Page 1306 - Veterinary Immunology, 10th Edition
P. 1306

coding for tumor necrosis factor (TNF-α) receptors and other co-
  VetBooks.ir  stimulatory molecules also result in loss of helper T cell function.

                  Cases of common variable immunodeficiency have been recorded
               in horses. Although they resemble primary immunodeficiencies in

               their sporadic nature and severity, they usually occur in animals
               over 3 years of age. Typically, these horses present with recurrent
               infections that are not responsive to medical treatment. Bacterial
               meningitis may be a consistent feature. Their serum contains only

               trace levels of IgG and IgM, no detectable IgG3, and very low IgA
               levels. Sometimes individual IgG subclasses are deficient, whereas
               IgA levels are normal. T cell numbers are normal, but B cells are
               undetectable, and there is no response to the B cell mitogen

               lipopolysaccharide. On necropsy, there are no B cells in lymphoid
               organs, blood, or bone marrow. Some horses may have severe liver
               disease, a feature also seen in humans. It is suspected that these
               individuals have an underlying defect that is only expressed when

               the immune system is stressed by infection. Other cases have
               included horses between 2 and 5 years old with a selective IgM
               deficiency. Many develop a concurrent lymphosarcoma, and they
               may have excessive regulatory T cell function.



               Foal Immunodeficiency Syndrome


               This primary immunodeficiency syndrome was first described in
               the highly inbred Fell and Dales pony breeds. It presents as a B cell

               immunodeficiency accompanied by a profound anemia. Affected
               foals appear normal at birth but fail to thrive. Their hematocrit and
               B cell numbers decline over 4 to 12 weeks until clinical disease
               develops. Affected animals lack germinal centers and plasma cells.
               Their B cell numbers decline to less than 10% of normal and serum

               immunoglobulin levels drop rapidly once maternal antibodies are
               catabolized. The loss of these immunoglobulins coincides with the
               development of clinical disease. T cell numbers remain within the

               normal range. Animals develop severe respiratory disease caused
               by opportunistic pathogens such as adenoviruses and from
               diarrhea caused by Cryptosporidium. At the same time, they develop
               a profound progressive, nonregenerative anemia that alone may be
               sufficient to cause death. Foals inevitably die or are euthanized by 1






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