Feline herpesvirus (FHV) is a common pathogen of domestic cats. The virus is a ds DNA virus with a lipid envelope. The virus
primarily targets epithelia of the upper respiratory tract and conjunctiva, and only rarely spreads beyond these regions to
cause disease. As with all herpesviruses, after acute infection it enters a latent state in innervating sensory nerves. In
cats, this most commonly occurs in the trigeminal ganglion. From this latent state, the virus can be reactivated leading to
replication in the epithelia, virus shedding, and in a minority of cats, disease. Termed recrudescence, it can be stimulated
by any stressor, including trauma, concurrent disease, parturition, boarding, or changes in social hierarchy.
The typical presentation of FHV infection is that of upper respiratory tract disease: sneezing, nasal and/or ocular discharge,
depression, and decreased appetite. Conjunctivitis is not uncommon, and can progress to severe hyperemia and chemosis, with
mucopurulent ocular discharge. Infection may lead to corneal ulceration. Less common manifestations of FHV are ulcerative
dermatitis and stomatitis.
Diagnostics for FHV infection primarily involves virus detection, as most cats are seropositive from either natural exposure
or vaccination. Antigen detection using immunofluorescence is fast and inexpensive; however, sensitivity is relatively low,
especially in chronic infections. Virus isolation remains the gold standard. However, in chronic infections, notably chronic
conjunctivitis or other ocular disease, the virus may be neutralized by locally-produced antibody leading to false negative
results. Genetic detection using polymerase chain reaction (PCR) has high sensitivity, such that subclinical, and even latent
infections may be detected. Thus, positive results must be interpreted in light of other clinical information.
Advancements have been made in the treatment of FHV infection in cats. Nucleoside analogs developed for human herpesvirus
infections have shown some efficacy against feline herpesvirus, at least in vitro. Toxic side effects have been reported with
some, such as acyclovir, but others, such as ganciclovir may prove to be useful clinically. Topical administration of antiviral
medications has been used with some success, and include trifluridine and idoxuridine. Interferon (IFN) has been used with
some success, and has been shown to be efficacious in vitro (human alpha IFN – US; and feline omega IFN – Europe). L-lysine
given orally inhibits viral protein synthesis and restricts virus replication. It is optimal when used early in infection,
or as a means to prevent recrudescence during stress. Experimentally, lactoferrin has been shown to inhibit virus attachment
and entry, and may be eventually be available as an antiviral treatment for FHV.
Protection following recovery is not long-lived, and reinfections may occur. Antigenic variation is not a significant problem
with feline herpesvirus, thus, the antigenic coverage of vaccines is adequate. Non-adjuvanted modified live vaccines are recommended.
Vaccines do not prevent infection, nor production of the carrier state. They do offer protection from disease, however.
Feline calicivirus (FCV) continues to be an important respiratory pathogen of cats. It is a nonenveloped virus making it very
hardy in the environment, and easily spread by fomites. It is a ss RNA virus with a significant mutation rate. This may lead
to changes in antigenicity (many strains that vary antigenically exist) as well as virulence.
Clinical presentations with FCV infection can vary from mild upper respiratory tract disease to viral pneumonia to lethal
systemic disease. The typical presentation is similar to FHV infection, though the ocular discharge generally remains serous,
corneal ulcers do not occur, and oral ulcers are common. The majority of infections are mild and self-limiting. However, following
recovery, infection with shedding in oropharyngeal secretions may persist for periods of week to months, even in the face
of vaccination. Lameness, ulcerative dermatitis, and gingivitis have also been associated with FCV, though the pathogenesis
Virulent systemic disease (VSD) has been recognized relatively recently. In affected cats, signs may include high fever, depression,
anorexia, edema, particularly of the head and limbs, and ulcerative dermatitis of the face, pinnae, and feet. Systemic involvement
with multiorgan dysfunction has also been noted, and affected tissues included lungs, pancreas, and liver. In the majority
of these occurrences, the index case has originated from a shelter or rescue facility. Both vaccinated and unvaccinated cats
have been affected, with significant mortality rates reported. The specific viral factor(s) responsible for this virulent
phenotype have not been identified, and no molecular markers have been found. The mutation or mutations responsible appear
to evolve independently in each outbreak, and the isolates from VSD episodes characterized thus far are distinct from one