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- Author or Editor: Bruce A. Rideout x
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Summary
Between 1988 and 1991, feline immunodeficiency virus (fiv) infection status was evaluated in 1,160 cats examined at an oncology referral and general practice in Los Angeles, California. Twenty-nine (2.5%) cats were fiv positive. Neoplasia was present in 18 of the 29 (62%) cats. Sampling for neoplasia was intentionally biased in the oncology referral group. However, 33% (6/18) of fiv-infected cats with neoplasia originated from the general practice. Three neoplastic processes were observed; myeloproliferative disease (mpd; 5/18), lymphoma (lsa; 5/18), and squamous cell carcinoma (scc; 7/18). One cat had lsa and scc.
Extranodal sites of lsa were common (66%) in fiv-infected cats. Sites of lsa were submandibular and mesenteric lymph nodes, liver, kidneys, periorbital area, and diffuse (heart, pancreas, bladder). Sites of scc were sublingual (n = 2), nasal planum (n = 3), nasal planum and eyelids (n = 1), and mandible (n = 2). Feline leukemia virus co-infection was observed in 17% (5/29) of fiv-infected cats. The fiv-infected cats with mpd were young (range, 8 months to 13 years; median, 4 years) and had short survival duration (2, 6, 21, 134, 249 days) even in response to aggressive treatment. The fiv-infected cats with lsa were older (median age, 8 years; range, 4 to 14 years) and survived 60 days if untreated. Cats administered chemotherapy survived 39, 45, 217, and 243 days; the latter 2 cats had partial remission of 2 months' duration. Older fiv-infected cats had scc (median age, 12 years; remission range, 7 to 16 years) because of more frequent association of both diseases in older cats with outdoor environment.
Lymphocytic-plasmacytic lymphadenopathy was seen in 10 necropsied fiv-infected cats (4 without neoplasia, 3 with lsa, 1 with scc, and 2 with mpd). Lymphadenopathy associated with fiv may develop in one lymph node, and lymphoma may develop in another lymph node. Clinically, fiv-induced lymphadenopathy may be confused with progressive lymphoma.
Abstract
Objective—To investigate the effects of preexisting FeLV infection or FeLV and feline immunodeficiency (FIV) coinfection on the pathogenicity of the small variant of Haemobartonella felis (Hfsm, California variant) in cats.
Animals—20 FeLV infected, 5 FeLV-FIV coinfected, and 19 retrovirus-free cats.
Procedure—A client-owned cat, coinfected with FeLV and Hfsm, was the source for Hfsm. Inoculum 1 (FeLV free) was obtained by passage of source Hfsm through 4 FeLV-resistant cats. Inoculum 2 was obtained by further passage of Hfsm (inoculum 1) through 2 specific pathogenfree cats.
Results—A mild-to-moderate anemia started 21 days after inoculation, with its nadir occurring at 35 to 42 days after inoculation. Infection with Hfsm induced greater decrease in hemoglobin concentration in FeLV infected cats, compared with retrovirus free cats. Reticulocytosis, macrocytosis, and polychromasia of erythrocytes developed in anemic cats regardless of retrovirus infection status. Mean neutrophil counts decreased during the hemolytic episode. For most cats, the anemia was transient. Four FeLV infected cats, 1 of which was also FIV infected, developed fatal FeLV-associated myeloproliferative diseases. Of the surviving cats, 8 died over the next 24 months from other FeLV-related diseases. Hemolysis did not recur after the initial episode. Inoculum 1 induced more severe anemia than inoculum 2.
Conclusions and Clinical Relevance—Our results support the clinical observation that cats coinfected with FeLV and H felis develop more severe anemia than cats infected with H felis alone. Infection with Hfsm may induce myeloproliferative disease in FeLV infected cats. The small variant of H felis may lose pathogenicity by passage through FeLV-free cats. (Am J Vet Res 2002;63:1172–1178)
Abstract
Objective—To characterize infection patterns and identify factors associated with avian mycobacteriosis among zoo birds that were housed with infected enclosure mates.
Design—Matched case-control study.
Animals—79 birds with avian mycobacteriosis (cases) and 316 nondiseased birds (controls) of similar age and taxonomic group that were present in the bird collection of the Zoological Society of San Diego from 1991 through 2005.
Procedures—Inventory and necropsy records from all eligible, exposed birds (n = 2,413) were examined to determine disease incidence and prevalence in the exposed cohort. Cases were matched in a 1:4 ratio to randomly selected controls of similar age and taxonomic grouping. Risk factors for mycobacteriosis (demographic, temporal, enclosure, and exposure characteristics as well as translocation history) were evaluated with univariate and multivariable conditional logistic regression analyses.
Results—Disease prevalence and incidence were estimated at 3.5% and 8 cases/1,000 bird-years at risk, respectively. In the multivariable model, cases were more likely to have been imported into the collection, exposed to mycobacteriosis at a young age, exposed to the same bird species, and exposed in small enclosures than were controls. Odds for disease increased with an increasing amount of time spent with other disease-positive birds.
Conclusions and Clinical Relevance—The low incidence of mycobacteriosis and the risk factors identified suggested that mycobacteria may not be easily transmitted through direct contact with infected enclosure mates. Identification of risk factors for avian mycobacteriosis will help guide future management of this disease in zoo bird populations.
Abstract
OBJECTIVE To determine the incidence of and risk factors for clinical feline herpesvirus (FHV) infection in zoo-housed cheetahs and determine whether dam infection was associated with offspring infection.
DESIGN Retrospective cohort study.
ANIMALS 144 cheetah cubs born in 6 zoos from 1988 through 2007.
PROCEDURES Data were extracted from the health records of cheetahs and their dams to identify incident cases of clinical FHV infection and estimate incidence from birth to 18 months of age. Univariate and multivariable Cox proportional hazards models, controlling for correlations among cheetahs with the same dam, were used to identify risk factors for incident FHV infection.
RESULTS Cumulative incidence of FHV infection in cheetah cubs was 35% (50/144). No significant association between dam and offspring infection was identified in any model. Factors identified as significant through multivariable analysis varied by age group. For cheetahs up to 3 months of age, the most important predictor of FHV infection was having a dam that had received a preparturition FHV vaccine regimen that included a modified-live virus vaccine versus a dam that had received no preparturition vaccine. Other risk factors included being from a small litter, being born to a primiparous dam, and male sex.
CONCLUSIONS AND CLINICAL RELEVANCE This study provided the first population-level characterization of the incidence of and risk factors for FHV infection in cheetahs, and findings confirmed the importance of this disease. Recognition that clinical FHV infection in the dam was not a significant predictor of disease in cubs and identification of other significant factors have implications for disease management.