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I Maudlin

Publications and source records attributed to I Maudlin.

At least 37 records · Page 2Linked to original sources
PubMed1996

The origins, dynamics and generation of Trypanosoma brucei rhodesiense epidemics in East Africa.

The history of sleeping sickness in East Africa has provoked controversy not only about the origins and spread of the disease, but also the identity of the causative organisms involved. Molecular methodology(1) has shed new light on the genetic makeup of the organisms involved in recent epidemics. Here, Geoff Hide, Andrew Tait, Ian Maudlin and Susan Welburn discuss these new data in relation to previous theories about the origins of epidemics in East Africa which emphasized the importance of the introduction of new strains.

Journal Article↗
PubMed1995

Trypanozoon: infectivity to humans is linked to reduced transmissibility in tsetse. I. Comparison of human serum-resistant and human serum-sensitive field isolates.

The transmissibility of recent isolates of human serum-sensitive (HSS) and human serum-resistant (HSR) Trypanozoon was 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 times 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. rhodesiense in wild flies is discussed.

Animals↗
PubMed1995

Trypanozoon: infectivity to humans is linked to reduced transmissibility in tsetse. II. Genetic mechanisms.

Trypanozoon infections are less likely to mature in female tsetse than in males. Analysis of maturation data from 37 Trypanozoon isolates in Glossina m. morsitans showed 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% CI 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.

Animals↗
PubMed1995

The 1901 uganda sleeping sickness epidemic revisited: a case of mistaken identity?

The great sleeping sickness epidemic that occurred in Busoga at the turn of the century was caused by a trypanosome identified by Bruce as Trypanosoma gambiense. A study of trypanosomes from the recent epidemic in southeast Uganda has shed new light on the origins of the disease in Busoga. Thorsten Koerner, Peter de Raadt and Ian Maudlin suggest that the epidemic of the turn of the century was of T. p. rhodesiense sleeping sickness, brought about then, as now by social upheaval.

Journal Article↗
PubMed1995

The kinetics of maturation of trypanosome infections in tsetse.

Estimates of the time delay between the infective bloodmeal and maturation (incubation or maturation time) for 4 trypanosome stocks (2 Trypanozoon and 2 Trypanosoma congolense) show that maturation time in tsetse is not a parasite species-specific constant. The mean incubation time of a Trypanosoma brucei rhodesiense stock (EATRO 2340 - 18 days) was not significantly different from one T. congolense stock (SIKUDA88 - 15.5 days) but was significantly greater than another (1/148 FLY9 - 12.5 days). There was no significant difference in incubation times between male and female Glossina morsitans morsitans for any of the stocks but in both of the Trypanozoon stocks the proportion of female flies producing mature infections was significantly less than in males. However, estimates of gene frequency, assuming a model in which maturation is controlled by an X-linked recessive allele, gave inconsistent results indicating that maturation cannot be controlled by a single sex-linked gene. Maturation was shown to be a tsetse sex-dependent phenomenon in Trypanozoon but not in T. congolense infections. Incubation time was quite variable even for a single trypanosome stock (e.g., standard deviation of 5 days for one Trypanozoon stock); we discuss how this variability can affect disease transmission, and the interpretation of age-prevalence data.

Alleles↗
PubMed1994

Epidemiological relationships of Trypanosoma brucei stocks from south east Uganda: evidence for different population structures in human infective and non-human infective isolates.

This study represents an analysis of trypanosome strains circulating within a confined location over a short period of time during a sleeping sickness epidemic in S.E. Uganda. A large number of Trypanosoma brucei isolates (88) were collected from a variety of hosts (man, cattle, pigs and tsetse) from villages within a 10 km radius and were analysed for variation in isoenzyme patterns, restriction fragment length polymorphism (RFLP) in repetitive DNA sequences and susceptibility to human serum. The human infective stocks form a clearly distinguishable population when compared with other stocks circulating in the domestic cattle reservoir. The data here support the occurrence of genetic exchange between the cattle stocks while an 'epidemic' population structure involving limited genetic exchange is a characteristic of the human infective stocks. Furthermore, it is shown that when both RFLP and isoenzyme analysis are carried out most stocks appear to have individual genotypes. Stocks which were formerly grouped as zymodemes are better considered as a collected of distinct individuals.

Animals↗
PubMed1994

Midgut lectin activity and sugar specificity in teneral and fed tsetse.

Midgut infection rates of Trypanosoma congolense in Glossina palpalis palpalis and of Trypanosoma brucei rhodesiense in Glossina pallidipes are potentiated by the addition of D+ glucosamine to the infective feed, but not to the levels of super-infection reported for G.m.morsitans, G.p.palpalis and G.pallidipes are shown to possess two trypanocidal molecules: a glucosyl lectin which can be inhibited by D+ glucosamine and a galactosyl molecule inhibited by D+ galactose. Addition of both D+ glucosamine and D+ galactose to the teneral infective feed promotes super-infection of the midguts of G.p.palpalis. The glucosyl lectin is specific for rabbit erythrocytes and is present in guts of fed G.m.morsitans and G.p.palpalis, titres of lectin activity do not increase substantially after the second bloodmeal. The galactosyl specific molecule does not show any erythrocyte specificity, although haemolytic activity is observed only in G.p.palpalis and not in G.m.morsitans. The presence of two trypanocidal molecules in some species of tsetse may account for the innate refractoriness of these flies to trypanosome infection. As D+ glucosamine also inhibits the killing of procyclic trypanosomes taken as an infective feed, it is suggested that the midgut lectin is normally responsible for the agglutination of trypanosomes in the fly midgut by binding to the procyclic surface coat, prior to establishment in the ecto-peritrophic space.

Animals↗
PubMed1993

Rickettsia-like organisms and chitinase production in relation to transmission of trypanosomes by tsetse flies.

Rickettsia-like organisms (RLO) from testse midguts and mosquito cell cultures showed high levels of endochitinase activity. A line of Glossina morsitans morsitans highly susceptible to midgut trypanosome infection and with high incidence of RLO infection showed significantly greater chitinolytic activity than G. austeni which had low RLO incidence and were correspondingly refractory to midgut infection. Midgut infection rates of Trypanosoma brucei rhodesiense in G. m. morsitans showed a dose-related increase when flies were fed N-acetyl-D-glucosamine (GlcNAc) in the infective meal and for 4 subsequent days. A model is proposed for susceptibility to trypanosome infection based on the generation of GlcNAc by RLO endochitinase activity in tsetse pupae inhibiting midgut lectin in teneral flies.

Animals↗
PubMed1992

The nature of the teneral state in Glossina and its role in the acquisition of trypanosome infection in tsetse.

Teneral Glossina morsitans morsitans from outbred and susceptible stocks infected with Trypanosoma (Nannomonas) congolense developed, respectively, three and six times higher midgut infection rates than flies of the same stock which had previously taken a bloodmeal. Non-teneral G. m. morsitans remained relatively refractory to infection when infected at subsequent feeds. Differences in susceptibility to midgut infection between teneral flies from susceptible and outbred lines of G. m. morsitans disappeared in non-teneral flies, showing that maternally inherited susceptibility to midgut infection is a phenomenon restricted to the teneral state of the fly. Laboratory reared G. m. morsitans were found to have become significantly more susceptible to trypanosome infection than wild flies from the population from which the colony was derived. The likely role of rickettsia-like organisms (RLO) in potentiating teneral susceptibility to midgut infection is discussed. The addition of the specific midgut lectin inhibitor D-glucosamine to the infective feed of non-teneral flies increased midgut infection rates to levels comparable with those achieved in teneral flies. It is concluded that the peritrophic membrane does not act as a barrier preventing non-teneral flies becoming infected. The relative refractoriness of non-teneral flies suggests that they do not play a significant part in the epidemiology of Trypanozoon or T. congolense infections.

Animals↗
PubMed1991

Trypanosoma brucei rhodesiense: characterisation of stocks from Zambia, Kenya, and Uganda using repetitive DNA probes.

We have previously described a system for characterising the relationships between trypanosome stocks of the T.brucei group based on Southern blotting with repetitive DNA probes followed by cluster analysis of resultant banding patterns (G. Hide et al. Molec. Bioch. Parasitol. 39, 213-226, 1990). In this study, we extend this analysis to examine the relationships between trypanosome stocks isolated from major sleeping sickness foci in Zambia, Kenya, and Uganda. We show that the trypanosome strains responsible for disease in Zambia are quite distinct from those sampled from the Kenya/Uganda foci. Furthermore, the human serum resistant stocks isolated from the Kenya/Uganda foci which were isolated from man (or from animals) were found to form a tight group in the cluster analysis, while stocks isolated from nonhuman sources in the same area or stocks from elsewhere were found in separate groups. Thus, the human infective trypanosome strains found in these foci may have common origins and have, perhaps, arisen by clonal selection from a common source.

Animals↗
PubMed1991

Rickettsia-like organisms, puparial temperature and susceptibility to trypanosome infection in Glossina morsitans.

Maintaining the puparial stage of successive generations of a population of tsetse 3 degrees C lower than normal reduced the numbers of rickettsia-like organisms (RLO) carried by emerging flies. The susceptibility of these flies to midgut infection with Trypanosoma congolense was also significantly reduced compared with control flies held at normal temperature. These results support the view that the relationship between RLO and susceptibility is quantitative-teneral flies with heavier RLO infections being more susceptible to trypanosome infection.

Animals↗
PubMed1990

Salivary gland infection: a sex-linked recessive character in tsetse?

Male tsetse, when infected in the laboratory with trypanosomes of the subgenus Trypanozoon, usually produce greater salivary gland infection rates than females of the same species. We show that a single sex-linked gene model can be fitted to most recently published data for salivary gland infection rates in tsetse. The maturation of Trypanosoma congolense infections is shown to be independent of fly sex. The possible effects of genetic control of maturation of Trypanozoon infections in tsetse populations on the transmission of sleeping sickness are considered.

Animals↗
PubMed1990

Banished bugs.

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Comment↗
PubMed1990

Identification of midgut trypanolysin and trypanoagglutinin in Glossina palpalis sspp. (Diptera: Glossinidae).

A midgut trypanolysin and an agglutinin from Glossina palpalis subspecies were isolated and partially characterized using anion-exchange chromatography and polyacrylamide gel electrophoresis. FPLC fractions of midgut extracts of Glossina palpalis palpalis caused agglutination and lysis of two trypanosome species (Trypanosoma congolense and Trypanosoma brucei brucei), although Glossina palpalis gambiensis caused only agglutination. The trypanolysin and agglutinin were active only in the posterior midguts, were heat labile above 50 degrees C, had a periodic cycle of 'activity' in response to bloodmeal intake and were not affected by protease inhibitors or trypsin but were inactivated by pronase. The lytic substance contained two proteins with approximate molecular weights (Mr) of 12,000 and 10,000 Da respectively. The agglutinin had an approximate Mr of 67,000 Da. Gamma-irradiation of the two subspecies caused a temporary inhibition of trypanolytic and agglutinin activities in midgut extracts.

Agglutination↗
PubMed1990

The possible role of Rickettsia-like organisms in trypanosomiasis epidemiology.

A simple model of human and animal trypanosomiasis is proposed in which the Ross equation for disease transmission is supplemented by a differential equation describing the inheritance of susceptibility in the vector. The model predicts an equilibrium state of balanced polymorphism for the fraction, theta, of susceptible tsetse and the occurrence of periodic epidemics at roughly the observed intervals. A loss of infectivity to tsetse of mechanically transmitted strains of trypanosome would seem to be a good evolutionary strategy for the trypanosome. The main implication for disease control is that measures initially reducing trypanosomiasis incidence could trigger off subsequent epidemics. Since theta leads incidence, monitoring theta could give several years advance warning of major epidemics. The model leads to oscillations in prevalence which are only lightly damped. Other mechanisms producing periodic epidemics would interact with this mechanism, and result in only one sequence of recurrent epidemics. With typical random variation of tsetse numbers about the seasonal norm the model shows the behaviour of a narrow-band system excited by broad-band noise, i.e. predicted trypanosomiasis incidence exhibits an undamped series of oscillations of variable amplitude and phase, similar to what is actually observed.

Animals↗
PubMed1990

Haemolymph lectin and the maturation of trypanosome infections in tsetse.

The tsetse immune system has recently been shown to be involved in trypanosome maturation; lectin secreted in the midgut, normally responsible for preventing the establishment of midgut infections, induces established midgut trypanosomes to mature. We now show that a second lectin, present in tsetse haemolymph, is essential to complete the maturation process. Interactions between tsetse lectins and parasite surface coats probably determine trypanosome transmissibility and may be partly responsible for the distribution of trypanosomiasis in Africa.

Animals↗