Intestinal Microbiota Shifts towards Elevated Commensal Escherichia coli Loads Abrogate Colonization Resistance against Campylobacter jejuni in Mice

Background: The zoonotic pathogen Campylobacter jejuni is a leading cause of bacterial foodborne enterocolitis in humans worldwide. The understanding of immunopathology underlying human campylobacteriosis is hampered by the fact that mice display strong colonization resistance against the pathogen due to their host specific gut microbiota composition. Methodology/Principal Findings: Since the microbiota composition changes significantly during intestinal inflammation we dissected factors contributing to colonization resistance against C. jejuni in murine ileitis, colitis and in infant mice. In contrast to healthy animals C. jejuni could stably colonize mice suffering from intestinal inflammation. Strikingly, in mice with Toxoplasma gondii-induced acute ileitis, C. jejuni disseminated to mesenteric lymphnodes, spleen, liver, kidney, and blood. In infant mice C. jejuni infection induced enterocolitis. Mice suffering from intestinal inflammation and C. jejuni susceptible infant mice displayed characteristical microbiota shifts dominated by increased numbers of commensal Escherichia coli. To further dissect the pivotal role of those distinct microbiota shifts in abrogating colonization resistance, we investigated C. jejuni infection in healthy adult mice in which the microbiota was artificially modified by feeding live commensal E. coli. Strikingly, in animals harboring supra-physiological intestinal E. coli loads, colonization resistance was significantly diminished and C. jejuni infection induced enterocolitis mimicking key features of human campylobacteriosis. Conclusion/Significance: Murine colonization resistance against C. jejuni is abrogated by changes in the microbiot

An outbreak of avian tuberculosis in peafowl (Pavo cristatus) and pheasants (Phasianus colchicus) in a zoological aviary in Turkey

WOS: 000234011300005Avian tuberculosis was diagnosed histopathologically and microbiologically in two pheasants (Phasianus colchicus) and two peafowl (Pavo cristatus) kept in the same aviary. The incidence of avian tuberculosis in the aviary was 6%. Non-mineralized caseogranulomas were present in the liver (3 cases), spleen (3 cases), intestine (2 cases), lung (2 cases), and cloaca (1 case). Granulomas in the lung were present only in peafowl. The presence of granulomas in the lung of both infected peafowl suggests that peafowl were exposed to the agent via the respiratory route rather than the alimentary route. Histopathologic findings were typical of avian tuberculosis, including acid fast bacilli and centrally located caseo-necrosis surrounded by epitheloid macrophages, lymphocytes, and multinucleated giant cells. Mycobacterium avium subsp. avium was isolated from tissue samples of all infected birds

The prevalence, colonization sites and pathological effects of gastric helicobacters in dogs

Akan, Mehmet/0000-0002-7342-1450WOS: 000174792400025The prevalence and colonization sites of Helicobacter slap. in the stomachs of dogs, and their association with gastric pathology were investigated. Scraping cytology, culture, urease test and histology were used to detect helicobacters in the stomachs of necropsied dogs. Gastric Helicobacter spp. were detected in 103 (84.4%) of 122 dogs from I month to 14 years of age. The uncultured spiral organisms seen in the most of stomachs were designated as H. heilmannii. Microscopical examination of stained mucosal scrapings was found to be superior for the diagnosis of gastric helicobacters. Six (4.9%) spiral organisms were isolated from 122 stomachs and all were identified as H. felis. Helicobacter spp. were detected in the fundus, corpus and antrum of 103, 101 and 53 dogs, respectively. Organisms were denser in the fundus and corpus than in the antrum, Histological changes comparable to mild chronic gastritis or chronic active gastritis were found in 56.3% of Helicobacter positive dogs and 47.4% of Helicobacter-negative dogs. H. felis was found only in dogs with chronic active gastritis

Succinivibrionaceae is dominant family in fecal microbiota of Behçet's Syndrome patients with uveitis.

Behçet's Syndrome (BS) is a multisystem vasculitis with various clinical manifestations. Pathogenesis is unclear, but studies have shown genetic factors, innate immunity and autoinflammation to have an important role in the disease course. Diversity in the microbial community of gut microbiota may significantly contribute to the activation of the innate immune system. The clinical features of BS present themselves in clusters and each cluster may be a consequence of different disease mechanisms. For this reason we aimed to investigate the gut microbiota of BS patients with uveitis. In addition to healthy controls, we have aimed to compare the gut microbiota of BS with that of Familial Mediterranean Fever (FMF) and Crohn's Disease (CD) as both diseases have innate and autoinflammatory features in their pathogenesis. Seven patients with BS, 12 patients with FMF, 9 patients with CD and 16 healthy controls (HC) were included in the study. Total genomic DNAs were isolated from fecal samples of the patients. Partial 16S rRNA gene was sequenced using the PGM Ion Torrent (Thermo Fisher Scientific, Waltham, MA, USA) for microbiota analysis. Statistical analysis showed that significant differences were detected on the microbial community of four groups. Succinivibrionaceae is dominant and the signature family, whereas Bacteroides was absent in BS patients