The condition known colloquially as “Tree Man Syndrome” is medically identified as Epidermodysplasia Verruciformis (EV), a rare, lifelong disorder characterized by widespread, persistent skin lesions resembling warts and plaques. The name refers to the most severe manifestations, where the growths become large and bark-like, primarily on the hands and feet. EV is a genodermatosis, meaning it is a genetic skin condition. This condition is directly linked to an abnormal susceptibility to specific strains of the Human Papillomavirus (HPV), which is the primary cause of the skin growths. The core question regarding this disorder is whether the severe, wart-like growths that define the syndrome are contagious, and the nuanced answer lies in understanding the necessary underlying genetic defect.
The Inherited Susceptibility
The severity of Epidermodysplasia Verruciformis is not simply due to a common infection but is rooted in a specific and rare genetic predisposition. The condition is typically inherited in an autosomal recessive pattern, requiring a person to inherit a mutated gene from each parent to develop the disorder. The genetic defect most commonly involves mutations in the TMC6 (EVER1) and TMC8 (EVER2) genes, which are located adjacent to each other on chromosome 17. These genes encode proteins that are integral to the body’s intrinsic immune control of HPV infection within keratinocytes. When these genes are non-functional, the skin cells lose their ability to effectively suppress the replication of certain HPV types, leading to the chronic, widespread skin overgrowth characteristic of EV.
The Role of HPV and Transmission Risk
The syndrome itself, meaning the development of the massive, persistent growths, is definitively not contagious because it requires the combination of the transmissible virus and the necessary, rare genetic mutation. The underlying cause is an infection by specific Human Papillomavirus strains, primarily beta-HPV types, such as HPV 5 and HPV 8. These beta-HPV types are common and widespread, often detected in the skin of up to 20% of the general population without any clinical consequence. For an individual without the TMC6 or TMC8 gene mutations, exposure to these HPV strains simply results in no symptoms or, at most, transient, common warts that the immune system eventually clears. The virus itself is transmissible through skin-to-skin contact, similar to other HPV types that cause common warts, but transmission alone will not cause Epidermodysplasia Verruciformis unless the recipient possesses the compromised genetic defense mechanism.
Physical Manifestation and Disease Timeline
The physical symptoms of Epidermodysplasia Verruciformis usually begin in childhood or adolescence. The lesions present in two main forms: flat, wart-like lesions that resemble verruca plana, and reddish-brown, scaly patches, often found in sun-exposed areas like the face, neck, hands, and feet. The lesions are progressive and persistent, failing to resolve spontaneously and often growing into thickened, confluent plaques and nodules over time. In severe cases, these growths become highly verrucous, taking on the dark, hardened appearance that led to the “Tree Man” moniker. A major complication is the significantly heightened lifetime risk of non-melanoma skin cancer, specifically Squamous Cell Carcinoma, which develops in 30% to 70% of affected individuals.
Management and Ongoing Studies
Since Epidermodysplasia Verruciformis is a lifelong genetic disorder, there is currently no definitive cure to permanently eliminate the lesions. Current medical management focuses on preventing malignant transformation and reducing the bulk of the persistent growths. Strict sun avoidance and the use of high sun protection factor creams are the most important preventive measures, as ultraviolet light acts as a cofactor in skin cancer development. Treatment for existing lesions often involves a combination of surgical methods, including cryotherapy, electrosurgery, and surgical excision, to remove benign and premalignant tissue. Systemic retinoids, such as acitretin, are frequently used to help slow the growth and proliferation of the lesions, and patients require rigorous, regular dermatological surveillance due to the high risk of skin cancer.