Taenia solium Metacestode Factor as Probable Cause of Temporal Lobe Epilepsy

This article analyzes data from scientific publications (mainly reviews) concerning the link between human neurocysticercosis and epilepsy. Along with data from our own studies on experimental hippocampal sclerosis induced by a Taenia crassiceps metacestode factor in mice, it explores the connection between mechanisms that likely favor the development of epilepsy in cases of human neurocysticercosis. The data from both sources suggest the idea that the T. solium metacestode factor causes hippocampal sclerosis and later epilepsy in humans with neurocysticercosis.

Subcutaneous Taenia crassiceps Cysticercosis Mass Excision from an 11-Year-Old Mixed-Breed Dog

ABSTRACT An 11 yr old mixed-breed dog presented with a 2 × 3 cm semimovable subcutaneous soft-tissue mass overlying the right hip region that grew to 8 × 5 cm over a 6 mo period. Two separate fine needle aspiration cytology samples showed marked pyogranulomatous inflammation with no cytologically apparent infectious etiology or neoplasia. Computed tomography imaging revealed a well-marginated, heterogeneous, contrast-enhancing soft-tissue mass extending into the adjacent fat, suggestive of neoplasia. A 14G needle biopsy showed similar chronic inflammatory changes without evidence of neoplasia or infectious etiology. Excisional biopsy of the mass was performed, and ex vivo sectioning revealed Taenia crassiceps cysticerci. Histopathology confirmed severe chronic pyogranulomatous cellulitis and myositis with intralesional cysticerci. Anthelmintic treatment was administered postoperatively, and no evidence of local recurrence has been noted as of 6 mo after the operation. To our knowledge, this is the first case report describing the cytological, histological, cross-sectional imaging characteristics and treatment outcome of T crassiceps cysticercosis in a dog.

Hormones and Parasites, Their Role in Taenia solium and Taenia crassiceps Physiology and Development

The host’s hormonal environment determines the susceptibility, the course, and severity of several parasite infections. In most cases the infection disturbs the host environment, and activates immune responses that end up affecting the endocrine system. In the other hand, a number of reports indicate that parasites have reproductive systems, and some others have shown that these organisms synthetize sex steroid hormones. We have shown that cysticerci, the larval stage of Taenia solium and Taenia crassiceps ORF and WFU, synthesize steroid hormones. This capacity was modified by drugs that act inhibiting the steroid synthesizing enzymes, or blocking the parasite’s hormone receptors. We have also shown that the cysticerci of T. crassiceps WFU and T. solium have the capacity to synthesize corticosteroids as deoxicorticosterone and corticosterone. We also reviewed the effects of insulin on these parasites, and the receptors found for this hormone. A deep knowledge of the parasite’s endocrine properties will contribute to understand their reproduction and the reciprocal interactions with the host. Likewise, may also help designing tools to combat the infection in clinical situations.

Regulatory T Cells as an Escape Mechanism to the Immune Response in Taenia crassiceps Infection

Murine cysticercosis by Taenia crassiceps is a model for human neurocysticercosis. Genetic and/or immune differences may underlie the higher susceptibility to infection in BALB/cAnN with respect to C57BL/6 mice. T regulatory cells (Tregs) could mediate the escape of T. crassiceps from the host immunity. This study is aimed to investigate the role of Tregs in T. crassiceps establishment in susceptible and non-susceptible mouse strains. Treg and effector cells were quantified in lymphoid organs before infection and 5, 30, 90, and 130 days post-infection. The proliferative response post-infection was characterized in vitro. The expression of regulatory and inflammatory molecules was assessed on days 5 and 30 post-infection. Depletion assays were performed to assess Treg functionality. Significantly higher Treg percentages were observed in BALB/cAnN mice, while increased percentages of activated CD127+ cells were found in C57BL/6 mice. The proliferative response was suppressed in susceptible mice, and Treg proliferation occurred only in susceptible mice. Treg-mediated suppression mechanisms may include IL-10 and TGFβ secretion, granzyme- and perforin-mediated cytolysis, metabolic disruption, and cell-to-cell contact. Tregs are functional in BALB/cAnN mice. Therefore Tregs could be allowing parasite establishment and survival in susceptible mice but could play a homeostatic role in non-susceptible strains.

Taenia larvae possess distinct acetylcholinesterase profiles with implications for host cholinergic signalling

Larvae of the cestodes Taenia solium and Taenia crassiceps infect the central nervous system of humans. Taenia solium larvae in the brain cause neurocysticercosis, the leading cause of adult-acquired epilepsy worldwide. Relatively little is understood about how cestode-derived products modulate host neural and immune signalling. Acetylcholinesterases, a class of enzyme that breaks down acetylcholine, are produced by a host of parasitic worms to aid their survival in the host. Acetylcholine is an important signalling molecule in both the human nervous and immune systems, with powerful modulatory effects on the excitability of cortical networks. Therefore, it is important to establish whether cestode derived acetylcholinesterases may alter host neuronal cholinergic signalling. Here we make use of multiple techniques to profile acetylcholinesterase activity in different extracts of both Taenia crassiceps and Taenia solium larvae. We find that the larvae of both species contain substantial acetylcholinesterase activity. However, acetylcholinesterase activity is lower in Taenia solium as compared to Taenia crassiceps larvae. Further, whilst we observed acetylcholinesterase activity in all fractions of Taenia crassiceps larvae, including on the membrane surface and in the excreted/secreted extracts, we could not identify acetylcholinesterases on the membrane surface or in the excreted/secreted extracts of Taenia solium larvae. Bioinformatic analysis revealed conservation of the functional protein domains in the Taenia solium acetylcholinesterases, when compared to the homologous human sequence. Finally, using whole-cell patch clamp recordings in rat hippocampal brain slice cultures, we demonstrate that Taenia larval derived acetylcholinesterases can break down acetylcholine at a concentration which induces changes in neuronal signalling. Together, these findings highlight the possibility that Taenia larval acetylcholinesterases can interfere with cholinergic signalling in the host, potentially contributing to pathogenesis in neurocysticercosis.