1.A critical examination of the parasitological and clinical literature indicates that hyperinfection (internal autoinfection) is not only a necessary hypothesis, to explain the relatively frequent cases of human strongyloidiasis which have persisted for many years in the absence of external sources for reinfection, but is supported by substantial experimental, clinical and postmortem evidence.
2.The case reported in this communication provides additional evidence demonstrating a relatively heavy invasion of the deeper layers of the bowel wall and liver by filariform larvae derived from mother worms situated in the overlying mucosa. Except for a localized eosinophilic response around the migrating worms no cellular reaction was provoked by this invasion. This stands in marked contrast to the picture of leukocytosis with hypereosinophilia which characterizes the usual case of acute strongyloidiasis.
3.Self-infection in strongyloidiasis may result: (a) from the perianal invasion of filariform larvae; (b) from the invasion of the mucosa of the lower levels of the bowel by filariform larvae which have originated from sites of infection at higher levels; (c) from the penetration of filariform larvae into the deeper layers of the bowel at the same level where they were produced in the mucosa, or (d) from unmetamorphosed rhabditoid larvae massively penetrating through the muscularis mucosae into the deeper layers of the bowel wall.
4.Probably all persons harboring Strongyloides are potential subjects of self-infection.
5.Self-infection with Strongyloides stercoralis may be controlled, or at least measurably reduced, by heeding certain dicta of personal hygiene, by providing adequate nutrition and hematopoietic stimuli and by diagnosis and treatment of the infection.