Interaction of Hymenolepis diminuta and Hymenolepis microstoma with complement

Schmidt, Jürgen; Ruppel, Andreas

doi:10.1016/0020-7519(88)90103-8

Cited by 6 publications

(2 citation statements)

References 20 publications

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“…Robinson et al (1987) have suggested that this differential resistance may be due to quantitative and/or qualitative differences in the glycocalyx on the surface of the worms; indeed Schmidt (1988) showed that only the scolex and adjacent parts adsorb lectins specific for AT-acetylglucosamine and galactose. The tegumental damage observed in our studies is similar to that found in 4day-old parasites by Robinson et al (1987) and for 11-day-old parasites by Schmidt & Ruppel (1988), i.e. shedding of microtriches, vesiculation and loss of the tegument.…”

Section: Discussionsupporting

confidence: 88%

Repair ofHymenolepis diminutaafter complement-mediated damage

Andreassen

Hoole

1989

Parasitology

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Seven and 56-day-old Hymenolepis diminuta were exposed to complement by incubation in 50% normal rat serum (NRS) in modified Hanks' saline. Ultrastructural studies revealed that the scolex/neck region remained relatively intact whilst in the strobila region microthrix denudation and loss of distal cytoplasm were observed. When complement-mediated damaged worms were incubated in vitro in 50% heat-inactivated normal rat serum (hiNRS) plus M199 or implanted into the duodenum of NMRI mice repair occurred, although destrobilated parasites were only found in vivo. The regions undergoing repair contained tegumental protrusions, vesicles, large electron-lucent areas and large quantities of lipid. Microtriches were formed parallel to the parasite surface and were raised into a perpendicular position. It is suggested that the regenerative process exhibited after complement-mediated damage does not mimic totally the embryological development of the surface layer.

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Section: Discussionsupporting

confidence: 88%

Repair ofHymenolepis diminutaafter complement-mediated damage

Andreassen

Hoole

1989

Parasitology

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“…It is less clear how H. polygyrus infection may affect liver mass. Some intestinal parasites elicit complement responses by their hosts (Schmidt & Ruppel 1988; Shin et al . 2001).…”

Section: Discussionmentioning

confidence: 99%

Intestinal nematode infection affects host life history and offspring susceptibility to parasitism

Kristan

2004

Journal of Animal Ecology

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Summary1. The effects of experimental infection with a naturally occurring intestinal nematode ( Heligmosomoides polygyrus , Dujardin 1845) on reproduction and on offspring growth, morphology and susceptibility to parasitism for wild-derived house mice ( Mus musculus , Linnaeus 1758) that were two to three generations captive-born were examined. 2. Parasitized females averaged 2·8 more pups per litter at weaning and, after adjusting for the effects of litter size on offspring mass, parasitized females had slightly larger offspring than unparasitized females (by 1-2%). 3. Heligmosomoides polygyrus did not affect mean values of other measures of host reproductive output (time to first litter production, interlitter intervals, sex ratio, offspring loss from birth to weaning) but parasitized mice were more variable than unparasitized mice in the number of days to first litter production and for numbers of pups that died between birth and weaning. 4. Offspring growth was not affected by either maternal parasite infection or direct parasite infection. Body mass of all pups at sexual maturity was equivalent but there were differences in body composition (fat mass, organ masses) between parasitized and unparasitized pups and between males and females. 5. Only offspring from parasitized mothers cleared their own infection but for offspring that retained their infection there were no effects of either offspring sex or maternal parasite infection on infection intensity. 6. These results clearly demonstrate that infection with an intestinal nematode affects host life history, primarily litter size but also offspring mass at weaning, and susceptibility of offspring to infection with the same parasite.

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Ultrastructural studies on the plerocercoid ofSpirometra erinacei in experimental sparganosis

Osaki

1990

Parasitol Res

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The gland cell and the tegument of the Spirometra erinacei plerocercoid following parasite migration in hamsters were observed by electron microscopy. Gland cells released secretory granules mainly into the frontal pit during each stage of migration. The density of the perinuclear secretory granules decreased markedly just after parasite penetration through the host intestinal wall. Therefore, gland cells seem to play an essential role in penetration. During migration in the host, lipid-like droplets appeared in the subtegumental cells and tegument and increased in number and size during migration in the abdominal cavity, but they had disappeared from plerocercoids recovered from subcutaneous tissues. Myelin-like bodies also occurred in the tegument, subtegumental cells and medullary matrix; they were released directly through the tegument into the frontal pit. Discoidal bodies gathered in the distal part of the tegument, where filamentous microtriches appeared in regions from which microtriches had been peeled off during penetration.

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Interaction of Hymenolepis diminuta and Hymenolepis microstoma with complement

Cited by 6 publications

References 20 publications

Repair ofHymenolepis diminutaafter complement-mediated damage

Repair ofHymenolepis diminutaafter complement-mediated damage

Intestinal nematode infection affects host life history and offspring susceptibility to parasitism

Ultrastructural studies on the plerocercoid ofSpirometra erinacei in experimental sparganosis

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