Faecal egg counts and nematode fecundity: Heligmosomoides polygyrus and laboratory mice.

The results are presented of an experimental investigation of the relationship between faecal egg counts and worm burden in outbred MF1 mice infected with Heligmosomoides polygyrus (Nematoda). The sex-ratio of the adult parasites was found to be significantly female biased, but independent of parasite burden. Evidence was also found to suggest a significant association between parasite density and mating success. The linear logarithmic relationship (gradient of approximately 2) between the variance and mean of repeated egg counts from individual mice could not be disrupted by controlled experimental conditions, and is therefore concluded to be an inherent feature of the biology of helminth-host interactions. A significant positive association was detected between host faecal output and parasite fecundity; further investigation of the cause of this association is now required. Average faecal production was found to be inversely related to worm burden. In combination, the above two factors account partly, but not completely, for the observed density dependence in the absolute rate of parasite egg production. Two epidemiological consequences of the relationship between faecal production and parasite fecundity are discussed. First, absolute rates of egg production can only be estimated by temporal egg counts (epd). Secondly, measurements of egg production/g of faecal material (epg) are more reliable indicators of worm burden than measurements of epd. Both faecal output and worm fecundity respond as might be predicted to a period of host food deprivation; faecal egestion and measurements of epd are significantly depressed, and measurements of epg are significantly increased. The data are consistent with the hypothesis that egg production and faecal output are causally associated, but that other factors relating to parasite density also influence egg production. Of the possible causes for the high variability in parasite egg production between mice harbouring low number of worms, the most likely explanation seems to be host heterogeneity (possible genetic in origin). This is discussed in relation to similar patterns observed in data collected from human populations in areas of endemic helminth infection.