1. Oral Microbiology Immunology 2003: 18: 131±134
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Short communication
Concurrent oral shedding of feline M. J. LommerÃ, F. J. M. Verstraete
Department of Surgical and Radiological
Sciences, School of Veterinary Medicine,
calicivirus and feline herpesvirus
University of California, Davis, CA, USA
Ã
Current af®liation: Aggie Animal Dental
Service, San Francisco, CA, USA
1 in cats with chronic
gingivostomatitis
Lommer MJ, Verstraete FJM. Concurrent oral shedding of feline calicivirus and feline
herpesvirus 1 in cats with chronic gingivostomatitis.
Oral Microbiol Immunol 2003: 18: 131±134. ß Blackwell Munksgaard, 2003.
Oral mucosal salivary samples were collected from 25 cats with chronic
Key words: cats; feline calicivirus; feline
gingivostomatitis and 24 cats with periodontal disease. Viral culture and isolation of herpesvirus 1; stomatitis
feline calicivirus and feline herpesvirus 1 were performed. Eighty-eight per cent of cats
with chronic gingivostomatitis were shedding both viruses, compared to 21% of cats F J. M. Verstraete, Department of Surgical
.
without chronic oral in¯ammatory disease. Cats with chronic gingivostomatitis are and Radiological Sciences, School of
Veterinary Medicine, University of California,
signi®cantly more likely to concurrently shed both feline calicivirus and feline Davis, CA 95616, USA
herpesvirus 1 than are cats with classical periodontal disease. Accepted for publication June 25, 2002
In¯ammatory conditions affecting the oral (FORL) may be present (5). Histopatholo- this study was to determine the prevalence
mucosa and gingiva of cats are commonly gic examination of affected tissues typi- of concurrent feline herpesvirus and calici-
seen in veterinary practice. `Feline stoma- cally reveals in®ltrates of lymphocytes and virus infection in cats with chronic stomatitis
titis' consists of a number of syndromes plasma cells (5, 12), giving this complex compared to that in cats with routine period-
with the common presenting clinical sym- the name `lymphocytic-plasmacytic gingi- ontal disease.
ptom being severe in¯ammation of the vitis-stomatitis' (LPGS). The initiating Oral mucosal salivary samples were
gingiva and oral mucosa. These cases pre- cause is usually not identi®ed, and may collected from feline patients presented
sent a diagnostic and therapeutic challenge differ from case to case. It has been noted to the Veterinary Medical Teaching Hos-
to veterinarians. Clinical signs include ha- that oral tissue in¯ammatory responses may pital's Dentistry and Oral Surgery Service
litosis, ptyalism, dysphagia, pawing at the be similar despite different etiologies, and at the University of California, Davis be-
mouth, poor grooming, and weight loss. that secondary infection by oral microbes tween April 1997 and October 1999.
Oral examination may reveal proliferative often leads to a super®cial suppurative Twenty-four cats presented for periodontal
and/or ulcerative in¯ammation of the phar- process overlying the more chronic in®l- treatment of mild to moderate periodontal
ynx, the mucosa lateral to the palatoglossal trate (22), making determination of the disease (11), and 25 cats presented for
folds, gingiva, buccal or palatal mucosa, or initiating cause dif®cult. The underlying treatment of chronic gingivostomatitis
tongue. The area lateral to the palatoglos- pathophysiologic process leading to feline were included in the study. All cats under-
sal folds is commonly referred to as the gingivitis-stomatitishasnotbeen elucidated. went a complete oral examination includ-
`fauces' and in¯ammation in this area as Affected cats may be actively shedding ing periodontal probing and full-mouth
`faucitis'; however, the fauces is in fact the feline calicivirus, feline immunode®ciency radiographs. Cats in the periodontal dis-
area surrounding the tonsils, or the lateral virus, and/or feline leukemia virus in saliva ease group only had mild to moderate
walls of the pharynx, caudomedial to the (21, 22, 25, 26, 34, 38, 41). While the role plaque and calculus accumulation, mild
palatoglossal folds (1). The term `caudal of calicivirus in the pathogenesis of chronic to moderate gingivitis, and/or mild to mod-
stomatitis' will therefore be used, instead stomatitis has been investigated (14, 26, 34, erate increased probing depths without any
of `faucitis', to denote in¯ammation in 35, 38), feline herpesvirus has not been ex- other in¯ammatory lesions in the rest of
this area. Concomitant periodontal disease amined in conjunction with feline calicivirus the oral cavity. Cats in the chronic gingi-
and feline odontoclastic resorption lesions as a possible etiologic factor. The purpose of vostomatitis group were presented with a

2. 132 Lommer & Verstraete
history of dysphagia, weight loss, or signs Table 1. Results of viral isolation
of oral pain, and were found to have pro-
liferative or ulcerative in¯ammation of the Stomatitis Periodontal disease 95% confidence
(n ˆ 25) (n ˆ 24) interval
pharynx, the mucosa lateral to the palato-
glossal folds, the buccal or palatal mucosa, FHV positive à Ã
FCV positive 22 5 (0.4056, 0.8115)
and/or tongue, in addition to the severe
gingivitis typical of the disease. Cats po- FHV positive
sitive for either feline leukemia virus or FCV negative 1 1 (À0.1608, 0.1624)
feline immunode®ciency virus were ex- FHV negative
cluded. Immediately following anesthetic FCV positive 2 1 (À0.1325, 0.2114)
induction and prior to performance of any
FHV negative 0 17
Ã
(À0.9486, À0.5658)
Ã
dental procedures, a sterile cotton-tipped FCV negative
viral culture swab was rolled several times Ã
over the gingiva, buccal and caudal oral Statistically significant.
mucosa, then placed in viral culture med-
ium. Samples were inoculated on Crandell- odontoclastic resorption lesions were pre- chronic caudal stomatitis or generalized
Reese feline kidney (CRFK) cells (ATCC sent in 59.1% of the stomatitis cats and in stomatitis. However, there is evidence that
CCL-94; American Type Culture Collec- 45.8% of the control cats. Two of the the virus is present in cats with chronic oral
tion, Rockville, MD) and incubated at stomatitis cats were edentulous, and data disease: shedding of feline calicivirus has
378C in 5% CO2. Observation for cyto- on FORL were unavailable for one addi- been demonstrated in 50±92% of cats with
pathic effect was performed twice weekly. tional stomatitis cat, so FORL statistics chronic in¯ammation of the gingiva and
Negative cytopathic effect after three pas- were computed based on n ˆ 22 for the oral mucosa (14, 35). The site of persis-
sages (approximately 10 days) constituted stomatitis cats. There was no statistically tence has been found to be the tonsil and
a negative diagnosis. Observation of posi- signi®cant difference between the two adjacent mucosa (4, 37). In the current
tive cytopathic effect resulted in a positive groups with regard to breed status or pre- study, 96% of cats with chronic gingivos-
diagnosis, and was followed by serum-virus sence of FORL. tomatitis were shedding calicivirus. It was
neutralization, also on CRFK cells, with Because viral shedding may be in¯u- initially thought that different strains of
antisera against feline calicivirus (ATCC enced by steroid administration (20, 21, calicivirus may result in varying clinical
VR-956 AS; American Type Culture Col- 39), and gingivostomatitis is often treated syndromes: when a large sample of feline
lection) and feline herpesvirus 1 (Animal with corticosteroids, the medical history of calicivirus-shedding cats was divided into
Resource Services, University of Califor- each cat in the study was reviewed. Of the groups according to clinical signs (asymp-
nia, Davis, CA). Twice-weekly observa- 27 cats for whom results of viral isolation tomatic shedders, cats with acute oral and
tion for cytopathic effect was performed to of both herpesvirus 1 and calicivirus were respiratory disease, and cats with chronic
con®rm isolation of either or both viruses. positive, 13 (48.1%) had received either stomatitis), virus neutralization assays re-
Cats were also classi®ed according to injectable or oral corticosteroids in the vealed that isolates from chronic stomatitis
breed, and the presence of FORL was 6 weeks prior to viral culture. Cats who cats differed from the other clinical groups
noted. Statistical analysis was performed tested positive for both viruses were not (3). However, this is more likely to be the
using 95% con®dence intervals (a Wilson more likely to have received steroids than result of antigenic variation of the virus
procedure without correction for continu- not to have received steroids within the within the host during persistent infection
ity) to compare viral isolation ®ndings, 6 weeks prior to testing (Fisher exact prob- (15, 23). It is currently believed that spe-
breed status, and presence of FORL be- ability test, P ˆ 1.085). ci®c biotypes for distinct disease manifes-
tween the two groups. Feline calicivirus is a common upper tations are unlikely, but that the antigenic
Of 25 cats with chronic gingivostoma- respiratory pathogen, and has been impli- variation occurs related to the presence of
titis, 22 (88%) were actively shedding both cated in the pathogenesis of chronic oral hypervariable regions of the capsid pro-
feline herpesvirus and feline calicivirus in disease (26). It has been suggested that tein, which is typical for the Caliciviridae
saliva. One cat was shedding only herpes- calicivirus infection is responsible for the family (8, 23). A speci®c tissue af®nity for
virus, and two cats were shedding only development of in¯ammation in the caudal different strains could also not be demon-
calicivirus. None of these 25 cats was aspect of the oral cavity: 100% of a small strated (36). The antigenic variation is also
negative for both viruses. sample of cats with caudal stomatitis were likely to be responsible for the differences
Of 24 cats with periodontal disease, ®ve shedding calicivirus, compared with 61% between feline calicivirus isolates from
(21%) were actively shedding both feline of cats with oral disease and 19% of ran- different geographical origins (13, 16).
herpesvirus 1 and feline calicivirus in saliva. domly selected cats. Several different strains The second virus investigated in this
Seventeen (71%) were negative for both were identi®ed in these cases. Speci®c- study, feline herpesvirus 1, is most com-
viruses; one cat was positive for herpes- pathogen-free cats inoculated with any of monly associated with rhinotracheitis in
virus only, and one cat was positive for four calicivirus strains isolated from clin- cats. It has also been linked with many
calicivirus only. Cats with stomatitis were ical cases developed acute caudal stoma- other clinical syndromes, including
signi®cantly more likely than cats with titis (26). chronic conjunctivitis and keratitis, phar-
periodontal disease to be positive for both Although it is recognized that feline yngitis, ulcerative glossitis and palatitis,
viruses, and signi®cantly less likely to be calicivirus can cause acute caudal stoma- facial dermatitis, abortion, and neonatal
negative for both viruses (Table 1). titis and glossitis, its role in chronic oral mortality (9, 19, 21, 22, 31). Immunization
Of the stomatitis cats, six (24.0%) were in¯ammation has not been elucidated. does not prevent acute or latent infection
purebred; six of the periodontal disease None of the inoculated speci®c-patho- with feline herpesvirus, or virus shedding,
group (25.0%) were also purebred. Feline gen-free cats in the above study developed but clinical signs may be less severe in

3. Calicivirus and herpesvirus in cats 133
vaccinated cats (21, 28). During acute out stomatitis and are `predisposed by Acknowledgments
stages of illness, the virus may be easily LP(G)S to occur' (40). If the in¯ammatory
The authors wish to thank Dr N. C. Ped-
isolated from conjunctival, oropharyngeal, process leading to chronic gingivostoma-
ersen for his contributions to this project.
or nasal swabs of symptomatic animals titis were also implicated in the develop-
(22). Isolation of feline herpesvirus is more ment of FORL, one would expect a higher
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