12570 Kock, M.D., Mullins, G.R. & Perkins, J.S., 2002. Wildlife health, ecosystems, and rural livelihoods in Botswana. Conservation medicine: ecological health in practice, eds Aguirre A.A. et al., Oxford University Press, 2002, pp. 265-275.
Kock: 19 Oat Street, PO Box 106, Greyton, South Africa. [mdkock@kings ley.co.za]
The wealth of biogeographical habitats in Botswana and the biodiversity that these habitats carry are under threat from the measures used to control foot-and-mouth disease, contagious bovine pleuropneumonia and trypanosomiasis. Issues include the increase in cattle numbers, erection of fences for disease control, elephant population growth, habitat degeneration, drought and deep borehole drilling. The three diseases mentioned above are discussed in more detail, in respect of the alternatives that may be available to current control strategies. Botswana is urged to adopt an integrated approach to conservation that includes consideration of societal values and human-well-being, but also of wildlife health and ecosystem stability.
12571 Mapaure, I. N. & Campbell, B. M., 2002. Changes in miombo woodland cover in and around Sengwa Wildlife Research Area, Zimbabwe, in relation to elephants and fire. African Journal of Ecology, 40 (3): 212-219.
Mapaure: Tropical Resource Ecology Programme, Department of Biological Sciences, University of Zimbabwe, PO Box MP 167, Mount Pleasant, Harare, Zimbabwe. [[email protected]]
One of the consequences of impacts of elephants and fire on woodlands is a change in woody cover, which often results in major challenges for wildlife managers. Changes in miombo woodland cover in and around Sengwa Wildlife Research Area (SWRA), in Zimbabwe, between 1958 and 1996 were quantified by analyzing aerial photographs. Woody cover in SWRA decreased from 95.2 percent in 1958 to 68.2 percent in 1996, with a lowest mean of 62.9 percent in 1983. The annual absolute rate of woody cover change in SWRA increased from -1.1 percent per annum between 1958 and 1964 to a recovery of 1.6 percent per annum between 1993 and 1996, while the annual relative rate increased from -1.1 percent per annum between 1958 and 1964 to 3.3 percent per annum between 1993 and 1996. There was a strong negative correlation between elephant densities and woody cover in SWRA, suggesting that loss of woody cover was mainly due to elephants. Woodland recovery after 1983 was due to reductions in elephant populations through legal and illegal off-take and reductions in fire frequency. Surrounding areas experienced less woody cover losses than SWRA, mainly due to tree removal by locals whose densities increased after the eradication of tsetse fly in the 1970s.
12572 Rogers, D.J. & Randolph, S.E., 2003. Trypanosomiasis control: surmounting diminishing returns - Response. Trends in Parasitology, 19 (3): 113-114.
Rogers: Department of Zoology, South Parks Road, Oxford OX1 3PS, UK. [[email protected]]
While wishing success to large-scale campaigns to eradicate vectors such as triatome bugs and the vectors of onchocerciasis, the perils of pursuing tsetse eradication in Africa should not be ignored. Malaria eradication in India was ultimately frustrated after enjoying initial great advances. The prospect of a total tsetse eradication scheme that fails and leaves behind massive debt is worrying. If control, not eradication, of tsetse is the only realistic long-term result, then current proposals (concerning operation, infrastructure and training) should be re-examined by PATTEC.
12573 Vinhaes, M.C. & Schofield, C.J., 2003. Trypanosomiasis control: surmounting diminishing returns. Trends in Parasitology, 19 (3): 112-113.
Schofield: London School of Hygiene and Tropical Medicine, Keppel Street, London WC1 E7HT, UK. [[email protected]]
There are parallels to be drawn between the control of American trypanosomiasis and of HAT, and these argue for the adoption of the Pan-African Tsetse and Trypanosomiasis Eradication Campaign. It is reported that the area targeted by the Southern Cone Initiative (of South America) is about 6 million km2 which is comparable to the 10 million km2 considered for tsetse control intervention in Africa. By attacking the vector, Chagas' disease Brazil and parts of Argentina, Paraguay and Bolivia. While differences in control techniques apply in the struggle against respectively the triatome vectors of disease and the tsetse for HAT, at least in the case of tsetse a variety of techniques are available. One of these, the SIT, is more effective at lower vector densities. Using these techniques against HAT, as urged by PATTEC, could have great political, social and economic benefits.
12574 Aksoy, S., 2003. Symbiosis in tsetse. In Insect Symbiosis, 53-63, eds K. Boortzis, K. & Miller, T.A., CRC Press Inc., Boca Raton, USA.
Aksoy: Department of Epidemiology and Public Health, School of Medicine, Yale University, New Haven, CT 06510 USA.
The following topics are treated: Characterization of tsetse symbionts; Evolutionary histories of symbionts; Genomics of the obligate symbiont Wigglesworthia; Genomics of genus Sodalis; Functional role of tsetse symbionts; Symbiont-host interactions; Symbionts as gene-expression vehicles; and Trypanosomiasis control and the impact of parasite refractory tsetse on disease transmission. It is considered that two aspects of the current SIT technology have the potential for improvement. The first is the development of parasite refractory strains, which would be of use as the mass release of sterile males could otherwise increase the chances of disease transmission. The second is the use of Wolbachia-mediated cytoplasmic incompatibility as a method of inducing sterility as an alternative to irradiation. The competitiveness of such males would be expected to be much greater than that of irradiated males, so that fewer insects would need to be released in SIT campaigns.
12575 Krafsur, E.S., 2003. Tsetse fly population genetics: an indirect approach to dispersal. Trends in Parasitology, 19 (4): 162-166.
Krafsur: Department of Entomology, Iowa State University, Ames, Iowa 50011-3222, USA.
Tsetse populations are distributed discontinuously, particularly the morsitans group. Dispersal among diverse populations cannot easily be measured directly because the geographical distances between them can be too great to have a reasonable expectation of recapturing experimentally released flies. Moreover, reproductive success of widely dispersed flies might be poor. The question of dispersal rates in tsetse is of immediate importance because area-wide eradication plans involving the sterile insect technique are under consideration. Dispersal and gene flow are important from evolutionary and historical viewpoints. An indirect method of estimating dispersal is to measure gene flow. Genetic data indicate surprisingly low rates of gene flow in the morsitans and palpalis groups studied to date. The underlying assumptions in making such estimates need to be examined carefully, however, before accepting firm conclusions, and further research is needed. Of particular interest is the question of tsetse adaptation to local environments.
12576 Bance, A.Z., Ouedraogo, A.P., Bauer, B., Kabore, I. & Sidibe, I., 2002. Efficacité du triflumuron selon la nature et la couleur du tissu Glossina palpalis gambiensis Vanderplank, 1949. [Efficacy of triflumuron related to texture and colour of cloth against Glossina palpalis gambiensis Vanderplank, 1949]. Insect Science and its Application, 22 (4): 281-287.
Institut de l'Environnement et de la Recherche Agricole (INERA), Programme Bovin, Farakoba, 01B.P. 910, Bobo Dioulasso 01, Burkina Faso.
The efficacy of triflumuron was tested on three types of textiles (cotton, polyester and polypropylene) of two colours (blue and black) for application in self-sterilization of Glossina palpalis gambiensis. Three concentrations of triflumuron diluted with water to 3, 6 and 12 percent were used to impregnate each type of cloth, and two groups of tsetse flies were contaminated. Females aged 20 days were directly contaminated by exposure to impregnated cloth; younger females (3-day-old) were contaminated during mating by males that had been treated like the older females. The blue and black-coloured cloths had no significant differences in terms of reproductive parameters (P<0.05). On the other hand, the type of fabric and the concentration of triflumuron had significant effects on the efficacy of the product. Cotton and polypropylene, impregnated with triflumuron diluted to 6 and 12 percent respectively, sterilized the old females for five consecutive reproductive cycles in respect of normal pupa production. The two concentrations also sterilized the younger females for three consecutive reproductive cycles with respect to pupal hatching. Polyester that had been impregnated with the same concentrations sterilized the old females during the three first reproductive cycles after treatment, and young females on two reproductive cycles.
12577 Bourn, D., 2002. Why tsetse won't future. Available as pdf file in Tsetse control: the next 100 years. Report of meeting organised by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Bourn: Environmental Research Group Oxford Limited, PO Box 346, Oxford OX1 3QE, UK.
We believe that eradication is unachievable in the foreseeable future for many reasons. Instead of eradication, we would favour extended or enhanced control. Factors to consider are the very large size of the affected land; the natural resilience of the tsetse populations; government departments' eradication schemes; unreliability of much basic information about distribution of the tsetse and the disease as well as present-day human settlement; the large areas set aside as nature reserves of various kinds that are currently sources of employment and foreign exchange; and the many other more pressing needs and priorities in rural development in Africa. The way ahead is to forget about eradication of tsetse and trypanosomiasis and think instead about enhanced and extended control of the vector. Future disease management strategies should encompass a broad range of control options for use in different circumstances: animal husbandry, management of risk, avoidance of areas where animals are at risk, breeding of animals that are tolerant, and drug use.
12578 Budd, L., 2002. Is tsetse eradication desirable or feasible? Available as pdf file in Tsetse control: the next 100 years. Report of meeting organized by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Budd: Mystole Farm, Canterbury, Kent CT4 7DB, UK. [LenBudd1@aol. com]
While the provision of clean water and good sanitation are two of the highest priorities, improving agricultural productivity does not come far behind these: all of these things have to be done. "Back-of-envelope" calculations suggest that trypanosomiasis is causing a loss to agricultural production worth US$4.75 billion per year; if trypanosomiasis can be controlled, this would translate into an annual increase in income of just under US$20 per person. Furthermore on animal welfare grounds, man has a moral duty to care for the animals with which he has been provided. One hundred years is an ambitious but not an impossible target to eradicate flies from Africa. There have been very few economic studies of tsetse control projects. Some studies have indicated good economic returns. Generally speaking there are significant economies of scale for larger projects. To the question "Is tsetse control the best strategy for taking forward the war against trypanosomiasis in the priority areas within the next 25 years?", the reply would be that addressing trypanosomiasis problem is desirable - even essential, that vector control is technically and economically feasible, and that PATTEC is an African initiative and justifies further support.
12579 Feldmann, U., 2002. [Statement on behalf of FAO and IAEA.] Available as pdf file in Tsetse control: the next 100 years. Report of meeting organized by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Feldmann: [[email protected]]
The speaker summarized recent developments relevant to the present debate. In September, November 2001 the IAEA General Conference and the FAO Conference respectively passed resolutions in support of PATTEC. A workshop was held at FAO Rome in early May 2002, which developed criteria and guidelines for prioritizing areas of joint international action against tsetse and trypanosomosis. Thirdly, the workshop validated two earlier identified projects namely one in the border zone between Burkina Faso and Mali and the other one in the southern Ethiopian area. The workshop concluded that both projects met all criteria and both projects deserve full international implementation support. Considering these criteria the partners in PAAT and PATTEC are now aiming at assisting member states to initiate international collaboration in identified priority intervention areas. The strategy will be based on the "area-wide integrated pest management" concept (area-wide IPM concept). IAEA and FAO support PATTEC. We regard that this initiative as a historical opportunity to sustainably address the major development problem in tsetse and trypanosomosis affected areas during the next decades. Other partners are very welcome to join and support both the planning and implementation of field activities and the harmonisation process, through targeted research and methods development and methods refinement, in-kind and financial support to member states, contributions to field interventions and support to related agricultural development.
12580 Getachew, T., 2002. Simple and cost effective technologies to tackle tsetse. Available as pdf file in Tsetse control: the next 100 years. Report of meeting organized by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Getachew: ICIPE, Addis Ababa, Ethiopia.
From our experience in tsetse control and doing other development activities in Ethiopia, we find we are working in often inaccessible areas of difficult terrain, with a high risk of re-invasion. We have to look for simple methods of killing this enemy. To do the job, what do we have in Ethiopia? It is locally available resources and materials. We don't have a lot of money resources, the farming communities. What we require is a simple and cost-effective technology. We shouldn't complex initially. If we have to use them later on technology we have in our hand and see the result. The job can be done using locally available material, at low cost, using a participatory approach and an ecologically-friendly technology and bottom-up approach. The farmers themselves have to decide what system to use.
12581 Hargrove, J. 2002. Tsetse eradication: necessity, sufficiency and desirability. Available as pdf file in Tsetse control: the next 100 years. Report of meeting organized by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Hargrove: 9 Monmouth Rd, Avondale, Harare, Zimbabwe. [john@ zappuz.co.zw]
Regarding the mechanisms of tsetse eradication, we may look back to a time before we had any insecticides. Potts and Jackson took 600 square miles of country and they organized hunters to shoot everything the size of an impala or bigger. Total game destruction was shown to be a sufficient method for eradicating closed populations of tsetse but Potts and Jackson thought it neither necessary nor desirable because bush clearing was, in the long run, cheaper and more effective. Nagupande in the Western part of Zimbabwe was the site of an experiment where only four species were shot: warthog, bushpig, bushbuck, kudu. Good control was achieved but it was not going to be sufficient for eradication, regardless of the desirability of the method. A ground-spraying trial with DDT was started and the results were so impressive that ground spraying started to become the mainstay of tsetse control in that part of the country; however to achieve eradication it was found necessary and financially worthwhile to use selective hunting as well. Attention then turned to the use of traps, a much improved method environmentally, but reinvasion remains a recurring problem. Modelling shows that if a control campaign such as aerial spraying over an area of 16 000 km2 leaves 16 flies behind, then unless there is a very high natural mortality rate operating, eradication will not result. Detecting the last few flies is in practice extremely difficult. Does SIT therefore have special merit to be included in the arsenal of control methods? Concerning ecological arguments, if you remove tsetse flies from an area you change the ecological balance and we have to be very sure in our own minds that the resulting land use change is going to be favourable. It is not always clear that clearing the land for cattle and crops is actually the best route. Issues such as aid for tsetse eradication have to be closely linked to the issues of human rights and good governance.
12582 Hargrove, J.W., Torr, S.J. & Kindness, H.M., 2003. Insecticide-treated cattle against tsetse (Diptera: Glossinidae): what governs success? Bulletin of Entomological Research, 93 (3): 203-217.
Torr: Natural Resources Institute, University of Greenwich, Central Avenue, Chatham, Kent ME4 4TP, UK. [[email protected]]
The distributions of insecticide-treated cattle from sites in Tanzania and Zimbabwe were assessed from interviews with livestock owners, analysis of secondary livestock data and mapping technologies. The time-course of tsetse control operations at these sites were then simulated using a mathematical model that assumed diffusive movement and logistic growth in fly populations. A simulation of a tsetse control operation in Mudzi district, north-east Zimbabwe, was in accord with observations that the use of insecticide-treated cattle was unable to prevent substantial re-invasion of tsetse from Mozambique, due to the patchy distribution of cattle. The simulation was also consistent with the observed efficacy of a 10 km wide barrier of insecticide-treated targets deployed evenly at 4 km-2. Simulation of a control operation on Mkwaja Ranch in Tanzania was in accord with the observation that the use of insecticide-treated cattle reduced the tsetse population on the ranch by c. 90 percent. Insecticide-treated cattle were used to better effect in the Kagera Region of Tanzania. Simulation of this operation predicts that the deployment of 35,000 treated cattle in the area would result in > 99 percent control of the tsetse population, consistent with the observed decline, by 1-2 orders of magnitude, in cases of trypanosomiasis in the region. The greater success of the Kagera operation was due to the size and shape of the treated area and, particularly, to the restriction of re-invasion to 20 percent of the perimeter, compared with >80 percent on Mkwaja. Simulation was used to assess how tsetse control could have been improved at Mkwaja. The results suggest that splitting herds into smaller, more numerous, units could have achieved some improvement but, in general, the disease problem would not have been solved by the use of insecticide-treated cattle alone. Only by deploying odour-baited targets in ungrazed areas, or in a 1-3 km barrier around the ranch, could substantially better control (99-99.9 percent) have been achieved. Sensitivity analyses of the Mkwaja simulation showed that the general conclusions were robust to assumptions regarding cattle distribution and the rates of fly movement and growth. Properly managed and appropriately applied insecticide-treated baits are powerful weapons for tsetse control but should not be used without regard to potential levels of re-invasion, taking into account the size and shape of the treatment area and the density and distribution of the baits.
12583 Kabayo, J., 2002. [Statement from the Commission of the African Union] Available as pdf file in Tsetse control: the next 100 years. Report of meeting organized by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Kabayo: PATTEC Co-ordinator, Addis Ababa, Ethiopia. [[email protected]]
Some advise that we should just sit tight and do nothing claiming that in time autonomous control methods will be activated by the environmental changes induced by man's activities and lead to the disappearance of tsetse flies. Some argue that trypanosomosis is not Africa's most urgent problem and point out that the PATTEC initiative will consume the resources that would be more urgently needed to solve more pressing problems. Some people have referred to the PATTEC initiative as a multi-billion dollar project doomed to fail. Some have tended to exaggerate and misrepresent the aims and plans of the PATTEC initiative making it all sound too complicated and unachievable. We have never claimed that we are going to tackle Africa's entire tsetse belt at a go, in one massive, ambitious, quixotic undertaking. We have never suggested that the PATTEC initiative is going to replace all other current and planned intervention schemes. We do not advocate the use of one particular technique. We believe that whichever cost-effective method, or combination of methods, is appropriate to achieve the desired objective of eradicating the disease should be used. Further, no one in Africa is looking for billions of dollars to spend on the PATTEC initiative. We believe that this plan is within the means of African countries to execute because it is based on the principle of biting what we can chew and chewing what we can swallow, one bite and one step at a time.
12584 Kanyari, P. W. N., 2001. Efficacy of Alphamethrin (Dominex®) pour-on in the control of bovine trypanosomosis. Bulletin of Animal Health and Production in Africa, 49 (2): 130-133.
Faculty of Veterinary Medicine, Department of Pathology, Microbiology and Parasitology, University of Nairobi, P.O. Box 29053, Kabete via Nairobi, Kenya.
At Kulalu region in the hinterland of the North Coast of Kenya, the effectiveness of alphamethrin (Dominex) pour-on against tsetse and trypanosomiasis was tested. From a herd of one-year-old heifers, 60 were randomly selected and assigned to two groups of 30. One group received the pour-on treatment, and the other remained as a control group. Pastures were shared by the two groups, but they were housed in separate sheds. Trypanosomiasis sampling was by means of ear-vein bleeding, followed by packed cell volume and buffy coat examination. Tsetse monitoring was by four biconical traps, that were odour-baited with acetone/octenol and p-cresol. Two trypanosomiasis cases were detected, only in the control group. Tsetse flies captured were mainly G. pallidipes (84.5 percent) and G. longipennis (14 percent); G. brevipalpis and G. austeni were also present. Tsetse number decreased, but other factors might have been involved.
12585 Maudlin, I., 2002. [Introduction to the debate "Tsetse control - the next 100 years.] Available as pdf file in Tsetse control: the next 100 years. Report of meeting organized by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Maudlin: Manager, DFID Animal Health Programme, Edinburgh, UK. [[email protected]]
Sleeping sickness has been described as a calamity. We thought we had conquered it in the 1960s, but it is now again a serious health problem in Africa. Up to half a million people are thought to be infected and it is believed to cause about a hundred thousand deaths a year. It is this calamitous situation that caused the PAAT programme to be set up and subsequently PATTEC: Pan African Tsetse and Trypanosomiasis Eradication Campaign. Following this declaration by the African Heads of State it came to the attention of a much wider public through the press. The press presented both positive and negative sides to the eradication debate. The purpose of the present meeting is to discuss these issues, essentially to allow technical experts and environmental experts, sociologists and economic experts to debate freely and transparently in public the pros and cons of the case.
12586 Schofield, C., 2002. Control of American vs African trypanosomiasis. Available as pdf file in Tsetse control: the next 100 years. Report of meeting organized by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Schofield: London School of Hygiene and Tropical Medicine, Keppel Street, London WC1, UK.
Control of American trypanosomiasis is relevant to African trypanosomiasis control: the basic operational concepts are very similar. Direct control of the infection in people or in animals is extremely difficult, but vector control will interrupt transmission, and local elimination is possible. All attempts to kill tsetse flies have worked, until they have stopped. The key problem in terms of feasibility is reinvasion. And so how can you address the question of reinvasion? Africa is very large, but so is the area within which American trypanosomiasis has been eliminated. Concerning the vectors, both tsetse fly and triatomine bugs are K strategists, they have low genetic variability and they are the most vulnerable targets that we can think of in entomological terms. Economic analyses have been done for American trypanosomiasis: predictions were outstripped by the economic returns eventually realized. Trypanosomiasis control is necessary. It is feasible for the simple reason that the biology and the genetics are amenable like no other target vector of any disease. Trypanosomiasis control will never be sustainable unless there is political commitment. We know this from Latin America. We have it also for Africa.
12587 Shaw, A., 2002. The arguments against tsetse eradication (an economist's view). Available as pdf file in Tsetse control: the next 100 years. Report of meeting organized by the DFID Animal Health Programme, 9-10 September 2002, Edinburgh, UK.
Shaw: [email protected]
Considering the question of continent-wide eradication, even with the 100 year scenario we are not covering our costs, if we allow for possible regression of the fly habitat. From an economic point of view, if we take a continent-wide approach, Pan- African eradication is not economically viable taken as a single project. However, we can get very respectable cost-benefit ratios if we target areas where the demand for tsetse control already exists; this has been demonstrated again and again for many successful control operations and localised eradication. Even in a very long-run scenario, we cannot justify appropriating such a huge chunk of scarce resources just for tsetse clearance if we are looking at it on a continental scale. Tsetse eradication considered as a single project does not perform acceptably on economic criteria, but clearly targeted tsetse and trypanosomiasis schemes are very profitable. Therefore we should move towards identifying profitable schemes which involve farmers and are in line with national poverty alleviation strategies.
[See also 26: nos. 12595, 12601]
12588 Laveissière, C., Garcia A. & Sané, B., 2003. Lutte contre la maladie du sommeil et soins de santé primaire [Sleeping sickness control and primary health care]. Publ. IRD, pp 243 [see extended summary in Section A].
12589 Waiswa, C., Olaho-Mukani, W. & Katunguka-Rwakishaya, E., 2003. Domestic animals as reservoirs for sleeping sickness in three endemic foci in south-eastern Uganda. Annals of Tropical Medicine and Parasitology, 97 (2): 149-155.
Katunguka-Rwakishaya: Faculty of Veterinary Medicine, Makerere University. PO Box 7062, Kampala, Uganda. [[email protected]]
The persistence of sleeping sickness (human African trypanosomiasis) in some areas of southeastern Uganda has necessitated further investigations, focusing mainly on domestic animals as reservoirs of this disease in three agroecological zones. The interzone differences in the prevalences of trypanosome infection among cattle (P < 0.001) and pigs (P < 0.001) were significant. Overall, 5.0 percent of the cattle, 13.9 percent of the pigs and 0.4 percent of the small ruminants investigated were found to be infected with parasites of the Trypanosoma brucei subgroup. The results of blood incubation infectivity tests (BIIT) indicated that all of the T. brucei-subgroup isolates from cattle in Kamuli district (zone I) were human-serum-sensitive. Of the zone-I pigs found infected, however, almost all (82.5 percent) were considered to be infected with T. brucei and many (30.2 percent) carried human-serum-resistant T. brucei. Pig-tsetse-human appears to be a major transmission cycle in zone I. In Mukono district (zone II), 10.5 percent and 26.1 percent of the T. brucei isolates from cattle and pigs, respectively, were humanserum- resistant, indicating that cattle-tsetse-human and pig-tsetse-human are major transmission cycles in zone II. In Tororo district (zone III), 47.3 percent of the T. brucei isolates from cattle were human-serum-resistant but there were no T. brucei isolates from pigs, indicating that cattle-tsetse-human is the major transmission cycle. Interestingly, as the only T. brucei isolate from sheep in zone III was human-serum-resistant, there may also be a sheep-tsetse-human cycle. In southeastern Uganda, control efforts must be designed to eliminate the parasites not only from cattle but also from pigs and small ruminants.
12590 Girard, M., Bisser, S., Courtioux, B., Vermot-Desroches, C., Bouteille, B., Wijdenes, J., Preud'homme, J.L. & Jauberteau, M.O., 2003. In vitro induction of microglial and endothelial cell apoptosis by cerebrospinal fluids from patients with human African trypanosomiasis. International Journal for Parasitology, 33 (7): 713-720.
Jauberteau: Laboratory of Immunology, CNRS UMR 6101, University Hospital, 2 Avenue Martin Luther King, 87 042 Limoges, France. [[email protected]]
In human African trypanosomiasis, trypanosomes first develop in the blood and lymph (Stage 1), then spread to the central nervous system (CNS) (Stage 2). Disruption of the blood-brain barrier of unknown mechanism occurs in Stage 2 disease. The hypothesis that cerebrospinal fluids (CSF) from African trypanosomiasis patients might contain factor(s) able to induce apoptosis in endothelial cells led us to evaluate this effect by two methods, the TdT-mediated dUTP nick end labelling (TUNEL) method and the measurement of soluble nucleosomes released by apoptotic cells in culture supernatant by ELISA. Apoptosis induction by CSF was also studied with microglial cells, the resident macrophages in the brain, which participate in the blood-brain barrier in the perivascular area. In contrast with control CSF, African trypanosomiasis patients' CSF induced apoptosis in both microglial and endothelial cells. The results obtained with the two methods correlated well, and showed that Stage 2 CSF induced apoptosis at higher levels in microglial cells, whereas the disease stage was not decisive for apoptosis induction in endothelial cells. We measured soluble Fas ligand (sFasL) and anti-Fas antibodies levels, two potent inducers of the Fas signalling pathway leading to apoptosis, in CSF from African trypanosomiasis patients and controls. CSF from African trypanosomiasis patients contained sFasL, and anti-Fas antibodies at higher levels than in controls. Stage 2 CSF contained more sFasL than Stage I CSF, and anti-Fas antibodies were detected only in Stage 2 CSF. Caspase-8 inhibitor effect and statistical data suggest that other proapoptotic factors may be involved in some CSF-induced apoptosis. Apoptosis induction may participate in the pathogenesis during African trypanosomiasis, and the presence of sFasL and anti-Fas antibodies may provide new tools for diagnosis and prognosis of the disease.
12591 Eckart, W.U., 2002. The colony as laboratory: German sleeping sickness campaigns in German East Africa and in Togo, 1900-1914. History and Philosophy of the Life Sciences, 24 (1): 69-89.
Eckart: Institut für Geschichte der Medizin, Ruprecht-Karls-Universität Im Neuenheimer Feld 327, D-69120 Heidelberg, Germany.
This paper is on dangerous human experimentations with drugs against trypanosomiasis carried out in the former German colonies of German East Africa and Togo. Victory over trypanosomiasis could not be achieved in Berlin because animals were thought to be unsuitable for therapeutic laboratory research in the field of trypanosomiasis. The colonies themselves were necessarily chosen as "laboratories" and the patients with sleeping sickness became the objects of therapeutical and pharmacological research. The paper first outlines Robert Koch's trypanosomiasis research in the large sleeping sickness "laboratory" of German East Africa and then focuses on the escalating human experiments on trypanosomiasis in the German Musterkolonie Togo, which followed.
12592 Stich, A., Barrett, M.P. & Krishna, S., 2003. Waking up to sleeping sickness. Trends in Parasitology, 19 (5): 195-197.
Krishna: St. George's Hospital Medical School, Department of Cellular and Molecular Medicine, Infectious Diseases, Cranmer Terrace, London SW17 0RE, UK. [[email protected]]
Devastating epidemics of human African trypanosomiasis are currently reemerging in many sub-Saharan countries. In the past three decades, clinical research into this important disease has been neglected, as have urgently-needed initiatives on drug development, disease surveillance and vector control. Recent impetus has aimed to provide a free supply of antitrypanosomal drugs, to develop a new orally-active trypanocidal agent and to attack the tsetse vector with modern technology. In addition, pan-African initiatives to co-ordinate control efforts have begun. These all provide some hope for the future, but they might not be enough to reverse the resurgence of this deadly disease in the heart of Africa.
[See also 26: nos. 12597, 12630]
12593 Hanotte, O., Ronin, Y., Agaba, M., Nilsson, P., Gelhaus, A., Horstmann, R., Sugimoto, Y., Kemp, S., Gibson, J., Korol, A., Soller, M. & Teale, A., 2003. Mapping of quantitative trait loci controlling trypanotolerance in a cross of tolerant West African N'Dama and susceptible East African Boran cattle. Proceedings of the National Academy of Sciences of the United States of America, 100 (13): 7443-7448.
Hanotte: ILRI, PO Box 30709, Nairobi 00100, Kenya. [[email protected]]
Trypanosomosis is a major disease constraint on livestock productivity in sub- Saharan Africa. To identify quantitative trait loci (QTL) controlling resistance to typanosomosis in cattle, an experimental cross was made between trypanotolerant African N'Dama (Bos taurus) and trypanosusceptible improved Kenya Boran (Bos indicus) cattle. Sixteen phenotypic traits were defined describing anaemia, body weight, and parasitaemia. One hundred and seventy seven F2 animals and their parents and grandparents were genotyped at 477 molecular marker loci covering all 29 cattle autosomes. Total genome coverage was 82 percent. Putative QTL were mapped to 18 autosomes. The results are consistent with a single QTL on 17 chromosomes and two QTL on BTA16. Individual QTL effects ranged from ~6 percent to 20 percent of the phenotypic variance of the trait. Excluding chromosomes with ambiguous or nontrypanotolerance effects, the allele for resistance to trypanosomosis originated from the N'Dama parent at nine QTL and from the Kenya Boran at five QTL, and at four QTL there is evidence of an overdominant mode of inheritance. These results suggest that selection for trypanotolerance within an F2 cross between N'Dama and Boran cattle could produce a synthetic breed with higher trypanotolerance levels than currently exist in the parental breeds.
12594 Bastiaensen, P., Cisse, A., Gnofam, M., Bebay, C. E., Kouagou, N. T., Sonhaye, A., Napala, A. & Hendrickx, G., 2001. [Pratique vétérinaire privée rurale au Togo: appréciation socio-économique de sa viabilité.] Private rural veterinary practice in Togo: assessment of socio-economic viability. Bulletin of Animal Health and Production in Africa, 49 (2): 96-120.
Hendrickx: Projet Régional FAO de Lutte contre la trypanosomose animale, Togo, Burkina Faso.
In most West-African countries, governments are in the process of privatizing state veterinary services in order to restrain their public sector expenses. In Togo, this has led to an emerging private veterinary sector in rural areas. From the very beginning the animal trypanosomosis control project has encouraged and counselled these young private veterinarians in their attempts to impose themselves in this surrounding which was not familiar with paying animal health services. As has been shown recently, private vets, through a nationwide extension campaign and the enhanced availability of the basic animal health services they offer, have had a major impact on disease prevalence in Togo. In order to ensure sustainability and continued availability of these services, a socioeconomic study was set up in order to identify social, structural and economic constraints to the viability of rural private veterinary practice in the mid and long term. From the study, it appears that 8 out of 10 private practices included in the study, are both financially and structurally sound enterprises with prospects for substantial growth in the years to come. Private veterinarians in rural areas today cover approximately 50 percent of agricultural and livestock production areas in Togo. The major constraint would appear to be the limited access to credit when financial turnovers increase to such proportions that self-finance becomes insufficient. Another possible cause for worry is the reliance on trypanocide sales to nomadic herdsmen crossing Togo, which is a typical feature of animal husbandry in Togo, but which is also subject to social and political controversy.
12595 Machila, N., Wanyangu, S.W., McDermott, J., Welburn, S.C., Maudlin, I. & Eisler, M.C., 2003. Cattle owners' perceptions of African bovine trypanosomiasis and its control in Busia and Kwale Districts of Kenya. Acta Tropica, 86 (1): 25-34.
Machila: CTVM, University of Edinburgh, Easter Bush, Roslin, Midlothian, Edinburgh EH25 9RG UK. [[email protected]]
A study using a structured questionnaire was conducted in Busia District, Western Kenya and Kwale District, Coastal Kenya, to obtain qualitative and quantitative information from 256 cattle owners about their production systems, their perceptions of the diseases encountered in their cattle, the drugs used, and other measures adopted to control trypanosomiasis in cattle. The predominant production system was mixed croplivestock with farmers owning 2-11 local cattle on holdings between 2 and 5 ha. Approximately 15 percent of disease episodes in cattle were perceived to be trypanosomiasis, although the farmers' ability to make diagnoses was limited in that over half of the diagnoses were inconsistent with the clinical signs described. Drugs were generally obtained from agro-veterinary shops, and the farmers themselves administered slightly more than half of these. One third of drug treatments given to sick cattle were trypanocides, but over half of these trypanocidal treatments were given to cattle believed to have diseases other than trypanosomiasis.
12596 Chiejina, S., Goyal, P., Li, C. & Wakelin, D., 2003. Concurrent infections with Trypanosoma brucei and Nippostrongylus brasiliensis in mice deficient in inducible nitric oxide. Parasitology International, 52 (2): 107-115.
Wakelin: School of Life and Environmental Sciences, University of Nottingham, Nottingham NG7 2RD, UK. [[email protected]]
Concurrent infection with Trypanosoma brucei (Tb) delays the normal protective responses of mice to the gastrointestinal parasite Nippostrongylus brasiliensis (Nb). The course of such infections was followed in mice genetically deficient in inducible nitric oxide synthase (INOS) to assess the role of nitric oxide (NO) in this effect. The time course of trypanosome infection in INOS deficient (INOS -/-) mice was similar to that in wild type (WT) and heterozygote (INOS +/-) mice but did not result in NO production. Although concurrent infection with Tb increased initial susceptibility to Nb in INOS -/- mice, the immune-mediated loss of N. brasiliensis and the associated decline in faecal egg output occurred more rapidly then in WT and INOS +/- littermates. Concurrent infection with trypanosomes markedly suppressed Concanavalin A (ConA)-induced in vitro proliferation of splenic lymphocytes in all groups, but had little effect on the responses of mesenteric node lymphocytes. Trypanosome infection was also associated with increased early release of interferon- and reduced IL-5 from lymphocytes stimulated in vitro with ConA, but did not affect later release of IL-5. The overall similarity of proliferative and cytokine responses in WT INOS +/- and INOS -/- mice suggest that the suppressive effects of T. brucei on N. brasiliensis infection do not simply reflect depressed lymphocyte responsiveness or altered cytokine profiles. NO appears to be involved in suppression only of the later phases of the host responses to Nb.
12597 Lubega, G.W., Byarugaba, D.K. & Prichard, R.K., 2002. Immunization with a tubulin-rich preparation from Trypanosoma brucei confers broad protection against African trypanosomosis. [Mice] Experimental Parasitology, 102 (1): 9-22.
Lubega: Molecular biology Laboratory, Faculty of Veterinary Medicine, Makerere University, PO Box 7062, Kampala, Uganda. [[email protected]]
Tubulin from Trypanosoma brucei was purified to near homogeneity using a protocol which involved treatment with urea with subsequent renaturation and was then used to immunize mice. Renatured tubulin further purified by SDS-PAGE (denatured), synthetic tubulin peptides (STP), and rat brain tubulin (RbTub) were also used. Immunized mice were challenged with T. brucei, Trypanosoma congolense or Trypanosoma rhodesiense. Renatured T. brucei tubulin (nTbTub) induced protection in all mice tested, of which 60-80 percent (n = 81) was complete and the remainder partial. Denatured T. brucei tubulin (dTbTub), STP, or RbTub induced lower antibody levels than nTbTub and did not offer protection. However, in culture, the antibodies against dTbTub or STP killed trypanosomes although at lower dilutions than nTbTub, but those against RbTub did not. In Western blots anti-trypanosome antibodies recognized the tubulin of all the trypanosome species investigated but not vertebrate tubulin, whereas the anti-RbTUB antibodies recognized both trypanosome and vertebrate tubulin. Of the five mice given passive immunity by the transfer of anti-RbTub serum, four were completely protected and one partially protected. These data suggest that tubulin is the relevant immunogen in the preparation used and could therefore be a promising target for the development of a parasite-specific, broad spectrum vaccine.
12598 Xong, H.V., De Baetselier, P., Pays, E. & Magez, S., 2002. Selective pressure can influence the resistance of Trypanosoma congolense to normal human serum. Experimental Parasitology, 102 (2): 61-65.
Xong: Department of Immunology, Parasitology and Ultrastructure, Flanders Interuniversity for Biotechnology. 65 Paardenstraat, St. Genesius Rode B 1640, Belgium. [[email protected]]
Resistance and sensitivity to normal human serum (NHS) of Trypanosoma congolense, a parasite believed to cause disease in animals only, were investigated in vivo as well as in vitro. Our results indicate that like Trypanosoma brucei, T. congolense can be grouped into three different phenotypes according to its resistance to NHS. Some strains are completely resistant to NHS, like Trypanosoma brucei gambiense and the resistant form of Trypanosoma brucei rhodesiense. Other strains show a very low degree of resistance comparable to the sensitive form of T. b. rhodesiense, and some are completely sensitive to NHS. Continuous passaging in mice in the presence or absence of NHS shows that the resistance and sensitivity of T. congolense can be reversed like in T. b. rhodesiense. Our data suggest that T. congolense might be able to infect man in regions where animals may serve as reservoirs for the infection.
12599 Croft, S.L., Seifert, K. & Duchêne, M., 2003. Antiprotozoal activities of phospholipid analogues. Molecular and Biochemical Parasitology, 126 (2): 165-172.
Croft: Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK. [[email protected]]
The antiprotozoal activity of phospholipid analogues, originally developed as anticancer drugs, has been determined in the past decade. The most susceptible parasites are Leishmania spp. and Trypanosoma cruzi with activity also shown against Trypanosoma brucei spp., Entamoeba histolytica and Acanthamoeba spp. Miltefosine, an alkylphosphocholine, was registered for the oral treatment of visceral leishmaniasis (VL) in India in March 2002. This review focusses on the biological activities of phospholipid analogues. Biochemical and molecular targets and mechanism(s) of action have been studied extensively in tumour cells but have not been determined in protozoa.
12600 Heby, O., Roberts, S.C. & Ullman, B., 2003. Polyamine biosynthetic enzymes as drug targets in parasitic protozoa. Biochemical Society Transactions, 31 (2): 415-419.
Heby: Department of Molecular Biology, Umea University, SE-901 87 Umea, Sweden. [[email protected]]
Molecular, biochemical and genetic characterization of ornithine decarboxylase, Sadenosylmethionine decarboxylase and spermidine synthase establishes that these polyamine-biosynthetic enzymes are essential for growth and survival of the agents that cause African sleeping sickness, Chagas' disease, leishmaniasis and malaria. These enzymes exhibit features that differ significantly between the parasites and the human host. Therefore it is conceivable that exploitation of such differences can lead to the design of new inhibitors that will selectively kill the parasites while exerting minimal, or at least tolerable, effects on the parasite-infected patient.
12601 McDermott, J., Woitag, T., Sidibé, I., Bauer, B., Diarra, B., Ouédraogo, D., Kamuanga, M., Peregrine, A., Eisler, M., Zessin, K.H., Mehlitz, D. & Clausen, P.H., 2003. Field studies of drug-resistant cattle trypanosomes in Kénédougou Province, Burkina Faso. Acta Tropica, 86 (1): 93-103.
McDermott: ILRI, PO Box 30709, 00100 Nairobi, Kenya. [[email protected]]
Field studies were conducted to assess the occurrence of resistance to isometamidium chloride and diminazene aceturate in trypanosomes infecting cattle in Kénédougou Province of Burkina Faso. Forty-five of the 166 villages in Kénédougou were randomly sampled and visited to assess livestock numbers, trypanosomosis risk and tsetse challenge. The proportion of cattle infections associated with drug-resistant trypanosomes was assessed in the nine villages with the highest trypanosome infection prevalence and one village with a confirmed history of drug-resistant infections. These studies showed that resistance to both isometamidium and diminazene was widespread. However, there was considerable variation between villages in drug-resistance parameters, with the proportion of treated cattle with trypanosome infections three months after isometamidium prophylaxis varying from 6.9 percent to 63.8 percent and the proportion of cattle having infections two weeks after treatment with diminazene varying from 0 percent to 36.8 percent. The demonstration of widespread resistance to both isometamidium and diminazene has important implications, as administration of trypanocides is the most commonly employed method to control trypanosomosis in this area.
12602 Montalvetti, A., Fernandez, A., Sanders, J.M., Ghosh, S., Van Brussel, E., Oldfield, E. & Docampo, R., 2003. Farnesyl pyrophosphate synthase is an essential enzyme in Trypanosoma brucei - In vitro RNA interference and in vivo inhibition studies. Journal of Biological Chemistry, 278 (19): 17075-17083.
Docampo: Laboratory of Molecular Parasitology, Department of Pathobiology and Center for Zoonoses Research, University of Illinois at Urbana-Champaign, Urbana, Illinois 61802, USA. [[email protected]]
We report the cloning and sequencing of a gene encoding the farnesyl pyrophosphate synthase (FPPS) of Trypanosoma brucei. The protein (TbFPPS) is an attractive target for drug development because the growth of T. brucei has been shown to be inhibited by analogues of its substrates, the nitrogen-containing bisphosphonates currently in use in bone resorption therapy. The protein predicted from the nucleotide sequence of the gene has 367 amino acids and a molecular mass of 42 kDa. Several sequence motifs found in other FPPSs are present in TbFPPS, including an 11-mer peptide insertion present also in the Trypanosoma cruzi FPPS. Heterologous expression of TbFPPS in Escherichia coli produced a functional enzyme that was inhibited by several nitrogen-containing bisphosphonates, such as pamidronate and risedronate. Risedronate was active in vivo against T. brucei infection in mice (giving a 60 percent survival rate), but pamidronate was not effective. The essential nature of TbFPPS was studied using RNA interference (RNAi) to inhibit the expression of the gene. Expression of TbFPPS double-stranded RNA in procyclic trypomastigotes caused specific degradation of mRNA. After four days of RNAi, the parasite growth rate declined and the cells subsequently died. Similar results were obtained with bloodstream form trypomastigotes, except that the RNAi system in this case was leaky and mRNA levels and parasites recovered with time. Molecular modelling and structure-activity investigations of enzyme and in vitro growth inhibition data resulted in similar pharmacophores, further validating TbFPPS as the target for bisphosphonates. These results establish that FPPS is essential for parasite viability and validate this enzyme as a target for drug development.
12603 Yabu, Y., Yoshida, A., Suzuki, T., Nihei, C., Kawai, K., Minagawa, N., Hosokawa, T., Nagai, K., Kita, K. & Ohta, N., 2003. The efficacy of ascofuranone in a consecutive treatment on Trypanosoma brucei brucei in mice. Parasitology International, 52 (2): 155-164.
Yabu: Department of Molecular Parasitology, Nagoya City University, Graduate School of Medical Sciences, Nagoya 467-2076, Japan. [[email protected]]
Consecutive administration of ascofuranone without glycerol was found to have therapeutic efficacy against Trypanosoma brucei brucei infection in mice. A suspension of ascofuranone (25-100 mg/kg) was administrated intraperitoneally every 24 h for 1-4 consecutive days to trypanosome-infected mice and efficacy was compared with oral treatment. With intraperitoneal administration, all mice treated with 100 mg/kg ascofuranone for four consecutive days were cured. On the contrary, with oral treatment a higher dose of ascofuranone (400 mg/kg) was needed for eight consecutive days to cure the mice. With intraperitoneal treatment, parasitemia was strongly suppressed, with almost all long slender bloodstream forms of the parasite changed to short stumpy forms by day 3 and the parasites have been eliminated four days after the start of treatment. These ascofuranone-induced short stumpy forms were morphologically analogous to the stumpy forms two days after peak parasitemia of pleomorphic clone of T. b. brucei GUTat 3.1. However, the properties of ubiquinol oxidase activity, which is the target of ascofuranone, in mitochondria isolated from before and after treatment, were almost the same. The enzymatic activities of ubiquinol oxidase decreased to approximately 30 percent within a day after treatment, and then kept at nearly the same level. In the present study, we have improved the regimen for the administration of ascofuranone without glycerol, and demonstrated that consecutively administrated ascofuranone showed trypanocidal effects in T. b. brucei infected mice. Our present results strongly suggest that consecutive administration of ascofuranone may be an effective chemotherapy for African trypanosomiasis.
12604 Alphey, M.S., Gabrielsen, M., Micossi, E., Leonard, G.A., McSweeney, S.M., Ravelli, R.B.G., Tetaud, E., Fairlamb, A.H., Bond, C.S. & Hunter, W.N., 2003. Tryparedoxins from Crithidia fasciculata and Trypanosoma brucei - Photoreduction of the redox disulfide using synchrotron radiation and evidence for a conformational switch implicated in function. Journal of Biological Chemistry, 278 (28): 25919-25925.
Hunter: Division of Biological Chemistry and Molecular Microbiology, School of Life Sciences, University of Dundee, Dundee DD1 5EH, UK. [[email protected]]
12605 Bodley, A.L., Chakraborty, A.K., Xie, S.J., Burri, C. & Shapiro, T.A., 2003. An unusual type IB topoisomerase from African trypanosomes. Proceedings of the National Academy of Sciences of the United States of America, 100 (13): 7539-7544.
Shapiro: Division of Clinical Pharmacology, Departments of Medicine and of Pharmacology and Molecular Sciences, John Hopkins University School of Medicine, Baltimore, MD 21205, USA. [[email protected]]
12606 Bruderer, T., Tu, L.C. & Lee, M.G.-S., 2003. The 5 end structure of transcripts derived from the rRNA gene and the RNA polymerase I transcribed protein coding genes in Trypanosoma brucei. Molecular and Biochemical Parasitology, 129 (1): 69-77.
Lee: Department of Pathology, New York University, 550 First Avenue, New York, NY 10016, USA. [[email protected]]
12607 Budde, H., Flohé, L., Hecht, H.J., Hofmann, B., Stehr, M., Wissing, J. & Lünsdorf, H., 2003. Kinetics and redox-sensitive oligomerisation reveal negative subunit cooperativity in tryparedoxin peroxidase of Trypanosoma brucei brucei. Biological Chemistry, 384 (4): 619-633.
Lünsdorf: German Research Centre (GBF), Mascheroder Weg 1, D-38124 Braunschweig, Germany.
12608 Coller, S. & Paulnock, D.M., 2003. The soluble variant surface glycoprotein released by African trypanosomes fails to alarm the innate immune system. FASEB Journal, 17 (7 Suppl.): C55.
Coller: Medical Microbiology and Immunology, University of Wisconsin Medical School, 1300 University Avenue, Madison, WI 53706, USA.
12609 Comini, M., Menge, U. & Flohé, L., 2003. Biosynthesis of trypanothione in Trypanosoma brucei brucei. Biological Chemistry, 384 (4): 653-656.
Flohé: Department of Biochemistry, Technical University of Braunschweig, Germany.
12610 Domingo, G.J., Palazzo, S.S., Wang, B.B., Pannicucci, B., Salavati, R. & Stuart, K.D., 2003. Dyskinetoplastic Trypanosoma brucei contains functional editing complexes. Eukaryotic Cell, 2 (3): 569-577.
Stuart: Seattle Biomedical Research Institute, 4 Nickerson St, Seattle, WA 98109 USA.
12611 D'Orso, I., De Gaudenzi, J.G. & Frasch, A.C.C., 2003. RNA-binding proteins and mRNA turnover in trypanosomes. Trends in Parasitology, 19 (4): 151-155.
Frasch: Instituto de Investigaciones Biotecnológicas-Instituto Tecnológico de Chascomús, CONICET-UNSAM, Av. Gral. Paz s/n, Edificio 24, INTI, 1650-, San Martin, Buenos Aires, Argentina.
Trypanosomes, protozoan parasites of the order Kinetoplastida, control gene expression essentially through post-transcriptional mechanisms. Several motifs located mainly in the 3 untranslated region, such as AU-rich elements (AREs), were recently shown to modulate mRNA half-life, and are able to modify mRNA abundance in vivo through the interaction with specific RNA-binding proteins. Along with the detection of an active exosome, decapping activities and a regulated 3 to 5 exonuclease activity stimulated by AREs, these results suggest that modulation of mRNA stability is essential in trypanosomes. These regulatory processes are specific for different developmental stages and thus relevant for allowing trypanosomes to adapt to variable environmental conditions.
12612 Durand-Dubief, M., Kohl, L. & Bastin, P., 2003. Efficiency and specificity of RNA interference generated by intra- and intermolecular double stranded RNA in Trypanosoma brucei. Molecular and Biochemical Parasitology, 129 (1): 11-21.
Bastin: Unite INSERM U565 & CNRS UMR8646, Laboratoire de Biophysique, Museum National d'Histoire Naturelle, 43 rue Cuvier, 75231 Paris Cedex 05, France. [[email protected]]
12613 Ernst, N.L., Panicucci, B., Igo, R.P. Jr, Panigrahi, A.K., Salavati, R. & Stuart, K., 2003. TbMP57 is a 3´ terminal uridylyl transferase (TUTase) of the Trypanosoma brucei editosome. Molecular Cell, 11 (6): 1525-1536.
Stuart: Seattle Biomedical Research Institute, Seattle, Washington 98109, USA. [[email protected]]
12614 Fang, J. & Beattie, D.S., 2003. Alternative oxidase present in procyclic Trypanosoma brucei may act to lower the mitochondrial production of superoxide. Archives of Biochemistry and Biophysics, 414 (2): 294-302.
Fang: Department of Biochemistry and Molecular Pharmacology, West Virginia University, School of Medicine, PO Box 9142, Morgantown, WV 26506-9142, USA. [[email protected]]
12615 Ferreira, C. dos S., Martins, P. S., Demicheli, C., Brochu, C., Ouellette, M. & Frézard, F., 2003. Thiol-induced reduction of antimony(V) into antimony(III): a comparative study with trypanothione, cysteinyl-glycine, cysteine and glutathione. BioMetals, 16 (3): 441-446.
Departamento de Química, Instituto de Ciências Exatas, Rio de Janeiro, Brazil. [[email protected]]
12616 Gaunt, M.W., Yeo, M., Frame, I.A., Stothard, J.R., Carrasco, H.J., Taylor, M.C., Mena, S.S., Veazey, P., Miles, G.A.J., Acosta, N., Rojas de Arias, A. & Miles, M.A., 2003. Mechanism of genetic exchange in American trypanosomes. [cf T. brucei] Nature, 421 (6926): 936-939.
Miles: Department of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, London WC1E 7HT, UK. [[email protected]]
The kinetoplastid Protozoa are responsible for devastating diseases. In the Americas, Trypanosoma cruzi is the agent of Chagas' disease - a widespread disease transmissible from animals to humans (zoonosis) - which is transmitted by exposure to infected faeces of blood-sucking triatomine bugs. The presence of genetic exchange in T. cruzi and in Leishmania is much debated. Here, by producing hybrid clones, we show that T. cruzi has an extant capacity for genetic exchange. The mechanism is unusual and distinct from that proposed for the African trypanosome, Trypanosoma brucei. Two biological clones of T. cruzi were transfected to carry different drug-resistance markers, and were passaged together through the entire life cycle. Six double-drug-resistant progeny clones, recovered from the mammalian stage of the life cycle, show fusion of parental genotypes, loss of alleles, homologous recombination, and uniparental inheritance of kinetoplast maxicircle DNA. There are strong genetic parallels between these experimental hybrids and the genotypes among natural isolates of T. cruzi. In this instance, aneuploidy through nuclear hybridization results in recombination across far greater genetic distances than mendelian genetic exchange. This mechanism also parallels genome duplication. These findings imply that genetic exchange can take place in vertebrate reservoir hosts of T. cruzi; in contrast, genetic exchange in T. brucei takes place in the vector the tsetse fly and probably involves meiosis.
12617 Gruszynski, A.E., DeMaster, A., Hooper, N.M. & Bangs, J.D., 2003. Surface coat remodeling during differentiation of Trypanosoma brucei. Journal of Biological Chemistry, 278 (27): 24665-24672.
Bangs: Department of Medical Microbiology and Immunology, University of Wisconsin Medical School, Madison, Wisconsin 53706, USA. [[email protected]]
12618 Gunzl, A., Bruderer, T., Laufer, G., Schimanski, B., Tu, L.C., Chung, H.M., Lee, P.T. & Lee, M.G.S., 2003. RNA polymerase I transcribes procyclin genes and variant surface glycoprotein gene expression sites in Trypanosoma brucei. Eukaryotic Cell, 2 (3): 542-551.
Lee: Medizinisch-Naturwissenschaftliches Forschungsinstitut der Universität Tubingen, Germany.
12619 Hammarton, T.C., Clark, J., Douglas, F., Boshart, M. & Mottram, J.C., 2003. Stage-specific differences in cell cycle control in Trypanosoma brucei revealed by RNA interference of a mitotic cyclin. Journal of Biological Chemistry, 278 (25): 22877-22886.
Mottram: Wellcome Centre for Molecular Parasitology, Anderson College, University of Glasgow, 56 Dumbarton Road, Glasgow G11 6NU, UK. [[email protected]]
12620 Hill, K.L., 2003. Biology and mechanism of trypanosome cell motility. Eukaryotic Cell, 2 (2): 200-208.
Hill: Department of Microbiology, Immunology and Molecular Genetics, University of California at Los Angeles, 609 Charles E. Young Dr. Easr, Los Angeles, CA 90095, USA. [[email protected]]
12621 Hughes, A.L. & Piontkivska, H., 2003. Phylogeny of Trypanosomatidae and Bodonidae (Kinetoplastida) based on 18S rRNA: Evidence for paraphyly of Trypanosoma and six other genera. Molecular Biology and Evolution, 20 (4): 644-652.
Hughes: Department of Biological Sciences, University of South Carolina, USA. [[email protected]]
12622 Jackson, L.K., Goldsmith, E.J. & Phillips, M.A., 2003. X-ray structure determination of Trypanosoma brucei ornithine decarboxylase bound to Dornithine and to G418 - Insights into substrate binding and ODC conformational flexibility. Journal of Biological Chemistry, 278 (24): 22037-22043.
Phillips: Department of Pharmacology, The University of Texas South Western Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas, TX 75390, USA. [[email protected]]
12623 Kaiser, A.E., Gottwald, A.M., Wiersch, C.S., Maier, W.A. & Seitz, H.M., 2003. Spermidine metabolism in parasitic protozoa - a comparison to the situation in prokaryotes, viruses, plants and fungi. [Review] Folia Parasitologica, 50 (1): 3-18.
Kaiser: Institut für Medizinishe Parasitologie, Rheinische-Friedrich- Wilhelms-Universität Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. [[email protected]]
The metabolism of the triamine spermidine is reviewed with particular focus on the biosynthesis of hypusine and homospermidine in parasitic protozoa, i.e., Plasmodium, Trypanosoma and Leishmania, compared to that in prokaryotes i.e., Escherichia coli, a phytopathogenic virus and pyrrolizidine alkaloid-producing plants (Asteraceae) and fungi.
12624 Krauth-Siegel, R.L., Meiering, S.K. & Schmidt, H., 2003. The parasite-specific trypanothione metabolism of Trypanosoma and Leishmania. [Review] Biological Chemistry, 384 (4): 539-549.
Krauth-Siegel: Centre of Biochemistry, University of Heidelberg, Im Neuenheimer Feld 504, D-69120 Heidelberg, Germany.
12625 LaCount, D.J., Gruszynski, A.E., Grandgenett, P.M., Bangs, J.D. & Donelson, J.E., 2003. Expression and function of the Trypanosoma brucei major surface protease (GP63) genes. Journal of Biological Chemistry, 278 (27): 24658-24664.
Donelson: Department of Biochemistry, University of Iowa, Iowa City, Iowa 52242, USA.
12626 Li, J.-L., Ruyechan, W.T. & Williams, N., 2003. Stage-specific translational efficiency and protein stability regulate the developmental expression of p37, an RNA binding protein from Trypanosoma brucei. Biochemical and Biophysical Research Communications, 306 (4): 918-923.
Williams: Department of Microbiology and Witebsky Center for Microbial Pathogenesis and Immunology, 253 Biomedical Research Building, State University of New York at Buffalo, Buffalo, NY 14214, USA. [[email protected]]
12627 Li, Y., Li, Z.Y. & Wang, C.C., 2003. Differentiation of Trypanosoma brucei may be stage non-specific and does not require progression of cell cycle. Molecular Microbiology, 49 (1): 251-265.
Wang: Department of Pharmaceutical Chemistry, University of California, Genentech Hall, 600 16th Street, San Francisco, CA 94143-2280, USA. [[email protected]]
12628 Li, Z.Y. & Wang, C.C., 2003. A PHO80-like cyclin and a B-type cyclin control the cell cycle of the procyclic form of Trypanosoma brucei. Journal of Biological Chemistry, 278 (23): 20652-20658.
Wang: Department of Pharmaceutical Chemistry, University of California, San Francisco CA 94143-0446, USA. [[email protected]]
12629 Liang, X.-H., Liu, Q. & Michaeli, S., 2003. Small nucleolar RNA interference induced by antisense or double-stranded RNA in trypanosomatids. Proceedings of the National Academy of Sciences of the United States of America, 100 (13): 7521-7526.
Michaeli: Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel. [[email protected]]
12630 Lubega, G.W., Ochola, D.O.K. & Prichard, R.K., 2002. Trypanosoma brucei: anti-tubulin antibodies specifically inhibit trypanosome growth in culture. Experimental Parasitology, 102 (3-4): 134-142.
Lubega: Molecular Biology Laboratory, Faculty of Veterinary Medicine, Makerere University, PO Box 7062, Kampala, Uganda. [[email protected]]
12631 Miclet, E., Duffieux, F., Lallemand, J.-Y. & Stoven, V., 2003. Backbone HN, N, C, C, and C assignment of the 6-phosphogluconolactonase, a 266- residue enzyme of the pentose-phosphate pathway from human parasite Trypanosoma brucei. Journal of Biomolecular NMR, 25 (3) 249-250.
Duffieux: Institut de Chimie des Substances naturelles (ICSN), UPR CNRS 2301, Avenue de la Terrasse, 91198 Gif-sur-Yvette cedex, France. [[email protected]]
12632 Motta, M.C.M., de Souza, W. & Thiry, M., 2003. Immunocytochemical detection of DNA and RNA in endosymbiont-bearing trypanosomatids. FEMS Microbiology Letters, 221 (1): 17-23.
Motta: Laboratório de Ultrastrutura Celular Hertha Meyer, Instituto de Biofisica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS, BlocoG, Ulha do Fundão, 21940-900 Rio de Janeiro, RJ, Brazil. [[email protected]]
12633 Moyersoen, J., Choe, J., Kumar, A., Voncken, F.G.J., Hol, W.G.J. & Michels, P.A.M., 2003. Characterization of Trypanosoma brucei PEX14 and its role in the import of glycosomal matrix proteins. European Journal of Biochemistry, 270 (9): 2059-2067.
Michels: Research Unit for Tropical Diseases, Christian de Duve Institute of Cellular Pathology and Laboratory of Biochemistry, Université Catholique de Louvain, Brussels, Belgium. [[email protected]]
12634 Ogbadoyi, E.O., Robinson, D.R. & Gull, K., 2003. A high-order transmembrane structural linkage is responsible for mitochondrial genome positioning and segregation by flagellar basal bodies in trypanosomes. Molecular Biology of the Cell, 14 (5): 1769-1779.
Gull: Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK. [[email protected]]
12635 Palazzo, S.S., Panigrahi, A.K., Igo, R.P. Jr, Salavati, R. & Stuart, K., 2003. Kinetoplastid RNA editing ligases: complex association, characterization, and substrate requirements. [T. brucei] Molecular and Biochemical Parasitology, 127 (2): 161-167.
Stuart: Seattle Biomedical Research Institute, 4 Nickerson Street, Seattle, WA 98109, USA. [[email protected]]
12636 Pearson, B. & Campbell, A.G., 2003. Localization studies on the Trypanosoma brucei class I ribonuclease H. FASEB Journal, 17 (4 Pt 1 suppl.): A598.
Pearson: Pathobiology Department, Brown University, Box G-B6, Providence, RI 02912, USA.
12637 Persson, L., Jeppsson, A. & Nasizadeh, S., 2003. Turnover of trypanosomal ornithine decarboxylases. [T. brucei] Biochemical Society Transactions, 31 (2): 411-414.
Persson: Department of Physiological Sciences, BMC F:13, S-221 84 Lund, Sweden. [[email protected]]
12638 Price, H.P., Menon, M.R., Panethymitaki, C., Goulding, D., McKean, P.G. & Smith, D.F., 2003. Myristoyl-CoA:protein N-myristoyltransferase, an essential enzyme and potential drug target in kinetoplastid parasites. Journal of Biological Chemistry, 278 (9): 7206-7214.
Smith: Wellcome Trust Laboratories for Molecular Parasitology, Centre for Molecular Microbiology and Infection, Department of Biological Sciences, Imperial College of Science, Technology and Medicine, London SW7 2AZ, UK. [[email protected]]
12639 Priest, J.W. & Hajduk, S.L., 2003. Trypanosoma brucei cytochrome c1 is imported into mitochondria along an unusual pathway. Journal of Biological Chemistry, 278 (17): 15084-15094.
Hajduk: Departments of Biochemistry and Molecular Genetics, Schools of Medicine and Dentistry, University of Alabama at Birmingham, Alabama 35294 USA. [[email protected]]
12640 Quan, N., He, L.L. & Lai, W.M., 2003. Intraventricular infusion of antagonists of IL-1 and TNF attenuates neurodegeneration induced by the infection of Trypanosoma brucei. Journal of Neuroimmunology, 138 (1-2): 92-98.
Quan: Section of Oral Biology, Ohio State University Health Science Center, Columbus OH, USA. [[email protected]]
12641 Redmond, S., Vadivelu, J. & Field, M.C., 2003. RNAit: an automated webbased tool for the selection of RNAi targets in Trypanosoma brucei. Molecular and Biochemical Parasitology, 128 (1): 115-118.
Field: Wellcome Trust Laboratories for Molecular Parasitology, Department of Biological Sciences, Centre for Molecular Microbiology and Infection, Imperial College London, Exhibition Road, London SW7 2AY, UK. [[email protected]]
12642 Sbicego, S., Alfonzo, J.D., Estevez, A.M., Rubio, M.A., Kang, X., Turck, C.W., Peris, M. & Simpson, L., 2003. RBP38, a novel RNA-binding protein from trypanosomatid mitochondria, modulates RNA stability. Eukaryotic Cell, 2 (3): 560-568.
Simpson: MacDonald Research Laboratories, Howard Hughes Medical Institute, University of California, Los Angeles 6780, Los Angeles, CA 90095, USA.
12643 Serveau, C., Boulangé, A., Lecaille, F., Gauthier, F., Authié, E. & Lalmanach, G., 2003. Procongopain from Trypanosoma congolense is processed at basic pH: An unusual feature among cathepsin L-like cysteine proteases. Biological Chemistry, 384 (6): 921-927.
Lalmanach: Protéases et Vectorisation, INSERM EMI-U 00.10, Laboratoire d'Enzymologie et Chimie des Protéines, Faculté de Médecine, Université François Rabelais, F-37032 Tours, France.
12644 Sheader, K., Berberof, M., Isobe, T., Borst, P. & Rudenko, G., 2003. Delineation of the regulated Variant Surface Glycoprotein gene expression site domain of Trypanosoma brucei. Molecular and Biochemical Parasitology, 128 (2): 147-156.
Rudenko: The Peter Medawar Building for Pathogen Research, University of Oxford, South Parks Road, Oxford OX1 3SY, UK. [[email protected]]
12645 Steverding, D., 2003. The significance of transferrin receptor variation in Trypanosoma brucei. Trends in Parasitology, 19 (3): 125-127.
Steverding: School of Biological Sciences, University of Bristol, Woodland Road, Bristol BS8 1UG, Avon, UK. [[email protected]]
The transferrin receptor of Trypanosoma brucei is encoded by genes located in different expression sites. The various expression sites encode slightly different transferrin receptors, which differ substantially in their affinity for transferrin of different host species. It was proposed that T. brucei has developed multiple expression sites encoding different transferrin receptors not only to cope with the diversity of mammalian transferrins, but also to ensure sufficient iron uptake in the presence of anti-transferrin receptor antibodies. This article shows that calculations based on Kd values argue against the first part of the hypothesis, but might support the second part.
12646 Tiralongo, E., Schrader, S., Lange, H., Lemke, H., Tiralongo, J. & Schauer, R., 2003. Two trans-sialidase forms with different sialic acid transfer and sialidase activities from Trypanosoma congolense. Journal of Biological Chemistry, 278 (26): 23301-23310.
Schauer: Biochemisches Institut, Universität zu Kiel, Olhausenstrasse 40, Kiel 24098, Germany. [[email protected]]
12647 Triggs, V.P. & Bangs, J.D., 2003. Glycosylphosphatidylinositol-dependent protein trafficking in bloodstream stage Trypanosoma brucei. Eukaryotic Cell, 2 (1): 76-83.
Bangs: Department of Medical Microbiology and Immunology, University of Wisconsin-Madison Medical School, Madison, Wisconsin 53706, USA. [[email protected]]
12648 van Deursen, F.J., Thornton, D.J. & Matthews, K.R., 2003. A reproducible protocol for analysis of the proteome of Trypanosoma brucei by 2-dimensional gel electrophoresis. Molecular and Biochemical Parasitology, 128 (1): 107-110.
Matthews: School of Biological Sciences, University of Manchester, 2.14 Stopford Building, Manchester M13 9PT, UK. [keith.matthews@man. ac.uk]
12649 van Weelden, S.W.H., Fast, B., Vogt, A., van der Meer, P., Saas, J., van Hellemond, J.J., Tielens, A.G.M. & Boshart, M., 2003. Procyclic Trypanosoma brucei do not use Krebs cycle activity for energy generation. Journal of Biological Chemistry, 278 (15): 12854-12863.
Boshart: Department of Biology I, Genetics, University of Munich, Maria- Ward-Strasse 1a, D-80638 München, Germany. [[email protected]]
12650 Vassella, E., Bütikofer, P., Engstler, M., Jelk, J. & Roditi, I., 2003. Procyclin null mutants of Trypanosoma brucei express free glycosylphosphatidyl- inositols on their surface. Molecular Biology of the Cell, 14 (4): 1308-1318.
Roditi: Institut für Zellbiologie, Universität Bern, CH-3012 Bern, Switzerland. [[email protected]]
12651 Vogt, R.N. & Steenkamp, D.J., 2003. The metabolism of S-nitrosothiols in the trypanosomatids: the role of ovothiol A and trypanothione. Biochemical Journal, 371 (1): 49-59.
Steenkamp: Division of Chemical Pathology, Department of Laboratory Medicine, University of Cape Town Medical School, Observatory, 7925, South Africa. [[email protected]]
12652 Vruchte, D.T., Aitcheson, N. & Rudenko, G., 2003. Downregulation of Trypanosoma brucei VSG expression site promoters on circular bacterial artificial chromosomes. Molecular and Biochemical Parasitology, 128 (2): 123-133.
Rudenko: The Peter Medawar Building for Pathogen Research, University of Oxford, South Parks Road, Oxford OX1 3SY, UK. [[email protected]]
12653 Wang, B.B., Ernst, N.L., Palazzo, S.S., Panigrahi, A.K., Salavati, R. & Stuart, K., 2003. ThMP44 is essential for RNA editing and structural integrity of the editosome in Trypanosoma brucei. Eukaryotic Cell, 2 (3): 578-587.
Stuart: Seattle Biomedical Research Institute, 4 Nickerson Street, Seattle, WA 98109, USA. [[email protected]]
12654 Wang, C.C., Bozdech, Z., Liu, C.I., Shipway, A., Backes, B.J., Harris, J.L. & Bogyo, M., 2003. Biochemical analysis of the 20 S proteasome of Trypanosoma brucei. Journal of Biological Chemistry, 278 (18): 15800-15808.
Wang: Department of Pharmaceutical Chemistry, University of California, San Francisco, California 94143-0446, USA. [[email protected]]
12655 Wang, J., Böhme, U. & Cross, G.A.M., 2003. Structural features affecting variant surface glycoprotein expression in Trypanosoma brucei. Molecular and Biochemical Parasitology, 128 (2): 135-145.
Cross: Laboratory of Molecular Parasitology, The Rockfeller University, Box 185, 1230 York Avenue, New York, NY 10021-6399, USA. [[email protected]]
12656 Wilkinson, S.R. & Kelly, J.M., 2003. The role of glutathione peroxidases in trypanosomatids. [Review] Biological Chemistry, 384 (4): 517-525.
Wilkinson: Department of Infectious Diseases, London School of Hygiene and Tropical Medicine, London WC1E 7HT, UK.
12657 Zeiner, G. M., Sturm, N. R. & Campbell, D. A., 2003. Exportin 1 mediates nuclear export of the kinetoplastid spliced leader RNA. Eukaryotic Cell, 2 (2): 222-230.
Department of Microbiology, Immunology & Molecular Genetics, University of California at Los Angeles, 609 Charles E. Young Dr. East, Los Angeles, CA 90095-1489, USA.
