JPC SYSTEMIC PATHOLOGY

HEMOLYMPHATIC SYSTEM

April 2024

H-V07

 

Signalment: Young chicken

 

HISTORY: None

 

HISTOPATHOLOGIC DESCRIPTION: Bursa of Fabricius: Diffusely, there is atrophy of bursal follicles within both the cortex and the medulla characterized by marked lymphoid depletion. Undifferentiated epithelial cells that separate the cortex and medulla are prominent. Multifocally, follicular medullas often contain eosinophilic cellular and karyorrhectic debris (lytic necrosis) admixed with macrophages that occasionally contain phagocytized cellular debris. Multifocally, lymphoid follicles contain dilated and congested vessels, mild hemorrhage, and low to moderate numbers of infiltrating heterophils. Diffusely the interfollicular connective tissue and to lesser degree follicular cortical areas are markedly expanded by clear space and lymphatics are multifocally ectatic (edema). Scattered heterophils transmigrate the surface epithelium, which is multifocally mildly attenuated.

 

MORPHOLOGIC DIAGNOSIS: Bursa of Fabricius: Lymphoid depletion, acute, diffuse, moderate, with lymphoid necrosis and mild heterophilic bursitis, breed unspecified, chicken, avian.

 

ETIOLOGIC DIAGNOSIS: Avian birnaviral bursitis

 

CAUSE: Infectious bursal disease virus

 

CONDITION: Infectious bursal disease (IBD)

 

SYNONYMS: Gumboro disease, avian infectious bursitis

 

GENERAL DISCUSSION:  

• Worldwide disease of economic importance to poultry producers
• Highly contagious, lymphocytolytic, immunosuppressive disease of predominantly young chickens (3-6 weeks), with predilection for differentiating B-lymphocytes in the bursa of Fabricius
  1. Birds infected younger than 3 weeks do not show clinical signs but will suffer results of immunosuppression from destruction of bursa
• Non-enveloped, bi-segmented, double-stranded RNA virus of the Avibirnavirus genus and the family Birnaviridae
  1. Two genome segments: A and B
     • Segment A encodes polyprotein that is cleaved into viral proteins 2, 3, and 4 (VP2, VP3, VP4)
  2. Segment B encodes viral protein 1 (VP1), RNA-dependent RNA polymerase (RdRp)
• There are two serotypes (I and II) of IBDV; only serotype I is pathogenic
  1. Serotype 1 has antigenic variation due to antigenic drift resulting in emergence of new strains with implication for vaccines
  2. Serotype 1 strains further classified as subclinical, classic, or very virulent pathotypes
     • Variations in outer capsid protein VP2 and VP1 polymerase demonstrated to influence pathogenicity (Stoute, J Vet Diagn Invest 2019)

 

PATHOGENESIS:  

• Virus is transmitted from infected chicks, contaminated premises, or fomites (including feed, water, meal worms, etc); vertical transmission has not been documented
  1. Non-enveloped virus: Resistant to many disinfectants and environmental factors; can persist for weeks in feed, water, feces
• Virus is directly cytopathic to immature B cells -> lymphocytolysis/necrosis
• Age at infection correlates with severity of immunosuppression (younger chicks more severely affected)
• Maternal antibodies important and vaccination/field exposure useful for boosting antibody production by hens
• Vaccination in chicks necessary once maternal antibodies wane
• Chicks who survive infection can have a prolonged periods of immunosuppression leading to susceptibility to secondary infections 

 

TYPICAL CLINICAL FINDINGS:  

• Signs only observed in birds infected at 3 weeks of age and older
  1. Birds under 3 weeks of age will have increased susceptibility to subsequent pathogens due to destruction of bursa
• Sudden onset of signs:
  1. Tremors and unsteadiness
  2. Depression, anorexia, ruffled feathers, droopy appearance (can resemble coccidiosis)
  3. Diarrhea and dehydration +/- tenesmus and hematochezia
  4. Vent-picking
• High morbidity; mortality can approach 30-60%
• Age, strain, breed, husbandry affect mortality
• Disease tends to be more severe in leghorns than broilers

 

TYPICAL GROSS FINDINGS:  

• Bursa: Enlarged, edematous, with transmural or mucosal hemorrhage in acute phase; caseous necrosis may be noted, especially with virulent strains. Bursa will atrophy as swelling recedes (8-10 days post infection). 
• Hemorrhages may be found in thigh muscles, pectoral muscles, and at ventriculus/proventriculus intersection
• Mucosal folds are swollen and edematous and diffusely or focally hemorrhagic 
• Increased mucous may be noted in the intestine 
• The spleen and liver may be enlarged with small gray foci on the surface
• The kidney may be swollen because of accumulation of urates (dehydration)
• Other lymphoid tissues (thymus, Harderian gland, cecal tonsils, Peyer’s patches): necrosis or atrophy possible, especially with highly virulent strains

 

TYPICAL LIGHT MICROSCOPIC FINDINGS:  

• Bursa: 
  1. Acute phase: Lymphoid follicle necrosis, heterophil-rich cellular infiltrates, edema (interfollicular and intrafollicular), hyperemia
  2. Chronic phase: Atrophy, fibroplasia (intrafollicular), formation of cystic cavities within follicles
  3. Variant strains may cause lymphoid necrosis and atrophy of the bursa without inflammation or diffuse necrosis
• Spleen, thymus, cecal tonsils, Harderian gland: Transient lymphoid necrosis
• Kidney: Tubular protein casts +/- heterophilic infiltration (secondary to dehydration)
• Other lesions may present due to immunosuppression (coccidiosis, gangrenous dermatitis, etc.)

 

ADDITIONAL DIAGNOSTIC TESTS:  

 

DIFFERENTIAL DIAGNOSIS:

• Bursal atrophy:

• Physiologic atrophy 
• Chronic Marek’s disease (H-V01, Alphaherpesvirus)
• Chick infectious anemia (Circovirus): Bursal lesions are less severe than IBD; lymphocyte depletion and small necrotic foci with infolded epithelium, with no inflammation and no intracytoplasmic inclusion bodies; thymus is most severely affected organ in CAV with severe lymphoid depletion; intranuclear inclusion bodies have been reported in thymus and bone marrow

• Lymphoid necrosis in the bursa:

• Newcastle’s disease virus (Paramyxovirus, genus Rubulavirus)
• Duck plague virus (Alphaherpesvirus)
• Psittacine beak and feather disease (Circovirus): Only in Psittacines; bursal necrosis with intracytoplasmic inclusions in macrophages

• Immunosuppressive conditions:

• Chicken infectious anemia

• Reticuloendotheliosis 
• Lymphoid leukosis
• Marek’s disease

COMPARATIVE PATHOLOGY:  

• Similar virus identified in bursa of Fabricius in ostriches
• IBD in Turkeys and ducks: Subclinical infections occur without apparent immunosuppression
  1. Viruses are serologically distinct

 

References:    

1. Abdul-Aziz T, Fletcher OJ, Barnes HJ. Avian Histopathology. 4th Philadelphia, PA: American Association of Avian Pathologists; 2016: 20, 37-41.
2. Bolfa P, Callanan JJ, Ketzis J, et al. Infections and pathology of free-roaming backyard chickens on St. Kitts, West Indies. J Vet Diagn Invest. 2019;31(3)343-349.
3. Brochu NM, Guerin MT, Varga C, et al. A two-year prospective study of small poultry flocks in Ontario, Canada, part 1: prevalence of viral and bacterial pathogens. J Vet Diagn Invest. 2019; 31(3):327-335.
4. Crespo R, Franca MS, Fenton H, Shivaprasad HL. Galliformes and Colubriformes. In: Terio KA, McAloose D, St. Leger J, eds. Pathology of Wildlife and Zoo Animals. London, UK: Academic Press; 2018:751-752. 
5. Schmidt R, Reavill DR, Phalen DN. Pathology of Pet and Aviary Birds. 2nd ed. Ames, IA: John Wiley & Sons, Inc.; 2015; 180-181.
6. Sellers H, Ojkic D. Viral diseases. In: Boulianne M, ed. Avian Disease Manual. 8th ed. Jacksonville, FL: American Association of Avian Pathologists, Inc; 2019:53-56, 61-62
7. Stoute ST, Jackwood DJ, Crossley BM, et al. Molecular epidemiology of endemic and very virulent infectious bursal disease virus genogroups in backyard chickens in California, 2009-2017. J Vet Diag Invest. 2019; 31(3): 371-377.

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