Oral Candidiasis: Clinical Manifestations and Cellular Adaptive Host Responses

Ashman, R. B.; Farah, Camile S.

doi:10.1007/0-387-25445-5_4

Cited by 4 publications

(8 citation statements)

References 132 publications

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“…Approximately 65% of complete denture wearers are predisposed to candida infection. The possible explanations include enhanced adherence of candida to the acrylic, ill-fitted appliances, decreased saliva flow under the denture surfaces or inadequate hygiene ( Ashman and Farah, 2005 ; Martori et al, 2014 ).…”

Section: Factors Predisposing For Oral Candidiasis ( Table mentioning

confidence: 99%

“…Lastly, individuals affected by congenital conditions associated with defective immune system such as Di George’s syndrome, hereditary myeloperoxidase deficiency and Chediak–Higashi syndrome are commonly predisposed to candida infections ( Ashman and Farah, 2005 ).…”

Section: Factors Predisposing For Oral Candidiasis ( Table mentioning

confidence: 99%

“…These plaques consist of desquamated epithelial cells, tangled aggregates of fungal hyphae, fibrin, and necrotic material ( Lalla et al, 2013 ). The superficial pseudo-membrane can be removed by wiping gently, leaving behind an underlying erythematous and occasionally bleeding surface ( Ashman and Farah, 2005 ; Farah et al, 2010 ). The oral surfaces frequently involved include labial and buccal mucosa, tongue, hard and soft palate and oropharynx.…”

Section: Forms Of Oral Candida Infections ( Table mentioning

confidence: 99%

“…Erythematous candidiasis is relatively rare and manifests as both acute and chronic forms ( Ashman and Farah, 2005 ). Previously known as ‘antibiotic sore mouth,’ due to its association with prolonged use of broad-spectrum antibiotics ( Farah et al, 2010 ).…”

Section: Forms Of Oral Candida Infections ( Table mentioning

confidence: 99%

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Clinical Appearance of Oral Candida Infection and Therapeutic Strategies

et al. 2015

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Candida species present both as commensals and opportunistic pathogens of the oral cavity. For decades, it has enthralled the clinicians to investigate its pathogenicity and to improvise newer therapeutic regimens based on the updated molecular research. Candida is readily isolated from the oral cavity, but simple carriage does not predictably result in development of an infection. Whether it remains as a commensal, or transmutes into a pathogen, is usually determined by pre-existing or associated variations in the host immune system. The candida infections may range from non-life threatening superficial mucocutaneous disorders to invasive disseminated disease involving multiple organs. In fact, with the increase in number of AIDS cases, there is a resurgence of less common forms of oral candida infections. The treatment after confirmation of the diagnosis should include recognizing and eliminating the underlying causes such as ill-fitting oral appliances, history of medications (antibiotics, corticosteroids, etc.), immunological and endocrine disorders, nutritional deficiency states and prolonged hospitalization. Treatment with appropriate topical antifungal agents such as amphotericin, nystatin, or miconazole usually resolves the symptoms of superficial infection. Occasionally, administration of systemic antifungal agents may be necessary in immunocompromised patients, the selection of which should be based upon history of recent azole exposure, a history of intolerance to an antifungal agent, the dominant Candida species and current susceptibility data.

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Section: Factors Predisposing For Oral Candidiasis ( Table mentioning

confidence: 99%

Section: Factors Predisposing For Oral Candidiasis ( Table mentioning

confidence: 99%

Section: Forms Of Oral Candida Infections ( Table mentioning

confidence: 99%

Section: Forms Of Oral Candida Infections ( Table mentioning

confidence: 99%

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Clinical Appearance of Oral Candida Infection and Therapeutic Strategies

et al. 2015

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“…However, should something make the host vulnerable, the organism can proliferate locally and even cause invasive infections. In 1869, the French clinician Armand Trousseau described mucosal candidiasis as ‘the disease of the diseased’ (88). Over a century later, when first cases of acquired immunodeficiency syndrome (AIDS) were published in 1981 (89), the report described five homosexual men with pneumonia that was caused by a different opportunistic fungus, Pneumocystis carinii (90, 91).…”

Section: West Coast Studiesmentioning

confidence: 99%

α‐Defensins in human innate immunity

Lehrer¹,

2011

Immunological Reviews

364

377

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Defensins are small, multifunctional cationic peptides. They typically contain six conserved cysteines whose three intramolecular disulfides stabilize a largely β-sheet structure. This review of human α-defensins begins by describing their evolution, including their likely relationship to the Big Defensins of invertebrates, and their kinship to the β-defensin peptides of many if not all vertebrates, and the θ-defensins found in certain non-human primates. We provide a short history of the search for leukocyte-derived microbicidal molecules, emphasizing the roles played by luck (good), preconceived notions (mostly bad), and proper timing (essential). The antimicrobial, antiviral, antitoxic, and binding properties of human α-defensins are summarized. The structural features of α-defensins are described extensively and their functional contributions are assessed. The properties of HD6, an enigmatic Paneth cell α-defensin, are contrasted with those of the four myeloid α-defensins (HNP1-4) and of HD5, the other α-defensin of human Paneth cells. The review ends with a decalogue that may assist researchers or students interested in α-defensins and related aspects of neutrophil function.

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Spatial Distribution of a Porphyrin-Based Photosensitizer Reveals Mechanism of Photodynamic Inactivation of Candida albicans

et al. 2021

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The antimicrobial photodynamic therapy (aPDT) is a promising approach for the control of microbial and especially fungal infections such as mucosal mycosis. TMPyP [5,10,15, 20-tetrakis(1-methylpyridinium-4-yl)-porphyrin tetra p-toluenesulfonate] is an effective photosensitizer (PS) that is commonly used in aPDT. The aim of this study was to examine the localization of TMPyP in Candida albicans before and after irradiation with visible light to get information about the cellular mechanism of antifungal action of the photodynamic process using this PS. Immediately after incubation of C. albicans with TMPyP, fluorescence microscopy revealed an accumulation of the PS in the cell envelope. After irradiation with blue light the complete cell showed red fluorescence, which indicates, that aPDT is leading to a damage in the cell wall with following influx of PS into the cytosol. Incubation of C. albicans with Wheat Germ Agglutinin (WGA) could confirm the cell wall as primary binding site of TMPyP. The finding that the porphyrin accumulates in the fungal cell wall and does not enter the interior of the cell before irradiation makes it unlikely that resistances can emerge upon aPDT. The results of this study may help in further development and modification of PS in order to increase efficacy against fungal infections such as those caused by C. albicans.

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Oral Candidiasis: Clinical Manifestations and Cellular Adaptive Host Responses

Cited by 4 publications

References 132 publications

Clinical Appearance of Oral Candida Infection and Therapeutic Strategies

Clinical Appearance of Oral Candida Infection and Therapeutic Strategies

α‐Defensins in human innate immunity

Spatial Distribution of a Porphyrin-Based Photosensitizer Reveals Mechanism of Photodynamic Inactivation of Candida albicans

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