RNA with messenger activity has been extracted from both blood and culture (insect mid–gut) forms of Trypanosoma brucei and translated in a reticulocyte cell–free system. The products of this cell–free system have been compared, and many common polypeptides demonstrated. A major polypeptide of 58000–65000 molecular weight was made when both blood and culture from RNA was added to the cell–free system.

Antiserum raised against purified variant antigen from a cloned variant (MIAG 099) was used to detect specific products of this system. A major polypeptide of approximately 58000–65000 molecular weight was precipitated when the homologous trypanosome (MIAG 099) blood form RNA was used in the cell–free system. No such polypeptide was precipitated when RNA from a heterologous strain culture or blood form was used in the system. Competition experiments, in which excess purified variant antigen was added after incubation but before addition of specific antiserum, confirmed that the polypeptide of 58000–65000 molecular weight is the variant antigen.

Poly(A)–containing RNA from trypanosomes was shown to contain the mRNA for the variant antigen.

Relapse of infection after drug treatment of trypanosome infections under conditions precluding re-infection has usually been ascribed to drug resistance on the part of the parasite or to under-dosage of the drug. With Trypanosoma brucei infection in mice we have obtained evidence of another type of relapse. In infections resulting from the inoculation of 1 × 105 trypanosomes, derived from a stabilate T. brucei TREU 667, treatment with diminazene aceturate (Berenil) at 40 mg/kg at either 3 or 7 days after infection elicited a permanent cure. If, however, treatment was delayed later than 14 days after infection, then all the mice relapsed. These relapses generally occurred between 20 and 50 days after treatment, but some mice remained aparasitaemic for up to 60 days. The relapsed infections were apparently not due to the survival of ‘drug-resistant’ trypanosomes, as infections derived from a stabilate isolated from a relapsed Berenil-treated mouse were also permanently cured with Berenil if treated 3 days after infection; however, if treatment was delayed until 21 days post-infection, all the mice relapsed. The cause of relapse was not related to the number of parasites inoculated, as infection resulting from initial inocula of 1 × 105 to 1 × 108 trypanosomes were all cured if treated at 3 days after infection, and all eventually relapsed if treatment was delayed until day 21. This type of relapse phenomenon was not confined to T. brucei TREU 667 but also occurred with 5 other stabi-lates of T. brucei after Berenil treatment. Treatment of T. brucei TREU 667 infections with Ethidium and Prothidium at dose levels of 7.5 and 10 mg/kg respectively was also followed by relapse if treatment was delayed for 3 weeks after infection. The possible causes of relapse under these conditions, and its implications in the study of the natural disease, are discussed.

Chicks infected with the Weybridge strains of Eimeria maxima and E. acervulina were not protected by the normal levels of amprolium, but the sporulation of the oocysts was inhibited. With higher drug concentrations, fewer oocysts were produced. E. brunetti was not so markedly affected, although oocyst sporulation was reduced by the higher dosage levels. The effects were not enhanced by the inclusion of ethopabate.

With dinitolmide the phenomenon was not so marked, although oocyats of E. maxima and E. acervulina were reduced in numbers by the normal drug concentration and sporulation was reduced when this level was increased. Much higher drug levels were required to obtain these effects with E. brunetti. Monensin at 120 ppm affected neither oocyst numbers nor their sporulation in any of the species tested. The significance of the effects of anticoccidial drugs on gametogony and sporogony is discussed.

Eimeria acervulina var. diminuta was serially passaged 12 times in chicken embryos, but growth in cultured chick kidney cells was linmited to 2 generations of schizonts. After 7 embryo passages the sensitivities of E. acervulina var. diminuta and an embryo-adapted strain of E. acervulina var. mivati to the anticoccidial drugs amprolium, methyl parasites were sensitive to all the anticoccidials but E. acervulina var. diminuta was more sensitive to sulphaquinoxaline and amprolium. The chicken-maintained strain of E. acervulina var. diminuta was extremely sensitive to clopidol, sulphaquinoxaline and decoquinate. Electrphoretic analyses of several enzymes from E. acervulina var. diminuta revealed enzyme profiles with similarities and differences to the embryo-adapted strain of E. acervulina var. mivati.

During the course of a field study of coccidiosis in turkeys, Eimeria oocysts were found which had much smaller dimensions than any previously recorded isolate from the turkey. These oocysts were purified by single oocyst infection of a turkey. The first oocysts (mean dimensions 16.15 ×14.75 μm) were recovered 103 h later. Inoculation of between 0·5 and 2.5 ×105 oocysts of this isolate caused severe effects on body weight gain. Cross-immunity studies showed the parasite to be a strain of E. meleagrimitis. Electrophoretic analyses of two enzymes showed that the strain could be differentiated from another strain of E. meleagrimitis. (Weybridge strain B).

The results show that strain variation occurs within the species E. meleagrimitis and extreme caution should be used in identifying species of Eimeria from the turkey by their oocyst characters.

Activated oncospheres of Taenia ovis were incubated for 24 h or 48 h at 37.5°C in Medium 858 alone or in Medium 858 enriched with 20% lamb serum or foetal calf serum. Antigens contained in the supernatant medium from these incubations were concentrated, emulsified in Freund's incomplete adjuvant and injected intramuscularly into lambs. These lambs developed a very high level of immunity to subsequent challenge infection with T. ovis eggs.

As mice recover from infection with Babesia microti, abnormal forms of the parasite are present in some red cells. These forms are non-infective, indistinguishable by light microscopy from those present after treatment with amicarbalide, a babesicidal drug, and persist in splenectomized mice.

Electron microscopy confirmed that these abnormal forms are degenerating intra-erythrocytic parasites. In the absence of evidence for death of B. microti elsewhere in the body, it appears that infections of mice with this parasite are normally terminated by their death within circulating red cells. This has important implications for the mechanism of immunity to both this parasite and those Plasmodium spp. with which it cross-protects in this host.

Infection with the avirulent piroplasm Babesia microti in mice is accompanied by a marked depression in the ability of the mice to mount an immune response to sheep red blood cells. The period of immunodepression begins 3 days after peak parasitaemia and is maximal 4 days later. There-after, there is a slow return to normal immune responsiveness, correlated with the gradual disappearance of the parasites from the blood. Both IgM and IgG responses are depressed. Cell-mediated responses as determined by contact sensitivity to oxazolone and allograft survival are apparently unaffected. Phagocytic activity as measured by carbon clearance tests is increased, and is correlated with the parasitaemia.

Metacercarial cysts of Bucephalus haimeanus occur throughout the liver of Pomatoschistus microps, greater concentrations being found around the gall bladder, blood vessels and periphery of the liver. The cyst wall is composed of three layers, an inner granular, middle vacuolated and outer nucleated layer. The inner layer consists of three zones, an inner zone of irregularly compacted, granular material; a middle densely compacted zone and an outer moderately compacted zone. Vacuoles of the middle layer vary in appearance and appear to be discharging their contents into the cyst cavity. The cells of the outer layer are flattened and elongated with elongate nuclei but no other distinct organelles. Occasionally at the outer edge of the cyst are electron-dense cells which are in the process of degeneration. Only small amounts of collagen and very few leucocytes are associated with the cysts.

The cyst wall is carbohydrate in nature containing some free aldehyde groups, galactogen and neutral mucosubstances. The inner layer appears to consist of mainly acidic mucopolysubstances and weakly acidic sulphomucins. Large amounts of protein, carbohydrate-protein complexes and DNA are also present within the cyst wall. Alkaline and acid phosphatases, ATPase, β-glucuronidase and N-acetyl-β-glucosaminidase were detected. The origin and function of the cyst wall is discussed.

The desiccation survival of 4th-stage larvae of Ditylenchus dipsaci revived from dry worm aggregations (‘wool’ larvae) was compared with that of larvae extracted from narcissus bulbs (‘bulb’ larvae). Both sorts survived desiccation well, but ‘wool’ larvae survived desiccation at various humidities somewhat better than ‘bulb’ larvae. The rate of drying of the former was more rapid than that of the latter; the ability to control water loss, therefore, does not of itself ensure survival. The number of larvae reviving decreased with repeated cycles of desiccation and hydration, and also with the increase in the period during which the nematodes were kept dry. However, this was not associated with any loss of ability to control drying. The rate of drying of ‘wool’ larvae remained unaltered irrespective of previous desiccation treatment. In contrast, the rate of drying of ‘bulb’ larvae was more rapid after an initial desiccation with the result that ‘bulb’ larvae dried at the same rate as ‘wool’ larvae. While ‘wool’ and ‘bull’ larvae differed initially in both the rate of water loss and survival, a period of desiccation eliminated only the difference in water loss.

The results suggest that the rate of drying is dependent largely on physical factors. It was shown, however, that the cuticle of dead larvae was completely permeable to water in both directions. Therefore the ability to control water loss must, in some as yet unknown way, be connected with the nematode as a living system.

The number of adult Strongyloides ratti which developed in the guts of lactating rats after subcutaneous injection of 4000 L3 on day 18–20 post partum was taken to be a measure of the relative importance of alternative larval routes. When injection was carried out at different times before and after weaning, larvae were diverted from a route bypassing the gut in nursing mothers to one leading to the gut (‘migration reversal’) in mothers without young in a period of less than 10 h. Migration reversal was mostly completed in lactating females injected at the time of weaning when compared with nulliparous controls. A stimulus-sensitive period shortly after injection, predicted from these dynamics, was demonstrated. Worms injected into lactating females 10 h after removal from their pups showed complete migration reversal. In similarly treated rats, given 1 h suckling 3 h after injection, migration reversal was practically abolished. These inter-relationships, in conjunction with earlier findings, are used to deduce the possible humoral mechanisms involved and to develop a working hypothesis to account for larval orientation based on features of the mammalian pulmonary microvasculature.

Hymenolepis microstoma from secondary infections in mice were found to grow initially more slowly than H. microstoma from primary infections. Eventually a similar rate of growth was attained by both kinds of worm. After transplantation, young worms (≤4 days old) grew more slowly in previously infected than in naive mice. In contrast, 10-day-old worms grew equally well in naive or resistant mice. The administration of cortisone to mice during a secondary infection of H. microstoma inhibited the stunting of growth in young worms which were able to grow as well as those in a primary infection. The effects of the cortisone persisted for less than 4 days. Worms in a secondary infection given 4days after cortisone treatment were stunted in growth. These experiments suggest that the susceptibility of the worms to the resistance of the mouse applies to the first 4 days within the host. The loss or reduction of this susceptibility might be associated with the worms' entry into the bile duct which occurs 3–4 days after infection.

Filaroides hirthi lungworm infection was diagnosed by the recovery of 1st-stage larvae from the faeces of dogs with heavy, artificially induced infections using zinc sulphate flotation. Diagnosis of low-grade natural infections was infrequently achieved. Zinc sulphate flotation was demonstrated to be about 100 times as efficient as the Baermann technique in concentrating F. hirthi larvae from dog faeces. Larvae recovered from faeces proved to be infective when fed to a pup and it was concluded that F. hirthi infection can be transmitted directly and immediately by fresh faecal contamination. Mongrel dogs of diverse ancestry were readily infected by feeding 1st-stage larvae from lung tissue. This, F. hirthi infection was shown not to be limited to the Beagle breed by biological restrictions. The observations that 1st-stage larvae pass through the alimentary tract on their way out of the body and that larvae are found in the mesenteric lymph modes long after a single exposure to infection support the hypothesis that there is an autogenous re-infection of the host by a proportion of these larvae.