Advertisement

Effect of preexisting FeLV infection or FeLV and feline immunodeficiency virus coinfection on pathogenicity of the small variant of Haemobartonella felis in cats

Jeanne W. George DVM, PhD1,2, Bruce A. Rideout DVM, PhD3,4, Stephen M. Griffey DVM, PhD5, and Niels C. Pedersen DVM, PhD6
View More View Less
  • 1 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616.
  • | 2 Present address is Deptartment of Pathology, Microbiology and Immunology, University of California, Davis CA 95616.
  • | 3 Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616.
  • | 4 Present address is San Diego Zoological Park, 2920 Zoo Dr, San Diego, CA 92112-0551.
  • | 5 Department of Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616.
  • | 6 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616.

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)