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Predicting the level of herd infection for outbreaks of foot-and-mouth disease in vaccinated herds.
Foot-and-mouth disease (FMD) is a highly contagious virus infection of sheep, goats, cattle, pigs and other, non-domesticated species of artiodactyls, and causes both clinical and subclinical infection according to the natural or acquired immunity of the host. Within vaccinated dairy herds FMD may appear as an acute, mild or subclinical infection, dependent upon the immune status of the herd, the level of challenge and the efficacy of the vaccine used. In the large dairy herds of Saudi Arabia, sub-clinical FMD was on a number of occasions, found to have spread amongst the cattle before signs of disease were seen. Such undetected transmission resulted in a large incidence on the first day of diagnosis and curtailed the impact of post-outbreak vaccination (PoV). First day incidence (FDI) for these herds was found to correlate with the final cumulative incidence of clinical disease. Since FDI is available at the start of an outbreak it can be used as a predictive tool for the eventual outcome of an FMD outbreak. During the past 11 years 47 % of dairy herds examined in Saudi Arabia have experienced FMD initially as sub-clinical disease. For the remaining 53 %, waning vaccinal protection did not suppress clinical disease in the initially infected animals, and these showed severe rather than mild signs. Hence, in such herds there was a very low initial level of subclinical infection, so PoV was more effective, and the timing of PoV was found to give a good correlation with cumulative herd incidence: an early PoV resulted in low prevalence of clinically infected animals whilst late PoV permitted high prevalence. PoV timing can thereby be used in tandem with FDI as a predictive tool for future outbreaks, estimating the final cumulative incidence (or prevalence) of clinical FMD cases.
Histological and histochemical characterisation of mammary gland tissue of cows infected with foot-and-mouth disease by contact exposure.
Foot-and-mouth disease virus was observed to replicate in secretory epithelial cells of bovine mammary gland alveoli as a result of systemic infection initiated by exposure to infected animals. Viral antigens were demonstrated using fluorescent antibody and immunoperoxidase labelling techniques before the development of signs of clinical disease. In addition, labelled antigens were observed associated with cytoplasmic-like fragments in luminal membrane limited structures. Histologically, lesions of the alveolar secretory epithelium consisted of focal necrosis of these cells which eventually sloughed into the lumen.
Carcass disposal: lessons from Great Britain following the foot and mouth disease outbreaks of 2001.
The foot and mouth disease (FMD) outbreak that occurred in the United Kingdom in 2001 was of an unprecedented scale and severity and presented a massive logistical challenge to Government. Over 6.5 million animals were slaughtered and disposed of, over 4 million as a direct result of disease and a further 2.5 million on welfare grounds. On-farm burial and on-farm burning were the principal routes for disposal at the commencement of the outbreak. On-farm burial was limited by legislation to protect groundwater supplies and pyre burning came increasingly under attack from local communities concerned about health risks from smoke and emissions. Burning also painted a vivid but distressing picture of the war against disease. Increasingly, rendering capacity made an important contribution to disposal. The peak of the outbreak could only be managed by the development of a new disposal route--mass burial in engineered sites and by using licensed landfill where available. During the course of the outbreak, a disposal hierarchy was developed to reflect environmental and public health concerns, namely: rendering and incineration ranked first, licensed landfill next, followed by burning with mass burial or on-farm burial as the least preferred options. However, the campaign against the disease could not have been won without the tactical use of mass burial in addition to all the other available disposal routes. The authors describe the development and deployment of the disposal routes used in the 2001 outbreak.
A simulation model of intraherd transmission of foot and mouth disease with reference to disease spread before and after clinical diagnosis.
Intraherd transmission of foot and mouth disease virus (FMDV) was examined using a simulation model for a hypothetical 1,000-cow dairy, assuming clinical diagnosis was made when at least 1% (10 cows) or 5% (50 cows) had clinical signs of FMD, I index case cow, and transition state distributions for the latent, subclinically infectious, and clinically infectious periods of FMD calculated from published data. Estimates assumed for the number of animal-to-animal contacts (k) adequate for transmission ranged from 0.6 to 9.0 per hour (13.7-216.0 per day). A total of 40,000 iterations (5,000 for each scenario, assessing 4 adequate contact rates and 2 detection criteria) were run. The model predicted that FMD would not be diagnosed in the herd until 10.0-13.5 days after the index case cow had become infected, at which time between 65% and 97% of the cows (646-967 cows) to nearly 100% (978-996 cows) would already have become infected with the virus, if the number of cows showing clinical signs of FMD at the time of diagnosis were 10 or 50, respectively. At the time of diagnosis, the simulated number of infectious cattle varied substantially from 82-472 to 476-537 cows, depending on adequate contact rate and whether the diagnosis was made when 10 or 50 animals were showing clinical signs, respectively. The simulated number of infectious cows increased rapidly during the first few days after diagnosis. In the scenario where at least 10 cows showing clinical signs was necessary before a clinical diagnosis was made, each day after diagnosis, the number of infectious animals increased by nearly 100 to more than 200 cases per day up to day 5, assuming 0.57-9.0 animal-to-animal contacts per hour, respectively. Results obtained when it was assumed that at least 50 clinical cases were present at the time of diagnosis showed smaller relative increases because nearly one-half of the herd was projected to be infected at the time of diagnosis. From these results, it is clear that once an individual in a herd becomes infected with FMDV, herd infectivity is not static, rather it accelerates as would be expected as long as there are sufficient susceptible animals to sustain the increasing transmission rate, after which time the rate at which new infections occurs will diminish. Results indicate that biosecurity strategies aimed at minimizing both intraherd and interherd contact will be critical in minimizing the spread of FMD before the initial diagnosis is made. In addition, simulations suggest that very early clinical diagnosis of FMD and effective isolation or depopulation and disposal will be critical in limiting the number of infectious animals capable of transmitting the virus to other herds and thus in timely control of an epidemic. Early diagnosis will rely on early virus detection from animals in the preclinical phase of infection, rather than waiting for clinical signs to manifest in sufficient numbers to be noticed and to warrant investigation.
Linear hoof defects in sheep infected with foot-and-mouth disease.
During the epidemic of foot-and-mouth disease (FMD) in The Netherlands in 2001, a sheep farm was identified that had been subclinically infected with the disease. The FMD virus genome was detected in 12 of 16 probang samples collected from the sheep and the virus was isolated from four of these samples. Linear defects were observed, 1 to 3 cm from the coronary band, in the hooves of several of the sheep. The defects were thought to have been caused by the FMD infection. It was thought that the distance of the defects from the coronary band might be an indication of the time since the animals had been infected. To determine the growth rate of the claws of sheep, the growth of the hoof horn of uninfected lambs and ewes was measured; in the lambs the growth rate was 0.44 mm per day and in the ewes it was 0.29 mm per day.
Role of nonstructural proteins 3A and 3B in host range and pathogenicity of foot-and-mouth disease virus.
The genome of foot-and-mouth disease virus (FMDV) differs from that of other picornaviruses in that it encodes a larger 3A protein (>50% longer than poliovirus 3A), as well as three copies of protein 3B (also known as VPg). Previous studies have shown that a deletion of amino acids 93 to 102 of the 153-codon 3A protein is associated with an inability of a Taiwanese strain of FMDV (O/TAW/97) to cause disease in bovines. Recently, an Asian virus with a second 3A deletion (amino acids 133 to 143) has also been detected (N. J. Knowles et al., J. Virol. 75:1551-1556, 2001). Genetically engineered viruses harboring the amino acids 93 to 102 or 133 to 143 grew well in porcine cells but replicated poorly in bovine cells, whereas a genetically engineered derivative of the O/TAW/97 virus expressing a full-length 3A (strain A12) grew well in both cell types. Interestingly, a virus with a deletion spanning amino acid 93 to 144 also grew well in porcine cells and caused disease in swine. Further, genetically engineered viruses containing only a single copy of VPg were readily recovered with the full-length 3A, the deleted 3A (amino acids 93 to 102), or the "super" deleted forms of 3A (missing amino acids 93 to 144). All of the single-VPg viruses were attenuated in porcine cells and replicated poorly in bovine cells. The single-VPg viruses produced a mild disease in swine, indicating that the VPg copy number is an important determinant of host range and virulence. The association of VPg copy number with increased virulence in vivo may help to explain why all naturally occurring FMDVs have retained three copies of VPg.
The economics of foot and mouth disease.
The economic effects of foot and mouth disease (FMD) are summarised. Losses arise from the direct effects of the disease on production, costs of disease control and restriction of trade. Direct effects are of greatest importance in dairy and pig production systems. Costs of disease control, whether by stamping-out or vaccination are high. Even countries that are free of the disease incur prevention and emergency preparedness costs. The published studies indicate that where FMD eradication is feasible, this is the least-cost policy option, even allowing for the costs of prevention, emergency preparedness and the risk of outbreaks. Where eradication is not feasible, it is economically beneficial to protect high-producing livestock by vaccination. Vaccination of lower-producing animals may also be justified, especially where these animals produce milk or traction power, or where this would serve to protect high-producing livestock from disease challenge.
Selective lymphocyte depletion during the early stage of the immune response to foot-and-mouth disease virus infection in swine.
Foot-and-mouth disease virus (FMDV) is the causative agent of a highly contagious vesicular disease of cloven-hoofed animals. In the present study we use FMDV serotype C infection of swine to determine, by analytical techniques, the direct ex vivo visualization of virus-infected immune cells during the first 17 days of infection. We report, for the first time, that FMDV C-S8c1 can infect T and B cells at short periods of time postinoculation, corresponding with the peak of the viremia. There is a significant lymphopenia that involves CD3(+) CD4(-) CD8(+/-), CD3(+) CD4(-) CD8(+)Tc, and CD3(+) CD4(+) CD8(+) memory Th but not CD3(+) CD4(+) CD8(-) naïve Th lymphocytes. In addition, a profound depletion of the vast majority of peripheral T cells in lymph nodes and spleen is observed. This selective depletion of T cells is not due mainly to in situ death via apoptosis as visualized by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling (TUNEL) technique. Thus, early infection of T cells by FMDV may be the main cause of the observed T-cell depletion. Importantly, this lack of T cells is reflected in a reduced response to mitogen activation, which in many cases is totally eliminated. These data suggest a mechanism by which the virus causes a transient immunosuppression, subvert the immune systems, and spreads. These results have important implications for our understanding of early events in the development of a robust immune response against FMDV.
The fencing issue relative to the control of foot-and-mouth disease.
Certain livestock diseases in sub-Saharan Africa, such as foot-and-mouth disease are difficult to control because of the large numbers of infected wildlife hosts. These wildlife disease reservoirs form a continuous hazard of transmittal of the diseases to domestic livestock, which limits the access of livestock products from southern Africa to international markets. The disease reservoirs are often found in border areas between countries with susceptible species and infected reservoir animals continuously crossing the border. A regional approach to disease control is probably the only way to achieve any real progress. Here we review the positive and negative attributes of fencing as a control mechanism for disease transmission.
[The stabilizing and reactivating influence of trypsin on the virus of Teschen disease (swine paralysis) and inactivation of foot and mouth disease virus by this enzyme].
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Hand, foot, and mouth disease: a viral disease of importance to dentists.
Hand, foot, and mouth disease is a disease of viral origin that produces characteristic lesions in the mouth and on the hands and feet. Knowledge of the disease is important to dentists since the oral vesicular and ulcerative lesions are usually the first clinical signs of the disease, and the epidemiclike patterns of the disease make it likely that the dentist will contract the disease himself or possibly become a carrier of the virus. The lesions of hand, foot, and mouth disease usually regress in two to three weeks, and complications are rare. Treatment is basically palliative to reduce the pain and irritation. Differential diagnosis of the disease must include consideration of herpes simplex, herpangina, recurrent aphthae, erythema multiforme, and animal foot and mouth disease. A case involving a dentist and his family is reported.
New approaches to vaccination against foot-and-mouth disease.
The economically important foot-and-mouth disease has been successfully controlled in Western Europe by comprehensive immunization using killed vaccine. The author discusses the wisdom of abandoning this policy, and outlines research into alternative vaccines using recombinant DNA technology, in particular using synthetic peptides.
The foot-and-mouth disease situation in Iran.
Foot-and-mouth disease has been known in Iran since long ago. Typing of virus was done in 1950 at Mérieux Institute and since 1959 at Razi Institute. Type Asia 1 was isolated three times: in 1957, in 1964 and in 1973. In June 1962, FMD type SAT 1 entered Middle-Eastern countries; it was soon controlled, and completely eradicated by the end of 1963. At the present time, endemic types of FMD cause limited and sporadic outbreaks in some regions of Iran; their incidence is lowered every year. Except the endemic types A and O, all other types in Iran are considered as exotic. The control measures are: 1) stamping-out policy against exotic types, 2) mass-vaccination of all healthy susceptible animals by a polyvalent vaccine, 3) regular disinfection of premises and utensils, 4) strict application of sanitary measures.
Outbreak of central nervous system disease associated with hand, foot, and mouth disease in Japan during the summer of 2000: detection and molecular epidemiology of enterovirus 71.
Few outbreaks of the serious enterovirus 71 (EV71) infections, which affect the central nervous system (CNS), had been reported in Japan before 2000. During June through August 2000, a patient died of pulmonary edema caused by brainstem encephalitis accompanied by EV71-induced hand, foot, and mouth disease (HFMD), and many patients complicated by serious CNS disease, including paralysis, were hospitalized in a restricted area in Hyogo Prefecture, Japan (K-area). During the same period, endemics of HFMD were reported in other areas in Hyogo Prefecture, where EV71 was isolated from HFMD patients, but few patients developed aseptic meningitis. The isolations of EV71 from K-area patients were difficult with the use of Vero cells, so the strains were isolated by use of GL37 cells; Vero cells, however, could isolate EV71 strains from other areas in Hyogo Prefecture. We sequenced VP4 coding regions of these EV71 isolates and found that the isolates from K-area had the same sequence, which, except for one isolate, was different from the sequences of EV71 strains isolated from other areas of Hyogo Prefecture. Although these results were not enough to state that EV71 from K-area was a virulent strain, it seemed reasonable to conclude that serious CNS diseases in K-area were caused by EV71 because it was the only infectious agent detected in the inpatients of K-area.
Genome-wide CRISPR screen identifies RNF24 as a critical host factor for foot-and-mouth disease virus entry.
BACKGROUND: Foot-and-mouth disease virus (FMDV) causes substantial economic losses in global livestock production; however, the key host factors supporting its early infection process remain poorly characterized. METHODS: In this study, we performed an unbiased genome-wide CRISPR/Cas9 knockout screening using porcine cells to screen and identify host factors involved in FMDV infection. RESULTS: We identified that the E3 ubiquitin ligase RNF24 supports efficient FMDV entry. RNF24 depletion inhibits viral entry and replication, whereas its overexpression enhances viral infectivity. Mechanistically, RNF24 preferentially promotes K27-linked non-degradative polyubiquitination of leupaxin (LPXN) at lysine 162, driving LPXN's trafficking to the plasma membrane. At the membrane, LPXN assembles a ternary integrin-LPXN-VP1 complex that strengthens virus-receptor interactions and promotes viral adsorption and entry. Disruption of this ubiquitination event via the LPXN K162R mutation impairs complex formation and compromises viral entry. CONCLUSION: Together, our study reveals a ubiquitin-dependent RNF24-LPXN regulatory axis that supports FMDV entry, highlights the role of non-degradative ubiquitination in viral pathogenesis, and proposes this interface as a potential target for antiviral intervention.
Foot-and-mouth disease virus (FMDV) causes an acute disease that can be lethal for adult laboratory mice.
Foot-and-mouth disease virus (FMDV) is a picornavirus that causes an acute vesicular disease of cloven-hoofed animals. This virus continues to be threat to livestock worldwide with outbreaks causing severe economic losses. However, very little is known about FMDV pathogenesis, partially due to the inconveniences of working with cattle and swine, the main natural hosts of the virus. Here we demonstrate that C57BL/6 and BALB/C adult mice are highly susceptible to FMDV infection when the virus is administered subcutaneously or intraperitoneally. The first clinical signs are ruffled fur, apathy, humped posture, and wasting, which are followed by neurological signs such as hind-limb paralysis. Within 2-3 days of disease onset, the animals die. Virus is found in all major organs, indicating a systemic infection. Mice developed microvesicles near the basal layer of the epithelium, event that precedes the vesiculation characteristics of FMD. In addition, a lymphoid depletion in spleen and thymus and severe lymphopenia is observed in the infected mice. When these mice were immunized with conventional inactivated FMDV vaccine, they were protected (100% of vaccinated animals) against challenge with a lethal dose of FMDV. The data indicate that this mouse model may facilitate the study of FMDV pathogenesis, and the development of new effective vaccines for FMD.
Global perspective for foot and mouth disease control.
The world distribution of foot and mouth disease (FMD) is almost a mirror image of the global economic structure. In general, industrialised countries are free while the disease is endemic in developing countries. In recent years, several incursions of FMD have been recorded in countries belonging to the Organization for Economic Co-operation and Development (OECD), all of which have been financially and socially costly to eliminate. At the same time, this single disease bars many developing countries from participation in formal trade, both regionally and internationally. However, recent studies have predicted an unprecedented high demand for animal protein, which can only be met through enhanced participation of developing countries in trade in livestock products. Accordingly, globalisation trends will exacerbate the exclusion of poor communities and countries from markets unless a long-term strategy is implemented to progressively build market opportunities for these countries, without placing the livestock of industrialised countries at undue risk from FMD and other major transboundary animal diseases. The authors submit that there is sufficient knowledge of FMD to make an international initiative for the progressive control of FMD a viable objective. Consequently, a four-stage pathway is proposed for developing a global FMD programme. The proposed strategy involves a build-up of the epidemiology and global status of FMD, including establishing an international early warning system, a risk-reduction phase to lower the incidence of FMD in the primary endemic areas and a control phase leading to the creation of zones of assured FMD-freedom. The authors also propose that an international FMD programme be co-ordinated, based on the experience of the Global Rinderpest Eradication Programme, the Hemispheric Plan for the eradication of FMD for the Americas, the South-East Asia Foot and Mouth Disease control and eradication campaign and the European Commission for the Control of FMD.