Identification and characterization of immune complexes in the cerebrospinal fluid of patients with spinal cord schistosomiasis.

The pathogenesis of neuroschistosomiasis is largely unknown. Available evidence suggests that it depends on the presence of parasite eggs in the nervous tissue and on the host's immune response. We investigated the presence of immune complexes (ICs) in the cerebrospinal fluid (CSF) of four patients with spinal cord schistosomiasis (SCS), and performed their characterization. ICs containing soluble egg antigen of Schistosoma mansoni (SEA) were found in the CSF of all the SCS patients. To our knowledge, this is the first evidence of ICs containing schistosomal antigens in the CSF of patients with SCS. Further studies are necessary to confirm our findings and investigate the possible roles of ICs in the pathogenesis of this disease.

Detection of Toxoplasma gondii soluble antigen, SAG-1(p30), antibody and immune complex in the cerebrospinal fluid of HIV positive or negative individuals

Active infection by T. gondii was evaluated by immunoassay for soluble SAG-1 (p30), the major surface antigen from T. gondii, specific antibodies and immune complexes in human cerebrospinal fluid (CSF) samples. A total of 263 samples of CSF were collected from hospitalized patients presenting neurological disorders and analyzed for antibodies to HIV. Patients were divided into two groups: HIV positive (n = 96) or HIV negative (n =167). The results of the assays showed that 45 of all samples were positive for soluble SAG-1. Toxoplasma Ag/Ab immune complexes were detected in 19 of the CSF samples and 62 were positive for T. gondii- specific IgG. A combination of these assays in the presence of clinical findings consistent with active Toxoplasma infection may predict the presence of toxoplasmic encephalitis. Moreover, detection of soluble SAG-1 in the CSF of these individuals appears consistent with active infection.

Detection of Toxoplasma gondii soluble antigen, SAG-1(p30), antibody and immune complex in the cerebrospinal fluid of HIV positive or negative individuals.

Active infection by T. gondii was evaluated by immunoassay for soluble SAG-1 (p30), the major surface antigen from T. gondii, specific antibodies and immune complexes in human cerebrospinal fluid (CSF) samples. A total of 263 samples of CSF were collected from hospitalized patients presenting neurological disorders and analyzed for antibodies to HIV. Patients were divided into two groups: HIV positive (n = 96) or HIV negative (n =167). The results of the assays showed that 45% of all samples were positive for soluble SAG-1. Toxoplasma Ag/Ab immune complexes were detected in 19% of the CSF samples and 62% were positive for T. gondii- specific IgG. A combination of these assays in the presence of clinical findings consistent with active Toxoplasma infection may predict the presence of toxoplasmic encephalitis. Moreover, detection of soluble SAG-1 in the CSF of these individuals appears consistent with active infection.

Humoral immune response in patients with cerebral parenchymal cysticercosis treated with praziquantel.

The humoral immune response to treatment with praziquantel (PZQ) was studied in eight patients with parenchymal cerebral cysticercosis (CC). In the serum and in the cerebrospinal fluid (CSF) before, during and after the administration of the drug, the following were quantitated (a) levels of specific anticysticercous antibodies measured in optical densities by the ELISA method; (b) levels of IgG, IgM, IgA and IgE; (c) levels of complement fraction C3, C4; (d) presence of immune complexes; (e) total number of white blood cells in the CSF. It was found that after treatment with PZQ, the level of specific anticysticercous antibodies and the level of IgG rose significantly in the CSF but not in the blood. The levels of the fractions of the complement and the immunoglobulins IgM, IgA and IgE did not change significantly either in the serum or in the CSF. The blood-brain barrier was found ruptured in three patients before therapy and in five patients after the therapy as measured by the albumin index. Nevertheless, the IgG index showed that there was local production of IgG in five patients before treatment and in seven after the end of it. The relative specific antibody index was greater than 1.0 in five patients before therapy and in seven after therapy. This data strongly supports the idea that the specific antibodies are produced intrathecally and are not derived from the serum pool through a ruptured blood-brain barrier. It was concluded that patients with parenchymal CC have an elevation of specific anticysticercous probably due to a combination of a ruptured blood-brain barrier and intrathecal synthesis. The relatively small rupture of the blood-brain barrier and the high IgG and relative specific antibody index suggest that intrathecal synthesis is the most important mechanism. The humoral immune response may be of importance not only in the elimination of the parasite but also in the genesis of the illness.