In an attempt to determine the mechanisms of resistance to schistosome infection operative in bulinid snails, an histological study was carried out on batches of a refractory strain of Bulinus truncatus and two highly susceptible strains of B. africanus killed at various intervals of time, ranging from 7 h to over 3 months, after exposure to infection with Schistosoma mattheei miracidia.
It was found that only a small fraction (less than 1%) of the miracidia penetrated B. truncatus, and that they penetrated only a few of the snails exposed. Much larger proportions (up to 26%) of the miracidia penetrated B. africanus and they penetrated nearly all the snails exposed.
In the susceptible B. africanus only miracidia which settled in the loose tissues of the head-foot proceeded to develop: those settling in dense tissue failed to develop and degenerated within about 2 days.
A strong infiltration reaction of amoebocytes rapidly destroyed the few miracidia that successfully penetrated B. truncatus. In contrast, B. africanus did not respond to the presence of miracidia in its tissues, nor to mother or to daughter sporocysts before the onset of cercarial shedding: it reacted only to cercariae.
It is concluded (a) that the combination of an effective surface barrier and an active defence mechanism due to amoebocytes were responsible for complete resistance to S. mattheei infection in B. truncatus (b) that successful establishment of S. mattheei infection in B. africanus depended on the failure of the snail to recognize the schistosome miracidia and sporocysts as foreign material.
I am indebted to Professor George S. Nelson for advice and encouragement in this work which was carried out at the London School of Hygiene and Tropical Medicine. I am most grateful to Dr R. J. Pitchford, Dr C. A. Wright and Dr F. Arfaa for providing material for schistosome and snail cultures and to the East African Community and the British Ministry of Overseas Development for financial support.