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)
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
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)
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.
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)