Non-respiratory viral diseases in poultry

Question 1

Infectious bursal disease (IBD) is also called

Answer 1

Gumboro disease, is an acute contagious birnavirosis of chickens, characterized by atrophy of the bursa of Fabricius, nephrosis
and haematomas of the muscles.

Notifiable dz!

Question 2

Infectious bursal disease (IBD), also called Gumboro disease, is an acute contagious birnavirosis of chickens, characterized by

Answer 2

atrophy of the bursa of Fabricius, nephrosis
and haematomas of the muscles.

Notifiable dz!

Question 3

IBDV causative agent
genus, family, DNA type

Answer 3

Infectious Bursal Disease Virus (IBDV)

Genus Avibirnavirus,
family Birnaviridae

Nonenveloped double-stranded RNA virus

Notifiable dz!

Question 4

serotypes of IBDV

Answer 4

Infectious Bursal Disease Virus (IBDV)

2 serotypes:
Serotype 1 - clinical disease of chickens, at least six subtypes.

Question 5

Survival of IBDV in the environment.

Answer 5

Infectious Bursal Disease Virus (IBDV)

Very durable in the environment.

Inactivates in a strongly alkaline environment.

Question 6

Host range and age of IBDV.

Answer 6

Infectious Bursal Disease Virus (IBDV)

NOT zoonotic

Chickens of all ages are susceptible.
◦ 3-6 weeks old chicks are especially susceptible
◦ Adult birds are sub-clinically affected.

Question 7

Transmission of IBDV.

Answer 7

Infectious Bursal Disease Virus (IBDV)

Excretion: faeces
◦ Sick and recovered birds spread the pathogen, spread is fast.

Infection route in: alimentary

Question 8

Morbidity & mortality of IBDV.

Answer 8

Morbidity up to 100%, mortality up to 100%.

 Incubation period: 2 – 6 days
 IBDV is immunosuppressive

Question 9

Clinical signs of IBD.

Answer 9

Infectious Bursal Disease Virus (IBDV)

Acute course:
◦ Drowsiness, depression, not drinking or eating.
◦ Muscle tremors, nervous symptoms
◦ Slimy to bloody diarrhoea
◦ Ruffled feathers
◦ Itching of the cloacal area
◦ Enlarged bursa of Fabricius (palpation)

The course may be extremely acute and fatal without the clinical signs developing.

In the case of subacute disease, the clinical signs are not so well developed.

Question 10

Post mortem signs of IBD.

Answer 10

Infectious Bursal Disease Virus (IBDV)

 Dry skeletal muscles, cachexia of the carcass.

 Haematomas in myocardium and skeletal muscles.

 Enlarged, pale liver and kidneys

 Inflammation of the intestinal tract and lining of the gut.

 The bursa is 1.5-2 times larger, swollen, covered with bruises.

In recovered chicks, the involution of the bursa starts prematurely.

Histologically: destruction of the structure of the follicles in bursa.
 Glandular and interstitial tissue, atrophy

Question 11

Diagnosis, treatment and prevention of IBD.

Answer 11

Epidemiological situation, clinical signs and
pathological changes, results of virological and serological studies.

Diagnostic material and analyses:
◦ Cloacal bursa, spleen, liver and kidneys
◦ VNR and ELISA are used for virus identification and serodiagnostics

No treatment: culling

Prevention: biosecurity
◦ Avoid bringing sick or carrier birds in

Vaccination: live vaccine, can cause disease.
◦ Influenced by disease, other infections, maternal antibodies.

Question 12

Avian leukosis is a chronic retrovirosis characterized by

Answer 12

tumors formed in different organs and tissues by proliferation of hematopoietic cells.

Question 13

Causative agent of avian leukosis.
genus, family, DNA type

Answer 13

genus Alpharetrovirus
Family Retroviridae

Enveloped spherical single-stranded RNA virus.

Sensitive to high temperature, drying and formaldehyde, well maintained at low temps.

Question 14

Avian leukosis surface glycoproteins.

Answer 14

Subgroups: A, B, C, D, J

Endogenous subgroups: E, F, G, H, I → E in chickens, other subgroups not.

Question 15

Excretion of avian leukosis virus:

Answer 15

feces and eggs, nasal secretions

Question 16

Transmission of avian leukosis virus.

Answer 16

Vertically Inside the egg (immunologic tolerance),
and respiratory (direct, indirect)

Question 17

Target age demo for avian leukosis.

Answer 17

More often in 6-12-month-old chickens.

◦ Also turkeys, pheasants, quails and many other bird species.

Question 18

Forms of disease in avian leukosis.

Answer 18

Forms: according to the cellular composition involved.

◦ Lympholeukosis – persistent lymphocytosis and erythropenia, most common.

◦ Erythroblastosis – increased number of young erythrocytes.

◦ Myeloblastosis – increase in myeloblasts (immature WBC) in the blood, anaemia and leukemia.

◦ Other tumors

Question 19

Most common form of disease in avian leukosis.

Answer 19

Lympholeukosis – persistent lymphocytosis and erythropenia, most common.

(other forms include: tumors, erythroblastosis and myeloblastosis (immature WBCs))

Question 20

Clinical signs of avian leukosis.

Answer 20

Non-specific symptoms:
◦ Drowsiness, weakness
◦ Anaemia
◦ Diarrhoea, dehydration
◦ Loss of appetite, weight loss, cachexia
◦ Drop in egg production
◦ Enlarged cloacal bursa, liver

Increased abdominal organs or fluctuation may be found during palpation of the abdomen.

Question 21

Incubation period of avian leukosis.

Answer 21

Incubation may last for months

Question 22

Course of disease in avian leukosis.

Answer 22

chronic

Question 23

Post mortem signs of avian leukosis.

Answer 23

Tumors in the liver, spleen, oviduct, kidneys, pancreas, lungs, thymus.

◦ Tumorous tissue is fat-like, whitish
◦ Erythroblastosis: anaemic skin and muscles,
enlargement and hyperemia of spleen and kidneys.

 Damage to bursa of Fabricius
 Histologically: proliferation of low-differentiated young forms of cells.

Question 24

Sample material for diagnosis of avian leukosis?
Tests?

Answer 24

Sample material: blood, tumours, faeces

Identification: CLoFAL test, histological examination, virus neutralization, immunofluorescence test

◦ Antibodies: ELISA

Question 25

Tx and prevention of avian leukosis?

Answer 25

No effective treatment – eradication (cull). Prevention: biosecurity rules ◦ Buying chickens from ALV free flocks ◦ Breeding of resistant bird crosses/breeds ◦ No effective vaccine!

Question 26

AIE

Answer 26

Avian infectious encephalomyelitis

Question 27

Avian infectious encephalomyelitis is a contagious and acute avian picornavirosis characterized by

Answer 27

different nervous symptoms. Not a zoonotic disease!

Question 28

Causative agent of AIE. genus, family, DNA type

Answer 28

Avian infectious encephalomyelitis (AIE) Avian EncephalomyelitisVirus (AEV) genus Tremovirus Family Picornaviridae Non-enveloped single-stranded RNA virus. Very resistant in the environment.

Question 29

Describe Natural viral strains of AIE virus versus Embryo-adapted strains.

Answer 29

Natural viral strains: enterotropic, relatively low pathogenicity. Embryo-adapted strains: generally apathogenic.

Question 30

Host range and age demographic for avian infectious encephalomyelitis.

Answer 30

Present all over the world. Susceptible species: chickens, pheasants, quails, turkeys. 1-2 weeks old chicks are particularly sensitive Older birds (over 6 wks of age) have a light or latent form.

Question 31

Transmission of AIE.

Answer 31

Excretion: faeces Source of infection: sick and carrier birds. Transmission: transovarial, aerogenic and alimentary (feed, water, bedding, inventory).

Question 32

Morbidity & mortality of AIE.

Answer 32

Morbidity 40-60%, mortality 25-50%

Question 33

Clinical signs of AIE.

Answer 33

◦ Drowsiness, anorexia, depression, cataracts can occur ◦ Lack of movement, staggering, sitting on hocks with Later: paresis, instability, ataxia, paralysis, head and neck tremors. ◦ Decrease in egg production in adult chickens by 10-20%. ◦ Increased late embryonic death during the viremic period. Most serious outbreaks: first exposure after reaching maturity. ◦ Allows the virus to spread vertically ◦ Tremors in 7-14-day-old chicks

Question 34

Incubation period of AIE.

Answer 34

Incubation period: 1-7 days or min. 10 days

Question 35

Post mortem signs of AIE.

Answer 35

Pathological findings: unspecific ◦ Neurodegeneration of brain tissue ◦ Perivascular infiltration ◦ Gliosis (a fibrous proliferation of glial cells in injured areas of the CNS)

Question 36

Diagnosis of AIE.

Answer 36

Diagnosis: epidemiology, clinical signs, necropsy findings. Laboratory: ◦ Samples: brain tissue, blood ◦ Virus isolation: inoculation ◦ Virus identification: immunofluorescence test ◦ Antibodies: ELISA

Question 37

Treatment of AIE.

Answer 37

Not treated! but there is a vax

Question 38

Prevention of AIE.

Answer 38

vaccination, live vaccine ◦ With drinking water when aged 10-16 weeks. ◦ Chicks get immunity before hatching ◦ The antibodies obtained from the egg protect the chick for the first 4-6 (6-8) weeks after hatching.

Question 39

EDS-76 is

Answer 39

Egg drop syndrome 1976

Question 40

Egg drop syndrome 1976 is an acute to chronic adenovirosis of birds characterized by

Answer 40

a sharp decrease in egg production, deformation of eggs, soft-shelled and/or shell-less eggs.

Question 41

Causative agent of Egg drop syndrome 1976. genus, family, DNA type

Answer 41

Duck atadenovirus 1 (DAdV-1) genus Atadenovirus Family Adenoviridae Non-enveloped double-stranded DNA virus. ◦ Stable in pH 3-10 ◦ Chickens, quails, turkeys, wild birds ◦ A- and C-antigen: antibody formation

Question 42

Genotypes of EDS-76.

Answer 42

Egg drop syndrome 1976 Three genotypes: classic strain, duck EDS virus England strain, Australian strain. ◦ A- and C-antigen: antibody formation

Question 43

Prevalence and host range of EDS-76.

Answer 43

Egg drop syndrome 1976  Spread all over the world. ◦ Chickens, quails, turkeys, wild birds  Natural reservoirs: geese and ducks

Question 44

Epidemiology and course of dz in EDS-76.

Answer 44

Under natural conditions, all birds get the disease. ◦ Usually at the peak of the laying period (25-35 weeks) ◦ The course is often subclinical → birds become immune. ◦ Stressors → virus reactivation

Question 45

EDS-76 localizes in what tissues?

Answer 45

Localized in the oviduct, upper respiratory mucosa, secretions, leukocytes.

Question 46

EDS-76 transmission

Answer 46

Excretion: faeces, cloacal and nasal secretion. Infection via: faecal-oral, contaminated vaccines, alimentary, vertical.

Question 47

Clinical signs of EDS-76.

Answer 47

 Depigmentation, softening, and thinning of the eggshell.  Sharp drop in egg production  Cloudy and very liquid/watery albumin (egg white)  Decreased fertilization rate and hatchability As a rule, there are no other clinical signs. In some cases/exceptions to the rule: ◦ Diarrhoea, loss of appetite, reluctance in movement, ruffled feathers ◦ As the disease evolves, the comb and wattles may become cyanotic ◦ Respiratory disease in chicks (ducks, geese)

Question 48

Post mortem signs of EDS-76.

Answer 48

Not fatal; changes either missing or not characteristic. ◦ Inactive ovary ◦ Atrophy of the oviduct, the wall is swollen and infiltrated with lymphocytes. ◦ White exudate in the uterus ◦ Mild to moderate spleen enlargement ◦ Egg yolk peritonitis (material in the coelomic cavity)

Question 49

Diagnosis of EDS-76.

Answer 49

Epidemiological situation, clinical signs, pathological changes. Laboratory: ◦ Fresh carcasses or live birds, faeces, blood ◦ Viral isolation ◦ Antigen: ELISA, PCR ◦ Antibody: ELISA, HI, IFA ◦ Immunological monitoring: 160-180 days old birds, serum

Question 50

Prevention of EDS-76.

Answer 50

No effective treatment. ◦ Sick birds are separated and culled ◦ In the event of wide spread dz, the entire flock in culled. Recovered birds become immune to recurrent infection. Prevention: biosecurity ◦ Quarantine and testing the new birds ◦ When necessary, vaccination of 14-18 weeks old birds with inactivated vaccine.

Question 51

CIA

Answer 51

Chicken infectious anaemia

Question 52

Chicken infectious anaemia is chronic circovirosis of chickens, characterized by

Answer 52

anemia, atrophy of the lymphoid organs and immunosuppression. Damage to the immune system is more significant than clinical disease in chickens. Causes considerable economic damage.

Question 53

Causative agent of Chicken infectious anaemia. genus, family, DNA type, strains, survival

Answer 53

Chicken Anemia Virus (CAV) genus Gyrovirus Family Anelloviridae Non-enveloped single-stranded DNA virus. ◦ All isolated strains belong to one serotype. ◦ There are some differences between virus strains. ◦ Highly persistent in the environment, resistant to many disinfectants.

Question 54

Prevalence and host range (+ age) of chicken infectious anemia.

Answer 54

Worldwide, in large production farms. Chickens are the only natural host. Susceptibility: all ages, especially 1-3 weeks old chicks.

Question 55

Transmission of chicken infectious anemia.

Answer 55

The spread of infection is very fast. ◦ Spreads horizontally and vertically Contaminated eggshell, semen. Persists in reproductive organs for long periods. The virus is excreted with faeces 5-7 weeks after recovery. Antibody formation 2-4 weeks after infection.

Question 56

Morbidity and mortality of CIA.

Answer 56

Morbidity up to 100%, mortality up to 30%

Question 57

IP of CIA

Answer 57

Incubation period 10-14 days

Question 58

Clinical signs of CIA.

Answer 58

Risk of superinfection Symptoms depend on age, amount of the virus, immune status. Specific feature: anaemia ◦ Develops 10-14 days after infection ◦ Plus thrombocytopenia → haemorrhages Depression, loss of appetite Death: 12-28 days after infection

Question 59

Post mortem signs of CIA.

Answer 59

Cachexia, Haematomas on the wings, legs, internal organs, muscles. Thymus dark red in colour, cortical lymphocyte depletion, atrophy, in severe cases destroyed. Fat-yellow or pale bone marrow → atrophy. Hematopoietic cells are replaced by fat or stromal cells. Bursa of Fabricius → atrophy of the lymph follicles. Lymphoid tissue is lost in various organs.

Question 60

Diagnosis of CIA.

Answer 60

Epidemiological situation, symptoms and findings, lab test results. Sample material: spleen, bursa of Fabricius, blood. Lab Tests: ◦ Viral Isolation: cell cultures + PCR  HCT less than 27% → confirms the diagnosis ◦ Antigen: PCR ◦ Antibodies from serology

Question 61

Prevention of CIA.

Answer 61

◦ Good housing, biosecurity ◦ Live vaccines in many countries  given 4-6 weeks before the onset of lay  in Drinking water or injection  Attenuated, inactivated, recombinant DNA (most effective).

Question 62

CIA is the key component in many

Answer 62

multifactorial chicken diseases May co-occur with Marek's Disease Virus (MDV), Infectious Bursal Disease Virus (IBDV) and others.

Question 63

Marek’s disease (MD) is also called

Answer 63

chicken neurolymphomatosis.

Question 64

Marek’s disease (MD) is also called chicken neurolymphomatosis, and is a highly contagious herpesvirosis of chickens and turkeys, characterized by

Answer 64

lymphogranulomas in internal organs, skin and muscles, or paralysis, depigmentation of the iris of the eye and deformation of the pupil.

Question 65

Causative agent of MD. genus, family, DNA type

Answer 65

Marek's DiseaseVirus (MDV) genus Mardivirus Subfamily Alphaherpesvirinae Enveloped double-stranded DNA virus.

Question 66

Serotypes of MD virus.

Answer 66

Three serotypes:  Gallid alphaherpesvirus 2 (GaAHV-2, MDV-1) – all strains are virulent.  Gallid alphaherpesvirus 3 (GaAHV-3, MDV-2) – avirulent to chickens.  Meleagrid alphaherpesvirus 1 (MeHV-1) – turkeys. ◦ Cause cell lysis.

Question 67

Prevalence of MD and host range (+age).

Answer 67

Present in all poultry flocks. ◦ Except SPF flocks (specific pathogen free) Chickens, turkeys, pheasants ◦ Experimentally in ducks, quails, swans, etc. ◦ Chicks up to 2 weeks are more susceptible.

Question 68

Transmission of MD.

Answer 68

Excretion: feather follicles  Horizontal (aerogenic, alimentary) transmission Routes of infection: mucous membranes of the mouth and respiratory tract, feather follicles. Chicks are infected during the first few weeks of life, few get sick.

Question 69

Incubation period of MD.

Answer 69

Incubation period 2-5 weeks, max. 60 weeks.

Question 70

Forms of disease in MD.

Answer 70

classical and acute but there are other forms too, such as ocular and cutaneous.

Question 71

Clinical signs of classical form of MD.

Answer 71

nervous signs, limping, droopy extremities or paralysis on them, wry neck

Question 72

Clinical signs of acute form of MD.

Answer 72

signs similar to avian leukosis high, 80% mortality in young birds indigestion, weight loss, malaise, dyspnea, pale, limping, abnormal posture

Question 73

Clinical signs of ocular form of MD.

Answer 73

iris color changes, deformed pupils, photosensitivity, blindness (chicken pupils are normally round)

Question 74

Post mortem signs of MD.

Answer 74

Depends on the form but: hypertrophic nerves (thick) nerve discoloration nerve structure altered tumors organ tissue destroyed

Question 75

Diagnosis of MD.

Answer 75

Epidemiological situation, clinical signs, necropsy. Laboratory analyses using: Tumours from damaged tissues, feces, blood, dead birds. Typical histological changes aid diagnosis. ◦ Virus isolation - cell cultures, infecting chicken embryos. ◦ Identification of virus ◦ Antibodies

Question 76

Tx and prevention of MD.

Answer 76

No treatment ◦ Sick and susceptible birds are culled Prevention: biosecurity, hygiene. All in - all out, strict sanitation → reduced or delayed exposure. Vaccination: live vaccine, immediately after hatching or in ovo. ◦ Incomplete vaccination may lead to development of hyperpathogenic MDV strains. Or prevent by: Raise/breed resistant bird breeds/crosses.

Question 77

DVE, DP stand for?

Answer 77

Duck viral enteritis, duck plague Notifiable disease!

Question 78

Duck viral enteritis, or duck plague, is an acute contagious herpesvirosis of ducks, geese and swans, characterized by

Answer 78

vascular lesions, haemorrhages, inflammation of the gastrointestinal mucosa and degenerative changes in parenchymal organs. Notifiable disease!

Question 79

Causative agent of Duck viral enteritis, or duck plague. genus, family, DNA type, survival

Answer 79

Anatid alphaherpesvirus 1 (AnAHV-1), or Duck Enteritis Virus (DEV) genus Mardivirus Subfamily Alphaherpesvirinae Double-stranded, enveloped DNA-virus. ◦ Inactivates rapidly in a strongly acidic or alkaline environment. ◦ Freezing conserves the virus ◦ Disinfective solutions destroy it quickly

Question 80

Host range for duck viral enteritis.

Answer 80

Susceptible species: ducks, geese and swans. Source of the infection: sick or recovered birds. Outbreaks at every season, associated with stressors.

Question 81

Transmission of duck viral enteritis or duck plague.

Answer 81

Excretion: faeces, nasal, oral and ocular secretions. Transmission: contaminated water, feed, direct contact. Vectors: rodents, blood-sucking insects, cats, dogs, wild birds and humans. Infection routes in: alimentary, respiratory, or transcutaneous.

Question 82

IP of duck viral enteritis or duck plague.

Answer 82

Incubation period 3-7 days

Question 83

Morb. + mort. of duck viral enteritis or duck plague.

Answer 83

Morbidity 5-100%, mortality 30-60%

Question 84

Course of disease in duck viral enteritis or duck plague.

Answer 84

Peracute course: ◦ Sudden deaths ◦ No characteristic signs of disease ◦ Dead birds are in good nutritional condition. Acute course: ◦ Obvious signs of disease

Question 85

Clinical signs of duck viral enteritis or duck plague.

Answer 85

 Sluggishness, loss of appetite, polydipsia, ataxia, nasal secretion, and bloody to watery diarrhoea.  Ruffled plumage, droopy head and wings.  Tremors of the head, neck, and body ◦ Birds can no longer stand or swim, fall to the side.  Photophobia  Cyanosis of the beak and abdominal area, phallus prolapse.  Decline in egg production

Question 86

Post mortem signs of duck viral enteritis or duck plague.

Answer 86

 Weight loss, cachexia  Haematomas throughout the intestinal tract ◦ Haemorrhagic belt in intestinal submucosa (picture E). In later stages replaced with yellowish plaques.  The liver is enlarged, friable, uneven in colour, haematomas on the surface.  Ovarian follicle deformation  Haematomas in the oviduct

Question 87

Diagnosis of duck viral enteritis or duck plague.

Answer 87

Epidemiological situation, clinical signs, necropsy results. Laboratory investigation ◦ Material: liver, spleen, bursa, kidneys, cloacal swabs, blood. ◦ Virus isolation: cell cultures, day-old ducklings, duck embryos. ◦ Virus identification ◦ Antibodies

Question 88

Prevention of duck viral enteritis or duck plague.

Answer 88

No specific treatment. ◦ Depopulation/culling using non-bloody method, carcasses burned, premises thoroughly decontaminated. ◦ SPREADING MUST BE AVOIDED! Prevention: biosecurity ◦ Avoid contact with wild birds ◦ Ducklings or hatching eggs from SPF flocks Vaccination: attenuated live and killed vaccines ◦ At 4 weeks of age, repeated 2 weeks later ◦ Vaccinated ducks transfer resistance to unvaccinated ducks.