Biomedical subjects

M R Lappin

Publications and source records attributed to M R Lappin.

76 records · Page 5Linked to original sources

PubMedDate not supplied

Effect of feline immunodeficiency virus infection on Toxoplasma gondii-specific humoral and cell-mediated immune responses of cats with serologic evidence of toxoplasmosis.

Serum samples from 89 cats with serologic evidence of toxoplasmosis were identified by using an enzyme-linked immunosorbent assay (ELISA) that detected Toxoplasma gondii-specific immunoglobulin M (IgM) or T. gondii-specific immunoglobulin G (IgG). Concurrent feline immunodeficiency virus (FIV) infection was detected in 36 cats using an ELISA for detection of FIV-specific IgG. The majority of the cats in both the FIV-seropositive and FIV-seronegative groups were male and > 5 years of age. FIV-seropositive cats were more likely to have T. gondii IgM titers without IgG (P < 0.05) or any T. gondii IgM titer (P < 0.05) than were FIV-seronegative cats. FIV-seronegative cats (1328) had a higher T. gondii IgG geometric mean titer than did FIV-seropositive cats (724) and were more likely to have T. gondii IgG titers > 1:2048 than were FIV-seropositive cats (P < 0.05). Cats with serologic evidence of both T. gondii and FIV infections had persistent T. gondii IgM titers for > 12 weeks. Lymphoblast transformation in response to concanavalin A, T. gondii-specific intracellular antigens, and T. gondii-specific secretory antigens was compared in T. gondii seropositive and FIV-seronegative cats, cats with serologic evidence of T. gondii infection alone, and cats with serologic evidence of concurrent FIV and T. gondii infections. Lymphocytes from all but one cat in the FIV-seropositive group responded to concanavalin A. Whereas lymphocytes from FIV-seronegative cats with serologic evidence of toxoplasmosis responded to T. gondii-specific antigens, four of five of the FIV-seropositive cats with concurrent serologic evidence of toxoplasmosis did not.

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PubMedDate not supplied

Association of hepatic necrosis with trimethoprim sulfonamide administration in 4 dogs.

Hepatic necrosis in association with trimethoprim-sulfonamide (TMS) combination therapy was diagnosed in 4 dogs based on history, clinical presentation, and examination of histopathologic specimens collected postmortem. Duration of TMS therapy prior to onset of clinical signs ranged from 4 to 30 days. The dose of TMS ranged from 18 mg/kg to 53 mg/kg bid. Despite supportive medical therapy, all dogs died or were euthanized due to hepatic failure. This report highlights the potential for hepatotoxicity during TMS therapy. Duration of therapy, type of TMS combination, and dose did not appear related to the development of toxicity. The low number of dogs affected suggests an idiosyncratic drug reaction.

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PubMedDate not supplied

Pulmonary thromboembolism in 29 dogs: 1985-1995.

Pulmonary thromboembolism (PTE) occurs as a complication to a number of commonly encountered clinical diseases. Antemortem recognition of this life-threatening disorder is hampered by nonspecificity of clinical signs. This retrospective study was performed to analyze clinical features, laboratory findings, imaging abnormalities, and concurrent postmortem diagnoses in 29 dogs with confirmed pulmonary embolism. A variety of clinicopathologic and radiographic abnormalities were noted but there were no pathognomonic findings for PTE. Arterial blood gas analyses were performed in 15 (52%) of 29 dogs; 12 (80%) of 15 exhibited hypoxemia and 15 (100%) of 15 had increased alveolar-arterial oxygen gradients. Response to supplemental O2 was variable and did not correlate with the presence or absence of additional pulmonary pathology on postmortem. At postmortem, 25 (86%) of 29 dogs had grossly visible emboli, 17 (59%) of 29 dogs had multiple disease processes, and 16 (55%) of 29 dogs had additional pulmonary pathology. PTE was suspected antemortem in 11 (38%) of 29 dogs. In dogs with respiratory signs consistent with PTE, the condition was a differential diagnosis in 11 of 17 animals; all had diseases previously reported to be associated with PTE. Neoplasia, systemic bacterial disease, and immune-mediated hemolytic anemia were diagnosed most frequently.

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PubMedDate not supplied

Functional urethral obstruction in 3 dogs: clinical and urethral pressure profile findings.

Three dogs with dysuria and urine retention caused by excessive functional urethral resistance are described. All dogs had clinical histories and urologic signs that previously would have been classified as detrusor-urethral dyssynergia. Diagnosis of functional urinary obstruction was established by exclusion of anatomic urinary obstruction and confirmed by urethral pressure profilometry. In 2 cases, multiple pressure deflections recorded in the urethral pressure profile suggested spasm of urethral musculature, whereas in a 3rd dog, abnormally high pressures were recorded along a portion of the proximal urethra. Functional urinary obstruction was associated with prostatitis in 1 dog and with a history of urethral calculi in 1 dog, and no underlying disorder could be identified in the remaining dog. All 3 dogs improved with medical treatments that included alpha adrenergic antagonists. The etiology, diagnosis, and pharmacologic management of functional urinary obstruction are discussed.

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