Avian Encephalomyelitis Epidemic tremor Etiology Avian encephalomyelitis virus

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Avian Encephalomyelitis (Epidemic tremor)

Avian Encephalomyelitis (Epidemic tremor)

Etiology • Avian encephalomyelitis virus (AEV), Enterovirus, Picornaviridae Isolates are close serolojical There are

Etiology • Avian encephalomyelitis virus (AEV), Enterovirus, Picornaviridae Isolates are close serolojical There are 2 pathotype 1 - Field strains, enterotropic 2 - Embryo adapte strains, neurotrophic

Epidemiology • • Chicken, turkey and ducks are sensitive to disease There is a

Epidemiology • • Chicken, turkey and ducks are sensitive to disease There is a vertical infection Transmission is also shaped in the horizontal The incubation period is at least 11 days in vertical transmission at 1 -7 horizontal infections

Clinical and macroscopic findings • Depression in young people, ataxia and tremor • Decrease

Clinical and macroscopic findings • Depression in young people, ataxia and tremor • Decrease in egg production in laying hens Decrease in incubation yield in studs • Lenste single and / or double-sided opacity • Neurological manifestations occur within 1 week after the incubation • The disease is usually seen at the age of 5 -6 weeks, although it has been reported in older people

 • Morbitidy is up to 60%, mortality is 15% in affected poultry •

• Morbitidy is up to 60%, mortality is 15% in affected poultry • Clinical manifestations in turkey are more severe 5 -10% decrease in egg yield reaches normal level after 2 -3 weeks • About 5% reduction in incubation yield • Weekly death in animals with egg yield increased by 0. 2 -1% • Macroscopic finding is usually absent

Diagnosis • ND, MD, and nutritional encephalomalacies Clinical manifestations are not enough to diagnose

Diagnosis • ND, MD, and nutritional encephalomalacies Clinical manifestations are not enough to diagnose the disease. • Histopathological examinations made from affected organs help diagnosis • Virus isolation; ETY 5 -6 days inoculation in the egg yolk • VN, ELISA, FAT

Control • Vaccines; alive and inactive

Control • Vaccines; alive and inactive

Infectious Bursal Disease ( IBD, Gumboro)

Infectious Bursal Disease ( IBD, Gumboro)

 • Infectious bursal disease • Common in all over the world • Subclinically

• Infectious bursal disease • Common in all over the world • Subclinically immunosuppressive characterized by clinical depression and death, • Infectious disease causing significant economic loss

Etiology • The disease contains an influenza virus, double-stranded RNA. The virus is divided

Etiology • The disease contains an influenza virus, double-stranded RNA. The virus is divided into two serotypes • Serotype 1 • Serotype 2

 • Serotype 1 Antigenic and pathogenic variants exist Precursor B is interested in

• Serotype 1 Antigenic and pathogenic variants exist Precursor B is interested in lymphocytes Bursa Fabriciusa has affinity and limits the function of this organ • Serotype 2 Does not cause disease in chickens

 • • • Economic evaluation of the disease High mortality Decline in growth

• • • Economic evaluation of the disease High mortality Decline in growth rate Decrease in utilization rate of feed Sensitivity to secondary infection secondary to immunosuppression Bacterial infections Viral infections Parasitic infections Increase in destruction rate at the slaughterhouse

Epidemiology • • • Chicken, turkey and duck are susceptible to disease It is

Epidemiology • • • Chicken, turkey and duck are susceptible to disease It is a very contagious disease Infectious transmission Mouth (most common) Conjunctiva Respiratory The disease can be transmitted both directly and indirectly Indirectly infected equipment, clothing, dust and pads Black beetles, rodents, mosquito are bearer

 • No vertical transmission • In patients virus out 10 -14 days with

• No vertical transmission • In patients virus out 10 -14 days with the stools • Virus is highly resistant to environmental conditions • Leghorns are more susceptible to disease than other races • Hot weather and high humidity ıncrease death • Men are more sensitive than females • Formaldehyde and iodophores are highly effective

Resistivity • High temperature resistance (30 minutes at 60°C) • Resistant to p. H

Resistivity • High temperature resistance (30 minutes at 60°C) • Resistant to p. H changes • Resistant to some of the commercial disinfectants (such as phenol) • 100 days in contaminating poultry • Protect 60 days of life in infected feed and stool

Patogenesis • Necrosis in lymphoid cells, Bursa Fabricius, spleen and sacral tonsils • T-cells

Patogenesis • Necrosis in lymphoid cells, Bursa Fabricius, spleen and sacral tonsils • T-cells are not affected by virus • Within 4 -5 hours following the entry of the causative agent into the body by the oral route, the cells in the lymphoid cells in the septum, duodenum, jejunum and liver and • Viruses are detected in macrophages. • During the stage of viremia, the agent spreads to other lymphoid tissues, especially Bursa Fabricius. after virus infection, remains 9 -10 days in Bursa Fabricius

Clinical Symptoms • Factors affecting severity of clinical findings: Age Race Maternal antibody level

Clinical Symptoms • Factors affecting severity of clinical findings: Age Race Maternal antibody level Virus virulence

 • The disease is in two different forms; Acute form Subclinical form

• The disease is in two different forms; Acute form Subclinical form

 • Acute form Usually 3 -6 week old animals Incubation period 2 -3

• Acute form Usually 3 -6 week old animals Incubation period 2 -3 days Depression, white colored watery diarrhea, contaminated cloaca Decrease in feed consumption, increase in water consumption Discomfort in the fur, slow motion Shivering and lying on the side Close your eyes, death Morbitide is 10 -100%, mortality is usually 1 -20%, rarely 50% The course of the disease is short (5 -7 days) Mortality is highest in 3 -5 days

 • Subclinical form It forms early (up to 3 weeks) No specific clinical

• Subclinical form It forms early (up to 3 weeks) No specific clinical signs Regression to development Immunosuppression Increased sensitivity to viral and bacterial infections

Lezyonlar • Dehidrasyon, bacak ve göğüs kaslarında kanama Ender olarak ön mide mukozasında kanama

Lezyonlar • Dehidrasyon, bacak ve göğüs kaslarında kanama Ender olarak ön mide mukozasında kanama Bağırsaklarda artmış mukus, Karaciğerde ve dalakta büyüme Bursada önce büyüme, yangı, ödem, renk değişikliği İnfeksiyonun 3 -8’inci günlerde bursada atrofi Bursadaki büyüme klinik belirtilerin başlangıcının göstergesi Çok virulent suşların neden olduğu infeksiyonlarda, bursanın etrafında jelatinöz bir sıvı birikimi Böbreklerde nefrozis, solgunluk ve şişkinlik

Diagnosis • Acute form Anamnesis Clinical symptoms It is defined by necropsy

Diagnosis • Acute form Anamnesis Clinical symptoms It is defined by necropsy

 • Subclinical form Diagnosis is difficult due to lack of clinical findings This

• Subclinical form Diagnosis is difficult due to lack of clinical findings This is why laboratory examinations are used

Diagnosis • • Display of virus in tissues (IFT, IPT) Virus isolation (Cell culture,

Diagnosis • • Display of virus in tissues (IFT, IPT) Virus isolation (Cell culture, EY, DH) Serological tests (ELISA, AGID, VNT) Molecular techniques (PCR, RT / PCR / RE)

 • Miscible with many diseases coccidiosis ND HS Vitamin A deficiency

• Miscible with many diseases coccidiosis ND HS Vitamin A deficiency

Protection and Control • General protection Disinfection Good care-feeding Stress factors to be removed

Protection and Control • General protection Disinfection Good care-feeding Stress factors to be removed Correction of poultry conditions Implementation of training programs • Special protection Vaccinations