Diversity of the Gastric Microbiota in Thoroughbred Racehorses Having Gastric Ulcer

Abstract

Equine gastric ulcer syndrome is one of the most frequently reported diseases in thoroughbred racehorses. Although several risk factors for the development of gastric ulcers have been widely studied, investigation of microbiological factors has been limited. In this study, the presence of Helicobacter spp. and the gastric microbial communities of thoroughbred racehorses having mild to severe gastric ulcers were investigated. Although Helicobacter spp. were not detected using culture and PCR techniques from 52 gastric biopsies and 52 fecal samples, the genomic sequences of H. pylori and H. ganmani were detected using nextgeneration sequencing techniques from 2 out of 10 representative gastric samples. The gastric microbiota of horses was mainly composed of Firmicutes (50.0%), Proteobacteria (18.7%), Bacteroidetes (14.4%), and Actinobacteria (9.7%), but the proportion of each phylum varied among samples. There was no major difference in microbial composition among samples having mild to severe gastric ulcers. Using phylogenetic analysis, three distinct clusters were observed, and one cluster differed from the other two clusters in the frequency of feeding, amount of water consumption, and type of bedding. To the best of our knowledge, this is the first study to investigate the gastric microbiota of thoroughbred racehorses having gastric ulcer and to evaluate the microbial diversity in relation to the severity of gastric ulcer and management factors. This study is important for further exploration of the gastric microbiota in racehorses and is ultimately applicable to improving animal and human health.

Recommendations for the management of equine glandular gastric disease

“…Other bacterial species including Escherichia fergusonii, Streptococcus bovis and Enterococcus faecium are potentially pathogenic and have been identified in association with EGGD lesions; however, their pathogenicity remains unproven. The balance of bacteria within the stomach has been hypothesised to be relevant to the development of EGGD, although there was no difference between the microbiota of horses with EGGD and horses with no gastric disease in one study (Dong et al, 2016). Mucolytic enzymes produced by bacteria as they transit the gastric mucosa can contribute to barrier denudation in other species, but their role is unknown in the horse.…”

Other Helicobacters and gastric microbiota

“…In racehorses with gastric ulceration, 16S RNA‐based PCR was not able to detect Helicobacter species. After genomic DNA extraction from the gastric samples, next‐generation sequencing of the V1–V3 regions of the 16S rRNA gene indicated presence of H. pylori and H. ganmani in two horses . Mori et al.…”

“…After genomic DNA extraction from the gastric samples, next-generation sequencing of the V1-V3 regions of the 16S rRNA gene indicated presence of H. pylori and H. ganmani in two horses. 8 Helicobacter-free deer mice were obtained through neonatal fostering, as described in other rodents. 13 Hygienic and environmental measurements should also be taken into account to maintain the Helicobacternegative status, as Pritchett-Corning and Gaskill reported transmission of Helicobacter species to formerly Helicobacter-negative rodents that were cohoused with Helicobacter-positive rodents.…”

Effects of transportation on gastric pH and gastric ulceration in mares

“…[7][8][9] Possible causes of EGGD are less well characterized although, in common with ESGD, it is hypothesized that erosion and ulceration occur as a result of an imbalance between aggressive and protective factors such that mucosal integrity is compromised. In horses, as in people with peptic ulcer disease, factors that decrease prostaglandin production 6,10 and possibly altered gastric microbiota 11,12 may contribute to the development of disease.…”