The intestinal nematode Heligmosomoides bakeri has undergone 2 name changes during the last 4 decades. Originally, the name conferred on the organism in the early 20th century was Nematospiroides dubius, but this was dropped in favour of Heligmosomoides polygyrus, and then more recently H. bakeri, to distinguish it from a closely related parasite commonly found in wood mice in Europe. H. bakeri typically causes long-lasting infections in mice and in this respect it has been an invaluable laboratory model of chronic intestinal nematode infections. Resistance to H. bakeri is a dominant trait and is controlled by genes both within and outside the MHC. More recently, a significant QTL has been identified on chromosome 1, although the identity of the underlying genes is not yet known. Other QTL for resistance traits and for the accompanying immune responses were also defined, indicating that resistance to H. bakeri is a highly polygenic phenomenon. Hence marker-assisted breeding programmes aiming to improve resistance to GI nematodes in breeds of domestic livestock will need to be highly selective, focussing on genes that confer the greatest proportion of overall genetic resistance, whilst leaving livestock well-equipped genetically to cope with other types of pathogens and preserving important production traits.

The maturation of female Schistosoma mansoni depends on pairing with a male which induces mitotic activities in the reproductive organs of the female worm. Since in other organisms cell proliferation is regulated by well-conserved signal transducing molecules, we looked for such molecules on immunoblots of schistosomes, using antibodies against conserved epitopes of Ras, GAP and MAP kinases. We identified all 3 molecules in schistosomes and found that they are developmentally regulated. Furthermore, there is evidence for their involvement in the male-directed maturation of the female.

Full-length cDNAs encoding cytosolic (SODc) and putative extracelluar (SODe) Cu/Zn superoxide dismutases (SODs) from the ovine gastrointestinal parasitic nematode Haemonchus contortus have been isolated and characterized. The predicted sequences of the H. contortus SODs showed strong homology to other helminth SODs, the highest level of sequence similarity was with those of the free-living nematode Caenorhabditis elegans. The predicted amino acid sequence of the putative extracellular form contained an N-terminal extension with the characteristics of a signal sequence including a potential signal peptidase cleavage site. Transcripts of both classes of Cu/Zn SOD were detected in all life-cycle stages examined. The cytosolic SOD mRNA was approximately 6-fold more abundant than that of the extracellular enzyme in adult parasites. Immunoblotting with antisera raised to in vitro-expressed parasite SODs revealed the presence of 2 proteins in extracts of adult H. contortus, with molecular masses of approximately 19·8 and 18 kDa. An additional protein of approximately 16·8 kDa was detected in adult ES material. Immunofluorescent staining showed Cu/Zn SOD was localized in the body wall musculature and the pharynx in adult worms and in the uterine tract of adult females. The immunogenic properties of recombinant H. contortus Cu/Zn SODs was assessed in a challenge infection experiment in lambs.

A population of Gasterosteus aculeatus from Priddy pool in Somerset was infected with three species of parasites: Schistocephalus solidus, Diplostomum gasterostei and Echinorhynchus clavula. The variations in the incidence and intensity of the infections with the sex, age and size of the sticklebacks are described.

The infections with the three parasites were very similar in male and female sticklebacks. The weights of Schistocephalus were greater in the females, however;the mean weight of the plerocercoids was larger suggesting that they grew more rapidly in female fish.

The Schistocephalus infection increased in small fish, under 1 year of age, but in older larger ones the infection decreased. These changes can be related both to the feeding habits of the fish and to the weight relationships of host and parasite.It was found that the weight of Schistocephalus did not greatly exceed that of the fish, and also that the combined weight of fish plus Schistocephalus was rarely greater than 3 g. Therefore the proportional weight of Schistocephalus, or parasite index, was lower in sticklebacks heavier than about 1·5 g.

The Diplostomum and Echinorhynchus infections both increased with age and size of fish, but the largest sticklebacks were not the most heavily infected. These increases can be related to the feeding habits of the fish in the case of Echinorhynchus and to accumulation with time in the case of Diplostomum.

In all three species the largest and oldest fish were not the most heavily infected.It is suggested that the old fish are becoming senile and are therefore less able to support large parasite burdens.

I am very grateful to Dr H. D. Crofton for his constant advice and encouragement during this study, and to Dr R. A. Avery for useful discussions. This work was supported by a Science Research Council research studentship and by a NATO studentship.

1. The number of third stage larvae of Trichostrongylus retortaeformis on different portions of herbage was studied. Three plant-types were used: Festuca sp., Clover, and Carex sp.

2. On Festuca spp., 5·5 in. in height, 90% of the total number of larvae occurred on the lower 3 in. of the blades; 50% occurred on the basal 1·5 in. On the same species, 3 in. high, 90% were found on the lower inch. This showed that the distribution on the blades was not limited by the total distance the larvae were able to travel. Nor was it limited by the rate of movement, because the form of the distribution was not altered after 3 days.

3. Larvae were found to be evenly distributed vertically over the stems and leaves of clover.

4. On Carex vulgaris 10 in. high the larvae were limited to the lower 2 in.

5. The distribution of larvae in the soil, ‘mat’ and herbage was recorded monthly throughout the year. During the warmer months of June, July and August the majority of larvae were found on the grass blades, and more larvae occurred in the soil than in the ‘mat’. During September, October, April and May more larvae were found in the ‘mat’ and fewer were found on the blades and in the soil. From November to March nearly all the larvae occurred in the ‘mat’. From December to January no larvae were found on the grass blades or in the soil.

6. Climatic conditions in the herbage were studied.

7. It was shown that the temperature below the top of grass blades may differ considerably from the air temperature. Differences of 10° F. were recorded between the tips and bases of grass blades. In general, there was a gradient of temperature established between the upper and lower parts of the grass.

8. High humidities occurred in the lower parts of the grass, even when atmospheric humidity was low. The relative humidity at the tips was never higher than that at the base of the blades.

9. The rate of evaporation decreased towards the base of the blades.

10. The light intensity decreased towards the soil. Midway between the top of the grass and the soil the light intensity fell rapidly.

11. The height, density and type of herbage modified the effect of the climatic factors.

12. It was concluded that the vertical distribution of larvae could be explained without reference to geotropism and that most of the larvae occurred in that portion of the herbage in which there was least climatic change.

The writer wishes to thank Prof. A. D. Hobson for advice and criticism and Mr W. Lyle Stewart, M.R.C.V.S., for encouragement and the provision of facilities, and Dr G. Lapage for helpful criticism and advice in the preparation of the MS. Thanks are also due to King's College, University of Durham, for a grant from the College Post-Graduate Research Fund.

The weight gain and growth rate of Trichoplusia ni larvae were severely depressed following parasitization by the insect parasite, Hyposoter exiguae. The development of the host was also delayed and juvenile hormone esterase activity present at the normal time of moulting was absent in parasitized insects. Similar effects on growth and development were achieved by rearing host insects on nutrient-deficient media. Accompanying the above effects of parasitization were alterations in dry/wet weight ratio and host haemolymph osmolality. Parasitization resulted in immediate increases in the concentrations of haemolymph non-glycogen carbohydrate (composed of trehalose, maltose and glucose) and protein. The concentration of fat body glycogen also increased following parasitization. In contrast, the concentration of haemolymph non-glycogen carbohydrate and protein, as well as fat body glycogen, decreased in nutrient-deprived larvae. The significance of the above results as they relate to the insect parasite–host relationship is discussed.

1. In addition to the parasite of East Coast fever three other organisms were observed. The first of these is a “symbiont” and was found in the Malpighian tubules and ovaries of all the ticks examined; the second, a protozoan, was observed in about 50 per cent. of our ticks in the process of multiplication in the epithelial cells of the gut and in the large phagocytic cells of the body cavity; the third, from its very active movements, probably a ciliate, was seen only in dark field preparations of a few ticks recently engorged. Once recognised these organisms were always easily distinguished from Theileria parva. We were unable to confirm the assumption of Nuttall and Hindle (1913) that practically 100 per cent of ticks fed on blood containing parasites become infective and are thus capable of transmitting the disease. Approximately accurate figures on the survival of ingested parasites can only be secured from sections. Of the 290 ticks of our standard series examined in very complete serial sections, parasites were found in 178, or 60·1 per cent. In the first series of infective nymphae, in which we kept records of sex, 33 per cent. of the ticks containing parasites were females and 66 per cent. were males.

2. In the erythrocytes of the animals suffering from East Coast fever on which the ticks engorged large and small parasites were distinguishable (Figs. 29 and 30 and Fig. I, p. 32). Both showed signs of division.

3. Intra-erythrocytic parasites were observed in the gut of the ticks only up to the sixth day after engorgement (Table V). Liberation of parasites takes place at a different rate in different ticks.

4. Parasites were seen free in the lumen of the gut from the time of engorgement up to 10,13,14 and 8 days, as indicated in Tables I–IV. Beginning about 2 days after engorgement and until they disappear from the gut there is a marked tendency for the parasites to be arranged in clumps, the small ones together and the large ones together (see Fig. I at 2). But the small and large parasites are sometimes scattered indiscriminately. Both types tend to accumulate on the surfaces of the epithelial cells lining the gut (Fig. I at 3).

5. Many parasites are taken up by epithelial cells which stretch further into the lumen than their neighbours and are called “pedunculated.” They are accompanied by lymphocytes, leucocytes, platelets and a variety of foreign materials. Parasites were observed in this situation from engorgement to 14 days (Table I), from the second to thirteenth day after engorgement (Table II), from the sixth to the twenty-first day after engorgement (Table III), and from the first to the eighth day after engorgement (Table IV). The examinations listed in Table III began on the sixth day. The fact that parasites were not seen earlier in this series in the pedunculated cells does not mean that they were absent. On each day during these rather long periods large and small parasites were observed which stained brilliantly and some of which appeared to be dividing. Other individuals of both types stained but feebly and from their irregular outlines were clearly degenerating. How long individual parasites remained could not be determined. Table I shows their presence in pedunculated epithelial cells 4 days after disappearance from the lumen, and Table III, 5 days after. But in the ticks recorded in Tables II and IV they disappeared from the pedunculated cells on the same day that they could no longer be seen in the lumen.

6. It is the parasites which enter non-pedunculated epithelial cells which carry on the life cycle. They enter in smaller numbers and more slowly. Tables I, II and IV record their appearance in this commoner type of epithelial cells just 7 days after they were first noted in the pedunculated cells. They remain intra-epithelial for as long as 20 days (Table I), 25 days (Table II), 22 days (Table III), and 16 days (Table IV). As a rule they are not accompanied by leucocytes and different sorts of debris. The small forms soon disappear. Large forms like those seen in the lumen are at first present in considerable numbers and give rise to a parasite distinctly different from any previously seen, which we call a “zygote,” although we have been unable to demonstrate the process of fertilisation. These zygotes have rather irregular outlines, stain blue by Giemsa's method and are for a time without red-staining nuclei. In this condition they are represented in Figs. 1–5, 40 and 41 (a–d); also in Fig. I at 4 and 5. In this phase of the zygote the parasites have to resist the digestive action of the cell containing them and many succumb, but some grow; their diameter increasing 300 or 400 per cent. (compare Figs. 1 and 5).

The surviving ones begin to exhibit once more characteristically red-staining nuclei about 18 days after engorgement and at approximately the time of moulting (Figs. 6, 41, e–h). Coincident with this change their outlines become smooth and they are evidently less susceptible to digestion. Oökinetes develop very rapidly within their interior (Figs. 42–49 and Fig. I at 6). All stages in the formation of oökinetes from blue-staining zygotes to others which are fully differentiated and have escaped from the epithelial cells of the gut into the body cavity are frequently seen in a single tick. Oökinetes were observed from the first to the eighth day after moulting in sections and to the ninth day in smears (Table II), from the first day before moulting to the eleventh day after (Table III), and from the second day before to the ninth day after (Table IV). They are illustrated in Figs. 7, 11–14 and 49.

7. The oökinetes begin to enter the salivary glands about the time of moulting. Our failure to detect them in this situation in our larval series (Table I) until 11 days after moulting is a negative observation, possibly due to technical difficulties, and of little significance compared with their definite discovery in the salivary glands 1 day after moulting (Table II), 1 day before moulting (Table III), and 1 day after moulting (Table IV). But this entry is probably not restricted to the days mentioned, for typical ookinetes were observed 9 days (Table II), 12 days (Table III) and 10 days (Table IV) after they were first noted in the salivary glands. It is therefore probable that successive crops of oökinetes enter the salivary glands over a relatively long period and that this explains the discovery of parasites in different stages of development in the salivary glands of individual ticks. Soon after penetration they round up but can be recognised at least until 5 days after moulting by their intensely blue-staining cytoplasm and red-staining nuclei (Figs. 15, 50, 51).

The next stage, which we refer to as a beginning “sporont,” is represented in Figs. 16, 52, 54 and to the right in Fig. I at 8. The nucleus of the oökinete is lost, but the parasite can be identified within the salivary gland cells by its intense deep blue colour when stained by Giemsa's method, by the clear halo about it, and by its relatively large size. The salivary gland cell containing it is usually considerably distended. This condition persists for a variable time which we estimate at about 3 days. Approximately 8 days after moulting buds appear on the surface of the sporont (Figs. 17 and 53) and spherical masses within its interior (Fig. 55) which constitute the “sporoblasts.” At the same time the central part of the parasite stains less intensely and the halo about it becomes barely distinguishable (Fig. I at 10). A little later on the central part stains still less strongly and the sporoblasts become proportionally more clearly defined (Fig. 18). Red-staining chromatin reappears in irregular masses in the sporoblasts (Fig. I at 11). This, in our experience, is as far as the parasite develops before the ticks containing it are placed on animals with a view to transmitting East Coast fever. During the first 3 days of feeding on susceptible animals the parasites were examined in great detail.

After 1 day a total of ten ticks were studied in serial sections, of which three contained parasites in their salivary glands. All of them were in the sporont stage. The central area of the sporont shown in Fig. 19 is developed beyond the condition illustrated in Fig. 18. It is less dense, it is stained a light bluish green and the sporoblasts have moved from it to the periphery. A careful search was made of the digestive tracts of all three ticks. No blood cells could be detected. The lumina were not sufficiently dilated to suggest the intake of cell-free plasma or lymph.

After 2 days four out of ten ticks examined contained parasites. In three of them sporonts were observed which apparently did not differ from those just described; but in the fourth (an adult female) the sporoblasts were further separated from the parent mass—a change which seemed to be preliminary to the more radical development noted the next day. In this particular tick no blood cells could be detected in the lumen of the digestive tract, which, however, was slightly but distinctly dilated perhaps by fluid from the animal on which the tick fed.

After 3 days a striking alteration occurred in the organisms in all five of nine ticks parasitised as illustrated in Figs. 57 and 58. The red-stained chromatin represented in Fig. 57 which before (Fig. 56) was distributed irregularly is becoming arranged in small masses at the surfaces of the sporoblasts. The differentiation of these chromatin masses is still further advanced in Fig. 58, though it illustrates conditions in the same tick. The masses have in many cases broken loose from the sporoblasts, and each is seen to be made up of some blue-stained cytoplasm in which a single spherical or cup-shaped nucleus is embedded. These are the sporozoites. While this development of sporozoites in association with the sporoblasts was observed in all of the five ticks wellformed sporonts like those illustrated in Figs. 18 and 19 were only seen in one. All of the ticks seemed to contain a slightly increased amount of fluid in their digestive tracts, but in only one could ingested leucocytes be recognised.

The period from 4 to 18 days is divisible into two parts: before engorgement (Figs. 20–25, 60–67) and after engorgement (Figs. 26–28, 68, 69).

Before engorgement the maximum production of sporozoites takes place. At 4 days the process is going on with extreme rapidity. Figs. 66 and 67 show two active sporoblasts with sporozoites radially arranged about their periphery. The morphology of the sporozoites on the fifth day is well shown in Fig. 59. When first formed they are somewhat larger than when later on they are ready for discharge. This difference is illustrated in Fig. 23 and in Fig. I (compare stages 12 and 13).

At 5 days larger sporoblasts were noted (Figs. 60–65), and the sporonts are broken up by the spreading apart of the sporoblasts through the tremendous development of sporozoites (Figs. 20–22). Fig. 24 represents a mass of sporozoites apparently ready for discharge into the lumen of the acinus on the right.

The maximum number of salivary gland cells in any tick containing parasites at any stage in the cycle is about 50 per cent. Such an infestation is, however, very exceptional, occurring in only four or five of the fifty-nine ticks of our standard series possessing parasites in this location. The usual infestation is about 8 per cent. In some ticks, however, parasites are only to be found in one or two cells after long search; that is to say, in a percentage of, say, 0·1 per cent. But when the infestation is so small the individual cells involved may be charged with parasites just as heavily. By far the heaviest cellular charge with parasites, though not the highest percentage infestation, was discovered in five out of seventeen female ticks found naturally attached to an animal in a region in which East Coast fever was very common. The degree of infestation probably depends upon the number of ookinetes which settle in the salivary glands and the individual cellular charge upon adverse or favourable conditions in the salivary glands to the development of parasites.

After engorgement both the percentage infestation and the cellular charge are apparently reduced. The conditions 6, 8, and 11 days after attachment are illustrated in Figs. 27, 28 and 68 and 69. Many of the parasites are obviously degenerating, and the whole mass of parasites may be sloughed off from the cell into the lumen of the acinus (Fig. 29). The last parasites were seen 18 days after the tick containing them was placed on a susceptible animal (Table IV), which is long past the time of probable transmission of the disease. Our experiments do not show how much longer they persist and it is likely that they are soon destroyed, because it has been proved experimentally by other investigators that the ticks are cleansed by feeding.

8. Three of our four series of ticks, which contained parasites in their salivary glands, which were fed on susceptible animals, produced typical cases of East Coast fever. It is probable that the other series (Table II), which possessed parasites in equal abundance, would also have transmitted the disease if the animal infested had not died so soon under chloroform anaesthesia as we were removing a lymph gland for study.

Forty-five cattle, which had recovered from EOF and been kept free from reexposure to infection for periods of 1–43 months, were given a single uniform lethal challenge using a stabilate prepared from triturated infected ticks. All withstood the challenge which killed the five controls. There was an increase in the incidence of mild febrile reactions with time since last exposure to T. parva, indicating a gradual loss of immunity in the absence of reinfection. The duration of the immunity was not related to the severity of the initial reaction.

We are indebted to our colleagues on the Immunological Research on Tickborne Cattle Diseases and Tick Control Project, with whom we designed and carried out the experiment.

Toxoplasmosis, caused by the protozoan parasite Toxoplasma gondii, is one of the most common parasitic infections in humans. Primary infection in pregnant women can be transmitted to the fetus leading to miscarriage or congenital toxoplasmosis. Carefully designed nationwide seroprevalence surveys and case-control studies of risk factors conducted primarily in Europe and America, have shaped our view of the global status of maternal and congenital infection, directing approaches to disease prevention. However, despite encompassing 1 in 5 of the world's population, information is limited on the status of toxoplasmosis in China, partly due to the linguistic inaccessibility of the Chinese literature to the global scientific community. By selection and analysis of studies and data, reported within the last 2 decades in China, this review summarizes and renders accessible a large body of Chinese and other literature and aims to estimate the seroprevalence in Chinese pregnant women. It also reviews the prevalence trends, risk factors, and clinical manifestations. The key findings are (1) the majority of studies show that the overall seroprevalence in Chinese pregnant women is less than 10%, considerably lower than a recently published global analysis; and (2) the few available appropriate studies on maternal acute infection suggested an incidence of 0·3% which is broadly comparable to studies from other countries.

Cryptosporidium and Giardia are two important zoonotic intestinal parasites responsible for diarrhoea in humans and other animals worldwide. Rodents, as reservoirs or carriers of Cryptosporidium and Giardia, are abundant and globally widespread. In the present study, we collected 232 fecal specimens from commensal rodents captured in animal farms and farm neighbourhoods in China. We collected 33 Asian house rats, 168 brown rats and 31 house mice. 6·0% (14/232) and 8·2% (19/232) of these rodents were microscopy-positive for Giardia cysts and Cryptosporidium oocysts, respectively. All 14 Giardia isolates were identified as Giardia duodenalis assemblage G at a minimum of one or maximum of three gene loci (tpi, gdh and bg). By small subunit rRNA (SSU rRNA) gene sequencing, Cryptosporidium parvum (n = 12) and Cryptosporidium muris (n = 7) were identified. The gp60 gene encoding the 60-kDa glycoprotein was successfully amplified and sequenced in nine C. parvum isolates, all of which belonged to the IIdA15G1 subtype. Observation of the same IIdA15G1 subtype in humans (previously) and in rodents (here) suggests that rodents infected with Cryptosporidium have the potential to transmit cryptosporidiosis to humans.

A technique is described for obtaining consistent reinvasion and multiplication of the erythrocytic stages of Plasmodium falciparum from humans in vitro. Subsequent to this, P. falciparum was subcultured through almost three cycles in vitro, during which multiplication of the parasite was obtained in the first but maintenance or only slight increase in numbers was obtained in the second subculture. The effect of sera from adult Gambians on the reinvasion of P. falciparum was measured in vitro both morphologically and by the incorporation of [14C]isoleucine into parasite protein and by the incorporation of [3H]adenosine into parasite DNA and RNA. Two sera reduced the amount of reinvasion.

It is usual, when considering the trichostrongyle infections of sheep, to refer to parasitic stages in the host and free-living stages on pasture as two separate entities with ecological, structural and physiological differences emphasized by their temporal relationship. They are, however, interlinked phases in a continuous exchange process in which the host acts as a vehicle. The role of the host as a mediator in this exchange has received little attention until recently and has been mainly restricted to a more dynamic approach to problems of immunity. The behaviour of the host, as well as that of the parasite, is obviously of great importance, but there has been little work on the behaviour of sheep in relation to patterns of helminth infections, although Taylor (1954) discussed the problem in general terms.

1. A technique is described for the preparation of axenic cultures of protoscolices of Echinococcus granulosus.

2. Protoscolices removed aseptically from hydatid cysts are treated with 0·02% crystalline pepsin at pH 2·0 for 10 min. at 38°C. in order to remove (a) daughter cyst germinal membranes, and (b) dead or degenerating protoscolices.

3. Protoscolices may be maintained for more than 100 days in a variety of media. These include media containing various proportions of some of the following: chick embryo extract, beef embryo extract, hydatid fluid, bovine amniotic fluid, Parker 199, bovine serum.

4. 10–20 ml. of culture media was used at 38°C., either in roller tubes or shaken in a water-bath. Media were renewed every 48 hr.

5. Protoscolices developed into cysts by two routes, either (a) by becoming vesicular, gradually growing in size, and finally becoming enclosed in a laminated envelope, or (b) by forming a ‘posterior bladder’ which became relatively enormous and ultimately absorbed the scolex region, the whole forming a cyst within an envelope as in (a).

6. In the majority of media, after about 31–48 days' culture, a thin envelope was secreted which developed later into a thick laminated membrane.

7. Cysts with laminated membranes ultimately underwent fatty degeneration and became cytologically abnormal.

8. In the most successful experiments, cells or clusters of cells formed within the cysts and these may have represented the anlagen of the protoscolices.

9. In no case was segmentation, or any other sign of strobilar development, obtained.

10. These results show that the laminated membrane in E. granulosus is initially of parasite origin and not of host origin as believed by some workers to be the case.

11. Since there is evidence from the literature that E. multilocularis does not form such an envelope in vitro, a clear developmental difference appears to exist between the two species.

12. It is suggested that this difference offers an explanation for the formation of unilocular or multilocular cysts. Since E. granulosus secretes a laminated envelope, its development is limited to a single or unilocular type of cyst. In the case of E. multilocularis no such limitation occurs, so that the invasive multilocular type of cyst could more easily develop.

Dynamics of natural populations of Schistosoma mansoni were studied during 8 consecutive years among Rattus rattus populations from 8 transmission sites of the marshy forest focus of Guadeloupe (French West Indies). The schistosome population is over-dispersed (k = 0·119) within the murine hosts and ecological factors linked to the patchy environment may be responsible for such aggregated distribution. Analysis of the spatio-temporal variations in prevalences, intensities and abundances showed limited variations of the infection during the 8 years at the level of the whole parasite population but great spatial heterogeneity at the level of local schistosome populations. Inter-populational genetic variability linked to the degree of adaptation of this human parasite to the murine host may explain differences in transmission dynamics between the local populations of S. mansoni.

Infection with Schistosoma haematobium was studied in a rural community of approximately 500 persons in eastern Zimbabwe. The overall prevalence of infection, as determined by urine egg counts, was 40·1%, and of heavy infections (≥ 50 eggs/10 ml urine) was 11·0%. The prevalence of both heavy and all infections was highest in the 8 to 10-year-old age class. During 1987–88 data were obtained from 102 individuals on intensity of reinfection 14 weeks after treatment with praziquantel, the efficacy of treatment having been determined after 4 weeks. The water contact made by these individuals during 2-week periods immediately following treatment was recorded. The relative abundance of patent infected intermediate host snails, Bulinus globosus, was also monitored. An index of exposure was developed which weighted each water contact by its duration, the type of activity, the time of day, and the abundance of infected snails at the site used. The relationships between rates of reinfection, rates of exposure, and age were examined. Although only 13 individuals showed positive rates of reinfection, there were statistically significant and independent effects of both exposure and age on reinfection rate. Quantitative estimates of reinfection rates suggested that individuals aged 12 years or less acquired substantially more infection (measured as egg output) than individuals more than 12 years old.

There is substantial evidence that host genetic factors play a major role in determining the outcome of infection with many pathogens. Detailed analysis of malaria has identified twelve genes that affect susceptibility in various human populations. However, less attention has been paid to other major infectious diseases where twin studies have identified an important host genetic component to susceptibility. Recent progress in the analysis of the human genome offers exciting prospects for the mapping and identification of new susceptibility and resistance genes for common infectious diseases. Screening of the whole genome in affected sibling pair studies is now feasible by employing highly informative microsatellite markers. In addition, many polymorphic candidate genes have become available for analysis in case-control studies. It is proposed that these new genetic tools offer a powerful approach to the epidemiological analysis of many infectious diseases in humans and supersede traditional genetic approaches to identifying susceptibility genes in mouse models. Progress in characterizing the role of major histocompatibility genes in susceptibility to malaria and other infectious diseases is reviewed before outlining the methodologies for and progress in identifying non-MHC susceptibility genes.

The paper describes a longitudinal field study of canine leishmaniasis in sympatric domestic dog and crab-eating fox (Cerdocyon thous) populations. Dogs were studied in house-to-house surveys, and foxes were studied by live-trapping and radio-telemetry. Because serological tests (IFAT in this case) for leishmaniasis are often of uncertain sensitivity and specificity, we draw conclusions comparatively. Both cross-sectional (age–prevalence) and longitudinal analyses indicate that incidence in dogs was highest in the dry season. Seasonal changes in the age–prevalence relationship for dogs suggest that serological conversion and recovery rates decline with prior exposure to infection, where ‘recovery’ may be due to loss of a positive antibody titre or death from leishmaniasis. The mean incidence in dogs was higher in the rural than in the urban population and higher in hunting dogs than pet dogs. Cross-sectional and longitudinal analyses of fox serological data suggest that foxes remain positive for longer than dogs on average, either because detectable antibody is more persistent or because they experience a lower mortality rate due to leishmaniasis.

Host-parasite interactions are an integral part of ecosystems that influence both ecological and evolutionary processes. Humans are currently altering environments the world over, often with drastic consequences for host-parasite interactions and the prevalence of parasites. The mechanisms behind the changes are, however, poorly known. Here, we explain how host-parasite interactions depend on two crucial steps – encounter rate and host-parasite compatibility – and how human activities are altering them and thereby host-parasite interactions. By drawing on examples from the literature, we show that changes in the two steps depend on the influence of human activities on a range of factors, such as the density and diversity of hosts and parasites, the search strategy of the parasite, and the avoidance strategy of the host. Thus, to unravel the mechanisms behind human-induced changes in host-parasite interactions, we have to consider the characteristics of all three parts of the interaction: the host, the parasite and the environment. More attention should now be directed to unfold these mechanisms, focusing on effects of environmental change on the factors that determine encounter rate and compatibility. We end with identifying several areas in urgent need of more investigations.

The relationship between the ciliated epidermal cells and the subepidermal layer of the miracidium of Fasciola hepatica has been described. Non-ciliated ridge-like extensions of the subepidermal layer separate the ciliated epidermal cells from each other. The sunken portions of the subepidermal layer, each containing a nucleus, lie below the outer body wall muscles of the miracidium and open into the ridge by narrow neck-like connexions. Elongate vesicles, which may be a source of stored plasma membrane similar to that which occurs in the transitional epithelium of other animals, fill most of the ridge. In addition, characteristic round electron dense granules are found in the ridge but the majority are found in the sunken portions of the subepidermal layer.

The development and origins of the tegument of the sporocyst of F. hepatica have been described at the ultrastructural level. When the miracidium is in the process of penetrating the snail host, large vacuoles appear between the ciliated epidermal cells and the basal lamina which overlies the muscles of the body wall. These vacuoles have the effect of loosening the epidermal cells from the basal lamina of the body wall of the miracidium. Possible mechanisms involved in the formation of such vacuoles are suggested and discussed.

During penetration of the snail the ciliated epidermal cells of the miracidium are lost; the ridge, a syncytial layer between the epidermal cells which is connected with the subepidermal layer, spreads over the basal lamina and exposed body wall muscles of the metamorphosing sporocyst to form the new outer covering of the sporocyst.

Cytoplasm passes from the subtegumentary layer into the tegument during this stage of the development of the body wall of the sporocyst. Muscular contraction and microtubules may be involved in the outward movements of this cytoplasm. The nuclei of the subtegumentary layer remain below the muscles of the body wall.

Twenty-four hours after penetration of the snail the outer plasma membrane of the tegument forms folds, which greatly increase the surface area.

Sixty hours after penetration involutions between the folds, which may indicate pinocytosis, are present, and it is suggested that pinocytosis may play a role in food absorption.

The fully formed tegument is a syncytial layer containing numerous electron dense granules, vacuoles, mitochondria and lipid droplets.

The results on the formation of the tegument of the sporocyst have been discussed with reference to the controversy about the origins and terminology of the outer covering of the Platyhelminths.

Trypanosoma brucei is exposed to the adaptive immune system and complement in the blood of its mammalian hosts. The aim of this review is to analyse the role and regulation of the proteins present on the external face of the plasma membrane in the long-term persistence of an infection and transmission. In particular, the following are addressed: (1) antigenic variation of the variant surface glycoprotein (VSG), (2) the formation of an effective VSG barrier shielding invariant surface proteins, and (3) the rapid uptake of VSG antibody complexes combined with degradation of the immunoglobulin and recycling of the VSG.