ECHINOCOCCOSIS

Citation
Al. Taratuto et Sm. Venturiello, ECHINOCOCCOSIS, Brain pathology, 7(1), 1997, pp. 673-679
Citations number
56
Categorie Soggetti
Pathology,Neurosciences,"Clinical Neurology
Journal title
ISSN journal
10156305
Volume
7
Issue
1
Year of publication
1997
Pages
673 - 679
Database
ISI
SICI code
1015-6305(1997)7:1<673:E>2.0.ZU;2-6
Abstract
Echinococcosis is a human disease caused by the larval form of Taenia echinococcus, which lives in the gut of the dog, wild canides and othe r carnivorous animals which represent the definitive hosts and involve s as intermediate hosts both domestic and wild animals. Humans become accidental intermediate hosts by ingesting Taenia eggs. The main speci es pathogenic for man are E granulosus causing cystic echinococcosis w ith worldwide distribution and endemic in sheep and cattle breeding co untries, and E multilocularis causing alveolar echinococcosis, with pr eferential distribution in the northern hemisphere. After ingestion of contaminated food, hexacanth embryos migrate by the portal system to liver and later lung, brain and other tissues. Symptoms are related to both cyst location and size. E granulosus infection of the central ne rvous system (CNS) may be primary or secondary and has been estimated to be low (2%). Sharply demarcated, spherical and intraparenchymal, cy sts may reach a large size causing neurological symptoms. Spilling of cyst fluid due to trauma or surgery may trigger anaphylaxis as well as disseminated infection. Host reaction is minimal in the brain but a f oreign giant cell reaction may develop. E multilocularis develops with in the liver as a rapid invasive pseudomalignant growth and may metast asize to the CNS, where estimated incidence reaches 5%. Hydatid antige ns induce an immune reaction in the host which is helpful for the diag nosis. DNA probes and PCR may be applied to differentiate between Echi nococcus spp. Although the host develops an immunological protection f rom reinfection, the parasite evades host immune attack. A wide range of evasion mechanisms have been advanced, including a barrier for host cells due to hydatid cyst laminated cuticle, polyclonal activation of lymphocytes by parasite soluble antigens, and depression of host cell immune responses. Chronic stimulation of the host by cyst fluid antig ens leads to increased specific IgG4 production, which might act as bl ocking antibodies against anaphlaxis suggestive of host response immun omodulation.