Acquired immune deficiency syndrome (AIDS)-associated cholangiopathy is a biliary tract condition seen in AIDS patients who are severely immunosuppressed, contributing to significant mortality in this population, even in developed countries with access to highly active antiretroviral therapy (HAART).  We discuss a thirty-six-year-old human immunodeficiency virus (HIV)-positive male, non-compliant with HAART therapy, who presented with a one-year history of weight loss, persistent fatigue, and chronic diarrhea, which had worsened significantly in the past few weeks. Routine laboratory studies on presentation indicated elevated liver enzymes and alkaline phosphatase, a CD4 count of 2 cells/mm3, and a high HIV RNA count of 8.8 million. Imaging via CT of the abdomen and pelvis and ultrasound of the abdomen both displayed thickening and edema in the gallbladder without evidence of gallstones, raising concerns of acalculous cholecystitis. The patient subsequently decompensated, requiring intravenous vasopressors to maintain hemodynamic stability, broad-spectrum antibiotics, and resumption of antiretroviral therapy. Biliary fluid drainage was performed, and Cryptosporidium and cytomegalovirus (CMV) were detected via polymerase chain reaction (PCR) testing. The diagnosis of AIDS cholangiopathy was established; however, the patient\'s diarrhea worsened upon the introduction of tube feeds. Despite ongoing antimicrobial treatment, the patient developed a fever of 101.4°F, became asystolic and subsequently passed away. This case highlights the diagnostic, management, and therapeutic challenges of AIDS cholangiopathy. Also, it underscores the importance of thorough investigation into even mild or intermittent diarrhea and abnormal liver function tests in all HIV-infected patients, particularly in severely immunosuppressed patients. AIDS cholangiopathy should be considered in AIDS patients with diarrhea and abnormal liver function tests, irrespective of age, due to its associated morbidity across all age groups. Laboratory investigations often reveal markedly elevated alkaline phosphatase, gamma-glutamyltransferase, and mild to moderate liver enzyme elevations as hallmark findings of AIDS cholangiopathy. Ultrasonography is the first-line screening modality of AIDS cholangiopathy. Cryptosporidium parvum is the most common infectious etiology of AIDS cholangiopathy and can be identified by DNA-based polymerase chain reaction (PCR) testing of the stool or biliary fluid or acid-fast staining of stool specimens. Early detection of HIV infection and the prompt initiation and adherence to highly active antiretroviral therapy (HAART), which helps with maintaining a normal CD4 count and a low HIV viral load through HAART therapy, thereby significantly reducing the risk of developing AIDS cholangiopathy in HIV patients.

We present the case of a young male who was diagnosed with HIV in 2012. However, his initiation of antiretroviral therapy (ART) was delayed until 2018 due to issues related to his acceptance and acknowledgment of the disease. In April 2021, the patient presented with hemoptysis, shortness of breath, and constitutional symptoms. Initial extensive workup for tuberculosis (TB) and other respiratory pathogens returned negative. Despite this, he was treated for smear-negative pulmonary TB and pneumocystis pneumonia (PCP) and was subsequently discharged. He then had recurrent hospital admissions due to worsening respiratory symptoms, with short intervals between recovery and recurrence. Each admission saw an increase in his oxygen requirements. Throughout these hospitalizations, tests for coronavirus disease 2019 (COVID-19) were consistently negative. TB and PCP treatment continued throughout his admissions. Despite various treatments, his condition continued to deteriorate. A DNA polymerase chain reaction (DNA PCR) test for cytomegalovirus (CMV) was eventually conducted. Unfortunately, the patient succumbed to progressive respiratory failure, and the CMV DNA PCR returned positive a week after his death. In the era of COVID-19, this case underscores the importance of early diagnosis and timely antiviral treatment.

Tuberculosis (TB) is still one of the most challenging infectious diseases worldwide. Coinfection with HIV increases the likelihood of extrapulmonary involvement, including the tuberculosis of the central nervous system (CNS-TB). CNS-TB often presents as tuberculomas or tuberculous meningitis. Although tuberculomas can be single or multiple, asymptomatic carriage of numerous tuberculomas is seldom reported. We present a case of a 55-year-old man who carried at least 34 tuberculomas of different sizes asymptomatically before developing and succumbing to tuberculous meningitis. Furthermore, we highlight several possible public health challenges that might have complicated his clinical course, suggesting that future studies also focus on these variables alongside more traditional clinical issues.

Progressive multifocal leukoencephalopathy (PML) is a rare, demyelinating infectious disease of the central nervous system, primarily affecting immunosuppressed individuals, such as those with acquired immunodeficiency syndrome (AIDS) or undergoing immunosuppressive therapy. The causative agent is the dormant John Cunningham (JC) polyomavirus, which reactivates in immunocompromised patients. PML is diagnosed through clinical observations, imaging, and polymerase chain reaction (PCR) analysis, detecting JC virus deoxyribonucleic acid (DNA) in the cerebrospinal fluid (CSF). Here, we report a case of a 42-year-old male, recently diagnosed with human immunodeficiency virus (HIV), who presented with slurred speech, difficulty articulating, tingling in both feet, difficulty walking, and significant weight loss. Examination revealed absent reflexes, coordination impairment, and diminished vibration sense. Blood tests showed anemia, elevated D-dimer, and HIV-1 positivity with a low CD4 count. CSF analysis indicated a lymphocytic profile with elevated protein and marginally increased adenosine deaminase (ADA). Autoantibody testing was positive for antinuclear antibodies (ANA), but CSF culture and India ink staining were negative. Magnetic resonance imaging (MRI) of the brain revealed hyperintense lesions on T2-weighted and fluid-attenuated inversion recovery (FLAIR) images in the left peritrigonal and parietal white matter, suggesting demyelination. The diagnosis of PML was confirmed by a positive JC virus PCR result from the CSF. The patient was started on combination antiretroviral therapy (cART) and supportive measures to improve immune status. This case underscores the importance of considering PML in patients with new-onset neurological symptoms and immunosuppression.

Histoplasma capsulatum is a dimorphic fungus that grows in nature as a mold or in culture but converts to a small yeast during cellular invasion. While most histoplasmosis infections are primarily asymptomatic or mildly symptomatic, disseminated histoplasmosis is a relentlessly progressive granulomatous disease that can mimic other granulomatous diseases, such as tuberculosis, sarcoidosis or coccidioidomycosis, more so in the proper context of immunosuppression. The current global migrant crisis, particularly the United States migrant crisis conversation is mostly socio-political; however, it also has a public health implication as exemplified by the case of a 35-year-old male who migrated from Haiti via Chile and Mexico to the United States. He presented with a four-day history of fever, generalized body aches, and cough. This case underscores the importance of entertaining a myriad of differentials and avoiding the tendency for anchoring, especially when initial therapy yields little clinical response.

This case emphasizes the significance of recognizing and managing Brevibacterium species. Here, we present a unique case of Brevibacterium species isolated from the cerebrospinal fluid of a 60-year-old female with recently diagnosed human immunodeficiency virus (HIV) and small cell carcinoma of the lung. Management involved a two-week course of intravenous vancomycin. Brevibacterium species are infrequently encountered in clinical practice. Sharing this case report aims to enhance the limited understanding of Brevibacterium species infections and encourages discussion among healthcare professionals regarding its diagnosis and management.

Polyneuropathy, organomegaly, endocrinopathy, M-protein, and skin changes (POEMS) syndrome is a multisystem paraneoplastic disorder due to an underlying plasma cell neoplasm, and its occurrence among HIV patients is extremely rare. The diagnosis of POEMS syndrome can be challenging in this context, particularly if its disabling polyneuropathy is misdiagnosed as neuropathy related to HIV. Herein, we report the case of a female patient with treated HIV who later developed POEMS syndrome. After a misdiagnosis of chronic inflammatory demyelinating polyneuropathy related to HIV and unsuccessful corticosteroids and cyclophosphamide therapies, the correct diagnosis of POEMS syndrome was made. The patient achieved significant hematological and neurological improvement after six cycles of lenalidomide. Autologous stem cell transplantation was then scheduled to prevent eventual relapses.

The development of Hodgkin\'s lymphoma (HL) is a known complication in patients with human immunodeficiency virus (HIV) infection. Extranodal involvement, specifically primary bone marrow Hodgkin\'s lymphoma (PBMHL) is a rare manifestation that has been reported in HIV-positive patients and may represent a distinct entity from HIV-associated HL. We present a case of PBMHL presenting with hemophagocytic lymphohistiocytosis (HLH) in an HIV-positive patient. The 55-year-old male with HIV/AIDS presented with abdominal pain, diarrhea, and fever, leading to hospital admission. Despite initial treatment, he deteriorated, prompting re-admission and investigation revealing pancytopenia and elevated inflammatory markers, suggestive of HLH. Subsequent bone marrow biopsy unexpectedly revealed PBMHL. Treatment with HLH-directed therapy and the HLH-94 protocol resulted in significant clinical improvement. This case underscores the importance of recognizing atypical lymphoproliferative presentations in HIV/AIDS patients and the need for interdisciplinary collaboration in complex cases.

Pneumocystis jirovecii pneumonia (PCP) is a life-threatening condition found in immunocompromised individuals, especially in human immunodeficiency virus (HIV) positive patients. Here, we report a case of PCP in a presumably immunocompetent 25-year-old male patient who presented with a one-month history of chest pain, dyspnea, and a nonproductive cough with recent development of night sweats. The patient recently immigrated to the United States without any known medical or family history. A chest radiograph revealed moderate pneumothorax for which a chest tube was placed. A chest computed tomography (CT) scan revealed diffuse lung disease with multiple thin- and thick-walled cystic lesions on a background of diffuse ground-glass opacities. Based on these radiologic findings and subsequent positive HIV serology, there was a high suspicion of PCP. Bronchoalveolar lavage was performed, and PCR for Pneumocystis jirovecii was positive. Appropriate treatment was initiated, and the patient recovered well. Through this report, we aim to highlight the importance of recognizing the various clinical and radiologic findings of PCP even in patients with no overt risk factors. Prompt and targeted treatment could mitigate morbidity and mortality associated with this opportunistic pathogen.

It is known that there are several clinical forms that diseases can take when presented in patients living with HIV, especially those in the AIDS phase. Here, we present a case that demonstrates the peculiar capacity of diseases to assume the most varied forms, highlighting the limited research on neglected infectious parasitic diseases. This study aimed to underscore the ability of these diseases to mimic other pathologies, emphasizing the importance of infectious diseases as differential diagnoses in the most diverse clinical entities, as is the case of visceral leishmaniasis.