Abstract
Bird schistosomes, besides being responsible for bird schistosomiasis, are known as causative agents of cercarial dermatitis. Cercarial dermatitis develops after repeated contact with cercariae, mainly of the genus Trichobilharzia, and was described as a type I, immediate hypersensitivity response, followed by a late phase reaction. The immune response is Th2 polarized. Primary infection leads to an inflammatory reaction that is insufficient to eliminate the schistosomes and schistosomula may continue its migration through the body of avian as well as mammalian hosts. However, reinfections of experimental mice revealed an immune reaction leading to destruction of the majority of schistosomula in the skin. Infection with the nasal schistosome Trichobilharzia regenti probably represents a higher health risk than infections with visceral schistosomes. After the skin penetration by the cercariae, parasites migrate via the peripheral nerves, spinal cord to the brain, and terminate their life cycle in the nasal mucosa of waterfowl where they lay eggs. T. regenti can also get over skin barrier and migrate to CNS of experimental mice. During heavy infections, neuroinfections of both birds and mammals lead to the development of a cellular immune response and axonal damage in the vicinity of the schistosomulum. Such infections are manifest by neuromotor disorders.
Highlights
Despite their worldwide distribution, avian schistosomes were neglected by parasitologists who assumed that they have no or minor pathogenic impact on birds or mammals, including humans
Experimental infections of mice showed that T. regenti schistosomula can evade attack by immune cells in the skin of mammalian hosts allowing them to migrate further through the central nervous system (CNS) where immature worms die after several days [5, 6]
Cercarial dermatitis can occur after contact with water containing cercariae from snails infected by bird schistosomes
Summary
Avian schistosomes were neglected by parasitologists who assumed that they have no or minor pathogenic impact on birds or mammals, including humans. Many studies focus on these parasites since it has been recognized that they can be severe pathogens of birds Their larval stages (cercariae) frequently infect humans and cause cercarial dermatitis. The studies on mice infected experimentally with bird schistosomes showed that soon after the penetration, the cercariae transform to schistosomula Under certain circumstances, these schistosomula are able to resist host immune response, escape from the skin, and migrate further to target organs [2, 3]. Experimental infections of mice showed that T. regenti schistosomula can evade attack by immune cells in the skin of mammalian hosts allowing them to migrate further through the central nervous system (CNS) where immature worms die after several days [5, 6]. A major part of this review is dedicated to this species of schistosome
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