African Swine Fever
Definition
A highly contagious, viral disease with signs, lesions and other features that closely resemble swine fever (CSF). The disease is exotic to the US.
Occurrence
African swine fever (ASF) occurs naturally in wild, feral and domestic swine (Suidae). At present, ASF does not occur in the western hemisphere. It is endemic in several African countries and an outbreak of the disease has been occurring across several countries in Central Asia since 2007. Distribution among countries changes, depending on new infections, re-infections and the success of eradication programs.
Historical information
African swine fever first was described in Africa in 1921. It soon was endemic in eight African countries. In 1957, the disease occurred in Portugal, the first non-African country to be infected. Over a 28-year period, ASF spread to eight European countries, Brazil, Cuba, Haiti and the Dominican Republic.
In some countries, repeated outbreaks have discouraged eradication efforts. In many other countries, eradication efforts have been successful. Prohibiting importation of swine and pork from infected countries, and eliminating or regulating the practice of waste-food feeding to pigs are fundamental to most successful eradication programs. Several features of ASF, plus the high cost of eradication, make worldwide eradication unlikely. The United States has never experienced an outbreak although ASF has occurred several times in nearby Caribbean islands.
Etiology
Formerly classified as a member of the Iridoviridae, this DNA virus is currently the only member of a family called Asfarviridae. Strains vary markedly in virulence and no effective vaccines currently exist. It grows readily in several cell culture systems. ASF virus is exceptionally hardy in the environment but can be inactivated by many disinfectants.
Epidemiology
The virus often is introduced by feeding uncooked garbage containing scraps of infectious pork. ASF virus persists in pork for long periods of time. Once the virus is introduced, direct or indirect contact of healthy swine with it leads to outbreaks. Most outbreaks can be traced to contact with infected swine. African swine fever can be transmitted by direct contact with infected animals, indirect contact on fomites, and by tick vectors. Direct transmission usually is through oronasal secretions.
In many endemically infected countries, several species of soft ticks (predominantly genus Ornithodorus) act as reservoirs and vectors. In Africa, a cycle of inapparent infection is established between ticks and wild boars, warthogs and bush pigs. ASF virus is passed transovarially in some ticks and persists in successive generations of ticks. Difficulty in eradication of ticks interferes with eradication of ASF. The United States has ticks with a similar potential.
Pathogenesis
The primary infection usually starts in the tonsils and mandibular lymph nodes. Virus then spreads in lymph and blood to secondary replication sites (bone marrow, lung, spleen and kidney). A persistent viremia begins about one week after infection. The main target cells of the virus include monocytes, macrophages, cells of the reticuloendothelial (RE) system, endothelial cells, and platelets. Destruction of antigen processing cells in lymph nodes, spleen and bone marrow apparently interferes with formation of protective antibodies. Destruction of endothelial cells and vascular damage is responsible for hemorrhages, edema and transudate formation. The virus also causes a meningoencephalitis responsible for ataxia. The virus affects multiple organs of fetuses and causes fetal deaths.
Clinical signs
Clinical signs appear five to fifteen days after infection. Signs vary greatly, depending on the virulence of the virus, and can range from inapparent or subclinical to hyperacute with sudden death. Many initial outbreaks are acute and closely resemble outbreaks of acute CSF.
In acute outbreaks, signs include anorexia, high temperatures, listlessness, incoordination, leukopenia, cutaneous hyperemia, hemorrhages on the skin (especially on ears and flanks), and hyperpnea. Vomiting, diarrhea, dehydration and ocular discharge may occur. Morbidity and mortality are high and can approach 100%. Death usually occurs in four to seven days. In subacute or chronic cases, signs include abnormal respiration, abortion and low mortality.
Lesions
The lesions are similar to those of CSF. There are petechial and ecchymotic hemorrhages at many sites (skin, kidneys, lymph nodes, serosal and mucosal surfaces, epicardium, endocardium, larynx, bladder, gall bladder, lung), edema, hydrothorax, hydropericardium and ascites. The liver and spleen are congested. The spleen often is enlarged, friable, and may have infarcts. There often is congestion of meninges and brain. Lesions that are often present with ASF, but seldom with CSF, include hydrothorax, hydropericardium, ascites and pulmonary edema. Hemorrhages and edema usually are more severe than with CSF.
Gross lesions in chronic cases of ASF include fibrinous pericarditis and pleuritis, spleen and lymph node enlargement, caseous lobular consolidation of areas in the lungs, possibly with mineralization.
Histologic lesions of ASF include meningoencephalitis, periportal hepatitis, extensive necrosis with karyorrhexis (cell nucleus rupture) in lymphoid tissues, and degeneration and necrosis of endothelial cells and cells of the mononuclear-phagocytic system.
Diagnosis
Diagnosis can be made by detecting ASF virus, viral antigen, or antibodies to ASF. A hemadsorption test is widely used to identify the virus. Viral antigen can be identified in tissue by direct immunofluorescence on frozen sections and is widely used. Also, several techniques have been developed to identify ASF virus in paraffin-embedded tissue sections. Several tests are used to identify ASF antibody. These include indirect immunofluorescence, enzyme-linked immunosorbent assay (ELISA), complement fixation (CF), immunoblotting and radioimmunoassay. There is a sensitive dot immunobinding assay for field diagnosis.
Control
Control in most countries is limited to preventing entry of the ASF virus. Early diagnosis of suspected cases is important. State and federal disease control authorities should be informed immediately if an ASF or CSF outbreak is suspected. If ASF should gain entrance, early quarantine and restriction of movement of animals in the area are important. Vaccines are unsatisfactory both for control of clinical signs and preventing infection.
Massive amounts of virus are found in many tissues especially blood. Care must be taken when performing necropsies to prevent substantial environmental contamination.
Cooperative international laws prohibit the importation of swine and pertinent food products from countries where ASF is endemic. Most countries prohibit the dumping of food wastes from planes and ships.
Should outbreaks occur in the US, they probably will be handled by slaughter, followed by cremation or burial of infected pigs and pigs that had direct or indirect contact. Strict restriction of animal movement in the area, cleaning and disinfection of premises and the use of sentinel pigs prior to repopulation will also be necessary.
Blue Eye Disease (Paramyxovirus)
Definition
Blue eye disease (BED) is the common name for a disease caused by a porcine rubulavirus (Paramyxoviridae; La Piedad Michoacan virus) that is characterized in nursing or growing pigs by central nervous system (CNS) signs and, frequently, by corneal opacities. Signs in sows and boars include various forms of reproductive failure and corneal opacity.
Occurrence
Blue eye disease is only known to occur in swine. In Mexico, the only country that has reported cases, BED occurs throughout the year but is more common in the hotter, drier months (March to July). Swine diseases caused by other paramyxoviruses have occurred in several countries (Japan, Israel, Canada, United States, and Australia) but the diseases they cause are sporadic, rare, and are distinctly different from BED manifesting as transient outbreaks of pneumonia, encephalitis, or reproductive disease.
Historical information
Blue eye disease first occurred in 1980 in a large swine raising operation in central Mexico. Within a short time it had spread to eleven other states or districts and had become economically important. The first outbreaks occurred mainly in unweaned piglets less than 30 days old, frequently in piglets less than two weeks old. After 1983, severe outbreaks occurred in larger pigs (33-99 lb). Signs of reproductive failure were also observed in mature sows and boars. The scarcity of reports since 1990 suggest BED is less common now.
Etiology
The agent that causes BED is a paramyxovirus. It grows in chick embryos and hemagglutinates erythrocytes of mammalian and avian origin. It grows and causes cytopathic effect in PK-15 and several other cell culture systems. It stimulates formation of inclusion bodies in PK-15 cells. Formalin destroys infectivity of the virus.
Antisera against seven paramyxoviruses and six parainfluenza viruses do not affect infectivity of the BED virus. This suggests BED virus differs from other paramyxoviruses and causes a unique disease in swine. Other paramyxoviruses are infrequent causes of swine pneumonia and encephalitis.
Epidemiology
Subclinically infected pigs are the main reservoir of virus. Virus can also be disseminated by people and vehicles. On farms with a continuous production system, virus persists and is maintained in new groups of susceptible young pigs while adult stock remains well. The disease is largely self-limiting in closed herds. Infected animals develop protective antibodies that usually persist throughout their lifetime.
Pathogenesis
Natural infection is thought to occur by inhalation based on experimental exposures where intratracheal and intranasal exposure reproduced the disease. The initial site of viral replication is unknown but may be in the nasal mucosa or tonsils. Virus soon spreads to the brain, lung and many other organs, suggesting that viremia occurs. Reproductive problems in dams suggest that the virus crosses the placenta and infects the fetuses.
Corneal opacities (blue eye) sometimes occur late in the course of the disease. The opacities disappear spontaneously, presumably as inflammatory edema resolves. The opacities are, perhaps, the result of an immunologic reaction accompanied by inflammation. Virus may replicate in the eyes since inclusion bodies have been demonstrated there.
Clinical signs
Signs vary somewhat with the age groups affected but are mainly those of encephalomyelitis in both young and growing pigs. In young piglets, onset is sudden with prostration and fever. Other signs include ataxia, weakness, muscle tremors, rigidity, nystagmus, abnormal postures, hyperexcitability, squealing, and paddling movements; occasionally there is blindness. Often there is conjunctivitis with adherence of the eyelids. Corneal opacity (blue eye) may occur in 1-10% of young piglets and may be seen in the absence of other signs. Twenty to 65% of litters can be affected. Morbidity within litters is between 20-50%; mortality in affected pigs can reach 90%. Piglets affected early in an outbreak often die within 48 hours; those affected later usually die after a course of four to six days. Mortality occurs over a two to nine week -period.
In pigs greater than 30 days old, signs are more moderate and transient. They include fever, sneezing, coughing and anorexia. CNS signs include listlessness, ataxia and circling. Less than 5% of the pigs are affected and mortality usually is low. However, in pigs weighing 35 to 45 lb, outbreaks with 20% mortality and up to 30% corneal opacity have occurred. Adult animals occasionally develop corneal opacities.
In pregnant swine, returns to estrus may occur and persist in the herd for six to eight months. There also is an increase in stillbirths and mummified fetuses, and occasional abortions. In affected boars, there is a reduction in fertility and an increase in testicular size, usually unilateral, followed by atrophy.
Lesions
Gross lesions are limited and largely nonspecific. They may include mild anteroventral pneumonia, tonsillitis and mild ascites with some fibrin. Brain congestion and an increase in cerebrospinal fluid may be present. There is conjunctivitis and, perhaps, corneal opacity in one or both eyes. Pericardial and renal hemorrhages also have been reported. In affected boars there is orchitis, epididymitis and testicular atrophy.
Microscopic lesions include a nonsuppurative encephalomyelitis affecting mainly the gray matter of the midbrain, thalamus and cerebral cortex. Intracytoplasmic inclusions in neurons have been reported. Affected eyes have corneal edema and anterior uveitis, perhaps with exudate in the anterior chamber. Intracytoplasmic inclusions may be present in epithelial cells near the drainage angle of the corneoscleral junction.
Diagnosis
Clinical signs of encephalomyelitis, along with corneal opacity, suggest a diagnosis of BED. Reproductive problems in either or both sexes, along with numerous corneal opacities, are also suggestive. Microscopic lesions of encephalomyelitis and the presence of intracytoplasmic inclusion bodies in neurons or eyes strongly suggest BED.
The hemagglutinating virus usually can be isolated from the brain or tonsil in PK-15 cells and can be identified by hemagglutination inhibition (HI), virus neutralization (VN) or enzyme-linked immunosorbent assay (ELISA). The HI test is widely used. Direct immunofluorescence has been used to identify the virus in cell culture. BED must be differentiated from other causes of CNS disease, especially pseudorabies.
Control
A rigorous health control program to prevent introduction of virus is the best preventive measure. Maintaining a closed herd and use of the all in/all out system of production may be helpful. Essential replacement stock should be added only after negative serologic tests and a period of quarantine. Commercial vaccines have been produced but there is no report on their efficacy.
BED has been eliminated from infected sites by disposing of infected animals, cleaning and disinfecting the site and using sentinel pigs to confirm elimination of infection. There is no satisfactory treatment of BED and pigs with CNS signs usually die. Pigs having only corneal opacities frequently recover without treatment.
Classical Swine Fever (Hog Cholera)
Definition
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.
Occurrence
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.
Historical information
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.
Etiology
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.
Epidemiology
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.
Pathogenesis
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).
Clinical signs
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.
Lesions
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.
Diagnosis
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
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.
Foot-and-Mouth Disease (FMD)
Definition
Foot-and-mouth disease (FMD) is a highly contagious viral disease of many wild and domestic cloven-footed mammals and many other animals. In swine, the disease is characterized by vesicles on the feet, snout and in the mouth.
Occurrence
A wide range of wild and domestic animals, especially cloven-footed mammals, are susceptible to FMD. Horses are resistant, a fact useful in differential diagnosis. The disease occurs in most countries with a large livestock population unless those countries have eradicated it and maintained their disease-free status. In countries where FMD occurs endemically and pigs are present in large numbers, swine frequently are infected. All age groups are susceptible.
Historical information
Foot-and-mouth disease is an ancient disease. A description of a disease observed in 1546 probably is a description of FMD. Since FMD was first clearly delineated from other diseases, it has continued to cause major losses in livestock throughout the world. Losses have been greater from loss of productivity than mortality.
Nine outbreaks of FMD have occurred in the United States. All outbreaks were followed by eradication, often at great expense. Much of the livestock population now in the United States is highly susceptible. An outbreak of FMD could cause great loss, especially if the outbreak became widespread before it was recognized. The United States has remained free of FMD since the last outbreak in 1929.
Recent outbreaks in Asia and the UK have demonstrated the devastation and frustration wrought by FMD. Exports were embargoed and entire regional herds slaughtered, effectively destroying the swine industry in these countries.
Outbreaks of all vesicular diseases of swine are of concern because the lesions cannot be distinguished from those of FMD, except by laboratory means. Swine are of special concern because they are susceptible to more vesicular diseases than other species of livestock, and they often play a major role in the spread of FMD by producing large, infectious aerosols of virus.
Etiology
An Aphthovirus of the family Picornaviridae causes FMD. There are at least seven immunologically distinct types of virus: A, O, C, South African Territory (SAT) 1, 2, 3 and Asian 1. Among the seven types, one particular antigen (virus infection-associated antigen [VIA]) is group reactive and useful in serologic diagnosis of FMD infection.
Over 60 subtypes of virus have been identified and new subtypes continue to develop. Many differ enough antigenically to require preparation of subtype vaccines for their control. The antigenic variation of the virus and the limited cross protection among strains has made it impossible to prepare a single vaccine that protects satisfactorily against all strains. Effective disinfectants of FMD virus include sodium hydroxide, acetic acid, sodium carbonate and Virkon® (Durvet).
Epidemiology
Virus transmission occurs through respiratory aerosols and direct or indirect contact with infected animals. Aerosol transmission of FMD virus over distances as great as 30 miles is believed to occur under certain weather conditions. Infected swine are exceptional disseminators of virus. For some virus subtypes, they are able to produce aerosols many times greater in virus concentration than those produced by cattle or sheep. They are sometimes referred to as “amplifier hosts” for FMD virus.
Infected swine disseminate virus in their excretions and secretions. Food products containing infectious pork can also spread FMD virus. Virus persists for long periods of time in frozen meat products. In several notable FMD outbreaks, the index case has been associated with the consumption by pigs of uncooked waste food containing infectious meat scraps. Contaminated biologics, including vaccines, have been responsible for outbreaks. People with residual FMD virus in their respiratory tract can transmit the virus to livestock for a short time.
Some species of animals recover from FMD and remain carriers for weeks, months and possibly, years. Occasionally they disseminate virus that initiates new outbreaks. Swine are not believed to be long-term carriers of FMD virus.
Pathogenesis
Foot and mouth disease virus adheres to the mucosa of the respiratory tract, the usual site of virus entry. Macrophages are believed to transport virus to secondary sites that include epithelium, mucosa and myocardium. In secondary sites, the virus replicates, then a marked viremia develops and the virus infects epithelium at many other sites. Within a few days vesicles develop, usually at sites of mechanical stress. In swine, common vesicle sites include the snout, mouth, tongue, and especially the feet. In cattle, the FMD virus affects the mammary gland epithelium and virus is shed in milk for a prolonged period. Although unproven, similar shedding may occur in swine.
The lesions of the major vesiculating viral diseases are similar. Vesicles develop in the epidermis, and the epithelium over the vesicle soon sloughs. Enough of the stratum basale is preserved to regenerate the epidermis unless there is secondary infection of the lesions. Secondary infection occurs on the feet of some swine and leads to chronic lameness.
The FMD virus often causes severe myocardial necrosis in neonatal and young pigs. This often leads to sudden deaths from myocardial failure. The mottled myocardial lesions sometimes are referred to as “tiger-heart” lesions and are useful in diagnosis.
Clinical signs
An incubation period of one to five days precedes clinical signs. Lameness is often the first sign noticed. There is an initial acute rise in temperature; slobbering and chomping are common signs. Pregnant sows may abort or deliver stillborn, infected pigs. Sudden deaths may occur in neonatal pigs, sometimes before signs or lesions are apparent in the sow. The early stages of lesions appear as blanched, small foci in the skin on the snout, soft tissues of the feet, and perhaps the teats of lactating sows. By the time signs are readily apparent, there are usually cutaneous vesicles or bullae. Signs develop rapidly and morbidity rapidly increases. Mortality usually is less than 5% but there can be higher mortality in young pigs.
Lesions
Well-developed vesicles and bullae are soon apparent. They are frequently present on the snout, behind the rim of the snout, in the nares, on the tongue and lips, and on the soft tissues of the feet, including the coronary band, the bulbs of the toes and interdigital clefts. Lesions probably are more common on the feet than in the mouth. Less often the lesions are on the vulva, the teats of lactating sows, or the scrotum of boars. Extensive lesions on the coronary band may lead to sloughing of the hoof and lameness. Foot lesions may involve one or more of the feet. Vesicles usually rupture within 24 hours and the superficial epidermis sloughs to reveal hyperemia and hemorrhage on underlying tissue. Uncomplicated lesions usually heal within two weeks. In a virulent form of FMD, young pigs, and sometimes older animals, may have extensive mottled areas of myocardial necrosis on ventricles and in papillary muscles.
Diagnosis
Diagnosis cannot be made reliably on the basis of clinical signs and lesions since they are similar in all the vesicular viral diseases of swine. The state veterinary office should be contacted immediately if an outbreak is suspected. Differential diagnosis of vesicular viral diseases should only be completed in specifically-designated laboratories having specific arrangement to safely handle exotic disease organisms. Plans must be made for collecting and mailing specimens. The Foreign Animal Disease Diagnostic Laboratory (FADDL), Plum Island, NY, often does the diagnostic work.
Diagnostic techniques used include serologic tests to identify FMD virus infection-associated antigen (VIA), complement fixation (CF) and enzyme-linked immunosorbent assay (ELISA) tests to detect FMD viral antigen, virus isolation (VI) and neutralization (VN), electron microscope (EM), and animal inoculation studies. Polymerase chain reaction (PCR) tests have been developed and are frequently utilized. FMD must be differentiated from all other vesicular viral diseases and from other diseases that cause erosive/ulcerative lesions in the oral cavity. Positive diagnoses usually require less time than negative diagnoses. An ELISA is available that can differentiate antibody titers from infected versus vaccinated animals but is not yet officially recognized by many countries.
Control
In the United States, prevention of FMD depends on regulations that govern the importation of animals, animal products, semen, embryos, and on regulations related to the safety of vaccines and other biologic products. There are special regulations on both cooking and dumping of waste food to prevent spread of the virus. Reliance on the vigilance of veterinary practitioners and diagnostic laboratory personnel is important in early detection of outbreaks.
In countries where FMD has not been eradicated, vaccines are used for prevention. The recently developed subunit vaccines have been of value in preventing some types and subtypes of FMD infection but have not provided consistent protection for type O infection, the most prevalent form of FMD. In the event of an outbreak in the United States, vaccine use will be considered but control is anticipated to occur primarily through slaughter of infected animals. The disease will be managed through quarantine, restriction of movement of animals in quarantined areas, slaughter followed by burial or incineration of infected and exposed animals and disinfection of production sites. Eradication is considered to be less costly than living with FMD.
Japanese B Encephalitis
Definition
Japanese B encephalitis is an exotic, mosquito-borne disease affecting many animals, including wild birds, horses, swine and people. In swine, the only evidence of disease may be reproductive failure.
Occurrence
Japanese B encephalitis (JE) occurs in most domestic animals; also in wild birds, reptiles, perhaps chickens, and people. Swine can be infected and all ages are susceptible. Major epidemics have occurred in horses, donkeys and people.
Japanese encephalitis is confined largely to southeastern Asia, Indonesia, and major Pacific islands. At least 20 countries have reported occurrence of the disease. In many locales, epidemics correlate with the mosquito season.
Historical information
Japanese encephalitis was first described in 1933. Major epidemics in people have been reported from Japan, Korea, India and Nepal. The disease has not been reported in the western hemisphere. Abortion in women, and encephalitis in children, have been caused by JE so the virus is recognized as an important zoonosis.
Etiology
The etiologic agent is a single-stranded RNA Flavivirus and is related to West Nile virus. It is unstable in the environment and easily inactivated by many disinfectants. The virus can be grown in many cell culture systems, including cells derived from embryonic or larval mosquito tissues.
Epidemiology
Mosquitoes become infected by feeding on viremic hosts. The virus is then transmitted through the mosquitoes’ saliva when they subsequently feed on uninfected people or animals. The virus is transmitted mainly by mosquitoes of three genera (Aedes, Culex, and Anopheles) and can be transmitted vertically in some species of mosquitoes. Infected mosquitoes feed on a wide range of mammals, birds and reptiles. Infected pigs become viremic and are a major source of virus for mosquitoes. Often there is a correlation between outbreaks in people and the concurrent presence of infected mosquitoes and swine in the region. Other known or suspected reservoirs include snakes, lizards, many wild birds and chickens.
Pathogenesis
Infected pigs remain viremic for several days. On the basis of research largely in other animals, the virus is believed to induce suppressor T-cells to produce a factor that suppresses humoral and cell mediated responses. This makes animals less resistant to infection. In porcine fetuses, the virus often causes the development of anomalies in the brain as well as encephalitis and degenerative neuronal changes.
Transplacental infection in swine sometimes occurs. The effect of the virus depends on whether the fetuses are immunologically competent. When dams are infected between 40-60 days in gestation, fetuses often are killed and some are mummified. There may be no effect on fetuses if they are 85 or more days in gestation. Fetal deaths are believed to be caused by destruction of vital stem cells.
Clinical signs
Mature swine seldom show signs of infection other than those of reproductive failure. Signs may occur in fetuses or piglets if their dam was infected during pregnancy. Signs include stillborn and mummified fetuses or weak pigs that may have signs of central nervous system (CNS) disease. Subcutaneous edema and hydrocephalus may be present in stillborn pigs. Abortions seldom occur. Infected boars may have orchitis, reduced libido and disturbance of spermatogenesis. Young, susceptible pigs occasionally contract JE and show signs of CNS lesions.
Lesions
Gross lesions in stillborn or weak, infected piglets include hydrocephalus, subcutaneous edema, ascites, hydrothorax, hemorrhages on serous membranes, congestion of lymph nodes and necrotic foci in the liver and spleen. Other lesions may include congested meninges, hypoplastic areas in the cerebral cortex, hypoplasia of the cerebellum or spinal hypomyelinogenesis.
Histologically, in infected fetuses or piglets there is diffuse nonsuppurative encephalitis, neuronal degeneration and necrosis in the cerebrum and cerebellum. In mature boars there is excessive fluid in the tunica vaginalis, orchitis, epididymitis, and degenerative changes in seminiferous epithelium.
Diagnosis
A definitive diagnosis is often based on isolation and identification of the virus from fetuses or infected piglets. Virus usually is isolated from brain extracts inoculated into suckling mice or cell cultures. Virus can be identified by neutralization tests in suckling mice or cell culture. Alternatively, viral antigen in tissues from infected fetuses or stillborn pigs can be identified by fluorescent antibody (FA) or avidin-biotin staining using formalin-fixed tissues treated with trypsin. In suspected outbreaks, serial serum samples from pigs sometimes are used to show a rising titer against JE. Serologic tests that reveal antibody in fetuses also are useful in diagnosis.
Control
It may be possible to break the cycle of infection by controlling mosquito populations, but this often is impractical. The disease can be controlled by vaccinating the breeding stock; vaccines are common in parts of Asia. Young gilts and boars are vaccinated twice at two to three week intervals prior to the mosquito season. Growing pigs are also vaccinated in endemic areas.
Porcine Epidemic Diarrhea
Definition
A coronavirus causes this exotic viral diarrhea of swine that closely resembles transmissible gastroenteritis (TGE).
Occurrence
Porcine epidemic diarrhea (PED) occurs only in swine. In previously unexposed herds, all age groups are susceptible. The disease occurs in England, many European countries, China, Taiwan and Korea. Thus far the disease has not occurred in the western hemisphere.
Historical information
In 1971, outbreaks of watery diarrhea in feeder and fattening swine were observed in England. Suckling pigs did not sicken; otherwise, outbreaks closely resembled TGE. In 1976, a similar disease, but also affecting suckling pigs, was observed. Eventually the two diseases were referred to as PED type 1 and PED type 2.
During the 1980s a similar disease with two virulence types was prevalent in many European countries. Also, PED spread to China, Taiwan and Japan. In Europe, outbreaks now are rare, usually affect feeder and fattening pigs, and are not economically important. The disease in Asian countries, however, is highly virulent. Efforts there are under way to develop an oral vaccine for immunization of sows.
Its presence in the US was first confirmed in 2013.
Etiology
A coronavirus causes porcine epidemic diarrhea. The virus is unrelated to porcine coronaviruses that cause TGE, porcine respiratory coronavirus (PRCV) and hemagglutinating encephalomyelitis virus (HEV). It does have some antigenic determinants in common with feline infectious peritonitis virus. The virus can be grown in epithelial cells from the mucosa of the small intestine of hysterectomy-derived piglets and in Vero cells. Porcine epidemic diarrhea virus induces antibodies in swine that can be identified by various laboratory techniques.
Epidemiology
Coronavirus is disseminated in the feces of infected pigs for at least seven days post-inoculation. Fomites and vehicles can also spread virus indirectly. There is little information on the possible existence of carrier swine that could spread virus. On sites where PED is endemic and there is frequent or continuous farrowing, virus is maintained in successive generations of susceptible piglets.
Pathogenesis
The coronavirus of PED, like that of TGE, is in feces and usually is transmitted orally. It replicates primarily in enterocytes on villi of the small intestine, and to a lesser degree in cryptal cells of both small intestine and colon. In the small intestine, it causes degeneration and necrosis of enterocytes. Many enterocytes are destroyed and replaced by cuboidal or flat epithelial cells. Intestinal lesions of PED are similar to those of TGE but develop less rapidly and are less severe. Erosion and ulceration of enterocytes leads to loss of tissue fluid into the lumen and failure of the intestine to absorb adequate fluids. Diarrhea follows and leads to dehydration and depletion of electrolytes.
Clinical signs
The main sign in all age groups is watery diarrhea. The disease closely resembles TGE but spreads more slowly than TGE on a site and among adjacent farms. Infected piglets up to one week old die from dehydration after three to four days. Mortality averages about 50% but usually is lower than that of TGE. Older piglets recover in about one week. In other outbreaks, weaned pigs and older animals are severely affected but younger animals may not sicken and have little or no diarrhea. The severity of disease is quite variable.
Feeders, finishers and adult swine have diarrhea, depression, anorexia, and signs of abdominal pain. Outbreaks often start in these age groups. Morbidity may be high and affected animals are quite sick. Although recovery usually follows, there may be some mortality and occasional sudden deaths.
Lesions
In piglets with PED, there usually are few gross lesions other than dehydration and a distended intestine filled with yellow fluid. In fattening hogs that die suddenly, there may be extensive necrosis of back muscles, a unique lesion. Microscopically, villi in the small intestine of piglets are atrophic. Some villi are fused with adjacent villi or poorly covered with cuboidal to flattened epithelium.
Diagnosis
When all age groups are affected, a firm diagnosis cannot be made on the basis of clinical signs. Signs closely resemble those of TGE although PED spreads more slowly. A diagnosis of PED may be suggested by failure of baby pigs to become ill when adult animals are sick. Necrosis of back muscles in older swine is suggestive.
Diagnosis sometimes can be made after direct immunofluorescence tests on cryostat sections of the small intestine of acutely infected young pigs. The test is both rapid and reliable. It identifies virus or viral antigen in affected epithelial cells. In older, acutely infected animals, an enzyme-linked immunosorbent assay (ELISA) test on feces or intestinal content may be used to detect viral antigen. Direct electron microscope (EM) examination of feces may be helpful in identifying a coronavirus but does not differentiate PED from TGE because the viruses have similar morphology.
Several serologic tests can be used to demonstrate rising antibody titer to PED. Paired serum samples should be taken, the first at the onset of diarrhea and the second no sooner than four weeks later. Antibodies persist for at least one year.
Control
There are no vaccines available. Pregnant sows more than two weeks away from parturition can be intentionally exposed in the face of an outbreak. This can be done by feedback of watery feces or intestinal content from acutely affected pigs. This procedure has the obvious risk of spreading other diseases.
Sanitary and quarantine measures may slow the spread of PED. There is no effective treatment other than good care and the provision of adequate water to combat dehydration.
Vesicular Exanthema of Swine (San Miguel Sea Lion Viral Disease)
Definition
In swine, an acute, contagious disease caused by a Calicivirus and characterized by vesicles on the feet, snout, mucous membranes of the mouth and tongue, and non-haired skin. The disease in sea lions causes vesicles on the flippers.
Occurrence
Of the domestic animals, vesicular exanthema (VE) occurs only in swine. The disease has only occurred in the US; in swine shipped from the United States to Hawaii, and in swine fed raw garbage from a US military post in Iceland. The disease has never been reported from any other country. Vesicular exanthema has not recurred in domestic swine since it was eradicated in 1956.
San Miguel sea lion viral disease (SMSL) occurs in sea lions, fur seals, elephant seals, opal-eye fish and several other marine animals of the western coast of the United States.
Historical information
Beginning in 1932, a vesicular disease, now believed to have been VE, occurred repeatedly in California. The lesions closely resembled those of foot-and-mouth disease (FMD). Outbreaks were contained by slaughtering the infected herds. In 1951, uncooked garbage from a train originating in California was fed to swine in Wyoming. Those swine developed vesicular exanthema. The disease spread throughout many states. Eradication required five years. In 1959, VE was declared to be an exotic disease.
Beginning in 1973, caliciviruses indistinguishable from the virus that causes vesicular exanthema were isolated from sea lions, northern elephant seals, fur seals and certain kinds of fish. Each of the viruses can produce lesions in swine and certain sea mammals.
Etiology
The calicivirus that causes VE and SMSL is believed to be the same. However, spontaneous outbreaks of VE in swine caused by SMSL virus have not been substantiated. Caliciviruses have a cup-shaped morphology from which they are named. The calicivirus that causes VE is sensitive to many common disinfectants including 2% sodium hydroxide.
Antibodies to several other closely related caliciviruses have been detected in both marine and terrestrial animals. The latter include swine, cattle, donkeys, foxes and buffalo. The taxonomy and exact relationship between these various caliciviruses have yet to be agreed upon.
Epidemiology
The opal-eye fish (Girella nigricans) now is believed to be the primary host of the calicivirus that may be passed to pinnipeds and swine. The method of spread of the virus among sea lions and other sea mammals is speculative. It could be through ingestion of infected fish or small marine life, by coastal contamination, or direct contact.
Swine usually are exposed to the VE calicivirus by eating uncooked garbage containing infectious meat scraps from swine or certain fish. Although unproven, some marine origin feed supplements for swine may contain calicivirus. Vesicular exanthema is quite contagious among swine and spreads by direct contact and fomites. Neither long-term carriers nor aerosol spread have been demonstrated.
Pathogenesis
In swine, the VE calicivirus is ingested in uncooked garbage. Virus enters the epithelium through abrasions and multiplies in the basal layer of the epidermis. Intracellular and intercellular edema and coalescence of disintegrating cells leads to vesicle formation. Virus spreads cell to cell as lesions develop. A low-grade viremia occurs and leads to secondary lesions at other sites. Extensive lymphocyte destruction occurs in regional lymph nodes. Since much of the basal layer of epidermis survives, regeneration of epithelium in swine usually occurs within one to two weeks. Lesions in sea lions closely resemble those seen in swine.
Experimentally, it requires much more virus by oral exposure to produce VE than is required by intradermal injection. This suggests that the virus can be spread more readily through abrasions on the skin.
Most swine with VE probably would recover if allowed to do so. However, it is required that they be destroyed as a precaution to prevent the surreptitious entry of foot-and-mouth disease.
Clinical signs, lesions, diagnosis and control
See Foot-and-Mouth Disease and Vesicular Stomatitis. These aspects of the various vesicular viral diseases of swine are similar.
See the table Vesiculating Viral Diseases.