Intestinal dysbiosis is common in people living with HIV/AIDS (PLWH), yet fungal communities of the gut microbiota (mycobiota) remain poorly characterized, especially in severely immunosuppressed patients. We analyzed the gut mycobiota of 33 PLWH and 20 healthy controls from a public hospital in central Argentina. Most PLWH presented with severe immunosuppression (<200 CD4[+] T cells/μL) and acute or chronic diarrhea, with or without antibiotic exposure or antiretroviral therapy. Fecal DNA was extracted and the ITS2 region was sequenced using next-generation sequencing. Beta-diversity analyses revealed significant segregation between PLWH and controls (PERMANOVA, Adonis: p = 0.001, R[2] = 0.0989). LEfSe analysis identified 17 fungal species enriched in PLWH, predominantly Candida albicans, Candida dubliniensis, and Nakaseomyces glabratus, whereas 31 species were differentially represented in controls, including Penicillium spp., Candida sake, and Clavispora lusitaniae. Histoplasma capsulatum, an endemic pathogen in the region, was more prevalent in PLWH and associated with low CD4[+] T cell counts. Dirichlet multinomial mixture analysis revealed two mycobiotypes: M1, with a balanced fungal composition predominating in controls, and M2, dominated by Candida species and present in PLWH. These findings provide novel insights into gut mycobiota alterations in severely immunosuppressed PLWH in Argentina, highlighting Candida-driven dysbiosis and the regional relevance of H. capsulatum.

Opportunistic infections are common in patients with acquired immunodeficiency syndrome (AIDS) or advanced human immunodeficiency virus infection when adherence to anti-retroviral is poor. We present a case report of multiple opportunistic infections simultaneously present in a patient with AIDS who presented with fevers, abdominal pain, and diarrhea. He was ultimately diagnosed with Streptococcus pneumoniae pneumonia, oral thrush, esophageal histoplasmosis, cytomegalovirus esophagitis and herpes simplex esophagitis. This case is a reminder of the severity of illness in AIDS and the need for thorough workups to address all disease processes.

Hemophagocytic lymphohistiocytosis (HLH) is a severe hyperinflammatory syndrome caused by unregulated immune activation, leading to a "cytokine storm" and multisystem failure. In people living with HIV (PLWH), it is frequently triggered by opportunistic infections like Mycobacterium tuberculosis. This report describes a 28-year-old transgender woman with HIV (on ART, undetectable viral load) admitted with a 20-day history of high fever, diarrhea, and hepatosplenomegaly. Admission labs showed severe pancytopenia (Hb 6.2 g/dL, WBC 1,590/µL, platelets 102,000/µL) and a CD4 count of 164 cells/mm[3]. Investigation revealed extreme hyperferritinemia (peaking at 18,366 ng/mL) and a positive urinary lateral flow urine lipoarabinomannan assay (LF-LAM) test, indicating extrapulmonary tuberculosis (TB). Abdominal CT showed mesenteric and para-aortic lymphadenopathy. Bone marrow biopsy confirmed HLH through frequent hemophagocytosis figures. Despite immediate initiation of antituberculosis therapy (ATT) combined with intravenous immunoglobulin, methylprednisolone pulse, and cyclosporine, the patient developed acute kidney injury and severe hepatitis, progressing to refractory shock and death on the 37th day. This case highlights the diagnostic challenge of HLH due to clinical overlap with sepsis. The LF-LAM test was crucial for rapid TB identification. Although integrated immunomodulation and ATT are recommended, the prognosis remains poor in advanced immunosuppression. High clinical suspicion is vital for early intervention in HIV-positive patients with fever and cytopenias in TB-endemic regions.

We present the case of a 28-year-old male with diarrhea, headache, and significant weight loss. He was diagnosed with HIV in the AIDS stage (CD4: 3 cells/μL), Cryptococcus neoformans meningoencephalitis, and multisystemic tuberculosis. Given the persistence of diarrhea and negative coproparasitological studies, endoscopic studies were performed. Upper digestive endoscopy incidentally showed esophageal erosions coated with fibrin and punched-out ulcers; these findings were identified as herpetic esophagitis by histopathological and immunohistochemical analysis. Treatment with intravenous acyclovir was initiated, followed by oral administration for 14 days. This case highlights the importance of considering herpetic esophagitis in immunosuppressed patients, even in the absence of esophageal symptoms, and emphasizes the value of upper digestive endoscopy with biopsy in the comprehensive diagnosis of HIV/AIDS.

Histoplasmosis is a potentially life-threatening opportunistic fungal infection in patients with advanced human immunodeficiency virus (HIV), particularly in endemic regions such as the Ohio and Mississippi River valleys. Despite advances in antiretroviral therapy, delayed diagnosis, lack of linkage to care, and treatment nonadherence continue to contribute to severe opportunistic infections in individuals with untreated HIV. We present the case of a 43-year-old woman with a 23-year-long history of untreated HIV infection who presented with fever, weight loss, diarrhea, and malaise. Laboratory evaluation revealed a viral load of 327,000 copies/mL and severe immunosuppression with a Cluster of Differentiation (CD4) count of 8 cells/µL, hyponatremia, and elevated liver transaminases. Computed tomography imaging demonstrated extensive mesenteric and retroperitoneal lymphadenopathy. Biopsy of a retroperitoneal lymph node revealed granulomas containing fungal organisms consistent with disseminated histoplasmosis. The patient was initially treated with empiric broad-spectrum antibiotics and intravenous amphotericin B, followed by long-term itraconazole therapy and initiation of antiretroviral treatment, resulting in clinical and immunologic improvement. This case highlights the direct relationship between prolonged untreated HIV infection, advanced immunosuppression, and disseminated histoplasmosis, while underscoring the impact of stigma and barriers to care on delayed diagnosis and disease severity. Early HIV diagnosis, timely linkage to care, and sustained patient engagement remain essential to preventing severe opportunistic infections.

Immune reconstitution inflammatory syndrome (IRIS) is an uncoordinated hyperinflammatory response to latent or de novo active infection in immunocompromised individuals following immune recovery. More specifically, paradoxical IRIS refers to the deterioration of a pre-existing infection, whereas unmasking IRIS can be thought of as the unveiling of a previously undiagnosed infection as immune function reconstitutes. HIV-positive patients with advanced disease who are also coinfected with tuberculosis have a uniquely high risk for this complication once started on highly active antiretroviral therapy (HAART). We present a case of a 58-year-old HIV and tuberculosis (TB)-positive woman from Northern Tanzania who presented to a rural care and treatment clinic (CTC) after a 17-month lapse from HAART. She had previously undergone curative treatment for tuberculosis three years prior, which was also the time of her initial HIV diagnosis and initiation of HAART. She arrived in the clinic cachectic, unwell, and with complaint of malaise and diarrhea. Blood analysis confirmed advanced HIV disease (AHD), and consequently, she was immediately restarted on HAART. Almost three weeks later, she returned to the clinic febrile, severely fatigued, and with grossly evident cervical lymphadenitis. Given her coinfection (HIV and TB positive) history, depleted CD4+ count, new onset of clinical findings, and temporal relationship of symptom appearance from HAART reinitiation, a diagnosis of paradoxical TB-IRIS presenting as TB lymphadenitis was made.