Foot-and-mouth disease (FMD)
Foot-and-mouth disease (FMD) is a highly contagious viral disease of many wild and domestic cloven-footed mammals and many other animals. In swine, the disease is characterized by vesicles on the feet, snout and in the mouth.
A wide range of wild and domestic animals, especially cloven-footed mammals, are susceptible to FMD. Horses are resistant, a fact useful in differential diagnosis. The disease occurs in most countries with a large livestock population unless those countries have eradicated it and maintained their disease-free status. In countries where FMD occurs endemically and pigs are present in large numbers, swine frequently are infected. All age groups are susceptible.
Foot-and-mouth disease is an ancient disease. A description of a disease observed in 1546 probably is a description of FMD. Since FMD was first clearly delineated from other diseases, it has continued to cause major losses in livestock throughout the world. Losses have been greater from loss of productivity than mortality.
Nine outbreaks of FMD have occurred in the United States. All outbreaks were followed by eradication, often at great expense. Much of the livestock population now in the United States is highly susceptible. An outbreak of FMD could cause great loss, especially if the outbreak became widespread before it was recognized. The United States has remained free of FMD since the last outbreak in 1929.
Recent outbreaks in Asia and the UK have demonstrated the devastation and frustration wrought by FMD. Exports were embargoed and entire regional herds slaughtered, effectively destroying the swine industry in these countries.
Outbreaks of all vesicular diseases of swine are of concern because the lesions cannot be distinguished from those of FMD, except by laboratory means. Swine are of special concern because they are susceptible to more vesicular diseases than other species of livestock, and they often play a major role in the spread of FMD by producing large, infectious aerosols of virus.
An Aphthovirus of the family Picornaviridae causes FMD. There are at least seven immunologically distinct types of virus: A, O, C, South African Territory (SAT) 1, 2, 3 and Asian 1. Among the seven types, one particular antigen (virus infection-associated antigen [VIA]) is group reactive and useful in serologic diagnosis of FMD infection.
Over 60 subtypes of virus have been identified and new subtypes continue to develop. Many differ enough antigenically to require preparation of subtype vaccines for their control. The antigenic variation of the virus and the limited cross protection among strains has made it impossible to prepare a single vaccine that protects satisfactorily against all strains. Effective disinfectants of FMD virus include sodium hydroxide, acetic acid, sodium carbonate and Virkon® (Durvet).
Virus transmission occurs through respiratory aerosols and direct or indirect contact with infected animals. Aerosol transmission of FMD virus over distances as great as 30 miles is believed to occur under certain weather conditions. Infected swine are exceptional disseminators of virus. For some virus subtypes, they are able to produce aerosols many times greater in virus concentration than those produced by cattle or sheep. They are sometimes referred to as “amplifier hosts” for FMD irus.
Infected swine disseminate virus in their excretions and secretions. Food products containing infectious pork can also spread FMD virus. Virus persists for long periods of time in frozen meat products. In several notable FMD outbreaks, the index case has been associated with the consumption by pigs of uncooked waste food containing infectious meat scraps. Contaminated biologics, including vaccines, have been responsible for outbreaks. People with residual FMD virus in their respiratory tract can transmit the virus to livestock for a short time.
Some species of animals recover from FMD and remain carriers for weeks, months and possibly, years. Occasionally they disseminate virus that initiates new outbreaks. Swine are not believed to be long-term carriers of FMD virus.
Foot and mouth disease virus adheres to the mucosa of the respiratory tract, the usual site of virus entry. Macrophages are believed to transport virus to secondary sites that include epithelium, mucosa and myocardium. In secondary sites, the virus replicates, then a marked viremia develops and the virus infects epithelium at many other sites. Within a few days vesicles develop, usually at sites of mechanical stress. In swine, common vesicle sites include the snout, mouth, tongue, and especially the feet. In cattle, the FMD virus affects the mammary gland epithelium and virus is shed in milk for a prolonged period. Although unproven, similar shedding may occur in swine.
The lesions of the major vesiculating viral diseases are similar. Vesicles develop in the epidermis, and the epithelium over the vesicle soon sloughs. Enough of the stratum basale is preserved to regenerate the epidermis unless there is secondary infection of the lesions. Secondary infection occurs on the feet of some swine and leads to chronic lameness.
The FMD virus often causes severe myocardial necrosis in neonatal and young pigs. This often leads to sudden deaths from myocardial failure. The mottled myocardial lesions sometimes are referred to as “tiger-heart” lesions and are useful in diagnosis.
An incubation period of one to five days precedes clinical signs. Lameness is often the first sign noticed. There is an initial acute rise in temperature; slobbering and chomping are common signs. Pregnant sows may abort or deliver stillborn, infected pigs. Sudden deaths may occur in neonatal pigs, sometimes before signs or lesions are apparent in the sow. The early stages of lesions appear as blanched, small foci in the skin on the snout, soft tissues of the feet, and perhaps the teats of lactating sows. By the time signs are readily apparent, there are usually cutaneous vesicles or bullae. Signs develop rapidly and morbidity rapidly increases. Mortality usually is less than 5% but there can be higher mortality in young pigs.
Well-developed vesicles and bullae are soon apparent. They are frequently present on the snout, behind the rim of the snout, in the nares, on the tongue and lips, and on the soft tissues of the feet, including the coronary band, the bulbs of the toes and interdigital clefts. Lesions probably are more common on the feet than in the mouth. Less often the lesions are on the vulva, the teats of lactating sows, or the scrotum of boars. Extensive lesions on the coronary band may lead to sloughing of the hoof and lameness. Foot lesions may involve one or more of the feet. Vesicles usually rupture within 24 hours and the superficial epidermis sloughs to reveal hyperemia and hemorrhage on underlying tissue. Uncomplicated lesions usually heal within two weeks. In a virulent form of FMD, young pigs, and sometimes older animals, may have extensive mottled areas of myocardial necrosis on ventricles and in papillary muscles.
Diagnosis cannot be made reliably on the basis of clinical signs and lesions since they are similar in all the vesicular viral diseases of swine. The state veterinary office should be contacted immediately if an outbreak is suspected. Differential diagnosis of vesicular viral diseases should only be completed in specifically-designated laboratories having specific arrangement to safely handle exotic disease organisms. Plans must be made for collecting and mailing specimens. The Foreign Animal Disease Diagnostic Laboratory (FADDL), Plum Island, NY, often does the diagnostic work.
Diagnostic techniques used include serologic tests to identify FMD virus infection-associated antigen (VIA), complement fixation (CF) and enzyme-linked immunosorbent assay (ELISA) tests to detect FMD viral antigen, virus isolation (VI) and neutralization (VN), electron microscope (EM), and animal inoculation studies. Polymerase chain reaction (PCR) tests have been developed and are frequently utilized. FMD must be differentiated from all other vesicular viral diseases and from other diseases that cause erosive/ulcerative lesions in the oral cavity. Positive diagnoses usually require less time than negative diagnoses. An ELISA is available that can differentiate antibody titers from infected versus vaccinated animals but is not yet officially recognized by many countries.
In the United States, prevention of FMD depends on regulations that govern the importation of animals, animal products, semen, embryos, and on regulations related to the safety of vaccines and other biologic products. There are special regulations on both cooking and dumping of waste food to prevent spread of the virus. Reliance on the vigilance of veterinary practitioners and diagnostic laboratory personnel is important in early detection of outbreaks.
In countries where FMD has not been eradicated, vaccines are used for prevention. The recently developed subunit vaccines have been of value in preventing some types and subtypes of FMD infection but have not provided consistent protection for type O infection, the most prevalent form of FMD. In the event of an outbreak in the United States, vaccine use will be considered but control is anticipated to occur primarily through slaughter of infected animals. The disease will be managed through quarantine, restriction of movement of animals in quarantined areas, slaughter followed by burial or incineration of infected and exposed animals and disinfection of production sites. Eradication is considered to be less costly than living with FMD.