Translocation is defined as the human-managed movement of living organisms from one area for free release in another. Throughout the world, increasing numbers of animals are translocated every year. Most of these movements involve native mammals, birds and fish, and are made by private and national wildlife agencies to augment existing populations, usually for sporting purposes. The translocation of endangered species, often to reintroduce them into a part of the historical range from which they have been extirpated, has also become an important conservation technique. The main growth in reintroduction projects over the last decade has involved smaller animals, including amphibians, insects and reptiles. The success of potentially expensive, high-profile wildlife translocation projects depends to a large extent on the care with which wildlife biologists and their veterinary advisers evaluate the suitability of the animals and chosen release site, and on the ability of the translocated animals to colonise the area. The veterinary aspects of reintroduction projects are of extreme importance. There are instances of inadequate disease risk assessment resulting in expensive failures and, worse still, the introduction of destructive pathogens into naïve resident wildlife populations. In this paper, some of the disease risks attending wildlife translocation are described. Risk assessment, involving the examination of founder and recipient populations and their habitats, is now a pre-requisite of managed movements of animals.

We report surveillance for rinderpest virus in wildlife populations in three major ecosystems of East Africa: Great Rift Valley, Somali and Tsavo from 1994 to 2003. Three hundred and eighty wild animals were sampled for detection of rinderpest virus, antigen or genome and 1133 sampled for antibody in sera from Kenya, Uganda, Ethiopia and Tanzania from 20 species. This was done modifying for wildlife the internationally recommended standards for rinderpest investigation and diagnosis in livestock. The animals were selected according to susceptibility and preference given to gregarious species, and populations were selected according to abundance, availability and association with livestock. Rinderpest virus, antigen and/or genome were detected in Kenya; within Tsavo, Nairobi and Meru National Parks. Serological results from 864 animals (of which 65% were buffalo) from the region were selected as unequivocal; showing the temporal and spatial aspects of past epidemics. Recent infection has been only in or peripheral to the Somali ecosystem (in Kenya). Our evidence supports the hypothesis that wildlife is not important in the long-term maintenance of rinderpest and that wildlife are infected sporadically most likely from a cattle source, although this needs to be proven in the Somali ecosystem. Wildlife will continue to be a key to monitoring the remaining virus circulation in Africa.

In January 1997, Tanzania requested international assistance against rinderpest on the grounds that the virus had probably entered the country from southern Kenya. Over the next few months, a variety of attempts were made to determine the extent of the incursion by searching for serological and clinical evidence of the whereabouts of the virus. At the clinical level, these attempts were hampered by the low virulence of the strain, and at the serological level by the lack of a baseline against which contemporary interpretations could be made. Once it became apparent that neither surveillance tool was likely to produce a rapid result, an infected area was declared on common-sense grounds and emergency vaccination was initiated. The vaccination programme had two objectives, firstly to prevent any further entry across the international border, and secondly to contain and if possible eliminate rinderpest from those districts into which it had already entered. On the few occasions that clinical rinderpest was subsequently found, it was always within this provisional infected area. Emergency vaccination campaigns within the infected area ran from January to the end of March 1997 but were halted by the onset of the long rains. At this time, seromonitoring in two districts showed that viral persistence was still theoretically possible and therefore a second round of emergency vaccination was immediately organized. Further seromonitoring then indicated a large number of villages with population antibody prevalences of over 85%. These populations were considered to have been 'immunosterilized'. Although no clinical disease had been observed in them, it was decided to undertake additional vaccination in a group of districts to the south of the infected area. Serosurveillance indicated that rinderpest could have been present in a number of these districts prior to vaccination. Serosurveillance in 1998 suggested that numerous vaccinated animals had probably moved into districts outside the infected and additional vaccination areas, but did not rule out the continued presence of field infection.

Emergency preparedness planning for animal diseases is a relatively new concept that is only now being applied in Africa. Information can be drawn from numerous recent disease epidemics involving rinderpest, contagious bovine pleuropneumonia (CBPP) and Rift Valley fever. These examples clearly demonstrate the shortcomings and value of effective early warning with ensured early reaction in the control of transboundary animal disease events. In concert, the Food and Agriculture Organization (FAO), through the Emergency Prevention-System for Transboundary Animal and Plant Pests and Diseases (EMPRES), and Organisation of African Unity/Inter-African Bureau for Animal Resources (OAU/IBAR), through the European Commission-funded Pan-African Rinderpest Campaign (PARC), have been actively promoting the concepts and application of emergency preparedness planning and should continue to do so under the proposed successor of PARC, namely: the Pan-African Programme for the Control of Epizootics (PACE). The potential partnership between the normative function of the FAO in developing and promoting emergency preparedness and the implementation of improved national and regional disease surveillance by PACE and other partners could witness the commencement of more progressive control of epidemic diseases in Africa and greater self-reliance by African countries in coping with transboundary animal disease emergencies.

A severe epidemic of rinderpest, affecting mainly wild ruminants, occurred between 1993 and 1997 in East Africa. Buffalo (Syncerus caffer), eland (Taurotragus oryx) and lesser kudu (Tragelaphus imberbis) were highly susceptible. The histopathological changes, notably individual epithelial cell necrosis with syncytia formation, were consistent with an infection with an epitheliotrophic virus. Serology, the polymerase chain reaction, and virus isolation confirmed the diagnosis and provided epidemiological information. The virus was related to a strain which was prevalent in Kenya in the 1960s, of a second lineage (II), and distinct from isolations of rinderpest virus in the region since 1986. The source of the virus was presumed to be infected cattle from the Eastern region of Kenya and Somalia. The pathogenicity of the virus varied during the epidemic. The mortality in buffalo populations was estimated to be up to 80 per cent, and population data suggested that the virus had an adverse effect on a wide range of species. The virus caused only a mild disease in cattle, with minimal mortality. The results confirmed the importance of wildlife as sentinels of the disease, but although wildlife were important in the spread of the virus, they did not appear to act as reservoirs of infection.

An investigation was made into whether recent vaccination of cattle with tissue culture rinderpest virus would cause immunosuppression and lead to more frequent or more severe infection with trypanosomes in animals grazing in tsetse-infested areas. Herds of cattle on Galana Ranch in Kenya were divided, with approximately half of each herd being vaccinated with tissue culture rinderpest virus strain Kabete 'O', while the rest remained unvaccinated. The herds were then exposed to the risk of natural infection with trypanosomes on the ranch. Three experiments were performed during different seasons. Infections with Trypanosoma congolense and Trypanosoma vivax were frequently detected but there was no evidence that vaccinated animals were more likely to acquire trypanosome infections or to show a more severe disease than unvaccinated cattle. It is concluded that tissue culture rinderpest vaccine does not cause immunosuppression and can safely be used in cattle likely to be exposed to tsetse flies and trypanosomosis.

Rinderpest is an ancient plague of cattle and other large ruminants, with descriptions of its effects dating back to Roman times. It is caused by a morbillivirus closely related to human measles virus. Although a very effective vaccine is available, it is heat labile, and logistical and financial problems hamper its delivery to the remote areas of Africa and Asia where enzootic foci remain. Periodic epizootics emerge from these foci and spread into neighboring areas, mainly as a result of uncontrolled livestock movement and trading. This is particularly true during wars or civil disturbances when normal veterinary controls do not operate. The disease continues to cause devastating economic losses in domestic livestock in areas of the world where it remains endemic.

Between April 1994 and November 1995 the most severe epidemic of rinderpest reported in the world for over a decade affected domestic livestock in the Northern areas of Pakistan. Full article published in Veterinary Record (1998) 143, 39-42.

Veterinary RecordVolume 142, Issue 24 p. 669-671 Short Communication Rediscovery of the second African lineage of rinderpest virus: its epidemiological significance T. Barrett, T. Barrett Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorM. A. Forsyth, M. A. Forsyth Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorK. Inui, K. Inui Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorH. M. Wamwayi, H. M. Wamwayi Kenya Agricultural Research Institute, National Veterinary Research Centre, Muguga, PO Box 32 Kikuyu, KenyaSearch for more papers by this authorR. Kock, R. Kock Kenya Wildlife Service, PO Box 40241, Nairobi, KenyaSearch for more papers by this authorJ. Wambua, J. Wambua Kenya Wildlife Service, PO Box 40241, Nairobi, KenyaSearch for more papers by this authorJ. Mwanzia, J. Mwanzia Kenya Wildlife Service, PO Box 40241, Nairobi, KenyaSearch for more papers by this authorP. B. Rossiter, P. B. Rossiter Pan African Rinderpest Campaign, OAU/IBAR, PO Box 30486 Nairobi, KenyaSearch for more papers by this author T. Barrett, T. Barrett Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorM. A. Forsyth, M. A. Forsyth Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorK. Inui, K. Inui Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorH. M. Wamwayi, H. M. Wamwayi Kenya Agricultural Research Institute, National Veterinary Research Centre, Muguga, PO Box 32 Kikuyu, KenyaSearch for more papers by this authorR. Kock, R. Kock Kenya Wildlife Service, PO Box 40241, Nairobi, KenyaSearch for more papers by this authorJ. Wambua, J. Wambua Kenya Wildlife Service, PO Box 40241, Nairobi, KenyaSearch for more papers by this authorJ. Mwanzia, J. Mwanzia Kenya Wildlife Service, PO Box 40241, Nairobi, KenyaSearch for more papers by this authorP. B. Rossiter, P. B. Rossiter Pan African Rinderpest Campaign, OAU/IBAR, PO Box 30486 Nairobi, KenyaSearch for more papers by this author First published: 13 June 1998 https://doi.org/10.1136/vr.142.24.669Citations: 4Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume142, Issue24June 1998Pages 669-671 RelatedInformation

Between April 1994 and November 1995 the most severe epidemic of rinderpest reported in the world for over a decade affected domestic livestock in the Northern Areas of Pakistan. As many as 40,000 cattle and yaks died, more by some estimates, and mortality rates may have exceeded 80 per cent in these species in several villages. This report describes some of the clinicopathological and epidemiological features peculiar to the outbreak, including laboratory-confirmed rinderpest in a goat, and the difficulties encountered before the disease was eradicated. It also describes the human costs and emphasises the need to accelerate the global eradication of this most eradicable disease.

Veterinary RecordVolume 139, Issue 5 p. 118-119 Short Communication Peste des petits ruminants in goats in Pakistan H. Amjad Qamar-ul-Islam, Veterinary Research Institute, Lahore, PakistanSearch for more papers by this authorM. Forsyth, Institute for Animal Health, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorT. Barrett, Institute for Animal Health, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorP. B. Rossiter, Pan African Rinderpest Campaign, OAU/IBAR, PO Box 30786 Nairobi, KenyaSearch for more papers by this author H. Amjad Qamar-ul-Islam, Veterinary Research Institute, Lahore, PakistanSearch for more papers by this authorM. Forsyth, Institute for Animal Health, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorT. Barrett, Institute for Animal Health, Pirbright, Woking, Surrey, GU24 ONFSearch for more papers by this authorP. B. Rossiter, Pan African Rinderpest Campaign, OAU/IBAR, PO Box 30786 Nairobi, KenyaSearch for more papers by this author First published: August 1996 https://doi.org/10.1136/vr.139.5.118Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume139, Issue5August 1996Pages 118-119 RelatedInformation

Translocation is defined as the movement of living organisms from one area for free release in another. Throughout the world, increasing numbers of native and exotic species are translocated every year. Most of these movements involve native mammals, birds and fish, and are made by private and national wildlife agencies to augment existing populations, usually for sporting purposes. The translocation of endangered species, often to reintroduce them into a part of the historical range from which they have been extirpated, has also become an important conservation technique. The success of potentially expensive, high-profile wildlife translocation projects depends to a large extent on the care with which wildlife biologists and their veterinary advisers evaluate the suitability of the chosen release site, and on the ability of the translocated animals to colonise the area. The veterinary aspects of reintroduction projects are proving to be of extreme importance. There are already instances of inadequate disease risk assessment resulting in expensive failures and, worse still, the introduction of destructive pathogens into naive resident wildlife populations. In this paper, some of the disease risks attending wildlife translocation projects are described and suggestions are made for the development of systematic procedures to reduce these risks both at the source of the founder animals and at the proposed release site.

Cloned bovine lymphoblastoid cell lines, transformed by the protozoan parasite Theileria parva were infected with cell culture-attenuated rinderpest virus vaccine. The virus grew readily in lymphoid B cells, CD4+ and CD8+ alpha/beta T cells and gamma/delta T cells producing new infectivity, viral antigens, c.p.e. and total cell death. There did not appear to be a predilection for any particular phenotype of lymphoblast. The results imply that if the vaccine causes immunosuppression, it could do so through a variety of mechanisms.

Bovine T lymphoblast cell lines transformed by the protozoan Theileria parva were compared with bovine kidney (BK) and Vero cells for their ability to isolate various strains of rinderpest virus from tissues and infected secretions. All of the strains of rinderpest virus that were tested, including attenuated cell-culture, caprinised and lapinised vaccines, and both mild and virulent pathogenic strains, readily induced syncytial cytopathic effect (cpe) in T lymphoblasts. The cpe could often be detected within one day of inoculation of lymphoblasts, whereas it took three to 14 days to appear in Vero and BK cells. Using lymphoblasts it was possible to reisolate rinderpest virus from nine of 42 swabs collected from three cattle experimentally infected with an isolate from a recent outbreak of mild disease whereas the same swabs yielded only one reisolate on BK cells. It was also possible using the lymphoblasts to detect infectious virus in the ocular, nasal and oral secretions of goats and rabbits infected with caprinised and lapinised virus, respectively. Peste des petits ruminants virus appeared to grow as rapidly as rinderpest virus in the lymphoblasts whereas canine distemper virus readily induced cpe on first passage but less readily on subsequent passage. Measles virus induced relatively little cpe when inoculated into lymphoblasts and did not appear to passage in these cells. The lymphoblasts are easy to maintain in culture and since they rapidly recovered 11 isolates from 37 diagnostic samples could prove useful in laboratories carrying out rinderpest diagnosis.

Rinderpest was confirmed in Kenya in 1986, 1987, 1988 and 1989. Three epidemiologically distinct events appear to have occurred: repeated outbreaks in West Pokot district related to cross-border movement of stock, an outbreak in Marsabit district in 1987 (thought to have been caused by illegal movement of cattle, possibly in vehicles, from countries further north) and a series of related outbreaks in and near Nairobi between 1988 and 1989 due to the unauthorized movement from abattoirs and holding grounds of slaughter stock possibly introduced from West Pokot or Marsabit. In West Pokot the disease affected unvaccinated calves and yearlings. In Marsabit cattle of all ages were affected. In August 1988, a major outbreak was confirmed in Kiambu and Kajiado districts in central Kenya, near Nairobi. At the same time a provisional diagnosis of rinderpest was made in a herd of cattle at a slaughterhouse in Nairobi. Rinderpest virus was isolated from sick cattle in all the outbreaks. Experimental infection of susceptible cattle with the Kiambu isolate demonstrated this to be of low virulence. Emergency vaccination and quarantine measures instituted immediately after confirmation eliminated clinical disease within three to four weeks in West Pokot, Kiambu and Nairobi. In Kajiado, however, the disease persisted for at least nine months, during which time a series of virus isolates was recovered. There was no evidence of infection in susceptible wildlife. This increase in the incidence of rinderpest in Kenya in recent years serves to highlight the problems of control and the need for concerted efforts to eradicate the threat of the disease from East Africa.

A malignant catarrhal fever (MCF)-like syndrome was experimentally induced in three steers, which were under immunization trials with a herpesvirus previously isolated from a case of MCF in a cow in Minnesota USA. The clinical signs observed in the three steers, and the pathological and histological lesions observed in two of these steers which succumbed to the disease syndrome were indistinguishable from those described for MCF. Although seroconversion was readily demonstrated in the three animals, virus was not re-isolated from the blood leucocytes, secretions and tissues obtained from the two animals which succumbed to the syndrome during the course of the disease and after death. However, a herpesvirus which showed cell rounding cytopathic effects (cpe) in bovine thyroid cells (Bth), was re-isolated from the one steer which survived the disease.