Quorum sensing (QS) regulates the metabolic activity of planktonic cells, induces microbial biolm formation and contributes to virulence. In this type of intercellular communication, the microbes communicate via the synthesis and secretion of cell signaling molecules. Once the Secreted signaling molecule reaches a threshold level, the fungus can detect sufcient cell density (Padder etal. 2018). The impor­tance of QS is illustrated by the fact that its inhibition has become a focus in the development of new antifungal drugs. In addition to biolm formation, it also con­tributes to antibiotic resistance, virulence factors, bioluminescence and sporulation (Hogan 2006)

Polymorphism, another factor responsible for fungal virulence, can be observed in several fungal species, including C. albicans. Fungus can take the form of parallel­walled true hyphae, long elliptical cells with constricted septa, or ovoid budding yeast. Other morphologies include Aspergillus spp. spores and white-opaque cells that form during switching (Ni etal. 2010). Yeasts and hyphae have different func­tions and are commonly seen during an infection (Mayer etal. 2013). The ‘dimor­phism’ is the transition between the growth forms hyphae and yeast, which is crucial for pathogenicity. Attenuated pathogenicity is typically associated with mutants that cannot form hyphae invitro. Nevertheless, both forms have their advantages, as the hyphae form is more invasive and the smaller yeast form is most responsible for spread. Numerous elements, including nutrient deprivation, serum or N-acetylglucosamine, physiological temperature, and CO2, encourage the growth of hyphae during infection. Quorum sensing, which is required for microbial com­munication, also controls morphogenesis (Sudbery 2011). Factors such as the gene products, TUP1, CPH1 and EFG1, are important transcriptional regulators that regulate lamentous growth. EFG1 and CPH1 are the activators of lamentous growth in C. albicans, as the null mutants of CPH1 show a defect in normal hyphal growth at 37°C (Csank etal. 1997). Similarly, the null mutants of CPH1 and EFG1 show large and smooth colonies. Moreover, the deletion of both copies of the TUP1 gene shows the lamentous form in C. albicans, indicating the role of TUP1 as a negative regulator of lamentous growth (Braun and Johnson 1997). The switch from a budding yeast form to a lamentous form in Candida can be initiated by a MAP kinase cascade (Csank etal. 1997). Hyphal development is associated with the expression of several genes encoding virulence factors. The aspartic proteases Sap4, Sap5, and Sap6, the hyphal wall protein Hwp1, the agglutinin-like sequence protein Als3, and the hyphal-associated proteins Ece1 and Hyr1 are examples of these types of proteins (Mayer etal. 2013). The growth of Aspergillus spp. begins with the germination of the conidium, which leads to the formation of an undiffer­entiated mass of hyphal cells. The hyphal cells form a mycelium during sexual reproduction. On the other hand, these hyphal cells stop growing, which also leads to the formation of spores and conidiophores (Ni et al. 2010). The conidia of A. fumigatus are released into the atmosphere and are so small that they can be ingested by humans as soon as they reach the alveoli. In immunocompromised hosts, the conidia can germinate into invasive hyphae that can invade the blood ves­sels and migrate to distant sites. The hyphal cell wall’s rigidity, the synthesis of different fungal proteins including hydrophobins, melanin, and toxins, as well as the spores’ structural characteristics, all aid in the fungus’s ability to escape the host’s defences and increase A. fumigatus’ virulence (Yu 2010).

Both saprophytic and pathogenic fungal species require the digestion of lipids or proteins by lipases and proteases in order to survive and grow. In pathogenic fungi, hydrolytic enzymes are crucial for their virulence. Among these enzymes, proteases and lipases are the best known extracellular enzymes that can damage host tissues and promote the spread of infection (Park etal. 2013).