Acanthamoeba castellanii encephalitis in a patient with AIDS: a case report and literature review.

Amoebic encephalitis is a rare cause of CNS infection for which mortality exceeds 90%. We present the case of a 27-year-old man with AIDS who presented to a hospital in Atlanta (Georgia, USA) with tonic-clonic seizures and headache. His clinical condition deteriorated over several days. Brain biopsy revealed lymphohistiocytic inflammation and necrosis with trophozoites and encysted forms of amoebae. Immunohistochemical and PCR testing confirmed Acanthamoeba castellanii encephalitis, typically described as granulomatous amoebic encephalitis (GAE). No proven therapy for GAE is available, although both surgical and multiagent antimicrobial treatment strategies are often used. Most recently, these include the antileishmanial agent miltefosine. Here we review all cases of GAE due to Acanthamoeba spp in people with HIV/AIDS identified in the literature and reported to the Centers for Disease Control and Prevention. We describe this case as a reminder to the clinician to consider protozoal infections, especially free-living amoeba, in the immunocompromised host with a CNS infection refractory to traditional antimicrobial therapy.

Development of fatal acute liver failure in HIV-HBV coinfected patients.

Coinfection with hepatitis B virus (HBV) is not uncommon in human immunodeficiency virus (HIV)-infected individuals and patients with HIV-HBV coinfection are at high risk for progression of liver disease. Current guidelines regarding the treatment of HIV infection recommend that patients who are coinfected with HIV and HBV receive highly active antiretroviral therapy (HAART) with activity against hepatitis B. While HIV-HBV coinfected patients often experience liver enzyme elevations after starting antiretroviral therapy, acute liver failure (ALF) is rare and typically occurs with older antiretroviral agents with known potential for hepatotoxicity. We describe two cases of fatal ALF in the setting of HIV-HBV coinfection after initiation of HAART. These cases occurred despite treatment with antiretrovirals that have activity against HBV and highlight the challenges in distinguishing drug hepatotoxicity and HBV immune reconstitution inflammatory syndrome. HIV-HBV coinfected patients should be monitored closely when initiating HAART, even when treatment includes agents that have activity against HBV.

Human immunodeficiency virus-associated cytomegalovirus infection with multiple small vessel cerebral infarcts in the setting of early immune reconstitution.

Cytomegalovirus (CMV) infection is an important cause of neurologic disease in the context of advanced human immunodeficiency virus (HIV) infection and is recognized as a cause of immune reconstitution inflammatory syndrome (IRIS) after initiation of highly active antiretroviral therapy (HAART). Central nervous system vasculitis secondary to CMV has only rarely been described in the context of HIV, despite the established ability of CMV to infect microvascular endothelial cells in the brain. However, we report a case that demonstrates the association between CMV and multiple small vessel cerebral infarct lesions after initiation of HAART.

The menstrual cycle does not affect human immunodeficiency virus type 1 levels in vaginal secretions.

To determine whether the menstrual cycle affects human immunodeficiency virus (HIV) type 1 levels in vaginal secretions, vaginal lavage samples were collected at 7, 14, and 21 days after initiation of menses, to compare virus levels during the follicular, ovulatory, and luteal phases. During 33 menstrual cycles in 25 women, HIV-1 RNA levels in vaginal secretions ranged from <1000 to 5.3x10(7) copies per lavage, and weekly changes ranged from <0.5 to 2.5 log(10) copies per lavage. HIV-1 RNA levels in vaginal lavage samples from days 7, 14, and 21 were not significantly different. No discernible pattern was found in changes of vaginal virus loads (VVLs) during the menstrual cycle. VVLs were not correlated with plasma estradiol or progesterone levels (P>.05). These results suggest that hormonal changes during the menstrual cycle do not have a significant effect on HIV-1 RNA levels in vaginal secretions.