A membrane-bound monoamine oxidase (EC 1.4.3.4) was demonstrated in homogenates of Hymenolepis diminuta. The enzyme oxidized a variety of biologically active amines (in decreasing order: dopamine, adrenaline, noradrenaline, tryptamine, tyramine, octopamine), there was, however, no activity with 5-hydroxytryptamine or benzylamine. No diamine oxidase (EC 1.4.3.6) could be detected in H. diminuta (using histamine, cadaverine or putrescine as substrates). The monoamine oxidase from H. diminuta was not inhibited by azide, hydroxylamine or semicarbazide, but was inhibited by cupferron, α-α dipyridyl and iodoacetamide, and by the specific monoamine oxidase inhibitors pargyline, nialamide and iproniazid. Several anthelmintics were also found to be inhibitors of monoamine oxidase. The possible roles of monoamine oxidase in H. diminuta are discussed.

Ten variants of phosphoglucomutase were detected by starch-gel electrophoresis in extracts of the tick Ixodes ricinus. Agreement of phenotype frequencies with those predicted by the Hardy–Weinberg model indicated that the enzyme is coded by a single gene locus (Pgm) at which 10 alleles are segregating. Allelic proportions in 5 Irish tick samples indicated that both spatial and temporal genetic differentiation exist. It is suggested that this polymorphism may be of use as a marker for studying the relationships of I. ricinus populations in Europe, as well as in taxonomic studies. A hypothesis is advanced which offers a possible adaptive explanation of the very high Pgm heterozygosity in tick populations. It is suggested that if kinetic differences exist between the various enzyme variants, the polymorphism may act to maintain an array of individuals in each population with varying developmental rates and longevities. Such a genetic strategy could be one factor which determines that the host-infesting seasons are spread over several months, thus ensuring maximum feeding and reproductive rates in each population.

Vitamins A, E and K were incorporated into turkey starter rations at normal (1×), 5× and 50× the National Research Council recommended vitamin levels and evaluated for their effect on histomoniasis in turkeys. Infected as well as comparable uninfected poults were included in all trials. Each vitamin was also evaluated at normal and 50× the NRC level in combination with ipronidazole, a low-level antihistomonal agent. In addition to performance parameters, glutamate oxaloacetate transaminase (GOT) and lactate dehydrogenase (LDH) plasma enzyme levels were used to evaluate the vitamin effect. None of the vitamins tested alone were found to be effective in terms of reducing mortality and morbidity following a severe Histomonas meleagridis challenge, regardless of the vitamin dose. A significant improvement in performance was demonstrated with the vitamin E (50×)–ipronidazole combination and a numerical improvement with the vitamin A (50×)–ipronidazole combination over ipronidazole alone or the poults fed NRC recommended vitamin levels. The GOT and LDH plasma enzyme levels correlated well with the progressive pathological changes associated with the disease. At 11 days post-infection both enzymes were consistently and significantly elevated above those of the uninfected controls, irrespective of the vitamin levels provided. The presence of low level ipronidazole in most instances delayed the onset of clinical symptoms and was associated with a delay in enzyme elevation, indicating the excellent correlation and sensitivity of the enzyme method in assessing liver damage.

N, N′-bis (3,4 ditrifluoromethylphenyl) methylmalonamide (Sch18545) completely controlled a mild Eimeria necatrix infection at 50, 40 or 30 p.p.m. in the diet, and controlled E. tenella infections at 50 and 40 p.p.m. Slight oocyst passage was observed at each E. tenella treatment level with a marked increase at the 30 p.p.m. treatment level. Fifty p.p.m. were necessary to control E. acervulina infections; levels of 40 p.p.m. reduced E. acervulina oocyst production while 30 p.p.m. were ineffective. Evaluations of Sch 18545 using a mixed infection (Coccivac D®) further suggested that activity with this compound was weakest against E. acervulina. Weight gains decreased with increasing concentration of drug in the diet of treated, infected birds and thus the compound showed an insufficient safety margin to be of practical value. Sch 18545 administered at 35 p.p.m. in the diet was effective against amprolium, zoalene, aklomide or nicarbazin-resistant strains of E. tenella.

Eimeria dispersa was isolated from young, intensively housed turkeys in Britain. The parasite has morphological features in common with those of the original description. At least two generations of schizonts occur before gametogony and one or two more schizont generations are concurrent with gametogony. Four generations of schizonts are needed to account for the observed reproduction index of 2·08 × 106/oocyst inoculated. The first oocysts were discharged by 105 h and these sporulated. within 30 h at 30 °C. A single dose of between 1 × 102 and 1 × 106 oocysts depressed body weight gain of 3-week-old poults and 2 poults died 6 and 12 days after receiving 1 × 104 or 1 × 106 oocysts. A single dose of oocysts protected against a challenge inoculation given 14 days later. Poultsimmunized against E. dispersa were resistant to challenge with a strain of E. dispera obtained from the United States. Electrophoretic examination of 2 enzymes from both strains of E. dispersa showed that they had similar mobilities. Attempts to infect chickens, guinea-fowl and Japanese quail with E. dispersa were unsuccessful. The strain of E. dispersa isolated here is best referred to as E. dispersa (Briston).

The frontal and sub-parietal glands of the pentastomid Reighardia sternae elaborate lamellate secretion which is poured on to the cuticle. The entire surface of the cuticle, including the mouth, hook pits and reproductive apertures, is coated with secretion. Electron microscope studies indicate that the glands are continuously active, which implies a turnover of surface membranes. The postulated function of these membranes is to protect certain vital areas of the host–parasite interface, notably the pores of ion-transporting cells, from the host immune response. The available evidence suggests that pentastomids do evoke a strong immune response but since most are long-lived they must circumvent it. We believe the surface membrane system to be instrumental in this. Studies on another pentastomid, Porocephalus crotali in rats have shown that an immune response stimulated by a primary infection will kill subsequent infections and that the surface membranes are strongly immunogenic. Obvious parallels between this situation and that of schistosome infections in mammals are discussed. An alternative explanation of concomitant immunity is proposed.

Common marmosets were shown to be susceptible to Plasmodium knowlesi malaria. The morphology of the parasite was indistinguishable from that observed in the natural host (Macaca fascicularis) and the common laboratory model (Macaca mulatta). A differential susceptibility to P. knowlesi was observed in the 8 marmosets studied. Multiplication rates of parasites were variable over 24 h periods. Five animals died of a fulminating infection within 12–17 days after challenge. Three animals recovered spontaneously from infection and were subsequently resistant to challenge with homologous and heterologous variants and strains of P. knowlesi. This resistance was maintained for intervals up to 100 days between challenge infections.

The effect was compared in CBA mice of adding Corynebacterium parvum, saponin, and Bordetella pertussis to living or killed Trypanosoma cruzi (Y strain) epimastigote vaccines on the induction of protective immunity against subcutaneous (s.c.) challenge with blood trypomastigotes. The addition of C. parvum to a low dose of T. cruzi vaccine, which alone was non-protective, generated a greater degree of protection than did saponin or B. pertussis. C. parvum alone increased resistance to infection to a variable and usually weak extent. The addition of C. parvum to larger doses of T. cruzi vaccine, which were themselves sufficient to elicit some degree of protection, improved resistance when the challenge was given 1 or 12 weeks after immunization, but lowered it at 3 weeks. It is concluded that the comparative efficacy of adjuvants for T. cruzi vaccines needs to be assessed on 3 parameters: (1) the dose of antigen, (2) the dose of adjuvant and (3) the time interval between immunization and challenge.

The uptake of bloodstream forms of Trypanosoma cruzi, Y and CL stocks, by mouse peritoneal macrophages and their intracellular differentiation and multiplication has been compared in vitro. After 48 h the number of macrophages showing intracellular amastigote forms was higher when the Y stock was used. The number of parasitized cells increased with the time of contact between parasites and macrophages. Prior treatment of the parasites with anti-T. cruzi antibodies and/or complement increased the number of infected macrophages, but did not interfere with their subsequent differentiation within the macrophages. The number of parasitized cells was greater when macrophages were obtained from mice previously treated with lipopolysaccharide, peptone or thioglycollate. Uptake was not appreciably affected when macrophages were pre-treated with trypsin or anti-macrophage serum, or when the parasites and macrophages were incubated in the presence of cytochalasin B. In the same experimental conditions, epimastigotes of T. cruzi were not able to differentiate into amastigotes. Their uptake was potentiated by previous treatment with specific antibodies and/or complement and was blocked by cytochalasin B. These results confirm that epimastigotes derived from T. cruzi cultures are phagocytosed and suggest that bloodstream forms penetrate actively into macrophages.

Uptake by the tegument of metacercariae of Bucephalus haimeanus of both particulate material and small molecules in solution is demonstrated by the use of electron-dense tracers and autoradiographic techniques. Ruthenium red (RR) uptake involved pinocystosis and the formation of large, electron-lucent vesicles in the outer cytoplasmic tegument. RR lost its association with these vesicles and became freely dispersed within the cytoplasm as it passed through the outer cytoplasmic tegument, down the cytoplasmic bridges and into the tegumental cell bodies. Ferritin, iodinated insulin and iodinated human serum albumin were also located within the outer cytoplasmic tegument and ferritin collected beneath the inner plasma membrane of the outer cytoplasmic tegument. Horseradish peroxidase was not absorbed by the tegument although it bound strongly to the outer surface of the metacercariae. C-labelled glucose, phenylalanine, tryptophan and tyrosine were all detected in the outer cytoplasmic tegument.