Death of schistosome cercariae during penetration of the skin | Parasitology | Cambridge Core (original) (raw)

Extract

The seagull, a natural host of Austrobilharzia terrigalensis, was infected with cercariae through a small area of breast skin; 40% of the schistosomula recovered from the skin shortly afterwards were dead. In budgerigar skin 29% of the schistosomula were dead, but mortality in the skin of ducklings was much higher (85%). The budgerigar is a useful laboratory host for this schistosome, but ducklings are completely resistant to experimental infection mainly because of the barrier effect of the skin.

Rapid recovery of schistosomula from budgerigar skin established that the majority of deaths occurred during the first 15 min after application of cercariae. In sections of skin fixed after 10 min nearly all the schistosomula were in the epidermis between the narrow stratum corneum and the living cells of the Malpighian layer. In seagull and budgerigar skin most schistosomula succeeded in crossing the Malpighian layer in the next 5 min, but in ducklings nearly all schistosomula completely failed to penetrate this layer.

In vitro experiments in which cercariae were allowed to penetrate through several layers of dead epidermis, isolated from dried budgerigar skin, into balanced saline, showed that schistosomula are not killed by host cells or a soluble toxic substance. The possibility that the epidermis contains an insoluble toxic substance could not be excluded.

The proportion of schistosomula which died during penetration of dead epidermis was related to the number of layers in the barrier, suggesting that schistosomula may die owing to exhaustion caused by the intense activity of penetration.

About 30% of the glycogen reserves of cercariae were utilized during penetration of budgerigar skin. In dead schistosomula the glycogen reserve had been reduced by 80%, but the significance of this observation is uncertain because much of the glycogen may have been autolysed after death of the schistosomula. Exposure of cercariae to glucose before penetration did not affect the proportion which died in the skin.

Schistosomula adapt to the osmotic pressure in the skin, which is one-third that of sea water, and 30 min after penetration they are rapidly killed if returned to sea water. This process of adaptation is not related to mortality of schistosomula during penetration of the skin.

We wish to acknowledge the expert technical assistance of Mrs J. Morgan. This investigation was supported in part by research grant AI-04707 from the National Institute of Allergy and Infectious Diseases, United States Public Health Service.

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