•
Throat swab, stool exam, LP
Nursing Interventions
 Intestinal perforation -bleeding
DIAGNOSTIC EXAM
•
Stool Exam ( cyst, amoeba+++)
•
WBC – elevated
TR E ATMENTo
Amoebacides – Metronidazole(Flagyl)
800mg TID X 7days
o
Bismuth gylcoarsenilate combined with
Chloroquine
o
Antibiotic – Ampicillin, Tetracycline,
Chloramphenicol
o
Fluid replacement – IVF, oral
NUSING MANAGEMENT
•
Enteric precaution
•
Health education- boil drinking water (20-
30 mins), Use mineral water.
o •
Increase CHO, mod Fat, low CHON Cover leftover food.
o •
Intake of vits/minerals Avoid washing food from open drum/pail.
o •
Proper food preparation/handling Wash hands after defecating and before
o eating.
Handwashing to prevent transmission •
AMOEBIASIS Observe good food preparations.
• •
Involves the colon in general but may Fly control
involve ASCARIASIS
the liver or lungs as well •
• Helminthic infection of the small intestine
Etiologic agent: Entamoeba histolytica caused by ASCARIS LUMBRECOIDES
• •
Incubation: 3-4 weeks MOT: fecal-oral
• •
Period of communicability: duration of Incubation period: 4-8 weeks
illness •
• Communicability: as long as mature
MOT: fecal oral route fertilized female worms live in intestine
• •
Indirect - Ingestion of food contaminated Diagnostic exams: Microscopic
with identification of eggs in stool, CBC, Hx of
E.Histolytica cysts, polluted water supply, passing out of worms (oral or anal), Xray,
exposure S/S
to flies, unhygienic food handlers. o
• Stomachache
Direct contact – sexual, oral, or anal, o
proctogenital Vomiting
Clinical manifestations o
• Passing out of worms
Intermittent fever o
• Complications
Nausea, vomiting, weakness o
• Energy / Protein malnutrition,
Later : anorexia, weight loss, Anemia
jaundice o
• Intestinal obstruction
Diarrhea – watery and foul smelling Treatment:
stool often containingblo o d o
streaked mucus Pyrantel Pamoate
• o
Colic and abdominal distention Piperazine Citrate
• o
Mebendazole, Tetramizole o
o Spore forming, gram positive rod
Dicyclomine Hcl, NSAIDS for abdominal •
pain Sources:
o o
For intestinal obstruction Animal and human feces
 o
Decompression Soil and dust
 o
Fluid and electrolyte Plaster, unsterile sutures, rusty
therapy scissors, nails and pins
 •
If persistent, MOT
laparotomy Direct or indirect contact to
o wounds
FF up stool exam 1-2 weeks after o
treatment Traumatic wounds and burns
Nursing Intervention o
o Umbilical stump of the newborn
Isolation- not needed o
o Dirty and rusty hair pins
Enteric precaution o
o GIT- port of entry – rare
Handwashing o
o Circumcision/ ear pearcing
Proper nutrition •
o Incubation period: 3d-3week (ave:10d)
Maintenance of hydration / fluid balance / S/s:
boil •
of water persistent contraction of muscles in the
o same anatomic area as the injury
Improve personal hygiene •
o Local tetanus
Proper food prep/handling •
o Cephalic tetanus - rare form
Administer meds (NSAIDS, MEBENDAZOLE o
Diseases Acquired thru the Skin otitis media (ear infections)
• •
Diseases caused by Trauma and Generalized tetanus
Inoculation o
o trismus or lockjaw
Tetanus o
o stiffness of the neck
Rabies o
o difficulty in swallowing
Malaria o
o rigidity of abdominal muscles
DHF o
o elevated temperature
Leptospirosis o
o sweating
Schistosomiasis o
• elevated blood pressure episodic
Disease acquired thru Contact rapid heart rate
o •
Leprosy Neonatal tetanus - a form of generalized
tetanus that occurs in newborn infants
TETANUS Complications:
• o
An acute, often fatal, disease characterized Laryngospasm
by generalized rigidity and convulsive 
spasms of skeletal muscles caused by the Hypostatic pneumonia
endotoxin released by C. Tetani 
• Hypoxia
AKA: Lockjaw 
• Atelectasis
Etiologic Agent: Clostridium Tetani o
o Trauma
Anerobic 
Fractures o
o Adequate airway
Septicemia o
 ICU – ET- MV
Nosocomial infections •
o Provide cardiac monitoring
Death •
Diagnostic procedure: KVO
 entirely clinical •
CSF – normal Wound care (TIG, Debridement, TT)
WBC- normal or slight elevation •
Treatment: Administer antibiotics as ordered
• o
Wounds should be cleaned Penicillin
• •
Necrotic tissue and foreign material should Care during tetanic spasm/ convulsion
be o
removed Administer Diazepam – muscle
• rigidity/spasm
Tetanic spasms - supportive therapy and o
maintenance of an adequate airway Administer neuromuscular blocking
• agents (metocurin iodide) – relax
Tetanus immune globulin (TIG) spasms and prevent seizure
o •
help remove unbound tetanus toxin Keep on seizure precaution
o •
cannot affect toxin bound to nerve Parenteral nutrition
endings •
o Avoid complications of immobility
single intramuscular dose of 3,000 to (contractures, pressure sores)
5,000 units •
o WOF urinary retention, fractures
Contains tetanus antitoxin. RABIES
• •
Oxygen A viral zoonotic neuroinvasive disease that
• causes acute encephalitis
NGT feeding •
• Etiologic agent:R habdovirus
Tracheostomy •
• AKA: Hydrophobia, Lyssa
Adequate fluid, electrolyte, caloric intake •
• Negri bodies in the infected neurons –
During convalescence pathognomonic
o •
Determine vertebral injury Incubation period: 4-8 weeks; 10d-1yr
o •
Attend to residual pulmonary disability Period of communicability: 3-5 days before
o the
Physiotherapy onset of s/s until the entire course of
o disease
TT •
Nursing Interventions: MOT: contamination of a bite of infected
• animals
Prevention •
• Diagnostic procedures
DPT o
o History of exposure
Adverse Reactions o
o PE/ assessment of s/s
Local reactions (erythema, induration) o
o Microscopic examination of Negri
Fever and systemic symptoms not bodies using Seller’s May-Grunwald
common and Mann Strains
o o
Exagerated local reactions Fluorescent Rabies Antibody
Nursing interventions: technique / Direct Immunofluorescent
• test
Prevention of CV and respiratory
complications
 •
Spasm, progressively increasing
paralysis
•
Death due to respiratory paralysis
TREATMENT•
No cure
•
No specific – symptomatic/ supportive –
directed toward alleviation of spasm
•
Employ continuing cardiac and
pulmonary monitoring
•
Assess the extent and location of the
bite – biting incident/ status of the
animal
o
Severe exposure
o
Mild exposure
•
Wound treatment (local care)
o
Cleanse thoroughly with soap
Cl and water (or ammonium
inical Manifestations compounds, betadine, or
Prodromal Phase / Stage of Invasion benzalkonium cl)
• o
Fever, anorexia, malaise, Anti rabies serum
sorethroat, copious salivation, o
lacrimation, perspiration, irritability, Tetanus prophylaxis
hyperexcitability, restlessness, o
drowsiness, mental depression, marked Antibiotics
insomia o
• Suturing should be avoided
Sensitive to light, sound, and •
changes in temp Antirabies sera
• o
Myalgia, numbness, tingling, Heterologous serum obtained
burning or cold sensation along nerve by hyperimmunization of
pathway; dilation of pupils different animal species i.e.
Stage of Excitement horses
• o
Marked excitation, apprehension HRIG – Homologous reabies
• immunoglobulin – human origin
Delirium, nuchal stiffness, involuntary •
twitching Rabies Vaccine
• •
Painful spasms of muscles of mouth, Active immunization
pharynx, and larynx on attempting to o
swallow food or water or the mere sight Administered 3 years duration
of them –hy dro pho bi a o
• Used for lower extremity bites
Aerophobia o
• Lyssavac (purified protein
Precipitated by mild stimuli – touch or embryo), Imovax, Anti-rabies
noise vaccine
• •
Death – spasm from or from cardiac / Passive immunization
respiratory failure o
Terminal Phase or Paralytic Stage 3 months
• o
Quiet and unconscious Rabuman, Hyper Rab, Imogam
• Nursing Intervention
Loss of bowel and bladder control o
• Isolation of patient
Tachycardia, labored irregular o
respiration, steady rising temp Provide comfort for the patient by:
 Malarial smear – film of blood is
Place padding of placed on a slide, stained and
bedside or use examined
restraints •
 Rapid diagnostic test (RDT)–
Clean and dress wound done in field. 10 -15 mins result
with the use of gloves blood test
 Clinical Manifestions
Do not bathe the •
patient, wipe saliva or Rapidly rising fever with severe
provide sputum jar headache
o •
Provide restful environment Shaking chills
 •
Quiet, dark environment Diaphoresis, muscular pain
 •
Close windows, no faucets or running Splenomegaly, hepatomegaly
water should be heard •
 Hypotension
IVF should be covered o
 May lasts for 12 hours daily or every 2
No sight of water or electric fans days.
MALARIA •
• Complicated Malaria
Acute and chronic disease transmitted by •
mosquito bite confined mainly to tropical GIT
areas. o
• Bleeding from GUT, N/V, Diarrhea,
Etiologic agent – Protozoa of genus abdominal pain, gastric, tyhoid, choleric,
Plasmodia dysenteric
• •
Plasmodium Falciparum (malignant tertian) CNS or Cerebral Malaria
o o
most serious, high parasitic densities in Changes in sensorium
RBC with tendency to agglutinate and o
form into microemboli. Most common Severe headache
in the Philippines o
• N/V
P. Vivax - non life threatening except for •
the Hemolytic
very young and old. •
o Blackwater fever
Manifests chills every 48 hrs on the 3rd o
day onward if not treated, Reddish to mahogany colored urine
• due to hemoglobinuria
P. malarie (Quartan) – less frequent, non o
life Anuria – death
threatening, fever and chills occur every 72 •
hrs Malarial lung disease
on the 4th day of onset MANAGEMENT
• •
P. ovale- rare Antimalarial drugs –Chl o ro qui ne (all but
• P. Malarie), quinine, Sulfadoxine (resistant
Incubation period: P falciparum) Primaquine (relapse P
o vivax/ovale)
12days P. falciparum, 14 days P vivax •
and ovale, 30 days P. malariae RBC replacement/ erythrocyte exchange
• transfusion
Period of communicability Nursing management:
o •
If not treated /inadequate – more than Isolation of patient
3 yrs. P malariae, 1-2 yrs. P. vivax, 1 •
yr- P. falciparum Use mosquito nets
• •
Mode of transmission Eradicate mosquitos
Mosquito bite •
VECTOR – female Anopheles mosquito Care of exposed persons – case finding
DIAGNOSTICS •
• I and O
• o
BUN & creatinine – dialysis could be life N &V
saving •
• FEBRILE Phase
ABG o
• Fever persists (39-40 C)
TSB, ice cap on head o
• Rash - more prominent on the
Hot drinks during chilling, lots of fluid extremities and trunk
• o
Monitoring of serum bilirubin (+) torniquet test- petechia more than
• 10.
Keep clothes dry, watch for signs of o
bleeding Skin appears purple with blanched
• areas with varied sizes (Herm a n’s
PREVENTION sign)
o o
Mosquito breeding places should Generalized or abdominal pain
be destroyed Hemorrhagic manifestations –
o epistaxis, gum bleeding
Insecticides, insect repellant •
o CIRCULATORY Phase
Blood donor screening o
DENGUE FEVER Fall of temp on 3rd to 5th day
• o
Is an acute febrile disease cause by Restless, cool clammy skin
infection with one of the serotypes of o
dengue virus which is transmitted by Profound thrombocytopenia
mosquito ( Aedes aegypti). o
• Bleeding and shock
Dengue hemorrhagic fever – fatal o
characterized by bleeding and hypovolemic Pulse - rapid and weak
shock o
• Untreated shock --- coma – death
Etiologic agent – Arbovirus group B – o
• Treated – recovery in 2 days
AKA: Chikungunya, O’ nyong nyong, west CLASSIFICATION
nile •
fever Grade 1
• •
Mode of Transmission: Bite of infected Grade 2
mosquito – AEDES AEGYPTI •
• Grade 3
Incubation period – 3-14 days •
• Grade 4
Period of communicability – mosquito all Treatment
throughout life •
Sources of infection No specific antiviral therapy for dengue
• •
Infected person- virus is present in the Analgesic – not aspirin for relief of pain
blood and will be the reservoir when •
sucked by mosquitoes IV fluid
• •
Stagnant water = any BT as necessary
Diagnostic Tests •
• O2 therapy
Torniquet test NURSING MANAGEMENT
• 1. Kept in mosquito free environment
Platelet Count 2. Keep pt. at rest
• 3. VS monitoring
Hematocrit 4. Ice bag on the bridge of nose and
Manifestations forehead.
• 5. Observe for signs of shock – VS (BP low),
PRODROMAL symptoms cold
o clammy skin
malaise and anorexia up to 12 hrs. PREVENTION
o •
Fever and chills, head-ache, muscle Mosquito net
pain •
Eradication of breeding places of mosquito- Convalescence – recovery
o MANAGEMENT
house spraying 1. IV antibiotic
o Pen G Na
change water of vases Tetracycline
o Doxycycline
scrubbing vases once a week 2. Dialysis – peritoneal
o 3. IVF
cleaning the surroundings 4. Supportive
o 5. Symptomatic
keep water containers covered Nursing Interventions
o o
avoid too many hanging clothes inside Isolation of patient – urine must
the house properly disposed
LEPTOSPIROSIS o
• Care of exposed persons – keep under
Infectious bacterial disease carried by close surveillance
animals whose urine contaminates water o
or food which is ingested or inoculated Control measures
thru the skin. 
• Cleaning of the environment/
Etiologic agent: spirocheteLeptospira stagnant water
interrogans 
o Eradicate rats
found in river, sewerage, floods 
• Avoid bathing or wading in
AKA: Weil’s disease, mud fever, contaminated pool of water
Swineherd’s 
disease vaccination of animals
• (cattles,dogs,cats,pigs)
Incubation Period: 6 -15 days SCHISTOSOMIASIS
• •
Period of Communicability – found in urine Parasitic disease caused by Schistosoma
between 10-20 days japonicum, S. mansoni, S. Hematobium
• •
MOT – contact with skin of infected urine or AKA: Bilharziasis, Snail fever
feces of wild/domestic animals; ingestion, •
inoculation Incubation period: 2-6 weeks
• •
Diagnostic tests: MOT: bathing, swimming, wading in water
o •
Clinical manifestations Vector: Oncomelania quadrasi
o o
Culture Cercariae: most infective stage
SOURCE OF INFECTION •
o Rats, dogs, mice Diagnostic test: ova seen in fecalysis
MANIFESTATIONS •
o Diagnostic procedures
Septic Stage 
 Fecalysis
Early •
 Identification of eggs
Fever (40 ‘C), tachycardia, skin
flushed, warm, petechiae Liver and rectal biosy
 
Severe Immunodiagnostic tests /
 circumoval precipitin test and
Multiorgan cercarial envelope reactions
 S/s
Conjunctival affectation, o
jaundice, purpura, ARF, Swimmers itch
Hemoptysis, head-ache, 
abdominal pain, jaundice Itchiness
o 
Toxic stage – with or w/o jaundice, Redness and pustule formation at site
meningeal irritation, oliguria– shock, of entry of cercariae
coma , 
CHF Diarrhea
o 
Abdominal pain Creation of a program on snail control –
 chemical or changing snail
hepatosplenomegaly environment
CLINICAL MANIFESTATIONS: LEPROSY
• •
Abdominal pain Chronic systemic infection characterized by
• progressive cutaneous lesions
Cough •
• Etiologic agent: Mycobacterium leprae
Diarrhea o
• Acid fast bacilli that attack cutaneous
Eosinophilia - extremely high eosinophil tissues, peripheral nerves producing
granulocyte count. skin lesions, anesthesia, infection and
• deformities.
Fever •
• Incubation period – 5 1/2 mo - eight years.
Fatigue •
• MOT – respiratory droplet, inoculation thru
Hepatosplenomegaly - the enlargement of break in skin and mucous membrane.
both Diagnosis
the liver and the spleen. •
• 1. Identification of S/s
Colonic polyposis with bloody diarrhea •
(Schistosoma mansoni mostly) 2. Tissue biopsy
• •
Portal hypertension with hematemesis and 3. Tissue smear
splenomegaly (S. mansoni, S. japonicum); •
• 4. Bloods – inc. ESR
Cystitis and ureteritis with •
hematuriaàbladder 5. Lepromin skin test
cancer; •
• 6. Mitsuda reaction
Pulmonary hypertension (S. mansoni,S. MANIFESTATIONS
japonicum, more rarely S. haematobium); •
• Corneal ulceration, photophobia –blindness
Glomerulonephritis; and central nervous •
system lesions. Lesions are multiple, symmetrical and
• erythematous– macules and papules
Complications •
o Later lesions enlarge and form plaques on
Pulmonary hypertension nodules on earlobes, nose eyebrows and
o forehead
Cor pulmonale •
o Foot drop
Myocardial damage •
o Raised large erythemathous plaques
Portal cirrhosis appear on
Treatment: skin with clearly defined borders. – rough
• hairless and hypopigmented – leaves an
Trivalent antimony anesthetic scar.
o •
Tartar emetic – administered thru vein Loss of eyebrows/eyelashes
o •
Stibophen (FUADIN) – given per IM Loss of function of sweat and sebaceous
• glands
PRAZIQUANTEL – per orem •
• Epistaxis
Niridazole TREATMENT
• •
Nursing Interventions: multiple drug therapy
o •
Administer prescribed drugs as ordered sulfone
o •
Prevent contact with cercaria-laden rehab
waters in endemic areas like streams •
o occupational Health
Proper sanitation or disposal of feces •
o isolation
•
moral support Major signs – loss of weight 10% BW,
PREVENTION chronic diarrhea 1month up, prolonged
1. Report cases and suspects of leprosy fever one month up.
2. BCG vaccine may be protective if given •
during Persistent lymphadenopathy
the first 6 months. •
3. Nursing Interventions: Cytopenias (low)
•
1. Isolation of patient – until causative PCP
agent is still present •
2. Care of exposed persons Kaposis sarcoma
1. Household contact – •
Diaminodiphenylsulfone for 2 Localized candida
years •
2. Observe carefully for Bacterial infections
symptoms of the disease •
Diseases Acquired Thru Sexual Contact TB
HIV /AIDS •
• STD
Chronic disease that depresses immune  Neurologic symptoms
function Criteria for Diagnosis of AIDS
• •
Characterized by opportunistic infections CD4 counts of 200 or less
when •
T4/CD4 count drops <200 Evidence of HIV infection and any of
• o
MOT – sexual contact with infected – Thrush
unprotected, injection of blood/products, o
placental transmission Bacillary angiomatosis
History of HIV / AIDS o
• Oral hairy leukoplakia
1959 - African man o
• Peripheral neuropathy
1981- 5 homosexual men o
• Vulvovaginal candidiasis
1982-Designated as disease by CDC o
• Shingles
1983- HIV 1 discovered o
• Idiopathic thrombocytopenia
1987- 1.5 million HIV-infected in USA o
• Fatigue, night sweats, weight loss
1994- WHO reports 8-10 mil. Worldwide & o
protease inhibitors introduced Cervical dysplasia, carcinoma in
• situ
1999-First clinical trials for HIV vaccine •
The immune system Evidence of HIV infection and any one of
o the
Macrophages following:
 Humoral response o
 Cell-mediated response Bronchial candidiasis
Diagnostic Tests o
• Esophageal candidiasis
ELISA o
• CMV disease
Western Blot o
• CMV retinitis
CD4 count o
• HIV encephalopathy
Viral load testing o
• Histoplasmosis
Home test kits o
Manifestations Kaposi’s Sarcoma
o o
Minor signs – cough for one month, Herpes simplex ulcers, bronchitis,
general pruritus, recurrent herpes pneumonia
zoster, oral candidiasis, generalized o
lymphadenopathy Primary brain lymphoma
o o
Pneumocystis Carinii Pneumonia
o Peripheral
Recurrent pneumonia neuropathy
o Lamivudine3TC, Epivir
Mycobacterium infection 150 mg
bid
o Used as
Progressive multifocal resistance
leukoencepalopathy develops
o Lamiduvine/
Salmonella septicemia Zidovudine
o Combivir
Toxoplasmosis 150/300
o mg
Wasting syndromes Bone marrow
Treatment toxicity
• Protease Inhibitors
Started in CD4 counts of <200 •
• Introduced in 1995
Viral load >10,000 copies •
• Acts by blocking protease enzyme
All symptomatic regardless of counts •
• Indinavir (Crixivan)
Note: CD4 reflects immune system CDC Guidelines
destruction. Viral load- degree of viral o
activity Combination of 2 NRTI + PI
• •
Nucleoside Reverse Transcriptase Nursing Management
Inhibitors o
• Administer Antiviral meds as ordered
Blocks reverse transcriptase o
NRT• Universal precaution
Acts by binding directly to the reverse o
transcriptase enzyme Reverse isolation
• 
Not used alone gloves, needle stick injury
• prevention
Rapid development of resistance o
• Assist in early diagnosis and
Acts by binding directly to the reverse management of complications
transcriptase enzyme •
• 4 C’so
Not used alone Compliance – info, + drugs
• o
Rapid development of resistance Counselling – education
Generic o
Trade Contact tracing – tracing out and tx for
Dose partners
Notes o
Zidovudine Condoms – safe sex
AZT, ZDV, GONORRHEA
Retrovir •
300 mg. A curable infection caused by the bacteria
Bid Neisseria gonorrhoea
Taken with food •
Didanosine AKA: Clap, Drip, G. vulvovaginitis
ddI, Videx •
200 mg MOT: transmitted during vaginal, anal, and
bid oral
Peripheral sex
neuropathy •
Zalcitibine Incubation period: 3-10 days initial
ddC,Hivid manifestations
.75 mg •
TID Period of communicability: considered
No antacids infectious from the time of exposure until
Stavudine treatment is successful
d4T, Zerit Manifestations:
400 mg •
bid Urethritis – both male and female
• a curable, bacterial infection, that left
S/S: dysuria and purulent discharge untreated will progress through four
• stages
Cervicitis with increasingly serious symptoms
• •
Upper Genital Tract – females (PID) Etiologic agent: Treponema pallidum
Endometritis, Salpingitis, •
Pelvic Abscess AKA: Lues, The pox, Bad blood
• •
Complications : Type of Infection: Bacterial
• •
PID Modes of transmission :
• o
Infertility Through sexual contact/ intercourse,
Complications: kissing
• o
Upper Genital Tract – male abrasions
o o
Epididymitis, Prostatitis, Seminal Can be passed from infected mother to
Vesiculitis unborn child (transplacental)
•
Disseminated Gonococcal Infection (DGI) Symptoms
o o
Tenosynovitis or Polyarthritis, skin Primary syphilis (10 – 90 days after
lesions and fever infection)
•  Chancre – a firm, painless skin
Anorectal Infection ulceration localized at the point
• of initial exposure to the
Pharyngeal Infection bacterium appear on the
• genitals
Gonococcal Conjuctivitis •
o can also appear on the lips, tongue, and
Opthalmia Neonatorum other body parts
• o
Meningitis, Endocarditis Secondary syphilis (last 2 – 6 weeks)
Diagnosis:  syphilis rash - an infectious
• brown skin rash that typically
Culture & Sensitivity occurs on the bottom of the
• feet and the palms of the hand
Blood tests for N. gonorrhoeae antibodies  condylomata lata - flat broad
Treatment: whitish lesions
• 
ANTIBIOTICS Fever, sore throat, swollen
• glands, and hair loss can also
Penicillin be experienced
• •
Single dose Ceftriaxone IM + doxycycline Third stage
PO o
BID for 1 week Will manifest 1 – 10 years after the
• infection
Prophylaxis: Silver nitrate, Tetracycline, o
Erythromycin characterised by gummas - soft, tumor-
Nursing Interventions: like growths
o 
Case finding seen in the skin and mucous
o membranes – occurs in bones
Health teaching on importance of o
monogamous sexual relationship joint and bone damage
o o
Treatment should be both partners to increasing blindness
prevent reinfection o
o Numbness in the extremities, or
Instruct possible complications like difficulty in coordinating movements.
infertility Neurosyphilis
o •
Educate about s/s and importance of generalized paresis of the insane
taking antibiotic for the entire therapy which results in personality
SYPHILIS changes, changes in emotional
• affect, hyperactive reflexes
• Etiologic agent: hepatitis B virus (HBV)
cardiovascular syphilis •
• Source of infections: Blood and body
aortitis, aortic aneurysm, secretions
Aneurysm of sinus of valsalva and Risk factors
aortic regurgitation, - death •
Consequences in Infants multiple sex partners or diagnosis of a
• sexually
Congenital syphilis transmitted disease
• •
extremely dangerous Sex contacts of infected persons
• •
Deformities Injection-drug users
• •
Seizures Household contacts of chronically infected
• persons
Blindness •
• Infants born to infected mothers
Damage to the brain, bones, teeth, and •
ears. Infants/children of immigrants from areas
Test and diagnosis with
• high rates of HBV infection
Venereal Disease Research Laboratory •
(VDRL) test Health-care and public safety workerr
• •
Flourescent treponemal antibody Hemodialysis patients
absorption (FTA – Abs) Complications:
• •
Micro hemagglutination test (MHA - TP) Lifelong infection
• •
CSF examination Liver cirrhosis
Treatment •
• Liver cancer
Syphilis is easily treatable when early •
detected Liver failure
• •
Penicillin & other antibiotics Death
Prevention S/s:
• •
Abstinence Jaundice
• •
Mutual monogamy Pruritus
• •
Latex condoms for vaginal and anal sex Fatigue
• •
Nursing interventions RUQ - Abdominal pain
o •
Case finding Loss of appetite
o •
Health teaching and guidance along Nausea, vomiting
preventive measures •
o Joint pain
Utilization of community health Prevention:
facilities •
o Hepatitis B vaccine has been available
Assist in interpretation and diagnosis since
o 1982.
Reinforce ff up treatment o
o Routine vaccination of 0-18 year olds
VD control program participation o
o Vaccination of risk groups of all ages
Medical examination of patient’s •
contacts Immune globulin if exposed
HEPATITIS B MEDICAL MANAGEMENT
• •
serious disease caused by a virus that Interferon alfa-2b
attacks •
the liver Lamivudine
• •
Telbivudine Immunofluorescence assay, can detect
• antibodies 10 days after the onset of the
Entecavir disease
• o
Adefovir dipivoxil labour and time intensive test
Nursing Interventions: •
o Polymerase chain reaction (PCR) test that
Blood and body secretions precautions can
o detect genetic material of the SARS virus
Prevention- Hepa B vaccine in
o specimens ranging from blood, sputum,
Proper rest periods tissue
o samples and stools
Prevent stress – physio/psychological •
o CXR - increased opacity in both lungs,
Proper NTN, increase in CHO, high in indicative of pneumonia
CHON, low fats, Vit. K rich foods and •
minerals SARS may bes us pected
o •
Assistance to prevent injury, promote fever of 38 °C (100.4 °F) or more AND
safety AAT •
Either a history of:
o
o Contact (sexual or casual) with
WOF s/s bleeding, edema someone with a diagnosis of SARS
o within the last 10 days OR
Health education on safe sex o
SEVERE OF ACUTE RESPIRATORY Travel to any of the regions identified
SYNDROME by the WHO as areas with recent local
• transmission of SARS (affected regions
An acute and highly contagious respiratory as of 10 May 2003 were parts of China,
disease in humans Hong Kong, Singapore and the province
• of Ontario, Canada).
Etiologic agent: SARS coronavirus •
• probable case of SARS has the above
November 2002 and July 2003, with 8,096 findings
known infected cases and 774 deaths plus positive chest x-ray findings of
• atypical
Incubation period: 2-3days pneumonia or respiratory distress
• syndrome
MOT: Airborne Treatment
S/s •
o Supportive with antipyretics, supplemental
flu like: fever, myalgia, lethargy, oxygen and ventilatory support as needed.
gastrointestinal symptoms, cough, sore •
throat Suspected cases of SARS must be isolated,
o preferably in negative pressure rooms,
fever above 38 °C (100.4 °F) with full
o barrier nursing precautions taken for any
Shortness of breath necessary contact with these patients
o •
Symptoms usually appear 2–10 days steroids
following exposure •
o antiviral drug
require mechanical ventilation •
Diagnostic Test: SARS vaccine
•
Chest X-ray (CXR)- abnormal with patchy
Description
infiltrates
•
WBC and PLT CT. - LOW Hand, foot, and mouth disease (HFMD) is a
• common viral illness of infants and
ELISA test detects antibodies to SARS children. The disease causes fever and
o blister-like eruptions in the mouth and/or a
but only 21 days after the onset of skin rash. HFMD is often confused with
symptoms foot-and-mouth (also called hoof-and-
• mouth) disease, a disease of cattle, sheep,
and swine; however, the two diseases are
not related—they are caused by different
viruses. Humans do not get the animal
disease, and animals do not get the human
disease.
Illness
• The disease usually begins with a
fever, poor appetite, malaise
(feeling vaguely unwell), and often
with a sore throat.
• One or 2 days after fever onset,
painful sores usually develop in the
mouth. They begin as small red
spots that blister and then often
become ulcers. The sores are
usually located on the tongue,
gums, and inside of the cheeks.
• A non-itchy skin rash develops over
1–2 days. The rash has flat or
raised red spots, sometimes with
blisters. The rash is usually located
on the palms of the hands and
soles of the feet; it may also
appear on the buttocks and/or
genitalia.
• A person with HFMD may have only
the rash or only the mouth sores.
Cause
• HFMD is caused by viruses that
belong to the enterovirus genus
(group). This group of viruses
includes polioviruses,
coxsackieviruses, echoviruses, and
enteroviruses.
• Coxsackievirus A16 is the most
common cause of HFMD in the
United States, but other
coxsackieviruses have been
associated with the illness.
• Enteroviruses, including
enterovirus 71, have also been
associated with HFMD and with
outbreaks of the disease.
How It Is Spread
• Infection is spread from person to
person by direct contact with
infectious virus. Infectious virus is
found in the nose and throat
secretions, saliva, blister fluid, and
stool of infected persons. The virus
is most often spread by persons
with unwashed, virus-
contaminated hands and by
contact with virus-contaminated
surfaces.
• Infected persons are most
contagious during the first week of
the illness.
• The viruses that cause HFMD can
remain in the body for weeks after
a patient's symptoms have gone
away. This means that the infected
person can still pass the infection
to other people even though he/she
appears well. Also, some persons
who are infected and excreting the
virus, including most adults, may
have no symptoms.
• HFMD is not transmitted to or from
pets or other animals.
Factors That Increase the Chance for Infection or
Disease
• Everyone who has not already been
infected with an enterovirus that
causes HFMD is at risk of infection,
but not everyone who is infected
with an enterovirus becomes ill
with HFMD.
• HFMD occurs mainly in children
under 10 years old but can also
occur in adults. Children are more
likely to be at risk for infection and
illness because they are less likely
than adults to have antibodies to
protect them. Such antibodies
develop in the body during a
person’s first exposure to the
enteroviruses that cause HFMD.
• Infection results in immunity to
(protection against) the specific
virus that caused HFMD. A second
case of HFMD may occur following
infection with a different member
of the enterovirus group.
Diagnosis
• HFMD is one of many infections
that result in mouth sores.
However, health care providers can
usually tell the difference between
HFMD and other causes of mouth
sores by considering the patient’s
age, the symptoms reported by the
 patient or parent, and the
appearance of the rash and sores.
• Samples from the throat or stool
may be sent to a laboratory to test
for virus and to find out which
enterovirus caused the illness.
However, it can take 2–4 weeks to
obtain test results, so health care
providers usually do not order
tests.
Treatment and Medical Management
• There is no specific treatment for
HFMD.
• Symptoms can be treated to
provide relief from pain from
mouth sores and from fever and
aches:
o Pain and fever can be
treated with over-the-
counter medications
(caution: aspirin should not
be given to children).
o Mouthwashes or sprays
that numb pain can be
used to lessen mouth pain.
• Fluid intake should be enough to
prevent dehydration (lack of body
fluids). If moderate-to-severe
dehydration develops, it can be
treated medically by giving fluids
through the veins.
Prevention
• A specific preventive for HFMD is
not available, but the risk of
infection can be lowered by
following good hygiene practices.
• Good hygiene practices that can
lower the risk of infection include
o Washing hands frequently
and correctly (see Clean
Hands Save Lives! ) and
especially after changing
diapers and after using the
toilet
o Cleaning dirty surfaces and
soiled items, including
toys, first with soap and
water and then disinfecting
them by cleansing with a
solution of chlorine bleach
(made by adding 1
tablespoon of bleach to 4
cups of water)
o Avoiding close contact
(kissing, hugging, sharing
eating utensils or cups,
etc.) with persons with
HFMD
Vaccination Recommendations
• No vaccine is available to protect
against the enteroviruses that
cause HFMD.
Complications
• Complications from the virus
infections that cause HFMD are not
common, but if they do occur,
medical care should be sought.
• Viral or "aseptic meningitis can
rarely occur with HFMD. Viral
meningitis causes fever, headache,
stiff neck, or back pain. The
condition is usually mild and clears
without treatment; however, some
patients may need to be
hospitalized for a short time.
• Other more serious diseases, such
as encephalitis (swelling of the
brain) or a polio-like paralysis,
result even more rarely.
Encephalitis can be fatal.
• There have been reports of
fingernail and toenail loss
occurring mostly in children within
4 weeks of their having hand, foot,
and mouth disease (HFMD). At this
time, it is not known whether the
reported nail loss is or is not a
result of the infection. However, in
the reports reviewed, the nail loss
has been temporary and nail
growth resumed without medical
treatment.
Trends and Statistics
• Individual cases and outbreaks of
HFMD occur worldwide. In
temperate climates, cases occur
more often in summer and early
autumn.
• Since 1997, outbreaks of HFMD
caused by enterovirus 71 have
been reported in Asia and
Australia.
• HFMD caused by coxsackievirus
A16 infection is a mild disease.
 Nearly all patients recover in 7 to
10 days without medical treatment.

• HFMD caused by enterovirus 71

has shown a higher incidence of
neurologic (nervous system)
involvement. And fatal cases of
encephalitis (swelling of the brain)
caused by enterovirus 71 have
occurred during outbreaks.
However, these serious outcomes
are still very rare.