eMedicine Specialties > Dermatology > Viral Infections

Cowpox Infection, Human

Author: Nikki A Levin, MD, PhD, Associate Professor of Medicine, Division of Dermatology, University of Massachusetts Medical School
Contributor Information and Disclosures

Updated: Mar 12, 2009

Introduction

Background

More than 200 years ago, in one of the first demonstrations of vaccination, Edward Jenner inoculated a young English boy with cowpox material from a dairymaid and showed that the boy became resistant to smallpox. Today, cowpox is a rare disease, largely confined to small mammals on the European continent and in Great Britain, with occasional transmission to humans. Most cases present with a small number of vesicopustular lesions on the hands or face that subsequently ulcerate and develop a black eschar before spontaneously resolving. Rarely, cutaneous dissemination and even death may occur.

Pathophysiology

Cowpox is caused by the cowpox or catpox virus, a member of the orthopoxvirus family, which also includes smallpox and vaccinia.¹ The virus is believed to be acquired by direct contact with an infected animal, most often a cat in the case of humans, with lesions occurring where the virus gains access through broken skin.² Infection generally remains localized at the initial site of inoculation, although lymphatic spread in a sporotrichoid pattern and generalized skin infection have been reported.^3,4,5 Human-to-human transmission of cowpox has never been reported.

As a member of the Orthopoxvirus family, cowpox is a large double-stranded DNA virus that replicates in cell cytoplasm. Viral particles bind to plasma membrane receptors on host cells and then enter into the cytoplasm, where the viral genome is replicated and viral progeny are assembled. After new viral particles are assembled, the host cell lyses, releasing infectious virus, which can enter surrounding cells. Cowpox virus has no latent stage and does not integrate its DNA into the host genome.

Poxviruses use numerous strategies to evade the host immune system. These include production of homologues of mammalian tumor necrosis factor receptor, interleukin-1beta receptor, interleukin 18–binding protein, interferon-alpha/beta receptor, and interferon-gamma receptor, as well as a complement-binding protein and a caspase inhibitor.⁶ These proteins are thought to neutralize the host's antiviral response by binding to cytokines and complement proteins and inhibiting their function. In addition, cowpox virus has been shown to inhibit intracellular transport of major histocompatibility class I molecules, allowing it to evade cytotoxic T cells.^7,8

Frequency

United States

Cowpox has never been reported in the United States.

International

Cowpox is a rare infection of humans, with fewer than 150 human cases reported.^3,9 Historically, most cases have been reported in Great Britain, with a smaller number from Germany, Belgium, the Netherlands, France, Sweden, Finland, Norway, and Russia. In 2001, 60 cases of possible cowpox were reported in Egypt, but this has not been confirmed.⁹ Most cases occur in the late summer and fall.

Mortality/Morbidity

Human cowpox is usually a self-limited disease. The host immune response is usually sufficient to control the viral infection, and the only sequelae are scars at the site of the pox lesions. Of the 6 cases of severe generalized skin infection that have been reported, 4 of the patients had atopic dermatitis and a fifth patient had hay fever.^4,10 The only reported death associated with cowpox was in a patient with atopic dermatitis and allergic bronchial asthma who was receiving systemic steroids at the time of infection. After developing widespread cutaneous lesions, the patient died from pulmonary embolism. Autopsy failed to demonstrate viropathic effect in any internal organs, so it is unclear what role cowpox may have played in the patient's death.

Race

No racial predilection has been reported.

Sex

Equal numbers of male and female cases have been reported.

Age

Human cowpox is a disease of young people, with half of all cases occurring in individuals younger than 18 years. Young people may be at greater risk because of a propensity for close contact with animals, such as cats, or because of their not having been vaccinated for smallpox, which may confer some protection against cowpox.

Clinical

History

• Generally, patients are young; 50% of patients are younger than 18 years.
• Most cases occur in late summer to fall.
• Cases present in endemic areas of Europe.
• Contact with rodents, cats, or cows is reported in 50% of cases.^{11,12,13,14,15} One case was reported in an animal keeper who was exposed to an infected circus elephant.¹⁶
• Usually, only 1 or a small number of lesions occur on the hands (48%) and face (33%).
• Patients may report having a flat red lesion that became raised and then blistered over a period of 2 weeks. The blister subsequently became crusted, with the surrounding skin becoming red and swollen. The lesions are characteristically described as quite painful.
• Patients may have eye complaints.
• Patients may report fever, malaise, lethargy, vomiting, and sore throat, which usually lasts 3-10 days but resolves during the eschar stage of cutaneous lesions.

Physical

• Physical findings generally are limited to the skin, eyes, and lymph nodes.
• Cutaneous findings develop as follows:
  • Days 1-6 (after inoculation): An inflamed macule appears at the site of contact with the infected animal and at any secondary sites of accidental transfer.
  • Days 7-12: The inflamed lesion becomes papular, then vesicular.
  • Days 13-20: The vesicle becomes hemorrhagic, then pustular, and has a tendency to ulcerate, with surrounding edema and induration. Secondary lesions may form nearby.
  • Weeks 3-6: The vesicopustule progresses to a deep-seated, hard, black eschar, often surrounded by edema, induration, and erythema. Most patients present at this stage, which may appear similar to cutaneous anthrax.^17,18
  • Weeks 6-12: The eschar sloughs, and the lesion heals, usually with scarring.

• Rarely, the cutaneous lesions may become generalized before resolving.
• Ocular findings include conjunctivitis, periorbital edema, and corneal involvement.
• Enlarged painful local lymph nodes often are observed. Necrotizing lymphadenitis has been reported.¹⁹

Causes

The natural reservoir of cowpox virus is believed to be small woodland mammals, such as bank voles and wood mice, with humans, cows, and cats being only accidental hosts.

• Risk factors for infection with cowpox include exposure to potentially infected animals (eg, cats, cows, rodents) in an endemic area.
• Risk factors for dissemination of infection include atopic dermatitis and use of systemic corticosteroids.

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