Echinococcosis

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 other carnivorous animals which represent the definitive hosts and involves as intermediate hosts both domestic and wild animals. Humans become accidental intermediate hosts by ingesting Taenia eggs. The main species pathogenic for man are E granulosus causing cystic echinococcosis with worldwide distribution and endemic in sheep and cattle breeding countries, and E multilocularis causing alveolar echinococcosis, with preferential 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 nervous system (CNS) may be primary or secondary and has been estimated to be low (2%). Sharply demarcated, spherical and intraparenchymal, cysts 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 foreign giant cell reaction may develop. E multilocularis develops within the liver as a rapid invasive pseudomalignant growth and may metastasize to the CNS, where estimated incidence reaches 5%. Hydatid antigens induce an immune reaction in the host which is helpful for the diagnosis. DNA probes and PCR may be applied to differentiate between Echinococcus spp. Although the host develops an immunological protection from 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 antigens leads to increased specific IgG4 production, which might act as blocking antibodies against anaphlaxis suggestive of host response immunomodulation.

Pulmonary echinococcosis

“…The membranes and host capsule contribute to protecting the parasite from immune destruction [7]. Parasite-derived anticomplement factor may dampen host immune response [1].…”

Stage-Specific Expression and Targeting of Cyst Wall Protein–Green Fluorescent Protein Chimeras inGiardia

“…Encysting Giardia trophozoites undergo a series of developmental changes in the course of which they synthesize, export, and assemble an extensive fibrillar extracellular matrix composed of proteins but also a large proportion of carbohydrate, mainly in the form of N-acetylgalactosamine (Manning et al, 1992). Formation of environmentally resistant cysts is a key step in Giardia development as in other eukaryotic pathogens (Eichinger, 1997;Taratuto and Venturiello, 1997;Dubey et al, 1998) that has not been well characterized on a molecular level. Therefore, a better understanding of the mechanisms that govern stage-specific regulation of genes and the synthesis, transport, and assembly of the cyst wall is needed.…”

Cardiac Involvement with Parasitic Infections

“…Both humoral and cellular immune responses to the presence of the oncospheres and metacestodes develop. The parasite evades the host immune response by using a number of mechanisms, including the cyst-laminated cuticle as a barrier to host cells, polyclonal activation of lymphocytes by parasite soluble antigens, and depression of host cell immune responses (315). For instance, chronic stimulation of the host by cyst fluid antigens leads to increased levels of specific IgG4 production, which is suggestive of host response immunomodulation (315).…”

“…The parasite evades the host immune response by using a number of mechanisms, including the cyst-laminated cuticle as a barrier to host cells, polyclonal activation of lymphocytes by parasite soluble antigens, and depression of host cell immune responses (315). For instance, chronic stimulation of the host by cyst fluid antigens leads to increased levels of specific IgG4 production, which is suggestive of host response immunomodulation (315). Th1 cell activation appears critical for protective immunity, while a Th2 response is correlated with progressive disease (276).…”