Survival and Developmental Aberrations in Schistosoma mansoni following the Administration of Stilbestrol to the Hosts

Ej, Robinson

doi:10.1017/s0022149x0002037x

Cited by 6 publications

(2 citation statements)

References 7 publications

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“…Thus, Lewert & Mandlowitz (1963) suggested that steroid-induced changes in skin structure and metabolism, as well as direct effects of the drug on cercarial proteolytic enzymes, would impair parasite infection. Malnourishment (Knauft & Warren, 1969), hyperthyroidism (Abdel-Wahab, Warren & Levey, 1971), hypophysectomy (Knopf & Soliman, 1980) and injection of stilboestrol (Robinson, 1960) have all been shown to affect schistosome fecundity. The recent detection of ecdysteroids in S. mansoni worms, particularly in lung-stage schistosomula (Torpier, Him, Nirde, de Reggi & Capron, 1982), indicates that parasite growth could be under direct control of hormones, and therefore perhaps susceptible to disruption by administration of copious amounts of exogenous steroid.…”

Section: Discussionmentioning

confidence: 99%

Retarded development of Schistosoma mansoni in immunosuppressed mice

Harrison

Doenhoff

1983

Parasitology

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Previous observations, which showed that treatment of mice with hydrocortisone acetate around the time of their infection with Schistosoma mansoni reduced the mature worm burden, have been confirmed. The number of eggs produced by the surviving worms during early patency was also significantly reduced. Cyclophosphamide and another steroid immunosuppressant, betamethasone, also caused a reduction in fecundity of S. mansoni when given at the time of infection, as did T-cell deprivation of the mice by adult thymectomy and injection of anti-thymocyte serum 1 month before infection. There was no effect of these three treatments on worm numbers. In contrast, injection of mice with anti-thymocyte serum at the time of infection marginally increased the size of the mature worm burden. The deleterious effects of hydrocortisone acetate on S. mansoni worm numbers and fecundity were only apparent if the steroid was given within 1 week of infection. Indomethacin, a compound which inhibits tissue inflammatory reactions by inhibiting prostaglandin synthesis, and which therefore mimics one of the actions of corticosteroids, had no effect on S. mansoni worm maturation and fecundity.

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