J. A. House and C. A. House

“ Swine may produce up to 108 infectious doses contained in aerosols per day during peak viremia (Sellers et al. 1971) , which is up to 1500 times greater than that produced by cattle (Donaldson and Ferris 1980) . In hot, arid regions, the disease is mainly spread by direct contact, as aerosols cannot travel long distances due to low humidity and high temperatures. Other means of spread include contaminated semen, meat and milk products, and fomites. ”

“ Lesions in local lymph nodes are not extensive, and the virus is not readily isolated from them. Secondary lesions are believed to result exclusively from the spread of the virus from an existing lesion, not by a cellassociated viremia as in most other poxvirus infections. The virus has not been recovered from the blood (Kasza and Griesemer 1962; Shope 1940) , but this may be due to the fact that the SwPV is difficult to isolate, especially when in low concentrations. Viremia must occur, as evidenced by congenital infection in piglets. ”

“ Foot-and-Mouth Disease FMD is considered the most contagious disease of livestock. Essentially all cloven-footed species are susceptible to FMDV. In some texts, the possibility of human infection is stated, but this has yet to be documented. Infected animals shed large quantities of virus into their surroundings for at least 7 days. Aerosol exposure is the major means of spread, particularly in temperate climates, where high humidity and moderate temperatures can favor long-distance airborne spread (Sellers and Parker 1969; Thomson 1994) . ”

“ The SwPV is present in infected epithelium and in dry scabs produced in the later stages of infection. Abraded skin can serve as the route of entry for SwPV. The virus may persist for up to a year in the desiccated form, likely accounting for the persistence of SwP in affected herds.
The morbidity of SwP may approach 100% in young stock up to 4 months of age where poor hygiene occurs. The disease may have a seasonal incidence related to the prevalence of insects. Mortality is usually less than 5%.
CLINICAL SIGNS 23.1. Swine pox lesions on the belly of a pig. ”

“ The epithelium may separate from the stratum basale, leaving a red lesion with shreds of torn epithelium. Vesicular fluid may leak through the stratum corneum without the formation of a true vesicle (Seibold and Sharp 1960) . Since vesicles are most often seen at the site of mechanical stress, they usually rupture quickly, leaving a red erosion. Often, lesions are contaminated with dirt and debris (Fig. 25.2) , resulting in infection with opportunistic bacteria. ”

“ Swine do not develop high levels of neutralizing antibody (Shope 1940; Kasza et al. 1960) , and negative results on the virus neutralization test should not be interpreted as the absence of SwPV infection.
TREATMENT There is no known treatment for SwP, although antibiotics may diminish the complications caused by infection with secondary bacteria. Affected animals should be isolated. Ectoparasites should be controlled by the use of licensed insecticides, and the premises should be aggressively cleaned and disinfected. ”

“ Many SMSVs have been shown to produce vesicular disease in experimentally inoculated swine (Smith et al. 1973; Berry et al. 1990) . Low levels of antibodies to VESVs and SMSVs have been found in terrestrial mammals (feral swine, foxes, buffaloes, donkeys, and cattle) on the west coast of the United States and on Santa Barbara Channel Islands (Smith and Latham 1978) . The relationship of antibodies to natural disease is not clear. The infection of humans with SMSVs is inferred but not corroborated. ”

“ No genetically engineered vaccines for FMD are commercially available, and their practicality is uncertain. Experimentally, genetic sequences for the key immunogenic FMD VP1 were cloned into Escherichia coli, and VP1 was successfully expressed (Kleid et al. 1981) . The cloned protein protected vaccinated cattle and swine against a virulent challenge inoculation. The system was successful with selected subtypes of serotypes A and C, but for serotype O, the cloned proteins did not provide consistent protection. ”

“ Samples from acutely ill swine should include vesicular tissue and, if possible, vesicular fluid from gently washed, active lesions on the tongue, lips, gums, nares, feet, dewclaws, extremities, or teats. Heparinized and clotted blood should be collected for virus isolation and serology, respectively. Clotted blood for serum should be collected from recovered animals. Necropsy samples of tissues for virus isolation should include vesicular lesions and, particularly from newborn or young animals, skeletal muscle and myocardium. ”

“ The VSVs can cause clinical disease or subclinical infections in a wide range of animals, including swine, cattle, horses, and humans.
The origin of outbreaks and means of dissemination of VSV is not thoroughly understood. The ecological distribution of VS is river basins and wooded areas, pointing to insect transmission. Serotypes Indiana 1 and NJ have been isolated from sand flies (Lutzomyia shannoni) , and transovarial transmission was demonstrated (Tesh et al. 1971; Comer et al. 1990) . Sand flies infected with VSV NJ transmitted the virus to suckling mice (Comer et al. 1990) . ”

“ Viral nucleic acid, as detected by in situ hybridization, was widespread in epithelial tissues of cattle only 6 hours after aerosol exposures (Brown et al. 1992) . In swine following intradermal inoculation in the snout, widespread FMDV nucleic acid was detected by in situ hybridization on the first sampling 24 hours after infection (Brown et al. 1995) . Langerhans cells may be the primary means of this rapid distribution of virus. ”

“ Electron micrograph of an epidermal cell with cytoplasmic degeneration and numerous poxvirus particles (V) ; a second cell has marginated chromatin (MC) and a filamentous matrix (F) in the nucleus, which corresponds to the central nuclear clearing seen histologically. Insert shows typical poxvirus particles. ”

“ Swine Vesicular Disease SVD is a moderately contagious disease of swine. Mice may be infected experimentally. Persons working with or around infected pigs can harbor SVDV in their nasal passages (Sellers and Herniman 1974) , and human infection has been observed (Brown et al. 1976) . Swine vesicular disease virus is spread primarily by contact with infected swine or by garbage feeding of SVDV-contaminated meat products. Fecal transmission is not common (Chu et al. 1979; Mann and Hutchings 1980) , which is unusual for an enterovirus. ”

“ A fever, which persists for up to 5 days, essentially coincides with the development of a cell-free viremia and vesicular lesions. The peak viremia occurs 2-4 days postexposure and persists for about 7 days. The virus persists for at least 7 days in the tissues of the snout, tongue, coronary band, tonsil, cardiac muscle, and central nervous system. The stratum spinosum is the primary site of viral replication in the epithelium. A nonsuppurative meningoencephalitis most frequently occurs in the cerebrum, thalamus, brain stem, and olfactory lobes. ”

“ Vesicular Exanthema of Swine and San Miguel Sea Lion Viruses VES is a moderately contagious disease. Under certain management situations_namely, the feeding of infected seal meat or contaminated garbage_swine were the only livestock to show clinical VES. Marine animals (fish, sea lions, fur seals, elephant seals, etc.) along the Pacific coast from California to Alaska and likely along the coast of northeastern Russia are apparently the natural hosts of the numerous serotypes of VESVs and SMSVs. ”

“ Serum samples may be tested for precipitating antibodies to the FMD VIAA, for neutralizing antibodies to FMDVs, SVDV, VESVs, and VSVs, and for CF antibodies to VSVs, with results available in 1-3 days. Virus-neutralizing antibodies are serotype-specific for FMDV, and animals infected for the first time characteristically develop the highest titer against the homologous subtype. Antibodies to FMD VIAA were used historically to differentiate the immune response to active infection from that of vaccination. ”

“ The disease primarily affects horses and cattle, with an occasional spillover to swine. The 1982-83 VS NJ epizootic persisted into winter, causing speculation that VS may be altering its epidemiological pattern. Movement of infected animals extended the scope of this outbreak to Idaho and California. The 1995 outbreak of VS NJ was typical, being confined to western states and disappearing with the onset of cold weather. ”

“ In some cattle, however, the virus may be shed in the milk for up to 7 weeks, even in the presence of neutralizing antibodies in the serum (Burrows et al. 1971) . Similar patterns of virus shedding in milk probably occur in swine. The virus is found in large quantities in oral and respiratory secretions 2-7 days postexposure. In young animals severe myocardial necrosis may occur.
Swine Vesicular Disease Lesions are evident 3-11 days after eating contaminated food (McKercher and Graves 1981) and as early as 2-4 days after experimental inoculation (Burrows et al. 1973; Lai et al. 1979) . ”

“ Low mortality (<5%) is usually seen with vesicular diseases. In young animals infected with FMDV or SVDV, myocardial necrosis may occur and mortality may reach 50–100%. There have been occasional reports of specific FMD isolates causing high mortality in mature animals. ”

“ Foot-andmouth disease virus particles contain replicase protein 3D. Proc Natl Acad Sci USA 91:733-737.
Patterson, W. C.; Jenny, E. W; and Holbrook, A. A. 1955. Experimental infections with vesicular stomatitis in swine. I. Transmission by direct contact and feeding infected meat scraps. In Proc 59th Annu Meet US Livest Sanit Assoc, pp. 368-378. Pereira, H. G. 1977. Subtyping of foot-and-mouth disease virus. In Developments in Biological Standardization. Ed. ”

“ Rapid and sensitive detection of foot-andmouth disease virus in tissues by enzymatic RNA amplification of the polymerase gene. J Virol Methods 34:161-172.
Meyer, R. F.; Babcock, G. D.; Newman, J. F. E.; Burrage, T. G.; Toohey, K.; Lubroth, J.; and Brown, F. 1997. Baculovirus expressed 2C of foot-and-mouth disease virus has the potential for differentiating convalescent from vaccinated animals. J Virol Meth, in press. Montgomery, J. F.; Oliver, R. E.; and Poole, W. S. H. 1987. A vesiculo-bullous disease in pigs resembling foot-andmouth disease. I. Field cases. ”

“ Barlough, J. E.; Berry, E. S.; Smith, A. W.; and Skilling, D. E. 1987. Prevalence and distribution of serum neutralizing antibodies to Tillamook (bovine) calicivirus in selected populations of marine mammals. J Wildl Dis 23:45-51.
Beck, E., and Strohmaier, K. 1987. Subtyping of European foot-and-mouth disease virus strains by nucleotide sequence determination. J Virol 61:1621-1629.
Berry, E. S.; Skilling, B. S.; Barlough, J. E.; Vedros, N. A.; Gage, L. J.; and Smith, A. W. 1990. New marine calicivirus serotype infective for swine. ”