Trypanosoma (Megatrypanum) incertum Pittaluga 1905 was found in 33 out of 206 Pipistrellus pipistrellus caught at various sites in Britain. The trypanosome is described from blood smears. Development took place in laboratory-reared Cimex pipistrelli and Cimex lectularius. Epimastigote forms initially multiplied rapidly in the ventriculus and midgut of Cimex. Metacyclic trypanosomes were found in the rectum of both species of Cimex after 8 days when bugs were maintained at 20 °C and as early as 3 days at 30 °C. Electron microscopy of infected bugs revealed that there was no attachment to epithelial cells of the ventriculus or midgut, but within the rectum epimastigotes were attached by their flagella to the cuticle of the rectum by hemidesmosomes. Transmission was achieved by feeding experimentally infected bugs to bats kept in the laboratory. These bats were negative as judged by xenodiagnosis using laboratory-reared Cimex. Bats which had been caught in the wild demonstrated low-grade or sub-patent parasitaemias (positive in xenodiagnosis) for up to 400 days after the day of capture. Despite an extensive search of impression smears of tissues immediately after trypanosomes first appeared in the blood of experimentally infected bats no multiplicative stages were found.

Two groups of patients were examined for anti-Trypanosoma cruzi antibodies by immunofluorescence and ELISA (i) inhabitants of the village and surrounding rural area of Tibu, Norte de Santander, Colombia (n = 327) and (ii) employees of the Empresa Colombiana de Petroleos (ECOPETROL, n = 849). The latter group had a lower rate of positive serology (12 as compared to 29%) but the distributions of antibody titres were very similar in the two groups. A total of 119 serum samples (37 village and 82 ECOPETROL, including 25 seronegative controls) were analysed for their ability to immunoprecipitate the 7 major polypeptides of T. cruzi trypomastigotes of Mr > 72 kDa. Although 10 sera from positive patients showed no immunoprecipitation, all of the remaining positive sera contained antibodies which reacted with the 150, 90 and 85 kDa polypeptides. When the T. cruzi immunofluorescence positive, immunoprecipitation negative sera were retested by ELISA using GP90, all were negative thus suggesting that the patients had had a misdiagnosed T. rangeli infection. The new diagnosis was confirmed by immunofluorescence and ELISA with T. rangeli epimastigotes. Longitudinal studies were carried out on 19 patients from the ECOPETROL group for up to 3–5 years. Five seropositive patients showed a change in their anti-trypomastigote immunoprecipitation profiles over this period; one by loss of a previously recognized high molecular weight band and four others by conversion from a negative to a positive immunoprecipitation profile. These latter patients presented initially with uncomplicated T. rangeli infection but then acquired a T. cruzi superinfection. These patients represent the nucleus of a group in which prospective studies will identify the effect of T. rangeli infection on the course of subsequent South American trypanosomiasis and Chagas' disease.

Twenty-seven stocks of Nannomonas trypanosomes isolated from livestock in 1982 on a ranch at Kilifi on the Kenyan coast were characterized by isoenzyme electrophoresis and by the abilities of the parasite's DNA to hybridize to two repetitive sequence DNA probes. Allthe Kilifi stocks which were examined had isoenzyme patterns which were markedly different from the 75 patterns previously described from 78 stocks of Trypanosoma congolense. On average only 15% of the enzyme bands present in the Kilifi stocks were present in those stocks of T. congolense which had previously been surveyed for isoenzymes. The DNA from all the Kilifi stocks which had been examined for isoenzymes hybridized with only the repetitive sequence probe isolated from a clone of a Kilifi stock. In contrast, the DNA from all 27 Kilifi stocks failed to hybridize with a repetitive sequence probe isolated from a clone from a different stock of T. congolense. Thus, the trypanosomes in all the Kilifi stocks examined were both phenotypically and genotypically discrete. These genetically discrete trypanosomes have also been detected in 2 stocks isolated from livestock from another location on the Kenyan coast. The results show that there is a wide range of genetic heterogeneity within the trypanosomes currently classified as T. congolense. We suggest that the limits of this genetic heterogeneity could represent incipient speciation.

A total of 114 stocks of Trypanosoma congolense originating from Kenya, Uganda, Tanzania, Zambia and Sudan, but including, for comparison, stocks from The Gambia, Liberia, Ivory Coast, Nigeria and Cameroun, were compared by isoenzyme electrophoresis for 6 enzymes. The zymodemes were grouped, both from a dendrogram and using a cladistic method, after calculating the dissimilarity, or distance, between profiles. Previous observations are broadly confirmed, the zymodemes clustering separately according to geographical origin and ecological zone. Thus, one group was composed almost entirely of East African stocks, and another of stocks from both East and West Africa, although each group was of savanna origin. A third group was composed of stocks from the humid, rain-forest zones of West Africa, and was particularly characterized by isoenzyme variants of superoxide dismutase and glucose-phosphate isomerase. Two stocks from the Kenyan coast formed a markedly separate group, which may be taxonomically distinct.

The relationship between the density of lst-stage larvae of Elaphostrongylus rangiferi on the infection rate into the gastropod intermediate host, Arianta arbustorum, was studied experimentally. Within a range of densities between 30 and 1100 larvae/cm2 the experimental data gave a good fit to the conventional epidemiological assumption of direct proportionality between the net infection rate and the density of infective stages. The instantaneous rate of infection was estimated to be about 1 × 10−3/larvae/snail/2 h. At higher densities (> 1100 larvae/cm2) the instantaneous rate of infection showed a densitydependent decline.

The cercaria of Trichobilharzia ocellata finds and identifies its duck host with a seriesof different behavioural phases. Dispersal and selection of the water surface as microhabitat is achieved by an intermittent swimming behaviour, which is governed by the interplay of passive dropping with forward and backward swimming movements and includes a positive phototactic and a geonegative orientation. Then the cercariae tend to cling to the water surface in an energy-saving resting position. A movement towards the duck feet as the site of entry occurs when shadows evoke forward swimming movements, which are directed away from the source of light, i.e. normally downwards. Forward swimming movements are also stimulated by touch, but only in free-swimming cercariae and not when these are in the resting position. Attachments occur only when a substrate is touched during forward swimming movements. Attachments are stimulated by warm substrates (1 °C temperature difference triggers a nearly maximal response) and by chemical components of duck-foot skin, and the readiness to attach is increased when the forward swimming movement is started by shadow stimuli.

Trichobilharzia ocellata cercariae attach readily to the foot skin of their duck host, but poorly to preen-gland contents. The attachment to duck foot disappears when the skin surface lipids are extracted, and can be restored by reapplication of the lipids to the skin. Hydrophilic skin extracts are without any effect. Thin-layer chromatographic fractionation of duck-foot skin surface lipids reveals cholesterol and ceramides as attachment stimuli. A stimulation of cercarial attachment by these hydrophobic host signals is supported by the host identification pattern of the cercariae, which secures a close contact with encountered substrates.

Examples of the apparently stochastic nature of freshwater fish helminth communities illustrating the erratic and unpredictable occurrence and distribution of many species are provided for six species of fish from several localities throughout Britain. By focussing on parasite colonization strategies two categories of helminths are recognized: autogenic species which mature in fish and allogenic species which mature in vertebrates other than fish and have a greater colonization potential and ability. Three groups of fish are distinguished: salmonids, in which helminth communities are generally dominated by autogenic species which are also responsible for most of the similarity within and between localities; cyprinids, in which they are dominated by allogenic species which are also responsible for most of the similarity within and between localities; and anguillids, whose helminth communities exhibit intermediate features with neither category consistently dominating nor providing a clear pattern of similarity. Recognition and appreciation of the different colonization strategies of autogenic and allogenic helminths in respect of host vagility and ability to cross land or sea barriers and break down habitat isolation, and their period of residence in a locality, whether transient or permanent, provides an understanding of, and explanation for, the observed patchy spatial distribution of many helminths. Comparison with other parts of the world indicates that colonization is a major determinant of helminth community structure.

Trichinous mice were killed and their carcasses maintained at room temperature or subzero temperatures for varying lengths of time. Some worm parameters were measured after direct isolation from carcasses while others were measured following passage through a second round of hosts. Glycogen and trehalose levels in infective 1st-stage larvae (L1) isolated directly from carcasses maintained at room temperature were significantly less than controls (day 0) after day 4 post-kill (p.k.). By day 21 p.k. among L1 isolated directly from mouse carcasses those observed coiled or moving had decreased by around 20% compared to day 0 p.k. The percentage of L1 isolated from carcasses on several days p.k., used to infect mice and recovered as pre-adult worms declined significantly after they had remained in carcasses for 14 days. Only 2·6% of muscle larvae isolated from carcasses on day 21 p.k. and used to infect mice were recoverable as pre-adults. Pre-adult worms raised in mice infected with larvae from day 7 carcasses had about 50% less glycogen than worms raised in mice infected with larvae isolated from fresh carcasses (day 0 p.k.). The fecundity in vitro of adult worms isolated from mice on day 7 following infection with infective L1 larvae maintained in carcasses held at room temperature for 0–16 days declined only when adult worms developed from larvae recovered from carcasses at 3 days following host death. Following 24 h at temperatures below freezing, infectivity of L1 larvae isolated from frozen carcasses was reduced by 97%. Carbohydrate levels remained high in larvae from carcasses frozen for up to 4 days.

Two groups of H-2 congenic strains of mice were compared for their susceptibility to a primary infection with the nematode Trichuris muris. Mice of the BALB genetic background were markedly more resistant than mice of the BIO genetic background, as reflected by the rate of expulsion of T. muris from the large intestine. Within each of the two groups of H-2 congenic strains mice possessing the H-2k haplotype (BALB/k, B10.BR) were more susceptible to infection than mice expressing other haplotypes; B10 background strains expressing H-2b (B10) or H-2q (B10.G) alleles were the most resistant of the four congenic strains studied. Differential resistance was observed within three of the four BIO congenic strains and this is discussed in terms of rate of development of the protective immune response in relation to worm development. The results support the conclusion that both H-2-linked and non-H-2 genes play important roles in controlling the immune response which expels worms from the gut.

The first rigorous proof applicable to the migration pathway of an infective juvenile macroparasite inside its host is presented. Third-stage larvae of a homogonic strain of Strongyloides ratti applied in exact doses of less than 20 to the skin of the flank of young rats were recovered 16–40 h later in the naso-frontal part of the head. The peak proportion of the dose recovered between 20 and 25 h in this site had a mean value of 0·316 ± 0·021 in 48 animals. In 40 other rats infected simultaneously the mean proportion of the dose that reached the small intestine was at least 0·837+0·013. Proof resides in verification of the inequality > 1. With appropriate statistical tests the excess of the sum of the means of these two proportions over unity is shown to have a probability of occurring by chance of 1 in 3·5 × 106. Thus it is effectively certain that the naso-frontal portion of the head is part of at least one pathway taken by this parasite on its way from the skin to the intestine of its host. By suitable protection of the infection site it was confirmed that migration to the head was achieved by an internal route and not as a result of grooming. Larvae were recovered from the cranium in the same rats over the period 15–40 h, but the peak proportion of the dose occurred at 20 h, and < in this location. Whether the cranium is also part of the pathway is therefore still undecided. The significance of this novel analysis in the general context of in-host migration of infective stages is discussed and it is concluded, following its application to data sets from other authors, that the only cases in which proof can be demonstrated are the anterior skull of the rat for S. ratti (present data) and the lung of the same host for Nippostrongylus brasiliensis (Twohy, 1956).

Hookworm infections, as assessed by counting worms expelled following anthelmintic treatment and by egg output, were found to be of low prevalence and intensity in a South Indian fishing community. The initial overall prevalence of infection in the community was 43%, and the average burden was estimated at 2·2 hookworms per person. The age profiles of prevalence and intensity differed between males and females, with the latter harbouring significantly higher levels of infection. Children of both sexes under 10 years of age rarely harboured hookworms. Treatment with pyrantel pamoate was estimated to be 91% effective in clearing hookworm infections. Egg counts made on stools collected during an 11-month period of reinfection indicated that female patients became reinfected soon after treatment, while little hookworm egg excretion was observed in males during the observation period following treatment. Females acquired a significantly higher number of worms during the reinfection period compared with males, although the average burden in females reached only 28% of the initial, pre-treatment level. The hookworm population consisted of predominantly Necator americanus, and less than 10% of Ancylostoma duodenale. The parasites were highly aggregated within the host population with 10% of the community harbouring over 65% of the total hookworms. Low values of the negative binomial aggregation parameter, k, (indicating extreme over-dispersion) were recorded in groups stratified by age and sex. Highly significant positive correlations were observed between the initial (pre-treatment) and reinfection worm burdens of female (but not of male) patients. It is suggested that occupational practices related to walking through areas contaminated with hookworm larvae play an important role in generating the observed patterns of infection within this community.

Cerebral malaria in A/J and CBA/H mice infected with Plasmodium berghei ANKA is accompanied by mononuclear cell infiltration, haemorrhage and cerebral endothelial cell damage. This damage is presumably one of the causes of the breakdown of the blood—brain barrier which was detected by measuring the movement of the dye Evans blue and radioisotope labelled albumin and erythrocytes. The density of brain tissue, measured by a Percoll gradient technique, was significantly reduced in mice exhibiting cerebral symptoms, suggesting the occurrence of cerebral oedema.

Polychromophilus murinus, a malaria parasite of Chiroptera is reported from Myotis daubentoni in England. The vector was suspected to be the ectoparasitic Nycteribiid fly, Nycteribia kolenatii. N. kolenatii collected from wild-caught M. daubentoni were found to have oocysts on the midgut and sporozoites in the salivary glands. Wild-caught N. kolenatii were maintained on two wild-caught M. daubentoni harbouring heavy (patent) infections of P. murinus; both oocysts and sporozoites were found in these flies. The mature oocysts measured 52–71 μm in diameter. Sporozoites were straight or slightly crescentic and had a mean length of 7·4 μm. Electron microscopy of immature and mature oocysts revealed a morphology similar to that of malaria parasites. Sporozoites were also similar in structure to Plasmodium sporozoites and were found in the epithelial cells of the salivary gland and within the lumen; a cytostome was present and transverse sections revealed 21 microtubules arranged evenly around the periphery. Sporozoites were observed within the basement membrane of the salivary gland of N. kolenatii; such sporozoites appeared to be penetrating the gland, a process hitherto not described in malaria parasites. Rickettsia-like bodies were found within the cytoplasm of the epithelial cells of the salivary gland. Exflagellation of microgametocytes was achieved. An ultrastructural study of the gametocytes revealed a structure similar to that described in other Haemoproteidae. A common feature of infected erythrocytes was a projecting erythrocyte membrane. Attempts to find schizogony in impression smears and sections of tissues of two infected M. daubentoni were not successful.

Several species of malarial protozoans commonly parasitize the same host population and often the same individual host. This paper reviews the evidence for interactions among such host-sharing parasites. Field studies measuring the cross-sectional prevalence of malarial species often record fewer mixed infections than expected by chance, suggesting that one parasite has excluded another or suppressed its parasitaemia to undetectable levels. Prevalences may vary reciprocally between seasons, with one species increasing in prevalence while another decreases, despite parallel increases in the transmission rates of both, again suggesting suppression of one species by another. However, longitudinal studies of individual hosts indicate that malarial parasites may also favourably affect the host environment for each other, perhaps due to their depressive effect on the immune system: this is shown by the recrudescence of a latent malarial species immediately before or after the parasitic wave of another species. The suppression hypothesis is supported by data derived from the simultaneous inoculation of two Plasmodium species into laboratory animals; many studies have shown that one or both species are suppressed. This may be mediated by competition for host cells or nutrients, or by heterologous immunity. However, the suppressed species rebounds after the other species has abated, and may show a prolonged infection. Experimental evidence that one species can facilitate the recrudescence of another is minimal, but this may reflect the paucity of investigations of this phenomenon. Laboratory studies show only minor cross-resistance between host-sharing species, which is consistent with the hypothesis that their co-occurrence has led to antigenic divergence or that species showing strong heterologous resistance cannot co-exist in the same host population. Such complementarity occurs not only with the host immune response but also with many other life-history characteristics of host-sharing parasites, such as host cell preference. I conclude that malarial species have been important in each other's evolution, particularly in the tropics where multi-species complexes are common.