Hand, foot and mouth disease is a common childhood illness caused by several enteroviruses, most notably enterovirus A71 and coxsackievirus A16. While most infections resolve with mild fever, mouth ulcers and a characteristic rash on the hands, feet and buttocks, enterovirus A71 is notorious for its capacity to invade the central nervous system. Infected children can develop brainstem encephalitis, acute flaccid paralysis, pulmonary edema and cardiogenic shock, complications that can progress from first symptoms to death within hours. Vietnam has experienced repeated waves of severe hand, foot and mouth disease over the past two decades, and the 2023 outbreak raised urgent questions about which viral lineage was responsible and why the population appeared so vulnerable.

The investigation centered on enterovirus A71 subgenogroup B5, a variant that had been circulating elsewhere in the Asia-Pacific region before its appearance in Vietnam. Genomic analysis of viruses recovered from patients during the 2023 outbreak revealed a striking pattern: the Vietnamese B5 sequences were tightly clustered, indicating that the entire outbreak descended from a single introduction event rather than from multiple independent importations. This observation has important implications for outbreak preparedness, because it suggests that a single crossing of a border by one infected individual can be sufficient to seed a nationwide epidemic when the conditions are right.

One of the most intriguing questions the researchers addressed was whether subgenogroup B5 had evolved the ability to evade immunity generated by earlier enterovirus A71 strains. Vietnam had previously experienced outbreaks caused by other subgenogroups, including B5 viruses that circulated as far back as 2014. If the 2022 and 2023 viruses had drifted antigenically away from their predecessors, previously acquired immunity would offer little protection, explaining the severity of the new epidemic. To test this hypothesis, the team collected convalescent plasma from patients infected with subgenogroup B5 in both 2014 and 2023 and measured how effectively the antibodies in these samples could neutralize contemporary viruses in the laboratory.

The results were clear and, in a sense, reassuring. Plasma from patients infected in 2014 neutralized the 2023 viruses with titers comparable to those achieved by plasma from patients infected in 2023, and the same held true in the reverse direction. In other words, the antigenic properties of the virus had not appreciably changed over the nine-year interval, and there was no evidence of immune evasion. The severity of the 2023 outbreak therefore could not be attributed to a viral escape from pre-existing immunity. Instead, the explanation lay in the age structure of susceptibility within the population, particularly among the youngest children who had never encountered any enterovirus A71 strain.

Serological surveys conducted in Ho Chi Minh City revealed the scale of this vulnerability. At one month before the start of the outbreak, only 6.7 percent of children aged zero to under three years carried neutralizing antibodies against enterovirus A71. Even at six months before the outbreak began, the figure was similarly low. This meant that the vast majority of infants and toddlers in the city, the group at highest risk of severe disease, had no immunological defense against the incoming virus. When subgenogroup B5 arrived, it found an almost entirely susceptible cohort in the exact age bracket where infection is most likely to turn dangerous.

The study did not stop at documenting susceptibility before the outbreak. The researchers repeated their serological measurements as the epidemic unfolded, and the results traced the arc of the outbreak in real time. As the proportion of young children with neutralizing antibodies rose, the number of enterovirus A71 infected patients residing in Ho Chi Minh City fell. This inverse relationship, in which increasing population immunity coincided with declining transmission, suggests that the outbreak burned through the susceptible pool until so many children had been infected and immunized that the virus could no longer spread efficiently. It also demonstrates that serosurveillance, the systematic measurement of antibody levels in the population, can serve as a practical early warning tool.

The implications of this serosurveillance-based approach extend well beyond a single outbreak. Traditional disease surveillance relies on detecting clinical cases, which by definition identifies an outbreak only after substantial transmission has already occurred. Measuring the fraction of the population that lacks neutralizing antibodies, by contrast, can quantify the size of the susceptible reservoir before any cases appear. In the case of enterovirus A71, the Vietnamese data show that a seroprevalence of under seven percent in children under three years of age signaled an acute risk of severe epidemic emergence. Health authorities monitoring antibody levels in young children could, in principle, identify comparable windows of vulnerability in advance and intensify clinical preparedness, public communication and, where available, vaccination efforts accordingly.

Enterovirus A71 remains an active public health threat concentrated in the Asia-Pacific region, where periodic outbreaks of severe hand, foot and mouth disease continue to burden pediatric health systems. Vaccines against the virus have been developed and licensed in China, but coverage across the wider region remains incomplete, and no vaccine is universally deployed. The Vietnamese experience underscores how quickly a single imported lineage can exploit gaps in population immunity, and how the cyclical nature of enterovirus transmission creates recurring cohorts of susceptible infants between epidemic waves. The authors note that the virus has a high potential to become a global problem, and that it should therefore be closely monitored beyond its current geographic range.

Collectively, the study offers a model for investigating the emergence of any pathogen that causes severe disease in a defined age group. By integrating viral genomics, antigenic characterization and longitudinal serology, the researchers were able to rule out immune evasion, pinpoint the timing and origin of the introduction, quantify the susceptibility of the at-risk population and connect rising immunity to declining transmission. These insights into the epidemiological factors driving enterovirus A71 emergence are intended to inform outbreak preparedness and response, and to support the development of serosurveillance-based risk assessment frameworks that could be applied to enteroviruses and other emerging infectious threats alike.

Subject of Research: Virological and epidemiological investigation of a severe enterovirus A71 hand, foot and mouth disease outbreak in Vietnam in 2023

Article Title: Virological and epidemiological investigations of a severe hand foot and mouth disease outbreak, Vietnam, 2023

Article References: Nguyet, L. A., Anh, N. T., Quy, D. T., Hong, N. T. T., Minh, N. N. Q., Nguyen, P. N. T., Quang, P. V., Han, D. D. K., Ny, N. T. H., Nhu, L. N. T., Truc, T. H. C., Thuy, C. T., Hoang, N. N., Thien, T. B., Thanh, L. K., Hung, N. T., Khanh, T. H., Hiep, C. M., Ngoc, N. M., … Tan, L. V. (2026). Virological and epidemiological investigations of a severe hand foot and mouth disease outbreak, Vietnam, 2023. PLOS Neglected Tropical Diseases, 20(10), e0014789. https://doi.org/10.1371/journal.pntd.0014789

Image Credits: AI Generated

DOI: 10.1371/journal.pntd.0014789

Keywords: enterovirus A71, hand foot and mouth disease, subgenogroup B5, Vietnam, serosurveillance, neutralizing antibodies, outbreak, pediatric infectious disease, genomic epidemiology, immune evasion, public health, Asia-Pacific

The study, published in Virology Journal by Ying Li of Zhengzhou Railway Vocational and Technical College and colleagues at Zhengzhou University and Henan Children’s Hospital, focused on children of Han Chinese ethnicity who were infected with Coxsackievirus A6, an enterovirus that has increasingly displaced enterovirus 71 as the dominant cause of hand, foot, and mouth disease outbreaks in many regions. The research team enrolled 189 children from Henan Children’s Hospital, dividing them into 94 severe cases and 95 mild cases, and then asked whether specific single nucleotide polymorphisms, or SNPs, in complement-related genes were more common among the severely ill children than among those with milder disease.

The complement system is a cascade of plasma proteins that acts as one of the body’s first lines of defense against pathogens. When activated, complement proteins such as C3 and C5 mark microbes for destruction, recruit inflammatory cells to sites of infection, and in some circumstances directly punch holes in viral envelopes or infected cell membranes. Because the complement cascade sits at the interface between pathogen recognition and inflammatory damage, it represents a biologically plausible target for genetic studies of infection severity: too little complement activity might impair viral clearance, while too much might fuel the excessive inflammation that characterizes severe cases. The central complement protein C3, the terminal component C5, and the complement regulatory protein factor H, encoded by the CFH gene, each play distinct roles in this delicate balance, and common genetic variants in these genes have previously been linked to susceptibility to other infectious and inflammatory diseases.

To test whether such variants matter in Coxsackievirus A6 infection, the researchers extracted genomic DNA from peripheral blood leukocytes using a modified phenol-chloroform method and performed SNP genotyping by polymerase chain reaction followed by restriction fragment length polymorphism analysis, a classical technique in which PCR-amplified DNA fragments are digested with restriction enzymes whose cutting patterns differ depending on the nucleotide present at a given position. This approach allowed the team to determine each child’s genotype at candidate SNPs in the C5, C3, and CFH genes and to compare genotype frequencies between severe and mild cases using both crude and multivariable logistic regression models adjusted for age group and sex.

The results revealed several nominal associations. Children carrying the GA genotype at rs3761847 in the C5 gene had roughly two and a half times the odds of severe disease compared with those carrying the GG genotype, with an adjusted odds ratio of 2.523 and a 95 percent confidence interval spanning 1.036 to 6.143. At rs2250656 in the C3 gene, the TC genotype was associated with an adjusted odds ratio of 1.982, with a confidence interval of 1.061 to 3.704, relative to the TT genotype. The strongest signals emerged at rs1065489 in the CFH gene, where the TT genotype conferred an adjusted odds ratio of 3.125, with a confidence interval of 1.249 to 7.818, and the GT genotype an adjusted odds ratio of 2.499, with a confidence interval of 1.118 to 5.588, both relative to the GG genotype. Taken at face value, these findings suggest that children carrying particular alleles at these three loci face a substantially elevated risk of progressing to severe hand, foot, and mouth disease once infected with Coxsackievirus A6.

However, the authors are careful to emphasize a critical statistical caveat. When the analysis was corrected for multiple testing using the Bonferroni method, a conservative procedure that adjusts the significance threshold to account for the number of SNPs examined, none of these associations remained statistically significant. This is a common and important pattern in candidate-gene association studies, which typically examine a modest number of preselected variants in a limited number of participants. Nominal signals that vanish after correction may reflect true effects that the study lacked the statistical power to confirm, or they may simply be chance findings that arise whenever many genetic variants are tested simultaneously in a finite sample. Distinguishing between these possibilities requires replication in independent cohorts, which is precisely what the authors call for.

Beyond the individual SNP analyses, the team also evaluated whether a combined model incorporating multiple SNPs could discriminate severe from mild cases. The combined model showed limited discriminatory performance, achieving an apparent area under the receiver operating characteristic curve of 0.653, which declined to 0.631 after bootstrap-based optimism correction. An AUC of 0.5 indicates discrimination no better than chance, while 1.0 indicates perfect discrimination, so a corrected value of 0.631 suggests that complement-related variants alone, at least in this cohort, provide only modest predictive information about disease severity. This finding underscores a broader lesson in genetic epidemiology: complex clinical outcomes such as infection severity are rarely determined by a handful of variants in a single pathway, and even biologically plausible genetic associations often translate into weak predictive models when considered in isolation.

The study also reported exploratory differences in selected laboratory parameters across genotype groups, hinting that complement variants might correlate with measurable differences in the host response to infection, although the authors frame these observations as preliminary. Such genotype-phenotype correlations, if confirmed, could eventually help explain the biological mechanism linking specific variants to clinical outcomes, for example by altering complement protein levels, activation efficiency, or regulation of the inflammatory response during enterovirus infection.

The clinical context of this work is significant. Coxsackievirus A6 has emerged as a major cause of hand, foot, and mouth disease in China and elsewhere, and unlike enterovirus 71, for which vaccines have been developed and deployed, CVA6 has no licensed vaccine. Surveillance data have shown shifting patterns of enterovirus dominance, with CVA6 outbreaks producing atypical and sometimes severe presentations, including widespread eczema coxsackium in children with atopic dermatitis and occasional neurological involvement. Understanding the host-side determinants of severity therefore has practical value: if genetic risk factors could be reliably identified and validated, they might eventually inform risk stratification in clinical settings, helping clinicians identify which children warrant closer monitoring during outbreaks.

The study was conducted in accordance with the Declaration of Helsinki and approved by the Life Sciences Institutional Review Board of Zhengzhou University, with written informed consent obtained from the parents or legal guardians of all participants. Funded by the National Natural Science Foundation of China and several provincial and postdoctoral programs, the work exemplifies the growing effort to move beyond purely virological explanations of disease severity and toward an integrated view in which viral factors, host genetics, and immune status jointly shape clinical outcomes. For now, the message of this study is one of cautious hypothesis generation: complement-related variants in C5, C3, and CFH merit further investigation as potential modifiers of Coxsackievirus A6 disease severity, but larger, independent, and ideally multi-center cohorts will be needed before these genetic signals can be considered established or translated into clinical tools. In a field where most children recover uneventfully and only a minority deteriorate, even modest advances in understanding host susceptibility could ultimately sharpen the clinical response to one of the world’s most burdensome pediatric viral diseases.

Subject of Research: Association between complement-related gene polymorphisms and severity of Coxsackievirus A6-induced hand, foot, and mouth disease in Chinese Han children

Article Title: Complement-related gene polymorphisms and severity of Coxsackievirus A6-induced hand, foot, and mouth disease in chinese han children: a candidate-gene association study

Article References: Li, Y., Li, Z., Duan, G., Chen, S., Zhang, Y., Wang, F., Dai, B., & Jin, Y. (2026). Complement-related gene polymorphisms and severity of Coxsackievirus A6-induced hand, foot, and mouth disease in chinese han children: a candidate-gene association study. Virology Journal. https://doi.org/10.1186/s12985-026-03282-3

Image Credits: AI Generated

DOI: 10.1186/s12985-026-03282-3

Keywords: hand, foot, and mouth disease, Coxsackievirus A6, complement system, C5, C3, CFH, single nucleotide polymorphisms, genetic association study, disease severity, enterovirus, pediatric infectious disease, innate immunity

The clinical story began with symptoms that might easily have been mistaken for a routine ear problem. The young woman developed a headache, pain in the affected ear, and visible inflammation of the skin over the site where her cochlear implant had been placed. For most patients, such complaints would prompt a search for common bacterial culprits, typically organisms that colonize the skin or the external ear canal. But this patient’s medical history and her home environment pointed her care team toward a far less expected diagnosis, one that would only emerge after an extensive diagnostic work-up.

CHARGE syndrome is a rare genetic condition whose name is an acronym summarizing its hallmark features: coloboma of the eye, heart defects, choanal atresia, retardation of growth and development, genitourinary abnormalities, and ear abnormalities. The ear anomalies associated with the syndrome are among its most consistent features, and they frequently produce severe sensorineural hearing loss. Cochlear implants, which bypass damaged inner ear structures by converting sound into electrical signals delivered directly to the auditory nerve, are therefore a common and often transformative intervention for patients with CHARGE syndrome. Yet the same anatomical complexity that makes implantation necessary also makes these patients surgically challenging, with altered temporal bone anatomy and an increased likelihood of perioperative and postoperative complications.

When the teenager arrived with headache, ear pain and cellulitis over her implant site, her physicians pursued an aggressive and systematic evaluation. Imaging of the temporal bone with computed tomography using intravenous contrast allowed the team to assess the bony structures surrounding the implant and to look for evidence of bone involvement. Blood cultures were obtained to determine whether bacteria had entered the bloodstream, and cultures of the wound itself were sent to identify the organism responsible for the local infection. The results were striking: cultures grew Pasteurella multocida, and the imaging findings confirmed osteomyelitis, an infection of the bone adjacent to the implant. Blood cultures demonstrated a transient bacteremia, indicating that the organism had at least briefly circulated beyond the site of the wound.

Pasteurella multocida is a gram-negative coccobacillus, a small, rounded rod-shaped bacterium that occupies a distinctive ecological niche. It lives as part of the normal oral flora of many domestic animals, with cats being the most common carriers, and it is notorious among clinicians for producing rapidly developing cellulitis after bites and scratches. In typical zoonotic infections, the bacterium is introduced directly into the skin through a break in the epidermis, causing redness, swelling and pain within hours to days of the injury. What makes this case exceptional is the presumed route of inoculation and the destination of the infection: rather than a simple skin infection, the organism apparently colonized the surgical site of an implanted medical device and then invaded the underlying bone, a pattern of disease that has rarely been described in association with cochlear implants.

The exposure history proved to be the key that unlocked the diagnosis. The patient’s family had recently welcomed a new kitten into the home, and the teenager had sustained numerous excoriations, superficial scratches that break the skin, from the animal’s playful claws. In a patient with a permanently implanted device beneath the skin of the scalp and mastoid region, even minor scratches over the implant site can provide a pathway for oral bacteria from a pet to reach the device and the surrounding tissue. The authors of the report emphasize that a thorough exposure history, including questions about animal contact, should be part of the standard evaluation of any pediatric patient presenting with headache, ear pain and cellulitis, particularly when complicating factors such as a cochlear implant are present, so that zoonotic organisms are included in the differential diagnosis from the outset.

Management of the infection required both surgical and medical strategies, reflecting the seriousness of a device-related bone infection. The cochlear implant itself had to be removed, a difficult decision in any patient for whom the device represents their primary connection to the hearing world, but one that is often unavoidable when infection involves the implanted hardware. Biofilm formation, in which bacteria adhere to artificial surfaces and encase themselves in a protective matrix, makes device infections nearly impossible to eradicate with antibiotics alone. In addition to the explantation, the patient received four weeks of antibiotic therapy targeted at Pasteurella multocida, a duration consistent with the treatment of osteomyelitis, where prolonged therapy is needed to eliminate bacteria residing within bone tissue.

The clinical course was further complicated by the development of facial nerve palsy, a weakness of the facial muscles caused by dysfunction of the facial nerve, which runs through the temporal bone in close proximity to the structures involved in cochlear implantation. Inflammation and infection within this confined bony space can compress or irritate the nerve, producing facial drooping and difficulty closing the eye on the affected side. The patient was treated with corticosteroids, the standard approach to reduce inflammation around the nerve, and the report documents this complication as part of the cascade of events set in motion by the infection. The episode underscores how infections of the temporal bone can threaten not only hearing but also the cranial nerves that control facial movement.

Beyond its microbiological novelty, the case carries a broader message about the care of medically complex patients. The authors highlight the importance of a multidisciplinary team in managing patients with intricate medical and surgical histories. In this single admission, expertise was required from otolaryngology, which managed the implant and the temporal bone; from pediatric infectious diseases, which selected and monitored the antibiotic regimen; and from pathology and laboratory medicine, which identified the organism through culture. The patient herself consented to the publication of her case, having been an adult at the time of her care, and the authors express their appreciation for her willingness to share her experience so that other clinicians might recognize similar presentations more quickly.

For the wider community of cochlear implant recipients and their families, the report offers practical lessons without cause for alarm. Device infections remain uncommon, and Pasteurella multocida is an unusual cause even among those that do occur. But the case illustrates a simple preventive principle: minor wounds over an implant site deserve attention, and households with implanted medical devices should be mindful of scratches from pets, particularly cats. For clinicians, the message is equally direct. When a patient with an implanted device presents with unexplained cellulitis, headache and ear pain, asking about animal exposure may reveal the diagnosis that routine thinking would miss, and early recognition of zoonotic pathogens can spare patients the prolonged and invasive course that this teenager endured.

Subject of Research: A case report of Pasteurella multocida cochlear implant infection in a teenager with CHARGE syndrome

Article Title: Cochlear implant infection in a teenager with CHARGE syndrome: a case report

Article References: Pereira, N. M., Tarun, S., Johnson, C. L., Neu, N., Green, D. A., Wang, R., & Golub, J. S. (2026). Cochlear implant infection in a teenager with CHARGE syndrome: a case report. BMC Pediatrics. https://doi.org/10.1186/s12887-026-07624-6

Image Credits: AI Generated

DOI: 10.1186/s12887-026-07624-6

Keywords: Pasteurella multocida, CHARGE syndrome, cochlear implant, zoonotic infection, osteomyelitis, bacteremia, facial nerve palsy, pediatric infectious disease, cat scratch, multidisciplinary care, antibiotic therapy, case report

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