Final CRP Vienna-17042012

IAEA-314-D4-RC-1048.1 LIMITED DISTRIBUTION WORKING MATERIAL IMPROVING SIT FOR TSETSE FLIES THROUGH RESEARCH ON THEIR SYMBIONTS AND PATHOGENS FOURTH RESEARCH COORDINATION MEETING ORGANIZED BY THE JOINT FAO/IAEA DIVISION OF NUCLEAR TECHNIQUES IN FOOD AND AGRICULTURE 25 th – 30 th March, 2012 Vienna, Austria NOTE The material in this document has been supplied by the authors and has not been edited by the IAEA. The views expressed remain the responsibility of the named authors and do not necessarily reflect those of the government of the designating Member State(s). In particular, neither the IAEAA nor any other organization or body sponsoring the meeting can be held responsible for any material reproduced in this document. Contents 1.INTRODUCTION ......................................................................................................................................................... 4 1.1.T SETSE AND THE DISEASE ........................................................................................................................................ 4 1.2 TRYPANOSOMOSIS CONTROL AND THE SIT .............................................................................................................. 4 1.3. CONSTRAINTS AND TARGETS FOR IMPROVED EFFICIENCY OF TSETSE SIT .............................................................. 5 1.4 TSETSE SYMBIONTS .................................................................................................................................................. 5 1.5 TSETSE PATHOGENS .................................................................................................................................................. 6 2. CURRENT STATUS .................................................................................................................................................... 7 2.1. TSETSE SYMBIONTS .................................................................................................................................................. 7 2.2. TSETSE FLY PATHOGENS ....................................................................................................................................... 11 2.2. TSETSE FLY PATHOGENS ....................................................................................................................................... 11 3. INDIVIDUAL ACHIEVMENTS DURING THE CRP ........................................................................................... 14 4. LOGICAL FRAMEWORK ....................................................................................................................................... 45 5. AGENDA ..................................................................................................................................................................... 51 6- LIST OF PARICIPANTS .......................................................................................................................................... 55 ANNEX I: WORKING PAPERS .................................................................................................................................. 59 Page 3 Executive Summary Major efforts have been expended by a number of international scientists in a focused and coordinated manner to (i) elucidate the cause of the collapse of tsetse fly colonies and reduced fly yields in tsetse fly production facilities for SIT, and (ii) to put into practice an action plan to solve the problem by understanding the biological basis of the symptoms in the flies associated with the collapse. Through a coordinated action, it has been found that a virus is the culprit causing reduced fecundity and that the disease is characterized by the hypertrophy of the salivary glands, hence the name, salivary gland hypertrophy virus (SGHV). The virus genome has been sequenced and compared to a related virus in the house-fly. SGHV is vertically and horizontally transmitted. The incidence of the disease in the field throughout Sub-Saharan Africa ranges from 0-15%, but approaches 100% in laboratory reared colonies. Through this CRP, tsetse’s physiology including fecundity has been shown to depend upon fitness of its symbiotic fauna. Correlations and interactions between the presence of virus, disease symptoms, and the occurrence of bacterial symbionts ( Wigglesworthia , Sodalis and Wolbachia) has been explored. Strategies have been designed and partially validated to mitigate / control / eliminate the disease. These strategies are based on: (i) monitoring viral loads for colony quality control; (ii) blocking transmission using specific antibodies, and/or clean feeding practices; (iii) blocking virus replication by applying specific inhibitors of virus replication. Strategies have also been designed to: (i) monitor prevalence and loads of tsetse symbionts and pathogens; (ii) augment current feeding regiments to improve tsetse’s fecundity; (iii) improve the application of SIT by harnessing tsetse’s symbionts to develop pathogen resistant fly lines and by introducing natural sterility. The outcome of the research efforts provided the fundamental knowledge required on tsetse’s microbiome and SGHV to develop a solid and robust strategy to prevent colony collapses caused by SGHV. This will have a major impact on large-scale production facilities for SIT. Further experimentation is required, including efficacy testing, to make this strategy robust, reliable and applicable for large-scale production facilities. The anticipated outcome will help to improve SIT applications, which will be more efficacious and cost-effective. The program in addition has resulted in extensive capacity building and technology transfer to disease endemic countries (DECs). Concerted action has enabled the involvement of all participants in the research to ascertain the application of a well-orchestrated strategy and production process to secure high fly yields in the future for more sustainable SIT applications. Page 4 1.Introduction 1.1.Tsetse and the Disease Tsetse flies (Diptera: Glossinidae) are the cyclical vectors of the trypanosomes, which cause human African trypanosomosis (HAT) or sleeping sickness in humans and African animal trypanosomosis (AAT) or nagana in animals. It is conservatively estimated by the World Health Organization (WHO) that there are currently 10,000 – 45,000 cases of human African trypanosomosis (HAT) with 60 million people at risk in 36 countries covering ~40% of Africa (almost 10 million km²). After a devastating epidemic in the early 20 th century when a million people died of HAT the disease almost disappeared by the 1960’s from Africa. HAT has a disease burden of 1.47 million disability adjusted life years (DALY). Given that the disease affects hard to reach rural populations and that there is a lack of active surveillance in war-torn areas, the disease prevalence numbers are undoubtedly a gross underestimation. In addition to direct losses of human life and the financial cost of control, African trypanosomosis affects: • Human health, through protein deficiencies caused by shortage of meat and milk • Livestock production, since it causes morbidity and mortality • Agricultural production, through the lack of draught animals and manure • Rural economy, by preventing integrated agriculture and livestock production • National economy, through essential import of living animals and their products • Environment, though the use of insecticides. The tsetse and trypanosomosis (T&T) problem is a key obstacle for rural development. About 50 million cattle and tens of millions of small ruminants are at risk from AAT. T&T are the major factors preventing the establishment of sustainable agricultural systems in sub-Saharan Africa. The Programme Against African Trypanosomiasis (PAAT) estimates that AAT causes approximately 3 million cattle deaths per year. Farmers are required to administer approximately 35 million doses of costly trypanocidal drugs. Unfortunately, many of these chemicals fail because of development of resistance by the parasites. Direct losses in meat production and milk yield and the costs of programmes that attempt to control trypanosomosis are estimated to amount to between US$600 million and $1.2 billion each year. In the absence of the AAT problem, a family that is currently dependent on manual labour alone could use draught animals and thus increase its income from agricultural work by 45 percent per unit of land and by 143 percent per unit of labour. If one includes this potential in livestock and crop production, trypanosomosis is estimated to cost sub- Saharan Africa US$4 billion or more each year, equivalent to one-quarter of the area's total livestock production. 1.2 Trypanosomosis Control and the SIT Human sleeping sickness is a zoonosis caused by the protozoan Trypanosoma brucei rhodesiense in East Africa and T. b. gambiense in West and Central Africa. The nagana causing related trypanosomatids T. vivax and T. congolense are major pathogens of cattle and other ruminants, while T. simiae causes high mortality in domestic pigs and T. brucei affects all livestock. Vaccines are not available and are unlikely to be developed due to the antigenic variation in the trypanosome in the mammalian host. The drug treatment of HAT is in a perilous state and relies on old, often dangerous drugs and resistance is becoming an increasing problem. In contrast, disease control, via control of the tsetse vector, has been found to be highly effective. Current vector control efforts, which depend

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