Foot and Mouth in Animals - General Conditions - MSD Veterinary Manual (2023)

Different foot-and-mouth disease virus serotypes were unevenly distributed in endemic areas. About 70% of global epidemics are caused by serotype O of the FMD virus. Six of the seven serotypes appeared in Africa (O, A, C, SAT-1, SAT-2, SAT-3). , four in Asia (O, A , C, Asia-1), three in Comes in South America (O, A, C). North and Central America, Australia, New Zealand, Greenland, Iceland and Europe are now generally free of FMD (the last outbreak in Europe was in Bulgaria in 2011). Since 2004, foot-and-mouth disease serotype C has not been reported anywhere, and it can now be eradicated outside the laboratory. However, vaccination against this serotype still exists in some places, so it is difficult to prove that the virus is completely absent in the field.

Foot-and-mouth disease virus is transmitted by direct contact with infected animals or indirect contact with secretions or feces (including semen and milk) of infected animals or mechanical carriers (humans, horses, dogs, cats, birds, vehicles) or air flow over land or water Viruses they can enter the host by inhalation, ingestion or through cracks in the skin and mucous membranes. Breeding is a possible route of SAT virus transmission in the African buffalo population.

A potential scenario for the introduction of the virus into previously FMD-free areas is the supply of imported feed (meat or offal) from infected animals to susceptible populations such as pigs. The virus then spreads from pigs, which have 3,000 times more virus than cattle, to the more susceptible host cattle. The virus was recorded to travel more than 250 km (~150 miles) in waters from Brittany, France, to the Isle of Wight, UK in 1981, but usually did not travel more than 10 km (~6 miles) over land. Foot-and-mouth disease has a high potential for agroterrorism due to its infectious nature, large spread by wind and pollutants, and potential for large economic losses.

Humans can act as mechanocarriers of foot-and-mouth disease by transmitting the virus on their clothing or skin. However, foot and mouth disease is not considered a public health problem.

FMDV is resistant to the environment, but is easily inactivated outside the pH range 6-9 and by drying and temperatures >56°C. Resistant to lipid solvents such as ether and chloroform, but sodium hydroxide (lye), sodium carbonate (soda ash), citric acid and acetic acid (vinegar) are effective disinfectants. Iodophors, quaternary ammonium compounds, hypochlorites and phenols are less effective disinfectants, especially in the presence of organic substances.

The foot-and-mouth disease virus enters the milk of cows before clinical symptoms appear, so the virus has the opportunity to spread from farm to farm through raw milk and from cow to cow. Depending on the method (short-term high temperature, ultrahigh temperature, laboratory pasteurization), FMDV can survive pasteurization; the lipid components of milk protect the virus during heating. FMDV can survive up to 20 weeks in hay or straw, up to 14 days in dry manure in summer, up to 6 months in faecal sludge in winter, 39 days in urine and 3 days in soil (summer) up to 28 (winter) days. However, the extent to which viruses survive on these materials depends on the degree of initial contamination.

Like other picornaviruses, FMDV has a positive-sense RNA genome. The RNA sequence is approximately 8500 nucleotides long and includes a large open reading frame (ORF) that encodes a large polyprotein (approximately 2330 amino acids long). During and after the synthesis of this polyprotein, it is mainly processed by virus-encoded proteases to create mature proteins. The structural proteins of the virus (designated as VP1, VP2, VP3 and VP4) are produced from the capsid precursor P1-2A (see image of foot-and-mouth RNA genome). A nearly spherical viral particle (approximately 25-30 nm in diameter) includes 60 copies of each structural protein and one copy of the viral genome. Proteins VP1, VP2 and VP3 are exposed on the outer surface of the virus, while VP4 is completely inside the virus.

The viral capsid serves to protect the RNA genome when it is outside the host cell and facilitates entry into the cell by binding to specific receptors on the cell surface. After internalization of the virus, the RNA genome is released into the cytoplasm of the cell. It is translated into viral proteins, including several nonstructural proteins, some of which are then used to replicate the RNA genome (via negative-sense RNA copies). Capsid proteins package positive-sense RNA to form new viral particles. Within hours, thousands of new viral particles can be produced within infected cells.

The main site of infection and reproduction of the foot-and-mouth disease virus is the mucous membrane of the pharynx. Viruses can also enter through skin lesions or the gastrointestinal tract. After being distributed through the lymphatic system, the virus replicates in the epithelial cells of the mouth, snout, teats, feet, and areas of damaged skin (e.g., knees and hocks of pigs). Vesicles then develop and burst within 48 hours. More than 50% of ruminants that recover from disease and ruminants that have been vaccinated and then exposed to the virus may be carriers, that is, have low levels of infectious virus in the pharyngeal area. The carrier state can last up to 3.5 years in cattle, up to 9 months in sheep and >5 years in African bison. Surprisingly, this persistent infection does not occur in pigs. The risk from these vectors appears to be low (but not zero) as it is not possible (under controlled conditions) to transmit the disease from carrier cattle to young cattle through prolonged close contact. However, the disease is transmitted from infected buffalo to cattle and also by direct transfer of pharyngeal fluid from infected cattle to young calves.

The incubation period for FMD is variable and depends on the host, environment, route of exposure, and virus strain. The average incubation period of sheep and goats infected with plague virus is 3-8 days, pigs ≥ 2 days and cattle 2-14 days. The incubation period for host-adapted pig strains can be as little as 18 hours, especially under intense direct contact. It is important to note that animals can shed the virus before clinical signs appear, since the virus is present in the animal's throat and blood before the disease is noticed.

Clinical signs in cattle include a temperature of approximately 40°C followed by vesicular lesions on the tongue, hard palate, dental pads, lips, gums, muzzle, crown cords, interdigital fissures and teats in lactating cows. Severely affected persons may drool profusely (drool), stamp their feet and prefer to lie down. Bursted mouth blisters may coalesce to form erosions, but they heal quickly about 11 days after blistering. Foot blisters take longer to heal and are susceptible to bacterial infections, which can lead to chronic lameness. secondary bacteriamastitis Bovine mastitis With few exceptions, mastitis occurs when microorganisms enter the teat through the teat ducts. Almost any microorganism can opportunistically invade the milk ducts and cause mastitis. However, most infect... Read more » This is usually due to resistance to milking due to infected teat blisters. After blister disease, cows quickly lose health and milk production decreases, which can last for a long time. Occasionally, calves may die without clinical signs of disease due to virus damage to the developing heart muscle.

Infected pigs show mild lameness and pericoronal pallor and can develop a temperature of up to 41.5°C. Infected pigs become lethargic, huddle among other pigs and show no interest in food. Vesicles form on the crowns and heels, including the appendages, nose, jaw and tongue. Pigs raised on rough surfaces may develop additional blisters on the hocks and knees. Depending on the severity of the blister, the horns may fall off completely, causing chronic lameness in the recovering pig. Young pigs under 14 weeks of age may die without symptoms of viral myocarditis; this is more common in pigs than in calves.

Experimentally infected camels have been reported to often have mild, if any, clinical disease, but may develop severe infections, resulting in drooling and oral lesions, as well as loss of skin on the foot pads and joints, tarsus, and carpus. Buffalo may have lesions in the mouth and paws that heal faster and are less severe than cattle. Foot-and-mouth disease in wild animals resembles the clinical disease of their domestic animals, but more serious injuries, such as loss of horns or toe horns, have also been reported.

Aging of lesions is an important part of epidemiologic investigation of foot and mouth disease outbreaks. Government agencies and professional societies have produced brochures that can assist clinicians in estimating the age of clinical lesions in foot and mouth disease. All of this is freely available on the Internet.NAS.gEuropa.

In cattle and pigs, clinical signs of foot-and-mouth disease are associated withvesicular stomatitis vesicular stomatitis , and those pigsvesicular disease of pigs vesicular disease of pigs ,Herpes swine herpes and Seneca Valley virus infection. Therefore, laboratory confirmation is essential for the diagnosis of FMD and should be performed in a specialized laboratory that meets the OIE Class 4 pathogen containment requirements. Countries that do not have access to national laboratories or regional authorities that comply with these guidelines should send samples to the OIE Reference laboratory for FMD.

The tissue of choice for sampling was vesicular or liquid epithelium. At least 1 g of epithelial cells should be placed in the transport medium of phosphate-buffered saline (PBS) or equal parts glycerol and phosphate-buffered saline (pH 7.2–7.6). Samples must be refrigerated or shipped on ice. If no vesicles are present, oropharyngeal fluid can be collected using a test cup or throat swab for virus isolation or a reverse transcription-PCR (RT-PCR) test. Serum (blood) samples can also be tested in these ways (OIE Terrestrial Animal Health Code 2019), but the viremia is quite transient (several days); therefore, by the time the lesion heals, the virus has been removed from the blood and antibodies can be detected. Repeat oropharyngeal fluid samples may be required to identify carriers, as virus levels in such animals are low and variable.

Laboratory diagnosis is usually performed by real-time RT-PCR detection; two separate assays targeting two different regions of the RNA genome are usually used. These tests are so sensitive that they can detect FMDV genomes even in samples improperly preserved after loss of viral infectivity. The presence of the virus can also be proven by the ELISA antigen test, which enables determination of the serotype. This is the method of choice for virus detection and serotyping in foot-and-mouth endemic countries (OIETerrestrial Animal Health Code2019). In reference laboratories, the portion of the genome (encoding the capsid protein) is often sequenced to determine the serotype and lineage of the strain. Simultaneous virus isolation can be performed in a suitable cell culture system. Commercially available lateral flow devices for rapid pen tip detection of viral antigens have proven useful.

Serological tests for FMD are used to prove import or export of animals (i.e. trade), identify suspected cases of FMD, test vaccine efficacy and provide evidence of absence of infection. Herd-based surveillance and restrictions on tests to prove the absence of infection for commercial purposes can be set at different levels. The choice of serological tests depends on the animal's vaccination status. Serological determination of antibodies against viral structural (capsid) proteins is not informative in vaccinated animals because the foot-and-mouth disease vaccine induces antibodies against these proteins. However, detection of antibodies against nonstructural proteins produced only during viral replication can be used to determine past or current infection with any of the 7 serotypes, regardless of whether the animal has been vaccinated. However, they are less sensitive and may give false negative results in cases of limited viral replication, such as when vaccinated animals become infected because the vaccine inhibits viral replication (OIETerrestrial Animal Health Code2019).

OIE classifies countries and territories as: free from foot-and-mouth disease after vaccination; suspended FMD-free status with or without vaccination; and unrecognized (OIE Terrestrial Animal Health Code, 2019).

The current global status of foot-and-mouth disease distribution indicates geographic regions with chronically high foot-and-mouth disease prevalence. They are often found in economically difficult countries where veterinary services and resources are insufficient to control or eradicate foot-and-mouth disease.

Movement and trade restrictions on the combined use of animals and animal products have not fully prevented FMD from entering FMD-free areas. The invasion of these viruses into countries or areas that are not foot-and-mouth endemic is generally controlled by the destruction of all infected and susceptible animals in infected herds, strict restriction of the movement of animals and vehicles around infected facilities, proper handling of carcasses and disinfection of the environment, without the use of vaccines.

Inactivated virus vaccines provide protection for only 4 to 6 months against the specific serotypes contained in the vaccine. Billions of doses are used every year to protect animals from clinical disease, but the virus does not persist in the pharynx, so vaccinated animals can become carriers of the infectious virus. Furthermore, it is difficult to distinguish infected from vaccinated animals unless a purified vaccine is used. Therefore, vaccination is used more in countries with endemic animals to protect production animals, especially high-producing dairy cows, from clinical disease, since the destruction of all at-risk individuals may not be economically viable and may cause food shortages.

Rapid disease notification is essential to control FMD outbreaks in non-endemic countries. During an outbreak, surveillance is conducted through epidemiological surveys to help determine the source of disease introduction. Viral sequencing can also identify the source of closely related viruses. When mass destruction is carried out, infected carcasses should be disposed of by burning, burial or near the infected site. Scavengers and rodents must be avoided or eliminated to prevent mechanical transmission of the virus. Buildings should be cleaned and sprayed with a weak acid or alkaline disinfectant, and those who have been exposed to the virus should decontaminate their clothing and avoid contact with sensitive animals for a while.

In some regions, the persistence of FMD in wildlife populations, such as wild African buffalo, can make FMD eradication very difficult. Control measures, such as fencing off wildlife sanctuaries to prevent contact with domestic animals, have helped limit the spread of the virus in some areas. A buffer zone of twice-yearly vaccination among cattle near endemic wildlife reserves can also help reduce disease outbreaks. The Progressive Control Pathway (PCP), developed by FAO and endorsed by OIE, enables countries to improve their own control of foot and mouth disease and thereby improve the global disease situation.

There is no specific treatment for FMD, but supportive care may be allowed in endemic countries.