Non-respiratory viral diseases in poultry Flashcards
Infectious bursal disease (IBD) is also called
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!
Infectious bursal disease (IBD), also called 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!
IBDV causative agent
genus, family, DNA type
Infectious Bursal Disease Virus (IBDV)
Genus Avibirnavirus,
family Birnaviridae
Nonenveloped double-stranded RNA virus
Notifiable dz!
serotypes of IBDV
Infectious Bursal Disease Virus (IBDV)
2 serotypes:
Serotype 1 - clinical disease of chickens, at least six subtypes.
Survival of IBDV in the environment.
Infectious Bursal Disease Virus (IBDV)
Very durable in the environment.
Inactivates in a strongly alkaline environment.
Host range and age of IBDV.
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.
Transmission of IBDV.
Infectious Bursal Disease Virus (IBDV)
Excretion: faeces
◦ Sick and recovered birds spread the pathogen, spread is fast.
Infection route in: alimentary
Morbidity & mortality of IBDV.
Morbidity up to 100%, mortality up to 100%.
Incubation period: 2 – 6 days
IBDV is immunosuppressive
Clinical signs of IBD.
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.
Post mortem signs of IBD.
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
Diagnosis, treatment and prevention of IBD.
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.
Avian leukosis is a chronic retrovirosis characterized by
tumors formed in different organs and tissues by proliferation of hematopoietic cells.
Causative agent of avian leukosis.
genus, family, DNA type
genus Alpharetrovirus
Family Retroviridae
Enveloped spherical single-stranded RNA virus.
Sensitive to high temperature, drying and formaldehyde, well maintained at low temps.
Avian leukosis surface glycoproteins.
Subgroups: A, B, C, D, J
Endogenous subgroups: E, F, G, H, I → E in chickens, other subgroups not.
Excretion of avian leukosis virus:
feces and eggs, nasal secretions
Transmission of avian leukosis virus.
Vertically Inside the egg (immunologic tolerance),
and respiratory (direct, indirect)
Target age demo for avian leukosis.
More often in 6-12-month-old chickens.
◦ Also turkeys, pheasants, quails and many other bird species.
Forms of disease in avian leukosis.
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
Most common form of disease in avian leukosis.
Lympholeukosis – persistent lymphocytosis and erythropenia, most common.
(other forms include: tumors, erythroblastosis and myeloblastosis (immature WBCs))
Clinical signs of avian leukosis.
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.
Incubation period of avian leukosis.
Incubation may last for months
Course of disease in avian leukosis.
chronic
Post mortem signs of avian leukosis.
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.
Sample material for diagnosis of avian leukosis?
Tests?
Sample material: blood, tumours, faeces
Identification: CLoFAL test, histological examination, virus neutralization, immunofluorescence test
◦ Antibodies: ELISA
Tx and prevention of avian leukosis?
No effective treatment – eradication (cull).
Prevention: biosecurity rules
◦ Buying chickens from ALV free flocks
◦ Breeding of resistant bird crosses/breeds
◦ No effective vaccine!
AIE
Avian infectious encephalomyelitis
Avian infectious encephalomyelitis is a contagious and acute avian picornavirosis characterized by
different nervous symptoms.
Not a zoonotic disease!
Causative agent of AIE.
genus, family, DNA type
Avian infectious encephalomyelitis (AIE)
Avian EncephalomyelitisVirus (AEV)
genus Tremovirus
Family Picornaviridae
Non-enveloped single-stranded RNA virus.
Very resistant in the environment.
Describe Natural viral strains of AIE virus versus Embryo-adapted strains.
Natural viral strains: enterotropic, relatively low pathogenicity.
Embryo-adapted strains: generally apathogenic.
Host range and age demographic for avian infectious encephalomyelitis.
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.
Transmission of AIE.
Excretion: faeces
Source of infection: sick and carrier birds.
Transmission: transovarial, aerogenic and alimentary (feed, water, bedding,
inventory).
Morbidity & mortality of AIE.
Morbidity 40-60%, mortality 25-50%
Clinical signs of AIE.
◦ 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
Incubation period of AIE.
Incubation period: 1-7 days or min. 10 days
Post mortem signs of AIE.
Pathological findings: unspecific
◦ Neurodegeneration of brain tissue
◦ Perivascular infiltration
◦ Gliosis (a fibrous proliferation of glial cells in injured areas of the CNS)
Diagnosis of AIE.
Diagnosis: epidemiology, clinical signs, necropsy findings.
Laboratory:
◦ Samples: brain tissue, blood
◦ Virus isolation: inoculation
◦ Virus identification: immunofluorescence test
◦ Antibodies: ELISA
Treatment of AIE.
Not treated!
but there is a vax
Prevention of AIE.
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.
EDS-76 is
Egg drop syndrome 1976
Egg drop syndrome 1976 is an acute to chronic adenovirosis of birds characterized by
a sharp decrease in egg production, deformation of eggs, soft-shelled and/or shell-less eggs.
Causative agent of Egg drop syndrome 1976.
genus, family, DNA type
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
Genotypes of EDS-76.
Egg drop syndrome 1976
Three genotypes: classic strain, duck EDS virus England strain, Australian strain.
◦ A- and C-antigen: antibody formation
Prevalence and host range of EDS-76.
Egg drop syndrome 1976
Spread all over the world.
◦ Chickens, quails, turkeys, wild birds
Natural reservoirs: geese and ducks
Epidemiology and course of dz in EDS-76.
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
EDS-76 localizes in what tissues?
Localized in the oviduct, upper respiratory mucosa, secretions, leukocytes.
EDS-76 transmission
Excretion: faeces, cloacal and nasal secretion.
Infection via: faecal-oral, contaminated vaccines, alimentary, vertical.
Clinical signs of EDS-76.
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)
Post mortem signs of EDS-76.
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)
Diagnosis of EDS-76.
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
Prevention of EDS-76.
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.
CIA
Chicken infectious anaemia
Chicken infectious anaemia is chronic circovirosis of chickens, characterized by
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.
Causative agent of Chicken infectious anaemia.
genus, family, DNA type, strains, survival
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.
Prevalence and host range (+ age) of chicken infectious anemia.
Worldwide, in large production farms.
Chickens are the only natural host.
Susceptibility: all ages, especially 1-3 weeks old chicks.
Transmission of chicken infectious anemia.
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.
Morbidity and mortality of CIA.
Morbidity up to 100%,
mortality up to 30%
IP of CIA
Incubation period 10-14 days
Clinical signs of CIA.
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
Post mortem signs of CIA.
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.
Diagnosis of CIA.
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
Prevention of CIA.
◦ 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).
CIA is the key component in many
multifactorial chicken diseases
May co-occur with Marek’s Disease Virus (MDV), Infectious Bursal Disease Virus
(IBDV) and others.
Marek’s disease (MD) is also called
chicken neurolymphomatosis.
Marek’s disease (MD) is also called chicken neurolymphomatosis, and is a highly contagious herpesvirosis of chickens and turkeys, characterized by
lymphogranulomas in internal organs, skin and muscles, or paralysis, depigmentation of the iris of the eye and deformation of the pupil.
Causative agent of MD.
genus, family, DNA type
Marek’s DiseaseVirus (MDV)
genus Mardivirus
Subfamily Alphaherpesvirinae
Enveloped double-stranded DNA virus.
Serotypes of MD virus.
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.
Prevalence of MD and host range (+age).
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.
Transmission of MD.
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.
Incubation period of MD.
Incubation period 2-5 weeks, max. 60 weeks.
Forms of disease in MD.
classical and acute but there are other forms too, such as ocular and cutaneous.
Clinical signs of classical form of MD.
nervous signs, limping, droopy extremities or paralysis on them, wry neck
Clinical signs of acute form of MD.
signs similar to avian leukosis
high, 80% mortality in young birds
indigestion, weight loss, malaise, dyspnea, pale, limping, abnormal posture
Clinical signs of ocular form of MD.
iris color changes, deformed pupils, photosensitivity, blindness
(chicken pupils are normally round)
Post mortem signs of MD.
Depends on the form but:
hypertrophic nerves (thick)
nerve discoloration
nerve structure altered
tumors
organ tissue destroyed
Diagnosis of MD.
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
Tx and prevention of MD.
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.
DVE, DP stand for?
Duck viral enteritis, duck plague
Notifiable disease!
Duck viral enteritis, or duck plague, is an acute contagious herpesvirosis of ducks, geese and swans, characterized by
vascular lesions, haemorrhages, inflammation of the gastrointestinal mucosa and degenerative changes in parenchymal
organs.
Notifiable disease!
Causative agent of Duck viral enteritis, or duck plague.
genus, family, DNA type, survival
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
Host range for duck viral enteritis.
Susceptible species: ducks, geese and swans.
Source of the infection: sick or recovered birds.
Outbreaks at every season, associated with stressors.
Transmission of duck viral enteritis or duck plague.
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.
IP of duck viral enteritis or duck plague.
Incubation period 3-7 days
Morb. + mort. of duck viral enteritis or duck plague.
Morbidity 5-100%,
mortality 30-60%
Course of disease in duck viral enteritis or duck plague.
Peracute course:
◦ Sudden deaths
◦ No characteristic signs of disease
◦ Dead birds are in good nutritional condition.
Acute course:
◦ Obvious signs of disease
Clinical signs of duck viral enteritis or duck plague.
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
Post mortem signs of duck viral enteritis or duck plague.
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
Diagnosis of duck viral enteritis or duck plague.
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
Prevention of duck viral enteritis or duck plague.
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.
