The poor prognosis of infections associated with multidrug-resistant Pseudomonas aeruginosa can be attributed to several conditions of the patient and virulence factors of the pathogen, such as the type III secretion system (T3SS), which presents the ability to inject four effectors into the host cell: ExoS, ExoT, ExoU and ExoY. The aim of this study was to analyze the distribution of exo genes through multiplex polymerase chain reaction in P. aeruginosa strains isolated from patients at a third-level pediatric hospital and their relationships with clinical variables, e.g., the origin of the sample, susceptibility profile and outcome, through a multinomial logistic regression model. A total of 336 bacterial strains were obtained from cystic fibrosis (CF; n = 55) and bloodstream infection (BSI; n = 281) samples, and eleven presence (+)/absence (−) exo virulotype patterns were identified. The virulotype V3 (exoU−/exoS+/exoT+/exoY+) was observed in 64.28%, followed by V1 (exoU+/exoS−/exoT+/exoY+) with 11.60%. Additionally, V2 (exoU+/exoS−/exoT+/exoY−) was present in 11.60%, and V7 (exoU−/exoS+/exoT+/exoY−) was present in 4.17%. The remaining virulotypes (8.33%) identified were clustered in the other virulotype (OV) group (V4, V5, V6, V8, V9, V10 and V11). The clinical records of 100 patients and their outcomes were reviewed. Fifteen patients died (CF = 4; BSI = 11). V2 and V1 were the virulotypes most related to pandrug resistance (PDR), whereas the V1 relative risk of death was determined to be almost four-fold greater than that of V3, followed by V2 and OV. In summary, the virulotypes V1, V2 and CF are related to death. This study highlights the association of T3SS virulotypes with the susceptibility profile, clinical origin and their potential for predicting a poor prognosis.

Recent multidrug resistance in Pseudomonas aeruginosa has favoured the adaptation and dissemination of worldwide high-risk strains. In June 2018, 15 P. aeruginosa strains isolated from patients and a contaminated multi-dose meropenem vial were characterized to assess their association to an outbreak in a Mexican paediatric hospital. The strains were characterized by antibiotic susceptibility profiling, virulence factors’ production, and biofilm formation. The clonal relationship among isolates was determined with pulse-field gel electrophoresis (PFGE) and multi-locus sequence typing (MLST) sequencing. Repressor genes for the MexAB-OprM efflux pump were sequenced for haplotype identification. Of the strains, 60% were profiled as extensively drug-resistant (XDR), 33% as multidrug-resistant (MDR), and 6.6% were classified as sensitive (S). All strains presented intermediate resistance to colistin, and 80% were sensitive to aztreonam. Pyoverdine was the most produced virulence factor. The PFGE technique was performed for the identification of the outbreak, revealing eight strains with the same electrophoretic pattern. ST235 and ten new sequence types (STs) were identified, all closely related to ST233. ST3241 predominated in 26.66% of the strains. Twenty-five synonymous and seventeen nonsynonymous substitutions were identified in the regulatory genes of the MexAB-OprM efflux pump, and nalC was the most variable gene. Six different haplotypes were identified. Strains from the outbreak were metallo-β-lactamases and phylogenetically related to the high-risk clone ST233.

Dysbiosis plays an important role in the development of bacterial infections in the gastric mucosa, particularly Helicobacter pylori. The international guidelines for the treatment of H. pylori infections suggest standard triple therapy (STT). Nevertheless, because of the increasing resistance rates to clarithromycin, metronidazole has been widely considered in several countries. Unfortunately, the non-justified administration of antibiotics induces dysbiosis in the target organ. We characterized the gastric microbiota of patients diagnosed with follicular gastropathy and pangastropathy attributed to H. pylori infection, before and after the administration of STT with metronidazole. Dominant relative abundances of Cutibacterium were observed in pre-treatment patients, whereas H. pylori was observed at <11%, suggesting the multifactor property of the disease. The correlation of Cutibacterium acnes and H. pylori with gastric infectious diseases was also evaluated using quantitative real-time polymerase chain reaction. The dominance of C. acnes over H. pylori was observed in gastritis, gastropathies, and non-significant histological alterations. None of the microorganisms were detected in the intestinal metaplasia. Post-treatment alterations revealed an increase in the relative abundances of Staphylococcus, Pseudomonas, and Klebsiella. Non-H. pylori gastrointestinal bacteria can be associated with the initiation and development of gastric diseases, such as pathobiont C. acnes.