| Abstract: | Infective larvae of Dipetalonema viteae did not reach maturity in inbred Fischer rats. However, female adults of D. viteae when transplanted surgically into Fischer rats established and the resulting microfilaraemia from the transplanted worms persisted for about 120 days after infection. Sequential dissections showed that some of the female worms transplanted remained viable in rats for about 35 days after infection. After inoculation of infective larvae into rats a varying number transformed into stage-4 larvae but they did not develop into adult worms and were killed. However, when the rats were immunodepressed non-specifically by a pre-existing Schistosoma mansoni infection or by treatment with S. mansoni-derived substance(s), a number of stage-4 larvae renewed their development and reached sexual maturity. These worms produced microfilariae which were observed in the peripheral blood for about 40 days. The effect of previous infection with S. mansoni on the survival and growth of D. viteae in Fischer rats depends greatly on the relative timing of infection because infective larvae of D. viteae reached maturity only when rats were inoculated with infective larvae after 15 days of S. mansoni infection but not after 21 or 28 days of S. mansoni infection. D. viteae will also develop to maturity in congenitally athymic rats. In congenitally athymic rats (Nu/Nu) each given 75 infective larvae, both the microfilaraemia and adult worm recovery at post-mortem were higher than those which resulted in Nu/Nu rats given an infection of 200 larvae. These experiments show that in rats innate immunity to this filarial nematode reflects a very rapidly induced acquired immunity which kills the parasite before it reaches maturity. |
