Feline Viral Respiratory Disease: Etiology, Clinical Signs and the Carrier State
Feline herpesvirus-1 (FHV1) and feline calicivirus (FCV) are the two major viral causes of upper respiratory tract disease
(URD) in cats.
Feline herpesvirus 1 is a large, enveloped, DNA virus that causes feline viral rhinotracheitis, a disease with signs that
include sneezing, ocular and nasal discharges, conjunctivitis, and pneumonia. It has also been associated with oral ulceration,
keratitis, corneal ulceration, eosinophilic dermatitis and stomatitis, and abortion in pregnant cats. Severe generalized disease,
with necrotic hepatitis, and CNS signs, may also occur. After infection, the virus almost always establishes latency in the
neural tissues of the head, especially the trigeminal ganglia, and reactivation may occur following stress, with viral shedding
with or without clinical signs of disease. The first strain of FHV1 was isolated from kittens with URD in 1958 (C27). Since
then, many strains of varying virulence have been isolated worldwide, which cannot be differentiated antigenically. Although
genotypic differences between strains have been demonstrated (Hamano et al, 2005), more work is required to determine whether
these correlate with virulence. In the mid 1970s, an attenuated strain, F2, was evaluated for its ability to protect cats
against intranasal challenge, and was found to dramatically reduce the severity of signs in cats challenged shortly after
vaccination (Bittle and Rubic, 1975). Most of the early studies challenged cats a few weeks after the booster vaccination.
FCV is a nonenveloped RNA virus that is relatively resistant in the environment, surviving days to several weeks at room temperature.
There are over 100 different FCV strains that cross-react serologically. The degree of cross-reaction is sufficient to classify
them into a single serotype. A marked level of strain diversity exists in large cat populations, such as those found in shelters,
and cats can be simultaneously infected by several different strains. Typically, infection is manifested by fever, conjunctivitis,
rhinitis, oral ulcerations and/or chronic stomatitis, although occasionally skin ulcerations, lameness and pneumonia may occur.
Following infection, a small percentage of cats become chronic carriers, with virus being shed from the oropharynx for months
to years in the absence of clinical signs; this virus can mutate slowly over time, allowing it to evade the host immune response.
More recently, FCV has been rarely associated with a severe systemic disease (virulent systemic disease, VSD) characterized
by subcutaneous edema, and ulceration of the mouth and skin, especially on the pinnae and pawpads and nares. Other lesions
include pneumonia, pancreatitis, and necrosis of the liver and spleen. Adult, vaccinated cats have been most severely affected,
and in each outbreak, the strain of FCV appears to differ, although all VSD strains infect tissue culture more efficiently
than non-VSD strains (Ossiboff et al, 2007). Outbreaks have occurred in the US and the UK. Most have followed introduction
of cats from shelters into another population, and all have been self limiting. A vaccine for FCV was first introduced shortly
after that for FVR, and the two were combined and evaluated as both intranasal and parenteral vaccines in 1976 and 1977 (Scott,
1977). The FCV vaccine has always contained the F9 or 255 strains of FCV.
How effective are feline respiratory viral vaccines?
Based on the results of challenge studies, feline viral respiratory vaccines are generally effective against reducing respiratory
disease, but do not protect against infection or development of the carrier state. This is reflected by the fact that the
prevalence of FCV and FHV1 has not changed considerably in the cat population since the introduction of these vaccines. Factors
that may affect whether an individual cat contracts respiratory disease after vaccination may depend on factors such as the
virus strain, the challenge dose, environmental temperature and humidity, and the presence of underlying immunosuppressive
disease or other concurrent disease.
Vaccination for FHV1 has been shown to reduce shedding following challenge, but some FCV vaccines have been associated with
increased shedding after challenge.
The effect of vaccination on latency and reactivation for FHV1 requires further study. There is some evidence that vaccinated
cats may shed less virus following reactivation. Whether vaccination reduces the chance of reactivation of FHV1 is not known.
Intranasal vaccines can become latent, but whether this is the case for parenteral vaccines is not clear.