The study, conducted by Bao Linh Nguyen and Thanh Binh Ngo of the University of Medicine and Pharmacy at Ho Chi Minh City, enrolled adults with HIV and microbiologically confirmed pulmonary tuberculosis at a tertiary referral hospital for tuberculosis and lung diseases between December 2022 and September 2023. Rather than averaging findings across the cohort, the researchers deliberately stratified patients by CD4 count, the standard laboratory measure of immune destruction, and tracked how three separate axes of the disease shifted across those strata: the radiographic appearance of the lungs on chest X-ray, the microbiological yield of sputum tests, and the presence of additional pulmonary pathogens sharing the same airways.

The patients themselves tell much of the story. The median CD4 count in the cohort was a startling 40.5 cells per microliter of blood, a level at which the immune system is barely functional; healthy counts sit above 500. Most patients were not yet taking antiretroviral therapy, and many were learning of their HIV diagnosis for the first time when they arrived at the hospital. This is the face of late presentation, and it is common in settings where HIV stigma, fragmented testing services and limited access to care delay diagnosis until opportunistic infections force patients through the door. Vietnam’s HIV epidemic, concentrated in certain regions and populations, continues to feed such late presentations into its tuberculosis wards.

The radiographic findings were the study’s most striking result. Among patients in the highest CD4 stratum, every single patient showed cavitation on chest radiography, and nearly nine in ten showed consolidation, the dense opacities that mark the body’s attempt to wall off infection with an intact inflammatory response. Large nodules appeared in two-thirds of this group. In the lowest CD4 stratum, the picture inverted almost completely: cavitation was seen in just 3.8 percent of patients, consolidation in 30.8 percent, and large nodules in 9.6 percent. Instead, half of the most immunosuppressed patients displayed ground-glass opacity, a hazy, frosted-glass pattern that in this population strongly evokes Pneumocystis jirovecii pneumonia or other non-tuberculous pathology. All four of these radiographic trends remained statistically significant after correction for multiple comparisons, with adjusted q-values of 0.025 or lower.

The biological explanation is straightforward but consequential. Cavitation in tuberculosis is not the work of the bacterium alone; it is the work of the immune response to it. Caseous necrosis, the destruction of lung tissue into a cheese-like core that can liquefy and drain into airways, depends on a vigorous CD4 T-cell driven inflammatory reaction. When CD4 cells are scarce, the lung cannot mount that reaction, so the bacilli multiply diffusely without forming cavities, and the radiograph shows vague haziness rather than the textbook cavity. The practical implication is that clinicians who dismiss tuberculosis because the X-ray lacks classic features may be precisely wrong in the patients at greatest risk, since atypical, ground-glass-predominant disease is a marker of the deepest immunosuppression.

That overlap with Pneumocystis is where the study becomes clinically urgent. Ground-glass opacity showed an unadjusted association with Pneumocystis positivity, with an odds ratio of 5.67, meaning patients with this pattern were more than five times as likely to harbor the fungus. Yet the diagnostic workup for Pneumocystis was strikingly incomplete: among patients with CD4 counts at or above 200 cells per microliter, only four of nine were ever tested, and none of those tested was positive. Overall, at least one additional pulmonary organism was documented in 28 of 92 patients, or 30.4 percent of the cohort. In other words, nearly a third of these patients were fighting more than one lung infection simultaneously, a reality that complicates every treatment decision, from empiric antibiotic choices to the timing and composition of antiretroviral initiation, where immune reconstitution inflammatory syndrome looms as a hazard.

On the microbiological axis, the study delivered a clear verdict on diagnostics. Sputum smear microscopy, the century-old workhorse of tuberculosis diagnosis in high-burden countries, detected acid-fast bacilli in only 63.3 percent of patients. The molecular Xpert MTB/RIF assay, which amplifies Mycobacterium tuberculosis DNA and simultaneously screens for rifampicin resistance, was positive in 91.1 percent. The paired comparison, analyzed with exact McNemar testing, produced a p-value below 0.0001, leaving little doubt that the molecular assay outperforms smear across every level of immunosuppression. Notably, neither test showed a significant ordered trend across CD4 strata, suggesting that the well-known paucibacillary appearance of tuberculosis in advanced HIV does not translate into a simple, predictable gradient of test positivity in real-world sputum samples.

Perhaps the most pragmatic finding concerns a test that almost any district laboratory can perform. The researchers explored whether the absolute lymphocyte count, a routine component of a complete blood count, could serve as a proxy for CD4 depletion. In exploratory receiver-operating-characteristic analysis, the absolute lymphocyte count discriminated patients with CD4 counts below 200 cells per microliter with an area under the curve of 0.89, with a 95 percent confidence interval of 0.79 to 0.96. An AUC near 0.9 represents strong discriminatory power, approaching the threshold often considered excellent. The authors are careful to frame this correctly: the lymphocyte count may provide a supportive indicator of advanced immunosuppression where CD4 testing infrastructure is unavailable, but it must not substitute for direct CD4 measurement, which remains the gold standard for staging HIV disease and guiding prophylaxis against opportunistic infections.

The study’s limitations deserve honest weight, and the authors acknowledge them directly. This was a single-center, cross-sectional investigation at a specialized referral hospital, which means the patients may not represent the broader population of people with HIV and tuberculosis in Vietnam or elsewhere. The design captures a snapshot rather than a trajectory, so it can describe associations but cannot establish how individual patients’ disease evolves as immune function changes. The Pneumocystis findings rest on microscopy, an insensitive method, and the testing gaps among higher-CD4 patients make the true prevalence of coinfection uncertain. The lymphocyte count analysis was explicitly exploratory. The authors describe their conclusions as hypothesis-generating and call for prospective confirmation, a framing that reflects appropriate scientific caution rather than weakness.

Even with those caveats, the findings land at a consequential moment. Tuberculosis remains the leading cause of death among people with HIV worldwide, and the World Health Organization’s targets for ending the dual epidemic depend on finding cases earlier and treating them correctly the first time. This study from Ho Chi Minh City distills that challenge into concrete clinical rules of thumb: in a patient with advanced HIV, a hazy chest X-ray without cavitation should raise, not lower, suspicion of tuberculosis; molecular testing should replace smear wherever possible; a substantial fraction of patients harbor secondary pulmonary pathogens that demand broader diagnostic thinking; and where CD4 counters are scarce, a simple lymphocyte count can flag the patients most likely to be dangerously immunosuppressed. For the clinicians working on the front lines of the HIV-tuberculosis collision, these are not abstractions. They are the difference between a diagnosis made in time and one made too late.

Subject of Research: Clinical, radiographic and microbiological presentation of HIV-associated pulmonary tuberculosis across CD4 count strata

Article Title: Clinical, radiographic and microbiological manifestations of newly diagnosed pulmonary tuberculosis across CD4 strata in adults with advanced HIV disease: a real-world cross-sectional study in southern Vietnam

Article References: Nguyen, B. L., & Ngo, T. B. (2026). Clinical, radiographic and microbiological manifestations of newly diagnosed pulmonary tuberculosis across CD4 strata in adults with advanced HIV disease: a real-world cross-sectional study in southern Vietnam. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14507-9

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14507-9

Keywords: pulmonary tuberculosis, HIV, advanced HIV disease, CD4 count, chest radiography, ground-glass opacity, Xpert MTB/RIF, sputum smear microscopy, Pneumocystis jirovecii, coinfection, absolute lymphocyte count, Vietnam

Gastrointestinal nematodes are among the most economically consequential pathogens of grazing livestock worldwide. In cattle, species such as Haemonchus placei, a blood-feeding abomasal worm, and various Cooperia species that damage the small intestine cause weight loss, reduced milk yield, poor fertility and, in heavy infections, death. The global cost is measured in billions of dollars annually, and the burden falls disproportionately on smallholder and pastoralist communities across sub-Saharan Africa, where livestock are both income and insurance. Yet the epidemiology of these worms in Africa remains strikingly under-characterised. Most surveillance still depends on faecal egg counts, which estimate the number of eggs shed per gram of faeces, and on the microscopic identification of third-stage larvae cultured from faecal samples. Both approaches have fundamental limitations that the new study set out to address.

Faecal egg counts cannot distinguish between species, because the eggs of many strongylid nematodes are morphologically near-identical. Larval culture and identification improve on this, but the technique is laborious, requires skilled parasitologists, takes one to two weeks, and is subject to culture biases that can distort the apparent composition of an infection. Different species develop and survive in culture at different rates, meaning the larval population recovered in a petri dish may not faithfully represent the worm population inside the animal. In tropical settings, where ambient temperatures accelerate larval development and where laboratory infrastructure may be limited, these problems are compounded. The result is a sparse and potentially skewed picture of nematode diversity across much of the continent, precisely where that diversity matters most for designing effective control.

The nemabiome approach sidesteps these constraints by reading the parasites’ DNA directly. The method targets the internal transcribed spacer-2 region, or ITS-2, a stretch of ribosomal DNA that varies sufficiently between species to serve as a barcode. Using primers that amplify this region from any Clade V nematode, the strongylid group that includes the major livestock worms, researchers can sequence thousands of amplicons in parallel from a single sample. Bioinformatic pipelines then sort the resulting reads into species-level operational taxonomic units and estimate their relative abundances. Because the technique works on any life stage containing usable DNA, it can in principle be applied to eggs in faeces, to first-stage larvae hatched from those eggs, or to third-stage larvae recovered from culture, allowing researchers to compare what each sample type reveals.

That is exactly what the team did at Ol Pejeta, a conservancy where livestock grazing is deliberately integrated with wildlife conservation, including populations of elephants, rhinos and large predators. The study focused on adult cows and their calves, sampling faeces, first-stage larvae and cultured third-stage larvae from individual animals. The nemabiome analysis confirmed infections with eight species: Cooperia curticei, Cooperia pectinata, Cooperia punctata, Haemonchus placei, Haemonchus contortus, Teladorsagia circumcincta, Trichostrongylus axei and Trichostrongylus colubriformis. Several of these findings are notable in themselves. Haemonchus contortus, classically a parasite of sheep and goats, was detected in cattle, raising questions about cross-species transmission at the interface. Teladorsagia circumcincta, another small-ruminant worm, likewise appeared in the cattle nemabiome, a signal that would have been easy to miss with morphology-based methods alone.

Perhaps the most striking quantitative finding concerns coinfection. Mixed-species infections accounted for 77.4 percent of all infections detected in the study animals. In other words, the typical infected cow at Ol Pejeta was not carrying a single worm species but a community of them, with the composition varying from animal to animal. This matters because nematode species differ in their pathogenicity, their seasonal dynamics and, critically, their response to anthelmintic drugs. A treatment regimen informed only by faecal egg counts treats the infection as an undifferentiated mass; a regimen informed by metabarcoding can recognise, for example, that a Haemonchus-dominated infection may demand different management than one dominated by Trichostrongylus. The study’s authors argue that uncovering this diversity opens new opportunities to investigate interactions between worm species within the host, including competition, facilitation and their consequences for disease severity and drug efficacy.

Age emerged as a second axis of variation. Calves carried higher infection rates than their dams and harboured more diverse nematode communities. This pattern is consistent with the immunology of helminth infection: adult cattle gradually acquire partial immunity through repeated exposure, which suppresses worm establishment and fecundity, whereas young animals, still immunologically naive, accumulate infections more freely. From a control perspective, the finding reinforces the importance of monitoring calves specifically, since they are both the most heavily parasitized cohort and the one in which subclinical damage to gut and abomasum can permanently compromise growth. It also suggests that dam–calf pairs provide a natural experiment for studying the development of nemabiome diversity over time, a direction the authors see as promising for future work.

Equally consequential is the study’s practical demonstration of which sample types can carry the analysis. Faecal samples and first-stage larvae both proved reliable sources of nematode DNA, yielding species compositions consistent with the gold-standard cultured third-stage larvae. This is a significant result for tropical field settings. Third-stage larval culture requires incubation, careful moisture and temperature management, and weeks of waiting; faeces require a bag and a courier. If routine surveillance can be run on faecal or first-stage larval DNA, the barrier to implementing molecular monitoring in African veterinary services drops dramatically. The authors position this as offering a practical alternative to labour-intensive L3 culturing, and the implication for national control programmes is clear: species-level surveillance could become as routine as the egg counts it would complement.

The wildlife–livestock interface setting adds a further layer of significance. Ol Pejeta’s cattle graze land shared with wild ungulates, and several of the nematode species detected are known to infect multiple host species. Haemonchus contortus, for instance, circulates in wild ruminants as well as small livestock, and Trichostrongylus species have broad host ranges. Molecular barcoding of livestock parasites therefore offers a window into transmission dynamics that span the domestic–wild boundary, something morphology-based diagnostics have never been able to resolve at scale. The authors argue that in such complex ecosystems, nemabiome approaches provide strong potential for unbiased disease surveillance, capturing the full parasite community rather than only the species a technician expects to find. As land-use change brings livestock and wildlife into ever closer contact across East Africa, tools that can track parasite flow between them will become increasingly valuable for both conservation and animal health.

The study also serves as a proof of concept for building African nemabiome reference data. Metabarcoding is only as good as its reference database; reads can be assigned to species only when that species’ ITS-2 sequence has been catalogued. By generating and validating species assignments in a Kenyan herd, the team has contributed to the baseline needed for wider deployment across the continent. Funded in part by the Bill & Melinda Gates Foundation and UK aid through the Centre for Tropical Livestock Genetics and Health, the work reflects a growing investment in molecular epidemiology for African livestock systems. The immediate next steps, the authors suggest, include exploiting the revealed diversity to study inter-species interactions within hosts and to track how nematode communities shift with season, treatment and grazing management. For a class of parasites that has long been counted but rarely identified, the era of seeing the whole community has begun.

Subject of Research: Gastrointestinal nematode diversity and coinfection in Kenyan cattle at a wildlife–livestock interface, assessed by nemabiome metabarcoding

Article Title: Gastrointestinal nematode diversity in Kenyan cattle at wildlife–livestock interfaces: a deep-amplicon sequencing approach

Article References: Yalcindag, E., Karani, B. E., Vasoya, D., van Bunnik, B. A. D., Freeman, E. J., Ngulu, S., van Aardt, R., Toye, P., Sargison, N., Morrison, L. J., & Bronsvoort, B. M. D. C. (2026). Gastrointestinal nematode diversity in Kenyan cattle at wildlife–livestock interfaces: a deep-amplicon sequencing approach. Parasites & Vectors. https://doi.org/10.1186/s13071-026-07657-x

Image Credits: AI Generated

DOI: 10.1186/s13071-026-07657-x

Keywords: gastrointestinal nematodes, nemabiome, metabarcoding, Kenya, cattle, wildlife–livestock interface, Haemonchus, Cooperia, coinfection, parasite surveillance, ITS-2 sequencing, livestock health

The research team, led by Shi Dong and Haokun Mei of Nanjing Medical University alongside colleagues at several Chinese institutions, conducted a comprehensive search of PubMed and Web of Science that initially returned 301 studies. After rigorous screening according to pre-specified design criteria, 21 studies met eligibility requirements, encompassing 74,424 participants and 4,274 human bocavirus positive patients drawn from nine countries across five continents. The analysis was registered prospectively on PROSPERO under registration number CRD420261460519, and the review followed established PRISMA reporting guidelines with quality assessment using the Joanna Briggs Institute framework.

For the primary prevalence estimate, the authors applied strict inclusion rules: only cross-sectional or consecutive surveillance studies with a valid denominator were admitted, and studies that exclusively enrolled patients already known to be bocavirus positive were excluded to avoid inflating prevalence. Eighteen studies survived these filters. The pooled global prevalence of human bocavirus among patients tested, most of them presenting with respiratory tract infections, was 9.7 percent, with a 95 percent confidence interval spanning 6.4 to 13.1 percent. Notably, the 95 percent prediction interval stretched from 0.0 to 25.1 percent, an unusually wide range that signals profound heterogeneity across settings, populations, and study designs.

That heterogeneity is not merely a statistical nuisance; it is a central biological finding. The authors report that human bocavirus prevalence, seasonality, and coinfection patterns are significantly shaped by geographic region, age, and socioeconomic factors. Viral detection rates in a densely populated urban pediatric ward in East Asia may bear little resemblance to those in a European outpatient clinic, and the meta-analysis makes clear that any single-country estimate should be extrapolated with caution. The wide prediction intervals serve as a quantitative reminder that the virus’s behavior is embedded in local epidemiological contexts rather than governed by a single global pattern.

Seasonality emerged as one of the more intriguing dimensions of the analysis. Twelve studies initially contributed data on the timing of infections. The crude proportion of bocavirus positive cases occurring in summer was 17.2 percent, but after the authors excluded three statistical outliers, identified by pre-specified criteria of studentized residuals greater than 2.0 and a reduction in heterogeneity exceeding 20 percentage points, the adjusted summer proportion rose to 23.2 percent with a confidence interval of 17.2 to 29.1 percent. No outliers were detected for spring, autumn, or winter, suggesting that while the virus circulates year round, a meaningful fraction of its burden falls in the warmest months, a pattern that distinguishes it from strictly winter-peaked pathogens such as respiratory syncytial virus or influenza.

The COVID-19 pandemic left a detectable fingerprint on these seasonal rhythms. The analysis found that the seasonal peak of human bocavirus activity was delayed by 1.6 months after the pandemic, and the phase distribution of infections became more concentrated in the post-pandemic era. This observation aligns with broader reports of disrupted respiratory virus ecology following the widespread deployment of non-pharmaceutical interventions, which temporarily suppressed transmission of many common respiratory pathogens and subsequently reshaped the timing and intensity of their return. The authors note that the higher coinfection proportion observed in the post-pandemic subgroup was not, however, a statistically significant moderator effect, with meta-regression yielding a p value of 0.721.

The most clinically consequential finding concerns coinfection. Across 18 studies, the overall proportion of human bocavirus infections that involved at least one additional pathogen was 65.9 percent, with a confidence interval of 64.3 to 67.5 percent. Among specific co-pathogens, respiratory syncytial virus showed the highest coinfection rate, followed by other common respiratory viruses including human rhinovirus, adenovirus, human metapneumovirus, parainfluenza virus, influenza virus, and enterovirus. In other words, when clinicians detect bocavirus in a pediatric respiratory sample, roughly two-thirds of the time another virus is present as well, complicating any straightforward attribution of disease to a single agent.

Does coinfection matter for outcomes? The meta-analysis suggests it does. Patients with coinfections had a significantly higher risk of pneumonia than those with bocavirus monoinfections, with an odds ratio of 1.53 and a confidence interval of 1.08 to 2.18. Coinfection was also associated with an average of 0.80 additional days of hospital stay. These numbers, while statistically significant, come with important caveats that the authors themselves emphasize. The clinical analyses rested on only nine studies, the majority of which originated from China, and bacterial co-pathogens were not assessed at all. Because bacterial pneumonia is a frequent and serious complication of viral respiratory infections, its absence from the pathogen panel means the full clinical impact of mixed infections is likely underestimated.

The methodological transparency of the review deserves attention in its own right. By pre-specifying outlier exclusion criteria before running analyses, reporting both crude and adjusted estimates, and presenting prediction intervals alongside confidence intervals, the authors offer a model of cautious inference in a field where pooled estimates are often presented with more certainty than the underlying data warrant. The confidence intervals describe the precision of the average effect across studies, while prediction intervals describe the plausible range a new study might observe, and the gulf between the two in this analysis is a candid acknowledgment of how much local variation remains.

Looking forward, the authors call for research incorporating standardized protocols and comprehensive pathogen testing, including bacterial diagnostics and quantitative viral load measurements, to clarify the clinical impact of human bocavirus coinfections. Whether the virus acts as a primary pathogen, a passenger amplified by concurrent illness, or a cofactor that worsens disease driven by other agents remains one of the central unanswered questions in respiratory virology. As molecular multiplex panels become standard in clinical settings worldwide, the data needed to answer that question are accumulating rapidly, and syntheses like this one provide the essential baseline against which future studies can be measured.

Subject of Research: Global epidemiology, seasonality, and clinical impact of human bocavirus coinfections in respiratory tract infections

Article Title: Epidemiology and clinical patterns of human bocavirus coinfections: a systematic review and meta-analysis

Article References: Dong, S., Mei, H., Tan, B., Ren, H., Xu, Y., Yang, D., Dai, Q., Ji, M., & Dai, G. (2026). Epidemiology and clinical patterns of human bocavirus coinfections: a systematic review and meta-analysis. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14478-x

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14478-x

Keywords: human bocavirus, coinfection, respiratory syncytial virus, pneumonia, systematic review, meta-analysis, epidemiology, seasonality, pediatric respiratory infections, viral epidemiology, BMC Infectious Diseases, COVID-19 pandemic

The patient, who had been working in Malaysia, first fell ill with intermittent fever during his period of immigration there. Screening at that stage returned a positive result for dengue, a diagnosis that seemed unremarkable in a region where the dengue virus circulates intensely. Yet the fever refused to settle. Dengue is typically a self-limited, mosquitoborne viral illness in which the nonstructural protein 1, or NS1, antigen circulates in blood during the acute phase and clears within days to a couple of weeks as the immune response takes hold. In this patient, however, the fever persisted long enough that he was forced to return to Nepal, carrying with him a dengue label that would shape every subsequent clinical decision.

Back in South Asia, the diagnostic journey grew more tangled rather than less. During evaluation in India, clinicians confronting the patient’s prolonged febrile illness and laboratory abnormalities turned their suspicion toward a hematological malignancy, an understandable but ultimately erroneous interpretation. Visceral leishmaniasis, caused by the protozoan parasite Leishmania donovani and transmitted by phlebotomine sand flies, is famous for mimicking other conditions: it produces splenomegaly, hepatomegaly, pancytopenia, weight loss, and relentless fever, a constellation that can indeed resemble lymphoma or leukemia on superficial review. The misdirection meant that the true diagnosis remained unmade while the underlying parasitic infection continued its indolent destruction of the patient’s immune defenses.

It was only after a third discrete febrile episode that visceral leishmaniasis was finally identified. By that point, however, the case had acquired another layer of complexity: the dengue NS1 antigen was still detectable, a strikingly prolonged persistence for a protein that normally vanishes as acute infection resolves. The reporting team argues that the concomitant infections appear to have driven this prolonged persistence of dengue features and, in parallel, may have propelled a previously asymptomatic Leishmania infection into symptomatic, life-threatening visceral disease. The immunology of such an interaction is plausible if speculative: dengue and Leishmania both manipulate mononuclear phagocytes, and the profound cell-mediated immunosuppression of active visceral leishmaniasis could plausibly impair clearance of viral antigens, while the viral insult could tip a controlled parasitic infection toward clinical manifestness.

Treatment brought the next setback. The patient received liposomal amphotericin B, or LAMB, the recommended first-line therapy for visceral leishmaniasis in many endemic settings, prized for its potency against Leishmania parasites sequestered in the spleen, liver, and bone marrow. Six doses were administered, yet the patient demonstrated no adequate response. Relapse followed the initial course, an outcome that forced the clinical team to reconsider both the diagnosis and the therapeutic strategy. Drug failure in visceral leishmaniasis can arise from host immunosuppression, parasite resistance, inadequate drug exposure, or an incorrect initial diagnosis, and in a patient whose dengue serology remained abnormal, every one of those possibilities demanded attention.

The decisive moment in the odyssey arrived through careful serial testing. When repeat assays for dengue NS1 antigen, dengue-specific IgM, and dengue-specific IgG all finally returned negative results, the diagnostic fog began to lift. With the dengue infection definitively behind him and active visceral leishmaniasis confirmed as the driver of his ongoing febrile illness, the clinicians turned to miltefosine, an oral alkylphosphocholine originally developed as an anticancer agent and later repurposed as a leishmanicidal drug. The intervention proved highly effective: the patient’s visceral leishmaniasis resolved, closing a clinical narrative that had spanned Malaysia, India, and Nepal and involved misdiagnosis, failed therapy, and relapse along the way.

The case carries technical lessons that extend well beyond one patient. Rapid diagnostic tests for dengue, including NS1 antigen detection and IgM/IgG antibody assays, are cornerstones of febrile illness triage in low- and middle-income countries, but their performance assumes a typical immunocompetent, monoinfected host. When a second pathogen remodels the immune landscape, antigen clearance kinetics can change in ways that no single test anticipates. Conversely, the rK39 rapid diagnostic test for visceral leishmaniasis, which the authors highlight among their keywords, detects antibodies that may be absent early or inconsistent across the disease course. A febrile traveler or migrant whose work history spans multiple endemic regions therefore represents a diagnostic worst case for panel-based, single-pathogen thinking, and the authors argue that the case demonstrates a clear need for better diagnostic tools and management strategies specifically designed for coinfections.

Epidemiologically, the report sits at the intersection of two burdens of the same geography. Visceral leishmaniasis remains endemic in the lowland plains of Nepal, India, and Bangladesh, where elimination programs have driven incidence down but not to zero, and dengue has expanded dramatically across the same territories in recent decades, with Nepal experiencing increasingly large seasonal epidemics. Migrant workers such as this patient, who move between endemic countries for employment, occupy a distinctive risk niche: they may acquire one infection in one country, carry it across borders, and have it diagnosed or misdiagnosed in another, fragmenting the clinical record that any single physician depends upon. The three-country trajectory recorded in this report illustrates how health systems that do not share records can each hold a partial truth about the same patient.

The authors caution, appropriately, that a single case report cannot establish the mechanism by which dengue and Leishmania interacted in this individual, only that the association coincided with atypical antigen persistence, disease progression, and treatment failure. Still, the therapeutic implication is concrete: in patients with visceral leishmaniasis who fail liposomal amphotericin B, especially those with concurrent or recent viral infections, clinicians should consider rescue therapy with miltefosine and should pursue serial virological testing to clarify what is resolving and what is not. The patient’s consent, anonymization of identifying details, ethical approval from the Nepal Health Research Council, and adherence to the Declaration of Helsinki documented in the report reflect the care taken to convert one man’s prolonged illness into a lesson for the clinics of the tropical world.

Subject of Research: Leishmania-dengue virus coinfection with persistent NS1 antigenemia complicating visceral leishmaniasis diagnosis and treatment

Article Title: Persistent dengue NS1 antigen in a patient with visceral leishmaniasis: A diagnostic and therapeutic odyssey

Article References: Chalise, B. S., Shrestha, S., Sapkota, A. S., Bajracharya, M., Basaula, Y. N., Bras‑Goncalves, R., & Manandhar, K. D. (2026). Persistent dengue NS1 antigen in a patient with visceral leishmaniasis: A diagnostic and therapeutic odyssey. BMC Infectious Diseases. https://doi.org/10.1186/s12879-026-14469-y

Image Credits: AI Generated

DOI: 10.1186/s12879-026-14469-y

Keywords: visceral leishmaniasis, dengue virus, NS1 antigen, coinfection, miltefosine, liposomal amphotericin B, rK39 RDT, neglected tropical diseases, Nepal, migrant workers, case report, diagnostic challenges