No abstract

Summaryobjective To describe and compare the clinical impacts of neurocysticercosis (NC) caused by Taenia solium in humans and pigs.methods Comparative study of the brains of 16 asymptomatic pigs and 35 human NC cases (15 asymptomatic and 20 symptomatic).results In humans, cysticerci were more frequently located in the ventricles and subarachnoid space at the base of the brain (11.8% vs. 1.6%; P = 0.001 and 25.9% vs. 0%; P < 0.0001, respectively) while in pigs, cysticerci were more frequently found in the parenchyma (44.4% vs. 7.6%; P < 0.0001). In human brains, 75.9% of the cysticerci were calcified, while in pigs all cysticerci were in the vesicular stage.conclusion The duration of infection and the host-parasite relationship (such as immune reactivity and brain haemodynamics) differ between humans and pigs. This may account for the different distribution and stage of the cysticerci among humans and pigs.

Human neurocysticercosis (NC) is caused by Taenia solium larvae lodged in the central nervous system. This disease is usually diagnosed by radiology but the results are not always clear-cut and so immunological assays are often also used. A semi-nested PCR, based on the non-coding HDP2 sequence of T. saginata, has now been developed for detecting DNA from T. solium cysticerci and confirming NC. This PCR, which amplifies a 171-bp T. solium product, allowed the specific detection of just 174 attograms of T. solium DNA. The efficacy of the PCR was tested using cerebrospinal fluid (CSF) from neurological patients, including 46 confirmed Mexican cases of NC and 32 patients from non-endemic Spain. Eighteen of the confirmed cases [including 10 (71%) of the 14 with vesicular extraparenchymal cysticerci and four (17%) of the 24 with damaged cysticerci] and two (33%) of the six patients with 'uncertain' diagnosis (in whom a diagnosis of NC could not be established by radiological and immunological studies) were found PCR-positive. The 36 patients known to have neurological problems other than NC were found PCR-negative. The HDP2 PCR offers a new tool in the diagnosis of NC and in exploring the pathogenesis of this serious disease.

Neurocysticercosis, a clinically and radiologically pleomorphic parasitic disease, is still endemic to most non-developed countries of Latin America, Africa, and Asia. Anti-helminthic drugs (AHD) are generally effective and rapidly destroy parenchymal cysticerci. In contrast, several cycles of AHD are frequently necessary to damage extraparenchymally located parasites. The present study was designed to evaluate whether differences in the immunological profile of the patients is involved in the diversity of the response to AHD. To this end, a global gene expression microarray and a cytokine analysis were made. Responder patients were those showing a radiological reduction greater than 50 % in the parasite burden following AHD treatment. Microarray pre- and post-treatment comparisons showed that a total of eighteen immune-related genes were up-regulated in the five responder patients with respect the expression profile seen in the four non-responder subjects. The function of up-regulated genes exerted pro-inflammatory (RORγC, Sema4A, SLAMF3, SLAMF6), anti-inflammatory (TGFβ, TNFRSF25, TNFRS18, SLAMF1, ILF2), or immunomodulatory effects (CXCL2, RUNX3, SLAMF9, TGFBR3). To further explore the causes of the heterogeneity in the response to treatment, a wide ELISA cytokine analysis was performed in serum, PBMC supernatants, and CSF samples from 39 responder and 26 non-responder patients. Responder patients showed higher CSF IL-17A levels (P = 0.04) and higher supernatant IL-6 levels (P = 0.03) 60 days after treatment. These results suggest a possible influence of pro-inflammatory cytokines on the response to AHD as observed by radiological methods, and thus the possible participation of the host immunity in the effectiveness of AHD treatment.

Neurocysticercosis (NC) is caused by the establishment of Taenia solium cysticerci in the central nervous system. Previous studies have established that neuroinflammation plays a key role in the severity of the disease. However, the relationship between peripheral and local immune response remains inconclusive. This work studies the peripheral and local immune-inflammatory features and their relationships, toward the identification of potential peripheral immunologic features related to severity. A panel of cytokines was measured in paired cerebrospinal fluid (CSF) and in the supernatant of antigen-specific stimulated peripheral blood mononuclear cells samples (SN) in a total of 31 untreated inflammatory and non-inflammatory NC patients. Increased clinical and radiologic severity was associated with an increased cerebrospinal fluid cell count. A peripheral proliferative depression that negatively correlates with CSF cellularity and TNFα and that positively correlates with SN IL5 was observed in severe NC patients. These results provide evidences to support the systemic proliferative response as a biomarker to monitor the level of neuroinflammation, of possible value in the patients' follow-up during treatment.