classical swine fever
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PicturesTop of page
IdentityTop of page
Preferred Scientific Name
- classical swine fever
International Common Names
- English: hog cholera; hog cholera infection in utero - exotic; hog cholera, classical swine fever, pestivirus infection in pigs; swine fever
- French: peste porcine classique
Local Common Names
- Germany: klassische schweinepest
OverviewTop of page
Classical swine fever is also known as hog cholera. Classical swine fever (CSF) is most often used in Europe and its ex-colonies. Hog cholera is the American term. CSF is a highly contagious multisystemic viral disease of swine that can run an acute, subacute, chronic, or late-onset course. Swine can also be infected subclinically. Domestic pigs, wild boar and feral pigs are the only animals susceptible to classical swine fever virus (CSFV).
There is a wide range in virulence among CSFV strains. Highly virulent strains cause acute severe disease often resulting in mortality, whereas strains with low virulence give rise to mild disease or subclinical infection.
The first presumptive outbreaks were reported from the USA in the early nineteenth century, whereas CSF may first have appeared in Europe in the middle of that century. In 1888, the first outbreak was reported in Japan (Fukuhso, 1998) and in South Africa in 1900 (De Kock et al., 1940; Edwards and Sands, 1990). De Schweinetz and Dorset (1903) showed that CSF is caused by a virus. It belongs to the pestivirus genus, together with bovine viral diarrhoea virus (BVDV) and border disease virus (BDV), within the family of Flaviviridae.
Classical swine fever is on the list of diseases notifiable to the World Organisation for Animal Health (OIE). It is distributed in many countries in Asia, Eastern Europe and South America and thus hampers international free trade in pigs and pig products. Large areas of Europe, Australasia and North America are normally free of the disease. Outbreaks can cause huge economic damage.
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
Pigs and wild boar of all ages are susceptible to CSFV. The virus generally causes higher mortality in piglets than in older pigs, although an increase in mortality with age has been described in fattening pigs (Koenen et al., 1996). Foetuses can also become infected; the outcome depends mainly on the age of the foetus at infection (Oirschot, 1979). Breed-related and other, still unknown, host factors may influence the clinical course of infection (Depner et al., 1996, 1997).
DistributionTop of page
CSF is present in much of Asia, some Caribbean islands, the African countries of Madagascar and Mauritius, and much of South and Central America. The disease has been successfully eradicated from the United States, Canada, New Zealand, Australia and most of western and central Europe.
The situation concerning CSF in Europe since 2007 is reviewed by Postel et al. (2013). In several East-European countries CSF is still present in domestic pigs or the CSF status is at least uncertain, for example in Belarus, the Russian Federation, in the Ukraine, and in the Balkan and Caucasus regions. In the EU Member States, only sporadic CSF outbreaks in domestic pigs have occurred since 2009, two years after the extension of the EU in 2007. The reoccurrence of CSF in wild boar in Germany in 2009 shows that HCV can persist at very low levels in local wild boar populations and even intensive surveillance cannot exclude the presence of CSF.
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 never reported||OIE, 2009|
|Bahrain||Disease never reported||OIE, 2009|
|Bangladesh||Disease never reported||OIE, 2009|
|Bhutan||Disease not reported||2007||OIE, 2000; OIE, 2009|
|Brunei Darussalam||Disease not reported||OIE Handistatus, 2005|
|Cambodia||No information available||OIE, 2009|
|China||Restricted distribution||OIE, 2009|
|-Hong Kong||Disease not reported||OIE, 2009|
|Georgia (Republic of)||Last reported||1984||OIE Handistatus, 2005|
|India||Restricted distribution||OIE, 2009|
|Iran||Disease never reported||OIE, 2009|
|Iraq||Disease never reported||OIE, 2009|
|Israel||Disease not 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 not reported||OIE, 2009|
|Kuwait||Disease never reported||OIE, 2009|
|Kyrgyzstan||Disease not reported||OIE, 2009|
|Laos||Absent, reported but not confirmed||OIE, 2009|
|Lebanon||Disease not reported||OIE, 2009|
|-Peninsular Malaysia||No information available||OIE, 2003; OIE Handistatus, 2005|
|-Sabah||Last reported||1992||OIE Handistatus, 2005|
|-Sarawak||Reported present or known to be present||OIE Handistatus, 2005|
|Mongolia||Disease not reported||OIE, 2009|
|Oman||Disease never reported||OIE, 2009|
|Pakistan||No information available||OIE, 2009|
|Qatar||No information available||OIE, 2009|
|Saudi Arabia||Disease never reported||OIE, 2009|
|Singapore||Disease not reported||OIE, 2009|
|Sri Lanka||Present||OIE, 2009|
|Syria||Disease not reported||OIE, 2009|
|Taiwan||Reported present or known to be present||OIE Handistatus, 2005|
|Tajikistan||Disease not reported||OIE, 2009|
|Turkey||Disease never reported||OIE, 2009|
|Turkmenistan||Last reported||1991||OIE Handistatus, 2005|
|United Arab Emirates||Disease never reported||OIE, 2009|
|Uzbekistan||Last reported||1979||OIE Handistatus, 2005|
|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||Disease never reported||OIE, 2009|
|Burundi||Disease not reported||OIE Handistatus, 2005|
|Cameroon||Disease never reported||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||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||No information available||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|
|Malawi||Disease never reported||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||Disease never reported||OIE, 2009|
|Réunion||Disease not reported||OIE Handistatus, 2005|
|Rwanda||No information available||OIE, 2009|
|Sao Tome and Principe||Disease not reported||OIE Handistatus, 2005|
|Senegal||Disease never reported||OIE, 2009|
|Seychelles||Disease not reported||OIE Handistatus, 2005|
|Somalia||Disease not reported||OIE Handistatus, 2005|
|South Africa||Disease not reported||OIE, 2009|
|Sudan||Disease never reported||OIE, 2009|
|Swaziland||Disease never reported||OIE, 2009|
|Tanzania||Disease never reported||OIE, 2009|
|Togo||No information available||OIE, 2009|
|Tunisia||Disease never reported||OIE, 2009|
|Uganda||No information available||OIE, 2009|
|Zambia||Disease never reported||OIE, 2009|
|Zimbabwe||Disease never reported||OIE, 2009|
|Bermuda||Disease not reported||OIE Handistatus, 2005|
|Canada||Disease not reported||OIE, 2009|
|Greenland||Disease never reported||OIE, 2009|
|Mexico||Disease not reported||OIE, 2009|
|USA||Disease not reported||OIE, 2009|
Central America and Caribbean
|Barbados||Last reported||1971||OIE Handistatus, 2005|
|Belize||Disease not reported||OIE, 2009|
|British Virgin Islands||Disease never reported||OIE Handistatus, 2005|
|Cayman Islands||Disease never reported||OIE Handistatus, 2005|
|Costa Rica||Disease not reported||OIE, 2009|
|Curaçao||Disease not reported||OIE Handistatus, 2005|
|Dominica||Disease not reported||OIE Handistatus, 2005|
|Dominican Republic||Present||OIE, 2009|
|El Salvador||Present||OIE, 2009|
|Guadeloupe||Disease not reported||OIE, 2009|
|Guatemala||Disease not reported||OIE, 2009|
|Haiti||Present||NULL||OIE, 2000; OIE, 2009|
|Honduras||Disease not reported||OIE, 2009|
|Jamaica||Disease never reported||OIE, 2009|
|Martinique||Disease not reported||OIE, 2009|
|Nicaragua||Disease not reported||OIE, 2009|
|Panama||Disease not 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||Last reported||1974||OIE Handistatus, 2005|
|Argentina||Disease not reported||OIE, 2009|
|Bolivia||Restricted distribution||OIE, 2009|
|Brazil||Present||NULL||OIE, 2003; OIE, 2009|
|Chile||Disease not reported||OIE, 2009|
|Colombia||Disease not 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||Last reported||1995||OIE Handistatus, 2005|
|Peru||Restricted distribution||OIE, 2009|
|Uruguay||Disease not reported||OIE, 2009|
|Venezuela||Disease not reported||OIE, 2009|
|Albania||Disease not reported||OIE, 2009|
|Andorra||Last reported||1975||OIE Handistatus, 2005|
|Austria||Disease not reported||OIE, 2009|
|Belarus||Disease not reported||OIE, 2009|
|Belgium||Disease not reported||OIE, 2009|
|Bosnia-Hercegovina||Reported present or known to be present||OIE Handistatus, 2005|
|Cyprus||Disease not reported||OIE, 2009|
|Czech Republic||Disease not reported||OIE, 2009|
|Denmark||Disease not reported||OIE, 2009|
|Estonia||Disease not reported||OIE, 2009|
|Finland||Disease not reported||OIE, 2009|
|Former USSR||Present||OIE, 2000|
|France||Disease not reported||OIE, 2009|
|Germany||Disease not reported||OIE, 2009|
|Greece||Disease not reported||OIE, 2009|
|Hungary||Restricted distribution||OIE, 2009|
|Iceland||Disease not reported||OIE, 2009|
|Ireland||Disease not reported||OIE, 2009|
|Isle of Man (UK)||Disease never reported||OIE Handistatus, 2005|
|Italy||Disease not reported||200309||OIE, 2003; 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|
|Malta||Disease not reported||OIE, 2009|
|Moldova||Last reported||2002||OIE Handistatus, 2005|
|Montenegro||Disease not reported||OIE, 2009|
|Netherlands||Disease not reported||OIE, 2009|
|Norway||Disease not reported||OIE, 2009|
|Poland||Disease not reported||OIE, 2009|
|Portugal||Disease not reported||OIE, 2009|
|Romania||Disease not reported||OIE, 2009|
|Russian Federation||Restricted distribution||OIE, 2009|
|Serbia||Disease not reported||OIE, 2009|
|Slovenia||Disease not reported||OIE, 2009|
|Spain||Disease not reported||OIE, 2009|
|Sweden||Disease not reported||OIE, 2009|
|Switzerland||Disease not reported||OIE, 2009|
|UK||Disease not reported||OIE, 2009|
|-Northern Ireland||Last reported||1958||OIE Handistatus, 2005|
|Ukraine||Disease not reported||OIE, 2009|
|Yugoslavia (former)||Last reported||1996||OIE, 2000; OIE Handistatus, 2005|
|Yugoslavia (Serbia and Montenegro)||Reported present or known to be present||OIE Handistatus, 2005|
|Australia||Disease not reported||OIE, 2009|
|French Polynesia||Disease not reported||OIE, 2009|
|New Caledonia||Disease never reported||OIE, 2009|
|New Zealand||Disease not 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
The pathology of (sub)acute CSF is that of a septicaemic disease characterized by widespread multiple haemorrhages of various sizes, mainly in lymph nodes and kidneys. Lymph nodes also become oedematous and consequently often have a ‘marbled’ appearance. Histologically, lymph nodes show lymphocytic depletion and reticular hyperplasia. Infarcts are often observed; spleen infarcts are considered to be pathognomonic for acute CSF. (However, these are not considered a consistent field finding.) There is disseminated intravascular coagulation with microthrombi in small blood vessels. Catarrhal, fibrinous and haemorrhagic inflammatory reactions can be seen in the respiratory, digestive, and urogenital tracts. Most pigs with acute CSF show encephalitis with perivascular cuffing. In pigs that die from persistent CSFV infections, the most outstanding lesions are a general exhaustion of the lymphoid system, exemplified by atrophy of the thymus and severe depletion of lymphocytes in tonsil, lymph nodes and spleen. Further consistent findings in persistent CSF cases are degeneration of endothelial cells, button-ulcers in caecum and colon and rib lesions. Foetal infection can result in stillborn piglets having excessive amounts of fluid in body cavities, in limb malformations and defects in the central nervous system, such as cerebellar hypoplasia and hypomyelinogenesis.
DiagnosisTop of page
An outbreak of acute CSF can be tentatively diagnosed in the field on the basis of an anamnesis [the history of a patient and its relatives], and thorough clinical and post-mortem investigations. Clinical signs indicative of acute CSF are described under Disease Course; the most relevant are: high fever, depression, ataxia, and leukopenia. Absence of clinical improvement after antibiotic treatment can be considered a further indication for CSF. In cases of subacute, chronic or late-onset CSF it is much more difficult to make a tentative diagnosis on the basis of clinical signs. The presence of skin lesions and runt pigs is suspect for CSF. At post mortem, haemorrhagic lesions and infarcts throughout the body and severe lymphoid depletion are indicative for CSF.
The following diseases are relevant for differential diagnosis. Acute CSF cannot be reliably differentiated from African swine fever without laboratory tests. Splenomegaly, haematoma-like lymph nodes, oedema of the gall bladder and bile ducts, and lung oedema are more indicative for African swine fever than for CSF. Septicaemic diseases such as salmonellosis, streptococcosis, pasteurellosis, erysipelas, or Haemophilus parasuis infections are of differential diagnostic importance, as is the case for generalized haemorrhages in piglets. The latter lesions can also be caused by thrombocytopenia, or intoxications. Runt pigs can also be observed after malnutrition, enterotoxicosis by Escherichia coli or Clostridium perfringens infections, dysentery or campylobacteriosis. Abortions, mummifications, stillbirth can also be caused by infections with pseudorabies, parvovirus, or porcine reproductive and respiratory syndrome virus. It is very important to differentiate CSF from infections with other pestiviruses. Porcine dermatitis and nephropathy syndrome (PDNS) is another viral disease that closely resembles CSF.
Many countries have an eradication or control programme in progress for CSF, and therefore it is of the utmost importance to rapidly make a definite diagnosis or exclude the disease in case of suspicion. This can only be performed in the laboratory. For this purpose, tonsil, spleen, and kidney samples are collected and submitted, preferably on ice to the laboratory, where frozen tissue sections are prepared. The direct immunofluoresence test (IFT) is the established method to detect viral antigen (OIE, 1996). The tonsil is the most important tissue for detecting antigen. The results can be available in a few hours. A negative result does not exclude CSF as the cause, and where suspicion remains more samples should be examined. The IFT can yield false-positive results, because pigs can become infected with BVDV [bovine viral diarrhoea virus] and BDV [border disease virus], which share common antigens with CSFV. The differentiation can be made by staining tissue section with conjugated monoclonal antibodies that are directed against conserved epitopes of CSFV, which do not react with BVDV or BDV. In countries where vaccination is applied, it may be necessary to distinguish between vaccine and field virus. This can be performed with selected monoclonal antibodies or in the case of lapinized vaccine strains by their ability to induce fever and antibodies in rabbits. In countries where laboratory facilities are scarce, the diagnosis may be made by inoculating susceptible pigs and vaccinated pigs with tissue homogenates. Presence of CSF in susceptible pigs, and absence in vaccinated pigs indicates CSF.
Isolation of CSFV is usually performed by inoculating a 10% mixed tissue homogenate on PK-15 cells. After 24-72 hours these cell cultures are examined by the direct IFT. The polymerase chain reaction is used increasingly often to diagnose CSF (McGoldrick et al., 1999). Enzyme-linked immunosorbent assays (ELISAs) to detect antigen are increasingly applied. However, their sensitivity and specificity could still be improved (Depner et al., 1995).
Antibodies to CSFV appear between 10 and 21 days after infection and probably persist throughout the animal's lifetime. An CSFV-specific proliferation of T lymphocytes and a cytotoxic T-lymphocyte response have been described in infected pigs (Ishikawa et al., 1995; Pauly et al., 1995). In pigs with chronic CSF, neutralising antibodies can remain absent, be impaired or delayed, or only transiently detectable. Pigs with late-onset CSF do not produce antibodies against the virus.
Virus-neutralisation tests and ELISAs, in various modifications, are commonly used for the detection of antibodies to CSFV. ELISAs are more simple to perform, are rapid and suited for screening a large number of samples, and therefore cheaper. Although some ELISAs use monoclonal antibodies that only recognize CSFV strains and thus should only detect CSFV antibodies, positive results should still be confirmed in neutralisation tests to differentiate between antibodies directed against BVDV or BDV. For this purpose, sera are titrated for neutralising antibodies against CSFV or against BVDV or BDV. Higher antibody titres against CSFV than against BVDV or BDV indicate an CSFV infection (OIE, 1996).
List of Symptoms/SignsTop of page
|Digestive Signs / Anorexia, loss or decreased appetite, not nursing, off feed||Pigs:All Stages||Diagnosis|
|Digestive Signs / Ascites, fluid abdomen||Pigs:Piglet||Diagnosis|
|Digestive Signs / Bloody stools, faeces, haematochezia||Pigs:All Stages||Diagnosis|
|Digestive Signs / Congestion oral mucous membranes, erythema, redness oral mucosa||Pigs:All Stages||Sign|
|Digestive Signs / Decreased amount of stools, absent faeces, constipation||Sign|
|Digestive Signs / Diarrhoea||Pigs:All Stages||Diagnosis|
|Digestive Signs / Erythema, redness of pharynx||Pigs:All Stages||Sign|
|Digestive Signs / Malformation of jaw, brachygnathia, prognathia||Pigs:All Stages||Sign|
|Digestive Signs / Melena or occult blood in faeces, stools||Sign|
|Digestive Signs / Mucous, mucoid stools, faeces||Sign|
|Digestive Signs / Unusual or foul odor, stools, faeces||Sign|
|Digestive Signs / Vomiting or regurgitation, emesis||Sign|
|General Signs / Ataxia, incoordination, staggering, falling||Pigs:All Stages||Diagnosis|
|General Signs / Back atrophy, wasting||Pigs:All Stages||Diagnosis|
|General Signs / Cyanosis, blue skin or membranes||Pigs:All Stages||Diagnosis|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Dysmetria, hypermetria, hypometria||Sign|
|General Signs / Fever, pyrexia, hyperthermia||Pigs:Piglet||Diagnosis|
|General Signs / Forelimb lameness, stiffness, limping fore leg||Sign|
|General Signs / Generalized lameness or stiffness, limping||Sign|
|General Signs / Haemorrhage of any body part or clotting failure, bleeding||Pigs:All Stages||Diagnosis|
|General Signs / Head, face, jaw, tongue atrophy, wasting||Pigs:All Stages||Diagnosis|
|General Signs / Hindlimb lameness, stiffness, limping hind leg||Sign|
|General Signs / Hypothermia, low temperature||Pigs:All Stages||Sign|
|General Signs / Inability to stand, downer, prostration||Pigs:All Stages||Diagnosis|
|General Signs / Kyphosis, arched back||Pigs:All Stages||Diagnosis|
|General Signs / Lack of growth or weight gain, retarded, stunted growth||Pigs:All Stages||Diagnosis|
|General Signs / Lymphadenopathy, swelling, mass or enlarged lymph nodes||Pigs:All Stages||Diagnosis|
|General Signs / Orbital, periorbital, periocular, conjunctival swelling, eyeball mass||Pigs:All Stages||Sign|
|General Signs / Pale mucous membranes or skin, anemia||Pigs:All Stages||Diagnosis|
|General Signs / Paraparesis, weakness, paralysis both hind limbs||Pigs:All Stages||Diagnosis|
|General Signs / Petechiae or ecchymoses, bruises, ecchymosis||Pigs:All Stages||Diagnosis|
|General Signs / Polydipsia, excessive fluid consumption, excessive thirst||Sign|
|General Signs / Reluctant to move, refusal to move||Pigs:All Stages||Diagnosis|
|General Signs / Sudden death, found dead||Pigs:All Stages||Sign|
|General Signs / Swelling, mass external abdomen||Pigs:Piglet||Sign|
|General Signs / Tenesmus, straining, dyschezia||Sign|
|General Signs / Torticollis, twisted neck||Pigs:All Stages||Sign|
|General Signs / Trembling, shivering, fasciculations, chilling||Pigs:Piglet||Diagnosis|
|General Signs / Underweight, poor condition, thin, emaciated, unthriftiness, ill thrift||Pigs:All Stages||Diagnosis|
|General Signs / Weight loss||Pigs:All Stages||Diagnosis|
|Musculoskeletal Signs / Forelimb spasms, myoclonus||Pigs:All Stages||Diagnosis|
|Musculoskeletal Signs / Head, face, neck spasms, myoclonus||Pigs:All Stages||Diagnosis|
|Musculoskeletal Signs / Hindlimb spasms, myoclonus||Pigs:All Stages||Diagnosis|
|Musculoskeletal Signs / Relative shortening forelimb||Pigs:Piglet||Sign|
|Musculoskeletal Signs / Relative shortening hind limb||Pigs:Piglet||Sign|
|Nervous Signs / Circling||Pigs:All Stages||Sign|
|Nervous Signs / Coma, stupor||Pigs:All Stages||Diagnosis|
|Nervous Signs / Constant or increased vocalization||Sign|
|Nervous Signs / Dullness, depression, lethargy, depressed, lethargic, listless||Pigs:All Stages||Diagnosis|
|Nervous Signs / Head tilt||Pigs:All Stages||Sign|
|Nervous Signs / Hypertonia of muscles, myotonia||Pigs:All Stages||Diagnosis|
|Nervous Signs / Seizures or syncope, convulsions, fits, collapse||Sign|
|Nervous Signs / Tremor||Pigs:Piglet||Diagnosis|
|Ophthalmology Signs / Blindness||Sign|
|Ophthalmology Signs / Chemosis, conjunctival, scleral edema, swelling||Pigs:All Stages||Diagnosis|
|Ophthalmology Signs / Conjunctival, scleral, injection, abnormal vasculature||Pigs:All Stages||Diagnosis|
|Ophthalmology Signs / Conjunctival, scleral, redness||Pigs:All Stages||Diagnosis|
|Ophthalmology Signs / Lacrimation, tearing, serous ocular discharge, watery eyes||Pigs:All Stages||Diagnosis|
|Ophthalmology Signs / Purulent discharge from eye||Pigs:All Stages||Diagnosis|
|Pain / Discomfort Signs / Skin pain||Sign|
|Reproductive Signs / Abortion or weak newborns, stillbirth||Pigs:Sow||Diagnosis|
|Reproductive Signs / Lack of libido or erection||Sign|
|Reproductive Signs / Mummy, mummified fetus||Pigs:Sow||Diagnosis|
|Reproductive Signs / Small litter size||Sign|
|Respiratory Signs / Abnormal breath odor, foul odor mouth||Pigs:All Stages||Sign|
|Respiratory Signs / Abnormal breathing sounds of the upper airway, airflow obstruction, stertor, snoring||Sign|
|Respiratory Signs / Coughing, coughs||Pigs:All Stages||Sign|
|Respiratory Signs / Dyspnea, difficult, open mouth breathing, grunt, gasping||Sign|
|Respiratory Signs / Epistaxis, nosebleed, nasal haemorrhage, bleeding||Pigs:All Stages||Sign|
|Respiratory Signs / Increased respiratory rate, polypnea, tachypnea, hyperpnea||Pigs:All Stages||Sign|
|Respiratory Signs / Mucoid nasal discharge, serous, watery||Pigs:All Stages||Sign|
|Respiratory Signs / Purulent nasal discharge||Pigs:All Stages||Sign|
|Skin / Integumentary Signs / Alopecia, thinning, shedding, easily epilated, loss of, hair||Pigs:All Stages||Sign|
|Skin / Integumentary Signs / Cold skin, cool ears, extremities||Pigs:All Stages||Sign|
|Skin / Integumentary Signs / Rough hair coat, dull, standing on end||Sign|
|Skin / Integumentary Signs / Skin erythema, inflammation, redness||Pigs:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin necrosis, sloughing, gangrene||Pigs:All Stages||Diagnosis|
|Skin / Integumentary Signs / Skin pustules||Pigs:All Stages||Sign|
|Skin / Integumentary Signs / Warm skin, hot, heat||Pigs:All Stages||Sign|
|Urinary Signs / Haematuria, blood in urine||Pigs:All Stages||Diagnosis|
Disease CourseTop of page
Pigs normally become infected via the oronasal route, whereupon CSFV first replicates in the tonsil. Highly virulent strains induce acute CSF. Their spread throughout the body is characterized by a lymphatic, viraemic and visceral phase. The virus initially infects epithelial cells of the tonsil, invades the underlying lymphoreticular tissue, is transferred to regional lymph nodes, wherein it replicates and then gives rise to viraemia. Secondary target organs, such as spleen, lymphoid structures lining the intestine, and bone marrow, produce high amounts of virus leading to a high-titred viraemia. Late in the viraemic phase CSFV infects parenchymatous organs (Ressang, 1973). The virus has an affinity for vascular endothelium and cells of the immune system. A leukopenia and thrombocytopenia develop rapidly after infection and usually persist until death in acute CSF (Weiss et al., 1973). During acute CSF, there is a severe general depression of immune responsiveness (Oirschot et al., 1981). Strains of moderate virulence can induce persistent infections that can be distinguished as chronic or late-onset CSF. The first phase of chronic CSF resembles that of acute CSF, but lasts longer and virus titres are lower in serum and organs. There is a second phase of clinical improvement, wherein there is no or a low-level viraemia, and virus is restricted to epithelial cells of tonsil, ileum, salivary glands and kidney. In this phase there is excessive plasma cell formation, an increase in serum immunoglobulin concentrations and specific antibody production (Cheville and Mengeling, 1969; Mengeling and Packer, 1969). The simultaneous presence of virus and antibody can lead to deposition of antigen-antibody complexes in the kidney, resulting in glomerulonephritis (Cheville et al., 1970). During the third phase of chronic CSF the virus disseminates again throughout the pig, which may be initiated by the immune exhaustion that appears to develop and renders the pigs more susceptible to secondary bacterial infections. Pigs can recover from mild to severe infections with moderately virulent CSFV strains. Such pigs produce neutralising antibodies and a cell-mediated immune response.
Late-onset CSF has an initial period of virtual absence of clinical signs, and is the sequel of foetal infection with strains of low virulence. Pigs have a lifelong high-titred viraemia and viral antigen is widespread throughout epithelial, lymphoidal and reticulo-endothelial tissues. Pigs suffering from late-onset CSF are immunotolerant to the virus. Eventually they develop clinical signs and die (Oirschot and Terpstra, 1977).
The multiplication of CSFV strains with low virulence appears to be restricted to the lymphatic phase: tonsil and regional lymph nodes (Lin et al., 1969). These infections usually run a subclinical course accompanied with a transient leukopenia and followed by a specific immune response. After infection of pregnant sows, the virus infects the foetuses. The outcome of the foetal infection is largely dependent on the age of the foetus and the virulence of the virus.
CSF can range from an acute disease with high mortality to a subclinical infection. After an incubation period of 2-6 days, pigs with acute disease show a high fever, with peaks above 42°C, depression, loss of appetite, ataxia, coughing, conjunctivitis, constipation, diarrhoea, and cyanosis. Most pigs die between 10-20 days post-infection. In subacute CSF, pigs develop similar but less severe signs and succumb within 30 days (Dunne, 1975). Pigs infected with strains of moderate virulence show a great variation in clinical signs (Depner et al., 1996, 1997). They may die from (sub)acute disease, may recover or may survive the acute phase only to succumb later from chronic CSF, or may only suffer from mild disease and subsequently recover. Chronic CSF is characterized by intermittent disease periods with anorexia, fever, diarrhoea, dermatitis and leukopenia, and can result in runt pigs. Such pigs are severely retarded in growth, have skin lesions and stand with arched backs. Pigs with chronic CSF may survive for more than 100 days, but most eventually die. Pigs infected with strains of low virulence usually show only mild disease or remain healthy. A congenital infection can result in abortion, mummification, stillbirth, malformation or birth of weak and trembling piglets. Healthy looking, but infected piglets can be born that develop late-onset CSF, characterized by a long period of freedom from disease, followed by gradually aggravating signs of CSF, including runting. Pigs with late-onset CSF die weeks or months after birth (Oirschot and Terpstra, 1977).
EpidemiologyTop of page
The pig and the wild boar are the sole animals that become infected with CSFV under natural conditions, and thus are the source of virus spread. Pigs usually become infected by the oronasal route and shed virus from saliva, nasal and ocular discharges, urine and faeces, until they die or recover. Pigs with chronic CSF may excrete virus continuously or intermittently. A congenital infection may result in the birth of persistently infected immunotolerant piglets that may shed CSFV for months (Oirschot and Terpstra, 1977).
Direct contact between infectious and susceptible pigs is the most common route of transmission of CSFV. Pigs can become infected at markets and during transport in contaminated vehicles, and thus may introduce virus into a herd. However, the mode of introduction of CSFV into a herd can often not be established (Terpstra, 1987; Elbers et al., 1999).
Sows may become infected by artificial insemination and thus probably by natural mating (De Smit et al., 1999). Aerogenic transmission seems to take place within housing compartments (Laevens et al., 1999). Aerogenic spread between farms may occur in pig-dense regions, where large units with mechanical ventilation are located close together. Transmission of CSFV within and between herds has been estimated by simulation models (Stegeman et al., 1999a, b; Stärk et al., 2000). Man appears to contribute considerably to virus spread within and between herds: for example, through the use of contaminated instruments and medicine bottles. The possibility that insects, dogs, cats and birds act as mechanical vectors of the virus cannot be excluded. Wild boars are an important reservoir of CSFV and they appear to have been the source of many outbreaks (Fritzemeier et al., 1999).
Pork and pork products are an important indirect source of dissemination, because CSFV can survive in them after processing. When the meat is stored, cooled or frozen, the virus can survive for months. After such products are introduced in a country, and if kitchen leftovers (swill, garbage) are not properly treated before being fed to pigs, they may cause outbreaks (Dunne, 1975; Fritzemeier et al., 1999). Because of this potential danger, some countries prohibit the feeding of swill to pigs.
Recent advances in molecular epidemiology of CSFV have facilitated the tracing of the source of outbreaks and of transmission routes. The phylogenetic analysis of genome sequences can be exploited to detect or exclude a possible connection between outbreaks (Lowings et al., 1999; Widjojoatmodjo et al., 1999).
The Classical Swine Fever Database has been implemented as a tool to facilitate exchange of information concerning CSF (Dreier et al. 2007). After registration the database is accessible at: http://viro08.tiho-hannover.de/eg/eurl_virus_db.htm
In 2002, a working group on CSF in wild boar of the Directorate General Health and Consumer Protection (DG SANCO) of the European Commission initiated the establishment of a common database on the epidemiology of classical swine fever in wild boar. (See: http://public.csf-wildboar.eu/Default.aspx)
Impact: EconomicTop of page
CSF can cause enormous economic losses in countries with an intensive pig industry. The losses can be divided into losses for the government, mainly due to the strict stamping out and other control measures that have to be taken, and losses for the entire livestock-production chain, i.e. feed suppliers, breeding organisations, animal traders, slaughterhouses and processing industries (Horst et al., 1999). Severe outbreaks plagued Belgium, Germany, and the Netherlands in the 1990s. In the latter country, the 1997 epidemic resulted in destruction of more than 11 million pigs and estimated financial losses of about 2.3 billion US dollars (Meuwissen et al., 1999). In extensive pig-holding systems in developing countries the animal and economic losses may be less obvious.
Zoonoses and Food SafetyTop of page
CSF is not a zoonosis.
Disease TreatmentTop of page
Treatment for CSF is not available.
Prevention and ControlTop of page
In countries where CSFV is endemic, vaccination is often practiced (but not in the European Union). Only live attenuated vaccines are applied, which are based on either the lapinized Chinese strain, on the cell-culture-adapted Japanese GPE- or on the French PK-15 cell-culture-adapted Thiverval strain. These three vaccines are highly efficacious. They induce a rapid (within 4-5 days) and probably lifelong protective immunity, provided the vaccine does not contain too low a virus titre. Vaccination also reduced the replication of virulent CSFV upon challenge and may reduce transmission of CSFV in a vaccinated population (Biront et al., 1987; De Smit, 2000). Because maternal antibodies strongly suppress the generation of active immunity, pigs with maternal immunity should be vaccinated twice. Although the Chinese strain vaccine virus may sometimes spread to contact pigs and foetuses, it has been shown to be highly safe. Vaccination has also been used in cases of emergency to support eradication.
A great disadvantage of vaccination with the above vaccines is that the antibody response after vaccination cannot be distinguished from that after an infection, and as a result it is impossible to convincingly demonstrate absence of wild-type virus in vaccinated populations. To solve this problem, E2 subunit marker vaccines have been developed and shown to be efficacious and safe (Hulst et al., 1993; Moormann et al., 1996; Bouma et al., 1999; De Smit, 2000). Infected herds in vaccinated regions can be detected with an ELISA that detects antibodies against the Erns protein of CSFV (De Smit, 2000).
Controlling endemic infections in wild populations is difficult. Oral vaccination campaigns have been undertaken in wild boar in Germany to reduce the risk of transmission of CSFV to domestic pigs (Kaden et al., 2005; Staubach et al, 2013). It has been proposed that the same bait vaccine used for wild boar could be used for oral vaccination of pigs in backyard production systems, where the systematic implementation of parenteral vaccination proves to be difficult and alternative delivery mechanisms might be needed (Dietze et al., 2013; Milicevic et al., 2013).
In endemic countries, the introduction of CSFV into a herd can best be prevented by purchasing pigs only from free herds and by putting incoming pigs in quarantine. After having been tested negative at the end of a 4-week period they can be admitted. Strict hygiene cannot be emphasized too much as a very important control measure. Thorough cleaning, disinfecting of pens, vehicles and other objects are too often neglected as means to prevent CSF.
Many countries are free of CSF and they take various measures to prevent the introduction of the virus. Usually, they ban the import of live pigs, pork and insufficiently heated pork products from countries where CSF is endemic. In addition, kitchen leftovers from international means of transportation and swill are destroyed or adequately sterilised before being fed to pigs. However, improperly treated pig products are still often the cause of new outbreaks in CSF-free regions. If CSF is diagnosed in 'free' countries, often rigorous measures are taken to eradicate the virus as rapidly as possible. Such eradication programmes are based on notifying suspected cases to the authorities, rapid laboratory diagnosis and immediate destruction of infected herds. In addition, a ban on the movement of pigs in the neighbourhood, intensive surveillance of herds in the endangered area, tracing of the source of infection and of possible contacts is implemented. Sometimes preventive culling of neighbouring herds is performed. At the end of eradication programmes, a serosurvey should demonstrate that a region or country is indeed again free of virus, and contingency plans should enable rapid eradication of CSFV, if the virus should be re-introduced (Crauwels et al., 1999).
In spite of all the above efforts, CSF is still a serious threat for many countries, because of increases in pig density in many areas, the intensification of transport, the wild boar as reservoir for CSFV, the dissemination of CSFV in the food chain and the continuing practice of feeding improperly sterilised swill.
Among the member states of the European Union (EU) a harmonized strategy for diagnosis, control and eradication of CSF is applied (Postel et al., 2013). The EU minimum control measures require depopulation of infected farms, movement restrictions, zoning and surveillance (EU Minimum strategy). Emergency vaccination is authorised for densely populated pig areas although the EU Minimum strategy plus culling in a 1-km ring around infected premises is preferred (Ribbens et al., 2012). Alternative control measures such as antiviral agents, in particular small molecule inhibitors of the CSFV replication, are being explored (Backer et al., 2013; Newcomer and Givens, 2013; Ribbens et al., 2012).
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Distribution MapsTop of page
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