Porphyromonas spp., Fusobacterium spp., and Bacteroides spp. dominate microbiota in the course of macropod progressive periodontal disease

Abstract

Macropod progressive periodontal disease (MPPD) is a necrotizing, polymicrobial, inflammatory disease commonly diagnosed in captive macropods. MPPD is characterized by gingivitis associated with dental plaque formation, which progresses to periodontitis and then to osteomyelitis of the mandible or maxilla. However, the underlying microbial causes of this disease remain poorly understood. In this study, we collected 27 oral plaque samples and associated clinical records from 22 captive Macropodidae and Potoroidae individuals that were undergoing clinical examination at Adelaide and Monarto Zoos in South Australia (15 healthy, 7 gingivitis and 5 periodontitis-osteomyelitis samples). The V3-V4 region of the 16S ribosomal RNA gene was sequenced using an Illumina Miseq to explore links between MPPD and oral bacteria in these animals. Compositional differences were detected between the microbiota of periodontitis-osteomyelitis cases compared to healthy samples (p-value with Bonferroni correction < 0.01), as well as gingivitis cases compared to healthy samples (p-value with Bonferroni correction < 0.05) using Permutational Multivariate Analysis of Variance (PERMANOVA). An overabundance of Porphyromonas, Fusobacterium, and Bacteroides taxa was also identified in animals with MPPD compared to healthy individuals using linear discriminant analysis effect size (LEfSe; p = < 0.05). An increased abundance of Desulfomicrobium also was detected in MPPD samples (LEfSe; p < 0.05), which could potentially reflect differences in disease progression. This is the first microbiota analysis of MPPD in captive macropods, and these results support a polymicrobial pathogenesis of MPPD, suggesting that the microbial interactions underpinning MPPD may be more complex than previously documented.

Targeting the succinate receptor effectively inhibits periodontitis

“…This experimental periodontitis model was initiated by a 5-day placement of a ligature around the second maxillary molar tooth, followed by oral inoculation of Fusobacterium nucleatum to promote prolonged inflammation and dysbiosis. F. nucleatum can act as an anchoring perio-pathogen to initiate and support periodontitis biofilm formation ( Foster and Kolenbrander, 2004 ; Park et al, 2016 ; Thurnheer et al, 2019 ; Yamada et al, 2005 ; Yip et al, 2021 ) and induce chronic inflammation and immune evasion locally and systemically ( Hajishengallis and Chavakis, 2021 ; McIlvanna et al, 2021 ). Thus, by adapting the traditional ligature-induced PD model, we can examine initiating events in PD and later events because of prolonged inflammation and dysbiosis.…”

Postbiotic Metabolite of Lactiplantibacillus plantarum PD18 against Periodontal Pathogens and Their Virulence Markers in Biofilm Formation

“…Moreover, the S. mutans count appeared to be directly correlated with worsening periodontitis severity among patients who were older and not receiving treatment [ 62 ]. P. gingivalis is considered to be the keystone pathogen in human periodontal disease [ 10 , 63 ]. P. gingivalis can create effective oxidative stress defense systems to survive when exposed to intracellular ROS, enhancing their aerotolerance ability [ 64 , 65 ], which increases the severity of this pathogen and its biofilms when they disperse to other sites of the host or contaminate medical devices.…”

Pharmacokinetic profile and effect on the faecal microbiome of a single dose of pradofloxacin oral suspension in the rabbit(Oryctolagus cuniculus)

“…We used linear discriminant analysis (LDA) and effect size (LEfSe) (Segata et al, 2011) for identifying the significant differentially abundant bacteria after pradofloxacin administration (alpha value =0.05 and threshold of absolute logarithmic LDA score >2), as previously described (Yip et al, 2021). LDA analysis was carried out using the Galaxy platform (https://hutte nhower.sph.harva rd.edu/galax y/).…”