Epidermal Activity in Annular Dermatophytosis

Berk, Sanders H.; Penneys, Neal S.; Weinstein, Gerald D.

doi:10.1001/archderm.1976.01630280015004

Cited by 24 publications

(9 citation statements)

References 27 publications

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“…This process was a uniform finding in our staphylococcal model system and may well be involved in clearance of these infections as well. The process of shedding organisms located in the stratum corneum or crusts is likely enhanced by increased production, differentiation, and upward movement of keratinocytes [2, 20, 21, 35]. Stimuli that serve to promote keratinocyte differentiation also upregulate the production of keratinocyte antimicrobial proteins such as β -defensins, cathelicidins, and calprotectin [8, 22, 23].…”

Section: Discussionmentioning

confidence: 99%

“…Studies of other cutaneous infections, particularly superficial mycoses and bacterial skin infections, have implicated several clearance processes that may function somewhat differently in the skin; these include neutrophil accumulation into the superficial layers of the epidermis [10, 29, 33, 40], epidermal proliferation [2, 20, 21, 33, 35], and shedding of viable organisms from the skin [32, 34]. The goal of the present study was to carefully examine the S. aureus -infected skin at later time points in this model system to elucidate the mechanisms by which the organisms are cleared from the skin.…”

Section: Introductionmentioning

confidence: 99%

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Clearance of experimental cutaneous Staphylococcus aureus infections in mice

2010

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Staphylococcal skin infections are quite common in human patients. These infections often clear spontaneously, but may also progress locally and/or disseminate to cause serious and sometimes fatal deep infections. The present studies were undertaken to examine the clearance phase of experimental cutaneous Staphylococcus aureus infections in a mouse model system. Previous work in this system has shown that staphylococci applied to the skin rapidly disseminate to the spleen and kidney. In the present experiments the bacteria were found to persist at the skin infection site at a time (8 days after inoculation) when they had disappeared from the spleen and kidney. Examination of the infected skin at earlier times revealed rapid (within 6 h) invasion into the stratum corneum, stratum Malpighii, and dermis, but subsequent redistribution of bacteria (at 1-2 days) to more superficial sites, particularly crusts located just above the skin surface. The crusts seen in these infections were of two distinct types, which were termed type 1 and type 2. Type 1 crusts appeared first, consisted of bacteria, inflammatory cells, and debris, and developed over an intact epidermis. Type 2 crusts arose from the process of dermal necrosis previously reported to take place at 2 days in this model system. In the latter situation the bacteria were not really cleared from the epidermis and dermis; rather those layers were transformed into a superficial crust that contained the bacteria. Deep hair follicle infections in the dermis were found in these infections, but they did not persist and did not seem to be a reservoir for organisms in the dermis. Resolution of these experimental infections appeared to involve redistribution of invading bacteria to more superficial locations in crusts above the skin surface, marked proliferation of the epidermis, loss of the bacteria-laden crusts from the skin, and eventual healing of the cutaneous damage.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Clearance of experimental cutaneous Staphylococcus aureus infections in mice

2010

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“…Increased epidermal labelling has been demonstrated in the vicinity of dermatophyte infections using autoradiography (Berk, Penneys and Weinstein, 1976). A defect in epidermal growth would be important in determining chronicity of an infection.…”

Section: Discussionmentioning

confidence: 99%

Failure of treatment in chronic dermatophyte infections

Hay

1979

Postgraduate Medical Journal

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“…Although the cornified layers of the skin lack a specific immune system to recognize this infection and rid itself of it, nevertheless, both humoral and cell-mediated reactions and specific and nonspecific host defense mechanisms respond and eventually eliminate the fungus, preventing invasion into the deeper viable tissue. This array of defense mechanisms thought to be active against dermatophytes consists of ␣2-macroglobulin keratinase inhibitor (281), unsaturated transferrin (140), epidermal desquamation (27), and lymphocytes, macrophages, neutrophils, and mast cells (36).…”

Section: Immunologymentioning

confidence: 99%

The dermatophytes

1995

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The etiologic agents of the dermatophytoses (ringworm) are classified in three anamorphic (asexual or imperfect) genera, Epidermophyton, Microsporum, and Trichophyton. Species capable of reproducing sexually belong in the teleomorphic genus, Arthroderma, of the Ascomycota. On the basis of primary habitat association, they may be grouped as geophilic (soil associated), zoophilic, and anthropophilic. Adaptation to growth on humans by most geophilic species resulted in diminished loss of sporulation, sexuality, and other soil-associated characteristics. The dermatophytes have the ability to invade keratinized tissue (skin, hair, and nails) but are usually restricted to the nonliving cornified layer of the epidermis because of their inability to penetrate viable tissue of an immunocompetent host. However, invasion does elicit a host response ranging from mild to severe. Acid proteinases, elastase, keratinases, and other proteinases reportedly act as virulence factors. The development of cell-mediated immunity correlated with delayed hypersensitivity and an inflammatory response is associated with clinical cure, whereas the lack of or a defective cell-mediated immunity predisposes the host to chronic or recurrent dermatophyte infection. Chronic dermatophytosis is mostly caused by Trichophyton rubrum, and there is some evidence that mannan produced by this fungus suppresses or diminishes the inflammatory response. Since dermatophytes cause a communicable disease, modes of transmission and control are discussed as well as a survey of recent trends in therapy. Collection of specimens, culture media, and tests for identification are also presented. Genetic studies have led to an understanding of incompatibility mechanisms, pleomorphism and variation, resistance to griseofulvin, and virulence. Molecular biology has contributed to our knowledge of the taxonomy and phylogenetic relationships of dermatophytes.

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Epidermal Activity in Annular Dermatophytosis

Cited by 24 publications

References 27 publications

Clearance of experimental cutaneous Staphylococcus aureus infections in mice

Clearance of experimental cutaneous Staphylococcus aureus infections in mice

Failure of treatment in chronic dermatophyte infections

The dermatophytes

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