Pathogens最新文献

Background/objectives: The gut microbiome plays an important role in the colonization of an individual by Clostridioides difficile and in the development of Clostridioides difficile infection (CDI). The main purpose of this study was to compare the gut microbiomes of patients with CDI and healthy individuals.

Methods: We prospectively included 48 individuals: 32 patients with CDI and 16 healthy individuals. Microbiomes were analyzed by sequencing the hypervariable regions of the 16S rRNA gene using an Ion GeneStudio™ S5 System. Further statistical analysis of microbiome data was performed with the open-source programming language R version 3.5.2.

Results: Among the CDI patients, Firmicutes and Proteobacteria were the most abundant phyla, while Enterobacteriaceae and Enterococcaceae were the most abundant families. Genus-level analysis showed that Enterococcus was the dominant genus in CDI patients; in contrast, in healthy individuals, Faecalibacterium was the most abundant. The MaAsLin2 tool revealed that members of the family Enterococcaceae and the genus Enterococcus were more abundant in patients with CDI than in healthy individuals. Alpha and beta diversity did not reveal differences between the two study groups.

Conclusions: We observed differences in microbiome patterns between healthy individuals and CDI patients that were consistent with the literature. Further studies are needed.

Trypanosoma vivax is a hemoprotozoan parasite of major veterinary importance affecting domestic ungulates in Africa and the Americas. While traditionally addressed within cattle-centered paradigms, accumulating evidence indicates that water buffaloes (Bubalus bubalis) are both clinically susceptible and epidemiologically significant hosts. This structured narrative review provides a host-centered synthesis of global evidence on T. vivax infection in buffaloes, integrating pathogenesis, transmission biology, epidemiology, diagnostics, chemotherapy, and integrated control. The analysis encompasses literature from 2000 to 2025 and incorporates seminal experimental studies published prior to 2000 that established buffalo susceptibility and reservoir competence. Evidence from cyclical (tsetse-mediated) and mechanical transmission systems is comparatively interpreted to clarify host-parasite dynamics. The Amazon biome is discussed as a model system for high-density buffalo production under mechanical vector pressure, offering case-based contextualization without geographic restriction. Particular attention is given to immunopathological mechanisms, chronic low-parasitemia carriage, diagnostic sensitivity in subclinical infections, emerging trypanocide resistance, and ecological constraints on vector control. Controversies and buffalo-specific knowledge gaps are highlighted throughout. By adopting a buffalo-centered analytical framework, this review supports translational diagnostics, targeted surveillance, and sustainable control strategies for trypanosomiasis in tropical livestock systems.

Contagious bovine pleuropneumonia (CBPP) is a significant respiratory disease in cattle caused by Mycoplasma mycoides subsp. mycoides (Mmm). A better understanding of the pathogenesis of CBPP and the immune response of the host to infection will assist in the development of novel interventions to prevent disease progression. In this study, bovine lung explants (BLEs) were exposed to Mmm to investigate the upregulation and release of early inflammatory cytokines, mediators and receptors following tissue infection. Immunomodulatory molecules indicative of cell activation were investigated by immunoblotting on the BLEs and the tissue culture supernatants, and quantitative real-time PCR (RTq-PCR) was performed on the BLEs to determine the fold change in the expression of the respective mRNA. Immunoblotting indicated the production of inflammatory cytokines, mediators and receptors in Mmm-infected BLEs; however, this contrasted strongly with the mRNA expression profile, which did not show any significant fold increase. Infection of the BLEs with Mmm stimulated the production of some pro-inflammatory cytokines and mediators, including IL-1β, COX-2, 5-LOX and iNOS. Toll-like receptor proteins TLR2 and TLR4 were detected solely in the tissue culture supernatant of Mmm-infected BLEs. These receptors are considered to be involved in the recognition of Mmm by BLE tissue cells, thus triggering intracellular pathways that produce specific inflammatory cytokines and mediators, initiating the inflammatory response.

Computer devices in university settings are frequently shared and repeatedly handled, making them potential reservoirs for pathogenic bacteria. This study aimed to investigate the prevalence, virulence determinants, and antimicrobial resistance profiles of Staphylococcus aureus and Escherichia coli isolated from computer devices used by staff and students at a university in Northern Thailand. A total of 400 computer devices were sampled, with each device defined as a single sampling unit comprising both the keyboard and computer mouse. Bacterial identification was performed using PCR, while staphylococcal enterotoxin (se) genes and diarrheagenic E. coli (DEC)-associated virulence genes were detected by PCR. Antimicrobial susceptibility was assessed using the disk diffusion method. Overall, 74 (18.5%) S. aureus isolates and 6 (1.5%) E. coli isolates were recovered. The highest prevalence of S. aureus was observed among personal-use student computer devices (29%; p < 0.001), whereas E. coli was most frequently detected on public-use staff computer devices (4%). Among S. aureus isolates, 24.3% (18/74) carried at least one se gene, with sec being the most prevalent (13.5%). Half of the E. coli isolates harbored the astA gene. Low resistance rates (<10%) were observed among S. aureus; however, four isolates (5.4%) were classified as MRSA, three of which exhibited multidrug resistance. All E. coli isolates were resistant to ampicillin, and 50% displayed multidrug-resistant phenotypes. These findings suggest that computer devices can act as occasional reservoirs of potentially pathogenic and antimicrobial-resistant bacteria in university environments.

Methicillin-resistant Staphylococcus aureus (MRSA) produces virulence factors and causes hard-to-treat infections. This study aimed to evaluate the effect of trans-cinnamaldehyde (TC) on the selected virulence factors of MRSA: adhesion to host plasma and extracellular matrix proteins, protease, DNase and esterase production, and hemolytic activity. Our results showed that TC at ½ MBIC (Minimum Biofilm Inhibition Concentration) of 240 µg/mL or 60 µg/mL, depending on the isolate, significantly reduced MRSA adhesion. Inhibition varied between isolates, ranging from 26.1% to 41.3% (fibrinogen), 18.2% to 34.9% (elastin), 26.5% to 32.4% (laminin), and 17.1% to 30.5% (collagen). TC at ½ MIC (Minimum Inhibitory Concentration) of 30 µg/mL also significantly inhibited MRSA enzyme production, and reduced hemolytic activity (by 80.0-83.1%, depending on the isolate). TC may be an alternative to antibiotics for combating infections caused by S. aureus, as it not only reduces bacterial survival in the host but also reduces S. aureus virulence at subinhibitory concentrations. TC at higher concentrations exhibits cytotoxicity in human fibroblasts, limiting its topical use. Therefore, to exploit TC's antibacterial potential, it is necessary to identify substances that act synergistically with it, enabling reduced effective doses.

Plastic pollutants, including phthalates, bisphenol A (BPA), per- and polyfluoroalkyl substances (PFAS), and microplastics (MPs), are increasingly recognized as emerging environmental cofactors that intersect with infectious disease dynamics. These compounds, once considered inert, can alter immune function, reshape host-pathogen interactions, and directly influence viral survival and transmission. In this review, we compile current evidence on the chemistry, environmental occurrence, and biological activity of major plastic-associated pollutants with emphasis on their role in viral infections. Phthalates such as di(2-ethylhexyl) phthalate (DEHP) and its metabolite MEHP modulate innate immune signaling and have been shown to exacerbate infections, including Dengue and Coxsackievirus B3. Other DEHP-like phthalates, such as dibutyl phthalate (DBP), exhibit consistent infection-enhancing effects, while high molecular weight or cyclical phthalates such as polyvinyl acetate phthalate (PVAP) display conflicting results in their modulation of viral infections. BPA, widely detected in human tissues, acts through endocrine and immune disruption, worsening viral myocarditis, and altering influenza outcomes. PFAS, persistent "forever chemicals," reshape adaptive immune responses and are associated with increased susceptibility, viral persistence, or severity of infection of herpesvirus (HCMV, EBV, HSV-1), hepatitis virus, and influenza infection. Microplastics represent a distinct risk by acting as physical carriers for viruses and bacteria, stabilizing viral RNA, enhancing host cell uptake, and skewing immune responses. Together, these pollutants extend beyond toxicology into virology, providing novel insights into how environmental exposures converge with viral pathogenesis. We highlight mechanistic advances and critical knowledge gaps and propose future directions for integrating environmental health and infectious disease research.

Human papillomavirus (HPV) is a well-known carcinogenic DNA virus, responsible for about 4% of all cancer cases globally. Effective antiviral treatments for those who are already infected with HPV are still in their early stages, despite the fact that prophylactic vaccinations have shown impressive success in preventing new infections. Effective treatments for HPV-related malignancies are also hampered by the fact that current articles address a wide spectrum of pathways but lack thorough systematic studies. In this work, we use bibliometric techniques to examine research trends and innovative approaches in the development of HPV antivirals over the last 40 years. Our results are intended to offer insightful information and direct future research into effective antiviral treatments for HPV-induced cancers.

The protozoan pathogen Toxoplasma gondii is responsible for toxoplasmosis, a disease that can be deadly in immunocompromised patients and the developing fetus during pregnancy. Current treatments are widely considered to be suboptimal. We have recently reported that 5-fluoropyrimidines have highly promising anti-toxoplasmosis effects and are internalized by the parasite by a high-affinity uracil/uridine transporter, TgUUT1. Here, we attempt to identify the gene encoding this transport protein. The only nucleoside or nucleobase family identified in the T. gondii genome was the Equilibrative Nucleoside Transporter (ENT) family, with four members. Of these, TgAT1 is known to be purine-specific, and deletion of the TgENT2 and TgENT3 genes, either separately or jointly, did not affect uridine transport or sensitivity to 5-fluoropyrimidines. In contrast, depletion of TgENT1, an essential gene, resulted in a significant reduction in the uptake of both uracil and uridine but not of the amino acid tryptophan. Moreover, expression of TgENT1 in a Leishmania mexicana cell line with low endogenous uracil uptake rates significantly increased uracil uptake for these cells. We conclude that it is highly probable that TgENT1 encodes the T. gondii uracil/uridine transporter. On the basis of our previous results, we infer that TgENT1 likely also mediates the uptake of 5-fluoropyrimidines.

Background: To assess longitudinal changes in the in vivo confocal microscopy (IVCM) features during Acanthamoeba keratitis (AK) treatment and develop a prognostic model.

Methods: This retrospective study included 59 AK patients who underwent IVCM at baseline and 1 and 3 months. Fourteen morphological features covering pathogen-related characteristics, cyst arrangement patterns, and inflammatory markers were compared between good and poor prognosis groups, which were defined based on clinical outcomes including corneal perforation, the need for therapeutic keratoplasty, or final best-corrected visual acuity (BCVA) ≤ 0.05. Prognostic modeling was performed exclusively using baseline IVCM features and applied univariable and Firth-corrected multivariable logistic regression with collinearity assessment and clinical filtering, followed by 5-fold cross-validation.

Results: Among 59 AK patients, 45 (76.3%) had a good prognosis and 14 (23.7%) had a poor prognosis. Poor prognosis eyes showed a higher prevalence of double-walled cysts, trophozoites, and clustered cysts, along with higher cyst density and deeper stromal invasion. In contrast, good-prognosis eyes had more target-like cysts, immature dendritic cells, and mature dendritic cells. Clustered cysts independently predicted poor prognosis (OR = 2.98), whereas target-like cysts (OR = 0.26) and mature dendritic cells (OR = 0.37) were protective (AUC = 0.883; all p < 0.05).

Conclusions: IVCM provides a quantitative tool for early outcome prediction and individualized management. Higher cyst burden, clustered cysts, and persistent stromal involvement indicated poorer prognosis, whereas target-like cysts and mature dendritic cells indicated better prognosis.

Acanthamoeba castellanii, an opportunistic free-living amoeba, causes severe infections including Acanthamoeba keratitis. This exploratory study evaluated whether three non-steroidal anti-inflammatory drugs (NSAIDs)-acetylsalicylic acid, ibuprofen, and diclofenac (100 µM)-modulate pathogenicity-related processes in A. castellanii and explored the involvement of a gp63-like protein during encystment and adhesion. Trophozoites were continuously exposed to each drug and analyzed for adhesion, migration on host-derived discontinuous brain micropatterns, encystment efficiency, and parasite-induced cytoskeletal remodeling in MDCK epithelial cells. In silico docking was performed to assess potential drug-protein interactions. Drug exposure reduced adhesion with maximal inhibition at 60 min. After 1 h, migration decreased by 49%, 64%, and 38%, and encystment was reduced by 50%, 85%, and up to 90%, respectively, in cultures treated with acetylsalicylic acid, ibuprofen, and diclofenac. Co-incubation with untreated trophozoites lowered actin fluorescence to approximately 50%, whereas drug-treated co-cultures preserved fluorescence near control levels. Colocalization analysis showed increased spatial overlap between gp63-like protein and F-actin in cysts (~40%) and migrating trophozoites (~20%) compared with non-stimulated forms (~3.8%). Collectively, these findings suggest that NSAID-sensitive pathways influence host interaction, migration, and encystment in A. castellanii and allow for the proposal of gp63-like protein as a putative molecular component of the NSAIDs sensitive pathways.