A consistent and reproducible method is described for isolating pure populations of microfilariae of Litomosoides carinii, Brugia pahangi, B. malayi and Dipetalonema viteae, free of cells, from blood, by density gradient centrifugation on Percoll in 0.25M sucrose. The recovery of the microfilariae was 85 to 97%.

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Necator americanus was studied in neonatally infected hamsters in order to determine precisely the growth and migration of the parasite in this laboratory host. Most larvae stayed at the skin infection site for at least 48 hours following administration of larvae and the movement to the lungs commenced on day 3. There was no significant growth at the skin site or during the first two days in the lungs. 98% of the larvae were recovered from the lungs by day 6 and showed signs of some growth and development. Moulting larvae were seen in the lungs on days 7 and 8, but intestinal worms, which were first detected on day 7, were all L4 larvae. These worms were significantly longer than the lung stages and henceforth grew rapidly. Over 80% of the worms were recovered from the intestine on day 9, only small numbers of larvae persisting in the lungs until day 12. Moulting worms were observed in the intestine on days 17 to 21, after which growth continued and did not slow until about the fifth week. Small quantities of eggs were occasionally detected as early as day 34 and continuous egg production commenced in the seventh week of infection reaching a peak by about the 10th week.

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Groups of rats, infected 7 weeks previously with Fasciola hepatica, together with appropriate control groups, were challenged either orally or intraperitoneally with 30 metacercariae. The mean worm recovery from the previously infected, orally challenged rats was significantly lower than from their respective controls (2.2 ± 1.1 worms as opposed to 9.0 ± 2.6). There was no significant difference in mean worm recovery from the previously infected, intraperitoneally challenged rats and their respective controls (5.3 ± 3.2 worms as opposed to 6.2 ± 1.9). Livers of the orally challenged group appeared to be largely free from secondary damage but considerable damage was evident in rats which received an intraperitioneal challenge. This evidence supports the view that the gut acts as an important barrier to metacercariae of a challenge infection. In a further experiment, young flukes were recovered from the gut, abdominal cavity and liver of immune and control rats 9, 18, 27, 36 and 45 h after oral challenge. It was found that fewer flukes successfuly penetrated the guts of immune rats (3%) than those of uninfected controls (13%), again pointing to the gut as a barrier to metacercariae of a challenge infection. Protective mechanisms that may oprate at the level of the gut are discussed.