Clinical variation in foot and mouth disease: sheep and goats

Rev. sci. tech. Off. int. Epiz., 2002, 21 (3), 505-512 

Clinical variation in foot and mouth disease: 

sheep and goats 

R.P. Kitching & G.J. Hughes 

National Centre for Foreign Animal Disease, 1015 Arlington Street, Winnipeg, Manitoba R3E 3M4, Canada 

Summary 

Foot and mouth disease (FMD) in adult sheep and goats is frequently mild or 

unapparent, but can cause high mortality in young animals. The recent outbreak 

of FMD in the United Kingdom has highlighted the importance of sheep in the 

epidemiology of the disease, although there have been numerous examples in the 

past where small ruminants have been responsible for the introduction of FMD 

into previously disease-free countries. The difficulty in making a clinical 

diagnosis should encourage the development of more rapid screening tests to 

assist in future control programmes. 

Keywords 

Control – Diagnosis – Foot and mouth disease – Goats – Sheep. 

Introduction 

The outbreak of foot and mouth disease (FMD) that occurred 

in the United Kingdom (UK) in 2001 has provided a good 

example of how difficult it is to make a clinical diagnosis of the 

disease in sheep (3). The outbreak predominantly affected the 

sheep population, and the policy adopted by the UK 

Government of slaughtering infected animals within 24 h of 

suspicion of disease put intolerable pressure on field 

veterinarians to make a clinical diagnosis on the evidence of 

lesions indistinguishable from those produced by a variety of 

other causes. Where samples were collected, over 50% of the 

flocks slaughtered were not confirmed as positive for FMD 

virus, viral antigen or genome by the laboratory. 

The susceptibility of sheep and goats to FMD can vary with the 

breed of animal and strain of virus. For example, the Hong 

Kong topotype of serotype O FMD virus has only once been 

isolated from a species other than the pig, and although never 

specifically used to infect sheep or goats, the inability of this 

strain to grow in experimentally inoculated cattle would 

suggest that it would also not naturally infect small ruminant 

hosts either (9). Conversely, there are strains of serotype O FMD 

virus circulating in the Middle East where sheep and goats form 

the majority of the susceptible population, which appear very 

well adapted to small ruminants, and there are many examples 

of FMD being carried into countries previously disease-free by 

the movement of infected sheep and goats. In 1983, FMD 

spread from Spain into Morocco with infected sheep. In 1989, 

FMD was introduced to Tunisia by infected sheep, and was 

originally misdiagnosed as bluetongue, because of the signs of 

lameness; not until the disease had spread to cattle was it 

recognised as FMD, by which time it had already been carried 

into neighbouring countries. In 1994, FMD was transported by 

illegally imported sheep from Turkey onto the Greek island of 

Lesbos, from where it was taken onto the mainland; infection 

was certainly present on Lesbos from May, but was not 

positively diagnosed until August, which led to extensive 

spread of the disease in eastern Greece. There are other 

examples of sheep carrying virus from Turkey to Greece and 

Bulgaria, in 1994 and 1993, respectively. Saudi Arabia banned 

the importation of cattle from India in the early 1990s because 

of the threat of rinderpest, but continued to import sheep and 

goats. Nucleotide sequencing of isolates of serotypes O, A and 

Asia 1 collected in Saudi Arabia during this period showed 

them to be identical to those circulating previously in India 

(Figs 1, 2 and 3). In 1994, an isolate later to be known as the 

pan-Asian topotype was imported into Saudi Arabia by infected 

livestock, probably from India; the disease then spread 

throughout the Middle East, eventually causing the 1996 

outbreaks in Bulgaria and Greece. Today this strain is still 

present in the region, and has replaced all other strains of 

serotype O. A close relative of this strain, but probably 

imported from South-East Asia, caused the 2001 UK outbreak 

(20). 

Serotype O FMD virus has been recovered from over 90% of 

the positive samples from sheep submitted to the World 

Reference Laboratory for FMD, Pirbright, UK. Asia 1 serotype 

© OIE - 2002

506 Rev. sci. tech. Off. int. Epiz., 21 (3) 

A5/Allier/60 

A22/IRQ/24/64 

A22/IND/300/94 

A/SAU/16/95 

17.9% 

A/SAU/19/95 

A/SAU/24/95 

A/SAU/35/94 

A/TUR/3/95 

18 16 14 12 10 8 6 4 2 0 

Percentage nucleotide difference (nt 475-639 of VP1) 

Fig. 1 

Dendrogram showing the close genomic relationship between foot and mouth disease serotype A isolates from India and Saudi Arabia 

(N.J. Knowles, personal communication) 

has also been isolated from goat samples submitted from 

Bangladesh and goats imported from this country were 

responsible for an outbreak of Asia 1 in Kuwait. Isolation of 

other serotypes is rare, but does not necessarily indicate that 

infection of small ruminants with these serotypes does not 

occur; for example, Kuwait reported isolating South African 

Territories (SAT 2) virus from sheep during the incursion of 

FMD into Saudi Arabia during 2000. However, even in East 

Africa, where outbreaks due to serotypes O, A, C, SAT 1 and 2 

are common, predominantly serotype O virus was identified in 

clinically affected sheep and goats. 

Transmission 

As is the case with other ruminants, sheep and goats are highly 

susceptible to infection with FMD virus by the aerosol route, 

with as little as 20 TCID 50 (tissue culture infectious doses) being 

sufficient for infection. Aerosol production by infected pigs can 

be as high as log 10 8.6 TCID 50 per day, theoretically sufficient to 

infect over 20 million sheep. Aerosol production by infected 

sheep, however, is considerably less, and whereas there are 

reports of airborne virus spreading from pigs over 250 km to 

infect cattle (France to England in 1981) (5), aerosol 

PAK/1/54 

TAI/2/95 

IND/26/95 

14.8% 

IND/40/95 

IND/233/95 

IND/43/95 

SAU/39/94 

SAU/40/94 

IND/51/95 

18 16 14 12 10 8 6 4 2 0 


Fig. 2 

Dendrogram showing the close genomic relationship between foot and mouth disease serotype Asia 1 isolates from India and Saudi Arabia 


© OIE - 2002

Rev. sci. tech. Off. int. Epiz., 21 (3) 507 

O1/Kaufbeuren/66 

O1/Manisa/69 

15.4% 

O/IND/6/94 

O/IND/9/94 

O/SAU/15/94 

O/SAU/62/94 

O/SAU/65/94 

O/SAU/58/94 

O/SAU/72/94 

O/SAU/100/94 

O/SAU/28/95 

O/SAU/14/95 

O/SAU/20/95 

O/SAU/77/94 

18 16 14 12 10 8 6 4 2 0 


Fig. 3 

Dendrogram showing the close genomic relationship between foot and mouth disease serotype O isolates from India and Saudi Arabia 


transmission from infected sheep is unlikely to occur over 

distances greater than 100 metres (7, 26). Sheep are also less 

likely to become infected by airborne virus than cattle because 

of their lower respiratory volume. Sheep and goats are probably 

most often infected by direct contact with infected animals. The 

virus may infect sheep and goats through abrasions on the skin 

or mucous membranes, through contaminated food, as well as 

by the respiratory route. During the FMD outbreak that took 

place in the UK in 2001, disease spread was reported to occur 

frequently by mechanical carriage of virus between flocks by 

humans or vehicles. 

Sheep-to-sheep spread by contact appears to be restricted, to 

the extent that the rate of transmission within an affected flock 

is lower than that observed in infected pig or cattle herds. A 

good example of this phenomenon is illustrated by the 

outbreak of FMD that took place in Greece during 1994. 

Serological investigations showed that in many of the affected 

flocks not all individuals had sero-converted to the virus, 

indicating that the virus had not disseminated sufficiently to 

infect entire flocks. In some flocks affected towards the end of 

the outbreak, only 20% of the sheep were sero-positive (21). 

There was suspicion, but little firm evidence, that the 1993 

outbreak of FMD in Italy had also failed to maintain itself in 

affected sheep flocks. Similarly, evidence from the recent UK 

epidemic shows considerable variation in the level of intra-flock 

infection rates. On one farm visited, only 5% of 237 sheep that 

were blood tested were sero-positive, and 3% were viruspositive, 

whereas 91% of the 75 cattle present were clinically 

affected. On a second farm tested, 8% of 148 sheep were seropositive, 

24% virus-positive, whilst 98 of 100 cattle showed 

clinical signs (1). A recent study by Hughes (14) has provided 

supportive evidence for the observed difference between the 

dynamics of FMD transmission in sheep populations as 

compared with cattle and pigs. The study showed that, using 

the 1994 Greek outbreak strain, there was significant reduction 

in the level of infection and estimated transmission rates over 

time during serial passage through groups of sheep. These 

results infer that some, possibly most, strains of FMD virus may 

die out if they are restricted to sheep. Infection of cattle or pigs 

may be sufficient to increase the level of circulating virus and 

consequently the probability of transmission of infection to 

© OIE - 2002


in-contact sheep, thereby re-establishing the disease. This 

hypothesis requires further investigation using other strains of 

FMD virus. The limited transmission that may occur within 

closed sheep populations is also often masked by the lack of 

clinical signs (see above). 

The probability of transmission of FMD virus from infected 

sheep is highest during the viraemic phase and peaks at or just 

before the appearance of clinical signs. This period correlates 

well with the period of virus excretion (4) which ends at the 

point of sero-conversion (2). Levels of virus excretion are strainspecific 

(4). 

Clinical signs 

The incubation period in sheep following infection with FMD 

virus is usually between three and eight days (19), but can be 

as short as 24 h following experimental inoculation, or as long 

as twelve days, depending on the susceptibility of the sheep, the 

dose of virus and the route of infection. The duration of 

viraemia is between one and five days. Hughes et al. (15) were 

unable to detect viraemia in 8% of sheep that sero-converted in 

a series of transmission experiments. Clinical signs appear up to 

three days after the start of viraemia, approximately seven days 

after exposure to contact infection – giving the period between 

exposure to infection and the onset of viraemia as between 

three and seven days (13, 15). Vesicular disease may fail to 

develop in approximately 25% of infected sheep (12, 15), a 

further 20% may develop only a single observable lesion. In 

79 sheep infected with the 1994 Greek strain, lesions in those 

animals that developed vesicular disease were visible for less 

than three days (15). 

Lameness is usually the first indication of FMD in sheep and 

goats (Fig. 4). An affected animal develops fever, is reluctant to 

walk, and may separate itself from the rest of the flock. In the 

field situation, lameness due to other causes may already be 

present and may conceal the presence of FMD. Vesicles may 

develop in the interdigital cleft, on the heel bulbs and on the 

coronary band, but they usually rupture rapidly (Fig. 5) and 

their appearance may be hidden by the coexisting presence of 

foot rot. Hair or wool may have to be deflected upwards to 

render lesions on the coronary band visible, but, in sheep, 

lesions can easily be confused with the coronitis seen with 

bluetongue. Vesicles also form in the mouth, but they rupture 

easily and are usually only seen as shallow erosions, most 

commonly on the dental pad, adjacent to the incisors (Fig. 6), 

but also on the tongue, hard palate, lips and gums. In one study, 

of 57 sheep with foot lesions due to FMD, only 4 had mouth 

lesions and only 2 of these had mouth lesions without foot 

lesions (15). Vesicles may also be observed on the teats, 

particularly of milking sheep and goats and rarely, on the vulva 

Fig. 5 

Coronary band lesions due to foot and mouth disease are 

usually mild, and difficult to see 

Fig. 4 

Lameness is usually the first sign of foot and mouth disease in 

sheep 

Fig. 6 

A ruptured vesicle on the dental pad of a sheep infected with 

foot and mouth disease virus 

© OIE - 2002


and prepuce. Affected rams are unwilling to work, and lactating 

animals suffer a temporary loss of milk yield. Secondary 

infections may cause mastitis and persistent lameness and the 

compromised epithelium can predispose to rapid transmission 

of other viral infections such as sheep and goat pox and peste 

des petits ruminants. Uncomplicated infections with FMD virus 

are usually followed by rapid recovery in the adult animal. 

The clinical disease in young lambs and kids is characterised by 

death without the appearance of vesicles, due to heart failure. 

Affected flocks may lose up to 90% of the lamb crop, and the 

image of large numbers of lambs falling down dead when 

stressed, as may occur when a stranger walks into the flock, is 

dramatic. 

Pathology 

Local replication of FMD virus occurs at the site of entry, in the 

mucosa of the respiratory tract or at a skin or mucous 

membrane abrasion. The virus then spreads throughout the 

body favouring epithelial tissue in the adult and heart muscle in 

the juvenile. Lytic changes in the cells of the stratum spinosum 

and consequent oedema give rise to the characteristic vesicles 

and accumulation of granulocytes, and in the developing 

myocardium of young animals, to a lympho-histiocytic 

myocarditis (6). Depending on the speed with which the virus 

overwhelms the function of the heart, gross lesions may be 

apparent on post mortem as diffuse grey spots or more 

organised ‘tiger’ stripes, particularly in the left ventricle and 

interventricular septum. 

In adult animals, recovery from FMD uncomplicated by 

secondary pathogens, is usually rapid, but the virus will persist 

in the tonsillar tissue for up to nine weeks in sheep and for a 

shorter period in goats. 

Diagnosis 

Clinical diagnosis of FMD in sheep and goats is difficult because 

of the usually transient appearance of lesions and their 

similarity to those caused by other common diseases of small 

ruminants. Laboratory confirmation of a diagnosis of FMD is 

therefore essential. Samples of vesicle epithelium, if available, or 

heart muscle from a dead lamb or kid, should be collected into 

50% phosphate/glycerol, buffered to pH 7.4-7.6, and 

submitted together with whole and clotted blood to a 

laboratory equipped to handle the diagnosis and with the 

necessary disease-secure facilities. This will either be a 

designated government laboratory or the regional FMD 

reference laboratory. Alternatively, samples can be sent to the 

World Reference Laboratory for FMD at Pirbright in the UK, 

following the necessary procedures (23). In the laboratory, the 

tissue samples will be prepared as a 10% suspension for antigen 

detection enzyme-linked immunosorbent assay (ELISA) (23) 

or used directly in a polymerase chain reaction (PCR) (24) to 

serotype the virus. Sensitive tissue cultures, such as primary 

bovine thyroid or lamb kidney cells, will also be inoculated 

with the tissue suspension and/or the whole blood and serum, 

to grow the virus for further characterisation, and to amplify 

the antigen if insufficient quantities were present in the original 

sample to provide an initial diagnosis by ELISA. The antigenic 

characteristics of the strain will be compared with existing 

vaccine strains in order to identify a suitable vaccine if one is 

required, or to confirm the use of one that is already helping to 

control the outbreak (17). A segment of the viral genome (part 

of the 1D gene) can also be sequenced and compared in the 

reference laboratory database to determine the relationship of 

the virus to other viruses circulating in the region, which may 

give an indication of its origin (18). 

Due to the difficulty in detecting clinical FMD in sheep and 

goats, the disease may be present in the flock for a considerable 

time prior to discovery and samples may be collected from 

recovering animals. These animals will no longer have live virus 

in their tissues, except possibly in the pharynx, but antibodies 

to FMD virus will be detectable using either the liquid phase 

blocking ELISA (23), the solid phase competition ELISA (22) 

or the virus neutralisation test (23). However, if vaccine has 

been used in the flock, these tests will not distinguish between 

antibodies resulting from infection and those resulting from 

vaccination. Animals that have been infected with replicating 

virus develop antibodies to the non-structural proteins of FMD 

virus, and these may be detected using the 3ABC ELISA or 

enzyme-linked immuno-electrotransfer blot (EITB), although 

neither test has been fully validated for use in small ruminants 

(23). Alternatively, the presence of infection within the flock 

can be investigated by collecting samples using a probang 

sampling cup which recovers mucous and superficial epithelial 

cells from the pharynx, the site of virus persistence (16). The 

probang sample is then tested for the presence of FMD virus as 

for tissue and blood samples. 

A pen-side diagnostic test would have been particularly 

valuable during the recent UK outbreak to assist field 

veterinarians in their clinical diagnosis. One, similar to a test 

which had been developed for rinderpest diagnosis, was in the 

process of validation and was used with some success towards 

the end of the outbreak (11, 25). The test relies on FMD viral 

antigen being recognised by a monoclonal antibody (Mab) 

attached to a coloured latex bead. The antigen/Mab/bead 

complex is trapped by a fixed band of additional anti-FMD 

virus monoclonal antibody as it migrates along a 

chromatographic strip, creating an easily identifiable coloured 

line over the fixed band of Mab as the latex beads concentrate. 

The result can be read in 10 minutes. However, the test requires 

the amount of antigen usually found in the epithelium of a 

ruptured vesicle, but would not be sufficiently sensitive to 

detect antigen in a blood sample; in many cases of FMD in 

sheep, there may not be sufficient epithelium available for the 

© OIE - 2002


test to be used. Adaptations of the PCR could also provide a 

more rapid diagnosis, either to detect viral genome in nasal 

swabs before the development of clinical disease, or for use in 

portable machines taken to suspect premises (8). 

Once the sample is received by a competent diagnostic 

laboratory, and assuming the sample was properly collected 

and stored during transport, the available tests are extremely 

sensitive and specific, and for positive samples, the result can 

usually be available in a few hours. However, before the 

laboratory can report that no virus was detected, the sample 

must be passaged on tissue culture and then blind-passaged a 

further one or two times, each passage requiring 48 hours. 

Thus a week may elapse after receipt of a sample and before a 

final report is issued from the laboratory. This can and 

frequently does cause some frustration with the field staff, as 

quarantine and movement restrictions would probably have 

been kept in place until a result was available. However, there 

are many examples where preliminary negative results have 

been issued and restrictions prematurely removed, and then the 

final result has been reported positive. 

Control 

The control of FMD in sheep and goats follows the same 

principles as would apply to the disease in other susceptible 

farm livestock, i.e. movement restrictions, disinfection and 

either slaughter of affected and in-contact animals or 

vaccination. In countries previously free from FMD, an initial 

attempt is usually made to eradicate the disease by slaughter. 

However, most countries will retain the option to vaccinate and 

thus maintain membership of a vaccine bank which can 

provide vaccine at short notice. In countries that have endemic 

FMD, sheep may be included in regular vaccination campaigns, 

although they are rarely vaccinated more than once a year. 

Sheep and goats are usually given half or a third of the cattle 

vaccine dose, and either oil or aluminium hydroxide/saponin 

adjuvants can be used. The duration of immunity against 

disease will depend on the severity of challenge with live virus 

in the field, the antigenic relationship between the vaccine 

strain and the field virus and the potency of the vaccine used. 

The often silent nature of the disease in adult sheep and goats 

can also give the impression that the vaccination programme 

has been successful, when in reality the virus is circulating 

freely. The ability of the particular strain to maintain itself in the 

small ruminant population becomes critical in these situations, 

but, as discussed above, has so far received little attention. 

Attempts to vaccinate the national sheep population are usually 

hindered by the numbers involved, the cost of vaccination, and 

the resources required to administer the vaccine. The initial 

intention to include sheep and goats in the vaccination 

campaign throughout Turkey was recognised as unrealistic. 

Vaccination was therefore targeted at all susceptible stock in 

European Turkey (Thrace) and only certain areas of Anatolia. 

Similarly, Morocco concentrated on vaccinating sheep and 

goats on the border with Algeria, together with strategic 

vaccination around affected areas during the last outbreak of 

FMD in the country. Uruguay vaccinated only the cattle 

population during the final stages of the successful FMD 

eradication programme undertaken in the early 1990s, and left 

the approximately 20 million sheep unvaccinated during this 

period. 

Conclusion 

The recent UK experience has demonstrated the importance of 

sheep in the epidemiology of FMD caused by certain strains of 

virus. The difficulties encountered in identifying clinical disease 

resulted in large numbers of healthy animals being slaughtered, 

while other infected flocks went unrecognised, allowing the 

virus to spread. While some would argue that the policy 

adopted was effective and the overkill justified (10), a more 

traditional approach of methodical tracing and laboratory 

testing may have been equally effective, less expensive and 

morally more defensible. Both sides of the argument would 

however probably agree on the need for more rapid and reliable 

on-farm diagnosis, and a better understanding of the natural 

history of FMD in small ruminants. 

■ 

© OIE - 2002


Variation des signes cliniques de la fièvre aphteuse chez les ovins 

et les caprins 

R.P. Kitching et G.J. Hughes 

Résumé 

Alors que les manifestations de la fièvre aphteuse sont souvent peu ou non 

apparentes chez les ovins et caprins adultes, cette maladie peut provoquer une 

forte mortalité parmi les jeunes sujets. L’épizootie de fièvre aphteuse qu’a 

récemment connue le Royaume-Uni a souligné l’importance du mouton dans 

l’épidémiologie de la maladie, même si la responsabilité des petits ruminants 

dans l’introduction de la fièvre aphteuse en pays indemnes avait été maintes fois 

établie par le passé. Les difficultés que rencontre le diagnostic clinique devraient 

inciter à mettre au point des épreuves de dépistage plus rapides, qui 

deviendraient de précieux auxiliaires dans les futurs programmes de prophylaxie. 

Mots-clés 

Caprins – Diagnostic – Fièvre aphteuse – Ovins – Prophylaxie. 

■ 

Variación de las manifestaciones clínicas de la fiebre aftosa: 

ovinos y caprinos 

R.P. Kitching & G.J. Hughes 

Resumen 

Aunque en los ovinos y caprinos adultos suela revestir carácter benigno o 

subclínico, la fiebre aftosa puede provocar una elevada mortalidad entre 

animales jóvenes. El reciente brote en el Reino Unido puso de relieve la 

importante intervención de las ovejas en la epidemiología de la fiebre aftosa, 

aunque antes ya se habían producido muchos episodios en que pequeños 

rumiantes introdujeron la fiebre aftosa en países hasta entonces indemnes. Las 

dificultades inherentes al diagnóstico clínico deben servir de aliciente para crear 

pruebas de detección más rápidas y ponerlas al servicio de futuros programas de 

control. 

Palabras clave 

Caprinos – Control – Diagnóstico – Fiebre aftosa – Ovinos. 

■ 

© OIE - 2002


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© OIE - 2002

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