NAME OF DISEASE:     Piedra
                                        Erythrasma
                                        Tinea
                                        Dermatophytosis
                                        Ringworm
                                        Candidosis
 

ETIOLOGICAL AGENT:

        Microsporum  ) 37 species of which six
        Trichophyton  ) cause 95% of all
    Epidermophyton ) dermatophytosis
 

    Pityrosporon orbiculare (Malassezia furfur)             )
    Candida albicans                                                     ) non-dermatophytes
    Piedraia - causes Black Piedra and White Piedra      )
 

THE DISEASE:

    These are diseases that affect 8.9 million Americans and account for 5% of all diseases with a skin manifestation. The organism is transmitted to man from:

        1.     Other humans (anthropophilic)

        2.     Non-human animals (zoophilic)

        3.     Soil
 

    The fungi invade only the dead, cornified layers of the skin, nails and hair. Most of the resulting pathology is caused by the host's reaction to the infecting fungus. The fungus alone has only a minimal capacity to damage skin directly.
 

PATHOLOGY:

    The fundamental pathogenic mechanisms of dermatophytosis involve two distinct phases:

        1.     Colonization

        2.     Host-parasite interaction

    During colonization the surface of the tissue is infected with a fungal spore and invasion begins. The dermatophytes grow in typical filamentous form within the stratum corneum. The downward extension of these hyphae is restricted because certain micronutrients, principally iron, are not available below the stratum corneum. The iron present in the living cell layers of the epidermis and dermis where the dermatophytes fail to penetrate is firmly bound to transferrin.

    Lateral expansion of the microcolony within the stratum corneum continues for 10-35 days, during which time the infected skin appears to be either normal or only very slightly inflamed. The dermatophytes do not produce diffusible irritants or toxins. After two-three weeks, the advancing border of the infection may become inflamed (ringworm lesions).

    During the colonization phase the host begins to respond immunologically by undergoing sensitization to soluble fungal antigens (trichophyton). The first detectable immune response is cell-mediated immunity (CMI), which is characterized in colonized skin as an intense inflammatory process and demonstrated at a trichophyton skin test site by a delayed or tuberculin-type reaction. The genesis and expression of CMI to dermatophytic antigen in an infection occurs between the 10th and 35th days and heralds the beginning of the second distinct period in pathogenesis, the host-parasite interaction phase.

    During the host-parasite interaction phase. CMI produces most of the pathology as an acute inflammatory type of dermatophytosis. The immune inflammation which results extends in a spectrum from erythema and edema of the dermis and epidermis (spongiosis) to the formulation of vesicles and pustules. Epidermal integrity is breached; oozing and weeping of the tissue fluid occur. Invasion of hair follicles results in inflamed nodules, deep seated pustules, and abscesses.

    Cell-mediated immune damage to the skin is not entirely without benefit to the host. The inflammatory damage to the epidermis may internalize what began as an essentially extracorporal fungal colony. The parasitized stratum corneum is now exposed to the internal host defense mechanisms. Several of the host defense mechanisms which are critical for resistance to other microbial pathogens do not appear to be important either in limiting the invasion of dermatophytes or in eradicating them. There is no evidence that either antibody or lymphocytes can directly retard fungal growth. Phagocytes surely cannot dissect out and engulf the long fungal filaments that arborize through the compact stratum corneum. However, unsaturated transferrin diffuses into the stratum corneum and binds iron, rendering this essential micronutrient unavailable for fungal utilization. The net effect of damage to the skin from CMI is that lateral spread of the colony is abruptly halted and within one-two weeks the pathogen can no longer be recovered from the lesion. The outward growth of the epidermis, which may be accelerated by the inflammation, probably aids in elimination of the infection.

    If CMI to dermatophyte antigen does not develop or is suppressed by immune regulation or modulation, the skin will not become sufficiently inflamed to reject the infection. In patients who cannot express CMI to dermatophytic antigens, the chronically infected skin is only minimally inflamed. The result of minimally inflamed, chronic infection is dryness, erythema, scaling, pruritus, fissures, and cracks.

    Thus, there are two basic types of dermatophytic infection. The acute or inflammatory type of infection, which is associated with CMI to the fungus, generally heals spontaneously or responds nicely to treatment. The chronic or noninflammatory types of infection, which is associated with a failure to express CMI to the fungus at the site of infection, is relapsing and responds poorly to treatment.

    Several conditions predispose to dermatophytosis. Recurrent colonization is favored by moisture, as provided by the high humidity of the tropics or in certain anatomic sites. It is also favored when the skin is frequently bombarded by a heavy fungal inoculum. Any condition that impairs the expression of CMI in the skin, such as congenital immunodeficiency disorders, atopy, reticular malignancy, anti-metabolic or glucosteroid therapy (even topical), would lead to chronic infection once colonization occurred.
 

DIAGNOSIS:

    Diagnosis is based upon:

        1.     Anatomical site infected

        2.     Type of lesion

        3.     Examination with a Woods lamp (366 A°)

        4.     Examination of KOH-treated skin scales from the infected area

        5.     Culture of the organism (not too important)

    In a differential diagnosis you must consider:

        1.     Leprosy

        2.     Secondary syphilis

        3.     Pityriasis rosea - a dermatosis due to a virus and marked by oval, papulosquamous
                lesions occurring along the lines of skin cleavage. The distal extremities, palms and soles,
                and mucous membranes are usually spared. Often the generalized eruption is preceded
                by a single lesion, the herald lesion.

        4.     Psoriasis - a papulosquamous disease characterized by well-demarcated scaling plaques
                on an erythematous base. Lesions commonly involved the scalp, elbows, knees and
                sacrum. The nails may also be characteristically involved. Psoriasis may involve the glans
                penis as an erythematous macular or papular eruption without scaling.
 

        5.     Nummular eczema - a skin disease with itching, redness and infiltration and coin-shaped
                lesions.

        6.     Lichen planus - an inflammatory skin disease with wide, flat papules, often in
                circumscribed patches.

        7.     Alopecia areata - hair loss in sharply defined areas, usually the scalp.

        8.     Trichotillomania - neurotic plucking of the hair.

        9.     Dyshidrosis - an acute, recurrent, noninflammatory vesicular eruption limited to the palms
                and the soles.

    10.     Contact dermatitis.
 

TREATMENT:

    Topical agents include:

        1.     Tolnaftate (trade name - Tinactin)
                No effect on Candida or bacteria

        2.     Haloprogin (trade name - Halotex)

        3.     Miconazole (trade name - Micatin and Monistat)
                Most potent of all. Active against tineas, Candida, some bacteria and several other fungi.

        4.     Econazole

        5.     Clotrimazole

        6.     Nystatin (for Candida infection)

    Systemic agent:

        1.     Oral griseofulvin

        2.     Ketoconazole