Resistance of Mice to Secondary Infection with Schistosoma Mansoni

Da, Dean; Minard, P; Ma, Stirewalt; We, Vannier; Kd, Murrell

doi:10.4269/ajtmh.1978.27.951

Cited by 44 publications

(6 citation statements)

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“…Also, Dean et al (1981) found that transferred, irradiated 21-or 25-day liver or mesenteric worms which fail to persist induced significant but low levels of resistance. In contrast, infections with unattenuated single-sex cercariae consistently failed to induce resistance in mice (Dean, Minard, Stirewalt, Vannier & Murrell, 1978;Bickle et al 1979c;Bickle, Bain, McGregor & Doenhoff, 1979c). Moreover, the present and other studies have demonstrated that the resistance wanes in pre-infected rats, despite the persistence of stunted adults (Phillips et al 1978;Perez et al 1974).…”

Section: Discussionmentioning

confidence: 48%

“…infections. This contrasts with the mouse, in which unirradiated single-sex infections or pre-patent bisexual infections (Dean et al 1978;Bickle, 1982), and those exposed to low radiation doses (Minard et al 1978;Bickle et al 1979a) induce insignificant or comparatively low levels of resistance relative to highly irradiated infections which terminated at or before the lungs. Several explanations for this intriguing difference between the rat and mouse models can be suggested.…”

Section: Discussionmentioning

confidence: 88%

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Immunization of rats againstSchistosoma mansoniusing irradiated cercariae, lung schistosomula and liver-stage worms

1984

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In PVG rats a single immunizing infection with Schistosoma mansoni cercariae exposed to 0, 5, 10 or 20 krad. gamma radiation failed to induce more than minimal resistance (17-29%) to challenge 4 weeks later, whereas 4 immunizations with 20 krad.-irradiated cercariae, over several months, induced substantial resistance (75%). In contrast, significant protection was induced in Fischer rats by a single immunization with unirradiated cercariae or cercariae irradiated with up to 80 krad. Comparable resistance was induced by unirradiated and by 2, 5 and 20 krad.-irradiated cercariae (67-74%) and lower levels by 10, 40 and 80 krad.-irradiated infections (57, 48 and 33%, respectively). Although the resistance induced by a single dose of 1000 20 krad.-irradiated cercariae could be boosted by a second (88%), further immunizations failed to enhance this resistance. Also, increasing the number of immunizing cercariae in single or multiple vaccinations from 1000 to 3000 failed to increase the resistance. While the resistance induced by 20 krad.-irradiated cercariae persisted undiminished for at least 25 weeks (67%), the resistance induced by normal cercariae declined to insignificant levels by 25 weeks (21%). Comparison of the migration and survival of unirradiated and of 20 and 40 krad.-irradiated cercariae revealed dramatic differences in their fate: parasites exposed to 40 krad. remained in the skin, while the majority of 20 krad.-irradiated parasites died in the lungs after a sojourn of at least 14 days. Thus, although skin schistosomula alone could induce significant protection, optimal resistance was induced only by parasites which migrated to the lungs or beyond. The immunizing potential of these older parasites was investigated by exposing rats to lung- and liver-stage larvae injected into the tail and mesenteric veins, respectively. Irradiated 4-day lung schistosomula induced comparable resistance (79%) to that induced by a complete unattenuated cercarial infection (78%), whereas less resistance was induced by irradiated and unirradiated 11-day-old liver worms (30 and 27%) and by 25-day-old pre-adult worms (48%).

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Section: Discussionmentioning

confidence: 48%

Section: Discussionmentioning

confidence: 88%

Immunization of rats againstSchistosoma mansoniusing irradiated cercariae, lung schistosomula and liver-stage worms

1984

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“…3) mice were challenged 8 weeks after infection, there was no overt lung pathology and histological examination revealed live but not dead schistosomula. At similar challenge times, S. mansoni lung schistosomula counts did not differ significantly from controls, while adult worm counts were greatly reduced (Dean et al 1978a;Doenhoff et al 1978). Further, von Lichtenberg, Sher, Gibbons & Doughty (1976) reported insignificant pathology around S. mansoni lung schistosomula in reinfected mice.…”

Section: Groupmentioning

confidence: 91%

“…A high degree of resistance to reinfection with Schistosoma mansoni has been demonstrated in mice harbouring patent primary infections (Doenhoff, Bickle, Long, Bain & McGregor, 1978;Long, Doenhoff & Bain, 1978;Dean, Minard, Stirewalt, Vannier & Murrell, 1978a). This acquired resistance has been correlated with the number of eggs deposited in the tissues (Dean, Minard, Murrell & Vannier, 19786;Long, Harrison, Bickle, Bain, Nelson & Doenhoff, 1980) and may be a result of egg-induced pathology (Wilson, 1980;Dean, Bukowski & Cheever, 1981).…”

Section: Introductionmentioning

confidence: 99%

Factors affecting the acquisition of resistance to Schistosoma japonicum in the mouse: I. The correlation between egg deposition and worm elimination

1984

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Acquired resistance to Schistosoma japonicum was evident after the lung phase of migration of challenge schistosomula. 'Trickle' infections which gave similar primary worm burdens to single infections stimulated similar levels of resistance. There was a strong correlation between the size of the primary worm burden of individual mice and their ability to resist infection 8 weeks after exposure to S. japonicum. However, acquired resistance did not develop until 6 weeks, that is after the primary infection had become patent, and was maximal some 12 weeks after infection; thereafter resistance declined. The numbers of parasite eggs deposited in the tissues increased during acute infection (duration of 12 weeks or less) and tended to stabilize or decrease during chronic infection (longer than 12 weeks). There were good correlations between the resistance of mice to challenge and the numbers of eggs deposited in their livers, guts or lungs during acute infection, but these correlations were not evident during chronic infection. The inflammatory responses to tissue-bound eggs regress during chronic infection and this may influence the relationship between acquired resistance and egg burden. Comparable primary infections of S. japonicum or S. mansoni protected equally well against both heterologous and homologous challenges. However, unisexual infections of S. mansoni, which produced no overt pathology, failed to confer protection against a challenge of S. japonicum.

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“…This occurs throughout the period of egg accumulation in the host's liver, usually between 6 and 20 weeks after initial infection (Cheever & Warren, 1964;Dean, 1983;Dean, Minard, Murrell & Vannier, 1978a;Wilson, Coulson & McHugh, 1983). Single-sex infections generally fail to induce high levels of resistance (Dean, Minard, Stirewalt, Vannier & Murrell, 19786;Bickle, Bain, McGregor & Doenhof, 1979;Dean, 1983), suggesting that the resistance which develops is influenced by some aspect of the host's reaction to parasite eggs.…”

Section: Introductionmentioning

confidence: 99%

Pathologically induced alterations in the dimensions of the hepatic portal vasculature of mice infected with Schistosoma mansoni

1987

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Alterations in the hepatic portal vasculature of NMRI mice infected with Schistosoma mansoni were assessed using a microsphere injection technique. The accumulation of eggs in the livers of infected mice and the development of portal hypertension were closely related to the worm pair burden during the first 15 weeks of infection. Individual variation between mice harbouring identical patent worm pair burdens was partially explained by the reduced fecundity of females from sexually biased infections. As eggs accumulated in the liver and portal hypertension increased, the number of injected microspheres escaping from the hepatic portal system rose in rank order of diameter from 9 microns through 15 microns and 25 microns to 50 microns. There was a strong correlation between the numbers of parasite eggs in the lungs and injected microspheres recovered from the lungs. The pattern of detection of microspheres in the lungs indicated a progressive increase in diameter of intra-hepatic porta-systemic connexions, followed by development of large-bore extra-hepatic collateral vessels. An accurate temporal profile of the pathological state of the host and the extent of collateral vessel formation was obtained. Injection of 141-Ce-labelled microspheres demonstrated that the arterial supply to all organs of the body was affected by alterations in the microvasculature of the liver and lungs.

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Resistance of Mice to Secondary Infection with Schistosoma Mansoni

Cited by 44 publications

References 0 publications

Immunization of rats againstSchistosoma mansoniusing irradiated cercariae, lung schistosomula and liver-stage worms

Immunization of rats againstSchistosoma mansoniusing irradiated cercariae, lung schistosomula and liver-stage worms

Factors affecting the acquisition of resistance to Schistosoma japonicum in the mouse: I. The correlation between egg deposition and worm elimination

Pathologically induced alterations in the dimensions of the hepatic portal vasculature of mice infected with Schistosoma mansoni

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