Summary

In summary it is possible to connect these findings by proposing the following hypothesis for the development and persistence of dermatophyte infections.

• Dermatophyte infections are normally eliminated through a largely Th1 path involving effector mechanisms that range from accelerated epidermal turnover to production of adhesion molecule-directed neutrophil trafficking in the epidermis at the site of infection and subsequent phagocyte-mediated fungal cell destruction.

• A number of different factors can delay elimination of the organisms. These include gross thickening of the epidermis as seen in patients with forms of kera-toderma, immunosuppression that affects the function of T lymphocytes (therapeutic or disease-related), but fungal antigen-mediated modulation of T-cell responses may also play a role in blunting host defense.

• Persistence of these organisms in the face of immune-recognition is a key factor involved in triggering a Th2 switch, which in turn leads to a defective defense mechanism. This switch is more likely to occur in individuals with atopic background but is not exclusive to them - this explains the higher prevalence of dermatophyte infections seen in some, but not all, studies in atopic subjects.

Whatever the truth of this hypothesis it is clear that dermatophytosis provides an intriguing model for the adaptation of effective immune mechanisms in both human and experimental infections.

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The term vaginitis is one that is applied to any inflammation or infection of the vagina, and there are many different conditions that are categorized together under this ‘broad’ heading, including bacterial vaginosis, trichomoniasis and non-infectious vaginitis.

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