Abstract
3/2013
vol. 51
Original article
Complex immune-mediated mechanisms of vasculitis in cerebral toxoplasmosis in AIDS patients
Folia Neuropathol 2014; 52 (1): 86-91
Online publish date: 2014/04/01
The increasing population of patients treated with immunosuppressive and immunomodulatory drugs, as well as growing resistance to anti-retroviral therapy, has caused the reemergence of cerebral toxoplasmosis as a clinical problem. Encephalitis caused by Toxoplasma gondii (Tg) is the most common opportunistic infection in patients with acquired immunodeficiency syndrome (AIDS). The scarcity of data concerning vessel involvement in cerebral toxoplasmosis in AIDS impelled us to examine this process.
In 15 of 178 cases with AIDS cerebral toxoplasmosis was the only opportunistic infection. In these patients routine histological stains and immunohistochemical reactions against T and B lymphocytes, immunoglobulins IgG and IgM, and factors C4 and B, involved respectively in classical and alternative pathways of complement activation, were performed. Apart from morphological changes typical for cerebral toxoplasmosis, eosinophilic necrosis of the vascular media, and vascular inflammatory infiltrates containing T and B lymphocytes were seen. In some arterial vessels intramural deposits of immunoglobulin IgG and IgM, and complement factors C4 and B were found.
Presence of polyarteritis nodosa-like changes, deposits of immunoglobulins and complement factors in the vessel wall, as well as inflammatory infiltrates containing B lymphocytes indicate that vasculitis in cerebral toxoplasmosis in AIDS has a very complex pathomechanism involving not only cell-mediated but also humoral-mediated immunological reactions.
In 15 of 178 cases with AIDS cerebral toxoplasmosis was the only opportunistic infection. In these patients routine histological stains and immunohistochemical reactions against T and B lymphocytes, immunoglobulins IgG and IgM, and factors C4 and B, involved respectively in classical and alternative pathways of complement activation, were performed. Apart from morphological changes typical for cerebral toxoplasmosis, eosinophilic necrosis of the vascular media, and vascular inflammatory infiltrates containing T and B lymphocytes were seen. In some arterial vessels intramural deposits of immunoglobulin IgG and IgM, and complement factors C4 and B were found.
Presence of polyarteritis nodosa-like changes, deposits of immunoglobulins and complement factors in the vessel wall, as well as inflammatory infiltrates containing B lymphocytes indicate that vasculitis in cerebral toxoplasmosis in AIDS has a very complex pathomechanism involving not only cell-mediated but also humoral-mediated immunological reactions.
Keywords
AIDS, complement, HIV, toxoplasmosis, vasculitis
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