Orthopoxvirus infections in domestic cats have occurred sporadically in the UK and continental Europe. A single case of raccoonpox virus infection has been reported in a cat in Canada; the affected cat had a localized infection of the paw. Cats affected with cowpox usually have multiple skin lesions, although respiratory and other signs also may be seen.
Etiology and Epidemiology
To date, with the exception of all the case of raccoonpox infection, all orthopox isolates examined from domestic cats have been indistinguishable from cowpox virus (see Pox Diseases: Cowpox). Cowpox or infection with other closely related viruses also has been recorded in captive Felidae and in other species (eg, elephants, rhinoceros, and anteaters) in various European zoos. However, the relationship of some of these viruses to established species within the genus is not clear. Cowpox apparently does not occur in the USA, although another orthopoxvirus has been isolated from raccoons. It is possible that this virus may also infect other hosts. Cowpox virus is also infectious to humans, and cat-to-human transmission has been recorded. Owners should be advised accordingly.
Although traditionally described as infecting cattle, cowpox virus is in fact rare, and its reservoir hosts are believed to be small wild mammals. Cats, which are now the most commonly recognized host of cowpox virus, may become infected when hunting. Most affected cats come from rural environments and are known to hunt rodents; the initial lesion is often described as having originated as a small bite-like wound. Infection in cats has a marked seasonal incidence, with most cases occurring between September and November. Cat-to-cat transmission can also occur but usually results in only subclinical infection. Rare bovine cases presumably result from direct or indirect contact with the reservoir host, as do some human cases. However, cat-to-human and cow-to-human transmissions are also possible.
The significance of the disease and its relatively recent recognition in cats is an enigma. It may have always been present in the feline population but not recognized. Alternatively, the disease may be increasing in importance as a result of a change either in the epidemiology of the disease in the reservoir host or in the nature of the dominant biotype of the virus itself.
The most common route of entry appears to be through the skin, but oronasal infection is also possible. After local replication and development of a primary skin lesion, the virus spreads to local lymph nodes and a leukocyte-associated viremia develops. The viremic phase may be associated with pyrexia and depression and, during this period, virus can be isolated from various tissues, including the skin, turbinates (and sometimes lungs), and lymphoid organs. Widespread secondary skin lesions appear a few days after the onset of viremia, and new lesions continue to appear for 2–3 days, at which time the viremia subsides.
Most affected cats have a history of a single primary skin lesion, usually on the head, neck, or a forelimb. The primary lesion can vary from a small, scabbed wound to a large abscess. About 7–10 days after the primary lesion appears, widespread secondary lesions begin to appear. Over 2–4 days, these develop into discrete, circular, ulcerated papules ~0.5–1 cm in diameter. The ulcers soon become covered by scabs, and healing is usually complete by ~6 wk. Many cats show no signs other than skin lesions, but ~20% may develop mild coryza or conjunctivitis. Some cats may also be pyrexic, depressed, and inappetent during the viremic phase just before and during the early development of secondary lesions. Concurrent bacterial infection, particularly of the primary lesions, may give rise to systemic signs. However, most domestic cats recover uneventfully. More severe pulmonary disease is uncommon in domestic cats but frequently occurs in cheetahs and is often fatal in both species. More severe disease in domestic cats is often associated with immunosuppression, either after treatment with corticosteroids or associated with infection with feline leukemia or immunodeficiency viruses.
Because most cats survive, skin biopsies generally are the only tissue available for histologic examination. Early lesions consist of areas of epidermal hyperplasia and hypertrophy with vesiculation of the prickle cell layer. Many of the epidermal cells bordering such vesicles contain characteristic eosinophilic cytoplasmic inclusions. Later, there is ulceration and necrosis of the epidermis and replacement by an eosinophilic coagulum of necrotic cells and fibrin. A heavy, mixed inflammatory cell exudate is present in the dermis surrounding the lesion. As healing ensues, a thin layer of epidermis covers the skin beneath the scabs, early scar tissue is present, and there is a moderate, mainly mononuclear cell infiltrate.
In rarer cases, in which the disease has generalized, lesions may also be present in the liver, lungs, trachea, bronchi, oral mucosa, and small intestine.
If multiple, well-circumscribed skin lesions are present, and especially if there is a history of hunting or exposure to a rural environment, a presumptive diagnosis may be based on clinical signs. Cowpox virus infection also should be suspected when skin lesions do not respond to antibiotics. Differential diagnoses include miliary dermatitis, feline herpesvirus or calicivirus infection, eosinophilic granuloma, bite wounds, ringworm, and other chronic bacterial or fungal conditions.
Presumptive and rapid diagnosis can be made in most cases from unfixed scab, exudate, or biopsy material examined for characteristic brick-shaped orthopox virions by electron microscopy. A more accurate and sensitive method of diagnosis is isolation of virus in cell culture or on chick chorioallantois. If no virus is isolated, fixed biopsy material for histologic examination and serum for antibody determination also can be sent to the laboratory.
Treatment and Control
In both domestic cats and cheetahs, it is important that cowpox be diagnosed promptly because steroid treatment, which is often used in the therapy of other skin conditions, is contraindicated. Although the disease is often severe in cheetahs, in domestic cats, supportive treatment (broad-spectrum antibiotics, fluid therapy) is generally successful, and mortality is low.
Because it seems that infection in domestic cats is mainly sporadic and acquired from chance contact with an infected wildlife reservoir, control measures probably are not indicated. In wildlife parks, where big cats are at risk from contact with small wild rodents, and especially where the disease has already occurred, vaccination may be helpful. Vaccinia virus appears to be of low pathogenicity in domestic cats, and cheetahs appear to be refractive; no trials have yet been done with other orthopoxvirus vaccines. At present, management of outbreaks among large cats depends on prompt diagnosis and segregation of affected animals to reduce the possibility of cat-to-cat spread. Premises may be disinfected with hypochlorite bleach or detergents. At ambient temperatures, poxviruses are relatively resistant and may remain infective in dried crusts for months.
Last full review/revision July 2011 by Paul Gibbs, BVSc, PhD, FRCVS