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Presence of Candida tropicalis on Staphylococcus epidermidis Biofilms Facilitated Biofilm Production and Candida Dissemination: An Impact of Fungi on Bacterial Biofilms

ABSTRACT: While Staphylococcus epidermidis (SE) is a common cause of infections in implanted prostheses and other indwelling devices, partly due to the biofilm formation, Candida tropicalis (CT) is an emerging Candida spp. with a potent biofilm-producing property. Due to the possible coexistence between SE and CT infection in the same patient, characteristics of the polymicrobial biofilms from both organisms might be different from those of the biofilms of each organism. Then, the exploration on biofilms, from SE with or without CT, and an evaluation on l-cysteine (an antibiofilm against both bacteria and fungi) were performed. As such, Candida incubation in preformed SE biofilms (SE > CT) produced higher biofilms than the single- (SE or CT) or mixed-organism (SE + CT) biofilms as determined by crystal violet staining and fluorescent confocal images with z-stack thickness analysis. In parallel, SE > CT biofilms demonstrated higher expression of icaB and icaC than other groups at 20 and 24 h of incubation, suggesting an enhanced matrix polymerization and transportation, respectively. Although organism burdens (culture method) from single-microbial biofilms (SE or CT) were higher than multi-organism biofilms (SE + CT and SE > CT), macrophage cytokine responses (TNF-α and IL-6) against SE > CT biofilms were higher than those in other groups in parallel to the profound biofilms in SE > CT. Additionally, sepsis severity in mice with subcutaneously implanted SE > CT catheters was more severe than in other groups as indicated by mortality rate, fungemia, serum cytokines (TNF-α and IL-6), and kidney and liver injury. Although CT grows upon preformed SE-biofilm production, the biofilm structures interfered during CT morphogenesis leading to the frailty of biofilm structure and resulting in the prominent candidemia. However, l-cysteine incubation together with the organisms in catheters reduced biofilms, microbial burdens, macrophage responses, and sepsis severity. In conclusion, SE > CT biofilms prominently induced biofilm matrix, fungemia, macrophage responses, and sepsis severity, whereas the microbial burdens were lower than in the single-organism biofilms. All biofilms were attenuated by l-cysteine.

SUBMITTER: Phuengmaung P

PROVIDER: S-EPMC8569676 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundPolymicrobial infections are responsible for significant mortality and morbidity in adults and children. Staphylococcus epidermidis and Candida albicans are the most frequent combination of organisms isolated from polymicrobial infections. Vascular indwelling catheters are sites for mixed species biofilm formation and pose a significant risk for polymicrobial infections. We hypothesized that enhancement of biofilms in a mixed species environment increases patient mortality and morbidity.ResultsMixed species biofilms of S. epidermidis and C. albicans were evaluated in vitro and in a subcutaneous catheter infection model in vivo. Mixed species biofilms were enhanced compared to single species biofilms of either S. epidermidis or C. albicans. A mixed species environment increased catheter infection and increased dissemination of S. epidermidis in mice. Microarrays were used to explore differential gene expression of S. epidermidis in the mixed species biofilms. In mixed species biofilms, compared to single species S. epidermidis biofilms, 2.7% of S. epidermidis genes were upregulated and 6% were down regulated. Staphylococcal autolysis repressors lrgA and lrgB were down regulated 36-fold and 27-fold respectively. The role of biofilm extracellular DNA was investigated by quantitation and by evaluating the effects of DNAse in a concentration and time dependent manner. S. epidermidis specific eDNA was increased in mixed species biofilms and further confirmed by degradation with DNAse.ConclusionsMixed-species biofilms are enhanced and associated with increased S. epidermidis-specific eDNA in vitro and greater systemic dissemination of S. epidermidis in vivo. Down regulation of the lrg operon, a repressor of autolysis, associated with increased eDNA suggests a possible role for bacterial autolysis in mixed species biofilms. Enhancement and systemic dissemination of S. epidermidis may explain adverse outcomes after clinical polymicrobial infections of S. epidermidis and C. albicans.

Project description:Epidemiological studies comparing clinical and commensal Staphylococcus epidermidis isolates suggest that biofilm formation is a discriminant biomarker. A study showed that four non-biofilm-forming clinical S. epidermidis isolates could form an induced biofilm by trypsin treatment, suggesting that S. epidermidis can form biofilms in a protease-independent way and in a trypsin-induced way. In this study, the trypsin capacity to induce biofilm formation was evaluated in non-biofilm-forming S. epidermidis isolates (n = 133) in order to support this mechanism and to establish the importance of total biofilms (meaning the sum of protease-independent biofilm and trypsin-induced biofilm). Staphylococcus epidermidis isolates from ocular infections (OI; n = 24), prosthetic joint infections (PJI; n = 64), and healthy skin (HS-1; n = 100) were screened for protease-independent biofilm formation according to Christensen's method. The result was that there are significant differences (p < .0001) between clinical (43.2%) and commensal (17%) protease-independent biofilm producers. Meanwhile, non-biofilm-forming isolates were treated with trypsin, and biofilm formation was evaluated by the same method. The number of commensal trypsin-induced biofilm producers significantly increased from 17% to 79%. In contrast, clinical isolates increased from 43.2% to 72.7%. The comparison between clinical and commensal total biofilm yielded no significant differences (p = .392). A similar result was found when different isolation sources were compared (OI vs. HS-1 and PJI vs. HS-1). The genotype icaA- /aap+ was associated with the trypsin-induced biofilm phenotype; however, no correlation was observed between aap mRNA expression and the level of trypsin-induced biofilm phenotype. Studying another group of commensal S. epidermidis non-biofilm-forming isolates (HS-2; n = 139) from different body sites, it was found that 70 isolates (60.3%) formed trypsin-induced biofilms. In conclusion, trypsin is capable of inducing biofilm production in non-biofilm-forming commensal S. epidermidis isolates with the icaA- /aap+ genotype, and there is no significant difference in total biofilms when comparing clinical and commensal isolates, suggesting that total biofilms are not a discriminant biomarker.

Project description:The biofilm phenotype offers bacterial communities protection from environmental factors, as evidenced by its role in the viability, persistence, and virulence of cells under conditions in which flow is present, such as in riverbeds, industrial piping networks, and the human circulatory system. Here, we examined the hypothesis that temperature-an environmental factor that affects the growth of the Gram-positive bacterium Staphylococcus epidermidis-controls, through dual mechanisms, persistence of this bacterial strain in a shear environment characteristic of the human circulatory system. We demonstrated that temperature and antibiotics impact the surface-adhered biofilm and material disseminated downstream in different ways. Specifically, by means of three-dimensional (3D) confocal and scanning electron microscopy, an increase in surface-adhered biofilm heterogeneity was observed with increasing temperature. Additionally, we found a 4-log decrease in cell viability at the biofilm surface as the perfusate temperature was increased from 37°C to 50°C. Finally, the viability of cell-containing fragments that were disseminated from the substrate was assessed by downstream sampling, culture, and optical density measurement. We found that although temperature decreased the viability of the surface-adhered biofilm, the downstream material remained viable. And yet, in the presence of antibiotics, the growth of disseminated material was nearly completely inhibited, even though the addition of antibiotics had no significant impact on the viability of the surface-adhered biofilm. The mechanism involves both biofilm structural damage, as quantified by morphology of debrided material, and reduced cell viability, as quantified by assay of bacterial cells present in the surface-adherent biofilm and in the downstream effluent. The results potentially identify parameter ranges in which elevated temperature could augment current antibiotic treatment regimens.IMPORTANCE Bacterial biofilms are a leading cause of medical device infections. Staphylococcus epidermidis is commonly responsible for these types of infections. With increasing occurrences of antibacterial resistance, there has been a new push to explore treatment options that augment traditional antibiotic therapies. Here, we show how thermal treatment can be applied to both degrade bacterial biofilms on substrates and impede the proliferation of cells that detach from them. Understanding the response of both surface-adhered and dispersed bacterial cells under thermal stress conditions is a foundational step toward the development of an in situ treatment/remediation method for biofilm growth in medical devices; such an application could use oscillatory flow of heated fluid in a catheter as an adjuvant to antibiotic treatment. The work furthermore provides new insight into the viability of disseminated biofilm material.

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Presence of Candida tropicalis on Staphylococcus epidermidis Biofilms Facilitated Biofilm Production and Candida Dissemination: An Impact of Fungi on Bacterial Biofilms

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