The DNA content of Plasmodium falciparum gametocytes during intra-erythrocytic development and during gametogenesis was established by cytophotometric methods. Intra-erythrocytic micro- and macrogametocytes (Stage I-Stage VB) contain about twice the amount of DNA of haploid sporozoites and ringstages, indicating that DNA is synthesized during transformation of ringforms into Stage I gametocytes. Microgametocytes, after activation at pH 8, rapidly duplicate their genome several times, while the DNA content of macrogametocytes remains constant during gametogenesis.

Infection with Plasmodium vivax was established in splenectomized Callithrix jacchus marmosets by inoculation of parasitized blood from Aotus trivirgatus carrying the Vietnam Palo-Alto line of P. vivax. Subsequent blood passage through intact marmosets resulted in higher peak parasitaemias (about 1% of red cells infected) and the loss of stainable Schüffner's dots in infected cells. Primary infections with the adapted line were patent for 74 days or more, and induced both a substantial antibody response, as determined by indirect fluorescence, and some lymphocytosis, but no marked anaemia. Marmosets which had recovered from their primary infection (or in which it was drug-cured) suffered abbreviated patency with low-grade parasitaemia on re-infection.

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.

The proportion of blood meals taken on humans which are infectious to mosquitoes in the Madang area, Papua New Guinea was estimated by two methods. In the first, laboratory reared Anopheles farauti were fed on individuals of all ages at village surveys. The results showed that 3·8% of people were infectious and that the mean percentage of mosquitoes which became infected by feeding on these people was 37·9%. From the average proportion of mosquitoes infected, the probability that a mosquito feeding on a human would pick up infection was 0·013±0·005. In the second approach mosquitoes were fed on identified Plasmodium falciparum, P. vivax and P. malariae gametocyte carriers. The results indicated that 46% of gametocyte carriers were infectious and that the mean probability of a mosquito becoming infected after feeding on a gametocyte carrier was 0·151±0·029. Gametocyte prevalence rates in all ages measured over 18 months in three villages averaged 3·3% P. falciparum, 4·0% P. vivax and 0·7% P. malariae, totalling 8·0±0·7%. Combining gametocyte prevalence rates with the probability of a mosquito becoming infected from a gametocyte carrier, the probability of a mosquito becoming infected following a blood meal on a member of the human population was estimated to be 0·012±0·003.

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.

The homoxenous flagellate Blastocrithidia triatomae disturbs excretion in Triatoma infestans. During the first 4 and 24 h after feeding, infected 5th instars excreted approximately a 2·5-fold smaller volume of urine. Consequently, about double the normal volume of haemolymph could be obtained from these infected bugs 24 h after feeding. Surprisingly, the in vitro secretion rates of Malpighian tubules from uninfected and infected bugs were nearly identical. In addition, the storage and release of diuretic hormone in infected bugs was sufficient to induce normal secretion rates by isolated Malpighian tubules. Therefore, the previously observed ultrastructural alterations in the upper Malpighian tubules of infected bugs do not result in a disturbed in vitro secretion, although in vivo excretion is reduced.

This paper describes a compartmental model incorporating biological details of the transmission of canine visceral leishmaniasis in southern France. In contrast to earlier, empirical models (Jolivet, 1977; Rioux, Croset & Lanotte, 1977) the new model (1) predicts a threshold density of sandflies below which transmission cannot be sustained, (2) suggests that, until better data become available, the maximum prevalence of infection obtained at high sandfly density should be considered an unknown quantity.

A new method of computing the infectivity index of microfilariae (mf) for the mosquito population is proposed using the estimated mf density distribution in the human population. The observed density distribution is considered a compound of the Poisson and the gamma distributions. The former distribution describes the probability of a specimen containing a specified number of mf and the latter describes the density distribution of mf in the host population. The mf infectivity index is the probability that a blood meal will include at least 1 mf, conditional on the population-density distribution of mf as specified by the gamma distribution. Actual data indicate that this population-density-based infectivity index can be considerably different from the conventional index based on the survey-density distribution. The level of the carrier rate of mf in a survey is greatly influenced, apart from the sample variation, by the average volume of blood taken from each person. The rate computed on the estimated population-density distribution of mf is convertible to any base amount of blood.

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 monoclonal antibody against the circumsporozoite proteins of the Plasmodium berghei sporozoite was used to trace the synthesis and expression of these proteins, via the Lowicryl immunogold technique, within the developing oocyst. The proteins were detected on the endoplasmic reticulum of the oocyst and were present in the sporozoite membranes at the point of their formation.

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.

To determine if, as is the case with Trypanosoma brucei and T. congolense, serodemes of T. vivax could be distinguished on the basis of immunity to the metacyclic stages of the parasite, attempts were made to immunize goats by infection with infected tsetse, followed by chemotherapy or eventual ‘self-cure’. Thirty goats were infected by tsetse with either clones or stocks of T. vivax from East or West Africa. Twenty-four goats were treated with diminazene aceturate (Berenil, Hoechst A.G.) 2–6 weeks after infection and 6 goats were allowed to self-cure. Infection, followed by treatment, induced immunity to a first homologous challenge by infected tsetse in only 2 of 24 goats (one immune to the East African stock, and the other to a clone of the West African stock). Immunity to a clone of the East African stock was induced in 3 or 4 animals after a second infection and treatment and in the fourth animal of the group following a third infection and treatment. One of 2 goats infected with the clone of the East African stock was immune to challenge at 16 weeks, following self-cure without treatment, and 1 of 4 goats infected with the parent stock was similarly immune when challenged at 40 weeks post-infection. Goats susceptible to infection with East African T. vivax showed evidence of partial immunity by delayed pre-patent periods and depressed parasitaemias after challenge. Goats infected with the relatively more virulent West African T. vivax were, however, completely susceptible to infection after homologous challenge, and showed only a slight delay in pre-patent period. A similar result was obtained in a further 8 goats primed and challenged by large numbers of tsetse (20 or 100 infected tsetse/goat) with the West African T. vivax. In further experiments using a very short treatment interval, infections following challenge were clearly shown to be the result of a lack of immunity rather than relapse following treatment. Lytic antibody activity to cultured metacyclic trypanosomes could not be detected during infection but such activity against bloodstream forms was detected after 2 weeks of infection. It is suggested that the primary reason for the erratic induction of immunity to T. vivax employing this methodology is the low number of metacyclics transmitted by infected tsetse, and thus poor antigenic stimulus encountered by goats upon tsetse challenge.

The differential permeability of cell membranes to various electrolytes and non-electrolytes represents one of the most fundamental characteristics of life. In the context of parasitology, differences in transport properties when parasite and host cells are compared represent an important avenue for chemotherapy. For example, a recent success in this area exploits the difference in nucleoside transport systems between host and parasite to produce combination therapy of Schistosoma japonicum by tubercidin and nitrobenzylthioinosine-5′-monophosphate (Elkouni, Diop & Cha, 1983). The morning session of this symposium was devoted to various aspects of membrane structure and function, particularly in the context of characterizing parasite transport systems. It is therefore probably worth while to present a simple classification of membrane transport systems, based on their complexity, and energy requirements. Table 1 summarizes the principal types of transport to be considered, starting with simple (Stokesian) diffusion. This will depend on permeant size, charge and lipid solubility. Classically, transmembrane transport of such molecules as aliphatic alcohols, ureas and small sugars has been studied, in simple systems such as the red cell (see Stein (1986) for references). In fact this route is important for intracellular delivery of a variety of hydrophobic molecules, for example phenylalanine benzyl ester transport as an antisickling agent (Acquaye, Young, Ellory, Grecki & Wilchek, 1983), or quin-2 and fura-2 for intracellular calcium measurements (Tsien, 1981).

The consensus view of biomembrane structure is outlined. The present model is built upon a fluid lipid matrix, usually two molecules in length, into which the proteins are embedded. The lipid bilayer organization is discussed, such as their phase transition and fluid character and the effect of cholesterol upon the chain organization. The non-lamellar arrangement which some lipids adopt is described. The use of new physical techniques for obtaining information about the structure and dynamics of membrane proteins are described. These techniques include electron diffraction, electron microscopy and FTIR spectroscopy. Models of the structures of the Ca2+–ATPase and the glucose transporter from erythrocytes are shown, indicating the putative helices embedded in the lipid bilayer and the groups of amino acids in the aqueous environment. These models are based upon biochemical methods to obtain amino acid sequences using DNA cloning techniques. Finally, an experimental method using triplet probes is described for the study of the rotational dynamics of membrane proteins. Labelled monoclonal antibodies for studying the dynamics of the glucose transporter have been used.

Two strains of Eimeria tenella with different decoquinate sensitivity and different glucose phosphate isomerase (GPI) isozymes were used in genetic recombination experiments: a line derived from a laboratory strain (NIAH) was decoquinate-resistant (DR) and had the isozyme GPI-9, while a field isolate (Iwate strain) was decoquinate-sensitive (DS) and had GPI-1. Coccidia-free chickens were orally inoculated with mixed oocysts of the two strains and parasites of the F1 generation were recovered. The F1 progeny showed both forms of the isozyme. Next, oocysts of the F1 progeny were passaged through chickens given the decoquinate-containing diet. The F2 progeny also had GPI-1 and GPI-9, indicating crossfertilization between the two strains. Six single oocysts were isolated from F2 progeny; 1 showed both phenotypes of GPI, 1 had GPI-1 and the remaining 4 lines had GPI-9. Analysis of the amount of GPI in recombinant oocysts suggested that the proliferation rate of the DR strain was slower than that of the DS strain. We concluded that GPI isozymes in E. tenella can serve as useful markers in experiments on chicken coccidia.

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.

Liver samples from 10 Schistosoma mansoni-infected baboons all yielded eggs but neither their egg counts nor duration of infection (< 226 weeks) correlated with the slightly elevated liver collagen levels or minimal histological fibrosis observed. Approximately 10% of inert 9 and 15 μm diameter microspheres injected into the mesenterio veins of 2 baboons with acute, challenge S. mansoni infection reached their lungs (mainly 9 μm microspheres). Lung egg recoveries over 1000 were significantly less common among 175 baboons exposed once to S. monsoni infections than among 56 baboons exposed more than once. Among 221 S. mansoni-and S. haematobium-infected baboons, female worm, total tissue egg and lung egg recoveries were significantly correlated with each other but not with liver or (where available) spleen weights. Liver and spleen weights were strongly correlated with total body weight. Baboons did not develop significant liver fibrosis, even after prolonged schistosome infections. However, some liver ‘leakiness’ developed during acute primary and challenge infections, allowing small inert particles and eggs to pass to the lungs, but this ‘leakiness’ was not associated with resistance to challenge. In contrast to mice, such resistance in baboons cannot, therefore, be explained simply in terms of pathological changes due to previous infections.