transmissible gastroenteritis and porcine respiratory coronovirus infection
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- transmissible gastroenteritis and porcine respiratory coronovirus infection
International Common Names
- English: enzootic TGE; porcine respiratory coronavirus, tge-like virus; porcine respiratory coronovirus infection; transmissible gastroenteritis; transmissible gastroenteritis in pigs, tge; transmissible gastroenteritis of pigs
OverviewTop of page
Transmissible gastroenteritis (TGE) is a disease confined to pigs, which was first seen in the USA in the 1940s (Doyle and Hutchings, 1946). It has since been seen in most swine producing areas of the world. The causative agent is a coronavirus, an enveloped positive strand RNA virus similar to coronaviruses affecting other domestic animals, including dogs and cats, with which it cross-reacts in a variety of serological tests. TGE can be a significant cause of economic loss in breeding herds, primarily because of the very high piglet mortality, although it is of less importance in rearing and finishing herds. The main clinical features (Pritchard, 1982) are watery diarrhoea, vomiting and loss of appetite affecting all ages of pigs. Sucking piglets are the most severely affected group. When a naïve herd is first infected, the mortality in piglets aged less than two weeks can reach 100% primarily due to dehydration. There is no specific treatment and vaccines, although commercially available in some countries, are currently of limited value. The disease is usually seasonal, with outbreaks occurring mainly in the winter months in temperate climates. In some countries, such as the UK, large-scale epidemics have tended to occur at fairly regular intervals of a few years. However, this situation has changed since the widespread emergence, in the mid 1980s, of a closely related, but non-enteropathogenic and clinically inconsequential, porcine respiratory coronavirus (PRCV) (Pensaert et al., 1986) which has coincided with the declining incidence of TGE in the European pig population. In recent field studies, Pritchard et al. (1999) noted clinically silent seroconversion to TGEV in a number of herds in the UK and raised the possibility of further changes in the TGEV or PRCV genomes. The literature on TGE and PRCV was recently reviewed by Saif and Wesley (1999).
This disease is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). The distribution section contains data from OIE's WAHID database on disease occurrence. Please see the AHPC library for further information on this disease from OIE, including the International Animal Health Code and the Manual of Standards for Diagnostic Tests and Vaccines. Also see the website: www.oie.int.
Hosts/Species AffectedTop of page
The pig is the maintenance host. However, the virus is closely related to feline and canine coronaviruses and may be able to replicate subclinically in dogs, cats and foxes (Bohl, 1989). Birds may act as mechanical vectors but have not been shown to replicate the virus (Pilchard, 1965).
DistributionTop of page
TGE is widely recognized throughout the pig-keeping world although it is absent from Australasia and a few other countries. The distribution of PRCV is less certain, since infection with this virus causes mild or inapparent illness and tests for its presence are often not carried out or reported. However, it is believed to have a very widespread distribution.
For current information on disease incidence, see OIE's WAHID Interface.
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 not reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||Disease never reported||OIE, 2009|
|Bhutan||No information available||OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||Restricted distribution||NULL||Anon, 1997; OIE, 2009|
|-Hong Kong||Disease never reported||OIE, 2009|
|Georgia (Republic of)||Disease never reported||OIE Handistatus, 2005|
|India||Disease never reported||OIE, 2009|
|Indonesia||Disease not reported||OIE, 2009|
|Iran||Disease never reported||OIE, 2009|
|Iraq||Disease never reported||OIE, 2009|
|Israel||Absent, reported but not confirmed||OIE, 2009|
|Japan||Present||NULL||Kamogawa et al., 1996; Anon, 1997; 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 not reported||20070820||Anon, 1997; Chae et al., 1998; Chae et al., 2000; OIE, 2009|
|Kuwait||Disease never reported||OIE, 2009|
|Kyrgyzstan||Disease not reported||OIE, 2009|
|Laos||Disease not reported||OIE, 2009|
|Lebanon||Disease not reported||1998||Anon, 1997; OIE, 2009|
|Malaysia||Disease not reported||OIE, 2009|
|-Peninsular Malaysia||Disease not reported||OIE Handistatus, 2005|
|-Sabah||Disease never reported||OIE Handistatus, 2005|
|-Sarawak||CAB Abstracts data mining||OIE Handistatus, 2005|
|Mongolia||No information available||OIE, 2009|
|Myanmar||Disease not reported||2001||Anon, 1997; 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|
|-Russia (Asia)||Present||Rukhadze et al., 1993|
|Saudi Arabia||Disease never reported||OIE, 2009|
|Singapore||Disease not reported||OIE, 2009|
|Sri Lanka||Disease never reported||OIE, 2009|
|Syria||Disease not reported||OIE, 2009|
|Taiwan||Last reported||2003||OIE Handistatus, 2005|
|Tajikistan||Disease not reported||OIE, 2009|
|Thailand||No information available||OIE, 2009|
|Turkey||No information available||OIE, 2009|
|Turkmenistan||Disease not reported||OIE Handistatus, 2005|
|United Arab Emirates||No information available||OIE, 2009|
|Uzbekistan||Disease not reported||OIE Handistatus, 2005|
|Vietnam||Disease never reported||OIE, 2009|
|Yemen||No information available||OIE, 2009|
|Algeria||Disease not reported||OIE, 2009|
|Angola||No information available||OIE, 2009|
|Benin||No information available||OIE, 2009|
|Botswana||Disease never reported||OIE, 2009|
|Burkina Faso||No information available||OIE, 2009|
|Burundi||No information available||OIE Handistatus, 2005|
|Cameroon||No information available||OIE Handistatus, 2005|
|Cape Verde||No information available||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||No information available||NULL||Anon, 1997; OIE, 2009|
|Eritrea||No information available||OIE, 2009|
|Ethiopia||No information available||OIE, 2009|
|Gabon||No information available||OIE, 2009|
|Gambia||No information available||OIE, 2009|
|Ghana||No information available||OIE, 2009|
|Guinea||No information available||OIE, 2009|
|Guinea-Bissau||No information available||OIE, 2009|
|Kenya||No information available||OIE, 2009|
|Lesotho||Disease not reported||OIE, 2009|
|Libya||Disease never reported||OIE Handistatus, 2005|
|Madagascar||Disease never reported||OIE, 2009|
|Malawi||No information available||OIE, 2009|
|Mali||No information available||OIE, 2009|
|Mauritius||Disease not reported||OIE, 2009|
|Morocco||No information available||OIE, 2009|
|Mozambique||Disease never reported||OIE, 2009|
|Namibia||Disease not reported||OIE, 2009|
|Nigeria||No information available||OIE, 2009|
|Réunion||No information available||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||NULL||Williams et al., 1994; 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 not reported||OIE, 2009|
|Uganda||No information available||OIE, 2009|
|Zambia||No information available||NULL||Stafford et al., 1992; OIE, 2009|
|Zimbabwe||Disease never reported||OIE, 2009|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Present||NULL||Anon, 1997; OIE, 2009|
|-Ontario||Present||Wilson et al., 1999|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Present||NULL||Anon, 1997; OIE, 2009|
|USA||Present||NULL||Anon, 1997; OIE, 2009|
|-Iowa||Present||Wesley et al., 1997|
Central America and Caribbean
|Barbados||Disease not 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||No information available||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 not reported||OIE, 2009|
|Nicaragua||Disease never reported||OIE, 2009|
|Panama||No information available||OIE, 2009|
|Saint Kitts and Nevis||No information available||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||No information available||NULL||Anon, 1997; OIE, 2009|
|Brazil||Disease not reported||OIE, 2009|
|Chile||Disease never reported||OIE, 2009|
|Colombia||Disease not 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 not reported||Anon, 1997; OIE Handistatus, 2005|
|Paraguay||Disease never reported||OIE Handistatus, 2005|
|Peru||Disease never reported||OIE, 2009|
|Uruguay||Disease never reported||OIE, 2009|
|Venezuela||No information available||OIE, 2009|
|Albania||No information available||OIE, 2009|
|Andorra||No information available||OIE Handistatus, 2005|
|Austria||No information available||NULL||Anon, 1997; OIE, 2009|
|Belarus||Present||NULL||Anon, 1997; OIE, 2009|
|Belgium||Disease not reported||2004||Pensaert et al., 1986; Pensaert et al., 1993; Reeth and Pensaert, 1994; Anon, 1997; OIE, 2009|
|Bosnia-Hercegovina||Disease not reported||OIE Handistatus, 2005|
|Bulgaria||Disease not reported||1997||Anon, 1997; OIE, 2009|
|Croatia||Disease not reported||OIE, 2009|
|Cyprus||Disease not reported||200707||Anon, 1997; OIE, 2009|
|Czech Republic||Disease not reported||1998||Anon, 1997; OIE, 2009|
|Denmark||Disease never reported||OIE, 2009|
|Estonia||Disease not reported||OIE, 2009|
|Finland||Disease not reported||OIE, 2009|
|France||No information available||NULL||Anon, 1997; OIE, 2009|
|Germany||Disease not reported||200804||Anon, 1997; OIE, 2009|
|Greece||Disease not reported||OIE, 2009|
|Hungary||Disease not reported||OIE, 2009|
|Iceland||Disease never reported||OIE, 2009|
|Ireland||Disease not reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||No information available||OIE, 2009|
|Jersey||Disease never reported||OIE Handistatus, 2005|
|Latvia||Disease not reported||OIE, 2009|
|Liechtenstein||Disease not reported||OIE, 2009|
|Lithuania||Disease not reported||OIE, 2009|
|Luxembourg||Disease not reported||OIE, 2009|
|Macedonia||No information available||OIE, 2009|
|Malta||Disease not reported||OIE, 2009|
|Moldova||Disease not reported||OIE Handistatus, 2005|
|Montenegro||Disease not reported||OIE, 2009|
|Netherlands||Disease not reported||OIE, 2009|
|Norway||Disease never reported||OIE, 2009|
|Poland||Disease not reported||1997||Anon, 1997; OIE, 2009|
|Portugal||Disease not reported||OIE, 2009|
|Romania||Disease not reported||2004||Anon, 1997; OIE, 2009|
|Russian Federation||Disease not reported||OIE, 2009|
|-Russia (Europe)||Present||Rukhadze et al., 1993|
|Serbia||No information available||OIE, 2009|
|Slovenia||Disease not reported||OIE, 2009|
|Spain||No information available||NULL||Cubero et al., 1993; Anon, 1997; OIE, 2009|
|Sweden||Disease never reported||OIE, 2009|
|Switzerland||Disease not reported||1995||Bereiter et al., 1988; Anon, 1997; OIE, 2009|
|UK||Disease not reported||2001||Pritchard, 1982; Brown and Paton, 1991; Anon, 1997; OIE, 2009|
|-Northern Ireland||Disease never reported||OIE Handistatus, 2005|
|Ukraine||Disease not reported||2004||Anon, 1997; OIE, 2009|
|Yugoslavia (former)||No information available||OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Disease not reported||OIE Handistatus, 2005|
|Australia||Disease never reported||NULL||Mulland et al., 1994; 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
TGE is characterised by marked dehydration in baby piglets associated with villous atrophy of the small intestine with thinning and translucency of the gut wall and very watery, foul smelling flocculent, greenish-yellow intestinal contents. Undigested milk clots are usually present in the stomach. Gastritis is occasionally seen, particularly in enzootic TGE where secondary colibacillosis can be a complicating feature. Urate crystals are often prominent in the kidney pelvis of affected baby piglets. Uncomplicated cases of PRCV are characterised only by a mild interstitial pneumonia.
DiagnosisTop of page
Acute outbreaks of enzootic TGE are usually fairly characteristic because of the large number of pigs of different age groups affected, often simultaneously. The main differential diagnosis is porcine epidemic diarrhoea (PED). This is caused by a serologically unrelated coronavirus and produces a clinically very similar disease, although not usually as severe. Enzootic TGE in an endemically infected herd is much less characteristic and can be difficult to diagnose clinically. It needs to be differentiated from other causes of pre and post weaning diarrhoea, including enteric colibacillosis, rotavirus infection or coccidiosis. TGE outbreaks confined to finishing units may be confused clinically with other causes of high morbidity diarrhoea such as swine dysentery or salmonellosis, although blood and mucus are absent from the faeces in uncomplicated TGE outbreaks.
Laboratory diagnosis of TGE is based on the demonstration of virus, viral antigens, nucleic acids or virus-specific antibodies (Paton et al., 1996). For virus detection, samples should preferably be collected from neonates in the early stages of disease. Samples of faeces or ligated lengths of small intestine are suitable for virus detection which can be by means of electron microscopy, virus isolation, antigen capture ELISA, fluorescent antibody tests (FAT) on cryostat sections and RT-PCR. The virus is labile, and therefore samples must be kept cool and transported to the laboratory without delay. Where possible, portions of small intestine should be snap frozen on solid carbon dioxide, immediately after collection. A practical approach is to screen samples by electron microscopy, ELISA or FAT and to confirm positive results by virus isolation or RT-PCR. Immunocytochemistry on formalin fixed small intestine is also possible. Virus neutralisation tests or various ELISAs can be used for serological diagnosis. Antibodies develop within 10 days of infection and persist for many months.
Diagnosis of PRCV is rarely attempted in relation to clinical disease outbreaks since the agent is considered to be of minimal pathogenic significance on its own. The main importance of PRCV is that it complicates the laboratory diagnosis of TGE. PRCV can be detected in respiratory tissues by virus isolation, IFAT, RT-PCR and immunohistochemistry on formalin fixed sections. The virus is present at only low levels, if at all, in the gastrointestinal tract. PRCV and TGEV can be differentiated by means of monoclonal antibodies and genetic analysis. Serologically, the two viruses fully cross-neutralise one another rendering the serum neutralisation test of limited value other than for general disease screening. Differentiation is only possible by means of competitive ELISAs using monoclonal antibodies specific for TGEV.
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Pigs:Weaner,Pigs:Growing-finishing pig,Pigs:Gilt,Pigs:Sow,Pigs:Boar||Diagnosis|
|Digestive Signs / Diarrhoea||Pigs:All Stages||Diagnosis|
|Digestive Signs / Unusual or foul odor, stools, faeces||Pigs:All Stages||Diagnosis|
|Digestive Signs / Vomiting or regurgitation, emesis||Pigs:All Stages||Diagnosis|
|General Signs / Dehydration||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Sign|
|General Signs / Hypothermia, low temperature||Pigs:Piglet||Sign|
|General Signs / Inability to stand, downer, prostration||Sign|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|General Signs / Polydipsia, excessive fluid consumption, excessive thirst||Pigs:Piglet||Sign|
|General Signs / Reluctant to move, refusal to move||Sign|
|General Signs / Tenesmus, straining, dyschezia||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Pigs:Piglet||Sign|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Sign|
|General Signs / Weight loss||Pigs:Piglet,Pigs:Weaner,Pigs:Growing-finishing pig||Diagnosis|
|Nervous Signs / Coma, stupor||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Pigs:All Stages||Sign|
|Reproductive Signs / Agalactia, decreased, absent milk production||Pigs:Sow||Sign|
|Respiratory Signs / Coughing, coughs||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Pigs:All Stages||Sign|
|Skin / Integumentary Signs / Matted or dirty hair||Pigs:Piglet,Pigs:Weaner||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Sign|
Disease CourseTop of page
In a fully susceptible herd the disease usually presents as an explosive, high morbidity outbreak affecting all ages of pigs. Losses continue in unweaned piglets until sows develop lactogenic immunity, which protects sucking piglets in the face of further virus challenge. TGE is clinically much more severe in neonates and mortality is highest in this age group. Acute onset watery diarrhoea and occasional vomiting lead to rapid dehydration, weight loss, and death. Older animals also develop watery diarrhoea and may vomit, but recover after a few days illness. Lactating sows can become agalactic which exacerbates the losses in their piglets. Reproductive failure is not a specific feature. The length of the epizootic phase in breeding herds varies from 2 or 3 weeks to several months, depending mainly on the size of herd, the farrowing programme, rate of spread of infection, development of immunity and whether any naïve breeding stock are added.
In larger, continuously farrowing, herds, particularly those with over 500 sows, the disease often persists in a clinically milder enzootic form. The main features of enzootic TGE (Pritchard, 1987) are mild diarrhoea in unweaned piglets from about 6 days of age and in recently weaned pigs. In some herds, enzootic TGE remains virtually subclinical for long periods although there may be short-lived episodes of overt clinical recrudescence, particularly in purchased breeding replacements and their litters.
In the 1980s, a new variant of TGE, termed porcine respiratory coronavirus (PRCV) (Pensaert et al., 1986) appeared in Europe. This is a deletion mutant of TGE with an altered tissue tropism, which replicates in the respiratory rather than the enteric tract (Cox et al., 1990). Infection is mainly subclinical. Unlike TGE, PRCV spreads via respiratory aerosols and has become widespread in Europe and elsewhere. Although the emergence of PRCV complicated the laboratory diagnosis of TGE it appears to have led to the reduced prevalence of TGE seen in Western Europe. It is assumed that pigs recovered from infection with PRCV are at least partially protected against TGEV infection, although this has proved difficult to demonstrate experimentally.
EpidemiologyTop of page
TGEV spreads within and between farms primarily by infected faeces. The incubation period is short (12-72 hours). Virus is shed in the faeces for about 2 weeks after clinical recovery, although there remains some debate about whether pigs may excrete viable virus for longer periods. The virus is heat and light labile. In temperate climates, it survives much better in the winter, which partly accounts for its mainly seasonal occurrence. As well as direct pig to pig contact, virus may be disseminated via faecally contaminated equipment or by birds, particularly starlings, acting as mechanical vectors. In countries where epizootic outbreaks have occurred periodically, the virus is probably maintained in large endemically infected breeding herds (Pritchard 1987) or in large continuous throughput finishing units. In contrast to TGE, PRCV spreads aerogenically. In large herds, the infection is rarely self-limiting and consequently in pig dense regions, there is a high seroprevalence of PRCV infection.
Impact: EconomicTop of page
Outbreaks of TGE in naïve breeding herds almost invariably result in severe, albeit usually short-lived, economic losses. In 56 epizootic outbreaks investigated in the UK by Pritchard (1982) piglet deaths averaged 1.3 times the total number of sows in the herd (about 6% of the annual piglet production). This has led some countries to make the disease notifiable, whilst it is in the B list of the Office International des Epizooties (OIE). In fattening units, anorexia and diarrhoea cause a reduction in feed conversion efficiency and can extend the finishing period by about 2 weeks.
Disease TreatmentTop of page
No specific treatment is available. Although heavy losses are inevitable in unweaned piglets during the early stages of an outbreak, fluid replacement therapy helps mitigate dehydration and prevents some deaths. Good husbandry and nursing, especially warmth, are beneficial. Early weaning or cross suckling onto immune sows can sometimes be worthwhile (Pritchard, 1982).
Prevention and ControlTop of page
The International control of TGE relies on preventing trade in carrier pigs, by health certification and serological testing either side of a period of quarantine. The likelihood of introducing TGEV into a herd can be reduced by good biosecurity. This includes avoidance of visitors and vehicles, bird proofing (where feasible), purchasing pigs from a small number of reputable sources and quarantining them on arrival. Maintaining freedom from PRCV is difficult and demands an isolated location away from other pigs. TGE vaccines are available in some countries, such as the USA, but their efficacy is rather limited because it is difficult to elicit the necessary local mucosal (IgA) immunity using killed vaccines or attenuated live vaccines (Saif and Jackwood, 1990).
Once TGE enters a herd it is beneficial to try and infect all the pigs in the herd as soon as possible in order to generate immunity and ultimately bring the outbreak to an end. This can be achieved by spreading diarrhoeic faeces or viscera, adding it to feed and/or mixing unaffected and affected groups of pigs. Spreading infection to pregnant sows and purchased breeding stock is popularly termed 'feedback'. In particular, deliberately infecting pregnant sows or gilts with at least 2 weeks left before farrowing should ensure they have protective IgA antibodies in their colostrum and milk by the time their piglets are born. However, this method of live TGE inoculation has the risk of spreading other infections such as leptospirosis, classical swine fever. In some countries a permit is needed before infected material can be fed to healthy animals, for example, 'feedback' may come under regulations controlling swill (garbage) feeding to pigs. Conversely, in an attempt to reduce the otherwise inevitably high baby piglet mortality, simultaneous efforts can be made to isolate pregnant sows with less than 2 weeks before farrowing, and farrowing houses containing baby piglets less than about 3 weeks old. However, these attempts at isolation are usually very difficult to achieve in practice. An 'all-in, all-out' policy, with good cleansing and disinfection, will help to prevent disease perpetuation amongst growing and fattening pigs.
ReferencesTop of page
Bereiter M; Hasler J; Keller H, 1988. Transmissible gastroenteritis (TGE) in Switzerland: antibody persistence after infection and seroepidemiological studies on the importance of the TGE virus as cause of diarrhoea. Schweizer Archiv für Tierheilkunde, 130(5):237-248; 31 ref.
Bohl EH; Pensaert MB, 1989. Transmissible gastroenteritis virus. 1. (Classical enteric variant). 2. (Respiratory variant). Virus infections of porcines., 139-153, 154-165; many ref.
Chae C; Kim O; Min K; Choi C; Kim J; Cho W, 2000. Seroprevalence of porcine respiratory coronavirus in selected Korean pigs. Preventive Veterinary Medicine, 46:293-296.
Chae C; Kwon D; Kim O; Min K; Cheon DS; Choi C; Kim B; Suh J, 1998. Diarrhoea in nursing piglets associated with coccidiosis: prevalence, microscopic lesions and coexisting microorganisms. Veterinary Record, 143(15):417-420; 21 ref.
Cox E; Hooyberghs J; Pensaert MB, 1990. Sites of replication of a porcine respiratory coronavirus related to transmissible gastroenteritis virus. Research in Veterinary Science, 48(2):165-169; 16 ref.
Cubero MJ; León L; Contreras A; Astorga R; Lanza I; Garcia A, 1993. Transmissible gastroenteritis in pigs in south east Spain: prevalence and factors associated with infection. Veterinary Record, 132(10):238-241; 37 ref.
Doyle LP; Hutchings LM, 1946. A transmissible gastroenteritis of pigs. Journal of the American Veterinary Medical Association, 108:257-259.
FAO, 1997. Animal Health Yearbook 1996. FAO Animal Production and Health Series No 36.
Kamogawa O; Tomita Y; Kaneko M; Yamada S; Kubo M; Shimizu M, 1996. Isolation of porcine respiratory coronavirus from pigs affected with porcine reproductive and respiratory syndrome. Journal of Veterinary Medical Science, 58(4):385-388; 23 ref.
Mulland BP; Davies GT; Cutler RS, 1994. Simulation of the economic impact of transmissible gastroenteritis on commercial pig production in Australia. Australian Veterinary Journal, 71:151-154.
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
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