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Bruce Watt (Central Tablelands Local Land Services, Bathurst) and Colin Scrivener (Veterinary Consultant, Charles Sturt University, Wagga Wagga)

This paper was previously published in Skirting the Issues, The Official Newsletter of the Australian Sheep Veterinarians, Autumn 2014, pp 6-9.
Posted Flock & Herd June 2015


Capripoxvirus genus viruses generally cause host specific infections in sheep (sheep pox), goats (goat pox) and cattle (lumpy skin disease). However, some isolates infect both sheep and goats. Sheep and goat pox (SGP) infections cause high morbidity and mortality disease outbreaks although this depends on the strain of virus and host susceptibility (Bhanuprakash et al 2006). Animals that have recovered from infection with any one strain of SGP are resistant to infection with any other strain (Capstick 1961). Sheep and goat strains appear to lack the genes necessary to enable them to infect cattle (Tulman et al 2002).

Capripoxvirus infection is regarded as the most serious pox virus infection of livestock and, along with classical swine fever and foot and mouth diseases, was assessed as having a ‘high likelihood of entry and establishment in Australia with serious socioeconomic consequences on a livestock industry and/or the national economy’ (Geering 1990). 


SGP is highly contagious, spreading by aerosol from infected animals, from contact with the virus in the environment and from arthropod vectors, primarily biting flies. The virus can survive in a sheltered environment for six months and survives drying, freezing and thawing but succumbs to an hour of 600 heat, extremes of pH and 1% formalin (Radostits et al 2007). It usually spreads when infected stock migrate or are transported to a naïve area. However the traditional but hazardous practice of inoculating sheep with a suspension of infected scab material (ovination) is also implicated in the spread of the virus in many countries including India and Egypt (Bhanuprakash et al 2006).

Outbreaks occur regularly in north and central Africa, southwest Asia (including China) and the Indian subcontinent, the Middle East and southern Europe. Historically, a series of outbreaks occurred in Britain from 1847 to 1866 when the disease was eradicated (Bhanuprakash et al 2006).

It has been claimed that sheep breeds vary widely in their susceptibility to sheep pox and that young sheep and Merinos and some British breeds of sheep are more susceptible than native breeds (Bhanuprakash et al 2006). 


After an incubation period cited as from 4-8 days (Bhanuprakash et al 2006) to 12-14 days (Radostits et al 2007) affected sheep develop a fever, respiratory signs, lacrimation, a nasal discharge and 1-2 days later, skin lesions especially on the less woolled parts of the body, most notably the face, groin, axilla and perineum. The skin lesions follow a typical pox virus development from a macule to papule.  The ruptured lesions often form a hard, black, scab. These skin lesions render infected sheep prone to flystrike and the scabs may persist for several weeks. Kitching (2007) considered that the clinical signs of severe sheep pox are pathognomic. However, highly susceptible breeds and highly susceptible age groups such as young sheep and naive animals may die during the septicaemic stage before skin lesions develop.  Lung and abdominal lesions if present at necropsy are also pathognomic.

It has been claimed that adult sheep of more resistant breeds may develop a benign form of the disease, characterised by skin lesions under the tail and elsewhere, without septicaemia and with recovery in 3-4 weeks (Bhanuprakash et al 2006, Kitching 2007, and Radostits et al 2007). However, ‘resistant’ breeds or sheep may simply have a background of circulating virus in the population with a cycle that involved early lamb infection when the lamb has a high level of passive (antibody) immunity from colostrum. 


It has been assumed that an outbreak of SGP in Australia would be suspected when veterinarians are presented with sheep or goats with characteristic skin and mucosal lesions. However, as Australia’s sheep and goat population is naïve, it is likely that the first signs would be an outbreak of high morbidity, high mortality disease from the ‘malignant’ or ‘septicaemic’ form of the disease, with death occurring before skin lesions have developed.  

Peracute SGP would resemble anthrax with sudden death with few clinical signs. The main necropsy findings would suggest a septicaemic death including wet, hyperaemic lungs with pathognomic pox lesions. 

Less acute cases would present with an oedematous face, swollen, drooping ears, a muco-purulent nasal exudate and typical pox lesions –slightly raised 1-2cm irregular plaques - on the bare skin areas.

At necropsy, affected sheep would show widely dispersed discrete, generally circular, slightly raised, firm 1-2 cm papules on the lung surface, occasionally in the mucosa of the rumen and abomasum and rarely, small (2-5 mm) lesions in the renal cortex and liver. Kitching (2007) commented that ‘the large number of hard, pale, sometimes haemorrhagic lesions found throughout the lobes of the lung are usually the most obvious and the most likely cause of death.’ (See Figures 1 and 2).  In the experience of one author (CS) however, lung lesions are firm to soft rather than hard.   

Sheep recovering from the systemic disease or from a more benign form of the disease may exhibit mild skin lesions that could be mistaken for orf, photosensitisation or Dermatophilus.

Image of sheep lungs <em>post-mortem</em> with lesions
Figure 1. Lung of sheep pox case (photograph Colin Scrivener)
Image of sheep lungs <em>post-mortem</em> with lesions
Figure 2. Lung of sheep pox case with concurrent apical pneumonia (photograph Colin Scrivener)
Image of sheep rumen with lesions <em>post-mortem</em>
Figure 3. Pox lesions in the omentum and wall of the rumen (photograph Colin Scrivener)
Image of sheep abomasum lining with lesions <em>post-mortem</em>
Figure 4. Sheep pox lesions in the wall of the abomasum (photograph Colin Scrivener)
Image of sheep kidney with lesions <em>post-mortem</em>
Figure 5. Sheep pox lesions in the renal cortex (photograph Colin Scrivener)
Image of sheep rumen wall with lesions <em>post-mortem</em>
Figure 6. Pox lesions in rumen wall (photograph Colin Scrivener)


Indian reports of Capripoxvirus causing papular skin lesions in man (Geering and Forman 1987) have been discounted. Kitching (2007) stated that ‘Capripoxvirus does not infect people.’ 


A presumptive diagnosis of sheep or goat pox would be made on the basis of a contagious disease of high morbidity and mortality in sheep and/or goats, in less acute cases accompanied by pox type lesions on the skin and digestive and respiratory mucosa. 

The diagnosis would be supported most rapidly by electron microscopy (1-2 hours after samples were received in an appropriate laboratory) and confirmed by identifying the virus or viral DNA in tissue samples by PCR technology. The histopathological picture of extensive inflammatory, proliferative and necrotic changes accompanied by intracytoplasmic inclusion bodies and infiltrating epithelioid cells (Borrel cells), is also diagnostic. 

While serological testing would be used in surveillance during and after an outbreak, there are no good serological tests for SGP. Serum neutralisation, the test of choice has a low sensitivity as immunity to Capripoxvirus is largely cell mediated (AUSVETPLAN 2011).


In 1990, Geering 1990 suggested that “the introduction of sheep pox into Australia would have very serious socio-economic consequences, which may even approach or be on a par with those of FMD.” Given that sheep pox only affects sheep and goats while FMD affects all cloven hoofed animals, this claim seems exaggerated but the point remains that SGP represents a serious threat to Australia’s livestock industries and economy.

Unlike classical swine fever and FMD, sheep pox has not been recorded in Australia (Geering and Forman 1987). Bhanuprakash et al (2006) erroneously cited Garner and Lack’s 1995 paper describing predictions (from computer modelling) of the impact of exotic diseases, including SGP, on regional Australia as a report of its occurrence in Australia.

While Australia’s prohibition of the importation of live sheep and goats is an important step in excluding the disease it could be imported on contaminated material such as clothing.  The 2011 version of AUSTVETPLAN comments ‘there is considerable risk of introduction of sheep pox to Australia on fomites (such as in sheep vessels returning from the Middle East), and on clothing, equipment and unprocessed wool products brought in by people from endemic areas.’

Should Capripoxvirus enter Australia it is likely to infect both sheep and goats. ‘An uncontrolled outbreak of SGP in Australia would cause serious stock losses in the sheep and goat industries, and an epizootic would have the potential to cause continuing economic loss (AUSTVETPLAN 2011).’ Cattle are unlikely to be involved in an outbreak of SGP in Australia. Early in an outbreak of a pathogenic strain of SGP the differential diagnosis would include anthrax. In less acute cases the differential diagnosis would include orf, photosensitisation and Dermatophilus infection.

The strategy for the control of SGP in Australia, as outlined in AUSVETPLAN (2011), is to eradicate the virus in the shortest time possible. SGP are Category 2 diseases under the Emergency Disease Response Agreement meaning that 80% of costs are borne by government and 20% by industry. The eradication strategy would involve the slaughter of infected livestock, decontamination of infected premises and tracing and surveillance. 

As mentioned, Garner and Lack (1995) modelled the impact of foot and mouth disease, classical swine fever and sheep pox on regional Australia. They argued that while each of these diseases would have a substantial impact on Australia’s livestock and economy, that impact could be reduced if it could be demonstrated to Australia’s trading partners that the disease was contained to a region. They estimated that a severe outbreak of sheep pox in northern NSW for example might last for 19 weeks, with 49 infected properties, 204 restricted area premises and 120,942 sheep and goats slaughtered.


Two, highly effective, modified live virus vaccines are available in the Middle East that give long term protection and a killed vaccine is available that requires an annual booster. 


The authors would like to thank Deborah Finlaison for her constructive comments.


  1. AUSVETPLAN Disease Strategy, Sheep pox and goat pox Version 3.1, 2011, available on the internet at: www.animalhealthaustralia.com.au  (accessed 31 January 2014)
  2. Bhanuprakash V, Indrani BK, Horseman M and Singh RK (2006). The current status of sheep pox disease. Comparative Immunology, Microbiology and Infectious Diseases, 29, pp 27-60
  3. Capstick PB (1961). Annual Report, Kenya Veterinary department, Kenya 45-47, cited in AUSVETPLAN Disease Strategy, Sheep pox and goat pox Version 3.1, 2011
  4. Garner MG and Lack MB (1995) Modelling the potential impact of exotic diseases on regional Australia. Aust Vet J 72: 81 - 87
  5. Geering WA and Forman AJ (1987) Exotic Diseases, Australian Government
  6. Publishing Service, Canberra (Animal Health in Australia vol 9), p 111
  7. Geering WAG (1990). A Qualitative Assessment of Current Erotic Disease
  8. Risks for Australia Bureau of Rural Resources Discussion Paper, Canberra
  9. Kitching RP (2007). Chapter 43, Sheep pox, in Diseases of Sheep, fourth edition, edited by ID Aitken, pp 302-306.
  10. Radostits 2007
  11. Tulman et al (2002). The genomes of sheeppox and goatpox viruses. Journal of Virology 76: 6054-6061, cited by AUSVETPLAN Disease Strategy, Sheep pox and goat pox Version 3.1, 2011


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