Candida albicans in Association with Pathogenic Bacteria to Form Mono and Polymicrobial Biofilms
DOI:
https://doi.org/10.32792/utq/utjsci/v12i2.1451Keywords:
Biofilm, monospecies biofilm, multispecies biofilm, Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, Candida albicansAbstract
Abstract
Biofilm formation by the accumulation of various pathogens may be responsible for chronic and acute human infections. This research aimed to explain the role of Candida albicans in biofilm formation with pathogenic bacteria isolated from clinical samples. Ninety clinical samples were collected to isolate pathogenic bacteria and Candida albicans. The isolation and identification of these pathogens were performed using selective media and the VITEK 2 system. Flat-bottom microtiter plates were used to evaluate the ability of all isolates to form biofilms in case of monomicrobial and polymicrobial species. Three pathogenic bacteria, including Staphylococcus aureus (n=8), Pseudomonas aeruginosa (n=8), and Escherichia coli (n=4), as well as C. albicans (n=20), were isolated. All isolates were submitted to evaluate their ability to form monomicrobial and polymicrobial biofilms. In the case of monomicrobial species, C. albicans (100%) and bacterial species (80%) showed a high percentage of biofilm formation. However, C. albicans was prepared to make an adherence phase for each one of S. aureus, P. aeruginosa, and E. coli. In this experiment, all bacterial isolates improved their ability to form polymicrobial biofilms. in contrast, some bacterial isolates reduce their ability for forming polymicrobial biofilms if bacterial isolates are used as an adherence phase. In conclusion, the replacement of adherence phase of the polymicrobial biofilm causes either an increase or a decrease in the ability of organism to form a biofilm when compared to monomicrobial biofilms.
Received: 2025-07-22
Revised: 2025-09-20
Accepted: 2025-10-04
References
[1] G. Ramage, R. Rajendran, L. Sherry, and C. Williams, “Fungal biofilm resistance,” Int. J. Microbiol., vol. 2012, 2012.
[2] M. M. Zafer, G. A. Mohamed, S. R. M. Ibrahim, S. Ghosh, C. Bornman, and M. A. Elfaky, “Biofilm-mediated infections by multidrug-resistant microbes: a comprehensive exploration and forward perspectives,” Arch. Microbiol., vol. 206, no. 3, pp. 1–23, 2024.
[3] O. Grari et al., “A comprehensive review on biofilm-associated infections: Mechanisms, diagnostic challenges, and innovative therapeutic strategies,” Microbe (Netherlands), vol. 8, no. March, p. 100436, 2025.
[4] J. Talapko et al., “Candida albicans—The Virulence Factors and Clinical Manifestations of Infection,” J. Fungi, vol. 7, no. 2, p. 79, Feb. 2021.
[5] F. Chaabane, A. Graf, L. Jequier, and A. T. Coste, “Review on Antifungal Resistance Mechanisms in the Emerging Pathogen Candida auris,” Frontiers in Microbiology, vol. 10. 2019.
[6] C. E. Zago et al., “Dynamics of biofilm formation and the Interaction between Candida albicans and methicillin-susceptible (MSSA) and -resistant Staphylococcus aureus (MRSA),” PLoS One, vol. 10, no. 4, Apr. 2015.
[7] M. M. Harriott and M. C. Noverr, “Importance of Candida-bacterial polymicrobial biofilms in disease,” Trends in Microbiology, vol. 19, no. 11. Elsevier, pp. 557–563, 2011.
[8] J. F. MacFaddin, Biochemical tests for identification of medical bacteria - Ghent University Library, 3rd ed. Lippincott Williams & Wilkins, Philadelphia, 2000.
[9] M. Ligozzi, C. Bernini, M. G. Bonora, M. De Fatima, J. Zuliani, and R. Fontana, “Evaluation of the VITEK 2 system for identification and antimicrobial susceptibility testing of medically relevant gram-positive cocci,” J. Clin. Microbiol., vol. 40, no. 5, pp. 1681–1686, 2002.
[10] B. Willinger and M. Manafi, “Evaluation of CHROMagar Candida for rapid screening of clinical specimens for Candida species,” Mycoses, vol. 42, no. 1–2, pp. 61–65, 1999.
[11] M. B. Marak and B. Dhanashree, “Antifungal susceptibility and biofilm production of Candida spp. Isolated from clinical samples,” Int. J. Microbiol., vol. 2018, pp. 6–11, 2018.
[12] A. Singh, P. Prakash, A. Achra, G. Singh, A. Das, and R. Singh, “Standardization and classification of in vitro biofilm formation by clinical isolates of Staphylococcus aureus,” J. Glob. Infect. Dis., vol. 9, no. 3, pp. 93–101, Jul. 2017.
[13] S. Stepanović et al., “Quantification of biofilm in microtiter plates: overview of testing conditions and practical recommendations for assessment of biofilm production by staphylococci,” APMIS, vol. 115, no. 8, pp. 891–899, 2007.
[14] E. Kamali, A. Jamali, A. Ardebili, F. Ezadi, and A. Mohebbi, “Evaluation of antimicrobial resistance, biofilm forming potential, and the presence of biofilm-related genes among clinical isolates of Pseudomonas aeruginosa,” BMC Res. Notes, vol. 13, no. 1, p. 27, Jan. 2020.
[15] E. F. Kong, C. Tsui, S. Kucharíková, D. Andes, P. Van Dijck, and M. A. Jabra-Rizk, “Commensal protection of Staphylococcus aureus against antimicrobials by Candida albicans biofilm matrix,” MBio, vol. 7, no. 5, pp. e01365-16, 2016.
[16] G. Wall, D. Montelongo-Jauregui, B. Vidal Bonifacio, J. L. Lopez-Ribot, and P. Uppuluri, “Candida albicans biofilm growth and dispersal: contributions to pathogenesis,” Current Opinion in Microbiology, vol. 52. Elsevier, pp. 1–6, 2019.
[17] M. D. Macià, E. Rojo-Molinero, and A. Oliver, “Antimicrobial susceptibility testing in biofilm-growing bacteria,” Clinical Microbiology and Infection, vol. 20, no. 10. Elsevier, pp. 981–990, 2014.
[18] O. Ciofu and T. Tolker-Nielsen, “Tolerance and resistance of pseudomonas aeruginosabiofilms to antimicrobial agents-how P. aeruginosa Can escape antibiotics,” Frontiers in Microbiology, vol. 10, no. MAY. 2019.
[19] Y. Lim, H. J. Shin, A. S. Kwon, J. H. Reu, G. Park, and J. Kim, “Predictive genetic risk markers for strong biofilm-forming Staphylococcus aureus: FnbB gene and SCCmec type III,” Diagn. Microbiol. Infect. Dis., vol. 76, no. 4, pp. 539–541, 2013.
[20] E. O’Neill et al., “Association between methicillin susceptibility and biofilm regulation in Staphylococcus aureus isolates from device-related infections,” J. Clin. Microbiol., vol. 45, no. 5, pp. 1379–1388, 2007.
[21] F. Zhao, H. Yang, D. Bi, A. Khaledi, and M. Qiao, “A systematic review and meta-analysis of antibiotic resistance patterns, and the correlation between biofilm formation with virulence factors in uropathogenic E. coli isolated from urinary tract infections,” Microbial Pathogenesis, vol. 144, no. February. Elsevier Ltd, p. 104196, 2020.
[22] D. Balasubramanian, L. Harper, B. Shopsin, and V. J. Torres, “Staphylococcus aureus pathogenesis in diverse host environments,” Pathogens and Disease, vol. 75, no. 1. Oxford University Press, p. ftx005, 2017.
[23] H. Carolus, K. Van Dyck, and P. Van Dijck, “Candida albicans and Staphylococcus Species: A Threatening Twosome,” Frontiers in Microbiology, vol. 10. Frontiers Media SA, p. 2162, 2019.
[24] B. M. Peters et al., “Staphylococcus aureus adherence to Candida albicans hyphae is mediated by the hyphal adhesin Als3p,” Microbiol. (United Kingdom), vol. 158, no. 12, pp. 2975–2986, 2012.
[25] M. A. Pfaller, “Antifungal drug resistance: Mechanisms, epidemiology, and consequences for treatment,” Am. J. Med., vol. 125, no. 1 SUPPL., pp. S3–S13, 2012.
[26] T. Vila et al., “Therapeutic implications of C. albicans-S. aureus mixed biofilm in a murine subcutaneous catheter model of polymicrobial infection,” Virulence, vol. 12, no. 1, pp. 835–851,
2021.
[27] F. Nogueira, S. Sharghi, K. Kuchler, and T. Lion, “Pathogenetic impact of bacterial–fungal interactions,” Microorganisms, vol. 7, no. 10, Oct. 2019.
[28] R. Fourie, R. Ells, C. W. Swart, O. M. Sebolai, J. Albertyn, and C. H. Pohl, “Candida albicans and Pseudomonas aeruginosa interaction, with focus on the role of eicosanoids,” Frontiers in Physiology, vol. 7, no. FEB. Frontiers Media S.A., p. 64, 26-Feb-2016.
[29] M. Hamet et al., “Candida spp. airway colonization could promote antibiotic-resistant bacteria selection in patients with suspected ventilator-associated pneumonia,” Intensive Care Med., vol. 38, no. 8, pp. 1272–1279, 2012.
[30] A. Brand, J. D. Barnes, K. S. Mackenzie, F. C. Odds, and N. A. R. Gow, “Cell wall glycans and soluble factors determine the interactions between the hyphae of Candida albicans and Pseudomonas aeruginosa,” FEMS Microbiol. Lett., vol. 287, no. 1, pp. 48–55, 2008.
[31] J. L. da C. Lima, L. R. Alves, P. R. L. de A. Jacomé, J. P. Bezerra Neto, M. A. V. Maciel, and M. M. C. de Morais, “Biofilm production by clinical isolates of Pseudomonas aeruginosa and structural changes in LasR protein of isolates non biofilm-producing,” Brazilian J. Infect. Dis., vol. 22, no. 2, pp. 129–136, 2018.
[32] D. J. Cabral, S. Penumutchu, C. Norris, J. R. Morones-Ramirez, and P. Belenky, “Microbial competition between Escherichia coli and Candida albicans reveals a soluble fungicidal factor,” Microb. Cell, vol. 5, no. 5, pp. 249–255, 2018.
[33] H. Wissam and M. H. Al-Yasiri, “Cooperative interaction between Candida albicans and Escherichia coli isolated from urinary tract infections,” Chinese J. Ind. Hyg. Occup. Dis., vol. 39, no. 7, pp. 304–310, 2021.
[34] A. Trejo-Hernández, A. Andrade-Domínguez, M. Hernández, and S. Encarnación, “Interspecies competition triggers virulence and mutability in Candida albicans-Pseudomonas aeruginosa mixed biofilms,” ISME J., vol. 8, no. 10, pp. 1974–1988, 2014.
[35] H. M. H. N. Bandara, B. P. K Cheung, R. M. Watt, L. J. Jin, and L. P. Samaranayake, “Pseudomonas aeruginosa lipopolysaccharide inhibits Candida albicans hyphae formation and alters gene expression during biofilm development,” Mol. Oral Microbiol., vol. 28, no. 1, pp. 54–69, 2013.
Downloads
Published
License
Copyright (c) 2025 University of Thi-Qar Journal of Science

This work is licensed under a Creative Commons Attribution 4.0 International License.











