Disseminated histoplasmosis and tuberculosis: dual infection in a non-endemic region.

Histoplasmosis is a systemic fungal infection caused by Histoplasma capsulatum, a dimorphic fungus that spreads commonly by contamination of soil with bird and bat droppings. The infection remains latent in most patients until manifested by reduced immune status, for example, HIV/AIDS, corticosteroid/immunosuppressive therapy or in solid organ transplant recipients. Tuberculosis and histoplasmosis may cooccur rarely in HIV and the clinical resemblance of both diseases may hinder identification of patients' harbouring dual infection, especially in regions non-endemic for histoplasmosis. We report a case of disseminated histoplasmosis with disseminated tuberculosis in an incidentally detected patient with HIV-positive who presented with reports of fever and skin rash for 10 days. The Mantoux positivity and CT of chest and abdomen revealing multiple necrotic lymph nodes coupled with bone marrow and skin biopsy divulging histoplasmosis and tuberculosis helped us clinch the concurrent infection.

Acute paraparesis in HIV-infected patient after initiation of highly active antiretroviral therapy.

Neurological syndromes occur in around 40-70% of HIV-infected people. Direct central nervous system involvement by the virus usually manifests as HIV encephalitis, HIV leucoencephalopathy, vacuolar leucoencephalopathy or vacuolar myelopathy. Indirect involvement is usually associated with neurotropic opportunistic infections which include tuberculosis, toxoplasmosis, cryptococcosis and viral encephalitis such as herpes simplex, varicella-zoster, cytomegalovirus and Human polyomavirus 2. We report a case of transverse myelitis in a recently diagnosed HIV patient who was otherwise asymptomatic initially and developed paraparesis after 1 month of initiation of antiretroviral therapy. After ruling out opportunistic infections and other causes of compressive and non-compressive myelopathy, development of transverse myelitis was attributed to immune reconstitution inflammatory syndrome in view of baseline low CD4 count and their improvement after HAART initiation. Prompt treatment with corticosteroids successfully reversed the symptoms.