Trichobilharzia regenti
From Wikipedia, the free encyclopedia
| Trichobilharzia regenti | |
|---|---|
 | |
| Trichobilharzia regenti, cercaria | |
Scientific classification  | |
| Kingdom: | Animalia |
| Phylum: | Platyhelminthes |
| Class: | Trematoda |
| Order: | Diplostomida |
| Family: | Schistosomatidae |
| Genus: | Trichobilharzia |
| Species: | T. regenti |
| Binomial name | |
| Trichobilharzia regenti Horák, Kolářová & Dvořák, 1998 [1] | |
Trichobilharzia regenti is a neuropathogenic parasitic flatworm of birds which also causes cercarial dermatitis in humans.[2] The species was originally described in 1998 in the Czech Republic[1] and afterwards it was detected also in other European countries, e.g. Denmark,[3] Belgium,[4] Germany,[5] France,[6] Iceland,[7] Poland,[8][9] Switzerland,[10] or Russia,[11] and even in Iran.[12][13] For its unique neurotropic behaviour in vertebrate hosts, the host-parasite interactions are extensively studied in terms of molecular biology, biochemistry and immunology.[14][15][16]
The life cycle of T. regenti is analogous to that of human schistosomes. Adult flukes mate in a nasal mucosa of anatid birds (e.g. Anas platyrhynchos, Spatula clypeata or Cairina moschata) and produce eggs with miracidia which hatch directly in the host tissue and leak outside when the bird is drinking/feeding.[1] Once in water, the miracidia swim using their cilia and actively search for a proper molluscan intermediate host (Radix lagotis, Radix labiata, Radix peregra).[17] In the snail, the miracidia develop into a primary sporocyst in which secondary sporocysts are formed and give rise to cercariae later on.[18]
Cercariae, infective larvae, exit the snail and penetrate the skin of an avian host. After penetration of the host's skin, they shed the immunogenic surface glycocalyx[19] and transform to schistosomula (subadult stage, sg. schistosomulum). Schistosomula then look for peripheral nerves to use them to get to the spinal cord. Through it they continue their migration to the brain[20][21] and, finally, the nasal tissue in a bill. Here, they mature, copulate and lay eggs while causing pathology (inflammatory infiltration, haemorrhages).[22]
If mammals are infected by cercariae (instead of birds), the parasites die in the skin being entrapped by immune response.[23] The clinical manifestation of such infection is known as a neglected allergic disease called cercarial dermatitis (or swimmer's itch).[2][24] In mice, especially in immunodeficient ones, migration of the parasite to the spinal cord was observed.[25][26]
A complete life cycle of T. regenti can be maintained under laboratory conditions using Radix lagotis and the Domestic duck (Anas platyrhynchos f. domestica) as intermediate and definitive hosts, respectively.[1] Interestingly, domestic ducks can also serve as reservoir hosts in aquaculture sites, such as rice fields.[13] To study biology of T. regenti in mammals, C57BL/6, BALB/c a SCID mouse strains are used as accidental hosts.[26][27][28]
Migration in vertebrate hosts
When cercariae of T. regenti find either avian or mammalian host, they penetrate its skin. For this purpose, they are equipped with cysteine peptidases present in their excretory/secretory products, which are capable of keratin and collagen degradation.[29][30] Experiments with laboratory prepared recombinant form of the cysteine peptidase cathepsin B2 of T. regenti (TrCB2) confirmed its ability to cleave skin proteins (collagen, keratin and elastin).[31]
After penetration the skin, cercariae transform to schistosomula and start a migration through the host's body. They avoid penetration into blood capillaries and rather prefer entering peripheral nerves in host's limbs. Schistosomula are found in peripheral nerves of ducks and mice as soon as 1.5 and 1 day post infection (DPI), respectively.[21] In both types of hosts, schistosomula exhibit a high affinity to the central nervous system which they enter via spinal roots.[27] Based on recent observation by 3D imaging techniques (ultramicroscopy and micro-CT), schistosomula appear to migrate preferably through the white matter of the spinal cord in both birds and mammals.[28]
The next course of the infection differs in final and accidental hosts. In ducks, schistosomula are observed in synsacral segments of a spinal cord 3 DPI and 7–8 days later (10–11 DPI) they reach the brain. In their final localisation (the nasal tissue), they occur 13–14 DPI and laying eggs starts 15 DPI.[21][22] In mice, the first schistosomula are found in a lumbar spinal cord as early as 2 DPI and medulla oblongata is invaded the day after, but only in some individuals. Most of schistosomula stay localised in the thoracic and cervical spinal cord and only exceptionally migrate to the brain.[20][21] Neither the presence of worms has been detected in a nasal cavity nor has their maturation been noticed in the nervous tissue. Schistosomula development in mice is suppressed likely due to the host immune response and/or the presence/absence of some essential (nutritional, stimulatory) host factors.[26]
