The patient arrived at the emergency department with three days of high-grade fever, reaching 103 degrees Fahrenheit, accompanied by the classic hallmarks of dengue: headache, retro-orbital pain behind the eyes, and generalized body aches. He had no vomiting, diarrhea, cough, or any bleeding manifestations, and no chronic medical conditions, prior surgeries, or relevant family history. He did not smoke, drink alcohol, or use recreational drugs. On examination he appeared ill and febrile, with a pulse of 110 beats per minute and a blood pressure of 115/80 mmHg, but his heart, lungs, abdomen, and neurological status were otherwise unremarkable. In short, he presented as a textbook case of uncomplicated dengue.

Laboratory testing confirmed the diagnosis. The dengue NS1 antigen came back positive, malaria parasites were absent, and ELISA-based serology ruled out other viral infections. His hemoglobin stood at 13 g/dL and his platelet count at 192,000 per microliter, well within the normal range, which would later prove to be one of the most instructive features of the case. His leukocyte count was initially elevated at 12,000 per microliter before settling to 4,600. More ominous was the coagulation picture: while his standard coagulation profile was normal, his D-dimer, a breakdown product of cross-linked fibrin that serves as a molecular flag for active clot formation and dissolution, was dramatically elevated at 9,968 ng/mL, later declining to 4,068 ng/mL. Inflammatory markers told a similar story of a body under siege, with C-reactive protein at 142 mg/L against a normal threshold of 10, procalcitonin at 0.57 ng/mL, and an erythrocyte sedimentation rate of 54 mm/h.

The turning point came on the sixth day of hospitalization, roughly the ninth day of illness, when the patient developed sudden painful swelling of the right lower limb extending from calf to thigh, together with progressive shortness of breath on exertion. The limb was visibly swollen up to the groin, red, warm, and tender, with increased calf and thigh circumference, though peripheral pulses remained intact. He remained hemodynamically stable apart from mild tachycardia, with a blood pressure of 105/70 mmHg and an oxygen saturation of 93 percent on room air. Doppler ultrasonography confirmed deep vein thrombosis, and because his dyspnea worsened, the team proceeded to CT pulmonary angiography. The scan revealed bilateral pulmonary emboli and dilatation of the right cardiac chambers, a sign that the clots lodging in the pulmonary arteries were forcing the right side of the heart to pump against dangerous resistance.

Imaging then uncovered a further puzzle. A chest radiograph showed a cavitary lesion in the right lung with mild cardiomegaly, and high-resolution computed tomography revealed that cavity surrounded by pneumonic consolidation, minimal bilateral pleural effusions, and basal atelectatic changes. Cavitary lung lesions typically raise the specter of tuberculosis, lung abscess, fungal infection, or malignancy, each of which could independently predispose a patient to clotting. The team therefore cast a wide diagnostic net: sputum examination, acid-fast bacilli smears, and GeneXpert testing were negative for Mycobacterium tuberculosis, blood cultures grew no bacterial or fungal pathogens, and bronchoscopy with bronchoalveolar lavage found only mucopurulent secretions with no organisms on Gram stain, no growth on culture, and no malignant cells on cytology. Transthoracic echocardiography showed preserved left ventricular function with an ejection fraction of 64 percent, no intracardiac vegetations, and a positive McConnell sign, a regional pattern of right ventricular dysfunction considered suggestive of acute pulmonary embolism.

The authors argue that the most likely explanation for the cavity is pulmonary infarction, tissue death downstream of the embolic obstruction, which can occasionally cavitate when vascular blockage is severe. The temporal relationship between the dengue infection and the thrombotic event, combined with a negative thrombophilia workup and the patient’s young age, pointed toward a transient, infection-associated prothrombotic state rather than an inherited clotting disorder or occult cancer. The differential diagnosis nonetheless included septic pulmonary emboli, secondary bacterial pneumonia, and malignancy, and the authors note that unexplained or recurrent venous thromboembolism should always prompt consideration of hidden malignancy, citing a prior report in which deep vein thrombosis was the presenting feature of uterine leiomyosarcoma.

The mechanistic picture emerging from the dengue literature is one of coordinated disruption of hemostasis. The authors outline several converging pathways: molecular mimicry between viral antigens and coagulation factors generating cross-reactive autoantibodies; direct endothelial dysfunction driven in part by the dengue NS1 protein; infection-induced upregulation of tissue factor in monocytes and endothelial cells; and a cytokine storm that amplifies both inflammation and coagulation activation. Critically, this case demonstrates that clinically significant thrombosis can occur even when platelet counts remain normal. Previous analyses have documented venous thrombosis in dengue patients with median platelet counts as low as 52,000 per cubic millimeter, but this patient never developed thrombocytopenia during hospitalization, underscoring that the absence of low platelets offers no reassurance against the thrombotic complication.

The timing also fits an emerging pattern. In an analysis of 19 previously reported cases of spontaneous venous thrombosis in dengue cited by the authors, the median onset of thrombosis was six days after fever began, with serious thrombotic events generally clustering between days 5 and 10 of illness, the transition from the acute phase to recovery. Lower limb deep vein thrombosis was the dominant manifestation, accounting for 68 percent of cases, most often involving the right side and the external iliac, common femoral, and popliteal veins. This patient’s right lower limb clot extending from calf to thigh, with bilateral pulmonary embolism on top, represents an unusually severe expression of that same tendency. His markedly elevated C-reactive protein also aligned with evidence that more intense inflammatory responses accompany severe dengue, where mean CRP levels of roughly 50 mg/L have been recorded against about 22 mg/L in non-severe disease.

Treatment required navigating a genuine therapeutic dilemma: anticoagulating a dengue patient in whom bleeding is the classically feared complication. The team initiated weight-based therapeutic enoxaparin at 60 mg subcutaneously twice daily for the approximately 60-kg patient, alongside intravenous paracetamol, fluids, broad-spectrum antimicrobials with meropenem and linezolid given concern for secondary bacterial infection, and nebulized bronchodilators and corticosteroids for respiratory symptoms. In the published series, 57.8 percent of patients received low-molecular-weight heparin, anticoagulation was tolerated even amid thrombocytopenia, and all patients recovered without incident. Yet the literature still lacks formal guidelines for managing dengue-associated pulmonary embolism, and the authors emphasize that the decision to anticoagulate remains difficult in the face of bleeding risk. This patient improved steadily, was discharged on day thirteen with apixaban 10 mg twice daily tapering to 5 mg twice daily for a total of six months of anticoagulation, and at four-week follow-up his dyspnea and leg swelling had resolved, repeat Doppler ultrasound showed interval improvement, and chest CT showed partial resolution of the cavitary lesion.

The case carries two forward-looking warnings. First, because the patient demonstrated right ventricular dysfunction from bilateral pulmonary emboli, he faces a risk of chronic thromboembolic pulmonary hypertension, a disabling late complication that demands extended monitoring. Second, and more broadly, the authors urge clinicians caring for dengue patients to stay alert for thrombotic symptoms during the recovery phase, when vague complaints such as unilateral limb swelling or exertional breathlessness may be the only clues to a clot that imaging will confirm. Early recognition, timely diagnosis with tools such as D-dimer measurement, Doppler ultrasound, and CT angiography, and prompt anticoagulation can prevent life-threatening outcomes in a complication that remains poorly recognized but is, as this case shows, very much preventable.

Subject of Research: Venous thromboembolism as a complication of dengue fever

Article Title: Post‐Dengue Deep Vein Thrombosis Complicated by Pulmonary Embolism: A Case Report

Article References: Nisar, S., Mushtaq, H., Khan, M. H., Sajjad, F., Afridi, A., Fatima, N. E., & Kamil, K. A. (2026). Post‐Dengue Deep Vein Thrombosis Complicated by Pulmonary Embolism: A Case Report. Clinical Case Reports, 14(10), Article e73642. https://doi.org/10.1002/ccr3.73642

Image Credits: AI Generated

DOI: 10.1002/ccr3.73642

Keywords: dengue, deep vein thrombosis, pulmonary embolism, venous thromboembolism, hypercoagulability, D-dimer, anticoagulation, enoxaparin, apixaban, NS1 antigen, pulmonary infarction, case report

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