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Feline Viral Upper Respiratory Tract Disease
Yvonne Drechsler, PhD

College of Veterinary Medicine, Western University of Health Sciences, Pomona, CA, USA

Etiology/Pathophysiology Epidemiology

Feline viral infectious upper respiratory tract disease Infection with both FHV‐1 and FCV is widespread in the
is primarily caused by two viruses: feline herpesvirus general cat population. The prevalence of infection and
(FHV‐1) and feline calicivirus (FCV). Infection is com- clinical disease is higher in multicat households, colo-
mon in multicat environments, and most cats have nies, catteries or shelters. Viral reactivation may occur in
been exposed. FHV‐1 is an enveloped single‐stranded latently infected cats when they are stressed or if their
DNA virus belonging to the alpha‐herpesvirus family. immune system is compromised. FHV‐1 is short‐lived in
As such, the virus exists in a latent form in the trigemi- the environment, and transmission occurs mainly by
nal ganglia after initial infection and can be reacti- direct contact with an infected cat. However, transmis-
vated by stressors. This leads to shedding via secretions sion through fomites in crowded environments is also
from oral, nasal, and conjunctival membranes. Viral important.
replication is usually restricted to the upper respira- Cats infected with FCV may be carriers who shed virus
tory tract, due to viral preference for lower tempera- while appearing clinically healthy. Virus may be shed in
tures. However, in young kittens and possibly the urine and feces in addition to respiratory secretions.
immunosuppressed cats, more severe systemic disease FCV survives in the environment much longer than
can occur. FHV‐1 and is resistant to quaternary ammonium com-
Feline calicivirus belongs to the Caliciviridae family, pounds. Therefore, in addition to direct and aerosol con-
and consists of a single‐stranded positive RNA genome. tact with respiratory secretions, fomites are a very
This genome structure has a high mutation rate and important means of transmission for FCV.
therefore the isolates are highly variable. Strains can vary
in their pathogenicity. Like FHV‐1, transmission occurs
via secretions from oral, nasal, and conjunctival mem- Signalment
branes. FCV persists in tonsillar and other oropharyn-
geal tissues, leading to a carrier state, but the mechanism Cats of any sex and age can develop respiratory disease
of persistence is not well understood. In addition to caused by FHV‐1 or FCV, with kittens being more
causing upper respiratory disease, FCV can be associ- susceptible.
ated with lameness due to acute synovitis, possibly due
to antigen‐activated macrophages residing in the syno-
vial membrane. Rarely, FCV can cause virulent systemic History and Clinical Signs
disease (VSD). Lesions associated with VSD are severe
and include oral and dermal ulcerations, bronchointer- Cats from multicat households, colonies, catteries
stitial pneumonia, necrosis of the liver, spleen and pan- or shelters are commonly infected. A history of stress
creas, and death. The pathogenesis of VSD is not fully or immune suppression may be noted. FHV‐1 may
understood. cause severe respiratory disease, especially in

Clinical Small Animal Internal Medicine Volume II, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical