**4.7 Genus** *Prevotella*

The genus *Prevotella* is phylogenetically classified in the family *Prevotellaceae*, order *Bacteroidales*, class *Bacteroidia* and phylum *Bacteroidetes*. Representatives of this genus are Gram-negative, anaerobic, non-motile rods. The primary periodontal pathogen is species *Prevotella intermedia*. Within the *P. intermedia* strains, heterogeneity was found in terms of serology and DNA homology. In 1992, based on complex DNA-DNA hybridization, it was suggested that *P. intermedia* be reclassified into two species, *P. intermedia* and *P. nigrescens* [70]. *P. intermedia* and *P. nigrescens*, members of the "orange complex" described by Socransky et al., are among the most common species in subgingival plaque in humans. *P. intermedia* may under certain conditions increase the activity of degradation enzymes and promote the progression of periodontitis [71]. *P. intermedia* is also present in canine dental plaque. In dogs, the

counts of *P. intermedia* correlated with the amount of plaque and the degree of gingivitis [72]. *Prevotella dentalis* is also associated with periodontitis. *P. dentalis* (formerly *Mitsuokella dentalis*) was originally named after Japanese bacteriologist Mitsuok, who described this organism for the first time [38]. Mitsuoka isolates a large number of *P. dentalis* strains from humans, dogs and pigs that seem to be closely related to the *Bacteroides* genus [73].

### **4.8 Oral protozoa**

For several decades, research in periodontology is focused on the characterization of bacterial communities thought to be involved in canine periodontal diseases. However, other microorganisms are known to inhabit the oral cavity and could also influence the process of periodontal disease. There were identified two oral protozoa, *Entamoeba gingivalis* and *Trichomonas tenax*, which can inhabit the canine oral periodontium. Both were statistically associated to animals with periodontal disease [74].

The species *Entamoeba gingivalis* is phylogenetically classified in the genus *Entamoeba*, class *Archamoebae* and phylum *Amoebozoa*. The protozoan *E. gingivalis* resides in the oral cavity and is frequently observed in the periodontal pockets of humans and pets. The parasite *E. gingivalis* is more prevalent and more abundant in periodontal pockets, suggesting that this ecological niche is either propitious for its survival, or that the parasite induces changes leading to this environment [75]. *E. gingivalis* is an opportunistic pathogen, which, together with synergistic symbiotic bacteria, can cause periodontal diseases in hosts with low immunity [76]. Pathogenicity of protozoa *E. gingivalis* in the oral cavity is not completely understood [77].

The species *Trichomonas tenax* is phylogenetically classified in the genus *Trichomonas*, family *Trichomonadidae* and order *Trichomonadida*. *T. tenax* inhabits the oral cavities of various mammals, including humans, dogs, cats and horses [78]. *T. tenax*, an anaerobic motile-flagellated protozoan, is 12–20 μm long and 5–6 μm wide organism. It is either ellipsoidal or ovoid in shape and has four anterior flagella of unequal lengths [79]. *T. tenax* can ingest bacteria and various particles by phagocytosis necessary for their development. *T. tenax*, detected in periodontal cases, is likely to be related to the onset and evolution of periodontal disease [80]. This parasite has been reported to be involved in a number of cases of pulmonary trichomoniasis. Besides bronchopulmonary exudates the trichomonads have also been found in pleural fluid, submaxillary gland and infra-auricular lymph node [81]. Several mechanisms may explain the deleterious effects of the *T. tenax* parasite towards periodontal tissues. Recent studies have emphasized the ability of parasites to induce changes in some features of microbial communities. *T. tenax* can escape the host immune response via a complex strategy caused by an imbalance of the oral cavity microbiocenosis. Pathogenic bacteria involved in periodontal host colonization and immune subversion use complement and toll-like receptor (TLR) signaling pathways. Like bacteria, parasites are recognized by TLR. *T. tenax* also produce fibronectin-like proteins, responsible for tissue adhesion. Given this pathogenic property, host-tissue disruption and lysis may be induced by *T. tenax* secretion of peptidases such as cathepsin B-like proteinases for matricial type 1 collagen and gelatin hydrolyses or haemolysins for erythrolysis [79].
