[The pathophysiology and defense mechanism against superficial and subcutaneous fungal infection].
To determine the pathophysiology of the fungal infection and defense mechanisms against superficial dermatomycosis, two series of experimental infections of Trychophyton mentagrophytes were made on the forearm of a male volunteer. One series was applied topical steroid ointment, the other the vehicle alone. The infected sites were biopsied from each row weekly up to the 4th week, and the set of sites were studied and compared clinically, histopathologically and immunohistochemically. For the study against subcutaneous fungal infection, the same experiments were studied using the subcutaneous inoculation of Sporothrix schenckii. The pathophysiology of the superficial dermatophytosis was thought to be the same as those of the contact (allergic) dermatitis, including the physiodynamics of CD-1 cells. The principal mechanism of the defense lay in the removal of the foreign materials (fungi) together with keratinocytes whose turnover increased because of the eczematous reaction. It was proved that the topical application of steroid ointment suppressed the immune reactions locally, thus forming a paradoxical feature with little inflammatory reaction and abundant fungal elements (so-called atypical tinea). The pathophysiology of the subcutaneous fungal infection was thought to be a suppurative granulomatous reaction and pathologically showed a mixed cell granuloma. The neutrophils and macrophages engulfed and digested the fungi in the forefront, but the circumference was surrounded by epithelioid cells and/or foreign body granuloma. Transepithelial elimination also played some role in the defense. It was proved that when the defense mechanism was weakened by the topically applied steroid ointment, not only the clinical symptoms but also the fungicidal tissue reaction were subdued, and histocytes only engulfed fungi to protect them from dispersion. The trichophytin reaction turned positive on the 14th day, and the sporotrichin reaction on the 7th day.
Nakajima
Hiroshi
H
Yokohama City University, Matsuda-machi, Ashigarakami-gun, Kanagawa 258-0003, Japan.
D003877:Dermatitis, Contact / Q000382:microbiology; D003881:Dermatomycoses / Q000276:immunology / Q000473:pathology* / Q000503:physiopathology*; D006025:Glycosaminoglycans / Q000494:pharmacology; D006801:Humans; D007111:Immunity, Cellular; D008264:Macrophages / Q000502:physiology; D009504:Neutrophils / Q000502:physiology; D012867:Skin / Q000382:microbiology / Q000473:pathology; D014005:Tinea / Q000503:physiopathology; D014249:Trichophyton
D006025:Glycosaminoglycans; C012039:sporotrichin