The major pathways for cysteine catabolism in Hymenolepis diminuta have been investigated. The parasite has an active cystathionine-β-synthase and, as in other tissues, this enzyme has a wide substrate specificity. However, the enzyme from H. diminuta differs significantly from the mammalian enzyme in showing a high serine sulphydrase activity and a high serine lyase activity. There was only low γ-cystathionase activity in H. diminuta and again the enzyme showed a range of substrate specificities. Cysteine aminotransferase activity was readily demonstrated in the tapeworm, but there was no evidence for 3-mercaptopyruvate sulphotransferase activity. An oxidative pathway for cysteine catabolism in H. diminuta was shown by the presence of cysteine dioxygenase and cysteine sulphinate transaminase. The properties of the helminth cysteine dioxygenase were very similar to those of rat liver. H. diminuta was able to reduce cystine to cysteine via a glutathione-cysteine transhydrogenase system.

Parasitic helminths have an absolute requirement for carbohydrate for their energy metabolism, there being no significant contribution from fatty acid or amino acid catabolism. There is no significant synthesis of glucose or glycogen from non-hexose precursors in helminths and so they are dependent on dietary carbohydrate. Characteristically parasitic helminths break down glycogen or glucose via linear anaerobic pathways to give reduced organic end-products, usually acids such as lactate, acetate, succinate and propionate or more rarely alcohols such as ethanol, propanol and acetoin (Barrett, 1984).

Total DNAs, isolated from a range of taeniid cestodes (Taenia solium, T. saginata, T. pisiformis, T. crassiceps, T. hydatigena, T. ovis, T. multiceps and T. taeniaeformis), have been subjected to restriction enzyme digestion, Southern transfer and hybridization analysis using cloned fragments of the ribosomal RNA gene of Schistosoma mansoni. Substantial inter-specific genetic differences have been revealed on the basis of characteristic hybridization patterns for each of the taeniid cestode species. Furthermore, a random genomic DNA library has been constructed in the vector plasmid pAT153 using DNA extracted from a pig isolate (Indian origin) of T. solium. A panel of taeniid cestode DNAs including DNA from Echinococcus granulosus, has been used in conjunction with hybridization and restriction enzyme analysis to identify in the library a single recombinant plasmid with a T. solium-specific insert (coded pTS10) and two recombinant plasmids with T. solium inserts having selective specificities for T. solium and T. ovis (coded pTS17) and T. solium, T. saginata, T. ovis and T. multiceps (coded pTS28). These recombinant plasmids and the cloned fragments of the ribosomal RNA gene of S. mansoni have been used in restriction endonuclease, Southern transfer and hybridization analysis to detect intra-specific genetic variation in cysticerci of T. solium from India, Mexico and Zimbabwe. In addition, pTS10 and pTS17 have been used in a simple dot-blot assay to distinguish T. solium from T. saginata.

An official control programme against Echinococcus granulosus and Taenia hydatigena has been in operation in New Zealand for more than 28 years and against Taenia ovis for more than 18 years. This unique effort to control three metazoan parasites at the same time has led to a change from endemic to extinction status for E. granulosus but only a change from hyperendemic to endemic status for T. hydatigena and T. ovis. This has presented problems in determining the most cost-effective future control strategies. To facilitate this, a benefit/cost analysis of 20 options for the combined control of E. granulosus, T. hydatigena and T. ovis in New Zealand was undertaken. This showed that for E. granulosus a future change from the current non-targeted to a targeted approach is strongly indicated. For T. ovis 6 options were cost-effective using a discount rate of 10%. These were (1) a targeted control package using a vaccine in the non-targeted attack phase; (2) a targeted control package using a larvicide in the attack phase; (3) the transfer of all losses due to and responsibility for the control of T. ovis to the producer who administers a larvicide to sheep to be killed for dog food; (4) the transfer of all losses due to and responsibility for the control of T. ovis to the producer who administers praziquantel every 6 weeks to dogs; (5) and (6) two options involving the discontinuation of control. Control of T. hydatigena was assumed to be an incidental outcome of the policies for the other two parasites.

A general mathematical model of a vector-borne disease involving two vertebrate host species and one insect vector species is described. The model is easily extended to other situations involving more than two hosts and one vector species. The model, which was developed from the single-host model for malaria described by Aron & May (1982), is applied to the African trypanosomiases and allows for incubation and immune periods in the two host species and for variable efficiency of transmission of different trypanosome species from the vertebrates to the vectors and vice versa. Equations are derived for equilibrium disease prevalence in each of the species involved. Model predictions are examined by 3-dimensional phase-plane analysis, which is presented as a simple extension of the 2-dimensional phase-plane analysis of the malaria model. Parameter values appropriate for the African trypanosomiases are derived from the literature, and a typical West African village situation is considered, with 300 humans, 50 domestic animals and an average population of 5000 tsetse flies. The model predicts equilibrium prevalences of Trypanosoma vivax, T. congolense and T. brucei of 47·0, 45·8 and 28·7% respectively in the animal hosts, 24·2, 3·4 and 0·15% in the tsetse vectors, and a 7·0% infection of humans with human-infective T. brucei. The contribution to the basic rate of reproduction of the human-infective T. brucei is only 0·11 from the human hosts and 2·54 from the animal hosts, indicating that in the situation modelled human sleeping sickness cannot be maintained in the human hosts alone. The animal reservoir is therefore crucial in determining not only the continued occurrence of the disease in humans, but its prevalence in these hosts as well. The effect of changing average fly density on equilibrium disease prevalences is examined, together with the effect of seasonal changes in fly numbers on disease incidence. In a seasonal situation changes in fly mortality rates affect both future population size and infection rate. Peak disease incidence lags behind peak fly numbers, and that in the less favoured host lags behind that in the more favoured host. Near the threshold fly density for disease transmission disease incidence is more changeable than at higher fly densities and may even exceed equilibrium prevalence at the same average fly density (because most hosts are susceptible at the time that fly numbers begin their annual increase). The implications of the model for disease control are discussed. Identifying the precise role of the animal reservoir may suggest that treating such animals will achieve a greater reduction of human sleeping sickness than direct treatment of the humans alone. Statistically significant results of control campaigns may also be more easily shown by monitoring the non-human reservoirs. The model provides a means by which a correct perspective view can be obtained of the complex epidemiology and epizootiology of the African trypanosomiases.