No abstract

A 37-spined Egyptian echinostome, Echinostoma liei sp.nov., is described in adult and larval stages. The parasite develops readily in the laboratory in chicks and ducklings, hamsters and rats. Its natural final host in or near irrigation ditches of the Nile delta involves the roof rat, Egyptian giant shrew and aquatic bird hosts. Developmental forms are described from infection of the NIH strain of Biomphalaria glabrata in the laboratory. B. alexandrina, is infected in the normal habitat in Egypt and contains both developmental stages in the heart or aorta and the hepatopancreas, and metacercariae encyst in the pericardium and kidney. E. liei sp.nov. is one of six very similar species characterized by 37 collar spines with a pattern of (3 + 2) corner spines in each lappet, six laterals on each side, and 15 dorsals in alternating rows; two pairs of dorsoventral and one small pair of ventro-lateral finfolds on the cercarial tail; and rodlike cystogenous material filling the cercarial encystation glands. In addition to distinctive intermediate-host specificity, differentiating characteristics of E. liei cercariae include presence of six sets of three flame cells each per side (total 36), seven oesophageal cells, eight penetration gland outlets on the dorsal lip of the oral sucker, and an absence of paraoesophageal gland cells as determined by intravital dyes. Significance of these and other cercarial traits is emphasized to aid in defining highly similar, but none the less distinct, sibling species.

Echinostoma liei, a newly described 37-spined eehinostome from Egypt, was tested against two trematodes in paired infections in the snail host, Biomphalaria glabrata (NIH strain). E. liei, when matched with the highly predacious Brazilian echinostome Paryphostomum segregatum, was dominated by the latter's predatory rediae. Pre-existing E. liei infections were destroyed, although the P. segregatum infection was itself delayed in development by an unidentified ‘indirect antagonism’ elicited by the E. liei larvae. In concurrent exposures with the two species, or with E. liei challenge of an established P. segregatum infection, the E. liei miracidia penetrated the snail, but the infection did not become established. When E. liei and S. mansoni were paired, the former species dominated. Exposure of snails already infected with E. liei to miracidia of S. mansoni slowed growth of the latter and the schistosome sporocysts eventually disintegrated without producing cercariae. When E. liei miracidia were exposed to snails with S. mansoni infections of different ages, the echinostome became established but developed slowly. Subsequently, however, it destroyed the schistosome infection. Although E. liei is itself quickly eliminated by P. segregatum, the two species appear almost equal in anti-schistosome capacity. This can be credited in part to a deleterious or lethal effect of the E. liei-schistosome combination on the host snail, as well as to a direct anti-schistosomal effect. Greater knowledge of this host-inter-trematode balance may permit the use of trematodes to attack infected snails and their parasites in regions hyperendemic with human schistosomiasis.