Identification of candida albicans and nonalbicans candida resistant species in tobacco users and oral squamous cell carcinoma patients: Comparison of HiCrome agar and automated VITEK 2 system

Abstract

Introduction: Candida is most common fungal pathogen in the immunocompromised and medically ill patients. Higher prevalence of Candida albicans has been reported in tobacco users and oral squamous cell carcinoma (OSCC) patients which may be due to immunosuppression. Recently, emergence of nonalbicans candida (NAC) species resistant to conventional antifungal treatment has been observed that requires accurate identification of organisms at species level for reduction of progression of suspicious oral lesions toward malignancy. Aims and Objectives: To detect and compare the prevalence of C. albicans and NAC species smokeless tobacco chewers, histopathologically confirmed oral squamous cell carcinoma patients and the normal individuals. Effectiveness of automated Vitek 2 system in comparison to HiCrome agar color media in the identification of the candida species was also evaluated. Methodology: One hundred and fifty patients (90 males, 60 females) aged between 20 and 76 years were divided into three groups: Group I individuals with habit of chewing Gutka, and betel quid/pan masala with or without tobacco, Group II individuals with clinically and histopathologically confirmed oral squamous cell carcinoma and Group III comprised of controls. Salivary samples were cultured on HiCrome agar color media and results were compared with those of Vitek 2 system in the accurate identification of candida species. Data were statistically analyzed and Chi-square test was used to estimate the effectiveness of color and Vitek method in the identification of candida species in all the three groups. P < 0.05 was considered to be statistically significant. RESULTS: HiCrome agar color method identified six candida isolates C. albicans , Candida tropicalis, Candida krusei and Candida glabrata isolates in all the three groups, with 0.00 unidentified organisms ( P = 0.00001) whereas VITEK 2 system identified five isolates of candida; C. albicans , Candida famat, Candida ciferri, Candida gulleri, C. tropicalis , unidentified organisms were observed in 26% of subjects. Further confirmation by supplemental tests indicated the presence of two or three organisms of different species/or subspecies with low reactivity biopattern. Higher incidence of opportunistic infections was seen in Group II OSCC patients ( P = 0.00001). Conclusion: The results suggested that there is shift toward NAC species, with higher species diversity in OSCC patients followed by gutka, betel quid/pan masala with or without tobacco users. Conventional agar media culture methods of species identification should be used in conjunction with automated ...

Real-Time PCR Detection of Candida Species in Biopsy Samples from Non-Smokers with Oral Dysplasia and Oral Squamous Cell Cancer: A Retrospective Archive Study

“…Due to the complex and multifaceted nature of carcinogenesis, the role of specific or entire oral microbiomes in oral cancer development and prognosis is still a subject of ongoing research [24]. C. albicans is one of the primary oral microorganisms whose influence on the development of oral cancer has been under evaluation for several decades [11,21,23,[27][28][29][30][31][32][33][34][35][36][37]. The connection between oral mycobiome and carcinogenesis is underscored by the intricate mechanisms through which C. albicans invades keratinocytes and surpasses the innate local defense abilities of oral mucosa.…”

“…These pioneering reports were further supported by several epidemiological and descriptive studies that revealed significantly higher oral Candida carriage among patients with oral epithelial dysplasia (OED) and OSCC compared to healthy subjects [27][28][29][30][31]. The suggested mechanisms for fungal involvement in oral carcinogenesis include the secretion of potential carcinogens, conversion of pro-carcinogens such as acetaldehyde or nitrosamines, destruction of epithelial barriers by secreted proteolytic enzymes, and excessive chronic inflammation [21,[32][33][34]. Recent in vitro experimental studies reported that OSCC cells secreted significantly more pro-inflammatory cytokine IL-1β when treated with zymosan (ZYM), a component from the cell wall of C. albicans [35], and the progress of OSCC was promoted by the presence of living C. albicans via stimulating the production of matrix metalloproteinases (MMPs), tumor metabolites, and tumor-promoting signal pathways [36].…”

The evil companion of OSCC: Candida albicans

“…Nitrosamines, as EGFR activators, can also initiate the activation of a variety of signaling pathways, including the phosphatidylinositol 3‐kinase (PI3k)/Akt/mammalian target of rapamycin (mTOR) pathway, promoting carcinogenesis independently or synergistically (Sonis & Amaral Mendes, 2016). Cigarette smoke increases the susceptibility of oral mucosa to C. albicans by inducing oxidative and redox dysfunction of epithelial cells, which is closely related to the onset of oral cancer (Saxena et al, 2021; Ye et al, 2021). Significantly, Sanjaya et al (2011) proposed that the direct carcinogenic effect of nitrosamines produced by C. albicans is still controversial; for example, immunosuppression may contribute to the activation of the nitrosation potential of C. albicans , which in turn is involved in the induction of oral carcinogenesis.…”