In their retrospective study of 25 cases of cerebral sparganosis, Song et al. found that 12 patients (48%) had eaten raw or uncooked frog or snake that was infected with sparganum, 5 patients (20%) had applied an animals flesh as a poultice to an open wound, 4 patients had drunk contaminated water, and the cause of infection was not known for 4 patients. As a result of these findings, Song et al. conclude that health education about sparganosis and the importance of food sanitation should be implemented in all rural endemic areas. It has been recommended that water consumed in endemic areas should be boiled or treated to prevent ingestion of Cyclops or Spirometra larvae. Especially in areas where ponds or ditches provide potential habitats for infected copepods, public health strategies should include education campaigns about how to identify drinking water that could potentially be infected. Strategies should warn people against ingesting the raw flesh of the intermediate hosts, such as snakes and frogs, and against using them as poultices. Management
One treatment for sparganosis is praziquantel, administered at a dose of 120 to 150 mg/kg body weight over 2 days; however, praziquantel has had limited success. In general, infestation by one or a few sparganum larvae is often best treated by surgical removal.DNA analysis of rare worms removed surgically can provide genome information to identify and characterise each parasite; treatments for the more common tapeworms can be cross-checked to see whether they are also likely to be effective against the species in question.
Anthrax components: protective antigen (PA), edema factor (EF), and lethal factor (LF). PA plus LF produces lethal toxin, and PA plus EF produces edema toxin. These toxins cause death and tissue swelling (edema), respectively. To enter the cells, the edema and lethal factors use another protein produced by B. anthracis called protective antigen, which binds to two surface receptors on the host cell. A cell protease then cleaves PA into two fragments: PA20 and PA63. PA20 dissociates into the extracellular medium, playing no further role in the toxic cycle. PA63 then oligomerizes with six other PA63 fragments forming a heptameric ring-shaped structure named a prepore. Once in this shape, the complex can competitively bind up to three EFs or LFs, forming a resistant complex. Receptor-mediated endocytosis occurs next, providing the newly formed toxic complex access to the interior of the host cell. The acidified environment within the endosome triggers the heptamer to release the LF and/or EF into the cytosol. It is unknown how exactly the complex results in the death of the cell. Edema factor is a calmodulin-dependent adenylate cyclase. Adenylate cyclase catalyzes the conversion of ATP into cyclic AMP (cAMP) and pyrophosphate. The complexation of adenylate cyclase with calmodulin removes calmodulin from stimulating calcium-triggered signaling, thus inhibiting the immune response. To be specific, LF inactivates neutrophils (a type of phagocytic cell) by the process just described so they cannot phagocytose bacteria. Throughout history, lethal factor was presumed to cause macrophages to make TNF-alpha and interleukin 1, beta (IL1B).