Page 187 - AIDSBK23C

Page 187

There is acute onset of altered mental status with confusion, agitation, or decreased
consciousness along with fever and nonspecific constitutional symptoms. Meningeal signs are
usually absent. Lumbar puncture with CSF examination shows mild pleocytosis, with normal to
mildly elevated protein levels and normal to mildly low glucose levels. Organisms are unlikely
to be identified microscopically, and CSF culture for P marneffei is required for identification.
The course is typically rapid, with high mortality.[802]
Cysticercosis has been reported in HIV infected patients. Neurocysticercosis is the most
frequent helminthic infection of the central nervous system and is caused by Taenia solium
larvae. Giant cysts and racemose forms of neurocysticercosis seem to be much more frequent in
HIV-infected patients and may be secondary to an uncontrolled parasitic growth because of an
impaired cell-mediated immune response. Multiple masses are usually present.[803,804]
An infectious agent first called Mycoplasma incognitus, a strain of Mycoplasma
fermentans, has been identified in brain tissue of some AIDS patients with acute or subacute
encephalitis by use of immunohistochemical staining when no other opportunistic agent was
found. Inflammation and necrosis may or may not be present with M fermentans. This agent has
also been found in reticuloendothelial tissues and kidney.[531,805]
In the era of antiretroviral therapy (ART) with increasing long-term survival of persons
infected with HIV, an increase in beta amyloid deposition has been observed in the brains of
patients dying with AIDS. Distribution of increased beta-amyloid is seen primarily in the frontal
cortex, but also in hippocampus and basal ganglia regions. The beta-amyloid appears within
neuronal soma and axonal processes in most cases, and within vascular walls in a few cases.
Possible causes for this finding may include local intracerebral inflammatory responses to HIV
may with increased amyloid precursor protein (APP) production and susceptibility to amyloid
deposition, or ART therapy mediated by inhibition of insulin degradation enzyme.[806] In
addition, HIV Tat protein inhibits the major Aβ-degrading enzyme neprilysin, and the β
chemokine, CCL2/MCP-1, associated with HIV migration to the brain, also causes an increase in
Aβ.[807]