|
Deficiencies in Immunoglobulins |  |
| These may be acquired or congenital. Acquired deficiencies occur in neonates that do not receive adequate maternal antibodies (failure of passive transfer) or in older animals due to conditions that decrease active immunoglobulin synthesis. Failure of passive transfer of immunoglobulin occurs occasionally in all species that have colostrum as the major source of maternal antibodies. It is commonly associated with clinical problems in calves, lambs, and foals. Failure of passive
transfer can occur when the young animal fails to nurse properly during the first several days of life or when the dam’s colostrum contains low levels of specific antibodies. Theoretically, problems with the intestinal absorption of immunoglobulin in the milk also can occur. Immunoglobulin levels <400 mg/dL in a postnursing serum sample indicate a failure of passive transfer in foals. Removing calves from their dams too soon is a frequent problem in dairy herds and is a leading
cause of failure of passive transfer in dairy calves. Newborn animals that do not obtain adequate maternal antibodies often succumb to fatal bacterial or viral infections of the GI and respiratory tracts. |
|
Idiopathic (essential) hypogammaglobulinemia has not been described in animals other than humans, but undoubtedly it occurs. It is associated with excessive regulatory cell activity that depresses antigen-stimulated immunoglobulin synthesis to B lymphocytes. |
|
Hypogammaglobulinemia of clinical significance can be associated with any disorder that interferes with immunoglobulin synthesis. Tumors, such as plasma cell myelomas or lymphosarcomas that occasionally secrete large amounts of monoclonal antibody, can be associated with profound deficiencies of normal beneficial antibodies. This may be because the tumor cells are competing for necessary substrate substances with normal immunoglobulin-producing cells, or because
thymus-derived regulatory lymphocytes in the blood nonselectively inhibit the abnormal immunoglobulin production. Animals with tumors that produce monoclonal antibodies can have severe secondary infections. Some viral infections, eg, canine distemper and canine parvovirus, may damage the lymphoreticular system so severely that normal antibody production is virtually stopped. |
|
Congenital hypogammaglobulinemia (common variable immunodeficiency) has been recognized either by itself or in combination with deficiencies in cell-mediated immunity (combined immunodeficiency, see below). Deficiencies in IgG subclass synthesis have been seen in some breeds of cattle; IgM deficiency has been described in horses; and IgA deficiencies have been described in Beagles, German Shepherds, and Shar-Peis. Cattle with IgG subclass deficiency are
usually asymptomatic. Older foals with IgM deficiencies develop respiratory infections. Dogs with IgA deficiency, like their human counterparts, suffer mainly from chronic skin infections, chronic respiratory infections, and possibly allergies. The IgA deficiency of Beagles appears to be due to a defect in the secretion of IgA, because IgA-positive cells are present in normal numbers. Some German Shepherds seem to have lower IgA levels than other breeds and a higher incidence of GI
allergies. IgA deficiency in Shar-Peis is highly variable; some have negligible serum and secretory levels, and some have normal serum levels and low or negligible secretory levels. Like the German Shepherds, affected Shar-Peis have more problems than expected with allergies. Patients with common variable immunodeficiency have a higher than usual incidence of autoimmune disorders and autoantibodies (eg, autoimmune hemolytic anemia, thrombocytopenia, systemic lupus erythematosis).
Longterm treatment with broad-spectrum antibiotics is required and IV human g-globulin is usually needed. |
|
Transient hypogammaglobulinemia has been recognized most frequently in foals and puppies. It may be more common in Spitz-type puppies than in other breeds. It is congenital and manifest by a delay in development of active immunity associated with a maturational defect of both TH function and the B cell response to foreign antigens. Puppies with this condition develop recurrent respiratory infections at 1-6 mo of age but recover and are essentially
normal by 8 mo of age. Affected foals frequently develop clinical signs of hypogammaglobulinemia (usually respiratory infections) at ~6 mo of age when their maternal antibody reaches a very low level. After another 3-5 mo, they begin to produce immunoglobulin. Appropriate antibiotic treatment is often sufficient. |
