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Toxoplasma gondii-naive cats and cats previously infected orally with T. gondii tissue cysts were inoculated with soluble tachyzoite antigens plus adjuvant or adjuvant alone. Toxoplasma gondii-specific IgM and IgG were measured in serum, aqueous humor, and cerebrospinal fluid (CSF). The Goldman-Witmer coefficient (C value) for ocular or central nervous system (CNS) antibody production was calculated for aqueous humor or CSF samples positive for T. gondii-specific antibodies. Following inoculation with adjuvant plus soluble tachyzoite antigens, ocular and CNS T. gondii-specific IgG C values increased in the three previously infected cats. Following inoculation with adjuvant, the two previously infected cats had increases in ocular and CNS T. gondii-specific IgG C values. Ocular (2/3 cats) or CNS (1/3 cats) T. gondii-specific IgG C values of over 1 were detected in some T. gondii-naive cats following inoculation with adjuvant plus soluble tachyzoite antigens. The results of this study suggest that T. gondii-specific IgG C values of over 1 in aqueous humor or CSF do not prove active ocular or CNS infection in all cats.

Objectives: To develop Toxoplasma gondii B1 gene polymerase chain reaction (PCR) for use with aqueous humor of cats, and to report PCR and antibody detection results in naturally exposed cats with and without uveitis., Sample Population: Serum and aqueous humor samples from client-owned, healthy cats (n = 23) and client-owned cats with uveitis (n = 43)., Procedure: T gondii-specific IgM and IgG were measured in serum and aqueous humor from all cats. The Goldman-Witmer coefficient for ocular antibody production was calculated for cats positive for T gondii-specific IgM or IgG in aqueous humor. Aqueous humor from all cats was assessed by the B1 gene PCR., Results: T gondii was detected in aqueous humor by PCR from 2 of 23 (8.7%) healthy cats and 8 of 43 (18.6%) cats with uveitis. T gondii-specific IgM in either serum or aqueous humor was detected in 5 of 8 (62.5%) cats with uveitis and T gondii in aqueous humor. All cats with uveitis and T gondii in aqueous humor had anterior segment disease. In 5 of 8 (62.5%) cats with uveitis and T gondii in aqueous humor, ocular production of T gondii antibodies was not detected. T gondii was not detected in aqueous humor from 14 of 17 (82.4%) cats with ocular production of T gondii-specific antibody., Conclusions: The presence of T gondii in aqueous humor may correlate to clinical disease in some, but not all, cats., Clinical Relevance: T gondii-specific aqueous humor antibody tests and PCR should be used together to aid in the diagnosis of ocular toxoplasmosis in cats.

Normal and asymptomatic feline immunodeficiency virus (FIV)-infected adult cats were inoculated orally with Toxoplasma gondii tissue cysts to assess differences in clinical disease, T. gondii serologic test results, hematologic results, and oocyst shedding. There was no difference between FIV-naive and FIV-infected cats in terms of clinical illness and duration of oocyst shedding following primary exposure. Both groups of cats developed significant decreases in neutrophil counts following primary inoculation with T. gondii; FIV-infected cats that were neutropenic prior to inoculation with T. gondii developed the most profound decreases in neutrophil numbers. Both FIV-naive and FIV-infected cats became lymphopenic during acute T. gondii infection; however, only FIV-naive cats developed lymphocytosis in the recovery stage. FIV-infected cats had lower total CD4+ and higher total CD8+ T-lymphocyte counts than FIV-naive cats prior to inoculation with T. gondii, but changes in these lymphocyte subsets were similar between groups of cats during the first several weeks after inoculation. Toxoplasma gondii infection had neither an ameliorating nor enhancing effect on T-lymphocyte subset abnormalities in FIV-infected cats during acute or chronic infection. Both groups of cats developed comparable levels of T. gondii-specific IgM and IgG antibodies and T. gondii antigen-specific lymphocyte blastogenic responses following primary inoculation. Both groups of cats were fed T. gondii tissue cysts 66 wk following primary exposure and both groups were solidly immune as evidenced by a lack of oocyst shedding and only minor changes in IgM but not IgG antibodies.

Objective: To evaluate the long-term clinical outcomes and serologic changes in cryptococcal antigen and antibody titers in cats with confirmed Cryptococcus neoformans infection., Design: Prospective case series., Animals: 47 cats with cryptococcosis., Procedure: Cats included in this study were determined to have cryptococcosis on the basis of identification of C neoformans on histologic or cytologic examination, isolation of C neoformans in culture, or positive serologic test results for cryptococcal antigens. Information concerning the signalment, history, physical examination findings, FeLV and feline immunodeficiency virus status, serologic testing, treatment, and outcome for each cat was requested on a survey form. Follow-up measurements of serum cryptococcal antigen and antibody titers were requested for all surviving cats., Results: Signalment and clinical signs of cats with cryptococcosis reported here were consistent with previous reports. Treatment consisted primarily of azole antifungal drugs. All cats were seronegative for cryptococcal antibody titers, whether tested initially or at follow-up examination. All but 1 cat tested were seropositive for cryptococcal antigens when initially tested. Cats with and without clinical signs of C neoformans infection were seropositive for cryptococcal antigens months to years after initial diagnosis of cryptococcosis., Clinical Implications: The results of this study indicate that serum titers to cryptococcal antigens in cats can persist with or without clinical signs for months to years after an initial diagnosis of cryptococcosis is made. Repeated evaluation of serum cryptococcal antigen titers is advised during the treatment of cats to monitor progress, evaluate prognosis, and guide cessation of treatment.

Objective: To evaluate antigen recognition patterns of serum IgM, IgG, and IgA from queens and their kittens as a method of diagnosing neonatal toxoplasmosis., Animals: 5 pregnant queens were inoculated orally with Toxoplasma gondii tissue cysts during gestation (18 to 44 days). On various days after parturition (0 to 97), serum was obtained from queens and kittens (n = 19)., Procedure: Tissues from most kittens were assessed for T gondii infection by bioassay in mice. Serum samples were evaluated by IgM, IgG, and IgA western blot immunoassays for the presence of T gondii antibodies. Antigens recognized by kitten serum samples, but not by the corresponding queen serum sample, were considered to indicate neonatal infection with T gondii., Results: Using the results of western blot immunoassay, 8 of 19 kittens (age, 2 to 97 days) were determined to be infected with T gondii. Western blot immunoassay results correlated well with bioassay results, identifying 7 of 8 bioassay-positive kittens. Western blot immuno-assay additionally identified 1 kitten as infected, but tissues from the kitten had not been bioassayed. In each of the 5 kittens that developed clinical signs of toxoplasmosis, the diagnosis of neonatal toxoplasmosis was supported by results of the western blot immunoassays., Conclusion and Clinical Relevance: Comparison of queen and kitten T gondii antigen recognition patterns of IgM, IgG, and IgA can be used for antemortem diagnosis of neonatal toxoplasmosis.

Based on seroprevalence studies, approximately 30% of the cats in the United States have been infected by T gondii. Cats are the only species that pass the environmentally resistant oocyst in feces. Sporulated oocysts are infectious to humans and the organism can cause significant disease in immunocompromised people and transplacentally-infected babies. Clinical illness including liver disease, lung disease, central nervous system disease, fever, and uveitis occur in some infected cats. Veterinarians need to be able to identify T gondii infection in cats because of potential public health risks and during the workup of clinical diseased cats. Oocyst shedding by cats is of short duration, but can be detected by fecal examination. There are currently no serological tests that can accurately determine when a cat has shed oocysts in the past. The combination of serological test findings, clinical signs of disease, exclusion of other causes, and response to anti-Toxoplasma drugs is required to make the diagnosis of antemortem++ clinical toxoplasmosis in cats.

Cats were experimentally inoculated parenterally with the ME49 strain of Toxoplasma gondii to characterize the efficacies of two different dosages of orally administered clindamycin hydrochloride in the treatment of ocular toxoplasmosis. Concentrations of clindamycin hydrochloride at levels previously suggested to be inhibitory to T. gondii replication in vitro were achieved in the serum and aqueous humor but not in the cerebrospinal fluid. Antibiotic therapy, initiated 7 days after inoculation, resulted in no significant difference in the morphometric severity of ocular posterior segment lesions compared with that in the control groups. Treatment appeared to blunt T. gondii-specific immunoglobulin M production but had no significant effect on immunoglobulin G titers. Paradoxically, clindamycin administration was associated with increased morbidity and mortality from hepatitis and interstitial pneumonia, which are characteristic of generalized toxoplasmosis. Serum tumor necrosis factor alpha activity was detected at moderate levels in all groups of cats and correlated with the severity of clinical disease. The results of the study suggest that clindamycin, when administered at this specific time interval following inoculation, does not ameliorate ocular lesions and has a detrimental effect on the clinical course of acute, experimental toxoplasmosis in cats. The factors responsible for and the relevance of this detrimental effect to naturally occurring toxoplasmosis in humans and pet cats were not clear from the study but may relate to an antibiotic-associated decrease in the antitoxoplasmic activity of phagocytic cells responsible for the control of T. gondii.

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.

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.

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)

Sixteen pregnant queens were inoculated orally with tissue cysts of Toxoplasma gondii, and fetal membranes and offspring were examined for T gondii infection by bioassay in mice. Queens appeared clinically normal, although all shed T gondii oocysts. Toxoplasma gondii was isolated from tissues of 7 of 33 fetuses or kittens from 5 litters (at 13, 23, 26, 27, and 29 postinoculation days) from 8 queens euthanatized between 10 and 31 postinoculation days. Infection with T gondii was found in kittens from all 8 litters from the 8 queens that were allowed to undergo parturition and nurse their kittens. A total of 43 kittens were born to these 8 queens. Toxoplasma gondii was isolated from tissues of 26 of 40 kittens bioassayed; in 3 kittens, tissues were not available for bioassay. Toxoplasmosis was severe in full-term kittens born to 5 queens; all 25 kittens from these litters died or were ill by 24 days of age. Anorexia, lethargy, hypothermia, and sudden death were the most common manifestations. Cytologic examination of peritoneal fluid aspirate samples and determination of hepatic-associated enzyme concentrations in affected kittens, as well as measurement of anti-T gondii antibodies in serum of kittens and queens, were helpful in the diagnosis of neonatal toxoplasmosis. Transplacental transfer of anti-T gondii antibodies was not observed in cats. Toxoplasma gondii oocysts were found in fecal samples of 3 kittens from different litters at 16, 24, and 63 days of age.

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.

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.

Cytometrographic studies and urethral pressure profiles were performed to objectively assess the functional status of the urinary bladder and urethra in 9 dogs with congenital ectopic ureters. Functional abnormalities of the urinary bladder or urethra were detected in 8 of 9 (89%) dogs. Cystometrographic evidence of reduced bladder capacity was detected in 4 (44%) dogs, and abnormalities in urethral pressure profiles were consistent with urethral incompetence in 6 (67%) dogs. Dogs with urethral pressure profile abnormalities were treated with phenylpropanolamine hydrochloride, and the urethral pressure profile was reevaluated. Urethral pressure measurements obtained before surgery (3 dogs) and after phenylpropanolamine (6 dogs) were used to predict the likelihood of continence after surgery. Predicted outcomes included continence maintained without medication (3 dogs), continence maintained with phenylpropanolamine (2 dogs), and persistent incontinence despite phenylpropanolamine administration (4 dogs). After surgical repair of ectopic ureters, 2 of 9 (22%) dogs were continent without medication, and 2 (22%) maintained continence with phenylpropanolamine treatment. Various degrees of incontinence persisted in 5 of 9 (56%) dogs, 4 of which had urethral incompetence that had been documented as poorly responsive to phenylpropanolamine administration prior to surgery. Predicted outcomes were consistent with actual outcomes in 8 of 9 (89%) dogs, with predictions of incontinence proving accurate in 4 of 4 (100%) dogs and predictions of continence proving accurate in 4 of 5 (80%) dogs. Urodynamic assessment of dogs with ectopic ureters appears to be valuable for identifying concurrent functional abnormalities of the urinary bladder and urethra and for predicting postoperative outcome.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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.

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)

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.

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 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.

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.

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.

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.

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.

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.

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.

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.