Bovine Papillomavirus (BPV) is a group of DNA viruses of the family Papillomaviridae. The virus is known to induce Papillomas of cutaneous or mucosal epithelia in cattle. Infection from BPV is the known cause of warts (Papillomas and Fibropapillomas) of the skin and alimentary tract, and more rarely cancers of the alimentary tract and urinary bladder in cattle. Infections are also thought to cause the skin tumor Equine Sarcoid in horses, donkeys and other animals.

Warts located on the genitalia or in the genital area of a cow or bull require immediate treatment for breeding animals as they may be torn or broken during the mating process. This will result in reluctance to breed, susceptibility to bacterial infection of the open wound and can be painful for the animal.

The significance of infection in cattle or Equine Sarcoid skin tumor in horses and other animals is dependent on the purpose or use of the animal. For dairy cattle, warts on their teats may interfere with milking and may result in a degree of discomfort during the milking process. This can lead to reluctance to enter the milking parlor and/or a decrease in milk volume due to stress in the animals. Bovine Papillomavirus can also affect beef cattle. Beef cattle with teat warts may be resistant to allowing their calf to nurse, which can result in reduced growth rates and increase incidence of mastitis. For show animals, (i.e., horses) warts present during a competition can result in lower grades or scores for the animal.

Types of BPV:

Six types of BPV have been characterized, BPV-1 to BPV-6, which are divided into three broad subgroups.

• Deltapapillomavirus or Fibropapillomaviruses (formerly known as subgroup A), including types 1 and 2, have a genome of around 7.9 kb. Similar Papillomaviruses of ungulates (eg deer Papillomavirus, European elk Papillomavirus, Bovine Papillomavirus 1,2) are also found in this group. Like all members of the Papillomavirus class, these viruses infect only Keratinocytes (epithelial cells); however, unlike other Papillomaviruses, they cause proliferation of both Keratinocytes and fibroblasts, causing benign Fibropapillomas involving both the epithelium and the underlying dermis. The specificity of the types differs:
  • BPV-1 infects para genital areas, including penis, teats and udders
  • BPV-2 infects skin, alimentary canal and urinary bladder
• Xipapillomavirus or Epitheliotropic BPV (formerly known as subgroup B), including types 3, 4 and 6, have a smaller genome of around 7.3 kb and are unique among papillomaviruses in lacking the E6 oncoprotein. They infect keratinocytes (epithelial cells), causing pure Papillomas involving only the epithelium. The specificity of the types differs:
  • BPV-3 infects skin
  • BPV-4 infects the upper alimentary tract
  • BPV-6 infects teats and udders

• Epsilonpapillomavirus has the single member BPV-5, with features intermediate between the other two groups. BPV-5 infects teats and udders, and can cause both pure Papillomas and Fibropapillomas.

  A further thirteen putative BPVs have recently been identified; the novel viruses have yet to be assigned to subgroups.

Infection from BPV is the known cause of warts (Papillomas and Fibropapillomas) of the skin and alimentary tract, and more rarely cancers of the alimentary tract and urinary bladder in cattle. Infections are also thought to cause the skin tumor Equine Sarcoid in horses and donkeys, mules, zebras, and przewalksi horse and other animals.

In cattle, warts commonly are found on the head, neck, and shoulders, and occasionally on the back and abdomen. The extent and duration of the lesions depend on the type of virus, area affected, and degree of susceptibility. Warts appear approximately 2 months after exposure and may last for more than a year. Papillomatosis becomes a herd problem when a large group of young, susceptible cattle become infected. Immunity usually develops 3-4 weeks after initial infection, but Papillomatosis occasionally recurs, probably due to loss of immunity.

In horses, small, scattered Papillomas develop on the nose, lips, eyelids, distal legs, penis, vulva, mammary glands, and inner surfaces of the pinnae, often secondary to mild abrasions. They can be a herd problem, especially when young horses are kept together, but regress in a few months, as a foal’s immune system matures. When they develop in older horses, they often persist for more than a year. So-called aural plaques are also thought to be a flat form of Papilloma (Verruca Planum). Equine Papillomas are disfiguring but benign. They need to be distinguished from Verrucous Equine Sarcoid.

• It is wise to keep cattle with warts away from any horses that are also on the property, as prevention against the possibility of Sarcoid development.
• Bovine Papillomavirus is generally fought off by the immune system of cattle and the warts will spontaneously disappear in about 5-6 months without any treatment, but may last for more than a year. If warts are to be treated, surgical removal is generally the best option. This may be followed by the application of liquid nitrogen to ensure that all wart tissue has been killed from the site – this is a method known as cryosurgery.
• Horses who present symptoms of infection by the BPV, (the presence of even one lesion,) are by definition genetically liable to the disease and remain so for life and therefore new lesions and recurrences are to be expected. The only caveat to this rule is the few self-curing cases. Typically, the more Sarcoids a horse has, the more it will get and visa-versa, the fewer Sarcoids it has, the fewer the horse will get, which is why it is important to diagnose and treat horses properly.
• Prevention of Bovine Papillomavirus is often more successful and practical than treatment after an infection has occurred. It is possible to vaccinate un-infected animals. This vaccine has been successful in trials, but in order to be truly effective it must contain proteins of all the virus types, as there is no cross-protection between the types.
• The simplest method of prevention is to separate infected animals from normal healthy animals, and to minimize the use of equipment, feeders, waters, etc. that come into contact with both groups.

The Equine Sarcoid is the most commonly detected skin tumour in equids worldwide and has been reported in horses, donkeys and mules. Despite the similarity of terminology, the Equine Sarcoid is unrelated to human Sarcoidosis. Sarcoids can be defined as locally aggressive fibroblastic benign tumors of equine skin and can occur as single or multiple lesions in different forms, ranging from small wart-like lesions to large ulcerated fibrous growths. Lesions can occur all over the body but show sites of predilection particularly in the paragenital region, the thorax–abdomen and head and frequently occur at sites of previous injury and scarring. Sarcoids can sometimes be confused with other skin lesions; for example, their rapid growth and transference from one part of the horse to another is similar to that observed with Equine Papillomas. However, spontaneous regression, which is common in Equine Papillomas, is rarely seen in sarcoids.

• A horse that has even one lesion is by definition genetically liable to the disease and remains so for life and therefore new lesions and recurrences are to be expected. The only caveat to this rule is the few self-curing cases (see below.)
• The more Sarcoids a horse has the more it will get (and the fewer it has the fewer it will get) i.e. treat them early and treat them properly.
• Sarcoids multiply over the summer (control the flies) and grow over the winter (examine your horse carefully in the spring time!)
• The best possible treatment should be applied at the earliest available opportunity; inappropriate treatment is a potential disaster.
• Wounds (no matter how small they may seem to be) on horses with Sarcoids at other sites MUST be dealt with promptly using full veterinary support.

Sarcoids can develop in all equine species including the horse, donkey, mule, zebra, and Przewalksi horse.

Sarcoids can develop at any age. Although most cases are first noticed between 2 and 10 years of age, individual cases can start at any age up to the late thirties. This probably simply reflects the time that a genetically susceptible horse is challenged by the disease and is able to succumb.