- Volume 11, Issue 12, 2025

The Karelian region, which spans the border between Finland and Russia, presents distinct environmental exposures and lifestyles on either side of the governmental border. In the more urbanized Finnish Karelia, allergic diseases are markedly more prevalent than in the more rural Russian Karelia. Prior studies, based on amplicon sequencing, have demonstrated major differences in skin microbiotas between the two populations. However, compositional differences in microbiota between sensitized and non-sensitized (NS) individuals have not been characterized. Here, in a selected population of 112 allergen-sensitized and NS adolescents, we used shotgun metagenomics to characterize the prokaryotic, eukaryotic and viral species in the skin potentially involved in allergic sensitization via distinct environmental exposures. In the more urban Finnish Karelia, the microbiome species composition was associated with IgE-mediated allergen sensitization status, while in the more rural Russian Karelia, the composition was associated with exposure to furry pets. Finnish participants showing high IgE-mediated sensitization to common allergens (allergen-specific IgE >7.5 kU/L) had less Cutibacterium acnes and Malassezia in their skin and displayed weaker interconnectedness of the microbial co-occurrence network compared with NS participants. Moreover, Malassezia restricta strain-level differences were related to allergen sensitization in both Finnish and Russian participants. In summary, we found distinct skin microbiomes between allergen-sensitized and NS participants and tracked the bacterial and fungal species associated with the degree of allergic sensitization in the more urbanized part of the Karelian region. These findings provide new insights into the factors that shape the human skin microbiome and influence allergic diseases.

Pelvic inflammatory disease (PID), which involves infection and inflammation of the female reproductive tract, can lead to sequelae including chronic pelvic pain, ectopic pregnancy and tubal factor infertility. A causative pathogen is not identified in many PID cases (idiopathic PID) and does not develop in all women with a sexually transmitted infection or bacterial vaginosis. Therefore, there is a need to better understand the pathogenesis of PID. A case–control study was conducted to explore microbiome, antibiotic resistance and immune gene expression in PID. Microbial profiling using both 16S rRNA gene amplicon and metagenomic approaches revealed that bacterial vaginosis-associated bacteria such as Gardnerella vaginalis, Fannyhessea vaginae, Ureaplasma parvum and members of the Prevotella spp. were significantly enriched in PID cases, while healthy controls were associated with Lactobacillus (L.) crispatus. Quantitative analysis with species-specific quantitative real-time PCR (qPCR) indicated that a high copy number of L. crispatus (measured using calibrated copy estimates by qPCR) was strongly associated with cervical samples from women in the control group, whereas PID cases with this organism had low copies when measured using qPCR. Antibiotic resistance to tetracyclines was more frequently predicted in metagenome-assembled genomes from PID cases, and corresponding isolates cultured from cases were less susceptible to doxycycline (L. iners). Overall, this study supports that PID is associated with cervicovaginal dysbiosis and an absence or low quantity of L. crispatus.

Understanding the interactions between gut microbiota, bile acid (BA) metabolism and systemic health is critical for supporting gestational physiological stability in sows, especially during the physiologically demanding late gestation period. Although physiological advantages vary by breed in late-gestation sows, the microbiota-related mechanisms underlying these differences remain poorly understood. This study compared serum antioxidant enzyme activity, oxidative damage markers, inflammatory cytokine levels, gut microbiota composition (analysed via 16S rRNA sequencing), and BA profiles (assessed through targeted metabolomics) between purebred large white (LW) and large white×landrace (LW×LR) crossbred sows during late gestation. Results showed that LW×LR crossbred sows exhibited significantly higher serum superoxide dismutase (SOD) activity and IL-10 levels, alongside reduced IL-6 levels (P<0.05), indicating enhanced antioxidant and anti-inflammatory capacity. Gut microbiota analysis revealed greater alpha diversity (Shannon indices) and a lower Simpson index, along with distinct beta diversity (P<0.05) in crossbred sows, with notable enrichment of functional taxa such as Treponema and Prevotella. Additionally, faecal concentrations of modified BAs, specifically 3-oxolithocholic acid and 7-ketolithocholic acid, were significantly elevated, correlating with increased abundance of gut microbiota encoding BA: Na+ symporter (BASS family) proteins, as well as the increased 7-α-hydroxysteroid dehydrogenase activity (P<0.05). In contrast, LW sows exhibited enrichment of Terrisporobacter and Clostridium sensu stricto 1, alongside accumulation of primary (e.g. chenodeoxycholic acid) and unconjugated BAs (e.g. deoxycholic acid) (P<0.05). Correlation analysis demonstrated that the accumulation of Terrisporobacter and primary BAs was positively correlated with exacerbation of inflammation. In conclusion, under intensive production conditions, significant differences in the gut microbiota–BA axis between LW and LW×LR crossbred sows may underlie variations in oxidative stress and inflammatory status during late pregnancy. These findings provide valuable insights into microbiome–BA–host associations underlying the physiological advantages (enhanced antioxidant and anti-inflammatory capacity) of crossbred sows.

Introduction. Cholera, caused by Vibrio cholerae, remains a priority public health concern, particularly in developing countries. The first cholera outbreak in Zambia was documented in the 1970s, with recurring epidemics reported since then. In 2023, a cholera outbreak affected Zambia, particularly in districts bordering Malawi, Mozambique and the Democratic Republic of Congo, with significant cases reported in these neighbouring countries. This study aims to analyse cholera cases and isolates obtained during the 2023 epidemic, focusing on geographical distribution, genetic relatedness of isolates and their antibiotic resistance profiles.

Methods. Stool samples were collected from patients presenting with cholera-like symptoms across three provinces of Zambia. A total of 98 samples were cultured on thiosulphate citrate bile salts sucrose agar, resulting in 32 sequenced V. cholerae isolates. Whole-genome sequencing was performed using Oxford Nanopore Technology, and phylogenetic inference was also achieved by the analysis of SNPs. Phenotypic antimicrobial resistance testing was conducted following Clinical and Laboratory Standards Institute guidelines. The genomic data were analysed for virulence factors and antimicrobial resistance profiles.

Results. Of the 98 stool samples tested, 38 confirmed cholera cases were identified. A subset of 32 confirmed V. cholerae isolates, predominantly from the Eastern Province of Zambia (n=21), was selected for whole-genome sequencing. Genomic analysis revealed that all isolates belonged to the seventh pandemic El Tor lineage and the O1 serogroup, with two distinct clades identified corresponding to the 10th (T10) and 15th (T15) transmission events. Geographical analysis indicated a predominance of Ogawa serotypes in Eastern Province and Inaba in Northern Province. The virulence gene analysis confirmed the presence of key cholera toxin genes (ctxA and ctxB) and intestinal colonization factors. All isolates carried genes or mutations predicted to confer resistance to multiple antibiotics, including decreased susceptibility to ciprofloxacin, recommended for the treatment of cholera by the World Health Organization.

Conclusion. The findings highlight the critical need for enhanced surveillance and targeted interventions to mitigate cholera outbreaks in Zambia. The emergence of resistant V. cholerae strains necessitates innovative strategies, including improved water sanitation, vaccination efforts and novel therapeutic approaches to combat this enduring public health threat.

Translucent post-larvae disease (TPD) is a new emerging disease causing massive mortality in shrimp at the larval stage. A highly virulent strain of Vibrio parahaemolyticus is reported to be associated with TPD (Vp TPD). Although few genomes from VpTPD strains isolated from China have been characterized, no comprehensive genomic studies have yet to be carried out for VpTPD strains isolated from samples originating outside of China. This study characterized the whole-genome sequence of V. parahaemolyticus strain causing TPD (Vp TPD). The whole-genome sequence of VpTPD was ~5.5 Mb, consisting of two chromosomes and three plasmids. One of the three plasmids encodes three (VHVP) proteins, causing TPD in shrimp. Genomic characterization revealed that Vibrio High Virulent Protein(VHVP) is a Tc-like toxin complex. Laboratory bioassays conducted using Vp TPD revealed that bacterial isolate used in this study causes mortality at the late stage of post-larvae (PL10–PL20). The findings broaden our understanding of the pathogenicity of the Vp TPD strain and diagnosis of TPD.

Streptococcus pneumoniae (Sp) is an opportunistic pathogen that colonizes the mucosal surfaces of the human upper respiratory tract. While transcriptomic studies of Sp have become more common, most have focused on laboratory-adapted strains such as D39 or TIGR4. These strains, though widely used in research, may not fully capture the biology of clinical isolates, particularly the hypervirulent serotype 1 (S1). S1 is clinically significant due to its association with invasive disease, epidemic outbreaks and a distinct global distribution, particularly in regions with a high pneumococcal disease burden. Unlike many other serotypes, S1 is frequently linked to hypervirulence and a propensity for rapid spread, making it a high-priority target for understanding the molecular mechanisms underpinning pneumococcal pathogenesis. In this study, we conducted a comprehensive in vitro transcriptomic analyses of Sp S1 strains, positioning this work as a valuable resource for the pneumococcal research community. Using a straightforward approach, we cultured three distinct S1 strains – ST306, ST217 and ST615, representing European, African and South American S1 lineages, respectively – in Brain Heart Infusion medium and compared transcriptomic profiles during exponential growth to those of the well-characterized laboratory-adapted D39 strain. Our analysis revealed significant differential expression of 292 genes in all three S1 isolates compared to D39. Among these, 151 genes had higher expression, including those involved in competence pathways and purine metabolism, while 141 genes exhibited lower expression, particularly those linked to lactose metabolism and iron/amino acid transport. These findings underscore the distinct molecular features of S1 strains, which likely contribute to the unique pathogenic properties of this serotype. The identification of the distinct transcriptional signatures of hypervirulent S1 strains paves the way for future efforts to design targeted therapeutics against pneumococcal S1 infections.

Campylobacter jejuni is a commensal bacterium that colonizes livestock and wild animals and is responsible for more than 80% of campylobacteriosis cases in humans, which all ultimately have an animal source. Its high genome plasticity and recombination rate allow it to adapt to multiple hosts and lead to the rapid emergence of lineages, some of which can be antibiotic resistant. Our aim in this study was to examine the population structure of Campylobacter in California and assess its differentiation between animal hosts and humans. We sequenced 69 human clinical isolates of C. jejuni from California and collected a dataset of human and animal Californian genomes to contextualize them. By comparing groups of isolates, we detected significant levels of differentiation between the human and animal Californian isolates. Through phylogenetic reconstruction, we demonstrated that, as expected, the human C. jejuni clinical isolates were derived from both avian and ruminant sources but represented a distinct subset of those populations. By identifying the genomic regions that were contributing to population differentiation amongst the host groups, we were able to identify protein variants potentially responsible for host adaptation and propensity to cause infection in humans.

We conducted the first molecular epidemiological analysis of Morganella intermedius, a novel genospecies of Morganella morganii frequently isolated from environmental sources. We identified specific advantages unique to M. intermedius, including the presence of more flagellar-related genes, which may enhance its environmental adaptability. Additionally, we explained the reduced number of antimicrobial resistance genes in M. intermedius, which could be attributed to its possession of more type II and type III restriction–modification systems compared to M. morganii and Morganella sibonii. Most importantly, we propose that environmental M. intermedius strains may contribute to clinical infections, and clinical strains showed the potential to acquire important antimicrobial resistance genes. This underscores the urgent need for increased clinical awareness and enhanced surveillance of this emerging genospecies.