Secondary infections of Hymenolepis diminuta in mice: effects of varying worm burdens in primary and secondary infections

Abstract

In one (1c) and six (6c) cysticercoid primary infections of Hymenolepis diminuta in NIH (inbred) and CFLP (outbred) male mice 6±1 weeks old > 85% of the worms established but were rejected (destrobilated or expelled) subsequently. Rejection occurs more quickly in 6c infections than in 1c infections. Considerable worm growth occurs in 1c and 6c primary infections but worms from 6c infections weighed less than worms from 1c infections on all days studied.Expulsion of H. diminuta does not occur more rapidly in secondary infections than in primary infections; loss of 6c secondary worms occurs at the same rate as 6c primary worms but 1c secondary worms survive longer than 1c primary worms. Although worms are not lost more quickly in secondary than in primary infections, they are affected at an early age by the immune response which stunts their growth. Increasing the intensity of primary and secondary infections increases the severity of stunting of secondary worms.The results are discussed and it is suggested that immune responses to Hymenolepis spp. in rodents are common but that thresholds of worm numbers exist below which appreciable worm loss does not occur. Stunting due to crowding, which generally is attributed to inter-worm competition, may be in part immunologically mediated. For future immunological studies attempting to induce secondary responses to H. diminuta in mice, worm growth, not survival, is the criterion to evaluate.

Humoral and cellular response to infection withEchinostoma revolutumin the golden hamster,Mesocricetus auratus

“…The problem of mucosal infection with helminths has stimulated research directed at its solution. Current concepts of mucosal immunology have been reviewed by BIENENSTOCK & BEFUS, 1980;MCDERMOTT etal., 1982;andBEFUS &BIENENSTOCK, 1982a &b, 1984. It is probable that immune responses occur against most, if not all, intestinal parasites. Protective responses are often density-dependent in that there are thresholds in a host below which rejection does not occur (WAKELIN, 1976).…”

“…Protective responses are often density-dependent in that there are thresholds in a host below which rejection does not occur (WAKELIN, 1976). However, rejection may occur more rapidly at greater parasite densities (BEFUS, 1975). The strategy of a species may be to minimize the possibility of overpopulation in an individual host.…”

Hymenolepis citelli, H. diminutaandH. microstoma: immunoglobulin-containing cells in the lamina propria of the mouse gut during primary and secondary infections

“…The maintenance and techniques used in infections of the mice have been described in detail previously (BEFUS, 1975a). The strains of Hymenolepis citelli, H. diminuta and H. microstoma used are those described previously by ALGHALI (1980); BEFUS (1975a) and HOWARD (1976) respectively. Mice were each given six cysticercoids of the appropriate parasite during both primary and challenge infections.…”

“…Mice infected with the appropriate tapeworms were killed and the worms extracted as described previously (BEFUS, 1975a). Worms were then washed once in Hanks' solution to remove adherent debris and then again washed twice in PBS (pH 7-2).…”

In vitrotapeworm extract-induced proliferative responses of gut-associated lymphoid cells fromHymenolepis diminutainfected mice

“…Several lines of evidence indicate that rejection is the result of acquired host immunity. First, fewer worms become established in immune mice given a challenge infection (HOPKINS et al, 1972a;BEFUS, 1975) and rejection may be more rapid in challenged immune mice (HOPKINS et al, 1972a). Also, rejection is delayed in young mice given single H. diminuta as a primary infection (BEFUS & FEATHERSTON, 1974) and is blocked by immunosuppressive treatment of the host (HOPKINS et al, 1972b).…”