The pathophysiology of PNT is controversial. It is thought by most authors to represent an initial Arthus reaction to released tuberculosis antigens or intact bacilli, followed by a subsequent hypersensitivity reaction to the mycobacterial products present in the skin. Specifically, the released mycobacterial organisms or antigens are opsonized by antibodies resulting in the formation of immune complexes, which ultimately lodge in small cutaneous blood vessels. These immune complexes activate complement inducing a leukocytoclastic vasculitis with subsequent destruction of blood vessel walls and release of proteolytic enzymes, resulting in focal tissue necrosis. Other authors dispute this pathophysiology, having found no evidence of a leukocytoclastic vasculitis histologically, and propose that the primary lesion represents a subacute lymphohistiocytic vasculitis leading to vessel thrombosis and ensuing tissue necrosis.
Most recent cases come from areas with high endemic rates of tuberculosis.
A rare U.S. case, involving a previously healthy 9 year-old girl from Chicago, IL, was, however, reported in 1990. Reports indicate that young women and children are especially susceptible to this disorder. PNT-like lesions have been associated with other mycobacterial infections including M. bovis and M. kansasii as well as from BCG vaccination. With the increased incidence of TB infection in HIV patients, PNT may experience an increase in frequency, though this has not occurred to date. An additional 12 cases were reported in 1986 from England presenting over a 30-year period, though most of these patients were immigrants and had presumably acquired the infection outside of England.