Characterization of Clostridioides difficile ribotypes in domestic dogs in Rio de Janeiro, Brazil.

Clostridioides difficile is the major etiologic agent of nosocomial bacterial diarrhoea and pseudomembranous colitis. The pathogenesis of C. difficile infection (CDI)involves two cytotoxic enzymes (TcdA, TcdB) that cause colonic epithelial damage, fluid accumulation and enteritis. CDI has been demonstrated in a variety of animal species and some reports have recently raised the importance of wild animals as a reservoir of this pathogen and possible transmission to humans and domestic animals. The aim of this study was to characterize C. difficile isolates obtained from pet dogs in Rio de Janeiro, Brazil. A total of 50 faecal samples were obtained from healthy and diarrheic dogs. Five of fifty samples (10%) grew C. difficile. Of those, three belonged to the PCR ribotype 106 (ST 42) and were toxigenic (A+B+). The other two strains belonged to the PCR ribotype 010 (ST 15) and were not toxin producers (A-B-). None of the isolates tested positive for the binary toxin genes. Considering the antimicrobial resistance patterns of all isolates using EUCAST breakpoints, all strains were sensitive to metronidazole and vancomycin. However, two strains (ribotype 106 and ribotype 010), were resistant to clindamycin (≤256 µg/mL). All strains were strong biofilm producers. Our study provides evidence that dogs can act as reservoirs for C. difficile epidemic ribotypes.

The epidemiology of Clostridioides difficile infection in Brazil: A systematic review covering thirty years.

Clostridioides difficile is considered one of the main etiological agents of bacterial diarrhea associated with the use of antibiotics. It is an important nosocomial pathogen and the main cause of morbidity and mortality. In recent years, infections associated with C. difficile have led to numerous investigations. It is well known that C. difficile associated diarrhea (CDAD) is favored by the suppression or imbalance of the intestinal microbiome during or after antibiotic therapy. Other risk factors are, for instance, advanced age, long periods of hospitalization, chemotherapy, and other gastrointestinal infections. In the 2000's, the number of CDAD cases largely increased due to the emergence of the epidemic clone named BI/NAP1 ribotype 027, responsible for causing several outbreaks in developed countries, such as Canada, the United States, and the United Kingdom. The presence of the epidemic clone has been reported in Asia, Latin America and Australia, however, infections associated with C. difficile (CDI) in these geographic regions are usually caused by other ribotypes. In Brazil, for instance, epidemiological data on the incidence of CDI are still limited, especially regarding the spread of C. difficile within hospital units, the spectrum of toxigenic genes and the antimicrobial resistance profile. Some studies have demonstrated the importance of notifying cases related to CDI and taking special care measures in order to minimize the spread of epidemic strains in Brazil. Finally, epidemiological analysis of the prevalent and/or exclusive ribotypes circulating in Brazil can contribute to understand and to correlate characteristics associated with the biology of this pathogen with other globally circulating ribotypes. This review aimed to summarize all published work related to the isolation of C. difficile from human patients in Brazil, being the main focus, the methodologies used for identification of prevalent ribotypes, the antimicrobial susceptibility profile, and the diseases associated with the acquisition of CDI.

A Bacteroides fragilis surface glycoprotein mediates the interaction between the bacterium and the extracellular matrix component laminin-1.

The adherence of Bacteroides fragilis strains to immobilized laminin-1 (LMN-1) was investigated using this protein adsorbed onto glass. Among the 27 strains isolated from infectious processes and assayed, 13 presented strong adherence to LMN-1. Among them, two strains, MC2 and 1081, showed the strongest association, and for that reason they were selected for further studies in which adherence to this protein was confronted with both physical-chemical and enzymatic treatments, along with concurrence assays with the LMN-1 molecule itself and the LMN-1-residing amino acid sequences (RGD, IKVAV, YIGSR, AG73, A13 and C16). The chemical and enzymatic treatments resulted in sharp decreases in binding rates of those strains, and competition experiments with LMN-1- residing amino acids revealed that, except for RGD and A13, all the others were effective at reducing bacterial binding of the bacteria. The outer membrane proteins (OMPs) of B. fragilis were extracted and assayed onto dot-blotted LMN-1, and when the extracts were chemically treated, especially with metasodium periodate, a drastic reduction in bacterial binding occurred. Results of the latter assays clearly indicate that bacterial molecules involved in both recognition and binding of B. fragilis to LMN-1 are present in OMP extracts. Taken together, our results strongly indicate that a B. fragilis surface glycoprotein may play a key role in bacterial association with LMN-1.