porcine enterovirus infections
- Host Animals
- Hosts/Species Affected
- Systems Affected
- Distribution Table
- List of Symptoms/Signs
- Disease Course
- Impact: Economic
- Zoonoses and Food Safety
- Disease Treatment
- Prevention and Control
- Links to Websites
- Distribution Maps
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- porcine enterovirus infections
International Common Names
- English: benign enzootic paresis; encephalomyelitis; enterovirus encephalomyelitis; enterovirus, teschen, talfan disease in swine; polioencephalomyelitis; poliomyelitis suum; porcine entoviral encephalomyelitis; porcine polioencephalomyelitis; stillbirth, mummification , embryonic death and infertility; swine vesicular disease; swine vesicular disease - exotic; talfan disease; teschen disease
Pathogen/sTop of page porcine enterovirus 1
porcine enterovirus 2-6, 8, and 12-13
swine vesicular disease virus
OverviewTop of page
Porcine enteroviruses are widespread, and occur in many different serotypes. The pathology of porcine enterovirus infections varies greatly between the representative viruses. Not all enteroviruses are pathogenic, and many enterovirus infections pass subclinically. However, there are several distinct pathological syndromes associated with porcine enteroviruses, including encephalomyelitis (Teschen disease), reproductive disorders (SMEDI) and swine vesicular disease (SVD). Teschen disease (encephalomyelitis) is associated with a porcine enterovirus (recently classified in a separate genus Teschovirus). Teschen disease occurs sporadically, and seems geographically restricted. The impact of this porcine enterovirus infection does not consistently cause great economic losses, although occasionally severe outbreaks may occur. Stillbirth, mummification, embryonic death and infertility (SMEDI) are characteristic of reproductive disorders caused by enteroviruses in pigs. Swine vesicular disease virus (SVDV) is an unusual representative of a porcine enterovirus, causing fever, vesicles on the mouth and feet, and lameness. Clinically, swine vesicular disease (SVD) cannot be distinguished from foot-and-mouth disease. The enteroviruses display particular resistance in the environment, and are highly contagious.
Host AnimalsTop of page
Hosts/Species AffectedTop of page
Evidence for porcine enterovirus infections, including reproductive disorders, have been found only in swine (Derbyshire, 1989; Wang and Pensaert, 1989). Swine vesicular disease virus (SVDV) is the exception (Derbyshire, 1989). Natural SVDV infections are restricted to pigs. However, due to its close relationship with Coxsackie B-5 virus, studies have been carried out to examine the susceptibility of humans and pigs for the respective viruses. Humans have been infected with SVDV following exposure under laboratory conditions and have become ill, with fever and viral meningitis, but attempts to infect pigs with Coxsackie B-5 virus did not induce disease (Hedger and Mann, 1989; Hoey and Martin, 1994).
Systems AffectedTop of page nervous system diseases of pigs
reproductive diseases of pigs
skin and ocular diseases of pigs
DistributionTop of page
Porcine enterovirus infections occur worldwide, and are frequently subclinical and therefore not noticed or reported. The infection rate in pig populations is high.
Teschen disease appears to be geographically restricted to parts of Africa, such as Madagascar (Blood et al., 1979) and central Europe (Derbyshire, 1989; Hoey and Martin, 1994). The disease was first described in 1929 in Czechoslovakia (Hoey and Martin, 1994). Talfan disease, also caused by the previously named porcine enterovirus serotype 1 strains, may be caused by less virulent strains, that occur worldwide (Derbyshire, 1989; Hoey and Martin, 1994).
Porcine enteroviruses causing reproductive disorders occur worldwide (Wang and Pensaert, 1989).
Swine vesicular disease
Swine vesicular disease (SVD) was first recognized in Italy in 1966, and was reported subsequently in Hong Kong in 1971, and repeatedly in the UK and Italy from 1972 onwards (Hedger and Mann, 1989; Morgan-Capner and Bryden, 1998). Further outbreaks occurred in most European countries, and were reported in Japan (1975), Korea (1980), Nicaragua (1986), Macau (1989), Laos (1991), Bolivia (1991), Lebanon (1992) and in Taiwan (1998) (FAO Animal Health Yearbook 1971-1996; Hedger and Mann, 1989; Dekker, 2000). Strict control measures (Davies, 1994) have eradicated the disease in many countries, but the disease persists in southern Italy and incidentally flares up in that country, the last occurrence being in 1999 (Davies, 1994; Dekker, 2000). Africa, North America and Australia have remained free of SVD, due to strict import control measures.
Distribution TableTop of page
The distribution in this summary table is based on all the information available. When several references are cited, they may give conflicting information on the status. Further details may be available for individual references in the Distribution Table Details section which can be selected by going to Generate Report.
|Continent/Country/Region||Distribution||Last Reported||Origin||First Reported||Invasive||Reference||Notes|
|Afghanistan||No information available||OIE, 2009|
|Armenia||Disease not reported||OIE, 2009|
|Azerbaijan||Disease never reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||Disease never reported||OIE, 2009|
|Bhutan||Disease never reported||OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||No information available||OIE, 2009|
|-Hong Kong||No information available||OIE, 2009|
|Georgia (Republic of)||Disease never reported||OIE Handistatus, 2005|
|India||Disease never reported||OIE, 2009|
|Indonesia||Disease never reported||OIE, 2009|
|Iran||Disease never reported||OIE, 2009|
|Iraq||Disease never reported||OIE, 2009|
|Israel||Disease never reported||OIE, 2009|
|Japan||Disease not reported||OIE, 2009|
|Jordan||No information available||OIE, 2009|
|Kazakhstan||Disease not reported||OIE, 2009|
|Korea, DPR||Disease not reported||OIE Handistatus, 2005|
|Korea, Republic of||Disease never reported||OIE, 2009|
|Kuwait||Disease never reported||OIE, 2009|
|Kyrgyzstan||Disease never reported||OIE, 2009|
|Laos||No information available||OIE, 2009|
|Lebanon||Disease never reported||OIE, 2009|
|Malaysia||Disease never reported||OIE, 2009|
|-Peninsular Malaysia||Disease not reported||OIE Handistatus, 2005|
|-Sabah||Disease never reported||OIE Handistatus, 2005|
|-Sarawak||No information available||OIE Handistatus, 2005|
|Mongolia||No information available||OIE, 2009|
|Myanmar||Disease never reported||OIE, 2009|
|Nepal||No information available||OIE, 2009|
|Oman||Disease never reported||OIE, 2009|
|Pakistan||No information available||OIE, 2009|
|Philippines||Disease never reported||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||Disease never reported||OIE, 2009|
|Singapore||Disease never reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||Disease not reported||OIE, 2009|
|Taiwan||Disease never reported||OIE Handistatus, 2005|
|Tajikistan||Disease never reported||OIE, 2009|
|Thailand||No information available||OIE, 2009|
|Turkey||Disease never reported||OIE, 2009|
|Turkmenistan||No information available||OIE Handistatus, 2005|
|United Arab Emirates||No information available||OIE, 2009|
|Uzbekistan||Disease never reported||OIE Handistatus, 2005|
|Vietnam||Disease never reported||OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease never reported||OIE, 2009|
|Angola||Disease never reported||OIE, 2009|
|Benin||No information available||OIE, 2009|
|Botswana||Disease never reported||OIE, 2009|
|Burkina Faso||No information available||OIE, 2009|
|Burundi||Disease never reported||OIE Handistatus, 2005|
|Cameroon||Disease never reported||OIE Handistatus, 2005|
|Cape Verde||Disease never reported||OIE Handistatus, 2005|
|Central African Republic||Disease not reported||OIE Handistatus, 2005|
|Chad||No information available||OIE, 2009|
|Congo||No information available||OIE, 2009|
|Congo Democratic Republic||Disease not reported||OIE Handistatus, 2005|
|Côte d'Ivoire||Disease not reported||OIE Handistatus, 2005|
|Djibouti||Disease never reported||OIE, 2009|
|Egypt||Disease never reported||OIE, 2009|
|Eritrea||No information available||OIE, 2009|
|Ethiopia||No information available||OIE, 2009|
|Gabon||Disease never reported||OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||Disease never reported||OIE, 2009|
|Guinea||No information available||OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||Disease never reported||OIE, 2009|
|Lesotho||Disease never reported||OIE, 2009|
|Libya||Disease never reported||OIE Handistatus, 2005|
|Madagascar||Disease never reported||OIE, 2009|
|Malawi||Disease never reported||OIE, 2009|
|Mali||No information available||OIE, 2009|
|Mauritius||Disease never reported||OIE, 2009|
|Morocco||No information available||OIE, 2009|
|Mozambique||Disease never reported||OIE, 2009|
|Namibia||Disease never reported||OIE, 2009|
|Nigeria||Disease never reported||OIE, 2009|
|Réunion||Last reported||1970||OIE Handistatus, 2005|
|Rwanda||No information available||OIE, 2009|
|Sao Tome and Principe||Disease not reported||OIE Handistatus, 2005|
|Senegal||No information available||OIE, 2009|
|Seychelles||No information available||OIE Handistatus, 2005|
|Somalia||No information available||OIE Handistatus, 2005|
|South Africa||Disease never reported||OIE, 2009|
|Sudan||Disease never reported||OIE, 2009|
|Swaziland||Disease never reported||OIE, 2009|
|Tanzania||No information available||OIE, 2009|
|Togo||No information available||OIE, 2009|
|Tunisia||Disease never reported||OIE, 2009|
|Uganda||Disease never reported||OIE, 2009|
|Zambia||No information available||OIE, 2009|
|Zimbabwe||Disease never reported||OIE, 2009|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Disease never reported||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease never reported||OIE, 2009|
|USA||Disease never reported||OIE, 2009|
Central America and Caribbean
|Barbados||Disease never reported||OIE Handistatus, 2005|
|Belize||Disease never reported||OIE, 2009|
|British Virgin Islands||Disease never reported||OIE Handistatus, 2005|
|Cayman Islands||Disease not reported||OIE Handistatus, 2005|
|Costa Rica||Disease never reported||OIE, 2009|
|Cuba||Disease never reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||Disease not reported||OIE Handistatus, 2005|
|Dominican Republic||Disease never reported||OIE, 2009|
|El Salvador||Disease never reported||OIE, 2009|
|Guadeloupe||No information available||OIE, 2009|
|Guatemala||Disease never reported||OIE, 2009|
|Haiti||Disease never reported||OIE, 2009|
|Honduras||No information available||OIE, 2009|
|Jamaica||Disease never reported||OIE, 2009|
|Martinique||Disease never reported||OIE, 2009|
|Nicaragua||Disease never reported||OIE, 2009|
|Panama||Disease never reported||OIE, 2009|
|Saint Kitts and Nevis||Disease never reported||OIE Handistatus, 2005|
|Saint Vincent and the Grenadines||Disease never reported||OIE Handistatus, 2005|
|Trinidad and Tobago||Disease never reported||OIE Handistatus, 2005|
|Argentina||Disease never reported||OIE, 2009|
|Bolivia||Disease never reported||OIE, 2009|
|Brazil||Disease never reported||OIE, 2009|
|Chile||Disease never reported||OIE, 2009|
|Colombia||Disease never reported||OIE, 2009|
|Ecuador||Disease never reported||OIE, 2009|
|Falkland Islands||Disease never reported||OIE Handistatus, 2005|
|French Guiana||Disease never reported||OIE, 2009|
|Guyana||Disease never reported||OIE Handistatus, 2005|
|Paraguay||Disease never reported||OIE Handistatus, 2005|
|Peru||Disease never reported||OIE, 2009|
|Uruguay||Disease never reported||OIE, 2009|
|Venezuela||Disease never reported||OIE, 2009|
|Albania||No information available||OIE, 2009|
|Andorra||Disease never reported||OIE Handistatus, 2005|
|Austria||Disease not reported||OIE, 2009|
|Belarus||Disease never reported||OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Bosnia-Hercegovina||Disease not reported||OIE Handistatus, 2005|
|Bulgaria||Disease never reported||OIE, 2009|
|Croatia||Disease never reported||OIE, 2009|
|Cyprus||Disease never reported||OIE, 2009|
|Czech Republic||Disease never reported||OIE, 2009|
|Denmark||Disease never reported||OIE, 2009|
|Estonia||Disease never reported||OIE, 2009|
|Finland||Disease never reported||OIE, 2009|
|France||Disease not reported||OIE, 2009|
|Germany||Disease not reported||OIE, 2009|
|Greece||Disease not reported||OIE, 2009|
|Hungary||Disease never reported||OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease never reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||Restricted distribution||OIE, 2009|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Disease never reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease never reported||OIE, 2009|
|Luxembourg||Disease never reported||OIE, 2009|
|Macedonia||Disease never reported||OIE, 2009|
|Malta||Disease not reported||OIE, 2009|
|Moldova||OIE Handistatus, 2005|
|Montenegro||Disease never reported||OIE, 2009|
|Netherlands||Disease not reported||OIE, 2009|
|Norway||Disease never reported||OIE, 2009|
|Poland||Disease not reported||OIE, 2009|
|Portugal||Disease not reported||OIE, 2009|
|Romania||Disease not reported||OIE, 2009|
|Russian Federation||Disease never reported||OIE, 2009|
|Serbia||Disease never reported||OIE, 2009|
|Slovakia||Disease never reported||OIE, 2009|
|Slovenia||Disease never reported||OIE, 2009|
|Spain||Disease not reported||OIE, 2009|
|Sweden||Disease never reported||OIE, 2009|
|Switzerland||Disease not reported||OIE, 2009|
|UK||Disease not reported||OIE, 2009|
|-Northern Ireland||Disease never reported||OIE Handistatus, 2005|
|Ukraine||Disease not reported||OIE, 2009|
|Yugoslavia (former)||No information available||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Disease not reported||OIE Handistatus, 2005|
|Australia||Disease never reported||OIE, 2009|
|French Polynesia||Disease never reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease never reported||OIE, 2009|
|Samoa||Disease never reported||OIE Handistatus, 2005|
|Vanuatu||Disease never reported||OIE Handistatus, 2005|
|Wallis and Futuna Islands||No information available||OIE Handistatus, 2005|
PathologyTop of page
At necropsy a non-suppurative encephalomyelitis is present. However, this is not pathognomonic for Teschovirus. Histologically changes are most consistently seen in the grey matter of the ventral horns of the spinal cord, and in the dorsal root ganglia, medulla, pons, cerebellum, cerebral peduncles, thalamus, motor cortex and the olfactory lobes (Blood et al., 1979; Hedger and Mann, 1989; Derbyshire, 1992). Histological lesions vary in distribution, extent and severity depending upon the strain of porcine enterovirus involved (Hedger and Mann, 1989). The principal histological changes include neuronal degeneration, neuronophagia, lymphocytic perivascular cuffing and focal areas of gliosis. The virus targets the endoplasmic reticulum in the infected neuron, as has been shown by electron microscopy, which results in degeneration of the infected cells. The lesions are more severe and extensive in Teschen disease than in Talfan disease.
Few lesions are found in stillborn or neonatal piglets, but a mild nonsuppurative encephalomyelitis may be present (Derbyshire, 1992). Histologically focal areas of gliosis, perivascular cuffing and neurophagia may be present (Wang and Pensaert, 1989).
Swine vesicular disease
The coronary band, and the skin over the metacarpus, metatarsus, snout, tongue and lips can be affected. Virus replication starts in the stratum spinosum and in a later stage also occurs in the stratum granulosum (Hedger and Mann, 1989; Dekker, 2000). Histopathology shows inflammation of the skin, and microscopic lesions in the tonsils, gastrointestinal tract, lymphatics, spleen, liver, striated muscle, adrenal and thyroid glands (Hedger and Mann, 1989; Dekker, 2000). Virus replication does not only occur in the skin, but virus cells can be recovered from the myocardium and brain.
DiagnosisTop of page
Demonstration of a Teschovirus species in any pig that died after showing nervous signs is conclusive. Tissue suspensions of brain and spinal cord from affected pigs can be inoculated into primary swine kidney cell cultures (OIE, 1996). The identity of the virus can best be confirmed by the use of specific antisera. Virus neutralization (VN) and indirect fluorescent antibody (IFA) tests are preferred techniques for this.
The reproductive effects of the disease are hard to distinguish from parvovirus infections without laboratory tests (Taylor, 1999). Clinical signs may point towards an enterovirus infection, such as farrowing of small litters, mummified fetuses of different sizes, and stillborn and weak piglets. Identification of the virus from the lungs, intestine or brains of stillborn fetuses may be attempted. Isolation is most successful in primary swine kidney cells (Wang and Pensaert, 1989). Isolation of virus cells from mummified foetuses is seldom successful. Otherwise, detection of porcine enterovirus-specific antibodies in the serum of stillborn piglets, or weak piglets which survive for a short time, is conclusive, provided the piglets did not receive colostrum from the sow.Antibody detection in paired sera of the sows is not helpful, because the infection will have taken place long before birth, and a seroconversion will not be detected (Wang and Pensaert, 1989; Derbyshire, 1992). Also, because many enterovirus infections pass subclinically, demonstration of a seroconversion would not be conclusive for the reproductive problems.
Swine vesicular disease
The clinical symptoms of swine vesicular disease (SVD) do not allow a definitive diagnosis, and laboratory examination is needed in the cases of lameness and vesicle formation in pigs in order to distinguish between foot-and-mouth disease and SVD. The most sensitive detection method is virus isolation on IBRS-2 cells, but the amounts of virus in vesicular material is very high and allows accurate and rapid diagnosis by an antigen ELISA (Dekker, 2000). Vesicle material must be collected from diseased animals, and transported to the laboratory. Virus isolation may also be performed on SK cells, PK-15 cells, or primary or secondary swine kidney cells. By reverse transcriptase polymerase chain reaction (RT-PCR) SVDV can also be detected, but this method has not yet been approved by the Office International des Epizooties (OIE) (OIE, 1996; Callens and Clercq, 1999). Detection of SVDV-specific antibodies in serum is also possible, and may be appropriate when the material collected has absent or insufficient virus cells for virus detection (Hedger and Mann, 1989).
List of Symptoms/SignsTop of page
|Cardiovascular Signs / Arrhythmia, irregular heart rate, pulse||Sign|
|Cardiovascular Signs / Jugular pulse||Sign|
|Cardiovascular Signs / Peripheral venous distention, jugular distention||Sign|
|Cardiovascular Signs / Tachycardia, rapid pulse, high heart rate||Sign|
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Pigs:All Stages||Sign|
|Digestive Signs / Ascites, fluid abdomen||Sign|
|Digestive Signs / Diarrhoea||Pigs:All Stages||Sign|
|Digestive Signs / Oral mucosal ulcers, vesicles, plaques, pustules, erosions, tears||Sign|
|Digestive Signs / Tongue ulcers, vesicles, erosions, sores, blisters, cuts, tears||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Pigs:All Stages||Diagnosis|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Exercise intolerance, tires easily||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Pigs:All Stages||Sign|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Sign|
|General Signs / Forelimb weakness, paresis, paralysis front leg||Pigs:All Stages||Sign|
|General Signs / Generalized lameness or stiffness, limping||Pigs:All Stages||Diagnosis|
|General Signs / Generalized weakness, paresis, paralysis||Pigs:All Stages||Diagnosis|
|General Signs / Hemiparesis||Sign|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Sign|
|General Signs / Inability to stand, downer, prostration||Pigs:All Stages||Diagnosis|
|General Signs / Opisthotonus||Pigs:All Stages||Diagnosis|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Pigs:All Stages||Sign|
|General Signs / Reluctant to move, refusal to move||Sign|
|General Signs / Sudden death, found dead||Pigs:All Stages||Diagnosis|
|General Signs / Tetraparesis, weakness, paralysis all four limbs||Pigs:All Stages||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Pigs:All Stages||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Sign|
|General Signs / Weakness of one hindlimb, paresis paralysis rear leg||Pigs:All Stages||Sign|
|General Signs / Weight loss||Sign|
|Nervous Signs / Coma, stupor||Pigs:All Stages||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Pigs:All Stages||Sign|
|Nervous Signs / Excitement, delirium, mania||Pigs:All Stages||Sign|
|Nervous Signs / Hyperesthesia, irritable, hyperactive||Pigs:All Stages||Sign|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Pigs:All Stages||Sign|
|Nervous Signs / Tremor||Pigs:All Stages||Sign|
|Ophthalmology Signs / Blindness||Pigs:All Stages||Sign|
|Ophthalmology Signs / Nystagmus||Pigs:All Stages||Sign|
|Pain / Discomfort Signs / Forefoot pain, front foot||Sign|
|Pain / Discomfort Signs / Hindfoot pain, rear foot||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Sign|
|Reproductive Signs / Female infertility, repeat breeder||Sign|
|Reproductive Signs / Mummy, mummified fetus||Pigs:Gilt,Pigs:Sow||Diagnosis|
|Reproductive Signs / Small litter size||Pigs:Gilt,Pigs:Sow||Diagnosis|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Sign|
|Skin / Integumentary Signs / Nail, claw, hoof sloughing, separation||Sign|
|Skin / Integumentary Signs / Skin edema||Sign|
|Skin / Integumentary Signs / Skin ulcer, erosion, excoriation||Sign|
|Skin / Integumentary Signs / Skin vesicles, bullae, blisters||Pigs:All Stages||Diagnosis|
Disease CourseTop of page
Teschen disease may occur at all ages, with high morbidity and high mortality (Derbyshire, 1989). Early signs are fever, anorexia and dullness, followed by symptoms of the central nervous system such as ataxia, convulsions and paralysis. Experimental infection leads to disease after an incubation period of 10-12 days. Morbidity is usually about 50% and mortality 70-90% (Blood et al., 1979). Affected pigs show fever, anorexia, stiffness, inability to stand and falling to one side. This is followed by tremors and convulsions, frequently accompanied by loud squealing (Blood et al., 1979). The convulsive period may last 24-36 hours and death may occur the third or fourth day of the disease, preceded by a drop in temperature (Blood et al., 1979; Derbyshire, 1989). Vomiting may occur. Paralysis of the larynx may result in partial or complete loss of voice, and facial paralysis has also been observed. Between convulsions, stiffness and opisthotonus may be apparent. Convulsions are easily provoked by sudden noise. Milder cases may be restricted to stiffness and weakness, followed by flaccid paralysis.
Talfan disease is milder than Teschen disease, with less morbidity and mortality and is frequently restricted to young pigs (Blood et al., 1979; Derbyshire, 1989). The disease is most common in young pigs of less than 2 weeks with high morbidity and mortality. 50-100% of a litter may be affected (Taylor, 1999). Piglets show anorexia, loss of condition, constipation, vomiting and slightly elevated body temperature. Nervous signs follow characterised by hyperaesthesia, muscle tremor, ataxia, walking backwards, and finally lateral recumbancy, and nystagmus before death. Older pigs are less severely affected, and may show transient anorexia and paresis of the hind limbs, but they recover quickly and completely (Blood et al., 1979). Differential diagnosis for both diseases includes hemagglutinating encephalomyelitis virus, classical swine fever virus, pseudorabies virus and intoxications.
Porcine enteroviruses are only pathogenic for pigs in their embryonic or fetal stages. Even primary infections of gilts and sows do not lead to disease of the animals, but may cause significant losses due to reproductive problems. Reproductive disorders occur when susceptible pregnant gilts or sows are infected. The virus crosses the placenta and infection of the foetuses may lead to stillbirth, mummification, embryonic death and infertility, indicated with the acronym SMEDI (Derbyshire, 1989). Abortion does not occur. The virus appears to spread from fetus to fetus in the uterus through the fetal membranes, and progresses rather slowly. The clinical symptoms depend on the stage of pregnancy at the time of the transplacental infection. Early infection leads to embryonic death and return to oestrus after a regular (18- to 24-day) or irregular interval. If the infection occurs between 40-70 days of gestation, mummification will occur and small litters result. In the second trimester infections lead to weak newborn piglets, which may die shortly after birth. If all fetuses are mummified, the gilts may farrow 2-3 weeks after the expected date. These piglets usually have developed antibodies against the virus that can be used for the diagnosis. Differential diagnosis includes porcine parvovirus, African swine fever virus, classical swine fever virus, and porcine circovirus 2 (Derbyshire, 1992; West et al., 1999).
Swine vesicular disease
Swine vesicular disease (SVD) infection may be subclinical (Hedger and Mann, 1989; Dekker et al., 1995). The disease is mostly only recognised when several young pigs show lameness. For close examination the animal will have to be sedated, and the feet will have to be cleansed. Vesicles may be present on one or more of the feet, initially on the coronary band but later the infection may spread across the foot. In severe cases claws may even slough off (Hedger and Mann, 1989; Dekker, 2000). Vesicles may also appear on the snout, tongue and lips. Lesions in the thin epithelium of the ventral part of the tongue have not been observed. After experimental infections and daily observation, early signs are fever, and whitening of the coronary band. Fluid accumulation between the dermal and epithelial layers causes vesicles that can easily be ruptured. The differential diagnosis is foot-and-mouth disease, which is clinically indistinguishable from SVD. Housing conditions have great influence on the severity of the lesions. Soft bedding decreases the severity of the symptoms, with animals kept on concrete floors showing the most severe lesions. Secondary infections may result in chronic lameness, otherwise pigs recover in 2-3 weeks (Hedger and Mann, 1989; Dekker, 2000). Mortality is not observed.
EpidemiologyTop of page
In general, transmission of porcine enterovirus infections occurs via the faecal-oral route, but the high stability of the virus also allows indirect infection through infected material and fomites (Derbyshire, 1989). Many infections with porcine enteroviruses may pass subclinically and therefore the true incidence of infections is not known.
The incidence of infections is not known but appears to be rather uncommon. Because of the widespread occurrence of porcine enterovirus, young piglets frequently posses maternal antibodies. Piglets are most susceptible at an age of 4-5 weeks (Hoey and Martin, 1994).
In the field, infections with porcine enteroviruses are considered to occur much less frequently than with porcine parvoviruses (Wang and Pensaert, 1989) which also cause stillbirth, mummification, embryonic death and infertility (SMEDI).
Swine vesicular disease
The main risk of introduction of swine vesicular disease virus (SVDV) is by importation of infected animals, contaminated vehicles, or feeding of contaminated waste pork products containing SVDV. These are risks due to the long survival time of SVDV (Hedger and Mann, 1989). The skin is the most susceptible tissue for SVDV, and infection may easily occur through damaged skin and abrasions. Swine vesicular disease may pass subclinically and infected animals can be easily overlooked. This may lead to slaughter of pigs that shed the virus and result in pork products that contain significant amounts of the infectious virus. The particular resistance of SVDV favours long-term survival in transport trucks, and loading of susceptible pigs into contaminated trucks may rapidly lead to infection. Pigs may show SVDV lesions as soon as 2 days after being housed in an SVDV-infected environment (Dekker et al., 1995). Outbreaks of SVDV have mostly been reported in winter (Derbyshire, 1992; Hoey and Martin, 1994). Although SVDV is contagious, the disease does not rapidly spread on a farm, and close contact between pigs seems necessary for efficient transmission. Pens with infected animals may thus exist next to pens without pigs positive for SVDV. Therefore, SVDV is considered a ‘pen disease’, rather than a ‘farm disease’ (Derbyshire, 1992; Terpstra, 1992; Dekker and Terpstra, 1996).
Impact: EconomicTop of page
Teschen disease does not occur frequently, but outbreaks may cause severe losses due to the high mortality and morbidity (Derbyshire, 1992).
The losses due to stillbirth, mummification, embryo death and infertility (SMEDI)-like disease may be considerable, when an infection occurs at a farm with many serologically negative pregnant gilts and sows. However, many farms with intensive pig farming have serologically positive animals, and when gilts become infected before they are entering the reproductive cycle, no losses occur.
Swine vesicular disease
Outbreaks of swine vesicular disease virus (SVDV) cause mass economic losses due to the trade restrictions and the costs of control measures. In Europe from 1982 to 1999 more than 100 outbreaks occurred (Hedger and Mann, 1989; Davies, 1994; Dekker, 2000). The subsequent stamping out measures and mass serological testing of pigs leads to huge economic losses following an SVDV outbreak (Davies, 1994; Dekker, 2000). The Netherlands perform a large-scale and costly serosurveillance programme for SVDV, to convince trade partners of the continuous absence of SVDV in the national pig population. This is important in view of the large volume of pig products exported from the Netherlands.
Zoonoses and Food SafetyTop of page
Porcine enteroviruses are restricted to swine and pose no risk for humans. Although infections with swine vesicular disease virus (SVDV) have been demonstrated in humans, these were associated with extensive laboratory exposure to the virus, which seems highly unlikely under natural conditions. Furthermore, illness in farmers or veterinarians who have been associated with outbreaks of SVD have not been reported.
Disease TreatmentTop of page
There is no treatment possible for Teschen or Talfan disease.
If SMEDI-viruses are confirmed, management procedures are usually sufficient to control the disease. Most breeding farms harbour enzootic porcine enterovirus, and gilts should be exposed to adult animals prior to entering the breeding cycle. Gilts should not be isolated from the other animals. When an outbreak occurs the immunity of the herd can be raised by dosing gilts and sows with ground faeces, foetal membranes and mummified foetuses approximately three weeks before service (Taylor, 1999).
Swine vesicular disease
Pigs are culled when the diagnosis is made to control the disease spread.
Prevention and ControlTop of page
Prevention of porcine encephalomyelitis is not possible, because the spread and transmission of the causative viruses is not known. However, control of the disease has been achieved by slaughter of infected herds, and ring vaccination (Derbyshire, 1992).
Infection with a particular porcine enterovirus provides protection against homologous enterovirus strains, and this is the basis of protection within a herd. Young piglets are protected by maternal antibodies in colostrum and milk; however, when maternal antibodies have waned around weaning, piglets may become susceptible to infection. It is important that gilts are infected prior to breeding. Repeated exposure of gilts and newly purchased animals to faeces of sows in a herd is recommended to induce infection with as many enterovirus strains as possible and subsequently induce protective immunity through the build-up of antibodies to the virus (Wang and Pensaert, 1989). Spreading infection to pregnant sows and purchased breeding stock is popularly termed 'feedback'.
Swine vesicular disease
Prevention of swine vesicular disease can be achieved by stringent import controls. Introduction of the virus in an SVD–free country may occur through import of live animals, contaminated trucks or contaminated swine products. Pigs and pig meat should only be imported from countries that are free of SVDV and trucks used for animal transport should be disinfected and cleansed before entering a country. When SVDV is confirmed, stringent control measures must be taken to eradicate the disease. Most countries follow the recommendations of the Office International des Epizooties (OIE) for disease control. European Union member countries must follow the European directives for disease control. The pigs on the farms where SVDV is identified must be culled and a protection zone of at least 3 km is installed around the so-called index case meaning the first farm where the disease is identified (Horst et al., 1998). In addition, a surveillance zone is installed with a diameter of 10 km around the index-case. In the protection zone all farms are visited and the animals are inspected for signs of SVDV, and in the surveillance zone animals are serologically monitored for presence of SVDV-specific antibodies. Furthermore, epidemiological tracing of the source of infection is important. Therefore, an effective identification and registration (I&R) of animals must be in operation, together with an effective registration of animal movements. It is important that the high-risk period is short, which is the period between introduction of the disease and its diagnosis (Horst et al., 1998). If the high-risk period is long, more farms will be infected, and the eradication of the disease will be much more costly and difficult.
ReferencesTop of page
Blood DC; Henderson JA; Radostits OM, 1979. Viral encephalomyelitis of pigs (Teschen Disease, Talfan disease, poliomyelitis suum) In: Veterinary Medicine, 5th ed. New York, USA: Baillière Tindall, 690-692.
Callens M; Clercq Kde, 1999. Highly sensitive detection of swine vesicular disease virus based on a single tube RT-PCR system and DIG-ELISA detection. Journal of Virological Methods, 77(1):87-99; 32 ref.
Dekker A, 2000. Pathogenesis, diagnosis and epizootiology of swine vesicular disease. Thesis. University of Utrecht.
Derbyshire JB, 1989. Porcine enterovirus (polioencephalomyelitis). Virus infections of porcines., 225-233; 42 ref.
Derbyshire JB, 1992. Enteroviruses [pigs]. Veterinary diagnostic virology: a practitioners guide., 222-223; 3 ref.
FAO Animal Health Yearbook, 1971-1996. Rome, Italy: FAO publisher.
Hedger RS; Mann JA, 1989. Swine vesicular disease virus. Virus infections of porcines., 241-250; 30 ref.
Hoey EM; Martin SJ, 1994. Animal enterovirses. In: Webster RG, Garnoff A, eds. Encyclopedia of virology. London, UK: Academic Press, Harcourt Brace & Company, Vol. 1, 384-391.
Horst HS; Dijkhuizen AA; Huirne RBM; Leeuw PWde, 1998. Introduction of contagious animal diseases into the Netherlands: elicitation of expert opinions. Livestock Production Science, 53(3):253-264; 33 ref.
Morgan-Capner P; Bryden AS, 1998. Foot-and-mouth disease, vesicular stomatitis, Newcastle disease, and swine vesicular disease. Zoonoses: biology, clinical practice and public health control., 319-329; 41 ref.
Office International des Epizooties, 1996. Manual of standards for diagnostic tests and vaccines: lists A and B diseases of mammals, birds and bees. Manual of standards for diagnostic tests and vaccines: lists A and B diseases of mammals, birds and bees., Ed. 3:xxxii + 723 pp.
OIE Handistatus, 2002. World Animal Health Publication and Handistatus II (dataset for 2001). Paris, France: Office International des Epizooties.
OIE Handistatus, 2003. World Animal Health Publication and Handistatus II (dataset for 2002). Paris, France: Office International des Epizooties.
OIE Handistatus, 2004. World Animal Health Publication and Handistatus II (data set for 2003). Paris, France: Office International des Epizooties.
OIE Handistatus, 2005. World Animal Health Publication and Handistatus II (data set for 2004). Paris, France: Office International des Epizooties.
OIE, 2009. World Animal Health Information Database - Version: 1.4. World Animal Health Information Database. Paris, France: World Organisation for Animal Health. http://www.oie.int
Rueckert RR, 1996. Picornaviridae: The viruses and their replication. In: Fields BN, Knipe DM, Howley PM et al., eds. Virology. Philadelphia, USA: Lipincot-Raven publishers, 609-654.
Taylor DJ, 1999. Pig Diseases, 7th Edition, ISBN 09506932 6X, 18-23.
Wang JT; Pensaert MB, 1989. Porcine enterovirus (reproductive disorders). Virus infections of porcines., 235-239; 17 ref.
West KH; Bystrom JM; Wojnarowicz C; Shantz N; Jacobson M; Allan GM; Haines DM; Clark EG; Krakowka S; McNeilly F; Konoby C; Martin K; Ellis JA, 1999. Myocarditis and abortion associated with intrauterine infection of sows with porcine circovirus 2. Journal of Veterinary Diagnostic Investigation, 11(6):530-532; 13 ref.
Distribution MapsTop of page
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