Gastric Non-Helicobacter pylori Urease-Positive Staphylococcus epidermidis and Streptococcus salivarius Isolated from Humans Have Contrasting Effects on H. pylori-Associated Gastric Pathology and Host Immune Responses in a Murine Model of Gastric Cancer.

In populations with similar prevalence of Helicobacter pylori infection, cancer risk can vary dramatically. Changes in composition or structure of bacterial communities in the stomach, either at the time of exposure or over the course of H. pylori infection, may contribute to gastric pathology. In this study, a population of 37 patients from the low-gastric-cancer-risk (LGCR) region of Tumaco, Colombia, and the high-gastric-cancer-risk (HGCR) region of Túquerres, Colombia, were recruited for gastric endoscopy. Antral biopsy specimens were processed for histology and bacterial isolation. Fifty-nine distinct species among 26 genera were isolated by aerobic, anaerobic, and microaerobic culture and confirmed by 16S rRNA analysis. Urease-positive Staphylococcus epidermidis and Streptococcus salivarius were frequently isolated from gastric biopsy specimens. We asked whether coinfection of H. pylori with urease-positive S. salivarius and/or S. epidermidis had a demonstrable effect on H. pylori-induced gastritis in the germfree (GF) INS-GAS mouse model. Coinfections with S. salivarius and/or S. epidermidis did not affect gastric H. pylori colonization. At 5 months postinfection, GF INS-GAS mice coinfected with H. pylori and S. salivarius had statistically higher pathological scores in the stomachs than mice infected with H. pylori only or H. pylori with S. epidermidis (P < 0.05). S. epidermidis coinfection with H. pylori did not significantly change stomach pathology, but levels of the proinflammatory cytokine genes Il-1ß, Il-17A , and Il-22 were significantly lower than in H. pylori-monoinfected mice. This study demonstrates that non-H. pylori urease-positive bacteria may play a role in the severity of H. pylori-induced gastric cancer in humans. IMPORTANCE Chronic infection with H. pylori is the main cause of gastric cancer, which is a global health problem. In two Colombian populations with high levels of H. pylori prevalence, the regional gastric cancer rates are considerably different. Host genetic background, H. pylori biotype, environmental toxins, and dietary choices are among the known risk factors for stomach cancer. The potential role of non-H. pylori gastric microbiota in gastric carcinogenesis is being increasingly recognized. In this study, we isolated 59 bacterial species from 37 stomach biopsy samples of Colombian patients from both low-gastric-cancer-risk and high-gastric-cancer-risk regions. Urease-positive S. epidermidis and S. salivarius commonly cultured from the stomachs, along with H. pylori, were inoculated into germfree INS-GAS mice. S. salivarius coinfection with H. pylori induced significantly higher gastric pathology than in H. pylori-monoinfected mice, whereas S. epidermidis coinfection caused significantly lower H. pylori-induced proinflammatory cytokine responses than in H. pylori-monoinfected mice. This study reinforces the argument that the non-H. pylori stomach microflora play a role in the severity of H. pylori-induced gastric cancer.

Detection of Myocoptes musculinus in Fur Swab and Fecal Samples by Using PCR Analysis.

Current methods for detecting mites in mouse colonies have limitations in terms of cost, accuracy, and throughput. To address these limitations, we developed PCR assays to detect Myocoptes musculinus in fecal samples. Using a newly generated ribosomal RNA sequence of M. musculinus (MC28S), we developed PCR and qPCR assays capable of detecting M. musculinus mites or eggs ingested during grooming. To determine our ability to detect mites, we tested fur swabs and feces from mouse colonies experimentally infested with M. musculinus and Demodex musculi, 2) Myobia musculi and Radfordia affinis, 3) M. musculinus and M. musculi, and 4) no mites (negative control). The MC28S PCR and qPCR assays positively identified M. musculinus in groups 1 and 3. The MC28S PCR assay detected M. musculinus in 9 of 10 fecal samples from known-positive animals, whereas the qPCR assay correctly identified M. musculinus in all 10 fecal samples. To our knowledge, this report is the first description of PCR-based detection of murine mites in feces. By eliminating the need for pelt examinations, mite detection from fecal samples can facilitate mite detection in sentinel or quarantine programs.

Cutaneous Dermatophilosis in a Meadow Jumping Mouse (Zapus hudsonius).

A laboratory-housed, wild-caught, subadult, male meadow jumping mouse (Zapus hudsonius) presented with extensive scaling of the face, limbs, and tail and severe edema of the paws. Postmortem examination revealed marked distal limb edema with focal digital hematomas and white scales, scabs, and crusts affecting the majority of nonhaired skin. Histopathologic analysis revealed severe, multifocal, chronic-active exudative and proliferative dermatitis characterized by multilaminated crusts covering the epidermis. The epidermis was expanded by hyperkeratosis, acanthosis, and hyperplasia. The superficial dermis contained moderate edema, hemorrhage, and pigmentary incontinence, and was infiltrated by granulocytes and mononuclear cells. The laminated crusts contained numerous branching filaments of gram-positive coccoid bodies arranged in parallel rows, consistent with cutaneous Dermatophilus congolensis infection. This diagnosis was confirmed through bacterial culture and 16S rRNA PCR analysis. In the presented case, factors that might have contributed to disease progression include climatic conditions at the capture site and stress associated with trapping and laboratory housing.