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)
Objective—To determine whether the active metabolite of leflunomide, A77 1726 (A77), inhibits replication of feline herpesvirus-1 (FHV-1) in cell culture.
Study Population—Crandell Rees feline kidney (CRFK) cell cultures.
Procedures—Cell cultures were inoculated with FHV-1 and treated simultaneously with concentrations of A77 ranging from 0 to 200μM. The antiviral effect of A77 was determined by use of conventional plaque reduction assays. The effect of A77 on viral load was determined via real-time PCR analysis, and transmission electron microscopy was used to evaluate the effect of A77 on viral morphology. To determine whether the antiviral effect was attributable to alterations in CRFK cell viability and number, CRFK cells were treated with various concentrations of A77 and stained with Annexin V and propidium iodide to assess apoptosis and a mitochondrial function assay was used to determine cell viability.
Results—Concentrations of A77 ≥ 20μM were associated with substantial reduction in plaque number and viral load. Concentrations ≥ 100μM were associated with complete suppression of plaque formation. At low concentrations of A77, clusters of intracytoplasmic virus particles that appeared to lack tegument and an external membrane were detected. Treatment of uninfected CRFK cell monolayers with A77 was associated with reduction in mitochondrial function with minimal evidence of apoptosis.
Conclusions and Clinical Relevance—Leflunomide may be an alternative to current calcineurin-based immunosuppressive protocols used in feline organ transplantation because of its antiherpesviral activity.