The behaviour of Eimeria acervulina in relation to macrophage activity in chickens was investigated by in vitro and in vivo techniques, with special consideration of the excystation of sporozoites and the fate of intact oocysts and sporocysts inoculated parenterally. In vitro: macrophages obtained from peritoneal washings phagocytosed mechanically released sporocysts or previously excysted sporozoites after 30 minutes incubation. In vivo: phagocytic activity of macrophages against intact oocysts and sporocysts in diffusion chambers implanted subcutaneously and intraperitoneally was observed as early as 4 h after implantation. Changes in the oocyst wall (corrugation, thinning, indentation and increased. fragility) as well as activation and excystation of sporozoites in situ was observed 24 h after implantation. Interaction in vivo between the invasive sporozoite and the phagocytic cell was recorded. Disintegration of the parasite was noticed 72 h after implantation.

Sheep in which abomasal fundic pouches had been made were infected with Ostertagia circumcincta (150000 larvae in one sheep, 100000 in three sheep). Subsequently studies were made on pouch secretion, food intake, plasma pepsinogens and abomasal pouch secretory responses when the sheep first ate. A functional abomasal lesion was apparent within 4 days of infection judged by the changes in plasma pepsinogen levels and the sodium concentrations of abomasal contents. Whereas the secretory activity of the abomasal fundic pouches (never exposed to parasites) was maintained or increased, the pH and sodium concentration of contents taken from the infected part of the abomasum were indicative of either a failure to secrete or of a permeability reabsorptive lesion. Ultrastructural studies demonstrated that parietal cells of the pouches had the appearance of cells subjected to strong secretory stimuli, but those of infected abomasa were similar to cells of gastric mucosa subjected to agents suppressing secretion. Factors which might operate, on the one hand, to stimulate secretion from separated fundic abomasal pouches, and on the other to inhibit or modify the secretory activity of the fundic mucosa of the infected abomasa, are discussed.

In a survey of animal trypanosomiasis in Musoma District, carried out in October and November 1970, 6344 G. swynnertoni were collected from six different localities of the Ikoma-Serengeti area and 623 G. pallidipes from Ikoma. These were dissected and examined for trypanosome infections. The mean infection rates of vivax-type in G. swynnertoni and G. pallidipes were 12.6% and 7.5%, respectively. The congolense group infection rates were 2.0% in G. swynnertoni and 1.8% in G. pallidipes. No salivary gland infection was encountered. The incidence of vivax- and congolense-type infections in general increased with age of both the tsetse species, suggesting that the latter can become infected with these trypanosome types at all ages. The infection rate among female tsetse was higher than among males in the six wing-fray categories. This was due to the slower rate of fraying of the wings with age of the former, so that at each wing-fray category the females were generally older than the males. Vivax-type greatly exceeded congolense-type infection rate in both G. swynnertoni and G. pallidipes. It is suggested that this probably reflects the known greater infectivity of the former group of trypanosomes to Glossina. It is concluded that in Ikoma, where game functions as the reservoir of animal trypanosomiasis and where infected tsetse are abundant, the domestic animals are exposed to a continuous trypanosome challenge.

Trypanosomes were isolated before and after the formation of infected detectable antibody from various brain sites and the blood of Microtus montanus. All isolates were serotyped by the agglutination reaction, and the isolates obtained prior to antibody formation were serologically identical to the original inoculum. Later isolates obtained from separate sites of an infected animal were serologically different from the original inoculum and also from each other. It was therefore concluded that in a single chronically infected animal there are numerous different antigenic populations of trypanosomes each occupying separate brain sites. A hypothesis to account for this antigenic diversity is given.

Lipid levels of infective larvae of Ancylostoma tubaeforme are reduced and their behavioural activity declines with age. We have measured behavioural activity using the percentage active, rate of activity, and the percentage of larvae able to penetrate a membrane. Neostigmine bromide, a cholinergic drug, increased larval activity in all tests. Larvae, stored at 4 and 10 °C and in hypertonic saline, were inactive but consumed lipid. When returned to isotonic saline at 26 °C, these larvae were no more active than those at 26 °C throughout. We found no evidence that such inactive larvae had entered a state of quiescence. All our results, and those of other workers, have been used to emphasize that larval ageing is related directly to decreased metabolic rates, and not primarily to lipid levels.

The encapsulation of Trichinella spiralis larvae in host striated muscle was studied.

Capsule formation starts at 13 days post-infection. Between days 20–50 p.i. the largest increase in capsule formation was observed. The capsule is exclusively, or almost exclusively, formed from and by the infected muscle fibre, as might be concluded from the presence of the sarcolemmal basal lamina surrounding the capsule substance during the initial stages of capsule formation. A collagen nature of the capsule cannot be excluded.

A study of electrophoretic forms of a selection of enzymes has been made in strains of subspecies of the rodent malaria parasites Plasmodium berghei and P. vinckei. Considerable electrophoretic variation of these enzymes occurred among the strains studied. On the basis of the results it was possible to identify groups of parasites within each species. While generally substantiating the classical taxonomy the identification of groups provided further information on the relationships between the subspecies.

Crosses have been made between two lines of Plasmodium berghei yoelii differing in drug-sensitivity and enzyme-type. The two lines used were line A, which is pyrimethamine-resistant and contains an electrophoretic form of glucose phosphate isomerase termed GPI-1, and line C, which is pyrimethamine-sensitive and contains enzyme-form GPI-2. Equal numbers of blood forms of lines A and C were mixed and injected intravenously into a mouse. Mosquitoes were fed immediately on the mixture, and the resulting sporozoites used to infect further rodents. After treating these animals with pyrimethamine, drug-resistant parasites characterized by GPI-2 could be detected in the remaining infections. Controls showed that these parasites were recombinant forms, which had arisen by cross-fertilization of gametes in the mosquitoes, and not by mutation or ‘synpholia’. By cloning the products of crosses between lines A and C by dilution, parasite lines of two recombinant classes (resistant GPI-2 and. sensitive GPI-1) were isolated, together with lines of parental characteristics.

The development of the epidermis of the oncomiracidium larva of Entobdella soleae was studied in embryos dissected from the egg and processed for electron microscopy. At first (7- to 8-day embryos at 15 °C) the embryo is covered with a nucleated primary epidermis of flattened cells which are closely associated with the viteUine cells and may take up nutrients from them. This layer is either replaced by or develops into the secondary epidermis which consists of ciliated cellular regions joined by an apparently syncytial interciliary cytoplasmic layer. Both ciliated cells and interciliary cytoplasm are at first nucleated but later both lose their nuclei. There may be a turnover of ciliated epidermal cells at the surface of young embryos. Between days 16–20 a discontinuous presumptive adult epidermis appears beneath the ciliated cells which has connexions to cell bodies lying in the parenchyma. This layer, apparently fuses with the syncytial (?) interciliary regions which have by this time lost their nuclei. After shedding of the ciliated cells, the presumptive adult epidermis spreads out to form a continuous syncytial covering to the post-larva. The ciliated epidermal cells apparently lose their nuclei between days 20 and hatching. This may be associated with the ‘programmed life’ of the ciliated cells. Details of the food reserves and morphology of the ciliated cells are discussed in connexion with the energetics of these cells.

Experimentally we have demonstrated what Lee (1969, 1971 a, b) postulated on the basis of morphological considerations. The female heterakid is capable of transmitting H. meleagridis from the bird to the caecal worm egg without the intervention of the male except for fertilization. If the male is otherwise involved in the transmission of H. meleagridis, it seems unlikely that its role is of appreciable significance in the life-cycle of the histomonad as we know it now. However, if as believed by many, the histomonad was originally a parasite of a nematode that may not have been an obligatory parasite, the role of the male worm may have been considerably more important to the survival of the histomonad.

Mouse peritoneal macrophage cells suspended in a TC 199 calf serum medium and cultured in Leighton tubes, were infected with Trypanosoma (Schizotrypanum) cruzi culture forms in order to study the development of this parasite in vitro. Three cycles of development were thought to occur: 1. Epimastigotes or trypomastigotes were taken up by macrophages and transformed into amastigotes. These multiplied by binary fission and ruptured the infected cell after 4‐5 days. Released amastigotes were taken up by uninfected macrophages and the cycle was repeated. 2. A small proportion of intracellular amastigotes developed into ‘ovoid forms’ which transformed progressively into promastigotes, epimastigotes and trypomastigotes. 3. Some amastigotes became ‘round forms’ from which sphaeromastigotes developed. These transformed directly into trypomastigotes without the formation of epimastigotes.

The effect of oxyclozanide (2,2′-dihydroxy-3,3′,5,5′,6-pentachlorobenzanilide) on Hymenolepis microstoma in the bile duct of mice, and H. diminuta in the small intestine of mice and rats was measured. Oxyclozanide at doses as low as 4mg/kg removed 13-day-old H. diminuta and caused no obvious harmful effect to the rat host up to the maximum level (256 mg/kg) tested. Worms were displaced and degenerating within 1 h. Results in mice were more difficult to assess because of the immune response, but similar total amounts of oxyclozanide caused destrobilation and loss of 7-day-old H. diminuta. Oxyclozanide was less effective against 21-day-old H. microstoma attached in the bile duct. Approximately half the strobila was lost following dosing at 5 mg/kg and progressively greater amounts as the dose level was increased. At 50 mg/kg worm loss commenced but even at 150 mg/kg 25 % of worms survived. The time taken to regrow to the original adult size varied but was complete within 7–9 days at levels up to 25 mg/kg. Double dosing at 5-day intervals did not enhance the effect of a single dose. The apparent existence of a sensitivity gradient down the strobila in H. microstoma is discussed.