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INFECTIOUS DISEASES
EMERGENCY
dr. Andi Sulistyo Haribowo, SpPD
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Diphtheria
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Gram +ve Bacilli and Colonies
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Case-fatality rate
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Selected RecentDiphtheria
Outbreaks in Great
Britain
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The Scandinavian Outbreak
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The Seattle Outbreak
1971-82
72 cases, nine deaths (four from obstruction)
Important roles of skin infections, Native Americans, Skid
Row residents
Diphtheria Dick ,alone cost $11,000
Total cost in $millions
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Back in the (former) USSR
Outbreak began in 1990 in
Russia
All NIS affected by 1994 >50,000 cases and 1,500
deaths in 1995
Adults predominant
Exported to Europe and UK
Cases of diphtheria - New Independent States of the
former Soviet Union, 1965-1995.
(Source MMWR, 45:32, August 16, 1996.)
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Diphtheria Epidemiology
Reservoir Human carriersUsually asymptomatic
Transmission Respiratory
Skin and fomites rarely
Temporal pattern Winter and spring
Communicability Up to several weekswithout antibiotics
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Diphtheria Clinical Features
Incubation period 2-5 days(range, 1-10 days)
May involve any mucous membrane
Classified based on site of infectionanterior nasal
pharyngeal and tonsillar
laryngeal
cutaneous
ocular
genital
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Pharyngeal and Tonsillar Diphtheria
Insidious onset of exudative pharyngitis
Exudate spreads within 2-3 days and may form
adherent pseudo membrane
Membrane may cause respiratory obstruction
Fever usually not high but patient appears toxic
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Thick Membrane
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Pseudo membrane
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Bull Neck
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Skin Lesions
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Diphtheria Complications
Mostly attributable to toxin
Severity generally related to extent of local
disease
Most common complications are myocarditis
and toxic neuritis with palsy
Death occurs in 5%-10% for respiratory disease
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Laboratory findings
Routine examination
Leukocytosis, 10~20 G/L, neutrophil is dominant.
Low platelet count (thrombocytopenia), riseprofiles of the serum enzyme tests and
proteinuria were found in serious cases.
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Laboratory findings
Bacteriological examinations
Smear and gram stain can found C. diphtheriae,
but can not identify from the diphtheroids.
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Laboratory findings
Bacteriological examinations
Fluorescent antibody-stain can found toxigenic C.
diphtheriae, favourable for early diagnosis, but
definitive diagnosis (false positive).
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Laboratory findings
Bacteriological examinations
C. diphtheriae can be cultured from the swabs
from nose, pharynx or other sites.
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Laboratory findings
Immunological examinations
Schick test (not to be used any more), positive
result supports diagnosis
Specific antibody detection. Positive results deny
the diagnosis since it is a protective antibody.
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Complications
Most complications of diphtheria, including death,
are attributable to effects of the toxin. The severity of the disease and complications are
generally related to the extent of local disease. The most frequent complications of diphtheria are
myocarditis and neuritis.
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Complications
Myocarditis
Present as abnormal cardiac rhythms and can
occur early in the course of the illness or weeks
later, and can lead to heart failure and abruptdeterioration (sudden death).
If myocarditis occurs early, it is often fatal.
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Complications
Neuritis
Most neuritisoften affect motor nerves andusually recovers completely.
Paralysis of the soft palate is most frequent
during the third week of illness.
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Complications
Neuritis
Eye muscles, limbs, and diaphragm paralysis can
occur after the fifth week.
Secondary pneumonia and respiratory failuremay result from diaphragmatic paralysis.
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Complications
Other complications Include otitis media and respiratory insufficiency
due to airway obstruction, especially in infants.
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Diagnosis
Clinical diagnosis is usually made based on the
epidemiological data and clinical presentation since
it is imperative to begin presumptive therapy
quickly.
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Diagnosis
Gram stain of material from the pseudomembrane
can be helpful when trying to confirm the clinical
diagnosis.
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Diagnosis
Culture of the lesion is even important to confirm
the clinical diagnosis. It is critical to take a swab of
the pharyngeal area, especially any discolored areas,
ulcerations, and tonsillar crypts.
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Diagnosis
If diphtheria bacilli are isolated, they must be testedfor toxin production by ELISA or Elek test.
If toxin test is positive, the definitive diagnosis canbe made.
The presence of staphylococci and streptococci donot rule out diphtheria.
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Diagnosis
In patients with negative culture and priorantibiotic therapy, the presumptive diagnosismay be confirmed with evidences:
(1) isolation of the C. diphtheriae from culturingof close contacts, and/or (2) a low or non-protective diphtheria antibody titer in sera (
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Differential diagnosis
Dyspnea
Acute laryngitis; foreign body in trachea;
laryngeal edema Pseudomembrane
Streptococcal pharyngitis
Oral candidiasis
Infectious mononucleosis
Vincents angina
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Differential diagnosis
Streptococcal pharyngitis
The pus covering on the tonsils sometimes is
misunderstood as the pseudomembrane of
diphtheria. Its usually yellow in color, and easy
to remove.
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Differential diagnosis
Oral candidiasis
The oral candidiasis often occurs in infants. The
general conditions of such patients are very well.
The membrane is very white, and easy to remove
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Differential diagnosis
Infectious mononucleosis and Vincents angina
Sometimes also have things like membranes on
the surface of tonsils or pharynx. However, they
can be remove without bleeding of the tissues.
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Prognosis
The overall case-fatality rate for diphtheria is about
5%, with higher death rates (up to 20%) in persons
40 years of age.
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Treatments
Strict isolation
Use antitoxin and antibiotics for neutralization offree toxin, elimination of further toxin productionand to control local infection.
Use supportive interventions during disintoxication.
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Treatments
General measures
Relax on bed for more than 3 weeks, 4-6 weeks
for patients with myocarditis.
Provide adequate energy and nutriments
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Treatments
Diphtheria antitoxin
Diphtheria antitoxin, produced in horses.
It will not neutralize toxin that is already fixed
to tissues, but will neutralize circulating toxin.
Early use will prevent progression of disease. The earlier, the better.
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Treatments
Diphtheria antitoxin
Dose: 3-5 104 U for early (3-4d)or grave patients; reduce in larynx diphtheria
1-2 104 U is given intravenously and the rest isgiven intramuscularly.
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Treatments Diphtheria antitoxin
The patient must be tested for sensitivity
before antitoxin is given.
Respiratory support and airway maintenanceshould also be administered as needed.
(Pseudomembrane shedding often happens
during disintoxication)
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Treatments
Antibiotics
Prevention of further toxin production.
Control local infection.
Reduction of transmission.
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Treatments
Antibiotics
Procaine penicillin G daily, intramuscularly
(300,000 U/day for those weighing 10 kg or less
and 600,000 U/day for those weighing more than10 kg) for 7-10 days.
Erythromycin orally or by injection (40-50
mg/kg/day; maximum, 2 gm/day) for 14 days.
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Treatments
Antibiotics
The disease is usually not contagious 48 hours
after antibiotics are used.
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Preventions
Management of infection sources
Isolation of patients (>7d), or elimination of the
organism should be documented by two
consecutive negative cultures after therapy iscompleted.
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Preventions
Management of infection sources Persons with suspected diphtheria should be
given antibiotics and antitoxin in adequate
dosage and placed in isolation (7d) after theprovisional clinical diagnosis is made and
appropriate cultures are obtained.
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Preventions Management of infection sources
For close contacts, especially household contacts,
a diphtheria booster, appropriate for age, should
be given.Antitoxin 1000-2000 U, intramuscularly
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Preventions
Management of infection sources Contacts should also receive antibiotics
benzathine penicillin G or a 7- to 10-day course
of oral erythromycin.
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Preventions
Interruption of the transmission routes by
disinfections of discharges and articles of patients
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Preventions
Protect the susceptibles by vaccination
The effective measure
Primary series (DTP, multivalent vaccine) given at
age of 3, 5, 6 months. Boosters (DTP) given at 15 months and 4-6 years
old, and booster (DT) every 10 years after then.
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Summary of the definition
Acute, communicable, toxin-mediated, sometime
life-threatening bacterial disease
Preventable with widespread immunization
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Summary of the definition
Pseudomembrane usually in the throat or nose
The typical pseudomembrane is adherent to the
tissue, and forcible attempts to remove it cause
bleeding.
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Diphtheria Antitoxin (DAT)
Produced in horses
First used in the U.S. in 1891
Used only for treatment of diphtheria
Neutralizes only unbound toxin
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Tetanus
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Tetanus Epidemiology
Uncommon in the US but not worldwide
1 million cases worldwide per year
Mortality rate of 20-50%
Highest prevalence in developing countries
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Epidemiology
Fewer than 50 cases per year in the US
Majority of cases in temperate climates (Texas,California, and Florida)
Mortality rate of 11%
Most who develop it have an inadequate immunizationhistory
Only 27% of Americans older than age 70 haveadequate immunity to tetanus
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Pathophysiology
Wound contamination with Clostridiumtetani
Motile, nonencapsulated, anaerobic, grampositive rod
Spore forming and ubiquitous in soil andanimal feces
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Pathophysiology
Usually introduced in the spore forming state,then germinates to the toxin producingvegetative form
Requires decreased tissue oxygen tension togerminate
Vegetative state produces two exotoxins Tetanolysin
Tetanospasmin
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Toxins
Tetanolysin
clinically insignificant
Tetanospasmin Neurotoxin responsible for the clinical
manifestations of tetanus
Reaches peripheral nerves by hematogenousspread and retrograde intraneuronal transport
Does not cross blood brain barrier
Reaches CNS by retrograde transport
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Tetanospasmin
Acts on the motor end plates of skeletalmuscle, in the spinal cord, and in thesympathetic nervous system
Prevents release of inhibitoryneurotransmitters glycine and gamma-
aminobutyric acid (GABA)
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Clinical Features
Tetanospasmin responsible for generalizedmuscular rigidity, violent muscular contractions,and instability of the ANS.
Typical wound is a puncture, but no wound isidentified in up to 10%
Other routes are surgical procedures, otitismedia, abortion, umbilical stump and drugabusers
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Four Clinical Forms
Local
Generalized
Cephalic
Neonatal
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Local Tetanus
Rigidity of the muscles in proximity to thesite of injury
Usually resolves completely in weeks tomonths
May develop into generalized
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Generalized Tetanus
Most common form
Most common presenting complaint is pain
and stiffness of the masseter muscles(Lockjaw)
Short axon nerves affected initiallytherefore starts in the face, then neck,trunk, and extremities
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Generalized Tetanus
Muscle stiffness leads to rigidity
Trismus and characteristic sardonic smile
develops (risus sardonicus)
Reflex convulsive spasms and tonic muscle
contraction create dysphasia, opisthotonos(arching of back and neck), flexing arms,clenching fists, and lower extremity extension
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Trismus and Sardonic Smile
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Opisthotonos
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Generalized Tetanus
Autonomic nervous system
Hypersympathetic state
Usually in the second week
Tachycardia
HTN
Diaphoresis
Increased urinary catecholamines
Significant morbidity and mortality
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Cephalic Tetanus
Results from an injury to the head or otitismedia
Cranial nerves affected most commonlythe seventh
Poor prognosis
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Neonatal Tetanus
400,000 worldwide deaths annually
Results from inadequately immunizedmothers
Frequent after unsterile treatment of thecord stump
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Neonatal Tetanus
Signs
Weakness
Irritability
Inability to suck
Presents in the 2nd week of life
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Diagnosis
Clinical diagnosis
No laboratory confirmatory tests
Wound cultures not very useful as C. tetanimaybe recovered without tetanus
Immunization history usually unknown orinadequate
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Tetanus Ddx
Strychnine poisoning
Dystonic reaction
Hypocalcemic tetany
Peritonsillar abscess
Peritonitis
Meningeal irritation
Rabies
TMJ
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Treatment
Admit to ICU
Be prepared for intubation with neuromuscularblockade as respiratory compromise may
develop
Minimal environmental stimuli to avoid reflexconvulsive spasms
Initial wound debridement to improveoxygenation
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Treatment
Tetanus Immunoglobulin (TIG)
Neutralizes wound and circulatingtetanospasmin
Does not neutralize toxin already bound to thenervous system
Does not improve clinical symptoms
Decreases mortality
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Treatment
TIG
Usual dose is 3,000 to 6,000 units
Administered IM opposite side as Td given
Give before wound debridement
T
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Treatment
Antibiotics
Questionable utility but usually given
Metronidazole
antibiotic of choice
Avoid penicillin
it is a GABAA antagonist and may worse symptoms
T t t
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Treatment
Muscle relaxants
Tetanospasmin
prevents neurotransmitter release at inhibitory
interneurons and therapy of tetanus is aimed atrestoring balance
Midazolam
preferred agent as it is water soluble
Baclofen specific GABAB agonist that has also been used
T t t
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Treatment
Neuromuscular blockade
Blockade often required to allow respirationand to prevent fractures and rhabdomyolysis
Succinylcholine recommended for initial airway management
Vecuronium
treatment of choice for long term blockade
T t t
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Treatment
ANS dysfunction treatment
Labetalol
useful for treatment due to combined alpha and
beta activity Magnesium sulfate
inhibits the release of epinephrine andnorepinephrine from the adrenal glands
Clonidine central alpha receptor agonist for cardiac stability
I i ti
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Immunization
Disease does not confer immunity so those thatrecover must undergo immunization
Tetanus toxoid 0.5 cc IM at presentation, 6 weeks, and 6
months
Local reactions are common
Less common serous reactions includeurticaria, anaphylaxis, or neurologiccomplications
I i ti d TIG id
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Immunization and TIG guide
Clean, Minor
wounds
All other
wounds
History of Td
Doses Td TIG Td TIG
Unknown or < 3 Yes No Yes Yes
Three or more No No Yes No
Td dose: 0.5cc IM TIG dose: 250 U IM
DPT given if under 7, Td given if over 7
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Rabies
R bi
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Rabies
Rabies ranks number 10 worldwide as acause of mortality
50,000
60,000 deaths annuallyworldwide
Rare human cases in US but 35,000people provided prophylaxis annually
Mi bi l
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Microbiology
Lyssavirus genus prototype Single-stranded, negative-sense,
nonsegmented RNA
7 rabies groups in genus
Classic rabies virus common rabies
6 others with less than 10 reported humancases of disease
P th h i l
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Pathophysiology
Virus course Initial uptake of virus by monocytes in 48-96
hours
Crosses motor end-plate to travel up the axonto the dorsal root ganglia to the spinal cordand the CNS
Then spreads outward via peripheral nervesto infect almost all tissue of the body
Pathoph siolog
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Pathophysiology
Histologically resembles other encephalitis
Monocellular infiltration with focal hemorrhage
Demyelination
Perivascular gray matter Basal ganglia
Spinal cord
Negri bodies
Eosinophilic intracellular lesions in cerebralneurons
Highly specific for rabies
Present in 75% of rabies cases
Negri bodies
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Negri bodies
Epidemiology
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Epidemiology
Primarily a disease of animals Human cases reflect the prevalence in animals
and degree of human contact with them Major vectors include
Dogs Foxes Raccoons Skunks Coyotes Mongooses bats
Epidemiology
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Epidemiology
Wild animals (93%)
Raccoons (37.7%)
Skunks (30.2%)
Bats (16.8%)
Foxes (6.2%)
Others (2.2%)
Domestic animals(7%)
Cats (3.4%)
Dogs (1.6%)
Cattle (1.1%)
Horses, donkeys, mules(0.71%)
Sheep, goats, camels(0.15%)
Others and ferrets0.06%
7,369 cases of animal rabies in the US in 2000
Epidemiology
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Epidemiology
Dogs
Less than 5% of animal cases in US, Canadaand Europe
Greater than 90% of animal cases indeveloping countries
Very rare documented rabies in:
Squirrels, hamsters, guinea pigs, gerbils,chipmunks, rats, mice, domesticated rabbitsand other small rodents
Almost never requires post exposure
prophylaxis
Epidemiology
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Epidemiology
Transmission Saliva though bite of an rabid animal most
common
Aerosolized in bat caves Mucus membrane transmission also reported
Bites and scratches
Risk of developing rabies dependant on thelocation injury, depth, an number of bites
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Infection Risk
Risk of infectionMultiple bites around the face 80-100%
Single bite 15-40%Superficial bite on the extremity 5-10%
Contamination of open wound by
saliva
0.1%
Transmission via fomites (e.g. treebranch, or animal)
0%
Epidemiology
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Epidemiology
32 cases reported from 1980 to 1996 inthe US 7 had a known animal bite
6 dog bites in a foreign country
1 bat bite
Animal contact identified in 12 8 with a bat
2 with a dog 1 with a cow
1 with a cat
No identifiable source in the other 13
Preexposure Prophylaxis
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Preexposure Prophylaxis
Prophylaxis Individuals with occupations or recreation that
place them at risk should receive the series
4 shot series with booster shots required Does not eliminate need for postexposure
prophylaxis
No need for HRIG and less doses of vaccine
Postexposure Prophylaxis
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Postexposure Prophylaxis
Indicated for all persons possibly exposed to arabid animal
Exposure is a bite, scratch, abrasion, openwounds, or mucous membrane exposure
Contact alone, and contact with blood, urine,or feces does not constitute and exposure
Cleansing wound with 20% soap and water hasbeen show in experimental animals to markedlyreduce the rate of infection
Bats
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Bats
Increasingly important wildlife vectors oftransmission of rabies
All cases of possible bat bites the batshould be collected and tested for rabies
Bat unavailable
Begin postexposure prophylaxis
Dogs Cats and Ferrets
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Dogs, Cats, and Ferrets
Observation CDC recommends 10 days of observation of a
healthy dog, cat, or ferret after a bite
Normal behavior No action needed
Unusual behavior
Sacrifice animal, test for rabies, and initiate HRIGand vaccine
Positive Complete course of vaccine
Negative Discontinue course
Possible animal exposure
Carnivore, bat or
salivary exposure
Bird, reptile, rodent or
nonsalivary exposure
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Dog or catBat, skunk, raccoon, cow,
bobcat, coyote, or fox
Captured and quarantined
Escaped
Vaccine + HRIG
Sacrifice and test
Initiate vaccine +HRIG
Rabid
Vaccine +HRIG
Not Rabid
Discontinue vaccine
Captured
Escaped
No epidemiologic
prevalence in area
No vaccine needed
Epidemiologic prevalence
Vaccine +HRIG
Normal behavior 10 days
No vaccine needed
Strange behavior
Sacrifice, initiatevaccine and HRIG
Rabid
Vaccine + HRIG
Not Rabid
Discontinue vaccine
No Vaccine needed
Bat, skunk, raccoon, cow,
bobcat, coyote, or fox
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Captured and quarantined Escaped
Vaccine + HRIGSacrifice and testInitiate vaccine +HRIG
Rabid
Vaccine +HRIG
Not Rabid
Discontinue vaccine
Dog or cat
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Captured Escaped
No epidemiologic
prevalence in area
No vaccine needed
Epidemiologic
prevalence
Vaccine +HRIG
Normal behavior
10days
No vaccine needed
Strange behavior
Sacrifice, initiate
vaccine and HRIG
Rabid
Vaccine + HRIG
Not Rabid
Discontinue vaccine
Postexposure Prophylaxis
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Postexposure Prophylaxis
Course HRIG (human rabies immune globulin)
One dose initially
May be given up to 7 days after an exposure Infiltrate as much as possible around wound
Give on the opposite side as the vaccine
Vaccine
5 doses over 28 days
Postexposure Prophylaxis
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Postexposure Prophylaxis
Vaccine reactions Minor reaction
Erythema, swelling, pain
30-74%
Systemic reaction Headache, nausea, abdominal pain, muscle aches
5-40%
Anaphylaxis and neurological symptoms Rarely reported
Vaccine should not be stopped for minoror systemic reactions
Special Circumstances
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Special Circumstances
Prior rabies immunization Either prior preexposure course or full
postexposure course
No HRIG Course shortened to 2 doses
One dose on presentation
One dose three days later
Special Circumstances
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Special Circumstances
Immunocompromised patient HRIG and vaccine usual course
Safe
Vaccine is inactivated so no danger of contracting
Stop all immunosuppressives if possible
Measure antibody titers to assure appropriate
response
Special Circumstances
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Special Circumstances
Travelers Preexposure prophylaxis
Recommended if prevalence and possible exposure
Veterinarians, animal handlers, spelunkers, certainlab workers
Non-FDA postexposure prophylaxis
If initiated in another country contact health
department for recommendations
Special Circumstances
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Special Circumstances
Pregnancy No adverse effects of the vaccine or HRIG
Follow usual course in pregnancy if indicated
Special Circumstances
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Special Circumstances
ChildrenVaccine
Same dose and same course
HRIG Dose is based on weight
If quantity of HRIG not sufficient to infiltrate allwounds may be diluted with saline
Clinical Disease
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Clinical Disease
Incubation period20 to 90 days
4 days up to 19 years have been reported
Greater than 1 year is well documented Prodrome
Fever, sore throat, chills malaise, headache,N/V, weakness
May report limb pain, weakness, andparesthesias
Nonspecific neurologic conditions such asanxiety, agitation, irritability or psychiatric
disturbances
Clinical Disease
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Clinical Disease
Acute neurologic phase Furious 80%
Hyperactivity, disorientation, hallucinations, bizarre
behavior Symptoms may alternate with calm
Autonomic dysfunction
Hydrophobia with pharynx spasms in 50%
Paralytic
20% Paralysis in the extremity, diffuse or ascending
Fever and nuchal rigidity
Clinical Disease
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Clinical Disease
ComaAlmost always present within 10 days
Death
Occurs from complications such as pituitarydysfunction, seizures, respiratory dysfunction,cardiac dysfunction, ANS dysfunction, ARF, orinfection
Outcome almost always fatal
No person without post-exposure prophylaxisin the US has survived since 1980
Diagnosis
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Diagnosis
Rabies should be in the differential of anyacute encephalitis
May be confused with poliomyelitis,Guillain-Barre syndrome, transversemyelitis, postvaccinial encephalomyelitis,
CVA, atropine-like poisoning, other viralencephalitis
Diagnosis
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Diagnosis
Lab testing No one test is completely informative
Test serum, CSF, and skin for antibodies in a
non-vacinated person Nuchal skin biopsy most sensitive early
PCR from saliva also useful
Treatment
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Treatment
Limited No specific treatment exists for clinical course
Treatment directed at the clinical
complications
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AVIAN INFLUENZA
AVIAN INFLUENZA
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Penyebab : Virus RNA, Fam. Orthomyxoviridae, Genus :
Orthomyxovirus : tipe A, B dan C.
Tipe A : unggas, manusia, kuda, babi, mamalia lain
Tipe B dan C : manusia
Beramplop, 2 permukaan antigen: hemaglutinin (HA)dan Neuraminidase (NA)
HA : 15 macam, NA : 9 macam
Kombinasi keduanya hasilkan lebih dari 100 tipe virus.
AI patogenik : H5 dan H7, contoh : H5N1
AVIAN INFLUENZA
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ILUSTRASI SEL VIRUS AI
AVIAN INFLUENZA
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SIFAT VIRUS
Hemaglutinasi pada unggas
Peka terhadap panas, pH yg ekstrim
Kondisi non isotonis dan udara kering
Peka terhadap pelarut lemak, spt : deterjen
Daya infeksi rendah oleh : formalin, oksidator,
-propiolakton, iodine, larutan asam, eter, ion
amonium dan klorida
AVIAN INFLUENZA
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Tahan dalam tubuh unggas sampai beberapa
bulan
Dikeluarkan dari tbh penderita lewat : sekresi
hidung, feses dan mata.
Dalam feses tahan thd usaha inaktiasi : pada
suhu 0-40C tahan 30 -35 hari dan pada suhu
200C tahan 7 hari.
Mati pada pemanasan 600C selama 30 menit,
800C selama 1 menit
Mati karena deterjen, formalin, alkohol 70%
AVIAN INFLUENZA
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Teori antigenic shift dari antigen permukaan Virus A: antigenic shift, B: antigenic drift, C:
relatif stabil
Adanya organisme sebagai mixing vessel,misalnya babi
Sampai 5 Agustus 2005: 112 kasus A pada
manusia(H5N1) di Hongkong, Vietnam,Thailand, Kambodia dan Indonesia
AVIAN INFLUENZA
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CARA PENULARAN
Kontak langsung
Tidak langsung ; udara tercemar oleh
muntahan, feses atau droplet penderita
Feses yg mengandung virus bs mencemari : air
minum, pakan, kandang, burung liar, pakaian,
sepatu, peralatan, kendaraan, serangga.
AVIAN INFLUENZA
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Sumber utama penularan :
1. Spesies lain dalam kelompok unggas
domestik (dari itik ke ayam).
2. Burung eksotik yg dipelihara
3. Burung liar (migrasi burung air).
4. Hewan lain (kalkun dapat tertular dari
babi)
Tidak ada indikasi penularan secara vertikal.
MANIFESTASI KLINIS
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Inkubasi: 3 hari (2-4 hari) Sistem respirasi : ringan s/d berat
ILI: influenza-like Ilness
Batuk, pilek, demam
Cephalgia, odynophagia, myalgia, malaise
Berat: Pneumonia s/d ARDS (progresif dan
fatal)
Lab: lekopenia, limfopenia, trombositopenia
CXR: progresif
DIAGNOSIS
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Uji konfirmasi: Kultur dan identifikasi H5N1
Real Time PCR
Serologi: IFA, Netralisasi (kenaikan titer 4x)
Uji penapisan: Rapid test, HI, ELISA
Lab lain : DL, AST/ALT, Ureum/Creatinine, BGA
Radiologis
OBSERVASI
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Panas >380C disertai 1 atau lebih:- Batuk
- Odynophagia
- Pilek- Nafas pendek/sesak nafas
- Pneumonia
Belum jelas ada tidaknya kontak dengan unggassakit/mati mendadak yang belum diketahuipenyebabnya dan produk mentahnya
Px diobservasi klinis, epidemiologis dan
pemeriksaan lab
SUSPECT
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Panas >380C disertai 1 atau lebih:
- Batuk
- Odynophagia
- Pilek
- Nafas pendek/sesak nafas
- Pneumonia
Disertai 1 atau lebih:- Pernah kontak dengan unggas sakit/mati mendadak yg tidak diketahui sebabnyadan produk mentahnya dalam 7 hari terakhir sebelum gejala
- Pernah tinggal di daerah yg terdapat kematian unggas yg tidak biasa dalam 14hari
- Kontak dg penderita AI terkonfirmasi dalam 7 hari
- Pernah kontak dg spesimen AI dalam 7 hari
- Lekopenia 3000
- Titer antibodi dg HI test menggunakan eritrosit kuda atau ELISA untuk influenza Atanpa subtipe
ATAU
Kematian akibat ARDS dengan 1 atau lebih:
- Lekopenia atau limfopenia dengan/tanpa trombositopenia
- Foto thorax men ambarkan neumonia ati ikal atau infiltrat ada kedua aru
PROBABLE
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Kasus suspek + 1 atau lebih:- Kenaikan titer AB minimum 4x terhadap H5 dg
HI test menggunakan eritrosit kuda atau ELISA
test- Hasil lab terbatas untuk influenza H5
menggunakan netralisasi test (ref lab)
- Dalam waktu singkat menjadi pneumoniaberat/gagal nafas/meninggal dan tidak
terbukti ada penyebab lain
CONFIRMED
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Suspect atau probable + 1 atau lebih:- Kultur virus poditif
- PCR positif
- IFA test positif dg antibodi monoklonal H5N1
- Kenaikan titer antibodi spesifik terhadap H5N1
sebanyak 4x pada paired serum sample
dengan uji netralisasi
HIGH RISK
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Pekerja peternakan/pemrosesan unggas Pekerja lab yang memproses sample
paien/unggas yang terjangkit
Pengunjung peternakan/pemrosesan unggas(7 hari)
Pernah kontak dg unggas sakit/mati
mendadak belum diketahui sebabnya danatau babi serta produk mentahnya dalam 7
hari
Pernah kontak den an enderita AI dalam 7
KRITERIA RAWAT
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Suspect dg gejala klinis berat: Sesak nafasdengan gangguan frek nafas 30x/menit, Nadi
100x/menit, ada gangguan kesadaran,
kondisi umum lemah Suspect dengan lekopenia
Suspect dengan gambaran radiologis
pneumonia Kasus probable dan confirmed
TATALAKSANA
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Supportif: Bed rest, imunomodulasi Antiviral
Antibiotik
Respiratory care
Antiinflamasi
ANTIVIRAL
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Paling efektif diberikan dalam 48 jam pertama Suspect: oseltamivir 2x75 mg 5 hari,
simtomatik dan antibiotik bila ada indikasi
Probable: Oseltamivir 2x75 mg 5 hari, broadspectrum Ab, steroid bila ada indikasi, ICU
(respiratory care)
Profilaksis: Oseltamivir 1x75 mg 7 hari s/d 6minggu
Alternatif: Zanamivir
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