Feline calicivirus: unveiling data on viral inactivation

01 December 2010
10 mins read
Volume 1 · Issue 3
Feline calicivirus: unveiling data on viral inactivation

Abstract

Feline calicivirus (FCV) is an important and widespread virus of the feline population. As a member of the Caliciviridae family, FCV mutates readily in nature, and this has resulted in the recent emergence of a highly virulent haemorrhagic systemic strain. Despite the increased concern about this feline pathogen, little is still known on potential FCV virucidal compounds. On the other hand several experiments on the inactivation behaviour of various surface disinfectants have used FCV as a surrogate to monitor norovirus survival in order to minimize their impact on public health. This has led to a considerable number of studies generating a huge amount of data on FCV inactivation. These findings are presented here and may be useful to veterinary nurses who can improve their practice by minimizing FCV transmission.

Feline caliciviruses (FCVs) are recognized as an important, highly infectious pathogen of cats, with a widespread distribution in the feline population (Radford et al, 2007; Patel and Heldens, 2009). FCV was first described in 1957 by Fastier and usually causes mild, acute, and self-limiting upper respiratory tract disease that causes frequent nasal and ocular discharge (Figure 1) (Fastier, 1957; Radford et al, 2007).

Other commonly found signs are oral vesicles/ulcers, conjunctivitis, rhinitis, tracheitis, pneumonia, fever, anorexia and lethargy. Morbidity is high, mortality may achieve 30% in very young kittens and recovery is followed by a prolonged carrier state. Aerosols and fomites are usually the transmission vehicle and the virus is often carried to susceptible cats by human handlers, including veterinary staff. The incubation period is 2 to 6 days and the virus is shed in large numbers by infected cats (Radford et al, 2007). Recuperating cats may continue to shed the virus for several months and stress is known to precipitate the recrudescence of the disease and therefore additional shedding (Murphy et al, 1999; Radford et al, 2007).

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