Acquired B lymphocyte deficiency and chronic enterocolitis in a 3-year-old quarter horse.

This case report describes a 3-year-old American Quarter Horse with acquired immunodeficiency. Clinical signs included chronic diarrhea due to Salmonella typhimurium and bacterial pneumonia. Characterization of the immunodeficiency involved in vivo phytohemagglutinin (PHA) intradermal testing, in vitro lymphocyte proliferation in response to concanavalin A, immunofluorescence flow cytometry data on blood lymphocytes, serum protein electrophoresis and immunoglobulin (Ig) quantification. A diagnosis of B lymphocyte deficiency with resulting deficiencies in serum IgG, IgA and IgM and a concurrent decrease in T cell function was made based on these tests. Postmortem examination revealed no evidence of lymphosarcoma. This case represents a variation of young adult-onset B cell deficiency not previously described in the literature.

Selective IgM deficiency and abnormal B-cell response in a foal.

Selective IgM deficiency was diagnosed in a 3-month-old Standardbred colt that was referred for chronic respiratory tract disease. Immunoglobulin quantification revealed normal IgG and IgA concentrations, but undetectable IgM concentration. Stimulation of blood lymphocytes with the T-cell mitogens concanavalin A and phytohemagglutinin yielded results within the normal range. However, stimulation with the B-cell mitogen lipopolysaccharide produced no response. A B-cell defect similar to that associated with several immunodeficiency disorders in people was suggested as the cause of the IgM deficiency in this colt.

Unusual selective immunoglobulin deficiency in an Arabian foal.

A 10-month-old Arabian foal was evaluated for a suspected immunoglobulin (Ig) M deficiency. Decreased to nondetectable concentrations of IgM, IgA, and IgG (T), and a normal concentration of IgG, were present. Results of in vitro testing of the blood lymphocyte blastogenesis showed a weak response to the B-cell mitogen, lipopolysaccharide (LPS), but normal responses to T-cell mitogens. Results of postmortem examination showed synovitis of the left tibiotarsal and both scapulohumeral joints. Atrophy and edema of the lymph nodes and lymphocyte depletion in the thymus and spleen were seen. A subacute inflammatory infiltrate was observed in the kidney, synovium, liver, and brain. Etiologic agents were not identified. This case represents a previously unreported form of immunodeficiency disease in the horse.

A lactogenic-immune-deficiency-syndrome in cows: unexplained phenomenon.

The majority of adult cows in a certain dairy herd, were found to have very low levels of immunoglobulins (Igs) in their colostrum. This phenomenon was defined by us as Lactogenic-Immune-Deficiency-Syndrome (LIDS). The mean IgG levels were 44.5 and 57.2 mg ml-1 respectively (on two different occasions) as compared to that of a control group which was 103.4 mg ml-1. The levels of Igs in the colostra of heifers from the same herd were found to be higher than those of adult cows. The degree of LIDS was found to be closely related to the age of cows in the herd. The low levels of Igs in the colostra were not directly linked to their concentrations in the sera of the affected cows. The relatively low amount of IgA in the affected colostra suggests that the local production in the lymph tissue associated with the mammary glands is impaired as well. In order to investigate the etiology of the phenomenon, tests were carried out to reveal whether bovine leucosis virus (BLV) infection or immune complexes were involved in the pathogenesis of LIDS. The results were negative. The etiology of LIDS remains for the time being unknown.

Relative IgA deficiency and small intestinal bacterial overgrowth in German shepherd dogs.

Serum immunoglobulin concentrations and densities of IgA-producing immunocytes in intestinal mucosa were compared in a group of clinically healthy dogs of various breeds, a group of clinically healthy German shepherd dogs, and a group of German shepherds with bacterial overgrowth in the proximal small intestine. Serum concentrations of IgA, but not IgM or IgG, were significantly lower in the clinically healthy German shepherd dogs than in other purebreed and mixbreed dogs, indicating that production of IgA by gut-associated lymphoid tissue might be relatively low in this breed. However, densities of IgA-producing cells were not significantly different comparing these two groups, suggesting that any impairment of mucosal IgA production is more likely to be related to defective synthesis or secretion of IgA than to reduced numbers of IgA-producing immunocytes. Comparable findings in German shepherd dogs with small intestinal bacterial overgrowth provided further indirect evidence that local immunity might be defective in this breed, since these luminal bacteria would be expected to stimulate mucosal IgA production. However, it is not clear whether such a defect is directly responsible for the overgrowth, or whether there is an indirect relationship between defective local immunity and bacterial overgrowth in German shepherd dogs.

Influence of parental serum immunoglobulins on morbidity and mortality of beagles and their offspring.

Serum IgA, IgG, and IgM concentrations were determined for Beagle sires and dams of 717 matings to assess the relationship of parental immunoglobulins with the morbidity and mortality of their pups. A significant relationship was not found between parental immunoglobulins and pup mortality. Pups born to dams with low serum IgA (P less than 0.001) and IgM (P less than 0.02) concentrations, however, were found to have an increased incidence of sneezing, coughing, nasal discharge, and conjunctivitis. Thirty-eight percent of pups born to dams with IgA less than or equal to 40 mg/dl developed these same conditions during the first 18 weeks of life, compared with 32% of pups of dams with IgA of 41 to 65 mg/dl and 27% of pups of dams with IgA greater than 65 mg/dl. Similarly, 41% of pups born to dams with low IgM (less than or equal to 135 mg/dl) developed abnormal respiratory tract signs, compared with 34% and 30% of pups born to dams with medium (136 to 175 mg/dl) and high (greater than 175 mg/dl) IgM, respectively. Serum IgA concentrations of the sires were also associated with abnormal respiratory tract signs in pups, but this influence was evident only at 10 to 18 weeks of age. To determine biologic variability of serum IgA, 60 Beagle dams were selected from 3 serum IgA categories, low (10 to 21 mg/dl), medium (60 to 80 mg/dl), and high (125 to 210 mg/dl). A second serum IgA was determined from a sample taken 2 years later.(ABSTRACT TRUNCATED AT 250 WORDS)

Survey of serum IgA, IgG, and IgM concentrations in a large beagle population in which IgA deficiency had been identified.

Concentrations of serum IgA, IgG, and IgM were determined for 829 adult Beagles from a commercial kennel in which several IgA-deficient dogs had been identified previously (index kennel). These values were compared with measurements of 100 adult dogs from another Beagle kennel (control kennel). After adjustment for differences in the ages and gender of the dogs, dogs from the index kennel had significantly (P less than 0.0001) lower IgA concentrations (mean, 46 mg/dl) than dogs from the control kennel (mean, 68 mg/dl). Regardless of kennel, males had significantly (P less than 0.01) higher IgA concentrations than did females. Dogs in the control kennel had significantly (P less than 0.04) higher IgG concentrations (mean, 2,649 mg/dl) than did dogs in the index kennel (mean, 2,478 mg/dl), and female dogs in the control kennel had significantly (P less than 0.05) higher IgM concentrations (mean, 189 mg/dl) than dogs of either sex in the index kennel (mean, 162 mg/dl) or male dogs in the control kennel (mean, 163 mg/dl). For both sexes, concentrations of IgA, IgG, and IgM increased with age.

Cryptosporidiosis associated with immunosuppression attributable to distemper in a pup.

Cryptosporidiosis, giardiasis, trichomoniasis, and distemper were diagnosed in a 6-month-old female Siberian Husky pup. Poor growth rate, mucopurulent ocular and nasal discharges, and diarrhea were observed. Results of immunologic studies revealed decreased serum IgG concentration and undetectable serum IgA concentration. Cultured lymphocytes yielded a less-than-adequate response to mitogen stimulation. The serum also contained a factor that suppressed mitogen stimulation in control cultured lymphocytes.

Acquired immunodeficiency in a seven-year-old horse.

A 7-year-old horse with no previous history of illness was determined to have a systemic infection of Rhodococcus equi. Rhodococcus equi was isolated from blood, tracheal fluid, and feces. Lymphopenia, failure to respond to concanavalin A and phytohemagglutinin lymphocyte stimulation testing, decreased concentrations of immunoglobulin (Ig)M, IgA, and IgG, low R equi antibody titer, histologic depletion of lymphoid tissue, and a failure to respond to antigenic stimulation led to the conclusion that both humoral and cell-mediated immunity were compromised. No cause for the acquired immunodeficiency could be determined.

IgA deficiency in shar-pei dogs.

Two shar-pei puppies examined because of signs of sinopulmonary disease, one of which also had skin disease, had deficient IgA concentrations. Deficient serum IgA concentrations also were confirmed in 30 of 39 (76.9%) clinically normal adult dogs in two colonies of shar-peis. Both courses of disease--sinopulmonary signs and chronic skin disease and a benign clinical course--have been reported in human patients with IgA deficiency. Thus, the shar-pei might be an appropriate model for studying the immunopathology of IgA deficiency in man.

Inherited dysgammaglobulinemia of chickens: reduced incidence of disease in parabiotic chimeras.

University of California, Davis (UCD) line 140 chickens develop a dysgammaglobulinemia characterized as selective 7S immunoglobulin (Ig) deficiency with elevated serum IgM levels. To study the role of bursal development on the expression of dysgammaglobulinemia in these birds, we examined the effect of bursacyte transfer to line 140 birds and parabiosis between UCD 140 and a control line of chickens on changes in serum IgM and 7S Ig levels. Bursacyte transfer was performed by injecting 18-day UCD 140 embryos (which had been cyclophosphamide treated on Day 15) with bursacytes from major histocompatibility complex B-matched control line (11 X 58) F1 birds. This transfer produced little change in the incidence of dysgammaglobulinemia in UCD 140 transfer birds (56%) compared to unmanipulated line 140 birds (60%). These data reflect a failure of line 140, rather than technique, because successful reconstitution was seen using line 11 X 58 birds injected with 11 X 58 bursacytes. In contrast, the generation of UCD 140/line 11 X 58 chimeras significantly reduced the incidence of dysgammaglobulinemia in line UCD birds. Indeed, fusion of the chorioallantoic vascular system (parabiosis) of UCD 140 and 11 X 58 embryos on Day 15 decreased the frequency of dysgammaglobulinemia of UCD 140 parabionts to 14% compared to 66% in unmanipulated line 140 controls. The success of parabiosis was 83% as determined by demonstrating chimerism with allogeneic blood groups. Moreover, the frequency of dysgammaglobulinemia in the 17% of parabionts that did not reveal chimerism was similar to unmanipulated UCD 140 chickens.

Biochemical and functional characterization of lymphocytes from a horse with lymphosarcoma and IgM deficiency.

Neoplastic lymphocytes from a horse with lymphosarcoma and IgM deficiency were analyzed for ability to grow in culture; surface and cytoplasmic IgM; functional activity in blastogenesis, cytoxicity, and suppressor assays; and activities of six enzymes involved in purine and pyrimidine metabolism. The cells lacked surface and cytoplasmic IgM. They had elevated activity of adenosine deaminase and reduced activity of purine nucleoside phosphorylase. Neoplastic cells were nonresponsive in blastogenesis assay and did not kill allogeneic lymphocyte target cells or YAC-1 targets in a lectin-dependent cytotoxicity assay, however, the cells were active in a suppressor assay. They were grown for 16 weeks in cultures supplemented with interleukin 2, during which time the cells retained suppressive activity. These results are consistent with a T cell lymphoma of suppressor cell origin, and may explain the deficiency of IgM observed in some horses with lymphoreticular neoplasms.

Suppressor lymphocyte activity in normal and immunodeficient horses.

Equine lymphocytes incubated with Con A and isolated on discontinuous BSA density gradients suppressed mixed lymphocyte reactions in a cell dose- and Con A dose-dependent manner. Suppressor lymphocytes were radiosensitive, even after the initial Con A incubation phase was completed. Suppressor activity was consistently demonstrated using peripheral blood mononuclear leukocytes from normal horses, but was absent in thymus cells and variably present in lymph node cells. Suppressor lymphocytes were present in horses with selective IgM deficiency, and within neoplastic lymph nodes from a horse with lymphosarcoma and concomitant IgM deficiency. Suppressor cells were not detected in 5 of 6 horses with severe combined immunodeficiency.