• Introduction
• Epidemiology
• Pathogenesis
• Diagnosis & differential diagnosis
• Control / Prevention
• Marketing & trade / Socio-economics
• Important outbreaks
• FAQs
• References

Important outbreaks

For reasons that are probably complex, FMD outbreaks in cattle in southern Africa have increased in frequency since the turn of the 21st Century. In the period 1981-2000 a significant decrease in the occurrence of FMD outbreaks in Botswana and South Africa was evident but in the period 2001-2010 the situation deteriorated significantly (Fig. 7). The reasons for this pattern of events are probably multifactoral.

Most recent SAT outbreaks have occurred in or near to the Kavango-Zambesi Transfrontier Conservation Area (KAZA TFCA – by far the largest in southern Africa) and the Greater Limpopo TFCA. About 1.5 million people and their livestock live in KAZA TFCA which is about 440 000 km² in extent and incorporates parts of 5 countries. This area also has a large (about 250 000) and growing elephant population which places increasing pressure on existing and planned fences designed to assist in controlling FMD. Some of the recent outbreaks have also proven difficult to manage, e.g. the so-called Habu outbreak in Ngamiland (northern Botswana) in 2008 persisted for about two years despite repeated rounds of vaccination. Spread of this outbreak south of the Kuki fence, i.e. into the Ghansi District ‒ part of Botswana’s recognized FMD-free zone ‒ resulted in temporary suspension of all Botswana’s beef exports to the European Union in 2009.

In 2011 an outbreak of FMD occurred in northern KwaZulu-Natal which apparently produced little clinical disease although SAT1 viruses were isolated from cattle with clinical disease (Fig. 8). At roughly the same time infection with SAT3 virus was detected in buffalo in the Ndumu Game Reserve which lies within the area of the cattle outbreak. This buffalo population was previously free from FMD. Unfortunately, little official information on these events has so far been provided by South Africa’s Directorate of Veterinary Services but laboratory data indicate that the viruses were related to SAT1 viruses endemic to the Kruger National Park (KNP) area and, more distantly, to viruses in southern Zimbabwe. Similarly, the SAT3 viruses obtained from the Ndumu game reserve buffalo are related to SAT3 viruses from the KNP and southern Zimbabwe. There is no direct connection between the KNP or southern Zimbabwe and northern KwaZulu-Natal. Therefore, how these SAT1 and SAT3 viruses spread to northern KwaZulu-Natal is not obvious (Fig. 8).

Also in 2011, Botswana suffered 3 SAT2 outbreaks in cattle – one in Ngamiland and the other two at locations close to one another on the border with Matabeleland South (Zimbabwe), i.e. in Botswana’s Zones 6 and 7. Viruses involved in the two Botswana outbreaks on the Zimbabwean border could not so far be matched with SAT2 viruses isolated in Matabeleland South in 2010 (Quarterly reports of the FAO World Reference Laboratory for FMD; Pirbright Laboratory - www.wrlfmd.org). Strangely, however, the Botswana SAT2 outbreak viruses from Zones 6 and 7 were closely related to viruses that caused outbreaks in Gaza and Maputo Provinces of Mozambique in 2010; possibly spread from Chicualacuala which is on Zimbabwe’s south-eastern border.

Collectively, the FMD incidents summarized above are indicative of a rapidly worsening FMD situation in southern Africa in the last 10-11 years. This is clearly a serious regional problem.

There have been assertions that inability to prevent and manage SAT2 outbreaks in the recent past in southern Africa was due to poor vaccine performance ‒ possibly as a result of poor matching between vaccine strains and field viruses. However, it is clear from investigations conducted on behalf of the Food, Agriculture & Natural Resources (FANR) Directorate of the SADC Secretariat and the Food & Agriculture Organisation (FAO) that poor vaccine administration and inadequate application of other zoosanitary control measures (including management of animal movement) were also important factors in the occurrence and persistence of these outbreaks (SADC, 2010). Nevertheless, recent evidence for greater antigenic variation occurring within the SAT2 serotype as compared with SAT1 has been provided despite the fact that the range of amino acid variation within the genomes of the two serotypes were similar (Maree et al., 2011). This may provide the technical basis for better understanding why SAT2 outbreaks have generally occurred more frequently and proven more difficult to control than outbreaks caused by SAT1 and SAT3 viruses.