Abstract
Previous studies have suggested the involvement of viral and bacterial components in the initiation and progression of feline chronic gingivostomatitis (FCGS), but the role of fungi remains entirely unknown. This pilot study aimed to investigate the bacteriome and mycobiome in feline oral health and disease. Physical exams, including oral health assessment, of privately owned, clinically healthy (CH) cats (n = 14) and cats affected by FCGS (n = 14) were performed. Using a sterile swab, oral tissue surfaces of CH and FCGS cats were sampled and submitted for 16S rRNA and ITS-2 next-generation DNA sequencing. A high number of fungal species (n = 186) was detected, with Malassezia restricta, Malassezia arunalokei, Cladosporium penidielloides/salinae, and Aspergillaceae sp. being significantly enriched in FCGS samples, and Saccharomyces cerevisiae in CH samples. The bacteriome was significantly distinct between groups, and significant inter-kingdom interactions were documented. Bergeyella zoohelcum was identified as a potential biomarker of a healthy feline oral microbiome. These data suggest that fungi might play a role in the etiology and pathogenesis of FCGS, and that oral health should not simply be regarded as the absence of microbial infections. Instead, it may be viewed as the biological interactions between bacterial and fungal populations that coexist to preserve a complex equilibrium in the microenvironment of the mouth. Additional investigations are needed to improve our understanding of the feline oral ecosystem and the potential interactions between viruses, bacteria, and fungi in FCGS.
Highlights
The prevalence of feline chronic gingivostomatitis (FCGS) is approximately 0.7–12% [1].Affected cats usually present with oral inflammation, pain, anorexia and dysphagia
Feline calicivirus (FCV) and feline herpesvirus-1 (FHV-1) have been implicated in the development of the disease, but it has been hypothesized that cats with FCGS may show an aberrant reaction to plaque bacteria that leads to oral inflammation beyond gingivitis and periodontitis [2]
The alpha-diversity measurements for clinically healthy (CH) and FCGS samples showed that the number of observed bacterial species was significantly higher than the number of fungal species
Summary
Affected cats usually present with oral inflammation, pain, anorexia and dysphagia. Feline calicivirus (FCV) and feline herpesvirus-1 (FHV-1) have been implicated in the development of the disease, but it has been hypothesized that cats with FCGS may show an aberrant reaction to plaque bacteria that leads to oral inflammation beyond gingivitis and periodontitis [2]. The exact cause of FCGS remains unknown, and there is no gold standard in terms of treatment besides partial and full-mouth tooth extraction and extensive medical management. Current therapeutic approaches include professional dental cleaning, tooth extractions (partial or full mouth), and extensive medical (antimicrobial, anti-inflammatory, immunosuppressive, immunomodulatory) management. Empirical treatment of FCGS with amoxicillin, amoxicillin clavulanate, clindamycin or metronidazole without proper diagnostic information can promote bacterial resistance and become ineffective
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