The Biology of Experimental Human Cutaneous Moniliasis (Candida Albicans)

Maibach, Howard I.

doi:10.1001/archderm.1962.01590020073009

Cited by 166 publications

(51 citation statements)

References 23 publications

(5 reference statements)

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“…Cytokine expression patterns observed in reconstituted human epidermis after treatment with allergic or toxic agents, or both, are similar to those seen after infection with C. albicans. In previous studies, the skin reactions seen in experimental C. albicans infection have been explained as a sort of biological contact dermatitis of the primary irritant or allergic type [22][23][24][25]. The present study found morphological alterations and a cytokine profile of reconstituted human epidermis induced by C. albicans infection, which are similar to that found in irritant/ allergic contact dermatitis [18].…”

Section: Discussionsupporting

confidence: 85%

Cytokine expression induced by Candida albicans in a model of cutaneous candidosis based on reconstituted human epidermis

Schaller¹,

Mailhammer²,

Körting³

2002

Journal of Medical Microbiology

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Skin equivalents based on reconstituted human epidermis have been used recently to establish models for allergic/irritant contact dermatitis and cutaneous candidosis. In the present study the cytokine expression pattern and the morphological alterations in experimental cutaneous candidosis were investigated by RT-PCR and histological analysis. In experimental cutaneous C. albicans infection the mRNA expression levels of interleukin (IL)-1AE, IL-1â, IL-8, GM-CSF, Exodus-2, tumour necrosis factor-AE and PSL (P-selectin ligand) were upregulated. Cytokine profile and histological features of infected skin (separation of keratinocytes, oedema, vacuolisation) were comparable to that seen in experimental contact dermatitis. These immunomodulatory and morphological similarities might reflect a common pathogenesis factor in both diseases.

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Section: Discussionsupporting

confidence: 85%

Cytokine expression induced by Candida albicans in a model of cutaneous candidosis based on reconstituted human epidermis

Schaller¹,

Mailhammer²,

Körting³

2002

Journal of Medical Microbiology

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“…The keratinous surface of intact skin is an important physical barrier to most pathogens, and the local acidic microenvironment of the dermis impedes microbial growth [13]. Investigations from the early 1960s revealed that healthy human skin is resistant to establishment of candidal infection unless maceration is induced [14]. Furthermore, organisms living on the skin as commensals suppress growth of pathogens by competing for nutrients, secreting toxins, and by metabolism of fatty acids that further lower the pH of the local microenvironment [13].…”

Section: Penetration Of Peripheral Defensesmentioning

confidence: 99%

The pathophysiology and treatment of Candida sepsis

Spellberg

Edwards

2002

Curr Infect Dis Rep

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Sepsis can occur during disseminated candidiasis, but its pathogenesis differs from that caused by typical prokaryotic pathogens. Complex interactions between defects in host defense and "relative" virulence factors expressed by Candida lead to dissemination of the saprophyte to parenchymal organs, and subsequently to onset of multiorgan failure. This review focuses first on the pathophysiology of Candida sepsis, detailing current understanding of host-pathogen interactions. We then consider the choice of antifungal and supportive treatments.

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“…In acute cutaneous candidiasis, organisms penetrate only the outer layers of the squamous stratum corneum of the skin. A pustular dermatitis results that actually more resembles a hypersensitivity reaction than an infection (68). Because of this, the term invasive candidiasis is commonly used to denote penetration of Candida spp.…”

Section: Definitions Of Invasive Candidiasismentioning

confidence: 99%

Laboratory diagnosis of invasive candidiasis

Jones

1990

Clin Microbiol Rev

183

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Severe infections due to Candida species have become more frequent during the past two decades because of the increasing numbers of immunosuppressed patients being treated in our hospitals. Distinguishing colonization from invasive disease requires knowledge of the pathogenetic mechanisms leading to invasion. To assist the clinician in therapeutic decisions, clinical microbiologists should identify to species Candida organisms isolated from immunosuppressed patients. Quantitative or semiquantitative cultures of urine, burn tissues, intravascular catheter tips, and bronchoalveolar lavage specimens may provide useful information. Immunofluorescent staining of certain specimens can enhance diagnostic yield. The lysis-centrifugation blood culture technique offers some advantages over traditional broth techniques in detecting Candida fungemia. Antibody testing is of limited diagnostic value in highly immunosuppressed patients. Developing simple and reliable tests for detecting antigens or metabolites of Candida spp. in the sera of infected patients has proven difficult. Methods for typing Candida albicans are evolving. Typing should prove useful for studying the epidemiology of candidiasis in hospitalized patients.

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The Biology of Experimental Human Cutaneous Moniliasis (Candida Albicans)

Cited by 166 publications

References 23 publications

Cytokine expression induced by Candida albicans in a model of cutaneous candidosis based on reconstituted human epidermis

Cytokine expression induced by Candida albicans in a model of cutaneous candidosis based on reconstituted human epidermis

The pathophysiology and treatment of Candida sepsis

Laboratory diagnosis of invasive candidiasis

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