Biomedical subjects
Publications and source records attributed to M R Lappin.
Monoclonal gammopathy associated with plasmacytic gastroenterocolitis was diagnosed in a dog. Treatment consisted of immunosuppressive drugs and dietary manipulation. The gammopathy resolved. Fifteen months after initial diagnosis, the dog had a relapse of intestinal disease and recurrence of the gammopathy. After inducing a second remission, the gammopathy again resolved.
Serologic evidence of infection by Toxoplasma gondii, feline leukemia virus, feline coronaviruses, or feline immunodeficiency virus (FIV) is commonly found in cats with uveitis. Serum samples from 124 cats with uveitis were assayed by use of ELISA for the detection of T gondii-specific immunoglobulin M (IgM), IgG, and circulating antigens (Ag), as well as an ELISA for feline leukemia virus Ag, an ELISA for antibodies to FIV, and an indirect fluorescent antibody assay for antibodies to feline coronaviruses. Serologic evidence of infection by 1 or more of the infectious agents was detected in 83.1% of the samples. Serologic evidence of T gondii infection, defined as the detection of T gondii-specific IgM, IgG, or Ag in serum, was found in 74.2% of the samples. The seroprevalence of T gondii infection was significantly greater in cats with uveitis than in healthy cats from a similar geographic area. Serum samples from cats with serologic evidence of both T gondii and FIV infections were more likely to contain T gondii-specific IgM without IgG than samples from cats with serologic evidence of T gondii infection alone. Cats with serologic evidence of FIV and T gondii coinfection had a higher T gondii-specific IgM titer geometric mean and a lower T gondii-specific IgG titer geometric mean than did cats with serologic evidence of T gondii infection alone. Serologic evaluation for T gondii infection should include assays that detect IgM, IgG, and Ag, particularly in cats coinfected with FIV.
Serum and aqueous humor samples, collected from 14 clinically normal cats and 96 cats with clinical evidence of intraocular inflammation, were assayed with ELISA for Toxoplasma gondii-specific immunoglobulin M (IgM), T gondii-specific IgG, T gondii-specific antigens, total IgG, and total IgM. Additionally, serum was assayed with ELISA for feline leukemia virus p27 antigen and antibodies against the feline immunodeficiency virus as well as with an immunofluorescent antibody assay for antibodies against feline coronaviruses. Calculation of the Goldmann-Witmer coefficient (C-value) for the T gondii-specific antibodies detected in aqueous humor established the likelihood of local antibody production. Serologic evidence of present or prior infection by an infectious agent was found in 81.9% of the clinically affected cats from which serologic results were available (77/94 cats). Seropositive results for toxoplasmosis were found in 74.0% of the clinically affected cats. Anterior segment inflammation was found in 93.1% (81/87 cats from which information was available) of the clinically affected cats, most of which were older males. Toxoplasma gondii-specific antibodies were not detected in the aqueous humor of 6 seropositive, clinically normal cats. The C-values for aqueous T gondii antibodies were greater than 1 in 44.8% of the cats and greater than 8 in 24.0% of the cats. Response to treatment with clindamycin HCl was positive in 15/20 (75%) of the T gondii-seropositive, clinically affected cats treated with this drug. In 13/15 (86.7%) T gondii-seropositive, clinically affected cats having a C-value greater than 1, response to treatment with clindamycin HCl was positive.(ABSTRACT TRUNCATED AT 250 WORDS)
Lymphoblast transformation in whole blood was assessed by 3H-thymidine incorporation after stimulation by concanavalin A and Toxoplasma gondii secretory and intracellular antigens in samples from cats with experimentally induced toxoplasmosis. Toxoplasma gondii-specific immunoglobulin M, immunoglobulin G, and circulating antigens were also measured throughout the study period. Lymphocytes from all cats were responsive to concanavalin A pre- and post-inoculation with T. gondii. Suppression of mitogen-stimulated lymphoblast transformation during the course of infection was not observed. Both the secretory and intracellular antigens stimulated lymphoblast transformation in many cats from Week 2 to Week 52 post-inoculation. Lymphoblast transformation was stimulated more frequently by intracellular antigens (66.25%) than by secretory antigens (48.75%). Lymphoblast transformation was not induced by T. gondii antigens in any cat prior to appearance of T. gondii-specific antibodies in serum or during the oocyst shedding period. Cats with persistent antigenemia had the most consistent lymphoblast transformation results induced by T. gondii-specific antigens.
The effect of primary phase feline immunodeficiency virus (FIV) infection on clinical signs, hematological values, Toxoplasma gondii oocyst shedding, T. gondii-specific serology, T. gondii-specific cell-mediated immune responses, non-specific cell-mediated immune responses, and lymphocyte subpopulations from cats with experimentally induced chronic toxoplasmosis was studied. No significant clinical or hematologic abnormalities were noted following inoculation with FIV. T. gondii-specific IgM was significantly increased, concanavalin A, T. gondii tachyzoite antigen and T. gondii secretory antigen induction of lymphocyte transformation were significantly suppressed, and CD4+ cell numbers were significantly decreased following inoculation with FIV. The changes were attributed to FIV effects on the immune system and resultant activated toxoplasmosis.
Lymphocytic-plasmacytic enteritis, a chronic inflammatory intestinal disease, was diagnosed in 2 cats. In 1 cat, recurrence of clinical signs after initiating treatment was attributed to relapse of the inflammatory intestinal disease, but was found to be attributable to relapsing toxoplasmosis secondary to immunosuppressive drug therapy. Treatment with clindamycin resolved the recurrent toxoplasmosis. In the second cat, clinical signs of toxoplasmosis did not develop, but serologic testing yielded evidence of active toxoplasmosis. Treatment with clindamycin caused the titers to decrease. Relapsing toxoplasmosis may be responsible for apparent resistance to treatment in cats for inflammatory intestinal disease being treated with immunosuppressive drugs.
Dysautonomia, or autonomic nervous system dysfunction, was diagnosed in a 1-year-old dog. Clinical signs of disease included diarrhea, vomiting, prolapse of nictitating membranes, and urinary incontinence. Bilateral keratoconjunctivitis sicca, xerostomia, and decreased anal sphincter tone were also observed. On the basis of response to atropine, results of intradermal histamine testing and gastric motility studies, and ocular response to parasympathomimetics and sympathomimetics (direct and indirect acting), autonomic nervous system function was determined to be abnormal. Treatment with metoclopramide hydrochloride and bethanechol chloride resulted in improved attitude, appetite, Schirmer tear test response, and decrease in frequency of vomiting within 24 hours. Bladder function and anal tone improved within 3 weeks.
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Serologic prevalence of Toxoplasma gondii infection was determined using enzyme-linked immunosorbent assays detecting immunoglobulin M (IgM), immunoglobulin G (IgG), and circulating T. gondii antigens (Ag) in 81 healthy cats and 107 cats with clinical signs referable to toxoplasmosis. A higher prevalence of infection was detected using the three assays together in healthy cats, clinically ill cats, and combined healthy and clinically ill cats than when IgG class antibody detection alone was used. IgM titers greater than or equal to 1:256 and IgG titers greater than or equal to 1:512 were present more frequently in cats with clinical signs of disease. Prevalence of present or prior infection as defined by these three assays combined increased with advancing age in both groups of cats.
Subclinical Toxoplasma gondii infection was induced in young and adult cats by oral administration of tissue cysts. An antibody-capture ELISA to detect anti-Toxoplasma IgM-class antibodies in the serum of cats was developed. The serologic response to experimental infection was followed in the 2 groups of cats by use of anti-Toxoplasma IgM and IgG detection. This study shows that anti-Toxoplasma IgM-class antibody titers develop early in the course of experimental infection in cats and that the combination of IgM- and IgG-class antibody titer measurement can aid in the detection of recent subclinical toxoplasmosis.
An ELISA was developed to detect circulating antigens of Toxoplasma gondii in the serum of cats. For the experiment, toxoplasmosis was induced in a group of cats by oral administration of bradyzoites. An ELISA that detects anti-Toxoplasma IgG, an ELISA to detect circulating antigens, and fecal examinations were performed on samples from each cat for 1 year after inoculation. When coupled with IgG-class antibody measurement, antigen detection can aid in the diagnosis of some cases of subclinical feline toxoplasmosis.
Renal tubular carcinoma was believed responsible for hematuria and extreme leukocytosis in a dog. Other paraneoplastic syndromes possibly associated with this neoplasm included fever, thoracolumbar hyperesthesia, and anemia attributable to myelophthisis. All clinical and clinicopathologic abnormalities resolved after unilateral nephrectomy. Neutrophil cytochemical stains were used to differentiate leukemoid reaction from myelocytic leukemia as the cause of the leukocytosis. The extreme leukocytosis in this dog may have been leukemoid reaction caused by production of colony-stimulating factor by the renal tubular carcinoma.
Idiopathic detrusor instability was diagnosed as the cause of urinary incontinence in 2 dogs and a cat. The diagnosis was based on abnormal cystometrographic findings and by exclusion of other causes of detrusor hyperactivity. Anticholinergic or combined anticholinergic, antispasmodic, and local anesthetic treatment resolved the clinical signs in all 3 animals. Increased threshold volumes after treatment were documented by cystometrography in one dog and in the cat.
A dog with severe pulmonary disease caused by Filaroides osleri (Oslerus osleri) infection was anesthetized with thiopental sodium IV for diagnostic bronchoscopy. The dog was ventilated continuously during bronchoscopy with a high-frequency jet ventilator (using a rate of 100 breaths/min, drive pressure of 20 psi, and inspiratory fraction of 0.30). High-frequency jet ventilation provided satisfactory ventilatory support during bronchoscopy despite the dog's pulmonary disease.
Sodium Tc-pertechnetate accumulated in the mammary glands of a male cat. It was determined that the uptake was attributable to gynecomastia induced by medroxyprogesterone acetate injections. Gynecomastia and pertechnetate uptake resolved following cessation of medroxyprogesterone acetate treatment.
Clinical toxoplasmosis was diagnosed in 15 cats by correlating serologic evidence of infection and clinical signs to either response to therapy or histopathologic demonstration of the organism. Ophthalmic manifestations, primarily involving the anterior segment, were common. Other common physical examination abnormalities included muscle hyperesthesia, fever, and weight loss. Response to therapy was variable, but administration of clindamycin hydrochloride resulted in resolution of all clinical signs not involving the eyes in surviving animals. This drug, alone or in combination with corticosteroids, led to total resolution of clinical signs in four of four cats with active retinochoroiditis and in six of nine cats with anterior uveitis. Four of the 15 cats had concurrent infection with feline immunodeficiency virus (FIV). Feline leukemia virus antigen or antibodies to feline infectious peritonitis virus were not detected.
The primary purpose of this study was to determine whether commercially available latex agglutination and indirect hemagglutination kits for the detection of Toxoplasma gondii-specific antibodies were capable of detecting T. gondii-specific immunoglobulin M (IgM) in the serum of cats. Serum samples from 35 cats containing either T. gondii-specific IgM, T. gondii-specific immunoglobulin G (IgG), or both were collected. Each serum sample was assayed using a latex agglutination kit, an indirect hemagglutination kit, an enzyme-linked immunosorbent assay (ELISA) for the detection of T. gondii-specific IgG, and an ELISA for the detection of T. gondii-specific IgM. When serum samples containing only T. gondii-specific IgM as determined by ELISA were assayed, the latex agglutination kit and the indirect hemagglutination kit detected antibodies in 33.3% and 13.3%, respectively. When T. gondii-specific IgG was present in a serum sample, the results from the latex agglutination kit, the indirect hemagglutination kit, and the IgG-ELISA were similar; however, there was a wide variation in titer magnitude results between the three assays. It was concluded that the latex agglutination kit and the indirect hemagglutination kit did not adequately detect T. gondii-specific IgM in feline serum.