Histopathology can be integrated with production, examining multiple birds at various ages, or comparing normal to affected. This allows assessment of the development and resolution of lesions, with consideration of severity, and the length of time that the disease presents a stress for the flock.

In consideration of the immune system, histopathology surveys can include only organs of the immune system, primarily bursa of Fabricius and thymus, but also spleen, bone marrow and cecal tonsil when appropriate. When the immune system pathology is examined relative to ongoing issues in the digestive or respiratory system, or skin or bone, it is possible to look at interactions of diseases as they develop relative to immune system injury.

Infectious bursal disease is the dominant immunosuppressive viral disease in broiler production. In broilers that are not vaccinated in endemic regions, infectious bursal disease virus infection can occur at a young age and cause permanent immunosuppression. With modification of the disease by passive immunity and acquired vaccinal immunity, it is possible to delay the age of infection to an older age, and to influence the recovery of the bursa from lymphocytolytic infection. In my experience, administering vectored Gumboro vaccine on day 1 proceeds without histopathologic lesions to the bursa and begins to establish acquired immunity. These factors become important in minimizing clinical immunosuppression, and the overall influence of infectious bursal disease.

Chicken infectious anemia virus is a common immunosuppressive cohort to infectious bursal disease. The classical form of chicken infectious anemia involves vertical transmission of virus from a seronegative hen. The chick hatches with no maternal immunity, and experiences severe damage to blood-forming elements in the bone marrow and to lymphocytes in the lymphoid tissues, primarily the thymus. This leads to anemia, leukopenia, thrombocytopenia and clinical blue-wing syndrome. In most broiler operations, maternal immunity to chicken anemia virus exists to some degree, and the classical form of chicken infectious anemia is mostly prevented. The common problem observed today with chicken infectious anemia occurs following the decline of maternal immunity. In this situation, broilers experience a secondary infection with chicken anemia virus, that can result in severe lymphocytic depletion in the thymus in a subpopulation. In this situation, the bone marrow is substantially spared, in contrast to the neonatal infection in an immunologically naïve chick. The occurrence of simultaneous infectious bursal disease and chicken infectious anemia can cause lesion patterns supportive of combined B- and T-lymphocyte immunodeficiency. This situation is variably expressed clinically as inclusion body hepatitis, gangrenous dermatitis, coccidiosis, and respiratory disease.

Additional viral diseases that are associated with the development of lymphocytic depletion in the bursa and thymus include viral enteritis, viral arthritis (reoviral tenosynovitis), Newcastle disease, and Marek’s disease. These observations are based on lesions observed in histopathology surveys of broiler production programs, but are also supported by experimental studies of the individual diseases. Experimental studies of mycotoxicosis have revealed that commonly encountered mycotoxins can cause also immunosuppression.

Understanding the age of onset and the severity of immunosuppression can provide insight to the application of mitigation strategies to improve immunesy.

Frederic J. Hoerr, DVM, PhD, Dipl. ACVP, ACPV
Veterinary Diagnostic Pathology, LLC, Fort Valley, Virginia 22652