In agreement with the negative immunomodulatory role suggested for AgB on human neutrophils, when accidentally released hydatid fluid activates neutrophils, AgB could act as an interference antigen allowing the released protoscoleces to develop into secondary cysts [96]. strategies and, when the immune response falls short, it may be necessary for the host to enter a damage limitation state, accommodating infection in order to minimize pathology. Parasite immune evasion mechanisms themselves depend on a form of molecular dialogue between pathogen and host and, in turn, many parasites depend on host molecular signals for their development [1]. During cystic echinococcosis (CE) the host-parasite relationship is interactive and the outcome of infection depends on the balance achieved by the combination of the different variables involved with the host immunity and the avoidance strategies [2]. An understanding of the biological events occurring during infection is necessary to visualize the diverse immune stimuli to which the parasite subjects the host and to define diagnostic and therapeutic tools. We discuss in detail these topics in this review. 2. Epidemiology CE, a chronic endemic helminthic disease caused by infection with metacestodes (larval stage) of the tapeworm is worldwide, with only a few areas such as Iceland, Ireland, and Greenland believed to be free of autochthonous human CE [6]. CE is prevalent in countries of the temperate zones, including South America, the entire Mediterranean region, Russia, central Asia, China, Australia, and parts of Africa [3, 7C9]. In KL-1 the USA, most infections are diagnosed in immigrants from countries in which echinococcosis disease is endemic. Sporadic autochthonous transmission is currently recognized in Alaska, California, Utah, Arizona, and New Mexico [10]. comprises a number of forms that exhibit considerable genetic variation [11]. Ten strains of (G1C10) have been described with molecular biology techniques using mitochondrial DNA sequences [12]. These include the common sheep strain (G1), a Tasmanian sheep strain (G2), two bovine strains (G3 and G5), a horse strain (G4), a camel strain (G6), a pig strain (G7), a cervid strain (G8), a Poland swine strain (G9) [12], and an Eurasian reindeer strain (G10). Recent molecular re-evaluation of species strongly suggests that is an oversimplified species. The Loviride genotypes G1 to G5 have been reclassified into (G1 to G3), (G4), and (G5). The genotypes G6 to G10 and the lion strain of (formerly Metacestodes 3.1. Biology The complex cycle of the parasite can explain the intricate host-parasite relationship. is a small tapeworm (rarely exceeding 7?mm in length) that lives firmly attached to the mucosa of the small intestine in definitive hosts, usually dogs, where the adult-stage reaches sexual maturity within 4 to 5 weeks. This is followed by Loviride the shedding of gravid proglottids (each Loviride containing several hundred eggs) and/or of released Loviride eggs in the feces of definitive hosts. After being ingested by the intermediate host, eggs release embryos (oncospheres) that penetrate the gut wall, travel via blood or lymph, and are trapped in the liver, lungs, and other sites where cystic development begins. This process involves transformation of the oncospheral stage to reach the metacestode stage. typically develops as a large unilocular, turgid cyst, which grows through an increase in diameter from less than 1 to 5?cm each year. This general structure can be thought to allow a permanent low ratio between total parasite cellular volume and host-exposed area, through linear growth that can exceed three orders of magnitude. Hydatid cyst is usually surrounded by a host-derived collagen capsule (adventitial layer), but can also been circled by host inflammatory cells. Metacestode (hydatid cyst) is bounded by the hydatid cyst wall, which comprises an inner cellular layer (germinal layer) and an outer Loviride protective acellular layer (laminated layer). The germinal layer (GL) gives rise towards the cyst cavity to cellular buds that upon vesiculation become brood capsules, and in turn bud towards their inside to.
In agreement with the negative immunomodulatory role suggested for AgB on human neutrophils, when accidentally released hydatid fluid activates neutrophils, AgB could act as an interference antigen allowing the released protoscoleces to develop into secondary cysts [96]
