Classical swine fever is a highly contagious, viral disease of swine that in its most virulent form causes morbidity and mortality approaching 100%. Viral strains of low to moderate virulence cause infections with a gradient of severity, some clinically inapparent.
Classical swine fever (CSF) occurs only in swine, and all age groups are susceptible. The disease occurs in most major swine-raising countries where eradication programs have not been successfully implemented. In the United States, CSF was once a frequent occurrence but was eradicated in 1976. Classical swine fever currently exists in many countries, including areas of Central and South America and the Caribbean, which present nearby threats to the US. Since 1997, epidemics of CSF have been reported in many European countries, including The Netherlands, Spain, Germany and Italy. Sporadic outbreaks continue to occur, particularly in Eastern Europe. The disease is endemic in much of Asia.
The historical record does not clearly indicate where CSF originated. A disease now believed to have been CSF occurred in Tennessee in 1810 and in Ohio in the early 1830s. Subsequently, CSF was reported from many other countries throughout the world. Classical swine fever has been eradicated from at least ten countries, but remains persistent in much of the world.
In the United States, there were many years when CSF was epidemic and caused huge losses. Losses were first reduced through vaccination with CSF antiserum/virus (serum/virus). When properly done on healthy swine, it resulted in strong immunity but was accompanied by several disadvantages. As examples, vaccination sometimes triggered outbreaks of other diseases and vaccinated swine commonly shed virus that could serve as a source of infection for other herds. Some of the later, attenuated vaccines had similar disadvantages. Vaccination with serum/virus or attenuated vaccines was prohibited as part of a national eradication program begun in 1962. This, along with other measures, resulted in eradication of CSF by 1976. Eradication was a remarkable achievement, considering the highly infectious nature of virus and extensive commerce in pigs and pork products.
Classical swine fever is a Pestivirus (family Togaviridae), related to the virus of bovine virus diarrhea (BVD) and sheep’s border disease (BD). Strains of CSF vary greatly in antigenicity and virulence. Virulence can increase in a single passage through pigs. Strains of high virulence cause classic outbreaks with high morbidity and mortality. Strains of moderate virulence cause subacute or chronic infections. Strains of low virulence can cause mild or inapparent infection, reproductive failure or neonatal losses.
CSF virus is moderately resistant to environmental influences. In pig houses, excreta and bedding, virus can persist for days to weeks, depending upon temperatures. The virus survives some curing processes as well as in frozen pork for months to years, and in chilled meats for months. The virus is inactivated by 2% sodium hydroxide or by lipid solvents.
Classical swine fever is highly contagious and infection spreads rapidly by direct or indirect contact between infected and susceptible pigs. Pigs with acute infection shed large amounts of virus before they are visibly ill, during illness, and after recovery. Live pigs infected as fetuses spread virus in their secretions and excretions. Uncooked waste food containing infectious pork scraps and subsequently fed to pigs has been well documented as initiating many outbreaks. Other methods of viral spread include farm equipment (contaminated wagons, trucks, tractors, machinery), personnel (careless farmers, salesmen, veterinarians), fomites, pets, birds and arthropods. Airborne transmission probably is of little significance.
After ingestion, the virus infects epithelial cells in the crypts of tonsils, spreads to adjacent lymph nodes and produces viremia within 24 hrs. Tonsils are the initial site of viral replication. Replication also occurs at other sites, especially in lymphoid tissues (spleen, Peyer’s patches, lymph nodes, thymus), in endothelial cells, bone marrow and circulating leukocytes. Within three to four days, virus spreads to many epithelial-type cells and is present in excretions and secretions.
The virus causes lymphoid depletion which makes the swine more susceptible to other infections. Bone marrow damage leads to leukopenia and thrombocytopenia. Thrombocytopenia, along with endothelial cell damage, results in petechial and ecchymotic hemorrhages at many sites. Swine with chronic CSF infection may develop glomerulonephritis from antigen-antibody complexes that damage glomeruli.
In pregnant sows and gilts, the virus may cross the placenta and infect some or all of the fetuses. The effect depends on the stage of pregnancy and can include abortion or production of mummified fetuses, stillborn piglets, or persistently infected live piglets. Fetal anomalies may result from in utero infection; a remarkable one is hypomyelinogenesis, a syndrome that results in shaking piglets (myoclonia congenita).
In typical acute outbreaks, clinical signs are nonspecific. These include: depression (a hunched posture with drooping head and a straight-hanging tail), anorexia, high fevers (106˚ F), conjunctivitis, and a strong desire to lie down and huddle or pile with other affected pigs. There may be diarrhea or constipation, and perhaps vomiting. Signs caused by central nervous system (CNS) lesions often are apparent and include reeling when forced to walk, eventual hindquarter paresis or paralysis and occasional tonic/clonic convulsions in young growing pigs. Most affected pigs die within three weeks of onset.
Outbreaks with less virulent virus or chronic cases seldom present with typical signs but often have conjunctivitis, diarrhea or constipation, and some degree of emaciation. Mildly virulent strains of the virus seem to be becoming more prevalent worldwide and present a significant opportunity for misdiagnosis by those veterinarians and producers unfamiliar with the disease. Pigs infected as fetuses or neonates may present no signs.
In typical acute CSF, lesions include petechial and ecchymotic hemorrhages at several common sites including the epiglottis, bladder mucosa, cortex and pelvis of the kidneys, gall bladder mucosa, on the lungs and heart, at the ileocecal junction and in the skin. Lesions sometimes considered of special value in diagnosis include single or multiple infarcts along the border of a spleen of normal size, subcapsular hemorrhage in many lymph nodes, and hemorrhages on the cortices of the kidneys and on the lungs. There usually is some degree of congestion in the fundus of the stomach and small intestine. Small foci of necrosis may be present in the tonsils.
Peracute cases may have no lesions. In chronic cases, ulcers with raised edges (‘button ulcers”) are often present in the cecum and/or colon. Grossly visible fetal lesions include ascites, hepatic nodularity, pulmonary hypoplasia, petechiation of the skin, microencephaly, hydrocephalus and cerebellar hypoplasia.
Microscopically, there is a panencephalitis more apparent in the medulla, pons, midbrain or thalamus. Glial cell nodules often cluster around destroyed capillaries. Vascular lesions are present at many sites, perhaps more pronounced in splenic follicular arteries.
Typical acute CSF should be suspected on the basis of history, clinical signs, temperatures and gross lesions. Numerous postmortem examinations will increase the accuracy of diagnosis. Leucopenia in several suspected cases is suggestive of CSF. The lesions of typical, acute cholera closely resemble and must be carefully differentiated from those of African swine fever, acute salmonellosis and acute swine erysipelas. Lesions sometimes resemble those of other septicemic diseases, including streptococcosis and Glasser’s disease. Infection with mildly virulent strains may be indistinguishable from many endemic systemic or respiratory pathogens. Diagnostic testing is imperative whenever the combination of gross pathology, clinical signs, and response to therapy suggest that CSF is on the list of possible etiologies.
Suspected outbreaks should be immediately reported to authorities to confirm diagnosis. Three laboratory procedures commonly used are: demonstration of CSF viral antigen in frozen tissue sections by immunoflorescence with preferred tissues being tonsil, pharyngeal lymph nodes, spleen, kidney and distal ileum; isolation of virus in cell culture and identification of viral antigen in the culture by the fluorescent antibody (FA) test; and identification of antibodies to CSF by virus neutralization tests. Regardless of the procedure used, it may still be necessary to differentiate CSF from BVD. A monoclonal antibody technique is available.
Control is possible through prevention of exposure, vaccination, or eradication. In most countries, prevention of exposure is attempted through banning/controlling importation of live pigs, fresh pork, insufficiently heated pork products, and other possible sources of virus (imported swine semen and embryos, biologics); and prohibiting the feeding of uncooked waste food and the dumping of garbage from ships in port.
In countries where the virus is endemic, attenuated vaccines often are used for preventing or reducing the prevalence of infection. A strain of virus attenuated by passage in rabbits (C strain) is widely used. Vaccination may be prohibited when eradication by slaughter is introduced. In the final stages of eradication, infected and exposed swine are slaughtered and buried or incinerated. Movement of swine in the area is controlled. Contaminated facilities are disinfected and not repopulated for a period of time.
Bovine viral diarrhea virus (BVDV) and border disease virus (BDV) of sheep
These two diseases and classical swine fever (CSF) are closely related members of the family Togaviridae. Naturally occurring infections with BVDV and BDV have occurred in swine. Their major importance in swine is that they both induce antibodies that can lead to serologic misdiagnosis of CSF. This can cause confusion in countries trying to eradicate CSF or maintain a CSF-free status. This confusion can be avoided if specific laboratory methods of CSF diagnosis are used.
Clinically apparent outbreaks of BVDV and BDV in swine are uncommon. Outbreaks that have been suspected are manifested in breeding herds as reproductive problems, such as poor conception rates, small litters, abortions, and an excessive number of dead and mummified fetuses. In infected, live piglets, the signs are expected to be similar to those of congenital CSF including deaths in piglets less than five weeks old, anemia, unthriftiness, congenital tremors and convulsions.