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Following a period characterized by severe epidemics of sleeping sickness, restoration of effective control and surveillance systems has raised the question of eliminating the disease from sub-Saharan Africa. Given sufficient political and financial support, elimination is now considered a reasonable aim in countries reporting zero or less than 100 cases per year. This success may lead health authorities across the affected region to downgrade the disease from 'neglected' to simply being ignored. In view of the significant levels of under-reporting of sleeping sickness mortality in rural communities, this could be a short-sighted policy. Loss of capacity to deal with new epidemics, which can arise as a consequence of loss of commitment or civil upheaval, would have serious consequences. The present period should be seen as a clear opportunity for public-private partnerships to develop simpler and more cost-effective tools and strategies for sustainable sleeping sickness control and surveillance, including diagnostics, treatment and vector control. [ABSTRACT FROM AUTHOR]

In July 2000, Heads of State of the 36th Session of the Organisation for African Unity signed a potentially important declaration on African trypanosomiasis, urging member states “to act collectively to rise to the challenge of eliminating the problem through concerted efforts in mobilising the necessary human, financial and material resources required to render Africa tsetse-free within the shortest time possible”. To many, such an ambitious dream is received with some scepticism, recalling the doubts that surrounded a similar declaration signed in Brasilia in 1991, which paved the way for the Southern Cone Initiative against American trypanosomiasis (Chagas disease). True, the two diseases are quite different. But the operational challenges are quite similar, and there are sufficient biological parallels to suggest that the Latin American experience in controlling Chagas disease may provide a useful model for the control of African trypanosomiasis.

Trypanozooninfections are less likely to mature in female tsetse than in males. Analysis of maturation data from 37 trypanozoonisolates in Glossina m. morsitansshowed that while the proportion of mature infections (salivary gland infections as a proportion of established midgut infections) varied from isolate to isolate, the proportion of mature infections in female flies was consistently smaller than the proportion in male flies. The log of the probability of maturation in females is, on average, twice the log of the probability in males (estimate of the ratio of the logged proportions is 2.09, 95% confidence interval (CI) 1.8 to 2.5). Human serum-resistant isolates were less likely to mature than human serum-sensitive isolates (ratio of logged proportions maturing was 1.5, 95% CI 1.3 to 1.8, in both male and female tsetse). Data for four other trypanosome stocks show that the probability of maturation decreases as the maturation time (the delay between the infected bloodmeal and maturation) increases. The decrease is approximately exponential with twice the half-life in male flies compared to that in female flies (estimate of the ratio of the exponential parameters is 1.97, 95% Cl 0.7 to 3.3). A model is proposed to explain these observations which assumes that product(s) from an X-linked gene(s) kills or otherwise prevents migrating parasites from establishing a mature infection. Longer maturation times are associated with a heavy penalty in terms of transmissibility as measured by the vectorial capacity.

Removal of certain components from pig or cow blood greatly reduces the maturation rate ofTrypanosoma congolense infections inGlossina morsitans fed on such diets. In particular, delipidation of serum has the same effect as complete removal of dietary serum with few midgut infections reaching maturity. The addition of gamma-globulin to red cells partially restores the ability of immature infections to transform suggesting that serum lipids or other serum factors are not acting directly on midgut trypanosome metabolism but indirectly through interactions between dietary constituents and the flies' metabolic processes. As susceptibility toT. congolense infection is known to be maternally inherited inG. morsitans, it is suggested that serum factors act through the flies' symbionts to induce maturation in midgut infections.

The distribution of chiasmata in the mouse was examined by measurement of a single metacentric bivalent in 173 oocytes taken from 36 mice of the Rb3Bnr stock. Frequency distribution analysis revealed a well defined pattern of chiasma formation in both arms of the metacentric and, as in other organisms, interference and localization were thought to be major factors influencing this pattern. Despite the tendency for bivalents to form terminal associations at metaphase in the mouse and reported differences in chiasma frequency between early and late stages of meiosis, analysis of bivalents at diakinesis has produced no quantitative support for the concept of terminalization of chiasmata during meiosis.

Studies of some vector-borne diseases have shown genetic factors to be involved in the vector-parasite relationships and these results have often influenced measures taken to control such diseases. Novel methods of vector control have emerged from genetical studies, such methods having the dual advantages of being species specific and of causing little environmental damage. However, genetics has made little impact on trypanosomiasis research or control when compared with other vector-borne diseases, for reasons which are related to the biology of the tsetse fly and the trypanosome. Despite these natural limitations, genetical studies may yet provide useful information for those engaged in trypanosomiasis research. For example, chromosome and isozyme studies have shown that there is a large amount of genetic variation within tsetse populations, but it is not known whether such variation is related to the distribution of the disease. The infection rates of flies are known to vary between species and are dependent on fly-trypanosome interactions but it is not known whether these interactions have a genetic component. It is suggested that studies of the genetics of natural populations of tsetse, combined with selection experiments in the laboratory, could provide answers to these questions which might be of importance to control programmes and to studies of the epidemiology of trypanosomiasis.

The transmissibility of recent isolates of human serum-sensitive (HSS) and human serum-resistant (HSR) Trypanozoonwas compared by transmission of 37 stocks through an inbred line of Glossina m. morsitans. As in previous studies maturation was found to be dependent on fly sex with males producing significantly greater proportions of salivary gland infections than females. HSS stocks were, however, 1.8 times more likely to mature to mammalian infective form than HSR stocks in male tsetse and 2.7 rimes more likely to mature than HSR stocks in female tsetse. Infectivity to man has apparently evolved at the expense of transmissibility in tsetse, The likelihood of sexual processes occurring in Trypanosoma b. rhodesiensein wild flies is discussed.

Summary.Female mice, induced to superovulate, were injected subcutaneously with progesterone or oestradiol near the time when hCG was given. The incidence of polyspermy in first-cleavage embryos following mating or in-vitro fertilization was then determined. There were no detectable differences in the incidence or degree of polyspermy between treated and control in either the in-vitro or in-vivo groups, although the mean incidence of polyspermy was higher in vitrothan in vivo. Furthermore, there was no detectable acceleration of egg transport after administration of either hormone.

Summary.Eggs obtained from young virgin and aged parous female mice were fertilized in vitroto compare the incidence of aneuploidy in the resulting first-cleavage embryos. There was a significantly higher incidence of aneuploidy in the aged group (7·5% versus 3·3% and this was due solely to a higher proportion of trisomic female chromosome complements; there was no difference in the incidence of monosomics. These results thus suggest that non-disjunction occurs more frequently in eggs from older females, leading to the production of aneuploid embryos.

Summary.A dose–response relationship between the incidence of polyspermy and sperm concentration was found by analysing chromosome preparations of first-cleavage mouse embryos derived from fertilizations in vitrowith 3 concentrations of mouse spermatozoa (2 × 104, 2 × 10 6and 1 × 107/ml).

Summary.Analysis of the chromosomes of 1-cell mouse embryos fertilized in vitroshowed that the incidence of polyploidy is independent of both sperm and egg genotype. No significant differences were detected between groups of eggs from 5 strains of mice fertilized by spermatozoa from a single strain, TO, or between groups of (C57BL/10 × CBA) F1eggs fertilized by spermatozoa from 2 strains, CBA/H-T6 and TO, although there was significant heterogeneity between individual males in the latter set of experiments. While the majority of polyploids were triploids resulting from dispermic fertilization, some derived from diploid spermatozoa were also found.

Summary.Chromosomal analysis of first-cleavage mouse embryos obtained by fertilization of TO eggs with TO spermatozoa in vitrorevealed that the incidence of polyploidy was proportional to the dose of PMSG given to the donor females. The dose-response was shown to be linear, with the level of polyploidy rising from 8·0% with a PMSG dose of 1·5 i.u./female to 20·8% with 10·0 i.u./female. A total of 64 polyploid embryos was found among the 452 examined and in all cases the polyploidy was the result of polyspermy or fertilization by diploid spermatozoa.

CONSIDERABLE progress has been made in developing the formal genetics and cytogenetics of several insect vectors of disease1,2, notably with mosquitoes, houseflies and tsetse flies in which the polytene chromosomes provide suitable material for detailed analysis of chromosome morphology. The triatomine bugs (Hemiptera, Reduviidae) are medically important as vectors of Chagas' disease in the Americas, yet cytogenetic information on these insects is meagre3–8. These bugs present the same problems which, until recently, limited developments in mammalian cytology in that they possess a large number (typically 2n = 22) of small, almost indistinguishable chromosomes7. Further, since their chromosomes are also holokinetic9(that is with non-localised centromeres) they do not show any primary constrictions and it is correspondingly difficult to recognise arms of a chromosome which are readily seen in chromosomes of organisms possessing discrete centromeres. This difficulty with triatomine material has now been overcome by applying the Giemsa staining methods, which have been effectively developed by mammalian cytologists10–13, to embryonic cells of bugs with metaphase configurations. The technique I describe here makes possible the identification of individual chromosomes within the complements of different species of triatomine bug.

MILLIONS of cases of Chagas' disease exist in Central and South America1. Apart from being virtually incurable, a major problem in this disease is symptomless carriers harbour trypanosomes all their lives but it is often difficult to demonstrate the parasite2. At present, the simplest and most sensitive method of diagnosis3is to feed uninfected triatomine bugs on the suspected case and subsequently to examine a faecal sample from the bug for the presence of trypanosomes. There is, however, great variation both within and between species of Triatominae, in their susceptibility to infection with Trypanosoma cruzi (see, for example, refs 4 and 5), and though a genetic basis for this variation in susceptibility has been suggested4, it has not been verified. Obviously, the production of a highly susceptible strain of triatomine bug that would provide a quick and accurate diagnosis of chronic Chagas' disease would be a distinct advantage. I report here on the selection of both susceptible and refractory lines of Rhodnius prolixus, and the results of this selection programme are related to the genetic control of susceptibility to infection with T. cruzi.