Is the oral fungal pathogen Candida albicans a cariogen?

Pathobiology of dental caries is complex. Data from recent molecular microbiologic studies have further redefined the role of the oral microbiome in the etiology of dental caries. This new information challenges the conventional view on the hegemony of classic cariogenic prokaryotes such as Streptococcus mutans in caries etiology, and raises the intriguing possibility of the participation of the eukaryotic oral fungal pathogen Candida in the caries process. The virulence attributes of Candida species such as their acidogenicity and aciduric nature, the ability to develop profuse biofilms, ferment and assimilate dietary sugars, and produce collagenolytic proteinases are all indicative of their latent cariogenic potential. Based on the above, oral candidal counts have been used by some as a caries risk indicator. On the contrary, other studies suggest that Candida is merely a passenger extant in an acidic cariogenic milieu, and not a true pathogen. In this review, we critically examine the varying roles of Candida, and traditionally accepted cariogens such as the mutans group of streptococci in the pathobiology of dental caries. The weight of available data tends to imply that Candida may play a pivotal role as a secondary agent perpetuating the carious process, especially in dentinal caries.

Extracellular phospholipase production of oral Candida albicans isolates from smokers, diabetics, asthmatics, denture wearers and healthy individuals following brief exposure to polyene, echinocandin and azole antimycotics

Abstract Objective Candida albicans is the primary causative agent of oral candidosis, and one of its key virulent attributes is considered to be its ability to produce extracellular phospholipases that facilitate cellular invasion. Oral candidosis can be treated with polyenes, and azoles, and the more recently introduced echinocandins. However, once administered, the intraoral concentration of these drugs tend to be sub-therapeutic and rather transient due to factors such as the diluent effect of saliva and cleansing effect of the oral musculature. Hence, intra-orally, the pathogenic yeasts may undergo a brief exposure to antifungal drugs. We, therefore, evaluated the phospholipase production of oral C. albicans isolates following brief exposure to sub-therapeutic concentrations of the foregoing antifungals. Materials and methods Fifty C. albicans oral isolates obtained from smokers, diabetics, asthmatics using steroid inhalers, partial denture wearers and healthy individuals were exposed to sub-therapeutic concentrations of nystatin, amphotericin B, caspofungin, ketoconazole and fluconazole for one hour. Thereafter the drugs were removed and the phospholipase production was determined by a plate assay using an egg yolk-agar medium. Results The phospholipase production of these isolates was significantly suppressed with a percentage reduction of 10.65, 12.14, 11.45 and 6.40% following exposure to nystatin, amphotericin B, caspofungin and ketoconazole, respectively. This suppression was not significant following exposure to fluconazole. Conclusions Despite the sub-therapeutic, intra oral, bioavailability of polyenes, echinocandins and ketoconazole, they are likely to produce a persistent antifungal effect by suppressing phospholipase production, which is a key virulent attribute of this common pathogenic yeast.

Extracellular phospholipase production of oral Candida albicans isolates from smokers, diabetics, asthmatics, denture wearers and healthy individuals following brief exposure to polyene, echinocandin and azole antimycotics

Objective Candida albicans is the primary causative agent of oral candidosis, and one of its key virulent attributes is considered to be its ability to produce extracellular phospholipases that facilitate cellular invasion. Oral candidosis can be treated with polyenes, and azoles, and the more recently introduced echinocandins. However, once administered, the intraoral concentration of these drugs tend to be sub-therapeutic and rather transient due to factors such as the diluent effect of saliva and cleansing effect of the oral musculature. Hence, intra-orally, the pathogenic yeasts may undergo a brief exposure to antifungal drugs. We, therefore, evaluated the phospholipase production of oral C. albicans isolates following brief exposure to sub-therapeutic concentrations of the foregoing antifungals. Materials and methods Fifty C. albicans oral isolates obtained from smokers, diabetics, asthmatics using steroid inhalers, partial denture wearers and healthy individuals were exposed to sub-therapeutic concentrations of nystatin, amphotericin B, caspofungin, ketoconazole and fluconazole for one hour. Thereafter the drugs were removed and the phospholipase production was determined by a plate assay using an egg yolk-agar medium. Results The phospholipase production of these isolates was significantly suppressed with a percentage reduction of 10.65, 12.14, 11.45 and 6.40% following exposure to nystatin, amphotericin B, caspofungin and ketoconazole, respectively. This suppression was not significant following exposure to fluconazole. Conclusions Despite the sub-therapeutic, intra oral, bioavailability of polyenes, echinocandins and ketoconazole, they are likely to produce a persistent antifungal effect by suppressing phospholipase production, which is a key virulent attribute of this common pathogenic yeast.(AU)

Extracellular phospholipase production of oral Candida albicans isolates from smokers, diabetics, asthmatics, denture wearers and healthy individuals following brief exposure to polyene, echinocandin and azole antimycotics.

OBJECTIVE: Candida albicans is the primary causative agent of oral candidosis, and one of its key virulent attributes is considered to be its ability to produce extracellular phospholipases that facilitate cellular invasion. Oral candidosis can be treated with polyenes, and azoles, and the more recently introduced echinocandins. However, once administered, the intraoral concentration of these drugs tend to be sub-therapeutic and rather transient due to factors such as the diluent effect of saliva and cleansing effect of the oral musculature. Hence, intra-orally, the pathogenic yeasts may undergo a brief exposure to antifungal drugs. We, therefore, evaluated the phospholipase production of oral C. albicans isolates following brief exposure to sub-therapeutic concentrations of the foregoing antifungals. MATERIALS AND METHODS: Fifty C. albicans oral isolates obtained from smokers, diabetics, asthmatics using steroid inhalers, partial denture wearers and healthy individuals were exposed to sub-therapeutic concentrations of nystatin, amphotericin B, caspofungin, ketoconazole and fluconazole for one hour. Thereafter the drugs were removed and the phospholipase production was determined by a plate assay using an egg yolk-agar medium. RESULTS: The phospholipase production of these isolates was significantly suppressed with a percentage reduction of 10.65, 12.14, 11.45 and 6.40% following exposure to nystatin, amphotericin B, caspofungin and ketoconazole, respectively. This suppression was not significant following exposure to fluconazole. CONCLUSIONS: Despite the sub-therapeutic, intra oral, bioavailability of polyenes, echinocandins and ketoconazole, they are likely to produce a persistent antifungal effect by suppressing phospholipase production, which is a key virulent attribute of this common pathogenic yeast.

Clindamicina para el tratamiento de infecciones dentales / Clindamycin for the treatment of dental infections

La clindamicina es un antibiótico de amplio espectro con actividad contra los aerobios grampositivos y una extensa gama de bacterias anaerobias, entre ellas los patógenos productores de betalactamasa. Los estudios in vitro e in vivo han demostrado que este fármaco alcanza una concentración elevada en el punto de infección, reduce la virulencia de las bacterias y refuerza las actividades fagocíticas de los linfocitos inmunitarios del huésped. La clindamicina por vía oral se absorbe con rapidez y eficacia, y su concentración permanece por encima de la concentración inhibidora mínima de la mayoría de los organismos por lo menos durante 6 horas. En este análisis, presentaremos pruebas de la eficacia e inocuidad de la clindamicina en el tratamiento de las infecciones odontogénicas con datos de estudios preclínicos y clínicos, los cuales avalan la aplicación general de este antibiótico como antiinfeccioso en el campo de la odontología.

Clindamycin is an antibiotic of wide range of action with a great activity against aerobic gram-positive germs and a broad spectrum of anaerobic bacteria, among which we can find the pathogenic agents that produce Beta-lactamase. The in vitro and in vivo have shown that this medicine reaches a high concentration at the infection point, reduces the bacteria virulence, and strengthens the phagocytic activity of the immunizing lymphocyte of the host. Clindamycin through oral ingestion is absorbed very quickly and effectively, and its concentration remains the same above the minimum inhibitory concentration of most of the organisms at least for six hours. In this analysis, we will introduce some proofs about the effectiveness and innocuousness of clindamycin in the treatment of odontogenic infections. This data is based upon clinical and pre-clinical studies that support the general use of this mentioned antibiotic as an anti-infectious agent in the field of odontology.

High oral prevalence of Candida krusei in leprosy patients in northern Thailand

Although Candida albicans is the most common human yeast pathogen, other Candida species such as C. krusei are now recognized as emerging agents, especially in patients with human immunodeficiency virus (HIV) disease. C. krusei is inherently resistant to the widely used triazole antifungal fluconazole and poses therapeutic problems, especially in systemic candidiasis. In a surveillance study of leprosy patients (with arrested or burnt-out disease) in a leprosarium in northern Thailand, we found a rate of oral carriage of C. krusei (36 per cent) significantly (P smaller 0.05) higher than that for a healthy control group (10 per cent). Among the Candida-positive patients, 16 of 35 (46 per cent) carried C. krusei, while C. albicans was the second most common isolate (12 of 35 patients; 34 per cent). The corresponding figures for the control group were 2 of 13 (15 per cent) and 6 of 13 (46 per cent), respectively. Studies of the antifungal resistance of the C. krusei isolates from patients indicated that all except one of the isolates were resistant to fluconazole, two isolates were resistant to ketoconazole, and all isolates were sensitive to amphotericin B. Evaluation of their genetic profiles by randomly amplified polymorphic DNA analysis with three different primers and subsequent analysis of the gel profiles by computerized cluster-derived dendrograms revealed that the C. krusei isolates from patients belonged to 10 disparate clusters, despite the origin from a single locale. These nascent findings indicate an alarmingly high prevalence of a Candida species resistant to a widely used antifungal in a part of the world where HIV disease is endemic.