In a recent survey of the health status of over 31,000 dogs and over 15,000 cats examined at veterinary practices in the United
States, the most commonly reported disorders were dental calculus (20.5% prevalence in dogs; 24.2% in cats) and gingivitis
(19.5% prevalence in dogs; 13.1% in cats) (Lund, Armstrong et al. 1999).
Chronic gingivostomatitis is a condition characterized by persistent inflammation of the oral mucosa. The mucosa and gingiva
may appear hyperemic, proliferative, and ulcerative with a bright red cobblestone appearance. It can be debilitating, frustrating
to treat, and may result in euthanasia. It may be referred to by other names, such as plasma cell stomatitis-pharyngitis,
chronic faucitis, lymphocytic plasmacytic gingivitis-stomatitis and others. Prevalence data is scarce, but in one study from
the U.K. involving 4,858 cats seen by primary care practices, the prevalence was 0.7% (Healey, Dawson et al. 2007).
The disease varies in severity and may include faucitis, pharyngitis, or palatitis. Clinical signs include drooling, halitosis,
bleeding gingiva, decreased grooming, and oral sensitivity. Severely affected cats may develop dysphagia, partial anorexia,
and weight loss. In addition, the chronic inflammation may contribute to progressive periodontal disease. The diagnosis is
based on clinical signs and histopathology. The most common histopathologic findings include abundant plasma cells, lymphocytes,
and occasional neutrophils and macrophages.
The etiology of chronic gingivostomatitis is unknown, but it is likely to be multifactorial. It has been proposed that the
disease is an exaggerated immune response to plaque and the tooth structure itself or the periodontal tissues as well as infectious
antigens. Other potential factors include genetic predisposition and nutritional factors.
Many organisms, including viruses and anaerobic bacteria, have been found in association with gingivostomatitis. The most
commonly suspected infectious etiology is feline calicivirus (FCV), but the feline retroviruses (FeLV and FIV), feline herpesvirus
(FHV), and Bartonella species have been implicated as well with variable results in different studies. A causal relationship is difficult to prove
because all these infectious agents may be harbored by both healthy and ill cats and the diagnostic methods used in various
studies are not standardized.
In a study of 78 British and 18 North American cats with chronic stomatitis and appropriate controls, FCV was more prevalent
in cases than controls. In the British cats, the prevalence of FIV was also significantly higher in cats with stomatitis (Knowles,
Gaskell et al. 1989). In another study of 25 cats with chronic gingivostomatitis, 88% of cats were shedding both FCV and FHV,
compared to 21% of cats without oral inflammatory disease (Lommer and Verstraete 2003). In a large study of 8,982 cats with
oral disease including gingivitis and stomatitis, 14.2% of the cats were positive for FeLV and/or FIV (data on file, IDEXX
Laboratories, 2006). A recent study of a colony of cats (9 affected cats, 36 unaffected controls) using blood samples and
oral swabs found no correlation between gingivostomatitis and Bartonella, FHV, FCV, FeLV, or FIV (Quimby, Elston et al. 2008).
The role of Bartonella species remains controversial. In a study of serum samples from 728 cats in Switzerland, there was an increased frequency
of stomatitis in sick cats positive for B. henselae (Glaus, Hofmann-Lehmann et al. 1997). In another study of 34 cats with stomatitis and 34 age-matched healthy controls, there
was no significant difference in the prevalence rates for Bartonella between the affected and control cats (Dowers and Lappin 2005). PCR testing for Bartonella was performed on oral biopsy samples
from 18 of the affected cats; Bartonella was identified in only one sample.