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  • Author or Editor: Niels C. Pedersen x
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Summary

Three commercial FeLV vaccines, (A, B, and C) were purchased on the open market and administered to 8- to 20-week-old specific-pathogen-free kittens, according to manufacturers' instructions. A similar group of nonvaccinated kittens served as controls. All kittens were challenge-exposed oronasally with virulent FeLV 4 weeks after the final vaccination. Serum samples were monitored for FeLV-p27 antigenemia using an elisa at 1- to 2-week intervals for at least 16 weeks after the last day of challenge exposure. Kittens that were either transiently (1 to 4 weeks) or never viremic during this period were counted as recovered, whereas kittens that became viremic and retained viremia for at least 10 weeks were counted as persistently viremic. The 3 vaccines were found to be 39% (vaccine C), 28% (vaccine B), and 17% (vaccine A) efficacious in preventing persistent viremia in immunized, compared with nonimmunized kittens.

Free access
in Journal of the American Veterinary Medical Association
in Journal of the American Veterinary Medical Association

Summary

Fifteen specific-pathogen-free cats were experimentally infected with FeLV; 8 cats recovered after transient or nondetectable viremia, and 7 cats became persistently viremic. Four additional cats served as noninfected controls. Antibodies to whole FeLV (elisa and immunoblot [western] analysis), antibodies to fixed FeLV-infected cells, and virus-neutralizing antibodies were monitored for as long as 3 years after infection. As a group, cats that recovered after acute infection developed higher titer of these various antibodies than did cats that became persistently viremic. However, specific combination or titer of antibodies was not always found in recovered cats or in persistently viremic cats. Six cats that had recovered from acute FeLV infection nearly 3 years earlier were reinfected with the same virus. Three of the cats appeared to be resistant to reinfection, 2 cats became transiently viremic, and 1 cat became persistently viremic. Slight and transient anamnestic elisa-detectable antibody response to whole virus was seen after reinfection; immunofluoresence- and western blot-detectable responses were not greatly enhanced. Five FeLV-recovered cats were monitored for 2 years; FeLV infection spontaneously recurred in 1 cat.

Free access
in Journal of the American Veterinary Medical Association

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)

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in American Journal of Veterinary Research

Objective—

To determine what risk factors, other than genetic predisposition, contribute to the incidence of feline infectious peritonitis (FIP) in private breeding catteries and animal shelters.

Design—

Cats from 7 catteries and a shelter were observed monthly for 1 year. At each visit, cats were examined, fecal samples were collected for determination of feline coronavirus shedding, and blood samples were collected for determination of coronavirus antibody titers. Diagnostic tests were performed on all cats that died of FIP.

Animals—

275 purebred or random-bred cats that were kept by private breeder-owners in homes.

Results—

24 cats died of FIP during the study. Development of FIP was not associated with cattery, mean cat number, mean age, sex, cattery median coronavirus antibody titer, husbandry and quarantine practices, caging and breeding practices, or prevalence of concurrent diseases. However, risk factors for FIP Included individual cat age, individual cat coronavirus titer, overall frequency of fecal coronavirus shedding, and the proportion of cats in the cattery that were chronic coronavirus shedders. Deaths from FIP were more frequent in fall and winter, and on the basis of analysis of cattery records, the number of deaths varied yearly. Epidemics (> 10% mortality rate) were reported at least once in 5 years in 4 catteries.

Clinical Implications—

Elimination of FIP from a cattery is only possible by total elimination of endemic feline enteric coronavirus (FECV) infection. The most important procedure to reduce FECV from catteries is elimination of chronic FECV shedders. (J Am Vet Med Assoc 1997;210:1313–1318)

Free access
in Journal of the American Veterinary Medical Association

Objective—

To determine, by use of a reverse transcriptase-polymerase chain reaction (RT-PCR) test, patterns of fecal shedding of feline coronavirus among cats.

Design—

Prospective observational study.

Animals—

275 purebred cats from 6 private catteries and 40 specific-pathogen-free (SPF) laboratory-reared cats.

Procedure—

40 SPF cats were experimentally inoculated with crude fecal extract containing feline enteric coronavirus (FECV). Fecal and plasma samples were collected every 4 days and evaluated by use of RT-PCR and indirect immunofluorescence assays, respectively, to correlate RT-PCR results with fecal infectivity and to determine patterns of FECV shedding and anti-FECV IgG production in acutely infected cats. The 275 cats in private catteries were monitored for 1 year. Fecal and blood samples were collected every 1 to 3 months and assayed by use of RT-PCR and serologic tests to determine patterns of coronavirus shedding and cofactors for high frequency shedding.

Results—

Results of the RT-PCR test in SPF cats were directly correlated with fecal extract infectivity. Overall, 370 of 894 (41%) fecal samples collected from cattery and shelter cats contained infectious levels of coronavirus. Of 121 cats from which multiple samples were collected, 11 never shed virus and 35, 65, and 10, respectively, shed virus with low, moderate, and high frequency. High frequency shedding was associated with age and cattery of origin, but not with sex or concurrent disease. Stress associated with parturition and lactation did not induce shedding in queens. Kittens did not shed coronavirus before they were 10 weeks old, even when nursed by shedding mothers.

Clinical Implications—

A large proportion of cats in multiple-cat environments shed coronavirus at any given time, but most undergo cycles of infection and shedding, recovery, and reinfection. Infection is acquired from chronically shedding cats and from infectious cats undergoing transient primary infection. Chronically shedding cats cannot be identified on the basis of antibody titer or signalment, but must be identified on the basis of the results of serial fecal RT-PCR tests. (J Am Vet Med Assoc 1997;210:1307–1312)

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective

To characterize 2 strains of Haemobartonella felis by use of molecular techniques.

Animals

35 specific-pathogen-free cats, 6 months to 4 years old.

Procedure

Intraperitoneal or IV inoculation with blood containing H felis small form (Hfsm, 18 cats) or H felis large form (Hflg, 11 cats); 6 cats were uninfected controls. Hfsm was evaluated for capability to cross-protect against the more virulent Hflg. Morphology of both strains was compared by light microscopy of Wright-Giemsa-stained blood smears, and the 16S rRNA genes were sequenced.

Results

Infection with Hflg induced signs of depression, fever, and severe macrocytic normochromic anemia with nucleated erythrocytes. More than 95% of erythrocytes were parasitized. Inoculation with Hfsm and uninfected control blood induced mild or no clinical signs and no hematologic abnormalities. Anti-Hfelis lgG was first detected on postinoculation day (PID) 21, and increased to maximal titer of 400 by PID 28. Reactivated infection was observed in 8 of 29 cats (4 Hfsm and 4 Hflg), with 5% parasitized erythrocytes during the later attack. On PID 8, Hflg-inoculated cats had positive results of polymerase chain reaction analysis (PCR) that persisted until cats were treated with doxycycline or oxytetracycline; Hfsm-inoculated cats had positive PCR results that persisted for duration of observation (3 months).

Conclusions

Genetically and morphologically distinct strains of H felis infect cats in the field. The level of genetic difference suggested that these strains may be different species or genera.

Clinical Relevance

PCR is a critical diagnostic aid to detect occult Haemobartonella spp infection, as well as response to treatment and clearance of the organism. (Am J Vet Res 1998;59:1581-1588)

Free access
in American Journal of Veterinary Research

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.

Free access
in Journal of the American Veterinary Medical Association

Summary

Although feline immunodeficiency virus (fiv) and the unrelated retrovirus feline leukemia virus (FeLV) are associated with acquired immune deficiency in cats, experimental and field evidence indicates that coinfection with both viruses may lead to more serious disease syndrome. A third feline retrovirus, feline syncytium-forming virus (FeSFV), which is far more prevalent than either fiv or FeLV and is considered nonpathogenic in nature, is consistently coisolated from sick, fiv-infected cats. To determine the potential role of FeSFV in enhancement of FIvV-mediated disease, persistent FeSFV infection was established in 14 of 24 nine-month-old cats. Four months later, half the FeSFV-infected and half the noninfected cats were inoculated with blood obtained from a cat persistently infected with the Petaluma strain of fiv. At postinoculation week 17, 1 male cat infected with only fiv died of bacterial bronchopneumonia that could have been attributed to fiv-induced acquired immune deficiency-like syndrome. However, none of the remaining cats had clinical illness, whether infected with either virus alone or coinfected with both viruses. As early as postinoculation week 6, decreases were observed in the CD4+ to CD8+ T-lymphocyte ratio of both groups of cats inoculated with fiv. Infection with FeSFV had no effect on the CD4+ to CD8+ T-cell ratio, Mitogen stimulation assays and total WBC count were unaffected by FeSFV infection, although an increase in numbers of neutrophils from FeSFV-infected cats was consistent, especially when compared with the decrease observed after fiv infection. Overall, results of the study indicate that coinfection with FeSFV may not enhance progression of the fiv-induced early stages of disease and that the positive correlation between FeSFV and fiv-induced acquired immune deficiency-like syndrome is attributable to a common mode of transmission, rather than to a synergistic effect of coinfection.

Free access
in American Journal of Veterinary Research