[2] In the history of fungi, the name of genus Candida, derived from the family Debaryomycetaceae,[3] comes from the Latin term "candidus" which has the meaning of “glowing white” and also refers to as smooth and glistening.

[8] Physiological profiles relating to carbon and nitrogen utilization are of value in determining species, as are the presence certain distinctive biochemical features.

[6] Increasingly, molecular genetic methods such as DNA sequencing are used as primary tools for the accurate determination of species identifications in this group.

[3] A mould exhibits dimorphism[8] forming a single-celled yeast or so-called blastoconidia which reproduces by simple budding.

[8] Conidia are types of simple and unicellular bodies that could also take the form of multicellular cells with different shapes, sizes, and colors.

[3][4] Under specific conditions of reduced oxygen level in host tissues, submerged colonies in agar medium, or in the presence of 5-10% CO2, true, septate hyphae may form.

[3] This test uses the azo dye, diazonium blue B which differentially stains cells from species affiliated with the Division, Basidiomycota.

[10] They are commonly found on plants and in the digestive system of mammals, especially in the gastrointestinal tract, and in the mucocutaneous membranes of humans.

[3] C. tropicalis is considered as an osmotolerant yeast; microorganisms that are able to survive in high salt concentration and able to develop fungal persistence in saline environments.

[5] C. tropicalis is the second most virulent Candida species[7] that can significantly affect by spreading through the weakened immune system host and can occupy the gastrointestinal tract within 30 minutes of inoculation, all this resulting in increased mortality.

[17] C. tropicalis is virulent due to its ability to produce biofilm, secrete lytic enzymes, adhere to epithelial and endothelial cells, and undergo transition of bud to hyphae.

[18][11][7] Biofilms are complex structures that are formed from the grouping of microorganisms on a local surface, either biotic or abiotic,[18] dependent on the ability of cellular adhesion to substrates.

[5] phospholipases will hydrolyze phospholipid; assist to break the epithelial cell membrane structure allowing the hyphal tip to enter into the cytoplasm.

[17] Although provided with oral cavity defenses such as epithelial cells, saliva, salivary immunoglobin (IgA), lysozyme, lactoferrin, histidine-rich polypeptide and lactoperoxidase to suppress C. tropicalis’ overgrowth,[17] C. tropicalis is reported to secrete additional products that can preferably target onto T-cell deficient host.

[5] Superficial and localized mucosal infections are mostly reported with a higher risk factor when combined with other diseases found in a patient.

[5] Only filamentous growth of C. tropicalis have the ability to invade and colonize orally in the epithelium,[11] commonly seen in cancer patients and higher risk for someone who subsequently develops disseminated invasive disease.

[17] C. tropicalis colonization is favoured in the gastrointestinal tract;[17] a common risk factor for individuals that are susceptible for invasive candidiasis development.

[5] Risk factors that contribute to the high rate are leukemia, anti-neoplastic chemotherapy, previous neutropenia, central venous catheters, long stay on intensive care and total parenteral nutrition.

[5] echinocandin are a type of non-competitive inhibitors of cell wall 1,3-b-D-glucan synthase complex mainly used to treat fungal infections.

[5][4][7] Azoles are agents that can deplete ergosterol, the main component of the fungus cell wall membrane,[7] in order to inhibit fungal growth.

[5] C. tropicalis can rapidly develop resistance towards fluconazole therefore it's not recommended to retreat fluconazole-treated patients with recurrent candidiasis.

[4] All of the mentioned treatments and drug therapies can also be applied onto neonates and premature newborns taking into account the amount of recommended dose.