Schistosoma mansoni: Alteration in ovipositing capacity by transplanting between heterologous hosts

Abstract

The guinea pig is considered a poor host for Schistosoma mansoni because the reproductive capacity of the worm in this rodent is so low that mature schistosome eggs are not excreted in the host feces. The reason for this is unknown. Experiments were designed to determine whether the guinea pig controls egg laying by specific damage to a specific organ during the worm's development, or whether it suppresses egg laying continuously or interferes with the development of the egg after it has been laid. Worms of various ages were transfered between the hamster (a host in which the majority of eggs laid by S. mansoni mature) and the guinea pig, and vice versa. Donor animals were infected with cercariae of S. mansoni (the life-cycle stage naturally infective to mammals) on day zero. Worms were transferred during four periods of their mammalian development. These were: (a) the lung phase (worms 7 and 8 days of age); (b) the phase of gut development (worms 16 days old); (c) the phase of organogeny (worms 27 days old); (d) the pase of oviposition (worms 34 and 35 days old). Control transplants were made between homologous hosts to determine whether transplantation per se interferred with normal sexual development. Experimental transplants were made between heterologous hosts. Lung forms were transplanted by ordinary intracardiac injection. Worms older than this were transplanted by intraportal injection. The methods developed for intraportal injection are described. The age of the recovered worms is the sum of the time spent in the donor and the recipient. Most of the recipients were autopsied when the worms reached the age of 58 days. Results in the recipients were based on fecal examination, worm recoveries, oograms, and histology of the recovered worms. Worms of all four ages were successfully transferred. The percentages of worms recovered after homologous transfer were higher (hamster to hamster, 61%; guinea pig to guinea pig, 32%) than recoveries after heterologous transfers (hamster to guinea pig, 18%; guinea pig to hamster, 25%). For the homologous transplants, the excretion of eggs by the recipient hosts were as expected. Recipient hamsters excreted eggs in their feces and recipient guinea pigs did not. All hamsters receiving worms donated by guinea pigs excreted eggs in their feces. The times eggs first appeared in the feces of these hamsters indicated that the guinea pig did not inhibit the rate of sexual development of S. mansoni. Mature eggs were excreted by guinea pigs which had received worms transferred from hamsters before the onset of the worm's sexual development. Thus, the ability of the guinea pig to inhibit egg maturation is not exerted directly on the developing egg. The finding that prior residence in the hamster increased the worm's reproductive capacity in the guinea pig, suggests that the guinea pig lacks one or more substances necessary for egg formation. Because of this lack, the rate of egg laying by S. mansoni is continuously suppressed by the guinea pig. On histological examination, there appeared to be fewer oocytes in the ovaries of female worms recovered from hosts in which schistosome eggs were not excreted in the feces than in the ovaries of worms recovered from hosts which did excrete schistosome eggs in their feces. It is not now known whether this is the specific lesion caused by the guinea pig. The number of sperm appeared similar in all male worms examined. Oograms confirmed the results of fecal examination. The reproductive capacity of sexually developed worms was not increased on transfer from the hamster to the guinea pig. The reason for this is not apparent. It was shown experimentally that sexually mature worms were not traumatized during transfer and that they probably were not shocked.