Vesicular Exanthema - Pig

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Also Known As: VES — Calicivirus infection — San Miguel Sea Lion Disease

Caused By: Calicivirus — San Miguel Sea Lion Virus — SMSV

This disease was eradicated globally in swine in 1959.


Vesicular Exanthema of Swine (VES) was a viral disease that affected pigs in America from 1932-1959, causing a similar presentation to that of the notifiable Foot and Mouth Disease and massive economic losses. The disease only ever occurred in the USA, originating from California, and is now eradicated. The pathogens involved were caliciviruses.

Related viruses are now isolated from marine mammal species along the USA’s pacific coast, now dubbed San Miguel Sea Lion Virus (SMSV) and are still capable of causing vesicular disease in swine under experimental conditions.[1]

There was only ever one case of VES in a human and it was acquired during laboratory work, rather than from an infected animal.


California was the origin of infection, which then spread across the USA.

Transmission of the virus was initially mainly due to the feeding of raw pork scraps to pigs. This was banned in the USA in 1956 and the virus was eradicated by 1959. The virus was also spread by direct contact with infected swine.

The only report of VES outside of the USA was in Iceland and no further incidence was ever reported. This incident was also linked to pigs fed raw garbage containing pork.

SMSV occurs along the USA’s pacific coast. It is unknown whether the range and movement of affected species has extended its reach to Russia and Japan but it is possible.


VES was only ever seen in pigs and its restricted host range was one of its distinguishing factors from FMD.

SMSV has a much broader host range and has now been isolated from a range of marine mammal species including pinnipeds and cetaceans. Other indistinguishable viruses from SMSV have been reported in reptiles[2], cattle[3], primates[4] and skunks[5].

Clinical Signs

Vesicular lesions in the oral cavity, snout and on the soles, coronary bands and interdigital areas of the feet were the hallmark of disease in all species affected by these caliciviruses.

The oral lesions caused excessive salivation, tongue protrusion, dysphagia and anorexia due to reduced food intake. Nasal lesions may have caused airway obstruction and associated signs. Once ruptured, the vesicles formed blisters, tears or erosions. Diarrhoea was also seen. Lesions on the limbs were usually at the coronary band and caused swelling, inflammation and lameness.

Pyrexia was a consistent feature in infected pigs.

Abortion also occurs in infected female sea lions.


Differentiation from Vesicular Stomatitis Virus, Swine Vesicular Disease and Foot and Mouth Disease was imperative.

Innoculation could be used as a method of differentiation but was time-consuming and innoculum supply was inconsistent. Thus, serological methods took over. Serum neutralisation, complement fixation and agar gel precipitation were all used. PCR is also now available.

Histopathology of lesions revealed squamous epithelial swelling, pyknosis and karryorhexis. As cells died, the virus spread to neighbouring cells. Epithelial cells that were left intact usually showed evidence of degeneration and intracellular oedema. Haemorrhage and oedema were also seen in the subcutaneous tissues. The malphigian layer of the dermis where the virus primarily replicated became infiltrated with neutrophils and was thus weakened and oedematous, causing the upward displacement of the epidermis above it and thus the characteristic vesicle.

Local lymph nodes showed extensive destruction of lymphocytes with congestion and oedema. Viral replication also occurred here and thus virus was readily isolated from these sites.


There was no treatment for VES but the disease ran its course in 10-14 days and mortalities were low. Palliative care aided and sped up recovery and antibiotics were useful against secondary infections of lesions.


The ban on feeding raw pork garbage to pigs and quarantine protocols were the key features of the successful VES eradication program in the USA.

Monitoring of SMSV in wild populations will be valuable and precautionary.

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  1. Smith, A. W., Akers, T. G., Madin, S. H., Vedros, N. A (1973) San Miguel sea lion virus isolation, preliminary characterization and relationship to vesicular exanthema of swine virus. Nature, 244:108-110
  2. Smith, A. W., Anderson, M. P., Skilling, D. E., Barlough, J. E., Ensley, P. K (1986) First isolation of calicivirus from reptiles and amphibians. American Journal of Veterinary Research, 47(8):1718-1721; 37
  3. Smith, A. W., Mattson, D. E., Skilling, D. E., Schmitz, J. A (1983) Isolation and partial characterization of a calicivirus from calves. American Journal of Veterinary Research, 44(5):851-855
  4. Smith, A. W., Skilling, D. E., Benirschke, K (1985) Calicivirus isolation from three species of primates: an incidental finding. American Journal of Veterinary Research, 46(10):2197-2199; 28
  5. Seal, B. S., Lutze-Wallace, C., Kreutz, L. C., Sapp, T., Dulac, G. C., Neill, J. D (1995) Isolation of caliciviruses from skunks that are antigenically and genotypically related to San Miguel sea lion virus. Virus Research, 37(1):1-12; 57


This article was originally sourced from The Animal Health & Production Compendium (AHPC) published online by CABI during the OVAL Project.

The datasheet was accessed on 20 July 2011.

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