The study also examined whether the microbial community associated with human skin changes between childhood and early adulthood. The team analyzed skin samples from 304 healthy volunteers: 150 children with a mean age of 5.45 ± 0.50 years and 154 young adults with a mean age of 19.48 ± 0.88 years. The overall microbial structure and alpha diversity differed significantly between the groups, and principal-coordinate analysis separated the cohorts.

Bacillota and Actinomycetota abundance did not differ significantly, whereas Bacteroidota was more abundant and Pseudomonadota less abundant in young adults. The study was cross-sectional, so it measured differences between age groups at one point rather than following individual microbiomes over time. At the genus level, Bacteroides was the predominant genus in both cohorts, accounting for an average relative abundance of 15.36% in children and 26.67% in young adults, as determined by 16S rRNA sequencing.

The abundances of Bacteroides and Alistipes increased significantly in young adults, whereas Prevotella 9 was more abundant in children. Several Pseudomonadota genera, including Klebsiella , Moraxella and Pseudomonas , were significantly less abundant in the adult group. In children, Bacteroidota and Pseudomonadota abundance were inversely correlated; the same association was not detected among young adults.

The authors proposed that the age-associated increase in Bacteroides might contribute to the exclusion of potentially pathogenic Gram-negative bacteria, although the human data establish an association rather than causation. To test that possibility, the researchers established a mouse skin co-colonization model using B. fragilis ATCC 25285 and bacterial isolates from skin or clinical specimens. Concurrent topical application of live B. fragilis and K. pneumoniae at a 1:1 ratio significantly reduced K. pneumoniae colonization.

The same bacterium also reduced the loads of Moraxella catarrhalis and Pseudomonas fulva . By contrast, colonization by the Gram-positive organisms Staphylococcus aureus and S. epidermidis was not significantly affected, indicating selectivity for the tested Pseudomonadota in this model. Timing also mattered: pre-inoculating mice with B. fragilis two hours before K. pneumoniae was effective, whereas introducing B. fragilis after K. pneumoniae was not.

Experiments with cultured cells indicated that the effect could not be explained simply by soluble antimicrobial products or impaired bacterial adhesion. Concentrated B. fragilis culture supernatant inhibited several organisms in vitro, but the pattern did not match the mouse results, and S. aureus was inhibited in culture without a corresponding reduction in vivo. In an immortalized human epidermal cell model, B. fragilis did not alter K. pneumoniae , M. catarrhalis or P. fulva adhesion to keratinocytes.

Exposure to K. pneumoniae , but not to B. fragilis alone, increased transcription of TNFα , IL36α and IL10 , while the antimicrobial peptide LL37 was inhibited by either bacterium. These observations pointed away from direct competition or inflammatory signalling in keratinocytes as the main explanation for the reduced colonization seen in mice. The central mechanistic evidence came from macrophages expressing LC3-GFP.

Cells exposed to B. fragilis alone or co-exposed to B. fragilis and K. pneumoniae accumulated more LC3-positive puncta than cells infected with K. pneumoniae alone. Western blotting showed increased LC3-II and reduced p62, a protein that is selectively degraded during autophagic flux, following co-infection. Transmission electron microscopy revealed double-membrane autophagosomes and vacuoles containing cellular debris.

Treatment with 3-methyladenine, an inhibitor of autophagy initiation, abolished the reduction in intracellular K. pneumoniae , M. catarrhalis and P. fulva , linking the antibacterial effect to the autophagic response under the tested conditions. Purified B. fragilis outer membrane vesicles reproduced several of these findings. The vesicles were spherical, had a bilayer membrane and averaged 162.1 ± 18.9 nanometres in size, with a mean zeta potential of −17.768 ± 2.238 millivolts.

Particle-to-protein ratios remained consistent across different protein concentrations, and the vesicle preparation displayed a different protein profile from whole-cell lysates. At 5 micrograms per millilitre, the vesicles increased LC3 puncta, LC3-II accumulation and autophagic structures in macrophages and reduced the intracellular loads of all three tested Pseudomonadota species. The effect disappeared when autophagy was inhibited with 3-methyladenine.

The vesicles did not significantly inhibit bacterial growth when tested directly in vitro, arguing against a simple direct-antibiotic explanation. Evidence from genetically modified mice extended the mechanism to skin colonization. Live B. fragilis lowered K. pneumoniae loads in wild-type C57BL/6J mice but not in homozygous lc3a -deficient mice, with six animals per group.

Heat-killed bacteria were ineffective. Skin immunohistochemistry showed increased LC3A immunoreactivity and reduced p62/SQSTM1 immunoreactivity after treatment with live B. fragilis , consistent with enhanced autophagic activity and substrate turnover. Purified intact outer membrane vesicles also reduced K. pneumoniae colonization in wild-type but not lc3a -deficient mice, with four animals per group.

Neither disrupted B. fragilis vesicles nor S. epidermidis extracellular vesicles had the same effect, suggesting that vesicle integrity and bacterial source were important under the tested conditions. Live B. fragilis and intact vesicles also reduced skin expression of the inflammatory cytokines TNFα and Il36α induced by K. pneumoniae . The authors described the mechanism as a possible explanation for the inverse relationship between Bacteroidota and Pseudomonadota observed in children.

The experiments also show that the response depends on the integrity of the outer membrane vesicles and on host LC3A-associated autophagy. Whether this mechanism operates at the same scale or strength in healthy human skin remains unresolved. Several limitations constrain how broadly the results can be applied.

The human study was cross-sectional, so differences in hygiene, lifestyle, hormonal development and other environmental or developmental factors may have contributed to the observed age-related pattern. Because 16S rRNA sequencing cannot establish bacterial viability, species identity, stable residence or the precise anatomical source of a sequence signal, transient deposition and gut-to-skin transfer could not be excluded. The animal work also relied on the laboratory-adapted B. fragilis ATCC 25285 strain because the researchers did not recover Bacteroides from healthy human skin samples under their culture conditions.

The occlusive dressings used in the mouse model may have increased local hydration and reduced oxygen exposure, potentially favoring the anaerobe. The specific vesicle-associated molecules that initiate autophagy remain unresolved, and their activity may differ among species or strains. Proteomic and lipidomic analysis of vesicles from skin-adapted isolates will be needed to identify the relevant components and determine whether this laboratory mechanism operates in healthy human skin.

Subject of Research: Bacteroides fragilis outer membrane vesicles, autophagy and skin colonization resistance

Article Title: Bacteroides fragilis outer membrane vesicle mediates Pseudomonadota colonization by inducing autophagy on the skin

Article References: Guo, Y., Nurxat, N., Wang, Q., Shen, Z., Zhao, N., Liu, Y., Jian, Y., Ye, B., Li, M., & Liu, Q. (2026). Bacteroides fragilis outer membrane vesicle mediates Pseudomonadota colonization by inducing autophagy on the skin. iScience, 29(11), Article 117969. https://doi.org/10.1016/j.isci.2026.117969

Image Credits: AI Generated

DOI: 10.1016/j.isci.2026.117969

Keywords: Bacteroides fragilis, outer membrane vesicles, autophagy, skin microbiome, Pseudomonadota, colonization resistance, Klebsiella pneumoniae, host–microbe interactions, murine skin model, 16S rRNA sequencing, Bacteroides, fragilis

Researchers conducted a comprehensive literature search to identify eligible studies examining bacterial urinary tract infections and common uropathogenic bacteria among people living with HIV/AIDS. They calculated pooled prevalence estimates with a random-effects model, assessed heterogeneity using the I² statistic and performed the statistical analyses in Stata version 14.0. The final analysis included 37 studies and 14,318 people living with HIV/AIDS. Because the overall I² value reached 98.5%, the 18% estimate should be understood as a pooled summary of the included studies rather than a uniform prevalence applicable to every population, location or clinical setting.

Regional subgroup analysis identified Asia as having the highest observed pooled prevalence, at 30% (95% CI: 17–43%; I² = 97.8%). The confidence interval was broad and heterogeneity within the Asian subgroup remained very high. The supplied results did not give comparable numerical estimates for the other regions, so the remaining regional differences could not be quantified. The Asian figure represents the highest prevalence among the reported subgroup estimates; it does not establish a global trend or a change over time.

Pathogen-specific meta-analysis yielded pooled proportions of 45% for Escherichia coli, 13% for Staphylococcus aureus and 12% for Klebsiella pneumoniae. The corresponding 95% confidence intervals were 37–53%, 9–17% and 8–15%, with I² values of 93.2%, 85.6% and 80.8%, respectively. Additional pooled proportions were 6% for Enterobacter species, 11% for Pseudomonas aeruginosa and 11% for Enterococcus species. These are pooled pathogen-specific proportions for the populations assessed; the supplied evidence does not establish that they are the probability of isolating a given organism from any individual urinary tract infection. The review was not a clinical trial and did not directly test a diagnostic strategy, antimicrobial treatment or prevention program. Its findings instead synthesize the reported burden and distribution of bacterial urinary tract infections in people living with HIV/AIDS, supporting the authors’ conclusion that these infections remain clinically important and require timely diagnosis and appropriate empirical treatment.

Subject of Research: Global prevalence and pathogen distribution of bacterial urinary tract infections among people living with HIV/AIDS

Article Title: Prevalence and distribution of common uropathogenic bacteria among HIV/AIDS patients worldwide: a systematic review and meta-analysis

Article References: Zomorodi, A. R., Askari, S., Aflakian, F., Bahrami, M., Farshi, Z. G., Mahmoodi, A., Azhdari, S., & Motamedifar, M. (2026). Prevalence and distribution of common uropathogenic bacteria among HIV/AIDS patients worldwide: a systematic review and meta-analysis. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14283-6

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14283-6

Keywords: HIV/AIDS, urinary tract infections, uropathogenic bacteria, Escherichia coli, Klebsiella pneumoniae, Staphylococcus aureus, systematic review, meta-analysis, prevalence, pathogen distribution, distribution, common

The overall difference was statistically significant, with p<0.001. Clinically true growth was also more frequent among patients with COVID-19. It occurred in 31.9% of COVID-19 culture sets, compared with 22.9% of sets from patients without COVID-19 during the pandemic and 16.1% of pre-pandemic sets.

Both comparisons produced p-values below 0.001. These percentages describe outcomes among the culture sets collected; they do not directly estimate an individual patient’s probability of developing a bloodstream infection. The distribution of individual microorganisms also differed across the three groups.

Acinetobacter baumannii was the most frequently detected organism among patients with COVID-19, appearing in 12.2% of culture sets, compared with 3.8% in the non-COVID pandemic group and 2.2% in the pre-pandemic group. All pairwise comparisons were statistically significant. The proportion ratio for A. baumannii in the COVID-19 group relative to the pre-pandemic group was 5.56, with a 95% confidence interval of 3.88–7.97.

Klebsiella pneumoniae was more frequent in both pandemic groups than before the pandemic. Staphylococcus aureus , coagulase-negative staphylococci and Stenotrophomonas maltophilia were also more frequent in the COVID-19 group than in the pre-pandemic group, although the supplied findings do not report the corresponding proportion ratios or confidence intervals for each of those organisms. Not every microbiological measure changed in parallel with the overall pattern.

The researchers detected no significant differences in the proportions of methicillin-resistant Staphylococcus aureus or vancomycin-resistant enterococci, and they found no significant difference in the frequency of Candida species. Comparisons were performed using the chi-square test or Fisher’s exact test, with Bonferroni adjustment for pairwise comparisons, and proportion ratios were calculated with 95% confidence intervals. The retrospective design and single-center scope limit the conclusions that can be drawn.

The analysis identifies associations between group membership, pandemic period and blood-culture outcomes but does not establish that COVID-19 caused the observed changes. The investigators noted that the COVID-19 pandemic required substantial reorganization of hospital services, with potential implications for infection prevention and blood-culture quality. They identified monitoring of blood-culture contamination during healthcare crises as an important implication of the findings and said that further patient-level studies are needed to clarify the underlying factors.

Overall, the study documents a distinct blood-culture profile among adult intensive care patients with COVID-19: more contaminated sets, more sets with clinically true growth, more polymicrobial infections and a particularly high frequency of A. baumannii , while the measured resistance markers and Candida frequency did not differ significantly across the groups.

Subject of Research: Blood-culture epidemiology in adult intensive care patients during the COVID-19 pandemic

Article Title: Shifting epidemiology of bloodstream infections during the pandemic era: a comparative analysis of blood cultures from adult intensive care unit patients

Article References: Yıldız Kaya, S., Kaya, A., Kurt, A. F., Çelik, Ö. F., Houssein, F. M., Kayhan, O., Bozbay, S., Karaali, R., Balkan, İ. İ., Mete, B., Saltoğlu, N., Tabak, F., & Aygün, G. (2026). Shifting epidemiology of bloodstream infections during the pandemic era: a comparative analysis of blood cultures from adult intensive care unit patients. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14680-x

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14680-x

Keywords: COVID-19, blood cultures, bloodstream infections, intensive care, culture contamination, polymicrobial infection, Acinetobacter baumannii, Klebsiella pneumoniae, antimicrobial resistance, pandemic epidemiology, Shifting, epidemiology

The results establish a regional genomic baseline for a selected high-risk clinical subset, rather than a population-wide estimate of resistance prevalence. The State Public Health Laboratory of Aguascalientes processed 3,454 E. coli and Klebsiella isolates from regional hospitals during the study period, including 683 E. coli, 679 K. pneumoniae and 92 organisms initially identified by MALDI-TOF mass spectrometry and phenotypic testing as K. oxytoca. Whole-genome sequencing reclassified two of the latter isolates as K. michiganensis.

Of the processed isolates, 246 met the study definitions for multidrug resistance or extensive drug resistance, and 65 were selected for sequencing after confirmation of species identity, availability of pure clinically relevant cultures and satisfaction of DNA-quality requirements. Almost all the sequenced isolates—94%—were recovered from patients in critical-care units, and clinical records classified 97.1% of Klebsiella cases and 93.3% of E. coli cases as severe illness. This referral pattern is central to interpreting the findings: the dataset represents severe, treatment-refractory or otherwise difficult-to-manage infections and is enriched for highly resistant organisms rather than representing community circulation.

p>Phenotypic susceptibility testing showed broad resistance across major antibiotic classes, including several drugs commonly used for urinary, respiratory and inpatient infections. Every sequenced isolate carried extended-spectrum beta-lactamase genes, consistent with cephalosporin resistance reaching 97.1% among the 35 Klebsiella isolates and 100% among the 30 E. coli isolates. Resistance to ciprofloxacin and levofloxacin exceeded 90% in both groups, while trimethoprim-sulfamethoxazole resistance was 82.8% in Klebsiella and 90% in E. coli.

Carbapenem resistance occurred in 31.4% of Klebsiella isolates and 13.3% of E. coli isolates. Amikacin retained activity against more isolates than most tested agents, although resistance was present in 11.4% of the Klebsiella group. Among Klebsiella respiratory isolates, tigecycline resistance increased from 0% in 2022 to 40% in 2023.

The study also found that E. coli XDR phenotypes were confined to the 2023 collection, while later Klebsiella isolates showed more dynamic carbapenem and tigecycline resistance patterns. p>Integrating phenotypic susceptibility results with genomic predictions produced 78.9% overall concordance across 689 antibiotic-class comparisons. Agreement exceeded 90% for fluoroquinolones, sulfonamides and macrolides, whose resistance determinants are comparatively well characterized, and reached 100% for E. coli against cephalosporins and for both macrolide results in Klebsiella. Concordance was substantially lower for aminoglycosides and carbapenems.

Some Klebsiella isolates were phenotypically resistant to carbapenems without carrying canonical blaKPC, blaNDM or blaOXA-48 genes; combinations of OXA-type beta-lactamases, porin disruption and efflux systems were instead associated with the phenotype. These findings identify possible non-classical contributors but do not directly prove their causal effects. Genomic predictions can also be affected by gene expression, regulatory mutations, epistasis, promoter efficiency and laboratory conditions, so the authors emphasize that gene detection alone cannot replace phenotypic susceptibility testing. p>Phylogenomic analysis placed the Aguascalientes genomes within a broader but unevenly sampled Mexican genomic landscape.

The comparative dataset included 268 public genomes: 139 E. coli, 85 K. pneumoniae and 44 K. michiganensis, the last comprising three Mexican isolates and 41 international reference genomes. Mexico City and Puebla were relatively well represented, whereas more than half of Mexico’s states were under-represented or absent. The 30 E. coli isolates from Aguascalientes fell into 15 sequence types and were distributed across the phylogeny rather than forming one local cluster.

They were interspersed with genomes from other states, indicating that the lineages detected locally overlapped with broader national patterns. Because sampling was neither population-based nor geographically uniform, the national comparison cannot establish population prevalence or a continuous national transmission route. The E. coli collection included established high-risk lineages such as ST131 and ST69, which also occurred most frequently among the public Mexican E. coli genomes.

Six isolates could not be assigned to a recognized sequence type; these untyped genomes carried the largest resistance-gene burdens, averaging more than 100 antimicrobial-resistance genes per genome. The blaCTX-M-15 gene was present in 90% of the Aguascalientes isolates, compared with 18% of public Mexican E. coli genomes. Polymyxin-associated regulators, including arnA, eptA, mgrB and members of the pmrB, pmrC and pmrF family, also occurred at higher frequencies in the referral collection.

Detection of these genes establishes their genomic presence, not phenotypic colistin resistance or the transfer of a particular plasmid. Across 169 E. coli genomes, the researchers identified 345 mobile genetic elements in the LESPA isolates, including 26 plasmid-associated elements and 319 of uncertain chromosomal origin. MITEEc1 had the largest number of reported associations, including links with ompT and virulence-associated loci.

p>Resistance genes were frequently located in mobile contexts, a pattern consistent with possible horizontal gene-transfer dynamics in clinical environments. The analysis catalogued 211 mobile genetic elements among the sequenced K. pneumoniae isolates and identified associations involving plasmids, transposons and insertion sequences. K. pneumoniae served as a principal sharing hub in the cross-species network, linking genes including the CTX-M-15, sul1, sul2, tetA, mphA and dfrA families with both E. coli and Klebsiella.

The two K. michiganensis isolates carried NDM-7, VIM-1 and MCR-9.1, which were absent from the sequenced E. coli and K. pneumoniae mobilomes. These observations identify mobile contexts and candidate routes of dissemination, but the study did not perform long-read sequencing or reconstruct complete plasmids. Genomic proximity alone therefore does not demonstrate patient-to-patient transmission or prove that a particular element transferred between species. p>The K. michiganensis isolates expanded the limited genomic record for an undercharacterized member of the K. oxytoca complex in Mexico.

One belonged to ST180 and clustered with genomes from China and the United States, while the other had an unknown sequence type and grouped with Mexican and North American isolates. Their phylogenetic positions were consistent with separate introductions into the regional collection, but the sample of two was too small to establish the species’ broader epidemiology. They were also the first multidrug-resistant K. michiganensis genomes reported from Aguascalientes and occupied separate resistance-gene clusters.

Pangenome analysis showed open, accessory-rich genomes for all three species. Cloud genes, defined as genes present in fewer than 15% of genomes, accounted for 81.7% of the E. coli pangenome, 76.1% of K. pneumoniae and 63.8% of the K. oxytoca complex dataset, illustrating substantial genomic diversity without directly demonstrating its origin or rate of evolution. p>Clinical complexity accompanied the molecular findings. Coinfections were recorded in 60% of Klebsiella cases and 36.7% of E. coli cases, with Acinetobacter baumannii, Enterococcus faecalis and Pseudomonas aeruginosa among the most frequent co-occurring organisms.

Among E. coli, virulence analysis identified seven units found only in the LESPA collection, including a shu hemin-uptake operon, afaC-VIII and galU; no K. pneumoniae virulence units exclusive to the new isolates were found. Temporal comparisons showed richer resistomes, more XDR phenotypes and more frequent coinfections among post-2020 isolates than in the older public collection, including a rise in carbapenem resistance among Klebsiella respiratory isolates from 0% in 2022 to 83% in 2023. These observations cannot be attributed to the COVID-19 pandemic or antibiotic use from this referral-heavy dataset, and they do not demonstrate population-wide temporal change.

The study instead supports routine whole-genome sequencing, standardized metadata and continued phenotypic testing as components of more representative antimicrobial-resistance surveillance across Mexico.

Subject of Research: Genomic surveillance of multidrug-resistant E. coli and Klebsiella in Aguascalientes, Mexico

Article Title: Genomic surveillance uncovers high-risk resistance profiles in Escherichia coli and Klebsiella spp. from Central Mexico

Article References: Lozano Gamboa, M. S., Muñoz Gomez, B., Maldonado Gonzaga, A. Y., Alejo Hernández, M. A., Cazares, A., Diaz, D., Marmolejo, A. P., & Ceapă, C. D. (2026). Genomic surveillance uncovers high-risk resistance profiles in Escherichia coli and Klebsiella spp. from Central Mexico. Frontiers in Cellular and Infection Microbiology, 16, 1939440. https://doi.org/10.3389/fcimb.2026.1939440

Image Credits: AI Generated

DOI: 10.3389/fcimb.2026.1939440

Keywords: antimicrobial resistance, genomic surveillance, Escherichia coli, Klebsiella pneumoniae, Klebsiella michiganensis, whole-genome sequencing, resistome, mobile genetic elements, Mexico, clinical microbiology, Genomic, surveillance

The study screened a library of phytochemicals selected for their reported potential to inhibit resistance enzymes rather than for direct antimicrobial activity. The researchers used ADMET profiling, or assessment of absorption, distribution, metabolism, excretion and toxicity, followed by molecular docking against the NDM-1 and KPC-2 β-lactamase enzymes. Quercetin, eriodictyol and luteolin produced favorable predicted docking scores: −9.1, −8.32 and −8.66 kcal/mol against KPC-2, and −8.74, −8.72 and −8.73 kcal/mol against NDM-1, respectively.

Molecular dynamics simulations were then performed for quercetin complexes with NDM-1 and KPC-2 to examine the predicted conformational behavior of those complexes. These computational findings supported further investigation of quercetin, but the docking and simulation results were predictions rather than direct measurements of enzyme inhibition. The reported in vitro assay showed potentiation of carbapenem activity against the CRKP isolate, while the abstract states that the assays did not directly assess β-lactamase inhibition.

The findings therefore identify quercetin as a preliminary carbapenem-adjuvant candidate under laboratory conditions, with supporting computational analyses and an observed improvement in antibacterial activity. The mechanism responsible for that potentiation remains unconfirmed, and the supplied evidence does not establish whether quercetin directly inhibits NDM-1, KPC-2 or another target. The results are also limited in scope because the reported laboratory testing involved one CRKP isolate; the abstract does not provide evidence about activity against a broader isolate collection or clinical effectiveness in people. The article was published on 12 October 2026 as an open-access, early version of peer-reviewed research and was described as subject to further edits before replacement by the final version of record.

Subject of Research: In vitro and computational evaluation of quercetin as a potential carbapenem adjuvant against a carbapenem-resistant Klebsiella pneumoniae isolate

Article Title: Phytochemical screening as an inhibitor of β-lactamases to overcome the carbapenem-resistant of Klebsiella pneumoniae

Article References: Azmal, M., Paul, J. K., Shohan, M. N. H., Haque, A. N. M. S. N. B., Mrinmoy, M., Talukder, O. F., Mishu, M. A., Mia, M. W., & Ghosh, A. (2026). Phytochemical screening as an inhibitor of β-lactamases to overcome the carbapenem-resistant of Klebsiella pneumoniae. Scientific Reports. https://doi.org/10.1038/s41598-026-68970-0

Image Credits: AI Generated

DOI: 10.1038/s41598-026-68970-0

Keywords: quercetin, Klebsiella pneumoniae, carbapenem resistance, β-lactamases, NDM-1, KPC-2, molecular docking, ADMET profiling, in vitro assay, Scientific Reports, Phytochemical, screening

The study reviewed records from the Second Affiliated Hospital of Zhejiang University School of Medicine, where 428 adult COVID-19 inpatients with microbiological surveillance data were admitted between November 2022 and February 2023. A total of 333 patients, or 77.8%, developed at least one additional infection. An infection detected within 48 hours of hospitalization was classified as a co-infection, while one first detected after 48 hours was classified as a secondary infection. Pathogens were grouped into Gram-negative bacteria, Gram-positive bacteria and fungi, with resistant isolates identified separately.

Resistant Acinetobacter baumannii was the most frequently detected pathogen, appearing in 55.9% of patients with infection, followed by resistant Klebsiella pneumoniae in 38.4%, fungi in 33.0% and resistant Pseudomonas aeruginosa in 14.1%. The researchers categorized patients into four pathogen-detection trajectories: no infection, sensitive-bacterial infection, resistant-bacterial infection and fungal-involved infection. They also examined the shape and burden of daily pathogen detections, then tested associations with death, total hospital stay, intensive-care stay and duration of mechanical ventilation.

After adjustment for age, Sequential Organ Failure Assessment score, the ratio of arterial oxygen tension to inspired oxygen fraction, admission to intensive care and underlying comorbidities, all three infection trajectories remained associated with in-hospital death. Compared with the no-infection group, adjusted odds ratios were 2.87 for sensitive-bacterial infections, 3.15 for fungal-involved infections and 4.69 for resistant-bacterial infections, with all 95% confidence intervals excluding one. The secondary outcomes followed the same broad gradient: total hospital stay, intensive-care stay and mechanical-ventilation duration were shortest in patients without additional infection and longest in the resistant-bacterial and fungal-involved groups.

Several analytic approaches supported the association. Propensity-score matching produced an odds ratio of 2.05 for a high-risk infection group compared with the no-infection group, while inverse-probability-of-treatment weighting yielded an adjusted odds ratio of 4.13 for resistant-bacterial infections. In time-dependent competing-risk analyses, infection onset was also associated with a higher instantaneous hazard of death for sensitive-bacterial, resistant-bacterial and fungal trajectories. These methods strengthen the robustness of the observed relationship, but the single-center, retrospective design cannot establish that infections caused the excess mortality. Differences in illness severity, treatment exposure, surveillance practices or unmeasured confounding could contribute to the findings, and the results describe a specific hospitalized population rather than all patients with COVID-19.

Subject of Research: Associations between secondary pathogen infections, clinical trajectories and mortality in hospitalized COVID-19 patients

Article Title: Pathogen trajectory and prognosis of co-infection and secondary infection in hospitalized COVID-19 patients

Article References: Wang, X., Yu, J., Zhang, K., Bai, S., Pan, W., Yang, W., Shao, X., Shen, Z., Zhen, N., Cui, W., Cai, J., Zhang, S., & Zhang, G. (2026). Pathogen trajectory and prognosis of co-infection and secondary infection in hospitalized COVID-19 patients. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14260-z

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14260-z

Keywords: COVID-19, co-infection, secondary infection, hospital mortality, antimicrobial resistance, Acinetobacter baumannii, Klebsiella pneumoniae, Pseudomonas aeruginosa, fungal infection, retrospective cohort, Pathogen, trajectory

The research team, led by Rameen Parvez and Mohsin Khurshid of the Institute of Microbiology at Government College University Faisalabad, with collaborators including James Jacob Sasanya of the International Atomic Energy Agency in Vienna, sampled three distinct tiers of the poultry economy between September 2024 and April 2025. By including commercial broiler operations, small-scale backyard flocks and retail markets, the design captured the full trajectory of poultry production from intensive rearing to point of sale. This matters because each tier represents a different interface between bacteria and humans, from farm workers exposed directly to birds and litter, to consumers handling raw meat in their kitchens.

Identification of the isolates was rigorous. The team combined conventional biochemical testing with API 20E strips, matrix-assisted laser desorption ionization time-of-flight mass spectrometry, a proteomic technique that fingerprints bacterial species by their protein profiles, and amplification of the rpoB gene, a molecular marker widely used to confirm species identity. This layered approach guards against the misidentification that has plagued some earlier surveys, since K. pneumoniae and its close relative K. oxytoca can be difficult to distinguish phenotypically. Of the 900 samples, 303, or 33.7 percent, yielded K. pneumoniae, a prevalence figure that underscores how thoroughly this organism has colonized the poultry environment.

The resistance picture that emerged was grim. Among the 303 isolates, 199, or 65.7 percent, qualified as multidrug-resistant under internationally accepted definitions, meaning they were nonsusceptible to at least one agent in three or more antibiotic classes. A further 48 isolates, 15.8 percent, were extensively drug-resistant, a category reserved for bacteria that have lost susceptibility to agents in all but one or two classes. Perhaps most tellingly, isolates from commercial broiler farms carried a heavier resistance burden than those recovered from backyard flocks or retail markets, a gradient consistent with the intensive antimicrobial use documented on industrial poultry operations in the region.

At the molecular level, polymerase chain reaction screening revealed a familiar but troubling cast of resistance genes. The dominant extended-spectrum beta-lactamase determinants were blaCTX-M-15 and blaTEM, enzymes that hydrolyze third-generation cephalosporins, workhorse antibiotics in both human and veterinary medicine. CTX-M-15 in particular is a global success story for the bacterium, having spread explosively through human clinical populations over the past two decades. Its prominence in poultry-associated isolates suggests that the farm environment is not merely a passive reservoir but an active participant in the circulation of the very genes that compromise treatment of urinary tract infections, bloodstream infections and hospital-acquired pneumonia.

More alarming still was the detection of carbapenemase genes among carbapenem-resistant isolates. The team identified blaNDM, blaKPC and blaOXA-48, three of the most clinically consequential carbapenemase families known. Carbapenems are often described as last-line antibiotics for infections caused by gram-negative bacteria, and the World Health Organization lists carbapenem-resistant K. pneumoniae as a critical-priority pathogen. The presence of NDM-type enzymes, which originated on the Indian subcontinent and have since spread worldwide, in bacteria recovered from poultry points to a plausible environmental bridge by which these determinants could move between animal, food and human compartments.

Colistin, a polymyxin antibiotic revived as a treatment of last resort when carbapenems fail, fared no better. Resistance to colistin was detected in 5.9 percent of the isolates, and the plasmid-mediated mcr-1 gene was identified among the resistant strains. The mcr-1 gene is of particular concern because, unlike chromosomal mutations that confer colistin resistance, it sits on mobile genetic elements that can hop between bacterial species and genera with relative ease. First described in Chinese pigs and pork in 2015, mcr-1 has since been reported on every inhabited continent, and its presence in poultry systems in Pakistan adds another node to its global distribution network.

One of the study’s most striking findings is the sheer combinatorial diversity of the resistance determinants. The researchers identified twenty-one distinct resistance gene combinations, including combinations that unite ESBL genes, carbapenemase genes and colistin resistance determinants within the same isolates. Co-occurrence of this kind is the molecular nightmare scenario for antimicrobial resistance control, because a single plasmid carrying multiple determinants can simultaneously confer resistance to front-line, last-line and reserve antibiotics. Such plasmids can be transferred laterally to other Enterobacteriaceae, including Escherichia coli and Salmonella, multiplying the number of pathogenic species that can acquire the resistance package in a single horizontal gene transfer event.

The authors frame their findings within a One Health perspective, the recognition that human, animal and environmental health are inextricably linked. Poultry production is a recognized amplifier of resistance: antimicrobials are used for growth promotion, prophylaxis and treatment in many low- and middle-income settings, selective pressure favors resistant clones, and resistant bacteria and their genes disperse through litter, wastewater, workers, carcasses and meat. Prior studies have documented intermingled K. pneumoniae populations between retail meats and human urinary tract infections, and the persistence of multidrug-resistant strains long after colistin withdrawal in poultry production, suggesting that contamination events can leave durable legacies in the food chain.

The study’s conclusions point toward concrete interventions: strengthened antimicrobial stewardship to curb unnecessary drug use, improved farm-level biosecurity to reduce the infection pressure that drives treatment, and integrated molecular surveillance that tracks resistance genes across the production chain rather than in isolated snapshots. The work was funded under an International Atomic Energy Agency Coordinated Research Project, and the authors report no competing interests. As resistance genes continue to accumulate in the animals that feed billions of people, the Faisalabad survey serves as a quantitative warning that the poultry sector, if left unmonitored, can function as both a reservoir and a launchpad for some of medicine’s most feared resistance determinants.

Subject of Research: Molecular characterization of antimicrobial resistance genes in Klebsiella pneumoniae from poultry production systems in Pakistan

Article Title: Molecular characterization and co-occurrence of ESBL, carbapenemase and mcr-1 genes in Klebsiella pneumoniae from poultry production systems in Pakistan

Article References: Parvez, R., Khurshid, M., Rasool, M. H., Aslam, B., & Sasanya, J. J. (2026). Molecular characterization and co-occurrence of ESBL, carbapenemase and mcr-1 genes in Klebsiella pneumoniae from poultry production systems in Pakistan. Molecular Biology Reports, 53(1), Article 1538. https://doi.org/10.1007/s11033-026-12718-6

Image Credits: AI Generated

DOI: 10.1007/s11033-026-12718-6

Keywords: Klebsiella pneumoniae, antimicrobial resistance, ESBL, carbapenemase, mcr-1, colistin resistance, poultry, One Health, Pakistan, multidrug resistance, food chain, molecular surveillance

The research team, led by transplant surgeons and microbiologists at the Affiliated Hospital of Qingdao University in China, enrolled 45 consecutive liver transplant donor–recipient pairs between May 2024 and January 2025. From each donor, the investigators collected up to three sample types within 24 hours before organ procurement: sputum or endotracheal aspirate, EDTA-anticoagulated peripheral blood, and organ preservation solution, the sterile fluid used to perfuse and flush the organ during recovery surgery. From each recipient, samples were taken within 24 hours after transplantation and included blood, respiratory specimens, ascites when abdominal infection was suspected, and occasionally preservation solution. In total, 124 donor samples and 97 recipient samples were tested in parallel by both mNGS and conventional microbiological culture, creating one of the most systematic matched-pair comparisons of these two diagnostic philosophies in the transplant literature.

Technically, mNGS works by extracting all nucleic acids from a specimen, sequencing them on an MGISEQ-200 platform, computationally stripping away human host sequences using the hg38 reference genome, and aligning the remaining reads against comprehensive microbial reference databases drawn from NCBI GenBank, RefSeq, and nt. Pathogen abundance was quantified in reads per 10 million raw reads, with positivity thresholds of RPTM ≥ 3 for viruses, RPTM ≥ 20 for bacteria and fungi, and RPTM ≥ 1 for special organisms such as Cryptococcus and Mycobacterium tuberculosis. Culture, by contrast, relied on growth-based identification by MALDI-TOF mass spectrometry with antimicrobial susceptibility testing under Clinical and Laboratory Standards Institute guidelines. The two methods embody fundamentally different diagnostic logics: culture requires organisms to be alive, cultivable, and abundant enough to grow, while mNGS requires only that their genetic fingerprints be present in the sample.

The clinical stakes were high. Among the 45 recipients, 29, or 64.4 percent, developed post-transplant infections, and the lung was by far the dominant battlefield, accounting for 89.7 percent of infections, followed by the abdomen at 24.1 percent and the bloodstream at 17.2 percent. Infected recipients spent dramatically longer in the intensive care unit, with a median of 91.0 hours compared with 53.9 hours for infection-free patients, and their total hospitalization stretched to a median of 44.0 days versus 23.0 days. These figures echo the broader epidemiology of solid organ transplantation, where more than 60 to 80 percent of recipients develop at least one clinically significant infection within the first year, and where early postoperative infection rates in liver transplant cohorts range from 44 to 71 percent.

When the researchers compared detection rates, the advantage of mNGS was striking. At the patient level, mNGS achieved positivity in 95.6 percent of donors versus 80.0 percent for culture, and in 64.4 percent of recipients versus just 22.2 percent for culture. The gap was widest for fungi and absolute for viruses: fungal detection in donors reached 40.0 percent by mNGS versus 15.6 percent by culture, and every viral pathogen identified in the study, including cytomegalovirus, Epstein–Barr virus, human parvovirus B19, and hepatitis B virus, was found exclusively by sequencing. In recipient samples, the contrast was even sharper in some matrices. Recipient blood samples yielded pathogens in 40.5 percent of cases by mNGS but in zero percent by culture, and donor blood showed 62.9 percent versus a mere 2.9 percent. Even after statistically accounting for the fact that multiple samples came from the same individuals using generalized estimating equations, the mNGS advantage remained highly significant in both donors and recipients.

Yet the study also revealed that the two methods are complementary rather than interchangeable. Among samples positive by both techniques, pathogen-level concordance was predominantly partial, with complete agreement in only 17.8 percent of donor samples and 22.2 percent of recipient samples. In other words, each method consistently uncovered a distinct subset of the microbial burden that the other missed. This trade-off was equally evident in diagnostic performance. Using the clinically adjudicated post-transplant infection diagnosis as the reference standard, mNGS achieved a sensitivity of 69.0 percent at the patient level, far exceeding the 31.0 percent of culture, but its specificity was only 43.8 percent, whereas culture reached 93.8 percent. The authors caution that because clinicians were not blinded to mNGS results in this retrospective setting, incorporation bias may have inflated the sensitivity estimates, and they emphasize that mNGS should never be interpreted in isolation from clinical, radiological, and other microbiological evidence.

The pathogen landscape that mNGS revealed included organisms that culture simply cannot reach. Most notably, Pneumocystis jirovecii, an opportunistic fungus responsible for severe and potentially fatal pneumonia in immunocompromised patients, was identified exclusively by sequencing. Rare invasive molds such as Rhizomucor pusillus, Lichtheimia ramosa, and Cunninghamella bertholletiae, which are notoriously culture-resistant and dangerous, were likewise detected only by mNGS in donor samples. In recipients, Staphylococcus aureus and Klebsiella pneumoniae led the bacterial detections, while Candida albicans, Candida tropicalis, and Aspergillus species dominated the fungal findings. The ability to detect these fastidious and culture-resistant organisms before clinical deterioration represents one of the most clinically consequential dimensions of the technology.

Perhaps the most novel contribution of the study was its systematic hunt for donor-derived pathogen transmission. By comparing matched donor and recipient microbiological profiles, the investigators identified 11 possible donor-to-recipient transmission events across 11 pairs, involving six distinct organisms, and six of the 11 affected recipients, or 54.5 percent, went on to develop clinical infections. Klebsiella pneumoniae was the most frequently transmitted pathogen, responsible for five of the 11 events, and three of the five recipients with donor-derived Klebsiella developed multi-site infections involving the lung, abdomen, or bloodstream. The study also documented possible donor-derived transmission of hepatitis B virus and human parvovirus B19, both invisible to culture-based screening. The authors stress that these events represent species-level concordance rather than genetically confirmed transmission, since no whole-genome sequencing or molecular typing was performed to establish clonal identity between donor and recipient isolates.

The impact on antimicrobial decision-making was equally significant. mNGS findings prompted treatment modifications in 24 of 45 recipients overall, including 20 of the 29 infected recipients, or 69.0 percent. In contrast, culture results alone informed no additional treatment changes beyond those already associated with mNGS findings. The spectrum of mNGS-informed modifications was notably broader than culture could support, including escalation in 40 percent of cases, addition of anti-Gram-positive agents in 35 percent, combination therapy in 35 percent, antifungal adjustments in 25 percent, and, critically, antiviral additions in 10 percent and de-escalation in 5 percent, categories that culture cannot inform given its inability to detect viruses and its characteristic diagnostic delay. Among the nine recipients whose treatment was adjusted based on both methods concurrently, the Jaccard similarity index between mNGS- and culture-informed modification categories was 1.00 in six cases and 0.50 to 0.67 in the remaining three, indicating that mNGS decisions extended rather than contradicted culture-confirmed findings.

The study also uncovered an unexpected epidemiological signal: recipients transplanted for liver cancer showed a markedly lower risk of post-transplant infection, with an univariate odds ratio of 0.10 and a p-value of 0.003. The authors interpret this cautiously, noting that patients with hepatocellular carcinoma are more likely to have compensated liver function, better nutritional status, and elective rather than emergency transplantation compared with those transplanted for acute liver failure or decompensated cirrhosis, so the association likely reflects confounding by underlying disease severity rather than any independent protective effect of cancer itself. Donor mNGS fungal detection and perioperative blood transfusion showed trends toward significance but did not reach statistical thresholds in this small cohort.

Despite its promise, the study carries important limitations. The cohort of 45 pairs limits statistical power, the retrospective design means clinicians were not blinded to mNGS results, and the absence of molecular typing means transmission events remain classified as possible rather than confirmed. The single-center setting in China may also limit generalizability to regions with different donor pools and local epidemiology. Nevertheless, the findings make a compelling case that mNGS, when deployed across multiple anatomical compartments in both donors and recipients, can substantially expand the visible pathogen spectrum, expose hidden donor-derived transmission risks, and drive more informed antimicrobial stewardship in a population where every diagnostic delay carries real clinical consequences. The authors conclude that mNGS should be regarded as an adjunctive peri-transplant diagnostic tool, pending prospective multicenter validation with standardized interpretation frameworks and genomic confirmation of transmission events.

Subject of Research: Metagenomic next-generation sequencing of matched liver transplant donor–recipient pairs reveals pathogen transmission dynamics and informs antimicrobial therapy

Article Title: Metagenomic next-generation sequencing of matched donor–recipient pairs reveals pathogen transmission dynamics and informs antimicrobial therapy in liver transplantation: a retrospective cohort study

Article References: Feng, S., Liu, J., Zhang, X., Zhang, L., Zhao, S., Jiang, N., Cai, J., Zheng, Y., Gai, W., & Xu, C. (2026). Metagenomic next-generation sequencing of matched donor–recipient pairs reveals pathogen transmission dynamics and informs antimicrobial therapy in liver transplantation: a retrospective cohort study. Frontiers in Cellular and Infection Microbiology, 16, Article 1919428. https://doi.org/10.3389/fcimb.2026.1919428

Image Credits: AI Generated

DOI: 10.3389/fcimb.2026.1919428

Keywords: liver transplantation, metagenomic next-generation sequencing, donor-derived infection, antimicrobial stewardship, post-transplant infection, Klebsiella pneumoniae, pathogen detection, transplant immunology, diagnostic microbiology, organ preservation solution, Metagenomic, next-generation

Carbapenems are last-resort antibiotics, deployed when other drugs fail against serious infections. When bacteria produce carbapenemases—enzymes that chemically dismantle these drugs—treatment options collapse to a handful of toxic or imperfect alternatives. The World Health Organization has classified carbapenem-resistant Enterobacterales among its critical priority pathogens, and in Brazil, Klebsiella pneumoniae alone accounts for a substantial share of carbapenem-resistant bloodstream infections. What makes the new findings alarming is not simply that resistant bacteria were found in wastewater, but which bacteria they were and what genetic weaponry they carried.

The research team, led by João Pedro Rueda Furlan of the Federal University of Paraíba and Universidade Federal de São Paulo, collected 500-milliliter samples of raw influent wastewater from four treatment plants between April and May 2024: Ribeirão Preto, Riacho Grande, Parque Novo Mundo, and Barueri. The samples were filtered, cultured in broth, and plated onto selective media containing meropenem and vancomycin to suppress ordinary susceptible organisms. Colonies were identified by mass spectrometry and then subjected to whole-genome sequencing on an Illumina platform, with draft genomes assembled de novo and interrogated using bioinformatic tools for resistance genes, plasmid replicons, virulence factors, and sequence types.

The twelve isolates comprised nine K. pneumoniae strains, two Enterobacter kobei, and one Enterobacter asburiae. Every single strain was multidrug resistant, with meropenem minimum inhibitory concentrations exceeding 64 milligrams per liter—a level far beyond what any clinically achievable drug concentration could overcome. Seventy-five percent were resistant to colistin, one of the few remaining salvage antibiotics, with minimum inhibitory concentrations ranging from 1 to greater than 64 milligrams per liter. Only ceftazidime-avibactam, a newer beta-lactam–beta-lactamase inhibitor combination, and tigecycline retained activity across the board. Phenotypic testing with boronic acid inhibitors pointed to serine carbapenemases, and genomic analysis confirmed the presence of blaKPC-2 in eleven of twelve strains, blaGES-5 in two E. kobei strains, and—remarkably—both blaKPC-2 and blaGES-16 cohabiting in a single E. kobei isolate.

The K. pneumoniae strains belonged to sequence types ST11 and ST307, clones recognized worldwide as high-risk lineages responsible for healthcare-associated outbreaks. ST11 appeared at multiple treatment plants and on different collection dates, indicating repeated environmental introductions rather than a single contamination event. Within ST11, two distinct capsular types were detected—KL64 and KL15—suggesting ecological plasticity and contributions from different source populations feeding into the sewage network. ST11-KL64 is typically associated with highly transmissible, virulent, carbapenemase-producing sublineages, while ST11-KL15 reflects broader environmental and community dissemination. ST307, found with capsular type KL102 at more than one plant, is strongly healthcare-associated yet demonstrably capable of spreading through urban wastewater systems.

The virulence profiles of these environmental isolates add a troubling dimension. All K. pneumoniae strains carried the mrk gene cluster encoding type 3 fimbriae, which mediate adhesion, colonization, and biofilm formation. The ST11 strains harbored the yersiniabactin siderophore locus embedded within integrative conjugative elements—ICEKp3 in the KL15 strain and ICEKp10 in the KL64 strain—machinery that enhances iron acquisition, immune evasion, and resistance to oxidative stress. Most strikingly, the ST11-KL64 strain also carried the colibactin gene cluster, specifically the clb3 variant, which encodes a genotoxin linked to DNA damage and disruption of epithelial barriers. The ST307-KL102 strains displayed the hypermucoviscous phenotype, an overproduction of capsule that shields the bacterium from host immune responses. In short, these are not attenuated environmental curiosities; they are bacteria with the genetic toolkit to cause serious human disease.

The Enterobacter isolates told a different but equally significant story. The E. kobei strains belonged to ST520, an international clone previously recovered from coastal waters in Brazil and from clinical samples in China, India, and Spain. The E. asburiae strain belonged to ST384, a lineage with no previous reports in the literature, suggesting that environmental genomic surveillance can uncover bacterial diversity that clinical sampling has entirely missed. Enterobacter species generally rely on basic fitness traits rather than specialized virulence systems, and the E. kobei strains carried no classical virulence determinants, while the E. asburiae strain carried adhesion and iron-acquisition genes consistent with an opportunistic lifestyle.

Beneath the species-level findings lies the real engine of concern: the mobile genetic elements shepherding the carbapenemase genes from cell to cell. In most K. pneumoniae strains, blaKPC-2 sat within the Tn4401a transposon, the classical vehicle that has driven the global spread of KPC-type resistance. One strain, however, carried blaKPC-2 within the Tn4401i isoform, an uncommon variant previously reported in Brazilian clinical and environmental K. pneumoniae but whose epidemiological risk remains unclear. In the Enterobacter strains, blaKPC-2 was embedded in structures involving ISKpn27 and ISKpn6 insertion sequences alongside Tn3-family transposases—platforms that may represent early stages of mobilization pathways before stabilization in clinically dominant vehicles. Meanwhile, blaGES-5 and blaGES-16 were both nestled within class 1 integrons, evolutionary capture systems whose intI1 integrase can seize, excise, and rearrange gene cassettes, promoting the accumulation and horizontal transfer of resistance genes across bacterial hosts and ecological niches.

The blaGES-16 gene deserves particular attention. GES-16 differs from GES-5 by a single amino acid substitution, glutamine 38 replaced by glutamic acid, yet it functions as a carbapenemase. First described in clinical Serratia marcescens from Rio de Janeiro and later found in Aeromonas veronii from hospital wastewater in Paraná, the gene appears to be geographically restricted to Brazil. A search of public genome databases conducted in January 2026 identified only five genomes carrying blaGES-16, all from Brazilian sources, spanning Aeromonas hydrophila, A. veronii, E. kobei, Enterobacter soli, and Pseudomonas aeruginosa from different states. Three of these genomes also carried KPC-2. In the new study, blaGES-16 was found on both chromosomal and plasmid contigs, consistently associated with class 1 integron machinery and flanked by additional resistance genes, including blaOXA-17, which encodes an extended-spectrum beta-lactamase. This integron association suggests the gene is being actively maintained and potentially mobilized within Brazilian bacterial populations.

The broader resistome of the isolates reinforced the picture of comprehensive multidrug resistance. All strains carried acquired and intrinsic genes conferring resistance to beta-lactams, fluoroquinolones, aminoglycosides, tetracyclines, sulfonamides, and phenicols. Extended-spectrum beta-lactamase genes blaCTX-M-2 and blaCTX-M-15 were present, along with rmtB, a 16S rRNA methyltransferase that obliterates the activity of aminoglycosides such as amikacin. Fluoroquinolone-resistant strains harbored the canonical GyrA S83I and ParC S80I mutations, while colistin-resistant K. pneumoniae strains carried multiple mutations in polymyxin resistance determinants, including disruption of the mgrB gene by an ISKpn14 insertion element and a deleterious R256G substitution in the PmrB sensor kinase. Genes conferring tolerance to quaternary ammonium disinfectants and to arsenic, copper, mercury, and silver were also detected, hinting at selection pressures beyond antibiotics alone. Plasmid replicons of the IncF type predominated, with IncN-pST15 and IncP6 also identified—plasmid types previously documented carrying blaKPC-2 in environmental K. pneumoniae and E. coli from southeastern Brazil.

The authors frame their findings within a One Health perspective: wastewater treatment plants are not merely passive conduits but active reservoirs and mixing vessels where clinically relevant resistance determinants, high-risk clones, and mobile genetic elements converge and evolve. When treatment is inadequate, resistant bacteria and their gene cargo can be discharged into receiving waters, bridging the clinical-environmental interface. Raw wastewater, the authors argue, functions as an early warning signal of high-risk lineages circulating within the human population—detectable before those lineages necessarily appear in hospitals. Continuous genomic surveillance in extra-hospital settings, they conclude, is essential to monitor emerging resistance genotypes and catch the early signs of clinically relevant dissemination. The complete genome sequences are publicly available under BioProject PRJNA1216268, offering researchers worldwide a resource for tracking these Brazilian lineages as the story of antimicrobial resistance continues to unfold at the intersection of human health and the environment.

Subject of Research: Genomic surveillance of carbapenemase-producing Enterobacterales in Brazilian wastewater

Article Title: Genomic characterization of carbapenemase-producing Enterobacterales from wastewater reveals the convergence of KPC-2 and GES-16 in Brazil

Article References: Furlan, J. P. R., Bueno, G. C., Sousa-Carmo, R. R., Silva, R. L. O., Barbosa, M. R. F., Sato, M. I. Z., Lincopan, N., & Schenkman, S. (2026). Genomic characterization of carbapenemase-producing Enterobacterales from wastewater reveals the convergence of KPC-2 and GES-16 in Brazil. Environmental Monitoring and Assessment, 198(9), Article 1014. https://doi.org/10.1007/s10661-026-15867-0

Image Credits: AI Generated

DOI: 10.1007/s10661-026-15867-0

Keywords: antimicrobial resistance, carbapenemase-producing Enterobacterales, Klebsiella pneumoniae, wastewater surveillance, KPC-2, GES-16, mobile genetic elements, class 1 integrons, whole-genome sequencing, One Health, Brazil, high-risk clones

The retrospective multicenter study, led by researchers at the Children’s Hospital of Chongqing Medical University and published in Frontiers in Cellular and Infection Microbiology, analyzed 5,618 pathogenic bacteria isolated from positive urine samples of children under 18 with community-acquired urinary tract infections. Children with congenital urinary tract anomalies, repeated infection episodes, or bacterial colonization without true infection were excluded, sharpening the picture of ordinary community-acquired disease. All susceptibility results were interpreted against the Clinical and Laboratory Standards Institute’s 2024 M100-S34 breakpoints, ensuring a uniform yardstick across the entire study window.

Gram-negative bacteria dominated the landscape, accounting for 71.0 percent of isolates, with Gram-positive organisms making up the remaining 29.0 percent. Escherichia coli was the undisputed leader, representing 37.3 percent of all isolates and ranking first in every age group and in both sexes. Its closest companions were Enterococcus faecium at 12.9 percent, Klebsiella pneumoniae and E. faecalis at 9.0 percent each, and Proteus mirabilis at 5.1 percent. In total, the team identified one hundred distinct uropathogenic species, a reminder that the urinary tract is anything but a single-pathogen disease niche.

The demographic patterns traced familiar developmental biology. Boys accounted for 53.9 percent of infections, with male susceptibility concentrated in the first year of life, where 59.8 percent of cases were male, and in the toilet-training years up to age three. The balance flipped with age: girls predominated from age four onward, likely reflecting the shorter female urethra and its proximity to enteric bacteria. Infancy carries particular risk for boys because of delayed ureteral maturation, congenital obstructive malformations, and physiological phimosis, all of which foster urinary stasis and bacterial colonization near the urethral opening.

Age stratification also shifted the microbial cast. E. coli peaked at 45.7 percent of pathogens in the four-to-six-year group, while E. faecium took second place in infants at 22.5 percent, and K. pneumoniae clustered most prominently in the youngest children. Notably, resistance to the fluoroquinolones ciprofloxacin and levofloxacin differed significantly across age groups for both E. coli and K. pneumoniae, reinforcing the authors’ argument that empirical treatment decisions should be calibrated to a child’s developmental stage rather than applied uniformly.

The resistance trends over time painted a mixed and sometimes counterintuitive portrait. E. coli resistance to sulbactam/ampicillin fell significantly from 57.9 percent in 2019 to 36.5 percent in 2024, and resistance to amikacin, gentamicin and nitrofurantoin also declined. Yet ciprofloxacin resistance climbed from 36.5 to 50.2 percent over the same period, and carbapenem-resistant E. coli rose from 2.7 to 4.9 percent. K. pneumoniae moved in the opposite direction on some fronts: its carbapenem resistance fell from a peak of 23.1 percent in 2019 to 18.9 percent in 2024, while its resistance to amikacin, the fluoroquinolones and nitrofurantoin rose significantly.

The enzymes that confer much of this resistance also diverged. The proportion of ESBL-producing E. coli, bacteria carrying extended-spectrum beta-lactamases that destroy penicillin-class drugs, crept upward from 54.0 percent to 62.2 percent, while ESBL-producing K. pneumoniae fell sharply from 66.2 to 52.7 percent. ESBL-producing strains of both species were consistently more resistant than their non-ESBL counterparts to nearly every agent tested, and carbapenem-resistant isolates showed broad resistance across the panel. For the enterococci, penicillin resistance averaged a striking 91.5 percent in E. faecium and 63.7 percent in E. faecalis, but no vancomycin- or linezolid-resistant E. faecalis was found anywhere in the cohort.

The pandemic’s influence emerged most clearly when the years were split into pre-COVID (2019), pandemic (2020 to 2022) and post-COVID (2023 to 2024) periods. Detection of E. coli, E. faecium and K. pneumoniae all declined after the pandemic, with E. coli dropping from 45.3 percent of isolates before COVID to 35.0 percent afterward, possibly reflecting more enduring hygiene habits. At the same time, resistance of E. coli and K. pneumoniae to piperacillin/tazobactam, cefepime, ciprofloxacin and levofloxacin rose post-pandemic, while penicillin resistance increased significantly in both enterococcal species. The authors suggest that reduced antibiotic consumption and altered healthcare-seeking behavior during the pandemic years plausibly drove these shifting dynamics.

A particularly subtle finding concerned the minimum inhibitory concentrations, the drug doses needed to halt bacterial growth. Vancomycin MIC values for the enterococci did not drift over the six years, but linezolid MICs did, with the proportion of isolates requiring concentrations of at least 2 micrograms per milliliter falling significantly in both species. The downward drift was more pronounced in E. faecalis, beginning around 2022, and by 2024 only 44.5 percent of E. faecalis isolates sat at or above that threshold, down from 93.3 percent in 2019. That vancomycin and linezolid remained fully effective against E. faecalis offers a rare reassuring note in the resistance literature.

The study’s practical message is sharpened by its limits: it covers only the Chongqing region, and its retrospective design could not confirm resistance mechanisms through molecular analysis. Even so, the surveillance data carry clear clinical guidance. Nitrofurantoin, with just 2.0 percent E. coli resistance, stands out as the only oral option below the 5 percent threshold recommended for empiric use, though it is suitable only for simple bladder infections since it penetrates kidney tissue poorly. Fluoroquinolone resistance rates well above 10 percent rule them out as first-line agents, and the authors argue that carbapenems, vancomycin and linezolid should be preserved as effective last-line options. Above all, they conclude, continued monitoring and age-stratified treatment strategies are essential, because the pandemic has shown that pediatric urinary infections are a moving target.

Subject of Research: Epidemiology and antibiotic resistance of pediatric urinary tract infections before, during and after the COVID-19 pandemic in China

Article Title: Changes in epidemiology and antibiotic resistance patterns isolated from paediatric urinary tract infections: a multicenter study in China pre-, during and post-COVID-19

Article References: Tang, L., Tian, R., Wei, X., Yu, X., Xiong, Z., Xiang, Y., Liu, F., & Jing, C. (2026). Changes in epidemiology and antibiotic resistance patterns isolated from paediatric urinary tract infections: a multicenter study in China pre-, during and post-COVID-19. Frontiers in Cellular and Infection Microbiology, 16, Article 1923862. https://doi.org/10.3389/fcimb.2026.1923862

Image Credits: AI Generated

DOI: 10.3389/fcimb.2026.1923862

Keywords: urinary tract infections, antibiotic resistance, pediatrics, COVID-19, Escherichia coli, Klebsiella pneumoniae, enterococci, ESBL, carbapenem resistance, surveillance, Chongqing, nitrofurantoin