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  • Author or Editor: Niels C. Pedersen x
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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

Abstract

Objective—To describe clinical and epidemiologic features of an outbreak of feline calicivirus (FCV) infection caused by a unique strain of FCV and associated with a high mortality rate and systemic signs of disease, including edema of the face or limbs.

Design—Observational study.

Animals—54 cats naturally infected with a highly virulent strain of FCV.

Procedure—Information was collected on outbreak history, clinical signs, and characteristics of infected and exposed cats.

Results—A novel strain of FCV (FCV-Kaos) was identified. Transmission occurred readily via fomites. Signs included edema and sores of the face and feet. Mortality rate was 40%, and adults were more likely than kittens to have severe disease (odds ratio, 9.56). Eleven (20%) cats had only mild or no clinical signs. Many affected cats had been vaccinated against FCV. Viral shedding was documented at least 16 weeks after clinical recovery.

Conclusions and Clinical Relevance—Outbreaks of highly virulent FCV disease are increasingly common. Strains causing such outbreaks have been genetically distinct from one another but caused similar disease signs and were resistant to vaccination. All cats with suspicious signs (including upper respiratory tract infection) should be handled with strict hygienic precautions. Sodium hypochlorite solution should be used for disinfection following suspected contamination. All exposed cats should be isolated until negative viral status is confirmed. Chronic viral shedding is possible but may not be clinically important. This and similar outbreaks have been described as being caused by hemorrhagic fever-like caliciviruses, but hemorrhage is uncommonly reported. Virulent systemic FCV infection is suggested as an alternative description. (J Am Vet Med Assoc 2004:224:241–249)

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in Journal of the American Veterinary Medical Association