Poultry pathology 5. Flashcards
Infectious chicken anemia
• Pathogen: chicken anaemia virus (CAV/CiAV))
• Circoviridae, Gyrovirus genus
- 15-20 nm, non-enveloped
- circular ssDNA, 2300 bp, 3 proteins
• ONLY CHICKEN
• infection:
- vertical (ovogenous)
- horizontal (orofecal route)
• Susceptibility: any age, but most sensitive at the first week, high mortality if unvaccinated
-rather sensitive between 1-3 week to clinical disease
-susceptibility decreases with age, asymptomatic but transmitting
-no age dependent immunity
• general immune status determines the outcome
-immunosuppression makes the susceptibility longer!
Infectious chicken anemia
Pathogenesis
SLOW
in real life
• clinical signs can appear as late as 3-4. week age
• immune status
-specific immunity (vaccine, parent flock)
-innate immunity and general health status
• The virus infects
-haemopoetic stem cells in the bone marrow
- stem cells in the thymus
• apoptosis 6-8 days PI
• anaemia (panmyelophtisis)
• atrophy of the thymus (and bursa Fabricii)
• T- (and B-) cellular immunosuppression
Infectious chicken anemia
Clinical signs
Clinical signs
• Retarded growth, increased mortality,
• secondary infections (Coli septicaemia)
Pathologic lesions
• severe anaemia (Ht <27)
• bright red, thin blood, the muscles appear pale yellowish
• coagulopathy » multiple haemorrhages (during viraemia)=> proventriculus, in the subcutaneous CT &
in fascia between muscles
+ Tip of the wings, ventral pectoral areas (most likely to take physical damage)
• immune organ atrophy
=> bone marrow, thymus, bursa Fabricii, spleen
• fatty infiltration of the liver (hypoxia)
Infectious chicken anemia
Losses
• direct loss: death
• heterogenous flocks - runting-stunting syndrome
Secondary infections often occur – index diseases
-bacterial
• septiceamia due to bacteria
• gangrenous dermatitis
-viral
• inclusion body hepatitis (IBH)
• transmissible (viral) proventriculitis (TVP)
Infectious bursitis
pathogen
• Pathogen: • Birnaviridae, Birnavirus genus • infectious bursal disease virus (IBDV) • 60 nm, nonenveloped • dsRNS, 6 kbp, 3 proteins • 1962, Gumboro, Delaware -classical virulent (vIBDV) ‘70-s -very virulent (vvIBDV) („hot strains”) • ’90-s • strains causing subclinical infection • strains of low virulence
Infectious bursitis
pathogenesis
• only chickens develop clinical disease
• most susceptible period: 3-6 weeks
• chickens are susceptible up to 4 months of age
• horizontal, per os
• very resistant in the environment
can remain infectious up to 4 months
Target organ: bursa of Fabricius
• target cells: dendritic cells of the follicles
„nursing” cells
• lack of nursing cells the competent & transforming B lymphocytes die and disappear during the disease
• lymphoclasia and lymphocyte depletion
Infectious bursitis
pathogenesis 2
1 per os / orofecal infection)
2 multiplies in the GI
3 transfers to the the liver
4 viraemia, final target: bursa Fabricii
Infectious bursitis
Effect
- Primary effect: -humoral immunocapacity is reduced
- Secondary effect:- due to the bone marrow destruction the T-cell immune response is also reduced
- consequences:
- mortality due to viraemia
- immunodeficiency >secondary infections
• the clinical-pathologic picture is versatile • depend on the virulence • classical strains (vBDV): classical lesions (serous bursitis), immunosuppression -mortality 15-20% • very virulent strains (vvBDV) -necrotic-haemorrhagic bursitis • expressed immunosuppression -high mortality • 30-50%
- subclinical strains
- variant strains
- strains of reduced virulence and vaccine strains
- depend on the age
- under 3 weeks
- after 3 weeks of age
• diseases caused by classical strains (vBDV)
•
Adenovirus diseases of poultry
Aviadenovirus (Grp 1)
Chicken, quail: Fowl Adenovirus (FAdV): 5spp, 1-12 serotypes
-Inclusion body heptatitis
Goose: Goose adenovirus (GoAdV) 1-3 serotypes
Inclusion body hepatitis IBH
pathogen
Pathogen: • Aviadenoviruses (FAdV A-E) • icosahedral, non-enveloped, dsDNA • multiplies in the nucleus > inclusion bodies • low virulence > predisposing factors are needed • immunosuppression • infectious bursitis • infectious (viral) chicken anaemia • mycotoxicosis • appears in 28-30 days old chicken (infection from 21 days, 4-7 days PP) • Other avian species susceptible are: -Young adult turkeys -Young guinea fowl, quail, pigeon • Main feature of the disease: viraemia -hepatitis is consequence of the viraemia!• hepatitis is severe • haemophilia due to hepatic disfunction
Inclusion body hepatitis
Pathologic lesions:
- multiple hemorrhages (per diapedesin)
- swollen, pale liver (fatty infiltration)
- with necrotic foci
- pale bone marrow
- anaemia
- in the pancreas:
- hemorrhages and necrotic foci
- Histopathology (liver):
- hemorrhages
- basophil and eosinophil inclusion bodies in the nuclei of the hepatocytes
Turkey haemorrhagic enteritis
pathogen
Pathogen TAdV3 = HEV • 70-90 nm in diameter • Siadenovirus dsDNA • Infection • per os, orofecal • Epidemiology • this form was observed in turkey poults • severe in young poults (1-2 weeks) • sometimes older age (7-9 weeks) • 10-15 (-60)% mortality in 2 weeks • immunosuppression • secondary infections • the whole flock becomes crippled, unable to perform as needed > the whole profit is lost
Turkey hemorrhagic enteritis
• Pathogenesis:
• the virus replicates in the enterocytes and enteric lymph follicules
• viraemia follows
• cytokine-mediated anaphylactic shock (in turkey the intestines are the shock organs)
• severe immunosuppression
Pathology:
• Bloody content and undigested feed in the intestines
• Mucous membrane of the small intestine are • swollen, dark-red w/ superficial necrosis • fibrinous pseudomembranes
• enlargement of the spleen (reticulum cell hyperplasia)
• „Marble spleen” disease
• in the nuclei of the reticulum cells inclusion bodies containing adenoviruses
• later atrophy of the spleen parenchyma follows
• the primary lymph organs atrophy too (thymus, bursa Fabricii)
Turkey hemorrhagic enteritis
Marble spleen disease / splenomegalia
- TAdV 3
- 3-8 months phaseants
- 2-3 (15) % mortality
- shock organ is the lung
- splenomegaly
- marble pattern
- lymphoreticularis hyperplasia
- lymphoid necrosis
Egg drop syndrome (EDS)
pathogen
Atadenovirus of duck origin (DAdV-1)
• 1974 NL, 1976 IRL (EDS ‘76), 1977 HU
• probably was spread by a vaccine for Marek’s
disease grown in duck-embryo fibroblasts
Infection:
• at the beginning: with vaccines (subcutaneous)
• later:
• vertically from layer flocks showing clinical signs (ovogenous infection)
• exogenous infection: the virus shed withthe feces can enter other layer flocks
