Candida tropicalis

C. tropicalis was originally isolated from a patient with fungal bronchitis in 1910 and called Oidium tropicale (Castellani, 1912).

C. tropicalis colonies form white to cream-coloured colonies on Sabouraud dextrose agar (SDA). These have a creamy texture and a smooth appearance and may have slightly wrinkled edges. Therefore this species is not distinguishable from other Candida species. After 7 days of microculture, spherical or ovoid blastoconidia develop, growing in pairs or alone in groups. Furthermore, pseudohyphs are formed in branched chains; from then on they can also grow into true hyphae (Silva et al. 2012).

It has been shown that Candida tropicalis is one of the most important pathogenic Candida species (Marcos-Zambrano L et al. 2014). C. tropicalis is a common trigger of candidemia (especially in Latin American countries and in Asia). C. tropicalis has a greater genetic similarity to C. albicans than other Candida species (Butler et al., 2009). This close evolutionary relationship is also reflected in the phenotypic and biochemical characteristics of both species. In terms of biochemical properties, it is known that C. tropicalis can ferment galactose, sucrose, maltose and trehalose and assimilate these and other carbohydrates via the oxidation pathway.

C. tropicalis is considered a strong biofilm former and adheres strongly to epithelial and endothelial cells (Marcos-Zambrano et al. 2014). This ability to form biofilms is an important determinant of virulence in Candida spp. and is considered to be an important component of microbial growth (Fanning and Mitchell 2012).

Adhesion of blastoconidia to host cells is regarded as a first step both for colonization and establishment of Candida infections and involves interactions between fungal cells and host surfaces (Cannon and Chaffin, 2001). It is a complex and multiphase process involving different factors such as the microorganism involved, the composition of the adhesion surfaces and various environmental factors (Silva-Dias et al., 2012).

Enzyme formers: To facilitate penetration into host tissue, several pathogenic microbes secrete lytic enzymes such as proteinases, phospholipases and haemolysins to destroy, alter or damage the integrity of host membranes, resulting in dysfunction or rupture of host cells. Pathogenic Candida species produce a variety of hydrolases, including secreted asparagine proteinases (saps). They have the ability to break down epithelial barriers, antibodies, complement and cytokines and are encoded by a large family of genes.

The cell wall structure of C. tropicalis consists of hydrophobic proteins embedded in a cellular matrix. Hydrophobic particles tend to bind to a variety of plastic materials and host proteins such as laminin, fibrinogen and fibronectin (Tronchin et al. 2008). These properties also appear to be a pathogenicity criterion.

Biofilm formation:

Biofilms are complex structures formed by a community of microorganisms adhering to solid surfaces of biotic or abiotic nature. The first step in the formation of biofilms depends on cellular adhesion cells to substrates and the further formation of a base layer. C. tropicalis adhesins are involved here. These are regulated by the BCR1 gene (also regarded as cell wall regulator). Other genes involved in the biofilm formation of C. tropicalis are WOR1, UME6, NRG1, ERG11 and MDR1. Besides morphogenesis and phenotypic change, WOR1 is one of the most important transcription factors in the formation of biofilms.

Furthermore, antifungal resistance to azoles, polyenes and echinocandins has been described in C. tropicalis (Choi et al. 2016). Furthermore, the species is considered an osmotic tolerant microorganism (ability to survive up to a high salt concentration - Zuza-Alves et al. 2016). This ability seems to have a role in the development of resistance.

With regard to the expression of resistance genes against antimycotics, the genes ERG11 (ergosterol biosynthesis) and MDR1 (multidrug resistance) are related to resistance to fluconazole. Bizerra et al (2008) reported increased expression of these genes in sessile cells of C. tropicalis isolated from vulvovaginal candidiasis (VVC) and urocultures resistant to both fluconazole and amphotericin.

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