Current authors:
S L BABIUK - Research Scientist, PhD, National Centre for Foreign Animal Disease,  Canadian Food Inspection Agency, 1015 Arlington Street, Winnipeg, Manitoba, R3E 3MA, Canada
J A W COETZER - Professor Emeritus, BVSc, BVSc (Hons), M Med Vet (Path), Faculty of Veterinary Science, University of Pretoria, Private Bag X04, Onderstepoort, Gauteng, 0110, South Africa
D B WALLACE - Senior Researcher, PhD, Agricultural Research Council, Onderstepoort Veterinary Research, 100 Old Soutpan Road, Gauteng, 0110, South Africa

A General Introduction has been added to each disease chapter in an attempt to give a brief updated overview of the taxonomic, biological and other characteristics of the virus family or group of bacteria /protozoa that cause disease in livestock and, where relevant, involve wildlife. As the text of the three-volume book Infectious Diseases of Livestock is currently under revision the Editors are aware that there are inconsistencies between the updated introductions to chapters and the content of the chapters themselves. Once the chapters have been updated – a process that is currently underway – these inconsistencies will be removed.

Poxviruses are classified in the family Poxviridae, which is divided into two subfamilies: Chordopoxvirinae, which infect vertebrates; and Entomopoxvirinae, infecting insects.

The poxviruses of vertebrates are grouped into ten genera which have been accepted by the International Committee for the Taxonomy of Viruses. There is one currently unassigned virus (squirrelpox) (see Table 1).

Poxvirus infections in domestic animals are, with a few important exceptions, generally of limited economic importance. The exceptions are lumpy skin disease in cattle, and sheep-and goatpox, and orf in sheep and goats. Camelpox may also cause severe losses in regions where dromedary camels (Camelus dromedarius) are important.

In Latin documents from the first and second centuries AD, a disease of sheep, which could have been sheeppox, is mentioned. However, reports from the seventeenth and eighteenth centuries describe an infectious disease of sheep, which was clearly sheeppox. Cowpox was presumably a common disease of cattle in England at the end of the eighteenth century when Jenner exploited the observation that milkmaids were resistant to the effects of smallpox by transferring ‘matter’ from lesions of milkmaids with cowpox to other individuals in order to immunize them against smallpox. This led to smallpox vaccination and initiated the science of immunology.

The poxviruses were the first virological agents for which criteria other than clinical signs could be applied to the diagnosis of the diseases they cause. By the end of the nineteenth century ‘elementary bodies’ (= virions) were seen by microscopic examination of stained smears, and cytoplasmic inclusion bodies, characteristic of poxviruses, could be demonstrated. Definite aetiological diagnoses became possible between 1930 and 1964 with the introduction of embryonated egg and cell culture techniques for growing viruses, as well as transmission electron microscopy for their morphological demonstration.4

Studies with mousepox (ectromelia) led to an explanation of the pathogenesis of generalized exanthematous viral diseases. The importance of cell-mediated immunity in recovery from viral infections was also demonstrated with this model.4

General characteristics of poxviruses

The characteristic size and morphology of poxviruses are traits often used for routine diagnosis by transmission electron microscopy (see Figure 1 in Lumpy skin disease, and Figure 1 in Orf). They are the largest and most complex viruses, brick-shaped and typically measure about 300 × 260 nm, although considerable variation exists. Parapox virions (see Figure 1 in Orf) are ovoid and smaller (approximately 300 × 170 nm in size). Mature virions are enveloped. Negative-staining shows that, within an outer double membrane, tubular protein ‘filaments’ are irregularly located on the surface of all poxviruses (see Figure 1 in Lumpy skin disease), except parapoxviruses which have a continuous regular arrangement, giving the false impression of a double helix (see Figure 1 in Orf). Two ‘lateral bodies’ are enclosed between this sheet of filaments and a second double membrane. A biconcave core in the form of a folded coil (‘triplet’), which contains the virus genome, is situated within a protein matrix in the centre of the virion (see Figure 2 in Lumpy skin disease).2, 12, 13

Chemically, poxviruses contain about four per cent lipids, three per cent carbohydrates and five per cent DNA. The genome is a double-stranded linear molecule with covalently cross-linked ends and has terminal inverted repeat sequences, an arrangement which bears a surprising similarity to the genome of African swine fever virus (an asfivirus). The molecular weight varies from about 85 × 106 Daltons in parapoxviruses to 240 × 106 Daltons in avipoxviruses. The G + C content is between 30 and 40 per cent, except for the parapoxviruses in which it is over 60 per cent.17 The general arrangement of genes within poxvirus genomes is similar between genera, with those genes coding for proteins involved in virion structure, replication, transcription etc. (“housekeeping” genes) clustering within the more conserved central region, while genes involved in host-range, pathogenicity, host immunomodulation etc. occur towards the less conserved termini.8

Restriction endonuclease analysis has been used extensively for the classification of poxviruses.6, 9, 14 Advances in genome sequencing confirmed the initial classification of poxviruses and have improved classification and knowledge of their genomes.

Virions contain more than 100 different polypeptides which account for about two-thirds of the theoretical coding capacity of the genome with variability in the number of coding genes between poxviruses. Several enzymes essential for establishing a DNA replication focus in the cytoplasm of infected cells are contained in the virion.

Although each genus is serologically distinct, the members of each share the majority of their antigens and usually show cross-neutralization. There are also antigenic differences between intracellular virus, which can be liberated by disrupting infected cells, and extracellular virus liberated into the medium by infected cells.

Orthopoxviruses can be distinguished from viruses in other poxvirus genera due to their coding for an immunologically-specific lipoprotein, haemagglutinin, separable from the virion, which agglutinates the erythrocytes of some avian species.

Genetic recombination has been demonstrated between members of different poxvirus genera; and genes from other organisms can be incorporated into poxvirus genomes by the method of in vivo recombination if they are presented with suitable homologous flanking sequences. Such ‘foreign’ genes can be expressed during infection and they present the possibility of constructing poxvirus-vectored recombinant vaccines which will protect against other diseases. Much progress has been made in this field over the past 30 years, especially against diseases of veterinary importance.1, 3, 14, 15 A number have been commercialised e.g. RABORAL V-RG is an oral bait using vaccinia virus as vector to control rabies in wildlife and RECOMBITEK Influenza is a canarypoxvirus-vectored vaccine providing immunity against equine influenza.11, 15

Poxviruses show a largely uniform reaction to physical and chemical influences. Some poxvirus species (e.g. cowpox) are resistant to ether, others (e.g. sheeppox) are partially ether-sensitive, but all are sensitive to chloroform. Inactivation is achieved by heating to 56 °C for 30 minutes. Higher temperatures and ultraviolet rays (245 nm wave length) are effective within a few minutes, but under natural conditions poxviruses are inactivated quite slowly. For example, the infectivity of dried material from lesions is stable for months even under unfavourable environmental conditions.

Sodium hydroxide (1 per cent), formalin (2 per cent) and quaternary ammonium compounds (0.5 per cent) are examples of effective disinfectants under field conditions.10

Pathogenesis and pathology

Animals may become infected with poxviruses through small abrasions of the skin (e.g. orf), by aerosol infection of the respiratory tract (e.g. sheep- and goatpox), or possibly by mechanical transmission by biting arthropods (e.g. lumpy skin disease and swinepox).5

Generally, poxviruses are epitheliotropic and may cause localized cutaneous (e.g. orf and pseudocowpox) or systemic disease (lumpy skin disease and sheeppox) involving the skin as well as many organs and tissues.

In both localized and systemic poxvirus diseases, initial multiplication of the virus occurs at the site of entry into the body. In those infections that are characterized by systemic disease, further viral multiplication in the draining lymph node(s) is followed by a primary viraemia and multiplication (and consequently amplification) of virus in many organs or tissues including the liver, spleen and lungs. This results in a secondary viraemia and subsequent infection and development of disseminated focal lesions in the skin.5

Classical lesions in the skin start as erythematous macules, which develop sequentially into papules and vesicles. In sheeppox the vesicular stage does not generally occur, papules changing directly into necrotic scabs, while in orf it is inconspicuous and transient or absent. Vesicles give rise to pustules with depressed centres and raised erythematous borders, the so-called pock. After the pustules have ruptured, they become covered by a crust, and, depending on the severity of the lesion, healing may either be complete or leave a scar. In contrast to the sequential development of skin lesions, mucosal lesions are briefly vesicular before ulcers are formed.7

Microscopically, pox lesions are characterized initially by swelling, vacuolation and ballooning of keratinocytes, particularly in the stratum spinosum of the epidermis. Rupture of these cells leads to the formation of vesicles. Marked hyperplasia of epithelial cells surrounding pustules contributes to the raised borders of umbilicated pustules.

Oedema, perivascular mononuclear cell (lymphocytes, macrophages) infiltrations, and variable numbers of neutrophils and eosinophils are often present in the dermis. In lumpy skin disease and sheep- and goatpox, vasculitis, sometimes accompanied by thrombosis, in the dermis may lead to ischaemic necrosis of the affected parts of the skin.7

Viral multiplication occurs in the cytoplasm of cells, where single or multiple inclusion bodies of varying size are formed. Acidophilic (A-type) inclusions are accumulations of viral protein and may or may not contain viral particles, whereas the basophilic (B-type) inclusions produced by all poxviruses are sites of viral synthesis and are the so-called viral factories.5 Some mature virus particles move to the Golgi complex to acquire an envelope before release from the cell. However, most are released by cell disruption and are not enveloped. Both enveloped and non-enveloped particles are infectious with enveloped viruses better suited to spread from the primary site of replication.5

Table 1 Important poxviruses of vertebrates (Chordopoxvirinae). Current classification of Chordopoxvirinae into genus, prototype virus and other members by the International Committee for the Taxonomy of Viruses





Sheeppox virus

Goatpox virus

Lumpy skin disease virus


Orf virus

Bovine papular stomatitis virus

Pseudocowpox virus (paravaccinia)

Sealpox virus


Swinepox virus


Vaccinia virus

Cowpox virus

Camelpox virus

Buffalopox virus

Monkeypox virus

Mousepox (ectromelia) virus

Raccoonpox virus

Uasin Gishu disease virus

Taterapox virus


Myxoma virus

Rabbit fibroma virus

Squirrel fibroma virus


Fowlpox virus

Canarypox virus

Pigeonpox virus

Turkeypox virus

Parrotpox virus and others


Yaba monkey tumour virus

Tanapox virus


Molluscum contagiosum virus


Mule deerpox virus


Nile crocodilepox virus


Squirrelpox virus


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