Rinderpest has been eradicated from the globe. This will be the joint message from the UN's Food and Agriculture
Organisation (FAO) and the World Organisation for Animal Health (OIE) during a meeting at FAO's Rome headquarters
in June 2011. This follows their announcement in October 2010 that rinderpest field operations had ceased.
Rinderpest (cattle plague) was the most devastating disease of domestic cattle, buffalo and other cloven-footed
animals, killing millions of animals.
Once responsible for untold human misery in Africa, Asia and Europe, the causative agent, rinderpest virus, was
most probably eliminated from its last stronghold in 2001; it has not been detected since then, despite active
surveillance. This is the first instance of the global eradication of an animal virus. Rinderpest virus is a
close relative of human measles virus, the elimination of which still eludes us.
The socio-economic impact of rinderpest was huge, as cattle, of many types, are kept for many purposes. In addition to meat and milk they provide leather, and in some countries they still provide dung for fuel or manure, and act as draft animals. Loss of the latter badly affected ploughing, which, in turn, led to famine.
That the battle against rinderpest has been so successful is a testament to the persistence and passion shown
by many people, comprising scientists and veterinarians in both developed and emerging countries, officials in
organisations such as the UN's Food and Agriculture Organisation
and World Organisation for Animal Health
and contributing governments, and, not least, the countless number of villagers who owned cattle, and their
Vaccination against the virus was at the heart of the eradication campaigns throughout the twentieth century. However, vaccines alone would have failed to do the job had it not been also for the development of diagnostic tests for rinderpest, such as those developed in The Pirbright Institute's Pirbright Laboratory. The development of these tests, whilst crucial for monitoring the ebb and flow of the virus and the success or otherwise of vaccination campaigns, would also have been insufficient were it not for the on-the-spot training in their use given by scientists from IAH Pirbright and elsewhere, as well as the scores of thousands of samples tested in laboratories such as Pirbright. In the 1990s genetic analysis of the rinderpest viruses isolated from various countries and regions within them enabled more precise detective work to be done, the better to understand why pockets of infection remained, instructive for deciding the final plays of the endgame, leading to the denouement of rinderpest.
This great achievement begs the question as to why the eradication of the closely related measles continues to lag behind that of rinderpest. The vagaries of human nature are perhaps responsible for the failure to finish-off measles. Nonetheless, the eradication of rinderpest virus, several decades after the only other virus to have been eliminated, smallpox (declared eradicated, by WHO, in 1980), is an inspiration to those attempting to achieve the same with measles and some other viruses e.g. poliovirus, that are genetically quite stable and which, therefore, make eminently achievable targets.
The Pirbright Institute is the FAO's World Rinderpest Reference Laboratory i.e. it is the world's principal laboratory and centre of expertise for diagnosis of this disease.
History of rinderpest
Tools for eradication
Scientists of The Pirbright Institute who have contributed to the eradication of rinderpest are briefly described below.
What is rinderpest virus?
Rinderpest virus (from the German for cattle plague) belongs to a group of viruses called the
, after the Latin for plague (morbus). The group also includes measles virus, peste des petits ruminants virus (PPRV) that causes plague in sheep and goats and other ruminants, canine distemper virus of dogs and some other carnivores, and viruses of seals and dolphins. Rinderpest virus not only infects cattle and buffalo but also grows in animals such as eland, giraffe, wildebeest, kudu and various antelopes.
The morbilliviruses are closely related to each other, so much so that measles vaccines have been used to
vaccinate animals against rinderpest virus.
has become of increasing importance, especially in Asia, since the cessation of vaccination against
rinderpest (following its eradication). PPRV does grow in cattle and other bovines but without causing
disease; it causes serious disease in small ruminants - sheep and goats. Rinderpest vaccination had not only
led to the elimination of rinderpest but it had also reduced the incidence of the closely related PPRV in
bovine species. Consequently less PPRV was shed into the environment, reducing the risk to goats and sheep.
What is rinderpest ?
(from the German for cattle plague) is one of the oldest known and most devastating diseases of cattle,
buffalo and other bovines, such as eland, giraffe, wildebeest, kudu and various antelopes. Domestic cattle,
water buffalo and yaks are very susceptible, mortality being 80 to 90% when infected with the more virulent
strains of the virus.
include fever, discharges from nose and eyes, ulceration and other damage in the upper digestive and respiratory
tracts, enteritis followed by diarrhoea, dehydration, and death.
The origins of rinderpest
Such have been the socio-economic consequences of rinderpest, it is one of the best documented diseases. It
originated in Asia and often broke out of its native area, either by infected cattle being traded, or by
invading armies accompanied by their oxen. Cattle were not only sources of food but also used for traction.
Descriptions suggest that it was present in Egypt 5000 years ago. The Huns, a nomadic pastoral people, are
credited with bringing the disease into Europe from Asia in the fourth century. There are many accounts of the
disease in Roman Europe and subsequently. The Mongol armies of Genghis Khan and his successors caused a series
of pandemics in Europe in the 13th century. Apparently their Grey Steppe oxen were little affected by the virus
but could excrete it for months, resulting in the death of European cattle wherever they went; unwitting
biological warfare. Since cattle were used to pull ploughs as well as for meat and milk, their loss had
ramifications that led to destabilisation of governments.
Disease in 18th century Europe: beginnings of the veterinary profession
The first scientific descriptions of the disease were in Europe in the early 18th century. Such were the
losses in the papal herds that Pope Clement ordered his physician, Lancisi, to take action. Lancisi introduced
control measures that have stood the test of time for many diseases, albeit augmented by vaccination in the
20th century; slaughter, movement restrictions, burial of animals in lime, and inspection of meat. These measures,
brutally enforced, were successful, and were rapidly adopted in other European countries, including Britain.
The first veterinary school (Lyon, 1761) was created in response to the need to train specialists, the first
veterinarians, in effect - to deal with rinderpest. Other European countries followed suit. This, in turn, led
to the creation of State Veterinary Services (SVS) e.g. in England in 1865. Despite an understanding that import
restrictions were key to control, relaxation of import controls in Britain resulted in further incursions of
rinderpest in the late 18th and early 19th centuries. Within two years of the creation of the SVS in England, when
the principles of Lancisi, with refinements, were properly applied and allied with import controls, the disease was
Not only were veterinary schools and SVSs created in response to rinderpest, so too was the World Organisation
for Animal Health (OIE). Following the very worrying introduction of rinderpest into Belgium in 1920, a conference
was held in Paris in the following year. One consequence was the creation, six years later, of the OIE.
The great African rinderpest pandemic of the 19th century
This pandemic started in 1887 in Eritrea, north-eastern Africa. It can be said that the arrival of rinderpest in
Africa was a consequence of European colonisation, and that subsequently colonisation was expedited. The virus is
believed to have been brought in by Italian imports of infected zebu cattle from Aden or Bombay. In 10 years it
had spread throughout the continent. It is recorded that 80-90% of susceptible domestic and wild animals died. In
Kenya, rinderpest led to starvation. This, exacerbated by subsequent smallpox, resulted in a massive reduction
in the population of the indigenous Masai, making colonisation by Europeans easier. F.J.D. Lugard, writing in 1893
about Masailand, said "never before in the memory of man, or by the voice of tradition, have the cattle died in
such numbers; never before has the wild game suffered." A Masai man is elsewhere recorded as saying, in regard
to the ground being littered with the corpses of animals and people "so many and so close that the vultures had
forgotten to fly."
Rinderpest in the 20th century: the era of vaccination
The disease ebbed and flowed in large parts of the world throughout the first half of the twentieth century, at times being as devastating as in earlier periods. Wars resulted in the collapse of control measures, leading to resurgence of the virus into vast areas, whilst during more peaceful times lax enforcement resulted in spread via trade.
For example, following the great African rinderpest pandemic of the late 19th century, West Africa had only pockets of disease by 1912. But by 1918 the situation had reversed, hundreds of thousands of cattle dying annually. Gradually the disease was brought under control again, this time with the added measure of vaccination. Sadly, consequent on this success, donor countries reduced their support. Coincidentally the boom in the Nigerian economy resulted in greatly increased trade in animals from far and wide; the second Great African Rinderpest Panzootic (late 1970s, early 1980s) was the result. A Pan-African Rinderpest Campaign was launched in the late 1980s. By the end of the century the infected area in Africa had shrunk to two regions: southern Sudan with contiguous areas of Kenya, Ethiopia and Uganda; and southern Somalia with eastern Kenya and southern Ethiopia (the southern Somali pastoral ecosystem). Genetic analysis had revealed that two different lineages of the virus were associated with these two areas. This showed that the circulation of the virus in the one area was independent from that in the other, with the implication that ad hoc solutions for control were required for each region.
The chaos of the Second World War resulted in resurgence of the disease in South and South-east Asia. More than one million cattle were killed by the disease in western China in 1938 to 1942, and the disease was widespread in China at the end of the 1940s. A control campaign, including vaccination, that Peter Roeder has described as "heroic", resulted in the elimination of the virus there by 1955. An FAO-coordinated campaign in South-east Asia achieved the same result by 1957.
In 1969 the virus spread from Afghanistan through Iran to the Mediterranean and into the Arabian Peninsula in what is known at the Near East Panzootic of 1969 to 1973. The disease is known to have occurred in Israel, Lebanon, Syria, Jordan, Kuwait and Yemen shortly afterwards. Iraq was affected by another epidemic in 1985. These and other incursions in the region, including into Turkey, were largely the result of trade, not conflict. Concerted efforts, orchestrated by the FAO, resulted in the elimination of rinderpest from West Asia and the Middle East by the mid-1990s.
The Indian sub-continent was severely affected by rinderpest throughout the 20th century, with peaks at various times. Each time vaccination campaigns shrunk the affected areas. The last large outbreak occurred in 1994, brought by buffaloes imported into northern areas from the Punjab. The virus caused huge losses in cattle, yaks and buffaloes. An intensive vaccination campaign by the Pakistan government, supported by FAO and the EU, was ultimately successful; the evidence indicates that the virus had been eliminated from the region by the end of 2001, perhaps earlier. This left the Somali ecosystem as the last bastion of rinderpest.
The endgame: the Global Rinderpest Eradication Campaign
The last big 'push' against rinderpest came in 1994, with the launching by FAO, in close association with the World Organisation for Animal Health (OIE), of the Global Rinderpest Eradication Campaign (GREP).
This was a time-bound programme, due to end in 2010, with the expectation of ultimate victory over the virus by that year, at the latest. By 1994 rinderpest was localised in four areas of Asia (Pakistan with Afghanistan; Asiatic Russia with Mongolia and China; Yemen with Saudi Arabia; and Turkey with Iraq and Iran), and two regions in Africa (southern Sudan with contiguous areas of Kenya, Ethiopia and Uganda; and southern Somalia with eastern Kenya and southern Ethiopia, known as the southern Somali pastoral ecosystem).
GREP was the most all-encompassing of the various campaigns against rinderpest, in that all measures needed for enduring success were incorporated, including: a thorough and ongoing, science-based understanding of why the disease was still present, including factors unique to each region e.g. wildlife reservoirs (epidemiology); mass vaccination with quality assured vaccines; training and management of national veterinary services to not only apply vaccines but also to undertake thorough surveillance, including for several years after the objective had been believed to have been achieved; support for national diagnostic services; proper risk analysis; contingency plans in the event of further outbreaks; and rules for the gaining of, from OIE, accreditation of freedom from rinderpest.
As the 21st century dawned, GREP had been successful in reducing the rinderpest enclaves from six to two, the latter being the two regions in Africa - southern Sudan with contiguous areas of Kenya, Ethiopia and Uganda; and southern Somalia with eastern Kenya and southern Ethiopia, known as the southern Somali pastoral ecosystem. Rinderpest was last detected, in samples sent from Kenya to the World Rinderpest Reference Laboratory at Pirbright, in 2001. There have been suspected cases of rinderpest since then, but all investigations, including the application of sensitive laboratory tests, have singularly failed to find any evidence for the involvement of rinderpest virus. Thus it is that FAO expects, in 2010 or shortly thereafter, to declare that the world is rid of rinderpest, that rinderpest virus has been eradicated.
The eradication of rinderpest from much of Europe in the 19th century (and the outbreak in Belgium in 1920) without the aid of vaccines proved that the strict application of sanitary measures could be sufficient. However, that required a degree of organisation and control that was not achievable in much of Asia and Africa. Vaccines provided a crucial piece of the rinderpest control jigsaw in the 20th century; vaccination produced lifelong immunity
In 1897 Robert Koch reported that the subcutaneous inoculation of blood and bile from an infected animal protected the inoculated animal from rinderpest infection. This, however, was a highly dangerous procedure. He also found that a mixture of virulent virus and serum (blood from which the cells had been removed) collected from recovered animals also induced immunity. Further research led to this serum-simultaneous virus approach being used widely in India and Africa.
A safer approach was to weaken (attenuate) virulent virus to make what today we would call a live attenuated vaccine strain. This was achieved by inoculating goats with virulent virus. The virus grew sufficiently well in the goats but they did not get sick. Virus recovered from the goats was used to inoculate more goats. Repetition of this process (serial passage) resulted in vaccine virus (caprinized vaccine) that grew in cattle, inducing protection without causing disease.
The next development was of inactivated rinderpest vaccines. Various chemicals were able to 'kill' the virus in tissues collected from infected animals, without destroying the integrity of the virus. When inoculated into animals these vaccines induced immunity. Inactivated vaccines were cheaper and less laborious to produce than the serum-simultaneous vaccines, and were widely used.
A disadvantage of the inactivated vaccines was that the protection they induced was not life-long. A single inoculation lasted for only six months. Two years' protection required two inoculations. More attention was paid to producing live attenuated vaccines, which did induce life-long immunity. Several more vaccines, using a variety of rinderpest virus strains, were made by passage in goats. These proved unsuitable for the more susceptible Asiatic livestock breeds, whereas rinderpest virus attenuated by passage in rabbits (lapinized vaccine) was suitable. Not all countries had sufficient rabbits to grow the lapinized virus. Fortunately the lapinized virus was able to grow in goats, sheep and calves, and even in Asiatic pigs (which were used for this purpose in Thailand). The Kabete O African strain of virus was used to make attenuated virus by passage in chick embryos, the resultant vaccine being used in some regions.
The next big advance came on the back of the development of being able to grow cells in the laboratory. If rinderpest vaccine virus could be grown in cell culture, rather than in animals, it would enable a much more consistent, quality controlled product, free from extraneous materials, to be made. A number of unsuccessful attempts were made to grow various vaccine strains of rinderpest in cell culture but then, in 1962, W. Plowright and R.D. Ferris made a breakthrough; they were able to grow the Kabete O strain in cell cultures of bovine kidney (BK). Moreover, further passage led to attenuation of the virus. (Already attenuated vaccine strains i.e. laprinized, caprinized and egg-adapted virus, did not grow in the BK cells.) After further research, this tissue culture rinderpest vaccine was demonstrated to be safe and efficacious for cattle of all breeds, ages and sex. Moreover, the potency of a batch of vaccine could be determined by measuring the infectivity of the virus in the laboratory; it was not necessary to test it in animals.
Live vaccines were not without disadvantages, however. One was the necessity for keeping the vaccine cold, or else the virus lost its infectivity, rendering the vaccine useless. Keeping the vaccine cold was logistically very difficult in hot climates. This problem was overcome after the Kabete O strain was adapted to Vero cells. This was a continuous cell line that could be maintained in the laboratory without going back to animals for fresh tissue, unlike bovine kidney cells, that were made on each occasion from freshly obtained kidneys. A high yield of infectious virus combined with a new freeze-drying regime resulted in a much more thermostable vaccine that did not have to be kept at low temperature. Indeed, it retained potency even in the extremely hot conditions met in many of the countries where it was needed. Production of the vaccine, called Thermovax, was successfully transferred to a number of vaccine manufacturers in Africa, and it was used in Sudan, Somalia, Uganda and Ethiopia, amongst the last strongholds of the disease.
Three other pieces in the rinderpest eradication jigsaw were robust methods for (a) the detection of antibodies to the virus (in hundreds of thousands of blood samples), and (b) for detecting the virus itself, rapidly, and without relying on the virus remaining infectious (difficult considering the temperatures where the samples originated). Thirdly, a procedure was required that would precisely identify the particular strain of virus in a given herd - by its genetic fingerprint.
A rapid turnover antibody detection test was required for the thorough, long term surveillance work after vaccination, to monitor the immunity of domestic herds, and to assess the presence of virus in susceptible wild animal populations. The virus detection test was used when tissue samples from animals suspected of having rinderpest were submitted, the virus itself being detectable before antibodies had formed against it. Moreover, detection of virus confirmed active infection whereas antibodies were indicative of infection at a largely indeterminate earlier time.
Detecting the virus
A big step forward in the detection of the virus in large numbers of samples was the development, in the 1990s, of the antigen- or immune-capture enzyme linked immunosorbent assay (immunocapture ELISA ). Briefly, a monoclonal antibody able to bind both rinderpest and the closely related peste des petits ruminants virus (PPRV) was coated onto the wells of standard diagnostic, high throughput 96-well plates. A sample of homogenised tissue, suspected of containing either virus, was added. Each sample was used in two wells. After washing, a second antibody, specific for rinderpest virus, was added to one of the pair of wells. An antibody specific for PPRV was added to the other well. Binding of the second antibody was revealed by an enzymatic colour-generating procedure. This simple procedure, the technology for which was transferred to countries in Asia and Africa, could not only detect rinderpest virus but could also detect and distinguish it from PPRV, whose presence would otherwise have been an impediment to the unequivocal diagnosis of rinderpest, the more serious of the two diseases in bovines.
The immune capture ELISA still required that samples were sent to a specialised laboratory, a time-consuming process. As speed was of the essence in curbing any resurgence of the virus during the final push to eradicate the virus, John Anderson at The Pirbright Institute Pirbright developed a pen-side (on farm) strip test based on the same technology as used for pregnancy tests. Eye swabs were shaken in a small volume of liquid, some of which was then applied to the lower window, which already contained dried reagents. These, and any virus particles present in the sample, then travelled upwards by wicking\capillary action. If virus was present then a coloured line appeared, within minutes, in the middle window, the top window being a control. When tested in the field in Pakistan, veterinary officers and technicians found the device easy to use. Moreover, it was more sensitive than the immune-capture ELISA. Subsequently the strip test was used to investigate potential outbreaks in Pakistan, where it did in fact reveal pockets of infection, contributing to the eradication of the virus in Pakistan. The Pirbright Institute has since used this technology to develop a commercially available pen-side test for the rapid detection of foot-and-mouth disease virus.
In the 1990s the late Tom Barrett of The Pirbright Institute's Pirbright Laboratory developed a procedure for detecting rinderpest by virtue of its genetic material, RNA. (The test is called a reverse transcriptase polymerase chain reaction, RT-PCR). Although not conducive for use in the field, and requiring a specialist laboratory, the product of the RT-PCR, a DNA copy of part of the genetic material of the virus, can be sequenced, providing a genetic fingerprint. This enables the most precise identification of a particular virus strain. The genetic fingerprint of a given strain of virus enabled its relationship with other strains to be established, providing evidence to identify the source of the virus in an outbreak, and the likely means by which the disease arrived to a region. In 1993 the technique was used to show that an outbreak of the disease on the Russian-Mongolian border had originated in Asia. In the following year there was an unexpected outbreak of rinderpest in buffalo and kudu in south Kenya. Sequence analysis after RT-PCR revealed that the virus in question was from a lineage that had been thought to be extinct, revealing the presence of another, previously hidden, endemic focus in the region.
Detecting antibodies to the virus
Following the resurgence of rinderpest in Africa in the 1980s, the Pan African Rinderpest Campaign (PARC) was undertaken. A major aspect of PARC was mass vaccination. Monitoring the effectiveness of that required the analysis of hundreds of thousands of serum samples. For this purpose, John Anderson and colleagues at The Pirbright Institute at Pirbright developed a high throughput indirect ELISA to detect antibodies to rinderpest. This assay was produced jointly as a kit by IAH and the Joint FAO/IAEA Animal Health Section in Vienna and distributed to all countries within PARC, together with the necessary training and support. It was used successfully between 1986 and 1990. However, the test could not distinguish between antibodies to rinderpest virus and those against the closely related peste des petits ruminant virus (PPRV). Poor water quality and serum quality in some affected areas also impacted negatively on the test.
These factors led John Anderson to develop the competitive ELISA which was specific for antibodies to rinderpest. Briefly, serum samples were added to the wells of 96-well plates which were coated with rinderpest virus. After washing, a rinderpest-specific monoclonal antibody was added, associated with a colour-generating system. If the serum samples had not contained antibodies to rinderpest virus, the monoclonal antibody bound to the wells and generated colour. If, however, the samples had contained rinderpest antibodies, the binding of those to the virus on the wells would have blocked (competed with) the subsequent binding of the monoclonal antibody; no colour meant that antibodies to the virus were present in the serum sample. This test proved to be more robust than the indirect ELISA in field conditions. Moreover, unlike the indirect ELISA, it could be used to look for rinderpest antibodies in any species, including wild animals, without modification. The competitive ELISA has been used very successfully throughout Africa, Asia and the Middle East. In recent years it has been used for monitoring purposes after the end of the GREP vaccination campaign, contributing evidence that the virus has indeed been eradicated.
Measles: awaiting eradication
Measles is a highly contagious viral disease, which affects mostly children. It is transmitted via droplets from the nose, mouth or throat of infected persons. There is no specific treatment for measles and most people recover within 2-3 weeks. However, particularly in malnourished children and people with reduced immunity, measles can cause serious complications, including blindness, encephalitis, severe diarrhoea, ear infection and pneumonia. Measles can be prevented by immunization.
The WHO is currently nearing the end of a 2006-2010 plan to reduce global measles deaths by 90% compared to 2000 estimates.
In 2008 there were 278,358 cases of measles reported to the WHO, similar to 2007 in which 197,000 measles-related deaths were reported to the WHO. Globally WHO estimates that 83% of infants were vaccinated against measles. Take-up of vaccine was >90% in North America, Australia and most of Europe, most of South America, and parts of Africa. India and many countries within Africa are where the lowest vaccination rates occur.
Within Europe it is notable that the UK and France had <90% vaccination coverage. The UK's Health Protection Agency reported in February 2009 that the number of confirmed cases of measles in the UK was 56; 437; and 1,348 in 1999, 2003 and 2008, respectively, a 24% rise over the decade.
The drop in uptake of the triple MMR (which contains live attenuated measles, mumps and rubella viruses) was in part related to research (subsequently discredited) that raised the possibility that this vaccine was linked to an increased risk of autism.
The source of most of the material on this webpage is from:
- Rinderpest and Peste des Petits Ruminants: virus plagues of large and small ruminants. (2006). Eds. Thomas Barrett, Paul-Pierre Pastoret and William Taylor. Elsevier, London.
This book, written and edited by scientists who, between them, were intimately associated with the eradication of rinderpest, is a most comprehensive and in-depth account of all aspects of rinderpest.
A concise account of the eradication of rinderpest is:
- Conquering the Cattle Plague: the global effort to eradicate rinderpest (2009). Peter Roeder and Karl Rich. In: Millions fed: proven successes in agricultural development. Eds, David J.Spielman, and Rajul Pandya-Lorch. Pages 109-116. International Food Policy Research Institute (IFPRI), Washington DC, USA. http://www.ifpri.org/contact
This is freely available online (Chapter 16) at http://www.ifpri.org/publication/millions-fed
Institute for Animal Health scientists who have contributed to the eradication of rinderpest
IAH scientists have been at the forefront of the fight against rinderpest for several decades.
Dr Walter Plowright , who, in the 1950s, developed one of the most successful vaccines against rinderpest
, for which he was awarded the World Food Prize, was Head of the Department of Microbiology at the
Institute's Compton Laboratory between 1978 and 1983.
In the 1960s Dr William (Bill) Taylor directed the production of the Plowright vaccine at the East African Veterinary
Organisation, Kenya. He continued to work on rinderpest, and the closely related peste des petites ruminants virus, after
he joined the Institute for Animal Health in 1978. In 1986 he joined the Pan African Rinderpest Campaign in Nairobi, working
for the FAO and EU, and three years later moved to New Delhi to advise the Indian Government on their eradication campaign.
He was then an FAO consultant on rinderpest for ten years. He currently helping several countries to draft their rinderpest
dossiers for submission to the OIE.
Whilst at IAH Pirbright between 1984 and 1985 Dr Peter Roeder OBE developed diagnostics for foot-and-mouth disease and
studied bluetongue. Having earlier been in Africa, he then returned there with the World Bank's Ethiopian Fourth Livestock
Development Project. This included a study of the epidemiology of rinderpest between 1989 to 1992. Following a number
of roles with the FAO, in 2000 he was appointed the Secretary of the Global Rinderpest Eradication Programme,
which led to the eradication of the virus. He is now involved in the process by which countries prove that
rinderpest has been eliminated.
Dr John Anderson MBE joined the IAH in 1968. Between 1971 and 1977 he was seconded by the Overseas Development Agency
to Nairobi, Kenya, working on foot-and-mouth disease. After his return to Pirbright he began working on rinderpest with Bill
Taylor, which included his development of an indirect ELISA to detect antibodies to rinderpest virus. Working with the
International Atomic Energy Agency, Vienna, in 1985 John set up, trained and assisted a network of laboratories in Africa
to use this test for monitoring of rinderpest. He then extended the training to the Middle East and Asia. In 1990 he
developed a competitive ELISA for antibodies to rinderpest, this test being used throughout the eradication programme. A
decade later he developed a pen-side test which could be used in the field, detecting the presence of the virus itself
within a few minutes. In 1994 IAH Pirbright was designated as the FAO World Reference Laboratory for Rinderpest, with John
as its Head until his retirement in 2008. In 2003 John was awarded an OBE for Services to Animal Health.
Dr Martyn Jeggo, currently Director of the Australian Animal Health Laboratory (AAHL), Geelong, worked at IAH Pirbright
from 1979 to 1986, where his research included aspects of the diagnosis of rinderpest . Then in 1986 he joined the Animal
Production and Health Science Section of the Joint FAO/International Atomic Energy Agency Division of Agriculture, Vienna,
becoming Section Head in 1996. Throughout this period in the United Nations (UN), he was intimately involved in the global
campaign to eradicate rinderpest with a focus on providing laboratory support at the national level in many rinderpest
infected countries. Using a variety of UN support mechanisms, these activities from the Joint FAO/IAEA Division ensured a
co-ordinated laboratory approach both to rinderpest diagnosis and sero-surveillance. This network of laboratories proved
a critical component in reaching the successful eradication of the disease. In 2002 Dr. Jeggo moved to Australia as Director
Professor Tom Barrett, who very sadly died on 19 September 2009, came to the Institute in 1985 and brought
molecular biological analysis to bear on rinderpest virus and peste des petits ruminants virus (PPRV). Amongst his many positions
Tom was a member of the Advisory Committee for the EU Pan African Control of Epizootics (PACE) Programme, and a member of
the Wellcome Trust review panel to decide priorities for their initiative on "Animal Health in the Developing world" in
2003. Research on PPRV continues within the Institute, under the leadership of Dr Michael Baron, whose investigations
include the mechanisms by which components of PPRV block host defence mechanisms.
The Pirbright Institute continues as the World Reference Laboratory for rinderpest, on behalf of the FAO and
OIE. Led by Dr Chris Oura, the rinderpest laboratory provides the
diagnostic kits (competitive ELISA kits ) that are being used in the final stages of the eradication programme. The
rinderpest laboratory still receives samples for testing, including from the Somali ecosystem , where the last
rinderpest virus was detected in 2001.
If you would like to speak with Drs Anderson, Baron, Jeggo, Oura or Taylor, contact Professor Dave Cavanagh, Institute
for Animal Health: Tel. (+44) (0)1635 577241 or mobile (+44) 07789 941568; firstname.lastname@example.org. The Institute for
Animal Health is an institute of the Biotechnology and Biological Sciences Research Council