Rotavirus (RV) remains a leading cause of paediatric acute gastroenteritis. COVID-19-associated non-pharmaceutical interventions (NPIs) profoundly altered enteric virus circulation. This single-centre hospital-based retrospective study aimed to describe ten-year epidemiological features among children aged ≤15 years with acute diarrhoea in Hangzhou, including both inpatients and outpatients, with attention to pandemic-related temporal changes, seasonal patterns, and burden of physician-documented clinical myocardial injury. We followed STROBE-RECORD reporting guidelines for electronic-health-record-based observational research. We analysed 71,115 rotavirus antigen test-episodes from children ≤15 years presenting with acute diarrhoea (≥ 3 loose or watery stools within 24 h, episode duration ≤14 days), January 2016-December 2025. Duplicate tests within a single diarrhoeal episode for one individual were excluded; distinct episodes separated by >14 days in the same child were retained. Selected physician-assigned clinical diagnostic labels from electronic medical records were extracted for exploratory secondary analyses, including myocardial-injury diagnoses obtained within 3 days of RV testing. Crude relative risks (RR), modified Poisson regression with robust standard errors, and Firth penalized logistic regression for sparse-event strata were implemented. Negative-binomial regression was applied for formal monthly seasonal inference; cosinor-harmonic regression failed to converge. Myocardial-injury analysis is exploratory because universal standardized cardiac screening was not implemented across the cohort. Sensitivity analyses included a hospitalized-only subset and models incorporating available comorbidity diagnostic tags. Patient-level clustering could not be performed because unique patient identifiers were not retained in the frozen analytical dataset. Electrolyte abnormality labels were unavailable, and cardiac testing frequency could not be quantified; these limitations preclude adjustment for electrolyte disturbances and precise assessment of surveillance bias. Overall RV test-positivity was 16.25
Abstract Background The role of Blastocystis in the pathophysiology of irritable bowel syndrome (IBS) remains controversial, with emerging evidence suggesting subtype-specific differences in pathogenicity. Interleukin-8 (IL-8), a key pro-inflammatory chemokine, has been implicated in mucosal immune activation in both IBS and parasitic infections. Objective This study aimed to investigate the association between Blastocystis subtypes and clinical manifestations of IBS, with a particular focus IL-8 as part of the systemic pro-inflammatory immune response associated with functional GIT disorders and intestinal infections. Methods In this cross-sectional study, 298 symptomatic patients attending a tertiary gastroenterology clinic were evaluated using Rome IV criteria for IBS diagnosis. Identification of Blastocystis in stool samples was done by direct microscopic examination. Subtype identification using PCR and subtype-specific sequence-tagged site primers were also performed. A balanced random selection was used to compare serum IL-8 levels between Blastocystis -positive IBS patients and an equal number of randomly selected Blastocystis -negative IBS patients. Clinical, biochemical, and demographic variables were analyzed in relation to infection status and subtype distribution. Results IBS was diagnosed in 197 out of 298 participants (66.1%), among whom 57 (28.9%) were positive for Blastocystis . Subtype analysis revealed a predominance of subtype (ST) 3 (86%), followed by ST1 (14%). Serum IL-8 levels were significantly higher in Blastocystis -infected IBS patients compared to non-infected controls (129.24 ± 56.28 vs. 26.28 ± 9.28 pg/mL, P < 0.001). Multivariate analysis identified younger age, diarrhea, and spring presentation as independent predictors of Blastocystis infection. Conclusions IBS is frequently associated with Blastocystis infection, particularly with subtype ST3. Serum levels of IL-8 are higher in Blastocystis -infected IBS patients as compared to uninfected ones. Statistical comparison between IL-8 levels in both subtype groups revealed no significant difference, despite the higher numerical values among the ST3 group. The potential aggravating effect of blastocystosis on IBS symptomatology and the relation between individual subtypes and the pro-inflammatory cytokine response require further mechanistic and longitudinal studies to clarify the causal relationship between Blastocystis subtypes and IBS pathogenesis. In addition, local inflammatory markers should be used to study local immune modulation and identify molecular effectors implicated in the pathogenesis of Blastocystis in IBS -infected patients.
The association between invasive infection caused by the Streptococcus bovis/Streptococcus equinus complex (SBSEC) and colorectal neoplasia is well established in international literature. However, evidence from Latin America and the Caribbean remains scarce, fragmented, and methodologically heterogeneous. To map the primary evidence published in Latin America and the Caribbean on invasive SBSEC infection, with emphasis on post-infectious colonic evaluation, reported neoplastic findings, microbiological characterization, and regional knowledge gaps. A scoping review was conducted following the Joanna Briggs Institute methodology and the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR). Five bibliographic databases were searched without date restrictions. Study selection and extraction of 44 variables were performed independently by reviewer pairs. Of 210 records identified, 29 studies published between 1984 and 2025 were included, comprising 25 case reports and 4 case series and representing 79 invasive SBSEC infection episodes in 78 patients from nine countries. Infective endocarditis was the principal presentation in 19 of 29 studies (65.5
Standard eradication therapy for Helicobacter pylori (H. pylori) induces substantial gastrointestinal dysbiosis. Here, we investigated whether probiotic supplementation mitigates these spatial microbial perturbations and facilitates ecological recovery post-eradication. C57BL/6 mice were assigned to five groups: uninfected controls, H. pylori PMSS1-infected mice, infected mice receiving two weeks of triple therapy (omeprazole, clarithromycin and metronidazole), and infected mice undergoing either four-week spontaneous recovery or probiotic supplementation (Enterococcus faecium R0026 and Bacillus subtilis R0179) after eradication. Paired gastric and fecal 16 S rRNA sequencing was utilized to assess microbial composition, cross-compartment co-occurrence networks and predicted functional profiles. H. pylori infection reshapes both the gastric and intestinal microbiota, with more pronounced perturbation on the stomach. However, eradication therapy triggered severe compartment specific dysbiosis that predominantly disrupted the intestine, characterized by near complete depletion of Bacteroidota and expansion of Escherichia-Shigella and Klebsiella. Spontaneous recovery remained incomplete four weeks post eradication. Interestingly, probiotic administration significantly accelerated gastrointestinal restoration and preferentially shaped the intestinal microbiota. It replenished depleted gastric dominant taxa such as Pseudomonas, norank_f_Muribaculaceae, and Ligilactobacillus and rescued the gut microbiota by enriching Bacteroidota and short chain fatty acid (SCFA) producers including Lachnospiraceae_FCS020_group and Ligilactobacillus. Paired analysis revealed that eradication severely disrupted the shared ASVs between the stomach and intestine, a trans-compartment connectivity that was effectively restored by probiotics. Notably, this microbial restoration coincided with enhanced cross-compartment network stability, enrichment of predicted SCFA metabolism and immune modulation pathways and improved intestinal barrier integrity. We delineate the distinct spatial ecological disruptions driven by H. pylori infection and eradication therapy. Probiotic intervention actively orchestrates the synergistic recovery of the gastrointestinal microbiome, providing compelling preclinical evidence for this adjunctive strategy to counter eradication induced dysbiosis.
The COVID-19 pandemic, caused by SARS-CoV-2, produced a global health crisis with disproportionate morbidity and mortality among older adults and medically vulnerable populations. Clostridioides difficile infection (CDI), a leading cause of antibiotic-associated diarrhea and health care-associated colitis, affects many of the same populations and is strongly influenced by antimicrobial exposure, hospitalization, immune status, and disruption of colonization resistance. This narrative mini-review synthesizes clinical and mechanistic evidence linking COVID-19, COVID-19-related care pathways, and susceptibility to CDI, while explicitly distinguishing established observations from hypotheses requiring experimental validation. We distinguish simultaneous SARS-CoV-2/CDI co-infection, CDI developing during hospitalization for COVID-19, and delayed or recurrent CDI after recovery from acute SARS-CoV-2 infection. The available evidence suggests that the interaction is multifactorial and may involve broad-spectrum antibiotic exposure, prolonged hospitalization, infection-prevention disruptions during pandemic surges, SARS-CoV-2-associated gut dysbiosis, epithelial barrier dysfunction, altered bile acid metabolism, and persistent inflammatory signaling. Particular emphasis is placed on angiotensin-converting enzyme 2 (ACE2), renin-angiotensin system imbalance, angiotensin II/AT1R signaling, NF-κB/MAPK activation, IL-6 production, nutritional vulnerability, ApoE-related immunometabolic pathways, and emerging extracellular vesicle-based biomarker frameworks as potential mechanistic interactions. Although direct longitudinal evidence remains limited, convergent clinical and experimental findings support a cautious, testable hypothesis that SARS-CoV-2 infection and COVID-19-related treatment pathways may create a biological context permissive to CDI or delayed intestinal recovery in susceptible individuals. Prospective studies with standardized CDI testing, antimicrobial exposure assessment, microbiome and metabolomic profiling, and mechanistic biomarker discovery are needed to clarify risk, prognosis, recurrence, and long-term consequences.
