The relationship between host dietary protein and intestinal helminth population biology during primary infection was studied using a mouse–T. muris experimental model. Uninfected CBA/Ca mice fed either a 4% (by mass) or 16% protein diet grew at a similar rate, but both suffered significant growth retardation when infected with T. muris. T. muris initial establishment and fecundity were unaffected by dietary protein content, but were significantly influenced by infection dose, declining at the higher level of infection. Dietary protein deficiency increased parasite survival at high infection levels. Heavily infected hosts fed the 16% protein diet were found to expel almost the whole of their infections around day 21 p.i. By contrast, this response appeared defective in hosts fed the lower 4% protein diet, resulting in the establishment and survival of large, chronic and patent infections. Mean faecal egg output per mouse increased with infection dose in animals fed a low protein diet, but was low and unrelated to infection exposure in hosts fed the 16% protein diet. It is concluded that low protein levels in diet, via alterations in host resistance, may have an important influence on the transmission of T. muris.

The results are presented of an experimental study of the population biology of chronic Trichuris muris (Nematoda) infection in cortisone-treated CBA/Ca mice. Attention is focused upon both the validity of the common use of faecal egg counts to demonstrate density dependence in helminth fecundity, and the identification of other possible density-dependent mechanisms that may regulate worm numbers in chronic trichuriasis. The results show that faecal egg counts, although demonstrating high daily variation, are not an artefact of host faecal output but a significant density-dependent function of worm burden. This finding contrasts with the observations on Heligmosomoides polygyrus infection in outbred MF1 mice, but accords with similar studies in a wide variety of host - helminth systems. Worm establishment in the murine host is found to be a density related function of infection dose. This is attributed to the probable existence of a physical gut-carrying capacity in the murine host for T. muris. Worm distribution in the gut is also shown to be density dependent, with worms being displaced from the caecum to the colon at increasing intensities of infection. The sex ratio of the adult parasites, however, is found to be both unitary and independent of worm burden. Evidence for a significant density-dependent decline in female T. muris growth or size is presented. The results also show a significant positive association between female T. muris weight and per capita fecundity. These findings indicate that the stunted growth of individual worms at high parasite densities may be a potential mechanism underlying density dependence in helminth fecundity.