Patterns of nematode fecundity were investigated for infections of the caecal worm Heterakis gallinarum in the ring-necked pheasant (Phasianus colchicus). Worm length was a good predictor of parasite fecundity. After controlling for worm length no other factors, including parasite intensity, were related to worm fecundity. Density dependence in worm size was detected in natural infections at parasite intensities above a threshold of 96 worms (worm size decreased with increasing parasite intensity). However, below this threshold, worm size actually decreased with decreasing parasite intensity (inverse density dependence). The interaction between density dependence and inverse density dependence in regulating the development and subsequent fecundity of H. gallinarum worms in ring-necked pheasants was demonstrated in an infection experiment. Density dependence was observed in the stunted growth of worms in heavily infected hosts, relative to worms in lightly infected hosts. Inverse density dependence in worm size was the common pattern across hosts by the end of the experiment, when parasite intensities were below the density dependence threshold. This is the first study to document both density dependence and inverse density dependence in parasite fecundity in the same host–helminth system.

Murine antibodies, raised against a purified recombinant 30 kDa laminin-binding protein from Echinococcus granulosus, were used to investigate the tissue distribution of the native protein in protoscoleces and brood capsules. Immunofluorescence, in combination with confocal microscopy, revealed that the protein was distributed in small annular foci near the peripheral regions of the protoscoleces. Immunoelectron microscopy of thawed cryosections demonstrated that the laminin-binding protein was present in the cytoplasm of tegumentary cytons and myocytons, but not in cells of the excretory system. The protein was associated with amorphous regions of the cytoplasm, and was not expressed at the surfaces of cells. This distribution resembles those of other invertebrate laminin-binding proteins, which are thought to act in the cell cycle and cell proliferation events. A low degree of label was consistently detected in extracellular matrices of the protoscolex.

The epidemiology and genetic variability of 2 parasitic nematodes Heligmosomoides polygyrus and Syphacia stroma of Apodemus spp. were investigated. Both are parasites of the same host, exhibit a direct life-cycle and are dioecious. However, H. polygyrus has a diploid and S. stroma a haplodiploid mode of reproduction. Haplodiploidy may lead to a more female biased sex ratio and reduced genetic variability. Levels of genetic diversity were analysed using both isoenzyme electrophoresis and RAPDs (random amplified polymorphic DNA). Both parasites showed a female biased sex ratio with a stronger bias for the haplodiploid parasite. Results showed significantly fewer genetic polymorphisms as measured by RAPDs for the haplodiploid parasite S. stroma in comparison with H. polygyrus. Despite the observed female biased sex ratio this could not be explained by a significant amount of inbreeding. Heterozygote deficiency for individual allozyme loci – which could indicate inbreeding – was not found in either parasite species. Other features of the particular life-history of these species are likely to have an impact on the sex ratio and genetic variability too.

This study presents new findings concerning the evolution of the human pathogens, Trypanosoma brucei and T. cruzi, which suggest that these parasites have divergent origins and fundamentally different patterns of evolution. Phylogenetic analysis of 18S rRNA sequences places T. brucei in a clade comprising exclusively mammalian trypanosomes of African origin, suggesting an evolutionary history confined to Africa. T. cruzi (from humans and sylvatic mammals) clusters with trypanosomes specific to Old and New World bats, T. rangeli and a trypanosome species isolated from an Australian kangaroo. The origins of parasites within this clade, other than some of those from bats, lie in South America and Australia suggesting an ancient southern super-continent origin for T. cruzi, possibly in marsupials; the only trypanosomes from this clade to have spread to the Old World are those infecting bats, doubtless by virtue of the mobility of their hosts. Viewed in the context of palaeogeographical evidence, the results date the divergence of T. brucei and T. cruzi to the mid-Cretaceous, around 100 million years before present, following the separation of Africa, South America and Euramerica. The inclusion in this study of a broad range of trypanosome species from various different hosts has allowed long phylogenetic branches to be resolved, overcoming the limitations of many previous studies. Moreover, T. brucei and the other mammalian tsetse-transmitted trypanosomes appear, from these data, to be evolving several times faster than T. cruzi and its relatives.

The monogenean (platyhelminth) skin parasite Entobdella soleae from the common sole (Solea solea) lays tetrahedral eggs. One of the 4 corners of the tetrahedron is a detachable operculum which is bonded to the rest of the egg-shell by cement. Most of this cement layer, beginning at the inner surface of the shell and running through almost to the outer surface (a distance of about 2 μm), is more or less uniform in thickness (30–38 nm), or tapers slightly. About 345 nm from the outer surface the cement layer narrows abruptly to about 10 nm. The cement is exposed on the inner surface of the shell, but in most eggs a layer of shell about 10 nm thick covers the narrow outer region of the cement layer. When experimentally perforated eggs were incubated with trypsin, the wide inner layer of cement was digested, but the narrow outer region initially remained intact. These observations are discussed in relation to the following (1) survival of the eggs during embryonic development, (2) hatching, (3) the ‘hinge’ often connecting the operculum to the empty egg-shell, (4) the rapid hatching that occurs in some other monogeneans.

The nematode parasite, Nippostrongylus brasiliensis, induces a biphasic anorexia in its rat host. The mechanisms, underlying this anorexia and its possible advantages to the host or parasite are unknown. We have investigated the effect of acute (12–24 h) and chronic (2–17 days) infections on plasma concentrations of leptin, insulin and corticosterone, and on hypothalamic expression of neuropeptide Y, galanin and corticotrophin-releasing factor genes. Plasma leptin was elevated in infected rats relative to uninfected ad libitum-fed controls and pair-fed controls in 12 h infections initiated at dark onset and in infections of 2 days' duration. At other times prior to parasite expulsion, plasma leptin in infected and pair-fed rats was lower than that of uninfected ad libitum-fed controls, reflecting the existing state of negative energy balance. Elevated plasma leptin concentrations in infected rats at day 2 post-infection were accompanied by reduced neuropeptide Y gene expression in the hypothalamic arcuate nucleus compared with both ad libitum control and pair-fed animals, and by lowered corticotrophin-releasing factor gene expression in the paraventricular nucleus relative to pair-feds. Twelve hour infections were characterized by a substantial increase in plasma corticosterone that was independent of reduced food intake, and in 12 h infections initiated at dark onset, where plasma leptin was elevated, there was also increased plasma insulin concentration in infected rats. In longer infections, differences between the groups in plasma insulin and corticosterone concentration were only observed at day 4 post-infection. In summary, perturbations to leptin, insulin and corticosterone signals early in infection may have a causative role and might feed back onto hypothalamic gene expression, whereas subsequent changes in these parameters are more likely to be secondary to negative energy balance.