The majority of patients with dermatophytosis are not immunosuppressed and have no underlying disease. Previous studies have occasionally revealed a number of underlying diseases in patients with dermatophytosis, notably hereditary palmoplantar keratoderma (Elmros & Liden, 1983) and Raynaud's phenomenon (Hay, 1982). But the former is likely to reflect a major change in the local environment in which dermatophytes grow and the latter vascular disease. In fact it is possible to see patients with dermatophytosis on one foot where there is poor vascular perfusion detectable clinically but not on the other normally perfused foot (Hay, 1982).
Atopy is an underlying disease syndrome which has been consistently connected with dermatophytosis. A high proportion of chronically infected individuals, over 40% in some surveys, have hay fever, asthma, or atopic eczema either on personal or family history (Hay, 1982; Jones et al., 1973). In addition a high proportion of individuals seen in dermatological clinics with peripheral dermatophyte infection either have negative or immediate-type hypersensitivity to dermatophyte antigens on intradermal testing. Increased prevalence of immediate-type responses to intra-dermally injected antigens is also a feature of atopic subjects. There is also evidence that some individuals with persistent dermatophytosis may also have sensitivity to environmental moulds suggesting a modified (atopic) immunological response to a family of antigens.
The other group of patients showing altered responses to dermatophyte infections are those who have certain defects of immunity. Patients with chronic mucocutaneous candidosis (CMC) are particularly susceptible to widespread intractable dermatophytosis as well as candidosis; human immunodeficiency virus (HlV)-infected individuals may also have chronic ringworm. These observations suggest that patients with impaired immunological defense mechanisms, in particular those affecting T-lymphocyte function, are prone to chronic or altered infection. However, in all these examples, whereas the clinical expression of infection may be modified by the patients' underlying condition, the prevalence of dermatophytosis in compromised patients is not significantly different to that seen in healthy subjects. In AIDS patients, the prevalence of infection has been no higher in some studies than in members of 'at risk' groups without HIV infection (Torssander et al., 1988) but there is an association with low CD4 counts (Munoz-Perez et al., 1998).
It is important to separate changes in prevalence, which also depends on the facility for transmission, from the clinical behaviour of the dermatophyte infection in immunosuppressed patients. Patients on chronic immunosuppressive therapeutic regimens, e.g. from solid organ transplant recipients, and patients with HIV/AIDS often have more widespread and difficult to treat dermatophyte infections. HIV positive women receiving antiretrovirals are less likely to have tinea pedis than those not receiving these drugs, irrespective of CD4 count (Maurer et al., 2004). There has been a report suggesting that patients receiving topical tacrolimus may develop widespread dermatophytosis (Siddaiah et al., 2004). These reflect the fact any prediposing condition that impairs T-cell function in the skin will affect the clinical expression of dermatophytosis in humans. But as stated previously, with the exception of atopy, underlying disease is not seen in the majority of patients with dermatophytosis (Svejgaard, 1985). This is in sharp distinction to patients with infections due to Candida albicans where there is usually some predisposing abnormality, ranging from occlusion of the skin surface to defects in neutrophil or T-lymphocyte function.
As stated previously, there is a correlation between inflammatory responses, T-lymphocyte activation, and recovery. In experimental infections, recovery occurs at the same time as lesions become inflamed and delayed-type hypersensitivity to the fungal antigen develops. Patients with persistent foot infections (T rubrum) or tinea corporis (T. concentricum) show reduced levels of lymphocyte blastogenesis to der-matophyte antigen (Jones et al., 1974; Hay et al., 1983). In chronic infections caused by T. rubrum compared to those more inflamed infections due to T. mentagrophytes, for instance, the lymphocyte transformation responses of peripheral blood lymphocytes from infected patients are low. There is little clinical inflammatory reaction and relapse or persistence of infection is common. In less than 15% of cases is there evidence of an underlying disease affecting the immune system that explains these findings. There is also evidence that some immune responses, such as absent delayed-type hypersensitivity to trichophytin, can be reversed by successful therapy (Elewski et al., 2002). In the rare disseminated forms of dermatophytosis where there is involvement of internal organs there may also be evidence of disturbance of immune function (Allen et al., 1977; Liautaud & Marill, 1984).
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