7-week-old, specific pathogen free, White Leghorn chickens, (Gallus gallus domesticus).The chickens were one component of an infectious bursal disease research project that included one group which had received topical ocular inoculations of infectious bursal disease virus (variant strain E) and another group of non-challenged control chickens. Four days post inoculation both groups of birds were euthanized. The challenged and control chickens were clinically normal throughout the duration of the study. Each slide contains tissues from one challenged animal and one age-matched control.

Gross Description:  

Subjectively, the bursa appeared approximately 10% smaller in the challenged group than the control group.

Histopathologic Description:

Bursa of Fabricius (cloacal bursa): In the affected tissue there is marked atrophy of bursal follicles due to loss of lymphocytes in the medulla and cortex. Numerous large, foamy, macrophages containing phagocytosed cellular debris are within the collapsed follicles. The endodermal epithelium separating the medulla from the cortex is prominent due to collapse of the follicles and mild epithelial hypertrophy and hyperplasia. The interfollicular epithelium covering the surface of the bursa is also mildly hyperplastic. Diffusely, the follicular cortex and interfollicular interstitium contain increased clear space (edema), congested vessels, and multifocal areas of mild hemorrhage. Multifocally, the lamina propria, muscularis, and serosa are expanded by edema with small numbers of lymphocytes, plasma cells, and macrophages.

Morphologic Diagnosis:  

Bursa of Fabricius (cloacal bursa): Lymphoid depletion, diffuse, severe, subacute, White Leghorn (Gallus gallus domesticus), avian.


Infectious bursal disease

Contributor Comment:  

Infectious bursal disease, or Gumboro disease, is an acute, highly contagious, immunosuppressive disease caused by serotype 1 infectious bursal disease virus (IBDV), a double-stranded RNA virus in the family Birnaviridae and genus Avibirnavirus.(2) Chickens are the only animals known to develop clinical disease and distinct lesions when exposed to IBDV, although other species may replicate the virus and develop neutralizing antibodies. Virtually all flocks in major poultry producing areas worldwide are exposed to the virus through natural infection or vaccination. Eliminating the virus from infected farms can be difficult, despite routine cleaning and disinfection, because the virus has been shown to survive in the environment for several months and it is relatively resistant to heat and certain disinfectants. Clinical signs of disease appear within 2-3 days after exposure and include soiled vent feathers, diarrhea, dehydration, anorexia, depression, ruffled feathers, trembling, prostration, and death. Clinical disease, although uncommon in the United States, is primarily seen in chickens 3-6 weeks old. Infection in chickens younger than 3 weeks of age is typically subclinical, but results in prolonged immunosuppression that can cause adverse economic impact to the producer due to secondary infections and poor response to routine flock vaccinations. Infected birds older than 6 weeks of age seroconvert but usually do not develop clinical signs.(2)

There are two serotypes: type 1 and type 2. The type 1 serotype is further divided into the standard (or classic) strain and variant strains. In Europe, Asia, Africa, and South America highly pathogenic serotype 1 strains have been identified and are termed very virulent infectious bursal disease (vvIBD).(2) Experimental inoculation elicits different responses depending on the strain of virus. Both the very virulent and classic strains induce typical clinical signs and gross lesions with mortality rates of 10-50% for classical strains and up to 50-100% during infections with vvIBDV.(2) Variant strains such as the type E strain used to infect this chicken typically cause bursal lesions to develop but rarely induce acute clinical signs or mortality.(5) In general, serotype 2 virus is not pathogenic and does not protect against challenge with serotype 1 viruses.(2)

Grossly the bursa initially increases in size due to edema and hyperemia, but then begins to atrophy due to lymphoid depletion and eventually decreases in size to one-third of its original weight.(1) The bursa may have necrotic foci with mild to extensive hemorrhage and the spleen may be mildly enlarged with uniform small gray foci on the surface.(2) Hemorrhages of the thigh and pectoral muscles are frequently present and severely dehydrated chickens commonly develop non-specific renal lesions.(2)

Microscopically the cloacal bursa is the most severely affected organ, but other lymphatic tissues, such as the spleen, thymus, and Harderian gland, have similar but milder lesions than the bursa.(3) Initially there is degeneration and necrosis of lymphocytes in the bursal medulla as early as 36 hours after infection.(1) As the disease progresses, heterophils, macrophages, and eventually fibroblasts accumulate in the follicular and interfollicular areas. In the spleen there may be hyperplasia of splenic reticuloendothelial cells along with lymphoid necrosis and the Harderian gland can have areas of necrosis.(1,3)

Multiple virus and host variables, including strain of virus, age and breed of chicken, and maternal immunity and vaccine status affect the development of infection/disease.(4) The pathogenesis of oral infection results in an initial viremia within five hours and a second massive viremia may occur following infection of the bursa.(2) The virus targets immature dividing B lymphocytes resulting in necrosis and apoptosis of B cells with activation of macrophages, T cells, and NK cells.(2,4) Recovery from complete immunosuppression can occur if large follicles capable of replenishing the B cell population are reconstituted from endogenous stem cells that survived the initial infection.(2,9) The long-term effect of IBD is frequently immunosuppression due to decreased humoral immunity, and to a much lesser degree, cellular immunity resulting in increased susceptibility to disease and poor immune response to vaccination.(7)

JPC Diagnosis:  

Bursa of Fabricius (cloacal bursa): Lymphoid necrosis and depletion, diffuse, marked, with stromal collapse and interstitial edema.

Conference Comment:  

Compared to tissue from the aged-matched control, there is increased prominence of reticular cells and macrophages in the section of bursa from the infected animal. One of the focal points of discussion among conference participants was the distinction between true inflammation versus increased prominence of resident reticular cells and monocytes due to follicular collapse. Additionally, some participants slides contained few discrete foci of heterophilic inflammation.

Based on the histomorphologic findings of lymphoid necrosis and depletion, conference participants were evenly divided between infectious bursal disease virus (IBDV) and chicken anemia virus (CAV) (Circoviridae, Gyrovirus) as the underlying etiology. Chicken anemia virus infects hemocytoblasts in the bone marrow and lymphoblasts in the cortex of the thymus, resulting in anemia with a hematocrit of 6-27% and pancytopenia. Gross lesions of CAV include thymic atrophy; bone marrow atrophy; hemorrhage in the proventricular mucosa, subcutaneous tissue, and skeletal muscle; and, less commonly, bursal atrophy. Panmyelophthisis and generalized lymphoid atrophy are commonly observed in chickens infected with CAV, with the thymus exhibiting the most severe lesions. When present, bursal lesions caused by CAV are less severe than those induced by IBDV, and include lymphofollicular atropy, few areas of necrosis, and infolding of the epithelium with hydropic degeneration and proliferation of reticular cells. In contrast, infection with IBDV frequently results in marked to severe lymphofollicular bursal atrophy, hemorrhage, edema, heterophilic inflammation, and hyperplasia of the bursal epithelium, sometimes resulting in a pseudoglandular appearance.(2,6)

The contributor discusses immunosuppression and decreased humoral immunity caused by IBDV infection, which renders infected chicks more susceptible to disease. Immunosuppression is most severe in chicks exposed to the virus within 2-3 weeks of hatch, and manifests clinically as impaired protective response to vaccination, increased incidence of secondary infections, poor feed conversion, and increased rates of carcass condemnation at processing. Interestingly, although T lymphocytes are resistant to infection with IBDV, the virus does cause thymic atrophy, thymocyte apoptosis, and impaired cell-mediated immunity, in addition to the expected impairment of humoral immunity that results from depletion of IgM+ B lymphocytes in the cloacal bursa, spleen, and cecal tonsils. Infection with IBDV is also thought to impair innate immunity, compromising the phagocytic activity of macrophages.(7) The Harderian gland is a component of the local immune system of the upper respiratory tract, and its function is also impaired by IBDV infection.(2)

The United States was considered free of the very velogenic (vvIBD) form of the disease; however, an outbreak of vvIBD was recently reported in 2009.(8) The source of the most recent disease outbreak has not been determined. Field veterinarians and diagnosticians should be aware of this report and consider vvIBD in the differential diagnosis when clinical signs, epidemiologic evidence, and diagnostic data indicate it as a potential etiology.


1. Cheville NF: Studies on the pathogenesis of Gumboro disease in the bursa of Fabricius, spleen, and thymus of the chicken. Am J Pathol 51:527-551, 1967
2. Eterradossi N, Saif YM: Infectious bursal disease. In: Diseases of Poultry, ed. Saif YM, 12th ed., pp. 185-208. Blackwell Publishing, Ames, IA, 2008
3. Ley DH, Yamamoto R, Bickford AA: The pathogenesis of infectious bursal disease: serologic, histopathologic, and clinical chemical observations. Avian Dis 27:1060-1085, 1983
4. M+�-+ller H, Islam MR, Raue R: Research on infectious bursal disease-the past, the present and the future. Vet Microbiol 97:153-165, 2003
5. Rodriguez-Chavez IR, Rosenberger JK, Cloud SS, Pope CR: Characterization of the antigenic, immunogenic, and pathogenic variation of infectious bursal disease virus due to propagation in different host systems (bursa, embryo, and cell culture). III. Pathogenicity. Avian Pathol 31:485 - 492, 2002
6. Schat KA, van Santen VL: Chicken infectious anemia. In: Diseases of Poultry, ed. Saif YM, 12th ed., pp. 211-249. Blackwell Publishing, Ames, IA, 2008
7. Sharma JM, Kim I-J, Rautenschlein S, Yeh H-Y: Infectious bursal disease virus of chickens: pathogenesis and immunosuppression. Dev Comp Immunol 24:223-235, 2000
8. Stoute ST, Jackwood DJ, Sommer-Wagner SE, Cooper GL, Anderson ML, Woolcock PR, BickfordAA, Senties- Cue CG, Charlton BR: The diagnosis of very virulent infectious bursal disease in California pullets 53:321-326, 2009
9. Withers DR, Young JR, Davison TF: Infectious bursal disease virus-induced immunosuppression in the chick is associated with the presence of undifferentiated follicles in the recovering bursa. Viral Immunol 18:127-137, 2005

Click the slide to view.

3-1. Bursa of Fabricius

3-2. Bursa of Fabricius

3-3. Bursa of Fabricius

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