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, pl.


(skis'tō-sō'myū-lŭm, -lă),
The stage in the life cycle of a blood fluke of the genus Schistosoma immediately after penetration of the skin as a cercaria; marked by loss of the tail and gaining of physiologic modifications allowing it to survive in a mammalian bloodstream.
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n. pl. schistosomu·la (-lə)
The immature form of a parasitic schistosome after it has entered the blood vessels of its host.
The American Heritage® Medical Dictionary Copyright © 2007, 2004 by Houghton Mifflin Company. Published by Houghton Mifflin Company. All rights reserved.
References in periodicals archive ?
Horn et al., "RNA interference in Schistosoma mansoni schistosomula: selectivity, sensitivity and operation for larger-scale screening," PLOS Neglected Tropical Diseases, vol.
Holzgrabe, "Anti-schistosomal activity of cinnamic acid esters: Eugenyl and thymyl cinnamate induce cytoplasmic vacuoles and death in schistosomula of Schistosoma mansoni," Molecules, vol.
Nakano, "Schistosoma mansoni: in vitro schistosomicidal activity schistosomicidal activity and tegumental alterations induced by piplartine on schistosomula," Experimental Parasitology, vol.
Ingram et al., "In vitro synergistic interaction between amide piplartine and antimicrobial peptide dermaseptin against Schistosoma mansoni schistosomula and adult worms," Current Medicinal Chemistry, vol.
In the early phase of the disease, macrophages act as immune system effectors cells killing schistosomula and promoting tissue repair [24].
Group 1: Uninfected native control, Groups 2-6: S mansoni infected mice and classified as follow: Group 2: S mansoni-infected animals (positive control), Group 3: infected-N sativa treated group immediately at the time of infection (immature schistosomula < 14 days post infection).
The best result was obtained in groups 3 and 4 in wwhich sativa seeds are eitheradministered at the time of infection, G3 (in the presence of immature larvae, schistosomula) or ten days after infection, G4 (during schistosomula maturation).
Clinical signs in people correlate with the life cycle of the parasite and are associated with the parasitic form: cercariae (cercarial dermatitis), schistosomula (producing symptoms such as cough and fever), adult worm (rarely pathogenic), and eggs (causing Katayama fever and schistosomiasis).
On locating a human host skin, the cercariae burrow into it, migrate into the blood through the liver and lungs and undergo transformation into schistosomula also called young worms.
The schistosomula mature within 4-6 weeks inside the portal vein, mate, and migrate to their destination, which is either the perivesicular or mesenteric venous plexus, to start the cycle again (Fig.
Mice infected with 50 cercariae (BH strain) were intraperitoneally treated at a dose of 50 mg/kg for 5 consecutive days, starting on the 1st, 14th, 28th and 45th days after infection, to evaluate the effect of [beta]-lap on skin schistosomula, lung schistosomula, young worms (before oviposition) and adult worms (after oviposition), respectively.
Between one and four weeks after infection, the migrating and maturing schistosomula can cause a systemic hypersensitivity reaction with fever, general weakness, headache, nausea, vomiting, diarrhea, and dry cough [2, 9].