Respiratory Viral Diseases in poultry

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Respiratory Viral Diseases in poultry:

Respiratory Viral Diseases in poultry Submitted to. Dr.H.C.Chauhan sir, Deptt. Of Microbiology (VLD-511) Submitted by: Prajapati M.D. Roll No. -41 Reg.No.-02-0111-2005

(Bird Flu / Fowl Plague) A threat to Indian Poultry Industry :

(Bird Flu / Fowl Plague) A threat to Indian Poultry Industry Avian influenza-

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Etiology Family Orthomyxoviridae Genus Influenzavirus Types A ► Man, Horse, Pig, Bird B ► Man C ► Man Subtypes 15 HA + 1 9 NA

Viral properties:

Viral properties Viral RNA Heamagglutinin –15 + 1 Neuraminidase - 9

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Inter species Transmission

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Pathogenesis Entry through aerosol/Inhalation Respiratory tract/ Intestinal tract Replication of virus Cell death & inflammatory response to infection

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Types of Avian Influenza Mild form – Low Pathogenic Avian influenza (LPAI) e.g. H9N2 - Variant 2) Sever form (100% Mortality) – Highly pathogenic Avian influenza (HPAI) – Mostly H5 & H7 subtypes. e.g. H5N1

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Out break of RD complicated with AI(H9) and E. Coli in North India Pakistan In Jan., 2002 Tarantaran near border of PAK Dist. Pathankot(pb) in Jan., 2003 Zirakpur town near Chandigarh Entering to Barwala in 10 th March, 2003

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Rajasthan Ajmer – 12,00,000 Uttaranchal Kashipura – 50,000 UP Lucknow – 50,000 80,000 M. Nagar- 20,000

Tracheal Lesions:

Tracheal Lesions

Egg peritonitis:

Egg peritonitis

Proventriculus Lesions:

Proventriculus Lesions



Clinical Signs:

Clinical Signs Incubation period: 3-14 days Birds found dead Drop in egg production Neurological signs Depression, anorexia, ruffled feathers Combs swollen, cyanotic Conjunctivitis and respiratory signs

Post Mortem Lesions:

Post Mortem Lesions Lesions may be absent with sudden death Severe congestion of the musculature Dehydration Subcutaneous edema of head and neck area

Swollen Head-Conjunctivitis:

Swollen Head-Conjunctivitis

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Cyanosis Edema Swelling

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Pin point hemorrhage on Heart Pin point hemorrhage on Trachea

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Pin point hemorrhage on mesentery & Intestine Fibrin clot in the sinus

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Haemorrhages of the intestine

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Diagnosis Virus Isolation Serological tests PCR Field diagnosis Clinical symptoms Laboratory diagnosis Differential diagnosis

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Virus Isolation Cell Culture (Mammalian or avian tissue) Embryonated Egg Inoculation Laboratory Diagnosis

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Heamagglutination tests Heamagglutination Inhibition tests ELISA Serological tests

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Treatment Amantadine & Rimantidine Inhibit viral uncoating by interacting with the M protein (interferes with ion channel function) Active against influenza A only Zanamivir & Oseltamivir A sialic acid analogue that inhibits viral replication - inhibits neuraminidase and is active against both type A and B viruses.

Infectious Laryngotracheitis :

Infectious Laryngotracheitis


Introduction Infectious Laryngotracheitis (ILT) is a viral infection of the respiratory tract (trachea - windpipe) of chickens, pheasants and peafowl. It can spread rapidly among birds and causes high death losses in susceptible poultry. The disease is not known to affect humans. Turkeys, ducks and geese do not get the disease, but can spread the virus.

Etiology of Disease:

Etiology of Disease Herpes virus Double stranded D.N.A virus Affect only Respiratory tract & Conjunctiva Virus doesn’t enter in blood ie no viremia Multiplication of virus is limited to respiratory tract only Disease become serious in presence of ND ,IB,FOWL POX virus, Hemophilus paragallinarum & Mycoplasma gallisepticum infections

Spread of infection:

Spread of infection Infection is spread by air. It enters in body through upper respiratory tract & cojunctiva. Virus is present in discharges from nostrils, mouth, trachea & cojunctiva. Movement of carrier birds, even mildly affected birds are important method of spread. Wild birds, vermin, dogs & cats can transmit the virus to susceptible host. Birds vaccinated with live virus, the virus can become latent & such birds become carrier of infection.


Pathogenesis ILT is caused by a Herpes virus that replicates within infected cells, specifically in the trachea. Incubation period of disease is 6-15 days. The virus kills the cells lining the airways, resulting in variable degrees of Inflammation and breathing difficulties. Birds that recover often develop a carrier state and are potential sources of the virus.

Clinical symptoms:

Clinical symptoms Per acute form Acute form Mild form Asymptomatic form

1.Per acute form:

1.Per acute form Bird may be found dead without showing any symptom Sudden severe respiratory distress with marked coughing & discharge of mucous and blood stained material and blood clots from mouth followed by death in 1-3 days. 2. Acute form Difficult breathing but not as severe as in per acute form Obstruction of trachea with exudate cause the bird to breath long gasp (quick deep breaths) with it’s head and neck upward & weak wide open. Usually accomplish with loud harsh cry. Abnormal respiratory sounds (rales), nasal discharge & conjunctivitis. Birds with severe respiratory distress, cyanosis of face & wattles, death occur with in 3-4 days Up to 100% of flock can be affected with 70% mortality In some birds recovery occur in 2-3 weeks.

Gasping in birds:

Gasping in birds

Post mortem findings:

Post mortem findings P.M findings vary with the severity of disease. Lesions are restricted to upper respiratory tract In per acute form haemorrhagic tracheitis, trachea is inflamed red & contains blood casts.

Prevention & control of disease:

Prevention & control of disease Use of sound biosecurity measures Rodent & dog control measures should also be followed. ILT live vaccine is used in most prevalent areas at 1-3 days age. In other areas at 3-18 weeks of age. Booster at 2-3 weeks interval Method of vaccination eye drop, drinking water, cloacal scarification. Disadvantage of live vaccine is possible spread of virus with in 10 days or a week. Disinfect the area before restocking the birds.

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Infectious Bronchitis (IB)

Introduction :

Introduction Infectious bronchitis is a sudden, rapid, highly contagious respiratory disease of chickens characterized by abnormal respiratory sounds, coughing and sneezing in young chicks. Besides causing disease of the respiratory tract, the virus may also affects kidneys, reproductive tract and muscles In laying birds, it cause great economic loss through reduced egg production, watery albumen, and poor eggshell quality.

Etiology :

Etiology Disease caused by Coronavirus, it’s a SS-RNA virus, there are 20 or more serotypes of the virus. Virus have a natural tendency to undergo genetic mutation, this can lead to new field strains against which present vaccines may not give protection. The best known serotypes include : Massachusetts Connecticut Holland Arkansas-99 JMK, Florida

Spread of the disease :

Spread of the disease By air, it takes just few of the virus particles to infect a bird. Spread by people and virus contaminated substances. Carriers, birds which carry infection without showing symptoms also spread the infection. THE VIRUS HAS NOT SHOWN TO BE EGG-TRANSMITTED The incubation period of IB is 18-36hrs, depending upon dose and route of infection.


Pathogenesis IB virus can replicate in tissues of the respiratory tract, intestinal tract, kidneys, and the oviduct. After replicating in respiratory tract it producing characteristic lesion in trachea. In reproductive tract it mainly affect the oviduct leads to it physiological abnormality and finally reduced egg production .

Symptoms :

Symptoms Respiratory form : Most common form in all ages of birds. Symptoms includes, Abnormal respiratory sounds, Gasping, Sneezing, Watery nasal discharge, Eye discharge (some time only ), Facial swelling. Mortality is slight, but may reach up to 30% in brooding chicks.

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Egg yolk with watery albumin

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Inferior quality egg with watery albumen compared with normal egg

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Shell less egg

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(2) The less common form of the reproductive form is associated with abnormal development of the oviduct following infection of young chicks. The oviduct may fail to develop completely or partially. At maturity affected birds ovulate normally but ova are not taken up by the badly formed oviduct, and are shed into the body cavity. Such birds go through the process of egg laying but fail to lay and are known as “blind layers”

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Nephrosis in broiler

Diagnosis :

Diagnosis Based on : History, Clinical signs, Postmortem examination, Histopathological examination- trachea is edematous, with loss of cilia, rounding and sloughing of epithelial cells, and minor infiltration of heterophills and lymphocytes with in 18 hrs of infection.

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Identification of IB virus by detection of IB RNA by PCR method Serological tests like ELISA, IFT, IDT can also be used VN and HI tests for IBV antibodies generally are considered to be type-specific, although there are cross-reaction between serotypes, especially in HI test.

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Provision of additional heat to eliminate cold stress, Elimination of overcrowding and attempts to maintain feed consumption to prevent weight loss are flock management factors that may help reduces losses from IB.

Control :

Control Because of mutating virus it is difficult to have appropriate vaccine strain. In developed countries region wise preveling IB strain are recognized and appropriate vaccine strains are suggested, which is not practiced in India. The Massachusetts serotypes of virus is the one most commonly included in commercial vaccines. In India only Massachusetts strain are available, which can take care of Respiratory & Reproductive form of disease.

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Repeated vaccination with repeated vaccine strain can cover the larger area. Both live and killed vaccine are available, live vaccine may be administered to day-old chicks. Schedule : Commercial broiler : Day old by dipping Booster on 14 th day by D/W, occulonasal, spray nasal.

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Commercial layer : Day old beak dipping, which is done with half dose . 4 th week occulonasal or D/W Boostering in D/W at 14 th weeks of age, Usually IB vaccine is done before laying starts and during lay it is avoided Parent stock : IB inactivated vaccine for parent stock in growing period as per commercial layers with IB killed vaccine. Broilers should be vaccinated only where the disease is a real problem, otherwise IB vaccination may cause greater flock morbidity (sickness) than the disease itself.




Synonyms Ranikhet disease Avian distemper Avian pneumo-encephalitis


Definition It is a sudden and severe, rapidly spreading disease of poultry The disease is characterized by rapid onset, respiratory symptoms, also nervous manifestations, and varying mortality. It is world wide in distribution. In India , it is most dreaded viral disease of poultry.


Etiology ` Order - Mononegavirales Family - Paramyxoviridae Subfamily - Paramyxovirinae Genus - Avulavirus Species – Avian paramyxovirus type -1 (PMV-1 To PMV-9)

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REPLICATION OF NDV Attachment Penetration Uncoating Biosynthesis of nucleic acid and proteins Assembly Release

ND viruses – Five Pathotypes :

ND viruses – Five Pathotypes Viscerotropic velogenic viruses. Highly powerful disease producing RDV. Causes most severe form of disease. Hemorrhagic changes are present in the intestine. Neurotropic velogenic viruses. Highly powerful disease producing RDV. Causes high mortality. Respiratory and nervous symptoms.

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Mesogenic viruses Moderately powerful disease producing RDV. Causes respiratory and sometimes nervous symptoms. Low mortality. Lentogenic respiratory viruses Mild or not clearly noticeable respiratory infection. Asymptomatic enteric viruses Causes intestinal infection. Without showing any symptoms .

Pathogenesis :

Pathogenesis Virulence of NDV strain varies greatly with the host. Chickens are highly susceptible. Ducks & geese may be infected and show few or no clinical signs. Chicken – pathogenicity depends on strain of virus, dose, route, age and environmental condition. Younger chicken, more acute disease with sudden death. Older bird-disease last longer with characteristic signs.

Transmission :

Transmission RDV spreads easily. The disease is highly contagious. Method Spread through the air (air born spread). Movement of people and equipment. Contaminated poultry feed. Contaminated water. Contaminated vaccine. Movement of poultry products. Movement of live birds – wild birds, pet birds, game bird, racing pigeons and commercial poultry. Movement of other animals.

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Clinical signs Depending upon pathotype the symptoms may vary considerable The factors influencing the symptoms are species of the bird, immune status, age management practices.

1. Viscerotropic velogenic ND (Doyle’s or Asiatic form) 2. Neurotropic velogenic ND :

1. Viscerotropic velogenic ND (Doyle’s or Asiatic form) 2. Neurotropic velogenic ND - 1 st indication is sudden death. - Depression, weakness and lying down. - Increased respiration and Diarrhoea. - Swelling of face and nervous signs . - Ending in exhaustion and death.

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Survived birds show green diarrhoea. Muscular tremors , Torticollis. Paralysis of legs and wings. Arched back position of body (opisthotonus). Mortality reaches 100% flock of fully susceptible chicks. Decreased egg production Shell-less or soft shelled eggs, followed by complete stoppage of egg laying in layer.

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Severe respiratory disease. Mortality up to 50% or more. Layer, marked drop in egg production- several weeks. Nervous symptoms may occur but are not common. Mortality is usually low, except in very young birds. 3.Mesogenic ND

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No disease or mild respiratory distress. With other organism or poor management may cause disease. Loss of weight gain in broiler. Young bird with severe respiratory problem causes mortality. Lentogenic respiratory and Asymptomatic enteric ND

Broiler flock showing high morbidity & mortality.:

Broiler flock showing high morbidity & mortality. Torticollis in an immature chicken infected with velogenic ND.

Typical posture of the bird during respiration, with tracheal rales.:

Typical posture of the bird during respiration, with tracheal rales. Acute outbreak in a broiler farm–heavy mortality, nervous convulsions, paralysis & death were noticed.

VVND - Edema and hemorrhage in the reflected lower eyelid. :

VVND - Edema and hemorrhage in the reflected lower eyelid. Edematous swellings of the head. Conjunctivitis.

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Bird unable to stand. Bird with twisted neck and unable to stand. Neurotropic form of ND

Gross lesions :

Gross lesions Inflammation of trachea with hemorrhages. Air sacs are inflammed, cloudy and congested. Hemorrhages in proventriculus is not a constant feature. Necrotic button ulcers in the intestine are frequently seen. Caeca with necrotic material exhibiting foul odour. Ovaries flaccid, peritonitis and watery yolk material in abdominal cavity.

VVND - Petechiae in the mucosa of the proventriculus. :

VVND - Petechiae in the mucosa of the proventriculus.

Hemorrhagic mucosa of proventriculitis - velogenic ND.:

Hemorrhagic mucosa of proventriculitis - velogenic ND.

VVND - Necrosis of a lymphoid area in lower small intestine. :

VVND - Necrosis of a lymphoid area in lower small intestine.

VVND - Necrosis of the cecal tonsils. :

VVND - Necrosis of the cecal tonsils.

Severe hemorrhagic enteritis-velogenic ND.:

Severe hemorrhagic enteritis-velogenic ND. Tracheitis Visceral hemorrhages associated with velogenic viscerotropic ND.

Inflammation of trachea with hemorrhages.:

Inflammation of trachea with hemorrhages. Necrotic ulcer visible from serosal surface.

Continuous long line formed by necrotic ulcers. :

Continuous long line formed by necrotic ulcers. Large size button ulcers in the intestine. Large size button ulcers visible from serosal surface.

Peritonitis & flaccid ova with creamy watery yolk material. :

Peritonitis & flaccid ova with creamy watery yolk material. Hemorrhages in the papillae of proventriculus.

Histopathology :

Histopathology It is of little value in diagnosis. Trachea – inflammation, cellular infiltration and hemorrhages are seen. Lung – proliferation and exudation. Lymphocytic infiltration in the air sac membrane, lung and trachea may be seen in milder form. Spleen – hypoplasia of lymphoid cells. Intestine – catarrhal enteritis with infiltration of mononuclear cells in the mucosa and submucosa with necrosis. Mucous membrane and lamina propria is infiltrated with mononuclear cells and congestion.

Spleen hypoplasia of lymphoid cells. :

Spleen hypoplasia of lymphoid cells. Intestine catarrhal enteritis with infiltration of mononuclear cells in the mucosa & sub mucosa with necrosis.

Intestine – mucous membrane & lamina propria is infiltrated with mononuclear cells with congestion. :

Intestine – mucous membrane & lamina propria is infiltrated with mononuclear cells with congestion.

Diagnosis :

Diagnosis Clinical signs & P.M. lesion. Isolation of virus and its characterization. Sample from live bird – faeces and tracheal swabs. Sample from dead bird - Spleen, Trachea, intestine, intestinal contents. Serological test- HI and ELISA. Value of serological test depends on immune status. HI used for measuring the immune status.

Control :

Control The basic objective of control To prevent susceptible bird from getting infected. To protect through vaccination.


Vaccination Commercially available vaccines. Live least harmful vaccines (live lentogenic). Moderate powerful vaccines (live mesogenic). Killed (inactivated) vaccines.

Live least harmful vaccines (live lentogenic).:

Live least harmful vaccines (live lentogenic). Derived from field viruses which have low disease producing power, but produce adequate immunity. Strains are LaSota, Hitchner B 1, F 1 strain LaSota and B 1 – most widely used. LaSota usually not used for 1 st vaccination, but booster after one or more B 1 or F strain vaccines. After LaSota based vaccine – mild spread bird to bird spread. Vaccine given by eye drop, in drinking water, or by machine producing sprays.

Moderate powerful vaccines (live mesogenic):

Moderate powerful vaccines (live mesogenic) Mukteswar (R 2 B), Roakin, Komarow, Hartfordshire (H) are prepared in Lab. From virulent strain. Vaccine given by drinking water or by intradermal inj. It causing severe disease & must only be given after primary vaccination with least harmful viruses. Capable of producing high secondary immune response.

Killed (inactivated) vaccines:

Killed (inactivated) vaccines Prepared from virus grown on egg, which is killed by treatment with formalin. Both virulent & avirulent viruses used in vaccine. Vaccine given by intramuscular or subcutaneous inj. Expensive than live vaccines.

Maternal immunity :

Maternal immunity It prevent effectiveness of primary vaccination. To avoid this problem, Bird are either not given primary vaccination until they are of 3-4 wks of age, vaccinated with live virus at one day old by eye drop or coarse spray. R2B vaccine used only in replacement pullet & breeder in basal immunity developed by lentogenic strain.

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