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Biomedical subjects

M R Lappin

Publications and source records attributed to M R Lappin.

At least 55 records · Page 3Linked to original sources

Comparison of clinical signs, diagnostic findings, organisms isolated, and clinical outcome in dogs with bacterial pneumonia: 93 cases (1986-1991).

Medical records were reviewed for 93 dogs with bacterial pneumonia from which transtracheal aspiration samples were obtained for culturing of Mycoplasma spp and aerobic bacteria. On the basis of culture results, there were 65 Mycoplasma-positive dogs, including 7 dogs for which only Mycoplasma spp were isolated, and 28 Mycoplasma-negative dogs. Most dogs were > 5 years old, and differences in breed or gender distribution among the 3 groups of dogs were not detected. Hematologic and serum biochemical analysis results did not differ significantly between Mycoplasma-positive and Mycoplasma-negative dogs. Fifty-three of 93 (57%) dogs had a concurrent medical problem that may have predisposed them to developing bacterial pneumonia as a sequelae to aspiration or immunosuppression. Mycoplasma-positive dogs were significantly (P < 0.005) more likely to have > 1 species of bacteria isolated from their transtracheal aspiration samples. Clinical outcome was favorable when antimicrobials were selected on the basis of antimicrobial susceptibility results for the other bacterial isolates and not on results of the antimicrobial activity against Mycoplasma spp. It could not be determined whether Mycoplasma spp were primary pathogens or only opportunists.

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Comparison of methods for estimation of Toxoplasma gondii-specific antibody production in the aqueous humor of cats.

Intraocular production of Toxoplasma gondii-specific antibody in cats has been estimated by comparing the ratio of T gondii-specific antibody in aqueous humor and serum with the ratio of total immunoglobulins in serum and aqueous humor (Goldmann-Witmer coefficient; aqueous antibody coefficient; C value). It has been proposed that in human beings, comparison of the ratio of T gondii-specific antibody in aqueous humor and serum with the ratio of antibodies against a nonocular pathogen in serum and aqueous humor is more accurate than methods using total immunoglobulin quantification. We developed an ELISA for detection of calicivirus-specific antibodies in the serum and aqueous humor of cats. By evaluating calicivirus-specific antibody concentrations in the aqueous humor of healthy and diseased cats, calicivirus was assessed as a nonintraocular pathogen. The ratio of T gondii-specific antibodies in the aqueous humor and serum and the ratio of calicivirus-specific antibodies in serum and aqueous humor were evaluated as a means of estimating intraocular T gondii-specific antibody production. A field strain of feline calicivirus was isolated, cultured, and purified. A calicivirus-specific IgG ELISA was developed for detection of feline calicivirus-specific IgG in serum and aqueous humor. Calicivirus-specific IgG was measured in the serum and aqueous humor from 3 groups of control cats. Results suggested that calicivirus is a nonintraocular pathogen in cats and that calicivirus IgG detected in aqueous humor is attributable to leakage across a damaged blood-ocular barrier.(ABSTRACT TRUNCATED AT 250 WORDS)

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Detection of Toxoplasma gondii-specific IgA in the serum of cats.

An ELISA for detection of Toxoplasma gondii-specific IgA in feline serum was developed. A group of cats (n = 7) was inoculated orally with T gondii bradyzoites. Toxoplasma gondii-specific serum IgM, IgG, and IgA responses were followed sequentially by use of the ELISA for 34 weeks. Serum IgA was detected later than IgM or IgG, and was detected in most cats on week 34 after inoculation. None of the cats was seropositive for IgA during the oocyst-shedding period. A group of client-owned cats with suspected clinical toxoplasmosis and a group of healthy cats were tested for T gondii-specific IgA in serum. A trend toward association of T gondii-specific IgA in serum of cats with ocular disease was observed.

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Detection of Toxoplasma gondii-specific IgA in the aqueous humor of cats.

Toxoplasma gondii-specific IgA, IgM, and IgG were measured by ELISA in the serum and aqueous humor of 29 client-owned cats with endogenous uveitis and 7 specific-pathogen-free cats tested sequentially for 20 weeks after inoculation with T gondii. Local antibody production in aqueous humor was estimated by multiplying the aqueous humor-to-serum T gondii-specific antibody ratio by the serum-to-aqueous humor total IgG (C value) or calicivirus-specific IgG (CTC value) ratio. Evidence for local production of antibody in aqueous humor was defined as C value greater than 8 or CTC value greater than 1. Toxoplasma gondii-specific IgM CTC values, IgG CTC values, or IgA CTC values greater than 1 were detected in the aqueous humor of 18 of 29 (62.1%) client-owned cats with endogenous uveitis; 2 cats had IgA CTC values greater than 1 without detectable IgM or IgG in aqueous humor. Toxoplasma gondii-specific IgM was not detected in the aqueous humor of experimentally inoculated cats before or after inoculation. Immunoglobulin G C values greater than 8 were detected in all 7 experimentally inoculated cats and ranged from 10.4 to 145.5. Immunoglobulin G C values greater than 8 were first detected 4 to 8 weeks after T gondii inoculation and were undetectable by week 16 after inoculation. Immunoglobulin A C values greater than 8 were detected in 4 of 7 cats and ranged from 12.7 to 264.3. Immunoglobulin A C values greater than 8 were first detected 4 to 8 weeks after inoculation, and were detected in 2 cats during week 20 after inoculation. It was concluded that some cats infected with T gondii develop detectable concentrations of T gondii-specific IgA in aqueous humor.

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Long-term antibody responses of cats fed toxoplasma gondii tissue cysts.

As part of a long-term study on immunity to oocyst shedding, 12 4-6-mo-old cats were inoculated orally with tissue cysts of the ME-49 strain (6 cats) or the TS-2 strain (6 cats) of Toxoplasma gondii. Two cats fed the ME-49 strain died or were killed because of acute toxoplasmosis 12 and 13 days after inoculation (DAI), respectively. On day 39 after primary infection, 5 cats (2 infected with the ME-49 strain and 3 infected with the TS-2 strain) were challenged orally with tissue cysts of the ME-49 strain. One cat died following rechallenge infection due to causes unrelated to toxoplasmosis. Seventy-seven months after primary infection, the remaining 9 cats were challenged orally with tissue cysts of the P89 strain of T. gondii. Blood samples were obtained weekly or monthly and sera were analyzed for antibodies to T. gondii using the modified agglutination test (MAT), the Sabin-Feldman dye test (DT), and the enzyme-linked immunosorbent assay (ELISA) for IgM (IgM-ELISA) or IgG (IgG-ELISA). The MAT was performed using both formalin-fixed (FF) and acetone-fixed (AF) tachyzoites. The MAT (FF) was the most sensitive test; cats seroconverted within 14 DAI and high titers (> 10,000) persisted > 6 yr, although cats had no clinical signs. The MAT titers using the AF detected recent exposure and titers declined sharply after 2 mo postinoculation. DT and ELISA titers were lower and developed slower than MAT titers. Fluctuations in antibody titers were limited to 8-fold during the 6-yr observation period. Anamnestic serum antibody responses were seen in 2 cats after the final challenge, but not after first challenge.

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Opportunistic infections associated with retroviral infections in cats.

Naturally occurring infection of cats with feline leukemia virus and feline immunodeficiency virus is common. A wide variety of clinical manifestations occur in retrovirus-infected cats including gastrointestinal tract disease, respiratory tract disease, central nervous system disease, ophthalmic disease, hepatic disease, urogenital tract disease, dermatologic disease, hematologic disease, and musculoskeletal disease. Clinical signs are often directly attributable to the primary viral infection, but because both feline leukemia virus and feline immunodeficiency virus can induce immunodeficiency, opportunistic secondary infections may cause the clinical manifestations of disease in some cats. Diagnosis, treatment, and zoonotic potential of the common opportunistic agents associated with feline retroviral infections are reviewed.

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Multifocal myositis associated with Sarcocystis sp in a horse.

Multifocal myositis was diagnosed in a 7-year-old Quarter Horse gelding on the basis of history and findings on physical examination, serum biochemical analysis, electromyography, and microscopic examination of frozen sections of muscle biopsy specimens. Histologic examination of the muscle specimen revealed multifocal accumulations of histiocytes, lymphocytes, and plasma cells, with attendant myofiber degeneration and necrosis. Parasitic cysts with morphologic characteristics of Sarcocystis sp were found in regions of myocyte degeneration and necrosis, and in regions of normal muscle. Based on a tentative diagnosis of Sarcocystis sp-induced myositis, the horse was treated with trimethoprim/sulfamethoxazole and pyrimethamine for 28 days, phenylbutazone for 5 days, and paddock rest for 30 days. At the end of treatment, the horse had gained 35 kg, its appetite had returned to normal, and muscle mass was returning to normal. Sarcocystis fayeri is the only Sarcocystis sp reported in equine muscle in the United States and is rarely associated with acute myositis or muscle atrophy. The development of clinical signs in this horse could have been the result of an underlying immunosuppression or infection with a particularly pathogenic strain or large infective dose of S fayeri.

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Dynamic cardiomyoplasty for treatment of idiopathic dilatative cardiomyopathy in a dog.

In a dog with advanced dilatative cardiomyopathy, dynamic cardiomyoplasty resulted in improvement in clinical status and systolic function. Dynamic cardiomyoplasty involved surgical isolation of the right latissimus dorsi muscle on its neurovascular pedicle, transposition of the muscle into the thoracic cavity, wrapping the ventricles with the muscle, and implantation of a myostimulator for cardiosynchronous stimulation of the muscle. After a 2-week period, the latissimus muscle underwent a 50-day period of progressive burst stimulation to transform the muscle to a fatigue resistant phenotype. Thereafter, the muscle received cardiosynchronous stimulation at a 3:1 R-wave-to-burst ratio. This procedure may offer hope for long-term treatment of dilatative cardiomyopathy in dogs.

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Clinical ehrlichiosis in a cat.

Clinical ehrlichiosis was diagnosed in a cat from Colorado on the basis of cytologic, serologic, and clinical findings. Clusters of gram-negative organisms that were morphologically similar to morulae of Ehrlichia spp were found only in mononuclear cells. The cat had clinical signs that were referable to infection by a rickettsial organism, and antibodies against E canis (titer, 1:80) and E risticii (titer, 1:40) were detected in serum. Exclusion of other obvious causes inducing similar clinical signs, and positive clinical response to doxycycline, an antibiotic with known antirickettsial actions, aided in diagnosis. The cat was clinically normal within days following initiation of treatment, and was clinically normal, as well as seronegative for antibodies against E canis and E risticii, 1,365 days after discharge.

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Pathogenesis and treatment of feline rhinitis.

Diagnosis and treatment of feline rhinitis, like canine rhinitis, can be a frustrating experience for the veterinary practitioner. Having sound knowledge of the possible etiologies involved and using a systematic diagnostic approach makes the workup of these challenging cases much easier. Selection of appropriate therapy based on a definitive diagnosis makes treatment rewarding. This article discusses the pathogenesis and treatment of a variety of causes of feline rhinitis.

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Toxoplasma gondii-specific antibodies in the aqueous humor of cats with toxoplasmosis.

We decided to determine whether Toxoplasma gondii-specific IgM or IgG is produced locally or is deposited in the aqueous humor of T gondii-naive cats after primary or secondary inoculation with T gondii. Cats were orally inoculated with T gondii tissue cysts during weeks 0 and 36. Aqueous humor and serum T gondii-specific IgM and IgG were measured, using ELISA, during weeks 0, 2, 4, 6, 8, 12, 16, 20, 26, 34, 38, 40, 42, 44, 48, 56, 62, 66, and 72 after primary oral inoculation. Total immunoglobulin-based Goldmann-Witmer coefficients were calculated to verify intraocular antibody production. Toxoplasma gondii-specific IgM was not detected in the aqueous humor of any cat. Data indicate that cats have transient local production of T gondii-specific IgG in the aqueous humor after primary and secondary oral inoculations with T gondii tissue cysts. The intraocular immune response to systemic T gondii infection may signal ocular recruitment of antigen-specific lymphocytes that function independently from the general humoral response to T gondii infection. Cautious interpretation of results that suggest intraocular production of T gondii-specific IgG in cats with uveitis is warranted.

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Feline serum antibody responses to Toxoplasma gondii and characterization of target antigens.

The Toxoplasma gondii-specific target antigens for feline immunoglobulin M (IgM) and immunoglobulin G (IgG) immune responses were studied longitudinally using western blot immunoassay in 8 cats experimentally inoculated with T. gondii strain ME49. Multiple antigens were recognized by IgM and IgG during the course of infection. Dense bands were associated with 12 antigens in the IgM western blot immunoassay and 30 antigens in the IgG western blot immunoassay. Immunoglobulin M responses were maximal on week 4 postinoculation (PI) and were greatly diminished by week 20 PI. Immunoglobulin G responses were maximal on week 12 PI. On week 20 PI, the 19-kDa (6/8 samples), 26-kDa (8/8 samples), 28-kDa (8/8 samples), 31-kDa (7/8 samples), 35-kDa (6/8 samples), 51-kDa (6/8 samples), 55-kDa (7/8 samples), and 65-kDa (7/8 samples) antigens were recognized most commonly in the IgG western blot immunoassay. When the western blot immunoassay results were compared to enzyme-linked immunosorbent assay (ELISA) results, there was no clear advantage to the development of IgM-ELISA, IgG-ELISA, IgM western blot immunoassay, or IgG western blot immunoassay using a single antigen instead of multiple antigens as the detection system for the diagnosis of recent infection.

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Feline zoonotic diseases.

Many of the feline zoonoses occur more frequently in veterinary personnel owing to their direct contact with cats and the potential for exposure to infected body tissue or fluids. Infection of humans with Afipia felis, Yersinia pestis, Francisella tularensis, and other aerobic/anaerobic bacteria may cause great discomfort and in some situations terminal illness. Although many systemic fungal agents infect humans and cats, only Sporothrix schenckii has been shown to infect humans following direct exposure to infected cats. Various parasites, enteric protozoans and bacteria, and Toxoplasma gondii infections also may cause significant human illness. Therefore, routine handling of cats may expose human personnel in a veterinary facility to an array of important or emerging feline-associated human illnesses that occur in the United States.

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Feline immunodeficiency virus predisposes cats to acute generalized toxoplasmosis.

This study was designed to examine the effects of a pre-existing, clinically asymptomatic feline immunodeficiency virus (FIV) infection on a primary challenge with Toxoplasma gondii. Parenteral challenge of FIV-infected cats with tachyzoites of the ME49 strain of T. gondii caused a precipitous drop in all lymphocytes (CD4+, CD8+, and B cells) and generalized severe toxoplasmosis. The predominant postmortem lesions included acute and often fatal interstitial pneumonia, dominated histologically by macrophages, and multifocal to coalescing hepatic necrosis. Immunohistochemistry revealed numerous T. gondii antigen and tachyzoites in macrophages and other cell types in the lung lesions. The proliferative response of peripheral blood mononuclear cells to specific (T. gondii antigen) and nonspecific (Concanavalin A) mitogens was defective in the dually infected cats, suggesting marked immunosuppression. In contrast to the dually infected cats, cats infected only with T. gondii developed a transient, mild clinical disease characterized by anorexia, lethargy, and multifocal chorioretinitis. Lymphocyte changes in T. gondii-infected cats included an early pan-lymphopenia followed by reestablishment of all lymphocyte subset profiles. These cats also showed a reduced proliferative response to Concanavalin A at 1 week after challenge, but a measurable in vivo response to T. gondii antigens, as evidenced by in vitro lymphocyte proliferation in the absence of a mitogenic stimulus. These results show that infection of cats with FIV-NCSU, markedly enhances their susceptibility to a primary T. gondii infection and provides a model to study the mechanisms of the underlying immunological defect(s) occurring early after HIV infection that may predispose individuals to development of acquired immunodeficiency syndrome and associated diseases.

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A feline model of ocular toxoplasmosis.

UNLABELLED: PURPOSE. This study was performed to characterize the clinical, serologic, histopathologic, and immunohistochemical features of an experimental model of ocular toxoplasmosis in cats. METHODS: Seven specific pathogen-free cats were inoculated in the right carotid artery with 5 x 10(3) tachyzoites of the ME49 strain of Toxoplasma gondii. Control cats received heat-killed tachyzoites. RESULTS: Progressive, bilateral, multifocal retinal, and choroidal inflammatory foci developed in the principal cats, beginning 5 to 8 days postinoculation (PI). Lesion development peaked 3 weeks PI, and the lesions varied in size from pinpoint to 5 mm, had a predilection for the central tapetal fundus, and were more numerous ipsilateral to the side of inoculation. Resolution of the lesions 21 to 70 days PI was characterized by foci of tapetal destruction and retinal degeneration. Fluorescein angiography showed disruption of the blood-retinal barrier at the level of the retinal pigmented epithelium, and occasional retinal vasculitis and perivasculitis. Mild anterior uveitis developed in four cats 10 to 13 days PI. Aside from a slight febrile response 2 to 3 days PI, no physical abnormalities were observed. T. gondii antigens were detected intermittently in the serum of four of seven cats as early as 8 days PI. T. gondii-specific immunoglobulin M titers were present on day 7 PI and continued to increase until 28 days PI. Immunoglobulin G production was documented on day 13 PI, and titers continued to increase throughout the study. Evidence of anterior uveal antibody production (mean Goldmann-Witmer coefficient [C value], 80.7; range, 13.4 to 236.6) was present in 11 of 14 eyes on day 70 PI. On histopathologic evaluation 70 days PI, multifocal granulomatous chorioretinitis, with retinal degeneration, retinal vasculitis, and lymphocytic-plasmacytic anterior uveitis, was documented. Tissue cysts in the retina and choroid were found with mouse inoculation of tissue suspensions, immunohistochemical studies, and histopathologic examination. CONCLUSIONS: This nonfatal, noninvasive method of inducing ocular toxoplasmosis may prove to be a useful model for investigation of toxoplasmi retinochoroiditis, particularly with the recent characterization of a naturally occurring, immunosuppressive feline lentivirus with properties similar to human immunodeficiency virus.

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Comparison of latex agglutination, indirect immunofluorescent antibody, and enzyme immunoassay methods for serodiagnosis of Rocky Mountain spotted fever in dogs.

Indirect immunofluorescent antibody (IFA), latex agglutination (LA), and enzyme immunoassay (EIA) methods were compared for evaluation of the serum antibody responses of dogs experimentally and naturally exposed to spotted fever-group rickettsiae. Selected sera (obtained on days 1, 42, 53, 124, 145, 236, 255, 264, and 292) were examined from three 8-month-old female Beagles inoculated with Rickettsia rickettsii on days 34 and 250 of the study. A second group of dogs comprised three 8-month-old female Beagles inoculated with R montana on days 34 and 102. Subsequently, these dogs were inoculated with R rickettsii on day 250. Serum samples were obtained from the second group of dogs on days 1, 96, 103, 132, 180, 215, 292, and 494. A third group consisted of 21 naturally exposed dogs, from which sequentially obtained serum samples were available, and which had clinical signs compatible with Rocky Mountain spotted fever. Clinical signs of disease in dogs of the third group resolved after treatment with tetracycline (22 mg/kg of body weight, PO, q 8 h) was instituted. At least 2 sequentially obtained serum samples from each dog were tested. In general, the first sample was obtained just prior to treatment and the convalescent serum samples were obtained at weekly or greater intervals thereafter. For correlation and reactivity data, an IFA test for IgG/IgM (using heavy and light chains-specific conjugate) was used as the reference standard for comparison of results with those of the other tests.(ABSTRACT TRUNCATED AT 250 WORDS)

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Detection of Toxoplasma gondii antigen-containing immune complexes in the serum of cats.

Enzyme-linked immunosorbent assays for the detection of Toxoplasma gondii antigen-containing IgM immune complexes (T gondii-specific IgM-IC) and IgG immune complexes (T gondii-specific IgG-IC) in the serum of cats were developed. Serum from clinically ill, naturally infected cats; healthy, naturally infected cats; and healthy cats experimentally inoculated with T gondii was assayed. All combinations of T gondii-specific IgM, IgG, antigens, IgM-IC, and IgG-IC were detected in naturally infected and experimentally infected cats. Clinically ill cats and cats with ocular signs of toxoplasmosis were more likely than healthy cats to have T gondii-specific IC in serum. It was concluded that T gondii-specific IC form in the serum of cats, may play a role in clinical disease development, and affect the results of T gondii-specific IgM, IgG, and antigen serologic assays.

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