A 20 years old bisexual male presented after collapsing at the airport, where he worked. Bladder and bowel incontinence occurred during the episode, and confusion and lethargy followed. Several days prior to admission, he had experienced headache, subjective fever, chills, nausea and vomiting. Physical exam revealed temperature of 38.2o C, lethargy, no meningeal signs or focal neurologic deficit. Neither rash nor lymphadenopathy was present.
Initial laboratory studies demonstrated leukopenia with neutrophil predominance, bandemia of 20%, and thrombocytopenia. Lumbar Puncture, performed after the first dose of antibiotics, revealed WBC 15/ µL with 88% PMN; normal protein and glucose. Gram stain showed no organisms, and bacterial, fungal, and mycobacterial cultures were negative. The CSF was negative for bacterial antigens, cryptococcal antigen and VDRL. CSF polymerase chain reaction tests for herpes simplex virus, varicella zoster virus, JC virus, and West Nile virus were negative. Serum antibodies were also negative for CMV, EBV, HBV, West Nile Virus and arboviruses. Enzyme immunoassay test for HIV was negative.
During hospitalization, the patient spiked high fevers, with a maximun temperature of 39.4o C. Leukopenia worsened to a WBC nadir of 1.3 x 109 /L with associated neutropenia (absolute neutrophil count 650), and 34% bandemia. Brain MRI with gadolinium showed a focal signal abnormality with associated diffusion restriction within the posterior corpus callosum, compatible with a demyelinating process. EEG was normal. CD4 count was 218 cells/µL, and HIV RNA PCR was > 10,000,000 copies/ml.
Antiretroviral therapy with darunavir, emtricitabine — tenofovir, and ritonavir was started on the fourth hospital day. Concurrently, the patient’s fever resolved, thrombocytopenia improved, and leukocyte count rose to 2.1 x 10 9 per liter.
Acute HIV infection often eludes accurate diagnosis due to the nonspecific nature of the symptoms and signs. Data suggest that the severity of symptoms at the time of seroconversion correlates with mortality risk. Despite some controversy, most experts favor initiation of antiretroviral treatment at the time of acute infection. Treatment may ameliorate symptoms, improve the chance of immune reconstitution, and decrease the risk of transmission by drastically lowering the viral load. Risks of early treatment include the development of drug resistance mutations, and toxicities of treatment.
This case of acute HIV infection demonstrates several rare laboratory and clinical features—neutrophilic pleocytosis in the CSF, neutropenia, bandemia, a seizure as the presenting complaint, and a demyelinating lesion in the corpus callosum. The case highlights the need for hospitalists to entertain a broad differential diagnosis in confusing cases and illustrates the importance of testing specifically for acute HIV infection even when features are atypical.