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PubMedDate not supplied

Modeling spatial and temporal transmission of foot-and-mouth disease in France: identification of high-risk areas.

Foot-and-mouth disease is one of the most contagious diseases of animal livestock. We used statistical tools to explore the dynamics of epidemics and to evaluate the consequences of virus reintroduction in France. We developed a stochastic farm-based model adapted to the French farm structure from previous modeling works following the 2001 epidemic in the United Kingdom. This model depends upon the distance between the 280,000 French farms and on species type (e.g. cows and sheep) and it tracks each animal's farm status at any given day. Since data were only available at the town scale, the farm location and the number of animals in each farm were simulated over the surface area of each French town, as well as the number of mixed farms. Based on 200 simulations of the model, our results allowed for the study of local disease transmission, since it begins simulations once limitation of movement is put into place. On average, the same 50 randomly chosen initially infected farms would lead to 1,110 infected farms (610; 1,590) when two control strategies (culling within 0.5 km from an infected farm and vaccination within 3 km) are put into place. Regions with high densities of cows and sheep (e.g. Pays-de-la-Loire) are high-risk zones, confirming that the epidemic process depends upon the location and the type of initially infected farms (size, species type). The results of this model highlight the importance of Geographical Information Systems (GIS) to obtain more precise data concerning herds.

Animals↗
PubMed2005

Foot-and-mouth disease: host range and pathogenesis.

In this chapter the host range of foot-and-mouth disease (FMD) under natural and experimental conditions is reviewed. The routes and sites of infection, incubation periods and clinical and pathological findings are described and highlighted in relation to progress in understanding the pathogenesis of FMD.

Animals↗
PubMed2003

Foot and mouth disease in Tanzania: an overview of its national status.

The presence of foot-and-mouth disease (FMD) in Tanzania is a major obstacle to the development of the national livestock industry because of its adverse effects on livestock production and on trade of animals and animal products into lucrative export markets. FMD is endemic in Tanzania, the affected area is extensive and lack of funding makes eradication unrealistic. Uncontrolled livestock movements, the presence of large populations of wildlife in regular contacts with livestock, and the general lack of enthusiasm for FMD control among the key stakeholders, are some of the factors favouring the persistence of FMD in Tanzania. This review examines the epidemiology, dynamics and socio-economic significance of FMD in the national herd. Various control options available in Tanzanian context are also explored.

Animal Husbandry↗
PubMed1995

Susceptibility of llamas (Lama glama) to infection with foot-and-mouth-disease virus.

An experimental trial was conducted to evaluate the ability of foot-and-mouth-disease (FMD) virus (serotypes A79, C3, O1) to infect susceptible llamas exposed either directly to affected livestock, or indirectly to llamas that had been directly exposed to affected livestock. In addition, susceptible livestock species (cattle, pigs, goats, and sheep) were exposed to those llamas that had been both directly and indirectly exposed to the FMD virus to further look at potential transmission possibilities. Of 30 llamas directly exposed to the FMD virus, only three (3/30) showed evidence of infection, and of those, only two (2/30) had mild clinical signs. No FMD virus was isolated from either oesophageal-pharyngeal (OP) fluid or blood samples collected from the infected llamas beyond 14 days post-exposure. There was no evidence of virus transmission between the directly exposed and indirectly exposed llamas or between both groups of llamas and susceptible domestic livestock, as determined by the lack of clinical signs, by virus isolation, and by serology results. These results provide further evidence that llamas are resistant to FMD infection, and that they play a minor role, if any, in transmitting the virus to domestic livestock.

Animals↗
PubMed2002

The economic impact of foot and mouth disease control and eradication in the Philippines.

The authors evaluate the impact of foot and mouth disease (FMD) and control of the disease in the Philippines using cost-benefit analysis. A scenario in which FMD control is maintained at recent levels with continued presence of the disease is compared to scenarios in which a publicly funded programme achieves eradication by 2005 (current policy objective), 2007 and 2010. Under varying assumptions regarding the development of exports of livestock products following eradication, estimated benefit-cost ratios for the investment in eradication range from 1.6 (2010, no exports) to 12.0 (2005, export of 5,000 tons each of low-value and high-value livestock products annually), indicating eradication to be an economically viable investment. The commercial swine sector is estimated to capture 84% of the benefits generated by the public investment in eradication, versus 4% by backyard swine producers. The implications of these results within the context of regional efforts to control FMD in South-East Asia are explored.

Animals↗
PubMed2001

Descriptive epidemiology of the 2001 foot-and-mouth disease epidemic in Great Britain: the first five months.

In February 2001, foot-and-mouth disease (FMD) was confirmed in Great Britain. A major epidemic developed, which peaked around 50 cases a day in late March, declining to under 10 a day by May. By mid-July, 1849 cases had been detected. The main control measures employed were livestock movement restrictions and the rapid slaughter of infected and exposed livestock. The first detected case was in south-east England; infection was traced to a farm in north-east England to which all other cases were linked. The epidemic was large as a result of a combination of events, including a delay in the diagnosis of the index case, the movement of infected sheep to market before FMD was first diagnosed, and the time of year. Virus was introduced at a time when there were many sheep movements around the country and weather conditions supported survival of the virus. The consequence was multiple, effectively primary, introductions of FMD virus into major sheep-keeping areas. Subsequent local spread from these introductions accounted for the majority of cases. The largest local epidemics were in areas with dense sheep populations and livestock dealers who were active during the key period. Most affected farms kept both sheep and cattle. At the time of writing the epidemic was still ongoing; however, this paper provides a basis for scientific discussion of the first five months.

Animals↗
PubMed2003

[Hand, foot and mouth disease, a not so benign affection: clinical reminder and potential complications].

Hand-foot-and-mouth disease is an infection appearing in epidemics and due, in most cases, to Coxsackie-virus A16 and/or Enterovirus 71 or, less often, to other Coxsackie-virus serotypes. The symptomatology mostly consists in vesicular eruption of the anterior part of the buccal mucosa as well as of hands and feet. Its evolution, although often benign, can include cardiopulmonary and neurological complications. The latter complications require a quickly detection and treatment, and prevention of virus transmission to other people must be adequate.

Cardiovascular Diseases↗
PubMed2004

The control of foot-and-mouth disease in Botswana: special reference to vaccination.

Botswana has a history of Foot-and-Mouth Disease (FMD) occurrence and control that dates far back into the 1930s. Conditions in the southern African region are favourable for spiking FMD outbreaks due to Southern African Territories (SAT) serotypes, because of the co-existence of the agent, hosts and a conducive environment. In the past these parameters were less controlled and FMD outbreaks were common in the region, causing tremendous social and economic losses. The inception of conventional FMD vaccines in the region in the 1970s led to a significant improvement in the control of the disease. Vaccination used with other appropriate strategies has been the cornerstone of FMD control strategy in Botswana. FMD vaccine used in Botswana is manufactured locally; it is effective and has been responsible for the elimination of FMD outbreaks since the early eighties. FMD vaccination is a costly exercise. The programme has been sustained for decades because there is political will and financial support from government. However, its economic value can only be determined through a cost-benefit analysis, which is not a subject of this paper. The experience of FMD control in Botswana, with special reference to vaccination, is discussed.

Animals↗
PubMed1997

An analysis of foot-and-mouth-disease epidemics in the UK.

There was a major epidemic of the foot-and-mouth-disease virus among cattle herds in the UK in 1967-68 which showed a very rapid early spread, a much slower later spread, and eventually infected 12% of herds in the core epidemic area. A simple discrete-time version of a susceptible-latent-infectious-removed epidemiological model is used to generate a set of estimates of the transmission rate. This parameter has high values over the first few days, then the values are lower and they subsequently decline. The early high values are consistent with the view that unusual meteorological conditions produced exceptionally good conditions for wind-borne spread of the virus over the first few days. The corresponding basic reproduction number, Rzero, is estimated as 38.4. Subsequent low values of the transmission rate correspond to a value of Rzero of 2.0; this is within the range of estimates made from the observed ratio of secondary to primary outbreaks for 25 other epidemics. Prophylactic control measures, such as vaccination, would have to be extremely effective to prevent epidemics with the higher Rzero value.

Animals↗
PubMed2001

The 3A non-structural-protein coding region of the southern African SAT type isolates differs from that of other foot-and-mouth disease viruses.

The 3A non-structural protein of foot-and-mouth disease viruses is a relatively conserved protein comprising 153 amino acids. Recent studies have demonstrated correlation between mutations in the 3A non-structural-protein-coding region, including a 10-amino acid deletion, and attenuation of the viruses in cattle. Although the 3A coding region of several type A, O and C isolates has previously been described, nucleotide sequence data of the 3A coding region of the South African Types (SAT) 1, 2 and 3 viruses are limited. Therefore, the 3A non-structural-coding region of different SAT serotypes was determined, analysed and compared to that of European, South American and Asian isolates. The 3A regions of the SAT isolates investigated differed markedly from that of types A, O, C and Asia-1, but were similar within the group.

Africa South of the Sahara↗
PubMed1976

[Serological study of several strains of foot-and-mouth disease virus type "O" isolated in Europe between 1971 and 1975: application of the biomathematical system of classification].

Nine strains of foot-and-mouth disease virus type "O" received in our laboratories since 1971 have been studied serologically by Osler's quantitative method of complement fixation (50% hemolysis). The results, submitted to the biomathematical system of bidimensional classification, allow to conclude that at present in Europe there are two groups of foot-and-mouth disease strains of type "O"; one has reference to our vaccinal strain "O Lausanne 1965" and the other to "O Romania 1972" strain, which has certain points of similarity with subtype "O2". In addition, strain "O Hungary 1975" has been studied on bovines; the immunological tests confirm the serological test.

Aphthovirus↗
PubMed1994

Antibody response to 146S particle, 12S protein subunit and isolated VP1 polypeptide of foot-and-mouth disease virus type Asia-1.

The antibody response to foot-and-mouth disease virus (FMDV) antigens of type Asia-1 in guinea-pigs was studied by micro-serum neutralization test (MSNT) and enzyme-linked immunosorbent assay (ELISA). One inoculation of as little as 1 microgram of binary ethyleneimine (BEI)-inactivated 146S virus particles in guinea-pigs elicited enough neutralizing antibodies to protect them against challenge with virulent virus. However, one inoculation of live 146S virus particles elicited higher levels of neutralizing antibodies in guinea-pigs than that of inactivated 146S particles. One inoculation of 12S protein subunits in guinea-pigs elicited only non-neutralizing anti-12S antibodies detected by ELISA. Similarly, non-neutralizing anti-VP1 antibodies were detected by ELISA after one inoculation of VP1. However, multiple inoculations of 12S or VP1 elicited measurable neutralizing antibodies in guinea-pigs that protected them against challenge.

Animals↗
PubMed2002

Change of major genotype of enterovirus 71 in outbreaks of hand-foot-and-mouth disease in Taiwan between 1998 and 2000.

Two outbreaks of hand-foot-and-mouth disease (HFMD) occurred in Taiwan between 1998 and 2000. Enteroviruses were isolated from a total of 1,892 patients in this laboratory during this period. Of the virus isolates, enterovirus 71 (EV71) was diagnosed in 44.4% of the patients (132 of 297) in 1998, 2% (13 of 646) in 1999, and 20.5% (195 of 949) in 2000. Genetic analyses of the 5'-untranslated and VP1 regions of EV71 isolates by reverse transcription-PCR and sequencing were performed to understand the diversity of EV71 in these outbreaks of HFMD. Most EV71 isolates from the 1998 epidemic belonged to genotype C, while only one-tenth of the isolates were genotype B. Interestingly, all EV71 isolates tested from 1999 to 2000 belonged to genotype B. This study indicated that two genogroups of EV71 capable of inducing severe clinical illness have been circulating in Taiwan. Furthermore, the predominant EV71 genotypes responsible for each of the two major HFMD outbreaks within the 3-year period in Taiwan were different.

5' Untranslated Regions↗
PubMed2004

VP1 of foot-and-mouth disease virus induces apoptosis via the Akt signaling pathway.

Foot-and-mouth disease virus (FMDV) binds to cellular integrins through an RGD motif in its capsid protein, VP1. It is unclear, however, what kind of cellular event(s) are triggered after the binding of VP1 to the cells. In this study, we show that aqueous soluble recombinant DNA-derived VP1 (rVP1) of FMDV induced apoptosis of BHK-21 cells after binding to integrins. In addition, treatment of BHK-21 cells with rVP1 resulted in deactivation of Akt and enhancement of several proapoptotic responses such as dephosphorylation of glycogen synthase kinase-3beta and cleavage of procaspase-3, -7, and -9. Additional studies revealed that the rVP1 treatment caused apoptosis of cancer cells, including MCF-7 (a breast carcinoma cell line with a functional deletion of the caspase-3 gene) and PC-3 (a sphingosine 1-phosphate receptor subtype 3-deficient androgen-independent prostate cancer cell line). These results suggest that rVP1 of FMDV may be used selectively as a potent apoptotic agent for human cancer by modulating the Akt signaling pathway and that its effect is not primarily dependent on either activation of procaspase-3 or deactivation of sphingosine 1-phosphate receptor subtype 3.

Amino Acid Sequence↗
PubMed1990

A study of antigenic variants of foot and mouth disease virus type A in India between 1977 and 1985.

The structural polypeptides of thirty-three field isolates of foot and mouth disease virus (FMDV) collected in India between 1977 and 1985 were analysed by SDS-polyacrylamide gel electrophoresis. They were placed in eleven groups based on their patterns and compared with results of conventional serological (virus neutralisation and complement fixation) tests. Variation occurred in the structural proteins of the viruses isolated between 1977 and 1981; however, the polypeptide patterns of viruses isolated in 1984 and 1985 were identical.

Animals↗
PubMed1996

Efficient infection of cells in culture by type O foot-and-mouth disease virus requires binding to cell surface heparan sulfate.

Foot-and-mouth disease virus (FMDV) enters cells by attaching to cellular receptor molecules of the integrin family, one of which has been identified as the RGD-binding integrin alpha(v)beta3. Here we report that, in addition to an integrin binding site, type O strains of FMDV share with natural ligands of alpha(v)beta3 (i.e., vitronectin and fibronectin) a specific affinity for heparin and that binding to the cellular form of this sulfated glycan, heparan sulfate, is required for efficient infection of cells in culture. Binding of the virus to paraformaldehyde-fixed cells was powerfully inhibited by agents such as heparin, that compete with heparan sulfate or by agents that compete for heparan sulfate (platelet factor 4) or that inactivate it (heparinase). Neither chondroitin sulfate, a structurally related component of the extracellular matrix, nor dextran sulfate appreciably inhibited binding. The functional importance of heparan sulfate binding was demonstrated by the facts that (i) infection of live cells by FMDV could also be blocked specifically by heparin, albeit at a much higher concentration of inhibitor; (ii) pretreatment of cells with heparinase reduced the number of plaques formed compared with that for untreated cells; and (iii) mutant cell lines deficient in heparan sulfate expression were unable to support plaque formation by FMDV, even though they remained equally susceptible to another picornavirus, bovine enterovirus. The results show that entry of type O FMDV into cells is a complex process and suggest that the initial contact with the cell surface is made through heparan sulfate.

Animals↗
PubMed2005

Analysis of a foot-and-mouth disease virus type A24 isolate containing an SGD receptor recognition site in vitro and its pathogenesis in cattle.

Foot-and-mouth disease virus (FMDV) initiates infection by binding to integrin receptors via an Arg-Gly-Asp (RGD) sequence found in the G-H loop of the structural protein VP1. Following serial passages of a type A(24) Cruzeiro virus (A(24)Cru) in bovine, via tongue inoculation, a virus was generated which contained an SGD sequence in the cell receptor-binding site and expressed a turbid plaque phenotype in BHK-21 cells. Propagation of this virus in these cells resulted in the rapid selection of viruses that grew to higher titers, produced clear plaques, and now contained an RGD sequence in place of the original SGD. To study the role of the SGD sequence in FMDV receptor recognition and bovine virulence, we assembled an infectious cDNA clone of an RGD-containing A(24)Cru and derived mutant clones containing either SGD with a single nucleotide substitution in the R(144) codon or double substitutions at this position to prevent mutation of the S to an R. The SGD viruses grew poorly in BHK-21 cells and stably maintained the sequence during propagation in BHK-21 cells expressing the bovine alpha(V)beta(6) integrin (BHK3-alpha(V)beta(6)), as well as in experimentally infected and contact steers. While all the SGD-containing viruses used only the bovine alpha(V)beta(6) integrin as a cellular receptor with relatively high efficiency, the revertant RGD viruses utilized either the alpha(V)beta(1) or alpha(V)beta(3) bovine integrins with higher efficiency than alpha(V)beta(6) and grew well in BHK-21 cells. Replacing the R at the -1 SGD position with either K or E showed that this residue did not contribute to integrin utilization in vitro. These results illustrate the rapid evolution of FMDV with alteration in receptor specificity and suggest that viruses with sequences other than RGD, but closely related to it, can still infect via integrin receptors and induce and transmit the disease to susceptible animals.

Amino Acid Sequence↗
PubMed2000

Neurological manifestations of enterovirus 71 infection in children during an outbreak of hand, foot, and mouth disease in Western Australia.

Enterovirus 71 (EV71) causes epidemics of hand, foot, and mouth disease associated with neurological complications in young children. We report an outbreak of EV71-associated neurological disease that occurred from February through September 1999 in Perth, Western Australia. Fourteen children with culture-proven, EV71-induced neurological disease were identified. Nine patients (64%) developed severe neurological disease; 4 of these patients developed long-term neurological sequelae. Neurological syndromes included aseptic meningitis, Guillain-Barré syndrome, acute transverse myelitis, acute cerebellar ataxia, opso-myoclonus syndrome, benign intracranial hypertension, and a febrile convulsion. Clinical and magnetic resonance imaging data indicated that immunopathology was a major factor in the pathogenesis of neurological disease in this outbreak. This finding is in contrast to reports of previous EV71 epidemics, in which virus-induced damage to gray matter was the most frequent cause of neurological disease.

Acute Disease↗