PRESENTED BY- GURPREET SINGH – 519 GAURAV KAUSHAL – 520 HIMANSHU NAUTIYAL – 522 IRA SHARMA...

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Transcript of PRESENTED BY- GURPREET SINGH – 519 GAURAV KAUSHAL – 520 HIMANSHU NAUTIYAL – 522 IRA SHARMA...

Page 1: PRESENTED BY-  GURPREET SINGH – 519  GAURAV KAUSHAL – 520  HIMANSHU NAUTIYAL – 522  IRA SHARMA – 523  ISHITA SHARMA – 524  KAMIA THAKUR - 526.
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PRESENTED BY-PRESENTED BY-

GURPREET SINGH – 519GURPREET SINGH – 519 GAURAV KAUSHAL – 520GAURAV KAUSHAL – 520 HIMANSHU NAUTIYAL – 522HIMANSHU NAUTIYAL – 522 IRA SHARMA – 523IRA SHARMA – 523 ISHITA SHARMA – 524ISHITA SHARMA – 524 KAMIA THAKUR - 526KAMIA THAKUR - 526

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MENTOR -MENTOR -Dr. ANJALI MAHAJANDr. ANJALI MAHAJAN

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CONTENTSCONTENTS INTRODUCTIONINTRODUCTION EPIDEMIOLOGYEPIDEMIOLOGY RISK FACTORS FOR SPREADRISK FACTORS FOR SPREAD CURRENT SITUATIONCURRENT SITUATION PANDEMIC ALERTPANDEMIC ALERT PREVENTION & CONTROLPREVENTION & CONTROL BIOSECURITYBIOSECURITY CONCLUSIONCONCLUSION

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Avian InfluenzaAvian Influenza

Infectious disease of birds caused Infectious disease of birds caused by Type A strains.by Type A strains.

First identified in Italy more than First identified in Italy more than 100 years ago, occurs worldwide100 years ago, occurs worldwide

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All birds are susceptibleAll birds are susceptibleMigratory waterfowl – most Migratory waterfowl – most

notably wild ducks are reservoirsnotably wild ducks are reservoirsDomestic poultry including Domestic poultry including

chickens and turkey are chickens and turkey are particularly susceptibleparticularly susceptible

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HISTORY OF BIRD FLUHISTORY OF BIRD FLU

SINCE 1901 AVIAN SINCE 1901 AVIAN INFLUENZA HAS BEEN INFLUENZA HAS BEEN RECOGNISED AS A RECOGNISED AS A HIGHLY LETHAL HIGHLY LETHAL DISEASE IN POULTRY DISEASE IN POULTRY INDUSTRYINDUSTRY

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HISTORY CONTD…..HISTORY CONTD…..

1955:TYPE “A” OF 1955:TYPE “A” OF INFLUENZA VIRUS INFLUENZA VIRUS RECOGNISED AS THE RECOGNISED AS THE CAUSAL AGENT AND CAUSAL AGENT AND TERMED AS “FOWL TERMED AS “FOWL PLAGUE”PLAGUE”

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The Influenza VirusFamily: Orthomyxoviridae

Type AInfect people, birds, pigs, horses, seals, whales, and other animals.wild birds are the natural hosts.

Type B

Found only in humans.

•Type CCause mild illness in humans and do not cause epidemics or pandemics.

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Surface proteins of influenza Surface proteins of influenza A/BA/B

Hemagglutinin (HA)Hemagglutinin (HA)– Rod-shapedRod-shaped– Binds virus to host cell Binds virus to host cell

to initiate infectionto initiate infection– Brings about fusionBrings about fusion– 16 types16 types

Neuraminidase (NA)Neuraminidase (NA)– Mushroom-shapedMushroom-shaped– Prevents viral Prevents viral

aggregation upon aggregation upon releaserelease

– 9 types9 types

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Virus killed by heat - (560C for 3 hrs & 600C for 30mts).

Common disinfectant like formaline, lodine compounds, gluteraldehyde

Survival of Virus

  Temp. Survival term

Contamination manure

Cool 3 months

Water 220C 4 days

00C 30 days

One gram of contaminated manure contain enough viruses to infect 1 million birds.

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Antigenic Drift• Accumulation ofnormal mutationsin RNA

• Minor changes that can make antigens ineffectual

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Hosts • Influenza A viruses have infected many different animals, including ducks, chickens, pigs, whales, horses, and seals. However, Highly pathogenic avian influenza (HPAI) isolates have been obtained primarily from chickens and turkeys.• It is reasonable to assume all avian species are susceptible to infection • Influenza A viruses normally seen in one species sometimes can cross over and cause illness in another species.

Sources of virus • Faeces, respiratory secretions • Highly pathogenic viruses may remain viable for long periods of time in infected faeces, but also in tissues and water .

EPIDEMIOLOGY

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COUNTRY COUNTRY SPECIESSPECIES TYPE TYPE AIAI

DATEDATE

Hong Hong Kong Kong

Peregrine Falcon Peregrine Falcon H5N1H5N1 Mar-03Mar-03

Cambodia Cambodia Wild birds in a zoo Wild birds in a zoo collectioncollection

H5N1H5N1 Feb-04Feb-04

Japan Japan Crows Crows H5N1H5N1 Mar-04Mar-04

Korea Korea MagpiesMagpies H5N1H5N1 Mar-04Mar-04

Thailand Thailand Pigeons, Open-Bill Pigeons, Open-Bill Storks, Little Storks, Little Cormorant, Red-Cormorant, Red-collar Dove, Scaly collar Dove, Scaly Breasted Munia, Breasted Munia, Black DrongoBlack Drongo

H5N1H5N1 Dec-04Dec-04

HOST

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COUNTRY COUNTRY SPECIESSPECIES TYPE AITYPE AI DATEDATE

China China Grey Heron Grey Heron H5N1H5N1 Dec-04Dec-04

China China Bar-headed geese, Bar-headed geese, Great black-headed Great black-headed gulls, Brown-headed gulls, Brown-headed gulls. Ruddy gulls. Ruddy shelducks and Great shelducks and Great cormorantscormorants

H5N1H5N1 Apr-05Apr-05

Mongolia Mongolia Bar-headed geese Bar-headed geese and Whooper swan and Whooper swan

H5H5 Aug-05Aug-05

Russia Russia (Siberia)(Siberia)

Wild birds Wild birds H5N1H5N1 Aug-05Aug-05

HOST

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Transmission Routes

• Certain birds, particularly water birds, act as hosts for influenza viruses by carrying the virus in their intestines and shedding it.

• Infected birds shed virus in saliva, nasal secretions, and feces.

• Susceptible birds can become infected with avian influenza virus when they have contact with contaminated nasal, respiratory, or fecal material from infected birds.

• Fecal-to-oral transmission is the most common mode of spread between birds

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PATHOGENESISPATHOGENESIS Respiratory tract (aerosols upto 3 viruses in Respiratory tract (aerosols upto 3 viruses in

exp. Animals)exp. Animals) Main site – Ciliated cells of Respiratory tractMain site – Ciliated cells of Respiratory tract Cell damaged/shed- laying bare basal cells in Cell damaged/shed- laying bare basal cells in

trachea & bronchitrachea & bronchi Vulnerable to Secondary Bacterial infectionsVulnerable to Secondary Bacterial infections IN SEVERE CASES- Pneumonia-hyperemia, IN SEVERE CASES- Pneumonia-hyperemia,

thickening of alveolar walls, intestinal thickening of alveolar walls, intestinal infiltration with leucocytes, capillary thrombosis infiltration with leucocytes, capillary thrombosis & leucocyte exudation& leucocyte exudationRARELY– Hyalin membrane- occupying alveolar RARELY– Hyalin membrane- occupying alveolar duct and alveoliduct and alveoliLATE STAGES– Infiltration with macrophages LATE STAGES– Infiltration with macrophages which engulf and remove desquamated alveolar which engulf and remove desquamated alveolar cellscellsVERY RARELY- 1957- epidemic- in spleen, liver, VERY RARELY- 1957- epidemic- in spleen, liver, kidney etc.kidney etc.

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Symptoms Bird flu (human Symptoms Bird flu (human infection)infection)

Common symptomsCommon symptoms Persistent fever, Persistent fever, cough, cough, sore throat, sore throat, muscle aches, muscle aches, shortness of breath and shortness of breath and acute respiratory distressacute respiratory distress

Patients can develop Patients can develop viral pneumonia, viral pneumonia, multiple organ failure, especially in the lungs and multiple organ failure, especially in the lungs and

kidneys, andkidneys, and other severe and life-threatening complications in a other severe and life-threatening complications in a

matter of days. matter of days.

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LABORATORY DIAGNOSISLABORATORY DIAGNOSIS

SAMPLESAMPLE– Good results- first 2-3 days, poor later– Good results- first 2-3 days, poor later Virus shed in secretions shortly before onset of illness to Virus shed in secretions shortly before onset of illness to

3-4 days thereafter3-4 days thereafter Throat Garglings in Broth Saline or Buffered Saline Throat Garglings in Broth Saline or Buffered Saline

solutionsolution Immediately or store -4degrees to -70 degreesImmediately or store -4degrees to -70 degrees Treat with antibioticsTreat with antibiotics

1.1. Virus IsolationVirus Isolation– eggs- Amniotic- 11-13 days or monkey – eggs- Amniotic- 11-13 days or monkey kidney cells -- 6 eggs / specimenkidney cells -- 6 eggs / specimen

--35 degrees C X 3 days--35 degrees C X 3 days

2.2. Virus Antigen-Virus Antigen- Rapid by Immunoflourescence Rapid by Immunoflourescence

Virus Antigen on the surface of Nasopharyngeal cells orVirus Antigen on the surface of Nasopharyngeal cells or

Viral RNA by RT-PCRViral RNA by RT-PCR

3.3. SerologySerology– CFT,HA1 tests– CFT,HA1 tests

parallel to see for increase in antibody parallel to see for increase in antibody levelslevels