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Biomedical subjects

I Maudlin

Publications and source records attributed to I Maudlin.

At least 55 records · Page 3Linked to original sources
PubMed1990

The relationship between rickettsia-like-organisms and trypanosome infections in natural populations of tsetse in Liberia.

A survey of natural populations of tsetse flies for rickettsia-like-organisms (RLO) has been carried out in Liberia. A population of G.p. palpalis showed a strong association between trypanosome and RLO infection; both infections were at low levels in this species suggesting that this population is highly refractory to trypanosome infection. A small sample of G. nigrofusca, considered the most effective vector of trypanosomiasis in Liberia, was found to have very high prevalence of RLO infection. The selection pressures which could determine RLO infection rate are discussed.

Animals↗
PubMed1989

Rate of trypanosome killing by lectins in midguts of different species and strains of Glossina.

The activity of lectins in different species of tsetse was compared in vivo by the time taken to remove all trypanosomes from the midgut following an infective feed and in vitro by agglutination tests. Teneral male Glossina pallidipes Austen, G. austeni Newstead and G. p. palpalis R-D. removed 50% of all Trypanosoma brucei rhodesiense Stephens & Fantham infections within 60 h. A 'refractory' line of G. m. morsitans Westwood took 170 h to kill 50% infections while a 'susceptible' line of the same species failed to kill 50%. Agglutination tests with midgut homogenates showed differences between fly stocks which accorded with differences in rate of trypanosome killing in vivo. Flies fed before an infective feed were able to remove trypanosomes from their midguts more quickly than flies infected as tenerals. Increasing the period of starvation before infection increased the susceptibility to trypanosome infection of non-teneral flies. Teneral flies showed little agglutinating activity in vitro, suggesting that lectin is produced in response to the bloodmeal. Feeding flies before infection also abolished the differences in rate of trypanosome killing found between teneral 'susceptible' and 'refractory' G. m. morsitans, suggesting that maternally inherited susceptibility to trypanosome infection is a phenomenon limited to teneral flies. Electron micrographs of midguts of G. m. morsitans suggest that procyclic trypanosomes are killed by cell lysis, presumably the result of membrane damage caused by lectin action.

Agglutination Tests↗
PubMed1989

Lectin signalling of maturation of T. congolense infections in tsetse.

The process of maturation of Trypanosoma congolense Broden in tsetse has been shown to be initiated by lectin secreted in the fly midgut. In the present study the duration of lectin signal required to induce maturation was determined by the sequential addition or removal of a specific lectin inhibitor (D+glucosamine) to the diet of infected male Glossina morsitans Westwood. An established midgut infection of T.congolense was found to require, at most, 72 h exposure to midgut lectin to begin the process of maturation. Longer exposure to midgut lectin increased the frequency of maturation, suggesting clonal variation in response to lectin stimulation occurs within trypanosome stocks. It is suggested that this variation corresponds to differences in lectin binding sites on the trypanosome surface. Midgut trypanosomes retained their ability to mature throughout their life in the fly; when lectin activity in the midgut was inhibited, the trypanosomes remained as procyclic forms but when this inhibition was removed maturation was able to proceed. This indicates that the process of maturation is dependent upon a signal from the fly and is not predetermined by the trypanosomes undergoing a fixed number of division cycles. The possible role of lectins in the maturation of trypanosomes in vitro is discussed.

Animals↗
PubMed1988

Tsetse immunity and the transmission of trypanosomiasis.

Cyclical transmission of African trypanosomes - Trypanosoma congolense and subspecies of T. brucei - depends on their uptake by and development within their tsetse fly vectors. Tsetse susceptibility to such trypanosome infection seems to be controlled by maternally inherited rickettsia-like organisms (RLOs) (Fig. 1) and it now seems that the RLOs may exert this effect by controlling midgut lectins in the fly. Ian Maudlin and Susan Welburn explain the latest findings.

Journal Article↗
PubMed1988

An estimate of the size of the metacyclic variable antigen repertoire of Trypanosoma brucei rhodesiense.

A group of 27 variable antigen type (VAT)-specific monoclonal antibodies (McAbs) have been made against metacyclic forms of a cloned stock of Trypanosoma brucei rhodesiense. In combination, these labelled in immunofluorescence 99.3% of trypanosomes in salivary probes from tsetse flies. The 0.7% of unlabelled trypanosomes were believed to be uncoated forms. The ability of a mixture of antibodies to kill metacyclics in vitro by complement-mediated lysis, thus neutralizing their infectivity for mice, was tested. The antibody mixture consisted of 24 McAbs plus 3 VAT-specific rabbit antisera. In 12 replicate experiments this mixture of antibodies prevented infection of mice. Parallel controls showed that neutralization was probably antibody-mediated and VAT specific. However, we have not been able to repeat these results on a long-term basis; this may be due to a loss of neutralizing activity by one of the McAbs. The successful neutralization experiments indicate that the number of VATs in the metacyclic repertoire of one stock of T. b. rhodesiense is limited to at most 27.

Animals↗
PubMed1988

Fluorescein conjugated lectins identify different carbohydrate residues on Glossina peritrophic membranes.

Fluorescein-lectin conjugates were used as markers to determine the presence of surface carbohydrates on the peritrophic membranes of 6 Glossina species. Inter- and intra-specific variation in exposed carbohydrate residues was observed. Peritrophic membranes from non-teneral flies appeared to have less exposed surface carbohydrates than those of tenerals. Teneral G. m. morsitans susceptible to trypanosome infection had exposed carbohydrate residues recognised by APA lectin, but these residues were absent in a line of this species refractory to trypanosome infection. It is suggested that at least some of the surface carbohydrates of the peritrophic membrane bind endogenous gut lectin and parasite-surface carbohydrates may influence trypanosome development in Glossina spp.

Acetylgalactosamine↗
PubMed1988

The role of lectins and trypanosome genotype in the maturation of midgut infections in Glossina morsitans.

Feeding D + Glucosamine to Glossina morsitans throughout their life significantly reduced the proportions of midgut infections which developed into mature infections with three different stocks of Trypanosoma congolense. In one stock of T. congolense, maturation was completely blocked by this carbohydrate, which is known to specifically inhibit tsetse midgut lectin activity. Similar experiments with T. brucei showed that D + Glucosamine also inhibited maturation and, when combined with results from previous experiments with the same carbohydrate, indicated that lectin inhibition also had significant effects on T. brucei infections. It is concluded that midgut lectin secreted by the fly is responsible for triggering maturation of procyclic T. congolense and T. brucei. The maturation response of midgut trypanosomes to lectin stimulation varies between species and between stocks of the same trypanosome species, probably reflecting differences in numbers of lectin binding sites which are determined by trypanosome genotypes.

Animals↗
PubMed1987

In vitro cultivation of rickettsia-like-organisms from Glossina spp.

A method is described for the in vitro cultivation of the rickettsia-like-organisms (RLO) from Glossina spp. which are believed to be associated with susceptibility to trypanosome infection. Cultures of RLO were established by infecting a mosquito cell line (Aedes albopictus) with haemolymph taken from teneral flies. RLO from nine species of Glossina have been isolated and maintained in continuous culture using this technique.

Animals↗
PubMed1987

Lectin mediated establishment of midgut infections of Trypanosoma congolense and Trypanosoma brucei in Glossina morsitans.

D+Glucosamine, which has been shown in vitro to specifically inhibit tsetse midgut lectin activity, when fed to Glossina morsitans morsitans with the infective feed significantly increased midgut infection rates of Trypanosoma congolense and T. brucei rhodesiense. All flies infected with T.b. rhodesiense and maintained on a diet of blood with D+Glucosamine throughout their lives developed midgut infections. Midgut extracts from flies bred for refractoriness to infection with trypanosomes showed significantly greater erythrocyte agglutinating activity and were more trypanocidal in vitro than flies bred for susceptibility to trypanosome infection. It is concluded that susceptibility to trypanosome infection in tsetse is mediated through midgut lectins.

Agglutination Tests↗
PubMed1986

Extrachromosomal inheritance of susceptibility to trypanosome infection in tsetse flies. II. Susceptibility of selected lines of Glossina morsitans morsitans to different stocks and species of trypanosome.

Two lines of Glossina m. morsitans, selected for susceptibility and refractoriness to infection with a single stock of Trypanosoma congolense, have now been shown to be susceptible or refractory to different stocks of T. congolense and, also, to different stocks of T. b. brucei and T. b. gambiense. The mean midgut infection rates of the susceptible line obtained in different experiments with T. congolense, T. b. brucei and T. b. gambiense were, respectively, 66%, 56% and 55%; the corresponding mature (hypopharynx or salivary gland) infection rates were 37%, 23% and 0%. The highest mature infection rates obtained in individual experiments with susceptible flies were 65% (T. congolense) and 40% (T. b. brucei). Mean T. congolense and T. b. brucei midgut infection rates obtained with the refractory line were 29% and 33% respectively, the mature infection rates being 12% and 7%, all significantly lower than the corresponding rates in the susceptible line. Development of midgut infections in susceptible flies appears to take place irrespective of trypanosome stock or form. There is some evidence to suggest that higher infection rates can be obtained with flies infected and maintained on mammals rather than on in vitro feeding systems. Susceptible flies matured a significantly greater proportion of their midgut T. congolense and T. b. brucei infections than did the refractory line, which suggests that maturation of infections is influenced by the susceptibility status of the fly. However, the apparent inability of these flies to develop mature infections of a major T. b. gambiense genetic grouping suggests that maturation of infections established in the midgut is a phenomenon primarily associated with trypanosome genotype.

Animals↗
PubMed1985

The behaviour of trypanosomes within the midguts of wild-caught tsetse from Zimbabwe.

Trypanosomes infecting the midgut of wild-caught tsetse from Zimbabwe were found on electron microscopic examination to be penetrating the peritrophic membranes and so entering the ecto-peritrophic space in the mycetome region of the midgut. Other trypanosomes entered midgut cells, behaviour similar to that previously reported in laboratory-infected tsetse colonies.

Animals↗
PubMed1985

Extrachromosomal inheritance of susceptibility to trypanosome infection in tsetse flies. I. Selection of susceptible and refractory lines of Glossina morsitans morsitans.

Differences in susceptibility to infection with Trypanosoma congolense between F1 families of Glossina morsitans morsitans indicated that susceptibility is maternally inherited in this species of tsetse fly. Twelve F1 families, six selected for susceptibility and six selected for refractoriness to infection, have been bred for up to 13 generations. The reciprocal differences demonstrated in the F1 generation persisted in these selected families over many generations, indicating that susceptibility/refractoriness to T. congolense infection is extrachromosomally inherited in G. m. morsitans. Repeated 'backcrossing' to males of the opposite strain showed that infection rates within families were independent of the contribution of the male parent. Susceptible families had a mean midgut infection rate of 76.9% and a mature (hypopharyngeal) infection rate of 47.9%. In the refractory families 88.9% of the flies failed to develop an infection, 11.1% had midgut infections and only 6.3% developed mature infections. Levels of midgut infection remained remarkably constant within families over generations, whether refractory or susceptible, while maturation rates varied between generations and between sexes. Males matured a significantly greater proportion of midgut infections than females in the susceptible families. It is suggested that the inheritance of susceptibility/refractoriness relates primarily to the establishment of midgut infections in G. m. morsitans, and that maturation of midgut infections is dependent upon environmental factors such as diet, and differences between sexes probably reflecting differences in rates of bloodmeal digestion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗