The connection between P. ovale and seborrhoeic dermatitis has been clearly demonstrated in a number of treatment studies but we still do not know how P. ovale induces skin lesions. An enhanced growth of P. ovale cannot be the cause, because a number of studies with quantitative determinations of P. ovale have not been able to show any difference in the number of yeast cells between patients and healthy controls. The number of P. ovale is probably only important for the individuals who are susceptible to seborrhoeic dermatitis. An abnormal immune response to P. ovale could be another explanation. Sohnle et al. have shown that P. ovale can activate complement by both the classical and the alternative pathway. A defective cell-mediated immunity to P. ovale in patients with seborrhoeic dermatitis has been demonstrated by Wikler et al. In patients with AIDS, who are known to have a diminished T-cell function, a high incidence of seborrhoeic dermatitis has been found. Activation of the alternative complement pathway by P. ovale, which does not require T-cell function, could be an explanation for the inflammatory response. I also believe that the skin lipids are important in the pathogenesis. An improvement of seborrhoeic dermatitis has been demonstrated after treatment with drugs that reduce the sebum excretion. Pityrosporum has lipase activity and may generate free fatty acids, which could also contribute to the inflammatory response. There are a number of factors which are probably important in the pathogenesis of seborrhoeic dermatitis, that is, the number of P. ovale, P. ovale lipase activity, skin lipids, immune function, heredity, atmospheric humidity and emotional state. A reduction in the number of P. ovale in patients suffering from seborrhoeic dermatitis and being treated with antimycotic treatment is, at the present state of knowledge, the best way to treat the disease.