Historic and economic significance of foot-and-mouth disease

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Foot-and-mouth disease (FMD) is endemic to most of sub-Saharan Africa, except in a few countries in southern Africa, where the disease is controlled by the separation of infected wildlife from susceptible livestock as well as by vaccination. Largely due to the endemicity of the disease, and the fact that FMD does not normally cause high rates of mortality in adult animals, FMD outbreaks are not perceived as important and are not reported or investigated further to determine the causative serotypes. However, a number of countries now realise that FMD is one of the transboundary diseases that should be controlled to ensure economic stability and access to lucrative international export markets for animal and animal products. Furthermore, they recognise that a regional approach would be needed to succeed. Knowledge about the epidemiology of FMD can greatly assist in developing control policies for such a regional approach. Foot and mouth disease was described for the first time during the XVI century (Bulloch, 1927). Bovines refused to eat as the internal parts of their mouths were covered with redness and small vesicles which then spread to the feet of the animals.
Most of the individuals that were affected showed the same clinical signs. However, the disease spread to several provinces around Verona, Italy, and it was believed that the infection spread through air but other vectors such as water and swamps were not excluded. This description, carried out more than 400 years ago, is absolutely comparable to what we know today as FMD. In 1898, Loeffler and Frosch proved the filterability of the pathogenic agent causing FMD through bacterial filters and started the notion of another living entity, viz., viruses (Bos, 2000; Brown, 2003). This was the first evidence of a virus causing an animal disease. Hence forth, a significant aspect in the field of FMD research was the discovery of the sensitivity of guinea pigs to FMD by Waldmann and Pape in 1920. During 1922 progress was made when Vallee and Carree proved that there were different antigenic types of FMD, thus explaining the possibility of successive infections in the same animal. They discovered 2 serotypes and named them after the place of origin, 0 for Oise and A for Allemagne in France. In 1926, Waldmann and Trautwein discovered the third antigenic type which they called C.
In the 1940s, 3 additional serotypes from Southern Africa were discovered at the Pirbright laboratory in England and named as South African Territories 1-3 (SAT-1, SAT-2, SAT-3) and the last serotype Asia I was discovered from Turkey in 1954 (Brown, 2003). At present 7 immunologically distinct serotypes of FMD viruses are known based on the fact that there is no cross protection between these serotypes (Brooksby, 1982). In addition, within each serotype a number of genetic and antigenic variants with different degrees of virulence exist (Vallee and Cam~~e, 1922; Pereira, 1977; Blood et a/., 1983; Chenug et a/., 1983; Kitching et a/., 1989). Vosloo et a/. (2002) reviewed the genetic and geographical distribution of FMD viruses in Africa and showed that the SAT-2 viruses appear to be more diverse in topotypes and prevalent in sub-Saharan African countries. The prevalence of the other serotypes of FMD viruses in Africa was also reported from high to low prevalence as 0 ~ A ~ SAT-1 ~ SAT-3~C. A break-through in the control of FMD was made when Vallee and co workers (1925) utilised formaldehyde-inactivated vesicular fluid from infected calves as a vaccine. In 1947, Frenkel started the large-scale production of virus on surviving bovine lingual epithelium to incorporate into the inactivated vaccine, which was subsequently adopted by a number of other laboratories (Fogedby, 1963). Since then various cell lines, e.g. Baby Hamster Kidney cells (Mowat and Chapman, 1962) have been investigated for virus propagation which opened a new era in vaccine production resulting in better control of the disease and fundamental studies on virus-cell interaction (cited in Bos, 2000; Brown, 2003). Foot-and-mouth disease has considerable economic consequences. Losses can be attributed to both direct and indirect costs. The direct effects of the disease are loss of milk production, loss of draught power, retardation of growth, abortion in pregnant animals, death in calves and lambs while indirect losses can be attributed to the disruption in trade of animals and derivative products. Its sequelae are found to be more important than the acute illness (Woodbury, 1995). A striking example is the recent outbreak of serotype 0 (the PanAsian strain) in Great Britain, a country which had been free of FMD since 1981.
This devastating epidemic of 2001 spread to Ireland, France and the Netherlands where the United kingdom alone were forced to slaughter about 4 million infected and in contact animals. The cost of this epidemic in the UK was estimated to be more than US $29 billion (Samuel and Knowles, 2001a). The virus causing FMD was defined in 1963 by the Intemational Committee of Taxonomy of viruses as belonging to the genus Aphthovirus, one of the genera of the family Picornaviridae. The name Picornaviridae is derived from the Latin word ‘pico’ (small) and ‘ma’ (RNA) which refers to the size and genome type while the genus name ‘aphth 0virus’ refers to the vesicular lesions produced in cloven hoofed animals. The Picornaviridae family consists of various virus species which cause diseases of medical and agricultural importance which are summarized as the various genera in Table 1.1.

Table of content: :

• Acknowledgments
• Abstract II
• Table of contents
• List of Tables
• List of Figures
• Abbreviations
• Chapter I: Literature review
  • 1.1 Introduction
  • 1.2 Historic and economic significance of foot-and-mouth disease
  • 1.3 Taxonomy of Picornaviruses
    • 1.3.1 Types (serotypes) and subtypes
    • 1.4 Foot-and-mouth disease virus
    • 1.4.1 Physico-chemical properties of the FMD viruses
    • 1.4.2 Virus morphology
    • 1.4.3 Genome organization and protein processing
    • 1.4.4 Genetic variation of FMD virus genome
    • 1.4.5 Antigenic variation
  • 1.5 Diagnosis of FMD
    • 1.5.1 Clinical signs
    • 1.5.2 Laboratory diagnosis
  • 1.6 Epidemiology and control of FMD
    • 1.6.1 Geographic distribution of FMD
    • 1.6.2 Serotype distribution of FMD in Africa
    • 1.6.3 Susceptible host range
    • 1.6.4 The role of carriers in the epidemiology of the disease
    • 1.6.5 Transmission of FMD
    • 1.6.6 Control of FMD
    • 1.6.6.1 Control by vaccination
    • 1.6.6.2 Control by stamping out
    • 1.6.6.3 Control of FMD in developing countries
    • 1.7 Molecular Phylogeny
  • 1.8 Summary and objective of the study
• Chapter II: Molecular epidemiology of serotype 0 foot-and-mouth disease viruses isolated from cattle in Ethiopia between
  • 2.1 Introduction
  • 2.2 Materials and Methods
    • 2.2.1 Viruses studied
    • 2.2.2 Nucleic acid isolation
    • 2.2.3 Complementary DNA synthesis (cDNA)
    • 2.2.4 Polymerase chain reaction (PCR)
    • 2.2.5 Agarose gel electrophoresis of PCR products
    • 2.2.6 Nucleotide Sequencing
    • 2.2.7 Data Analysis
  • 2.3 Results ‘ »
  • 2.3.1 Phylogenetic analysis of all serotype 0 isolates included in this study
  • Pair-wise comparison of partial VP1 gene sequences
  • Amino acid variability
  • Discussion
• Chapter III: Molecular epidemiology of serotype 0 foot-and-mouth disease viruses from East African countries in relation to the rest of the world
  • 3.1 Introduction
  • 3.2 Materials and Methods
    • 3.2.1 Viruses studied
    • 3.2.2 RT-PCR amplification of the 1D gene and nucleotide sequencing
    • 3.2.3 Sequence data analysis
  • 3.3 Results
  • 3.3.1 Genetic relationships of serotype 0 FMD viruses
  • 3.4 Discussion
• Chapter IV: Genetic heterogeneity of SAT -2 foot-and-mouth disease viruses in East Africa
  • 4.1 Introduction
  • 4.2 Materialsand Methods
    • 4.2.1 Virusesstudied
    • 4.2.2 Nucleicacid isolationandRT-PCRamplification
    • 4.2.3 DNApurificationandCycleSequencing
    • 4.2.4 PhylogeneticAnalysis
  • 4.3 Results
  • 4.3.1 Phylogeneticanalysis
  • 4.3.2 Sequencevariationsanddistributionof mutations
  • 4.4 Discussion
• Chapter V: Molecular epidemiology of SAT -1 foot-and-mouth disease viruses in East Africa isolated between 1971 and
  • 5.1 Introduction
  • 5.2 Materialsand Methods
    • 5.2.1 Virusesusedinthis study
    • 5.2.2 Nucleicacid isolationandRT-PCRamplification
    • 5.2.3 DNApurificationandCycleSequencing
    • 5.2.4 Phylogeneticanalysis
  • 5.3 Results
  • 5.3.1 Phylogeneticanalysis
  • 5.3.2 Sequencevariations
  • 5.4 Discussion
• Chapter VI: Serological survey to determine the role of small ruminants and wildlife in the epidemiology of foot and mouthdisease in Ethiopia and evaluation of serological tests
  • 6.1 Introduction
  • 6.2 MaterialsandMethods
  • 6.2.1 Studyarea
  • 6.2.2 Serumsamples
    • 6.2.3 Antibodydetectiontests
    • 6.2.3.1 LiquidphaseblockingELISA
    • 6.2.3.2 The UBI FMDVnon-structuralenzyme-linkedimmunosorbent assay . Dataanalysis
  • Results
  • Analysis of sera from small ruminants
  • 6.3.3 Analysis of sera from cattle
  • 6.4 Discussion
• Chapter VII: General discussion and recommendationsGeneral discussion and recommendation
  • References
  • Appendix I
  • Appendix II

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