Download pdf - Infectious Diseaseemergency

7/30/2019 Infectious Diseaseemergency

1/136

INFECTIOUS DISEASES

EMERGENCY

dr. Andi Sulistyo Haribowo, SpPD


2/136

Diphtheria


3/136

Gram +ve Bacilli and Colonies


4/136


5/136

Case-fatality rate


6/136

Selected RecentDiphtheria

Outbreaks in Great

Britain


7/136

The Scandinavian Outbreak


8/136

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


9/136

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.)


10/136


11/136

Diphtheria Epidemiology

Reservoir Human carriersUsually asymptomatic

Transmission Respiratory

Skin and fomites rarely

Temporal pattern Winter and spring

Communicability Up to several weekswithout antibiotics


12/136

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


13/136

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


14/136

Thick Membrane


15/136

Pseudo membrane


16/136

Bull Neck


17/136

Skin Lesions


18/136

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


19/136

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.

19


20/136

Laboratory findings

Bacteriological examinations

Smear and gram stain can found C. diphtheriae,

but can not identify from the diphtheroids.

20


21/136

Laboratory findings


Fluorescent antibody-stain can found toxigenic C.

diphtheriae, favourable for early diagnosis, but

definitive diagnosis (false positive).

21


22/136

Laboratory findings


C. diphtheriae can be cultured from the swabs

from nose, pharynx or other sites.

22


23/136

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.

23


24/136

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.

24


25/136

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.

25


26/136

Complications

Neuritis

Most neuritisoften affect motor nerves andusually recovers completely.

Paralysis of the soft palate is most frequent

during the third week of illness.

26


27/136

Complications

Neuritis

Eye muscles, limbs, and diaphragm paralysis can

occur after the fifth week.

Secondary pneumonia and respiratory failuremay result from diaphragmatic paralysis.

27


28/136

Complications

Other complications Include otitis media and respiratory insufficiency

due to airway obstruction, especially in infants.

28


29/136

Diagnosis

Clinical diagnosis is usually made based on the

epidemiological data and clinical presentation since

it is imperative to begin presumptive therapy

quickly.

29


30/136

Diagnosis

Gram stain of material from the pseudomembrane

can be helpful when trying to confirm the clinical

diagnosis.

30


31/136

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.

31


32/136

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.

32


33/136

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 (


34/136

Differential diagnosis

Dyspnea

Acute laryngitis; foreign body in trachea;

laryngeal edema Pseudomembrane

Streptococcal pharyngitis

Oral candidiasis

Infectious mononucleosis

Vincents angina

34


35/136


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.

35


36/136


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

36


37/136


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.

37


38/136

Prognosis

The overall case-fatality rate for diphtheria is about

5%, with higher death rates (up to 20%) in persons

40 years of age.

38


39/136

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.

39


40/136

Treatments

General measures

Relax on bed for more than 3 weeks, 4-6 weeks

for patients with myocarditis.

Provide adequate energy and nutriments

40


41/136

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.

41


42/136

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.

42


43/136

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)

43


44/136

Treatments

Antibiotics

Prevention of further toxin production.

Control local infection.

Reduction of transmission.

44


45/136

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.

45


46/136

Treatments

Antibiotics

The disease is usually not contagious 48 hours

after antibiotics are used.

46


47/136

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.

47


48/136

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.

48


49/136

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

49


50/136

Preventions

Management of infection sources Contacts should also receive antibiotics

benzathine penicillin G or a 7- to 10-day course

of oral erythromycin.

50


51/136

Preventions

Interruption of the transmission routes by

disinfections of discharges and articles of patients

51


52/136

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.

52


53/136

Summary of the definition

Acute, communicable, toxin-mediated, sometime

life-threatening bacterial disease

Preventable with widespread immunization

53


54/136

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.

54


55/136

55


56/136

Diphtheria Antitoxin (DAT)

Produced in horses

First used in the U.S. in 1891

Used only for treatment of diphtheria

Neutralizes only unbound toxin


57/136

Tetanus


58/136

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


59/136

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


60/136

Pathophysiology

Wound contamination with Clostridiumtetani

Motile, nonencapsulated, anaerobic, grampositive rod

Spore forming and ubiquitous in soil andanimal feces


61/136

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


62/136

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


63/136

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)


64/136

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


65/136

Four Clinical Forms

Local

Generalized

Cephalic

Neonatal


66/136

Local Tetanus

Rigidity of the muscles in proximity to thesite of injury

Usually resolves completely in weeks tomonths

May develop into generalized


67/136

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


68/136

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


69/136

Trismus and Sardonic Smile


70/136

Opisthotonos


71/136

Generalized Tetanus

Autonomic nervous system

Hypersympathetic state

Usually in the second week

Tachycardia

HTN

Diaphoresis

Increased urinary catecholamines

Significant morbidity and mortality


72/136

Cephalic Tetanus

Results from an injury to the head or otitismedia

Cranial nerves affected most commonlythe seventh

Poor prognosis


73/136

Neonatal Tetanus

400,000 worldwide deaths annually

Results from inadequately immunizedmothers

Frequent after unsterile treatment of thecord stump


74/136

Neonatal Tetanus

Signs

Weakness

Irritability

Inability to suck

Presents in the 2nd week of life


75/136

Diagnosis

Clinical diagnosis

No laboratory confirmatory tests

Wound cultures not very useful as C. tetanimaybe recovered without tetanus

Immunization history usually unknown orinadequate


76/136

Tetanus Ddx

Strychnine poisoning

Dystonic reaction

Hypocalcemic tetany

Peritonsillar abscess

Peritonitis

Meningeal irritation

Rabies

TMJ


77/136

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


78/136

Treatment

Tetanus Immunoglobulin (TIG)

Neutralizes wound and circulatingtetanospasmin

Does not neutralize toxin already bound to thenervous system

Does not improve clinical symptoms

Decreases mortality


79/136

Treatment

TIG

Usual dose is 3,000 to 6,000 units

Administered IM opposite side as Td given

Give before wound debridement

T


80/136

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


81/136

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


82/136

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


83/136

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


84/136

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


85/136

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


86/136

Rabies

R bi


87/136

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


88/136

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


89/136

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


90/136

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


91/136

Negri bodies

Epidemiology


92/136

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


93/136

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


94/136

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


95/136

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


96/136

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


97/136

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


98/136

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


99/136


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


100/136

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


101/136

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


102/136

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


103/136

Captured and quarantined Escaped

Vaccine + HRIGSacrifice and testInitiate vaccine +HRIG

Rabid

Vaccine +HRIG

Not Rabid

Discontinue vaccine

Dog or cat


104/136

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



105/136


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



106/136


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


107/136


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



108/136


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



109/136


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



110/136


Pregnancy No adverse effects of the vaccine or HRIG

Follow usual course in pregnancy if indicated



111/136


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


112/136

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


113/136

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


114/136

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


115/136

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


116/136

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


117/136

Treatment

Limited No specific treatment exists for clinical course

Treatment directed at the clinical

complications


118/136

AVIAN INFLUENZA

AVIAN INFLUENZA


119/136

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


120/136

ILUSTRASI SEL VIRUS AI

AVIAN INFLUENZA


121/136

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


122/136

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


123/136

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


124/136

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


125/136

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


126/136

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


127/136

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


128/136

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


129/136

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


130/136

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


131/136

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


132/136

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


133/136

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


134/136

Supportif: Bed rest, imunomodulasi Antiviral

Antibiotik

Respiratory care

Antiinflamasi

ANTIVIRAL


135/136

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


136/136