The team, led by A. O. Olalemi with colleagues O. O. Olaniyi, D. O. Olugbade and O. F. Olowoporoku, sampled the dam biweekly over a six-month period that spanned both wet and dry seasons. Crucially, they did not restrict their sampling to the water surface. Samples were collected both just below the surface and near the dam bed, a distinction that matters because microbial distributions in reservoirs are rarely uniform. Pathogens and fecal indicator organisms can settle into sediments, where they may persist longer than in the open water column, and resuspension during storms or disturbance can return them to the water that people draw for domestic use. Capturing both zones gives a more realistic estimate of the microbial population that users of the dam are actually exposed to.

The numbers reported for fecal indicator bacteria are striking. Escherichia coli, the standard benchmark organism for fecal pollution in water, was detected at concentrations ranging from 3.0 to 4.3 log10 colony-forming units per 100 milliliters. In practical terms, that means between roughly 1,000 and 20,000 viable E. coli cells in each 100-milliliter sample. Proteus species ranged from 3.6 to 4.5 log10 cfu/100 ml, and Shigella, one of the classic causes of bacillary dysentery, was present at 3.3 to 4.1 log10 cfu/100 ml. International guidelines for drinking water quality set the acceptable level of E. coli in treated drinking water at zero per 100 milliliters, so the measured concentrations represent contamination that is orders of magnitude above what would be considered safe for direct consumption.

Beyond the cultured indicator organisms, the researchers used molecular methods to characterize the broader bacterial community in the dam. Sequencing revealed that the water was dominated by two phyla: Proteobacteria, which accounted for 57.63 percent of the community, and Bacteroidota, which made up 26.63 percent. This composition is typical of freshwater systems influenced by organic matter and fecal inputs, since both phyla contain large numbers of organisms associated with the animal and human gut as well as with decaying organic material in aquatic environments. The dominance of these two groups is consistent with the picture painted by the culture data of a reservoir under continuous contamination pressure.

Drilling down further, the community analysis showed that at the order level Pseudomonadales was the most abundant group at 40.43 percent, followed by Cytophagales at 28.29 percent. At the family level, Pseudomonadaceae dominated with 39.17 percent of sequences, with Spirosomaceae close behind at 28.29 percent. The most prevalent individual species identified were Pseudomonas sp003428805, accounting for 27.61 percent of the community, and Arcicella rosea at 19.09 percent. Pseudomonas species are ubiquitous in soil and water and are not themselves typically fecal indicators, but their dominance alongside high fecal indicator counts suggests a reservoir rich in organic nutrients, conditions that allow both environmental organisms and gut-derived pathogens to survive and sometimes multiply outside their hosts.

Perhaps the most concerning findings concern the protozoan parasites. Cryptosporidium parvum was detected in 83.33 percent of the water samples, and Giardia lamblia was found in 50 percent of them. Both are single-celled parasites that cause prolonged diarrheal illness, and both are globally recognized as major causes of waterborne disease outbreaks. Cryptosporidium in particular is notorious in water treatment circles because its oocysts are highly resistant to chlorine disinfection, the mainstay of municipal water treatment in many places. An organism present in more than four out of five samples from a source used for domestic purposes represents a persistent and widespread exposure hazard, not an occasional anomaly.

To translate these measurements into estimates of actual health risk, the team applied a dose-response approach, the core of quantitative microbial risk assessment. This framework uses experimentally derived relationships between the number of pathogen cells or cysts ingested and the probability of infection, combined with estimates of how much water people consume and how contaminated that water is. The calculated risks of infection from the pathogens detected in the dam all exceeded 10 to the power of minus 4 per exposure, a benchmark often used in public health as the maximum acceptable annual risk of infection from waterborne pathogens. In other words, the estimated infection probabilities were above one in ten thousand, the level at which intervention is generally considered necessary.

The risk estimates also revealed a clear hierarchy among the pathogens. When ranked by infection risk, the order was Klebsiella, lowest, followed by Giardia lamblia, then Salmonella, then Cryptosporidium parvum, and finally Shigella, which carried the highest estimated risk. This ordering reflects both the concentrations at which each organism was present and the differing infectivity of each pathogen; Shigella requires very few cells to establish an infection, which makes even moderate concentrations in drinking water a serious concern. The finding that protozoan parasites ranked above most of the bacteria underscores the particular threat posed by Cryptosporidium and Giardia in untreated surface waters.

The authors interpret the consistently high bacterial and protozoan loads across the sampling period as evidence of continuous contamination of the dam rather than isolated pollution events. Multipurpose dams like Owena typically serve a range of functions, including domestic water supply, irrigation, fishing and livestock watering, and such multiple uses, combined with runoff from surrounding settlements and farmland during the wet season, create numerous pathways for fecal material to enter the reservoir. The fact that elevated counts persisted through both wet and dry periods suggests that contamination sources are not merely seasonal runoff but ongoing inputs, whether from human activity around the dam, animal access to the water, or the survival and regrowth of organisms within the reservoir itself and its sediments.

The practical message of the study is unambiguous: water drawn from the Owena dam must be adequately treated before it is consumed. For households and water managers in the region, that means treatment capable of addressing both bacteria and chlorine-resistant protozoa, such as filtration, boiling, or appropriately designed multi-barrier treatment systems. More broadly, the study illustrates the value of pairing traditional culture-based monitoring with molecular community profiling and formal risk assessment. Culture methods reveal viable indicator organisms and known pathogens, sequencing exposes the full ecological structure of the microbial community, and dose-response modeling converts both into estimates of human health risk that decision-makers can act on. As pressure on freshwater resources grows across sub-Saharan Africa, studies of this kind provide an evidence base for protecting the millions of people who rely on surface waters like the Owena dam for their daily needs, and they make clear that in the absence of treatment, the microbial hazards in such waters are neither marginal nor hypothetical.

Subject of Research: Microbial contamination and quantitative infection risk assessment of water from the Owena multipurpose dam in Nigeria

Article Title: Microbial risk assessment of enteric bacteria and protozoa in Owena multipurpose dam in Igbara-Oke, Nigeria

Article References: Olalemi, A. O., Olaniyi, O. O., Olugbade, D. O., & Olowoporoku, O. F. (2026). Microbial risk assessment of enteric bacteria and protozoa in Owena multipurpose dam in Igbara-Oke, Nigeria. PLOS Water, 5(7), e0000595. https://doi.org/10.1371/journal.pwat.0000595

Image Credits: AI Generated

DOI: 10.1371/journal.pwat.0000595

Keywords: water quality, microbial risk assessment, E. coli, Shigella, Cryptosporidium parvum, Giardia lamblia, faecal indicator bacteria, Nigeria, Owena dam, PLOS Water, quantitative microbial risk assessment, waterborne disease

The research was carried out by Jimena Camila Suárez, Ramiro Simonetti, Alejandro Mariñelarena and Joaquín Cochero of the Instituto de Limnología Dr. Raúl A. Ringuelet, a joint institute of the National University of La Plata and Argentina’s national research council CONICET. Their study area stretched along 78 kilometers of the southern coastal fringe of the estuary, a strip of shore that serves simultaneously as an economic resource, a freshwater supply and the principal recreational outlet for the largest population centers in Argentina. Because this fringe absorbs the pressures of millions of residents, untreated and partially treated sewage discharges, stormwater runoff and intense summer visitation, it offers an ideal natural laboratory for asking a deceptively simple question: if you want to know how polluted a beach really is, should you be testing the water, the sand, or both?

To answer it, the team sampled eight beaches and quantified two classic indicators of fecal pollution, Escherichia coli and Enterococcus, in both water and sand. Indicator organisms are used around the world as proxies for the presence of fecal matter and, by extension, for the possible presence of enteric pathogens. Water quality regulations, including the United States Environmental Protection Agency’s 2012 Recreational Water Quality Criteria, are built around thresholds for these very bacteria, which is why beach closures and advisories are typically issued on the basis of water samples alone. The Argentine study set out to test whether that water-only approach captures the true microbial picture of a beach, and the answer, in short, is that it does not.

The central technical result is stark: at all study sites, bacterial abundance was higher in the sediment than in the water column. This pattern is consistent with a substantial body of international literature showing that intertidal and foreshore sands can accumulate and sustain fecal indicator bacteria at densities far exceeding those of adjacent waters. Sand grains provide surfaces for bacterial attachment, shelter from ultraviolet radiation, and pockets of organic matter and moisture that support survival and even growth. In freshwater beaches on Lake Michigan, researchers famously showed that wet foreshore sand could act as a source of E. coli to nearshore water, and studies along the California coast have demonstrated that beach sands function as diffuse sources of fecal bacteria to coastal waters. The Río de la Plata results indicate that the same sand-to-water coupling operates along the Argentine estuary, where the combination of fine sediments, nutrient-rich waters and chronic sewage inputs creates favorable conditions for bacterial persistence in the beach matrix.

What controls where the bacteria concentrate? The study found a consistent spatial signature: microbial abundances in sand were negatively associated with distance from sewage discharges for both E. coli and Enterococcus, meaning that the closer a beach sits to an outfall, the more contaminated its sand tends to be. In the water, the same negative relationship with distance from sewage discharges held for Enterococcus, while E. coli abundance in water was additionally associated with dissolved oxygen, being higher where oxygen levels were lower. That second relationship makes physiological sense, since heavy organic loading from wastewater consumes oxygen as it decomposes, so low dissolved oxygen acts as a chemical fingerprint of sewage influence, coinciding with elevated indicator bacteria. Taken together, the spatial and chemical associations point to sewage outfalls as the dominant driver of the contamination pattern, rather than diffuse or naturalized sources alone.

The two indicator organisms did not behave identically. Across sand and water alike, E. coli was always more abundant than Enterococcus, leading the authors to suggest that E. coli may be a more generalized and sensitive indicator of fecal contamination in this system. The distinction matters for monitoring design. Enterococci are the preferred indicators in marine waters under many regulatory frameworks because they correlate well with swimming-associated illness in ocean settings, but in freshwater and estuarine systems the relative performance of indicators can shift. In the turbid, nutrient-rich, freshwater-dominated environment of the Río de la Plata, E. coli appears to track the fecal signal more faithfully, and a monitoring program that relied exclusively on Enterococcus could underestimate the extent of contamination at some sites.

Perhaps the most sobering finding came from a single site. At the Bagliardi beach, the researchers detected Salmonella choleraesuis and Shigella in water samples. These are not harmless indicator organisms; they are genuine enteric pathogens responsible for salmonellosis and shigellosis, diseases characterized by diarrhea, fever and abdominal cramps, and capable of causing severe illness in vulnerable populations. Their presence in recreational waters confirms what the indicator bacteria implied: where fecal pollution is intense enough, pathogens follow. While the study detected these pathogens at one location rather than across all sites, the finding illustrates the public health stakes of the broader contamination pattern and underscores why indicator-based surveillance, however imperfect, remains essential.

The implications for beachgoers extend beyond swimming. Epidemiological work published over the past two decades has linked sand contact itself to enteric illness among beach visitors. A study following beachgoers found that fecal indicators in sand, and the degree of sand contact, were associated with risk of gastrointestinal illness, independent of water exposure. Children, who dig, bury themselves and inevitably transfer sand to their mouths, are considered particularly exposed. Bacteria trapped in sand can also be resuspended into the water by waves, tides and the disturbance caused by bathers, meaning that a beach can fail water quality tests not only because of direct sewage input but because contaminated sand is continuously seeding the water column. Quantitative studies have shown that bathers themselves release bacteria from their bodies and from the sediment they stir up, complicating the interpretation of water samples taken during peak visitation.

All of this converges on the study’s principal recommendation: sand should be incorporated into routine beach monitoring programs. Current regulatory practice in most countries, including the frameworks that govern recreational water quality in Argentina, evaluates beaches almost exclusively through water sampling. The Río de la Plata results suggest that a water-only approach can paint a misleadingly reassuring picture, because a beach may show acceptable water counts while its sand harbors bacterial loads well above recreational guidelines, ready to be resuspended or picked up on the skin and hands of visitors. Monitoring sand alongside water, particularly at beaches near sewage outfalls, would give health authorities a more complete and precautionary basis for advising the public, and would help identify the sites where sanitation infrastructure investments, such as extending sewer networks or upgrading treatment, would deliver the greatest public health return.

The study also fits into a broader rethinking of how coastal pollution is assessed in urbanized estuaries. The Río de la Plata has previously been the subject of research on microplastics, cyanobacterial blooms and microbenthic communities, all of which point to the same underlying pressure: a colossal metropolitan population discharging its wastes into a shallow, slowly flushing estuary. By demonstrating that the sand itself is a reservoir of fecal bacteria that tracks sewage proximity and exceeds recreational guidelines at most beaches, the new work closes an important gap in that picture. For the millions of people who use these shores each summer, the practical message is nuanced rather than alarmist. The water is not uniformly unsafe, and the risks vary with location and proximity to discharges. But the comforting assumption that clean-looking water means a clean beach is no longer tenable. The ground beneath the towel, it turns out, deserves a place on the laboratory bench beside the sample bottles, and until monitoring programs catch up with the science, the humble sandcastle may be a better indicator of a beach’s microbial secrets than any water test.

Subject of Research: Fecal indicator bacteria contamination in beach sand and water along the Río de la Plata estuary

Article Title: Sand as a source of bacteriological pollution in recreational beaches of the Río de la Plata

Article References: Suárez, J. C., Simonetti, R., Mariñelarena, A., & Cochero, J. (2026). Sand as a source of bacteriological pollution in recreational beaches of the Río de la Plata. Environmental Monitoring and Assessment, 198(11), Article 1143. https://doi.org/10.1007/s10661-026-16012-7

Image Credits: AI Generated

DOI: 10.1007/s10661-026-16012-7

Keywords: Escherichia coli, Enterococcus, beach sand, fecal pollution, Río de la Plata, recreational water quality, sewage discharge, Salmonella, Shigella, water microbiology, public health, estuary

The urgency behind the search is difficult to overstate. According to recent estimates from the World Health Organization, bacterial antimicrobial resistance was associated with approximately 1.14 million deaths in 2021 alone. Between 1990 and 2021, deaths linked to antimicrobial resistance among adults aged 70 and older rose by more than 80 percent, and projections suggest that by 2050 resistance could be directly responsible for roughly 1.91 million deaths annually, with a further 8.22 million deaths associated with resistant infections. Gram-negative bacteria such as E. coli, Acinetobacter baumannii, Pseudomonas aeruginosa and Shigella are among the worst offenders, wielding structurally dynamic cell envelopes, antibiotic-inactivating enzymes, remodeled porins, efflux pumps and altered drug targets that render many existing drugs ineffective.

What makes the new study particularly compelling is its focus on biofilms, the dominant form of microbial growth in nature. Biofilms are structured communities of bacteria encased in a self-produced extracellular matrix of polysaccharides, proteins, nucleic acids and lipids. This matrix shields the inhabitants from antibiotics and immune attack, restricts drug penetration, and supports cell-to-cell communication, making biofilm-associated infections notoriously difficult to eradicate. Both E. coli and Shigella form robust biofilms that dramatically amplify their resistance. Most previous screens of natural products have tested only free-floating, planktonic bacteria, leaving antibiofilm activity largely unexplored. The Indian research team set out to close that gap by examining not just whether their fungal extract killed bacteria, but whether it could prevent biofilms from forming and dismantle those already established.

The journey began with leaves collected from healthy A. officinalis trees. After thorough washing and surface sterilization with ethanol and sodium hypochlorite, leaf segments were placed on potato dextrose agar supplemented with antibiotics to suppress bacterial contaminants. Fungal hyphae emerged only from the cut edges of the sterilized segments, confirming that the fungus truly lived inside the plant tissue rather than on its surface. Morphological examination under light and field-emission scanning electron microscopes revealed dense, septate, branched hyphae and a gray to grayish-green, velvety colony. Molecular identification followed: the researchers amplified the internal transcribed spacer region of the fungal genome with the universal primers ITS1 and ITS4, sequenced the product, and compared it against the Unite 9.0 database. The result was a 100 percent match with Daldinia sp., confirmed by a maximum-likelihood phylogenetic analysis built from the closest neighbors in the NCBI database.

To coax the fungus into releasing its chemical defenses, the team grew it in potato dextrose broth for 21 days in the dark, then extracted the culture filtrate with ethyl acetate and methanol. The ethyl acetate fraction, designated AO-EA, proved the more potent of the two and became the focus of all subsequent experiments. In agar well diffusion assays, the crude extract produced clear zones of inhibition ranging from 13.67 to 17.33 millimeters against E. coli and Shigella. Those zones are smaller than the 30 to 33 millimeters produced by the fluoroquinolone antibiotic ciprofloxacin, but the comparison is not straightforward. Ciprofloxacin is a purified single compound with a well-characterized target, whereas AO-EA is a crude mixture in which any individual active molecule is present at relatively low concentration, diluted among inactive constituents. Purification and enrichment of the active principles could substantially improve potency.

Quantitative testing reinforced the promise. Broth microdilution following Clinical and Laboratory Standards Institute guidelines yielded minimum inhibitory concentrations of 625 micrograms per milliliter for E. coli and 312.5 micrograms per milliliter for Shigella, with minimum bactericidal concentrations of 625 micrograms per milliliter for both organisms, indicating that the extract does not merely stall growth but kills the cells outright. Time-kill kinetics over 24 hours showed a significant, progressive decline in viable counts of both pathogens at the MIC, while untreated controls grew normally. Field-emission scanning electron microscopy then revealed what the killing looked like at the cellular level: after three hours of exposure, treated cells appeared deformed, wrinkled and broken, with altered shape and size, in stark contrast to the smooth, intact rods of the untreated controls.

The mechanism of action came into sharper focus through two complementary techniques. Flow cytometry with propidium iodide, a red fluorescent dye that enters only cells with compromised membranes, showed that after three hours at twice the MIC, 84.04 percent of E. coli cells and 62.15 percent of Shigella cells had lost membrane integrity, a rightward shift in fluorescence that signals catastrophic permeability failure. Confocal laser scanning microscopy confirmed the same pattern visually, with treated cells glowing red in the propidium iodide channel. The confocal experiments also used the dye DCFDA to probe for reactive oxygen species, and the results were striking: treated cells displayed a surge in fluorescence comparable to that produced by hydrogen peroxide, indicating that the extract floods the bacteria with oxidative stress. Membrane disruption and ROS-mediated damage together appear to form a two-pronged killing strategy.

The antibiofilm results may be the study’s most impressive contribution. In crystal violet staining assays, AO-EA at its MIC prevented new biofilm formation by 93.03 percent for E. coli and 89.38 percent for Shigella. More remarkably, when the researchers allowed mature 24-hour biofilms to establish first and then added the extract, biomass fell by 86.20 percent for E. coli and 83.02 percent for Shigella. Published criteria consider inhibition above 50 percent to be good antibiofilm activity, and the extract not only cleared that bar decisively but approached the performance of ciprofloxacin, which achieved just over 90 percent inhibition. An MTT assay, which measures the metabolic activity of living cells through a colorimetric reaction, showed that only around 10 to 15 percent of biofilm cells remained viable and metabolically active after treatment. Scanning electron micrographs of treated biofilms revealed scattered, loosely associated cells instead of the dense, layered architecture of untreated communities, pointing to impaired adhesion and destabilized cell-to-surface interactions.

Finally, high-resolution liquid chromatography mass spectrometry on an Orbitrap platform identified 15 distinct metabolites in the extract, spanning antimicrobial peptides, carboxylic acids, alkaloids, polyketides and phenols. Among the notable constituents were citrinin, a polyketide recently reported to show antimicrobial activity from other mangrove-derived fungi; radicinin, known to inhibit the grapevine pathogen Xylella fastidiosa; homovanillic acid, azelaic acid, xanthine, 5-hydroxyindole-3-acetic acid, gluconic acid and anthranilic acid, all of which have documented antibacterial credentials in other fungal systems; and peptide compounds including glycyl-L-leucine and two cyclic dipeptides of the octahydropyrrolo[1,2-a]pyrazine-dione family. Several of these molecules had not previously been reported from the genus Daldinia, although related phenols and carboxylic acids from Daldinia eschscholtzii have shown antibacterial and antibiofilm effects elsewhere. The extreme conditions of mangrove ecosystems, with their fluctuating salinity, tides and oxygen levels, are thought to drive these fungi toward chemically novel metabolism, and the competition among microorganisms packed into plant tissues likely selects for broad-spectrum defensive chemistry.

The authors caution that much work remains before any clinical application. The active compounds must be isolated and purified, their individual contributions disentangled, their mechanisms confirmed at the molecular level, and their safety and efficacy tested far beyond the culture dish. Nevertheless, the study demonstrates that a single fungus plucked from the leaves of an ecologically important, traditionally medicinal mangrove can simultaneously kill planktonic Gram-negative pathogens, shatter their membranes, provoke lethal oxidative stress, block nearly all new biofilm formation and dismantle the majority of established biofilms. As resistance continues to erode the value of existing antibiotics, such findings suggest that the world’s mangrove forests, among the most productive and least explored ecosystems on Earth, may hold a substantial share of the next generation of anti-infective drugs, provided they are studied before they disappear.

Subject of Research: Antimicrobial and antibiofilm activity of secondary metabolites from the mangrove endophytic fungus Daldinia sp. isolated from Avicennia officinalis

Article Title: Antimicrobial and Antibiofilm Activity of an Endophytic Fungus, Daldinia sp. Isolated From Avicennia officinalis

Article References: Dutta, N., Kumari, N., Lather, A., & Kumar, K. (2026). Antimicrobial and Antibiofilm Activity of an Endophytic Fungus, Daldinia sp. Isolated From Avicennia officinalis. MicrobiologyOpen, 15(5), Article e70422. https://doi.org/10.1002/mbo3.70422

Image Credits: AI Generated

DOI: 10.1002/mbo3.70422

Keywords: endophytic fungus, Daldinia, mangrove, Avicennia officinalis, antimicrobial resistance, antibiofilm, Escherichia coli, Shigella, secondary metabolites, LC-HRMS, membrane disruption, reactive oxygen species

The research team, led by scientists at Shahid Beheshti University of Medical Sciences in collaboration with Hakim Children’s Hospital, collected 79 Shigella isolates from the stool of pediatric patients suffering from diarrhea between September 2023 and April 2025. The children had all been referred to the hospital, one of Tehran’s major pediatric centers, making the sample a representative snapshot of clinically significant infections in the city’s young population. The study was approved by the ethics committee of Shahid Beheshti University of Medical Sciences and funded through a university grant.

Species identification revealed a familiar but shifting landscape. Shigella flexneri remained the predominant species, accounting for 59.5 percent of isolates, while Shigella sonnei made up the remaining 40.5 percent. This distribution matters because the two species differ not only in their epidemiology but also, as the study demonstrated, in their genetic armamentaria and their susceptibility to antibiotics. Globally, S. flexneri has traditionally dominated in low- and middle-income countries while S. sonnei has been more common in industrialized settings, so the near-even split observed in Tehran provides a useful epidemiological marker for a region in epidemiological transition.

The antimicrobial susceptibility testing, performed using the Kirby-Bauer disk diffusion method according to Clinical and Laboratory Standards Institute guidelines, tested isolates against twelve antibiotics. The results were grim. Resistance to ampicillin, a long-standing first-line option, stood at 92.4 percent. Trimethoprim-sulfamethoxazole, another mainstay of treatment in many settings, fared little better, with 91.1 percent of isolates resistant. Tetracycline resistance reached 86.1 percent. These three drugs, which in earlier decades formed the backbone of shigellosis therapy, are now effectively useless against the vast majority of circulating strains.

Not all news was bleak. The majority of isolates remained susceptible to meropenem, a broad-spectrum carbapenem, at 84.8 percent, and to tigecycline, a glycylcycline often held in reserve, at 82.3 percent. These agents thus retain considerable activity against Shigella in this setting, although clinicians must weigh the appropriateness of deploying such broad-spectrum drugs in children, particularly given concerns about preserving these last-line options. More troubling was the species-specific pattern that emerged for other drug classes: S. sonnei isolates demonstrated significantly greater resistance to azithromycin and to the fluoroquinolones than S. flexneri, a difference the authors flagged as statistically significant. Azithromycin and fluoroquinolones such as ciprofloxacin are among the most important oral options for treating shigellosis, so their erosion in S. sonnei narrows the therapeutic window considerably.

Beyond resistance phenotypes, the heart of the study lay in its molecular analysis. The researchers used polymerase chain reaction to screen every isolate for a panel of eleven virulence-related genes, including ipaH, ipaA through ipaD, ipgD, sen, virA, virB, virF, ial, sigA, icsA, and icsB. Many of these genes encode components or effectors of the type III secretion system, a syringe-like molecular apparatus that Shigella uses to inject effector proteins directly into human intestinal epithelial cells. This injection machinery allows the bacterium to invade host cells, escape immune detection, manipulate cell signaling, and spread from cell to cell, producing the colitis and bloody diarrhea characteristic of shigellosis.

The PCR results revealed a strikingly conserved virulence core. Every single one of the 79 isolates carried ipaH, a multicopy gene that is frequently used as a diagnostic target precisely because of its ubiquity and its presence in multiple copies on both the large virulence plasmid and the chromosome. More than 90 percent of isolates also harbored ipaB, ipaC, and ipaD, the genes encoding the invasion plasmid antigens that form the translocation pore and the effector proteins that trigger host cell uptake. The near-universal presence of this core set underscores that the invasive capacity of Shigella remains intact even as the bacterium accumulates resistance determinants; there is no apparent trade-off in which the bacteria sacrifice virulence for resistance.

Not every gene, however, was evenly distributed. The presence of ipgD, which encodes another type III secretion system effector involved in invasion, and sigA, which encodes an enterotoxin contributing to fluid secretion and tissue inflammation, differed significantly between the two species. These species-specific differences in virulence gene carriage suggest that S. flexneri and S. sonnei circulating in Tehran may cause disease through subtly different molecular mechanisms, and they complicate any one-size-fits-all approach to vaccine design or virulence-based diagnostics. A vaccine or therapeutic strategy targeting a single effector might protect against one species but leave the other untouched.

Perhaps the most conceptually significant finding involved the statistical associations between specific virulence genes and resistance phenotypes. The researchers found that resistance to levofloxacin, a fluoroquinolone, was linked to the presence of ipaB, while resistance to ampicillin was associated with ipaD. Even more broadly, sigA was associated with resistance across multiple drug classes. The authors interpret such correlations as evidence that virulence gene profiles could serve as indirect markers of resistance behavior, and they hint at underlying biological or epidemiological mechanisms. Plasmids carrying virulence genes can also carry resistance determinants, and particular genetic lineages that have succeeded in circulating may have acquired both traits together. Co-selection, in which the presence of one trait facilitates the maintenance of another on the same mobile element, is a well-established driver of resistance spread in enteric bacteria, and these associations are consistent with that framework.

The practical implications of the study extend in several directions. For clinicians in Tehran and comparable settings, the near-total loss of ampicillin, trimethoprim-sulfamethoxazole, and tetracycline as treatment options means that empirical therapy must lean increasingly on carbapenems, tigecycline, or whichever oral agents retain activity, decisions that should ideally be informed by species identification and susceptibility testing. For public health authorities, the distinct resistance and virulence profiles of S. flexneri and S. sonnei argue for species-specific surveillance programs that track the two organisms separately rather than lumping them together as generic Shigella. And for researchers, the demonstrated links between virulence genes and resistance phenotypes open a line of inquiry into whether molecular screening for genes such as sigA, ipaB, or ipaD could help predict resistance patterns before culture-based results become available. As the authors conclude, the findings underscore a need for vigilance: in this Tehran pediatric population, shigellosis has become not only a disease of poverty and sanitation but a showcase for how bacterial virulence and antibiotic resistance evolve together in a clinical setting.

Subject of Research: Virulence gene distribution and antimicrobial resistance in pediatric Shigella isolates from Tehran, Iran

Article Title: Distribution of virulence-related genes in Shigella isolates recovered from pediatric patients in Tehran, Iran: association with antimicrobial resistance

Article References: Kazemzadeh Anari, R., Sadredinamin, M., Hashemi, A., Houri, H., Taheri, M., Yousefi Nojookambari, N., Nikmanesh, A., & Ghalavand, Z. (2026). Distribution of virulence-related genes in Shigella isolates recovered from pediatric patients in Tehran, Iran: association with antimicrobial resistance. Gut Pathogens. https://doi.org/10.1186/s13099-026-00875-9

Image Credits: AI Generated

DOI: 10.1186/s13099-026-00875-9

Keywords: Shigella, antimicrobial resistance, multidrug resistance, Shigella flexneri, Shigella sonnei, virulence genes, children, diarrhea, Tehran, type III secretion system, pediatric infectious disease, public health

The analysis drew on more than 9,300 cases of moderate-to-severe diarrhea collected in Mali, Kenya, and The Gambia through the Global Enteric Multicenter Study, or GEMS, and its follow-up project, Vaccine Impact on Diarrhea in Africa, known as VIDA. Both studies generated extensive clinical, laboratory, demographic, and household data from children living in communities with differing levels of infrastructure and economic resilience. The researchers examined four major causes of severe childhood diarrhea: Cryptosporidium, Shigella, rotavirus, and enterotoxigenic Escherichia coli, or ETEC. Their objective was not simply to determine whether climate change increases disease, but to identify which climate variables matter for each pathogen and which populations are most likely to experience the greatest effects.

Diarrheal disease remains a major cause of childhood illness and death worldwide. The World Health Organization identifies it as the third leading cause of death among children younger than five and a leading contributor to malnutrition. Repeated infections can damage the intestinal lining, impair nutrient absorption, and create a cycle in which illness and undernutrition reinforce one another. Climate change may intensify these processes because many enteric pathogens are sensitive to temperature, humidity, water availability, and flooding. Warmer conditions can accelerate microbial replication or extend the period during which pathogens survive in the environment, while heavy rainfall can overwhelm sanitation systems and contaminate drinking-water sources. Drought can also force communities to rely on unsafe water or travel farther to obtain it.

The new study shows that these mechanisms operate differently depending on the organism and location. In Kenya, temperature was strongly associated with the risk of Shigella, Cryptosporidium, and ETEC. In Mali and The Gambia, rainfall-related measures were more influential for rotavirus, Cryptosporidium, and ETEC. These differences reflect the distinct biology and transmission pathways of the pathogens. Shigella spreads primarily through fecal-oral transmission and can move rapidly through contaminated food, water, and close household contact. ETEC produces toxins that disrupt intestinal fluid balance, while Cryptosporidium forms environmentally hardy oocysts that can persist in water. Rotavirus, an exceptionally contagious virus, can spread efficiently wherever sanitation is limited and susceptible children come into contact with contaminated surfaces or bodily fluids.

The researchers also investigated whether so-called adaptive capacity factors could modify climate-associated risks. Adaptive capacity describes the practical resources that allow households and communities to anticipate, withstand, and recover from environmental stress. In the analysis, children from households with access to transportation, electricity, or a television generally showed lower climate-associated risks for certain pathogens than children from households without those resources. These factors are not necessarily direct biological defenses against infection. Rather, they may act as indicators of mobility, economic stability, access to information, the ability to seek treatment, and the capacity to obtain safer water or food when environmental conditions deteriorate.

Access to improved drinking water emerged as particularly important for Cryptosporidium. Modeling indicated that a decline in access to improved water could substantially increase Cryptosporidium incidence under future climate scenarios across all three study sites. Conversely, expanding access to improved drinking water was projected to reduce incidence. The finding is consistent with the parasite’s transmission biology: Cryptosporidium oocysts can survive in water and are resistant to commonly used levels of chlorine, making filtration, source protection, sanitation, and reliable water infrastructure important components of prevention. For families living in areas where water sources are vulnerable to flooding, contamination, or seasonal shortages, even modest disruptions can increase exposure.

The climate projections examined in the study suggest that temperatures could rise substantially by 2055, but the resulting effect on precipitation and Cryptosporidium incidence was modest across the three study locations. This does not mean that climate change will have little effect on diarrheal disease. Rather, it demonstrates why broad assumptions about climate and infection can be misleading. A warmer future may alter risks through several pathways at once, while local precipitation patterns, sanitation conditions, pathogen ecology, and household behavior determine how those changes are expressed. A climate variable that predicts increased risk for one pathogen in one country may have a weaker association—or a different association altogether—in another setting.

The findings also reinforce the importance of vaccination as part of climate adaptation. Rotavirus vaccination can prevent severe disease caused by one of the most transmissible viral agents of childhood diarrhea, reducing the number of children who require hospitalization and protecting health systems during periods of heightened environmental pressure. Vaccination cannot eliminate every cause of diarrhea, and it does not replace clean water, sanitation, or clinical care. However, by lowering vulnerability to a major pathogen, immunization can reduce the consequences of climate-related disruptions. The researchers argue that vaccine delivery should be considered alongside infrastructure improvements, economic development, transportation access, and public-health surveillance when governments plan for a changing climate.

“This research highlights the importance of looking beyond environmental exposures alone,” said Stefan Kappe, director of the University of Maryland School of Medicine’s Center for Vaccine Development and Global Health. “Building resilience to climate change will require a combination of public health interventions, infrastructure improvements, economic development, and expanded access to lifesaving vaccines.” Megan Kowalcyk, the study’s lead author and a research associate at the center, said the results show that disease risk depends not only on temperature and rainfall but also on the factors that shape a family’s ability to adapt and respond to environmental stressors.

The study’s site-specific and pathogen-specific approach gives public-health planners a more precise way to anticipate future disease patterns. Instead of treating climate change as a single exposure with a uniform outcome, the analysis connects environmental conditions with biological mechanisms and household resilience. That perspective could help identify where water improvements, vaccine campaigns, transportation networks, or disease surveillance would have the greatest protective effect. The GEMS and VIDA programs were funded by the Gates Foundation and led by Myron M. Levine and Karen L. Kotloff. Together, their data suggest that protecting children from climate-driven diarrheal disease will depend not only on reducing greenhouse-gas emissions, but also on strengthening the social and public-health systems that enable vulnerable communities to withstand environmental change.

Subject of Research: People

Article Title: Vulnerability to climate-driven pathogen-specific diarrheal diseases: secondary analysis from the Global Enteric Multicenter Study and Vaccine Impact on Diarrhea in Africa follow-up

News Publication Date: August 19, 2026

Web References: University of Maryland School of Medicine Center for Vaccine Development and Global Health: https://www.medschool.umaryland.edu/cvd/ ; Global Enteric Multicenter Study: https://www.medschool.umaryland.edu/gems/ ; Vaccine Impact on Diarrhea in Africa: https://www.medschool.umaryland.edu/cvd/vaccines/studies–projects/vaccine-impact-on-diarrhea-in-africa-vida/ ; World Health Organization diarrheal disease fact sheet: https://www.who.int/news-room/fact-sheets/detail/diarrhoeal-disease

References: Nature Communications, DOI: 10.1038/s41467-026-76189-w. Initial analysis: Journal of Infectious Diseases, DOI: 10.1093/infdis/jiag306.

Keywords: climate change, childhood diarrhea, viral diseases, rotavirus, Cryptosporidium, Shigella, ETEC, sub-Saharan Africa, infectious disease, vaccination, drinking water, public health, epidemiology, climate resilience