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Learn more: PMC Disclaimer | PMC Copyright Notice BMC Microbiol . 2026 Mar 6;26:340. doi: 10.1186/s12866-026-04912-0 Search in PMC Search in PubMed View in NLM Catalog Add to search Phenotypic-genotypic characteristics of Corynebacterium striatum clinical isolates and diversified biofilm production capabilities in the presence of plasma proteins Jiajia Su Jiajia Su 1 Department of laboratory medicine, Affiliated hospital of Inner Mongolian Medical University, Hohhot, 010050 People’s Republic of China Find articles by Jiajia Su 1, # , Juan Wen Juan Wen 1 Department of laboratory medicine, Affiliated hospital of Inner Mongolian Medical University, Hohhot, 010050 People’s Republic of China Find articles by Juan Wen 1, # , Wenqi Zheng Wenqi Zheng 1 Department of laboratory medicine, Affiliated hospital of Inner Mongolian Medical University, Hohhot, 010050 People’s Republic of China Find articles by Wenqi Zheng 1 , Junrui Wang Junrui Wang 1 Department of laboratory medicine, Affiliated hospital of Inner Mongolian Medical University, Hohhot, 010050 People’s Republic of China Find articles by Junrui Wang 1, ✉ Author information Article notes Copyright and License information 1 Department of laboratory medicine, Affiliated hospital of Inner Mongolian Medical University, Hohhot, 010050 People’s Republic of China ✉ Corresponding author. # Contributed equally. Received 2025 Dec 12; Accepted 2026 Feb 27; Collection date 2026. © The Author(s) 2026 Open Access This article is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License, which permits any non-commercial use, sharing, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if you modified the licensed material. You do not have permission under this licence to share adapted material derived from this article or parts of it. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc-nd/4.0/ . PMC Copyright notice PMCID: PMC13078081 PMID: 41787264 Abstract Background Corynebacterium striatum is an opportunistic pathogen associated with a wide range of hospital-acquired infections, in which biofilm production plays a critical role in nosocomial transmission and pathogenicity. Although genotypic heterogeneity among C. striatum clinical isolates has been increasingly recognized, factors influencing isolate-specific biofilm formation, particularly host-derived factors, remain poorly understood. This study investigated the biofilm formation characteristics of C. striatum isolates with distinct genotypic and phenotypic profiles under exposure to human plasma proteins. Methods Sixty clinical C. striatum isolates were collected from inpatients at the Affiliated Hospital of Inner Mongolia Medical University between December 2013 and August 2022. The isolates, subcultured onto blood agar plates and the single colonies, were identified using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, and antimicrobial susceptibility testing was conducted using the microbroth dilution method. Whole-genome sequencing was performed to assess genetic relatedness and to identify virulence and antibiotic resistance genes. Biofilm formation was evaluated using Congo red agar and crystal violet assays in the presence or absence of fibronectin or fibrinogen. Results Phylogenomic analysis classified the 60 C. striatum isolates into five evolutionary clades (I–V), with Clade I as the dominant lineage (45%, 27/60). Biofilm assays showed that 95% (57/60) of C. striatum isolates were biofilm producers, of which 56.14% (32/57) were moderate or strong producers. Notably, 92.59% (25/27) of Clade I isolates exhibited moderate or strong biofilm formation. Multidrug resistance was observed in 95% (57/60) of isolates, with high resistance rates to ciprofloxacin, cefepime, and ceftriaxone. Virulence gene distribution varied significantly across clades, with spaDEF (96.30%) and whiB3 (100%) being highly prevalent in Clade I. Proteinase K showed the strongest biofilm-degrading activity. Exposure to fibronectin or fibrinogen (50 µg/mL) enhanced biofilm formation in 47.37% (27/57) of isolates, whereas biofilm density decreased significantly in most strong biofilm-producing Clade I isolates. Conclusions This study reveals significant genomic heterogeneity among C. striatum clinical isolates and their association with biofilm formation. Importantly, it demonstrates isolate- and genotype-dependent effects of human plasma proteins on C. striatum biofilm production, highlighting the potential roles of spaDEF and whiB3 in pathogenicity. Supplementary Information The online version contains supplementary material available at 10.1186/s12866-026-04912-0. Keywords: Corynebacterium striatum, Biofilm, Whole genome sequencing, Plasma proteins Background As a commensal of human skin and mucous membranes, Corynebacterium striatum has increasingly been recognized as an important opportunistic pathogen capable of causing a range of invasive infections, particularly in immunocompromised patients and individuals undergoing invasive procedures [ 1 – 5 ]. Although its pathogenic mechanisms remain incompletely understood, accumulating evidence indicates that biofilm formation is a key factor contributing to pathogenicity, nosocomial transmission, and antimicrobial resistance [ 6 – 8 ]. Biofilms are complex microbial communities adhered to biotic or abiotic surfaces and embedded in an extracellular polymeric substance (EPS) matrix [ 9 ]. The EPS has a complex composition that includes polysaccharides (composed of homopolysaccharides or heteropolysaccharides), proteins, extracellular DNA (eDNA), glycoproteins, and lipids. This matrix plays a critical role in biofilm formation and maturation by stabilizing the biofilm structure [ 10 ]. Regarding C. striatum , extracellular proteins, eDNA, and exopolysaccharides also play important roles in regulation of its biofilm formation [ 11 ]. Additional bacterial factors implicated in biofilm regulation include cellular and physicochemical heterogeneity, quorum sensing, and resistance-related mechanisms [ 12 ]. Biofilm formation is also influenced by host-derived factors originating from innate and adaptive immune processes [ 13 ]. Plasma components, such as fibrin or fibronectin, may contribute to stabilization of extracellular matrix of biofilm [ 6 ]. Despite growing interest in the mechanisms underlying biofilm formation in C. striatum , several important knowledge gaps remain. Only a few genes, such as spaDEF , are associated with the initial stages of biofilm formation in C. striatum [ 11 ], and correlations between genotypes and biofilm production capacity have been explored in only a few studies [ 8 , 14 ]. The definite genetic mechanisms determining biofilm production capacity in C. striatum , but it remains poorly defined. Moreover, although exposure to plasma proteins has been reported to enhance biofilm production in C. striatum [ 6 ], its effects on isolates with different genomic backgrounds have not been elaborated. In this study, the phenotypic and genotypic characteristics of C. striatum clinical isolates collected at a teaching hospital in China were analyzed, and their biofilm production capabilities were evaluated in the presence and absence of human plasma proteins. Methods Isolate identification Sixty clinical isolates of C. striatum were collected from inpatients admitted to the Affiliated Hospital of Inner Mongolia Medical University, China, between December 2013 and December 2022. Isolates were stored at − 80 °C until use. For analysis, isolates were thawed, streaked onto Columbia blood agar plates, and incubated at 35 °C under 5% CO 2 for 24–48 h. Species identification was confirmed using matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS; EXS3000, Chongqing Zhongyuan Biotechnology Co., Ltd., China). Antimicrobial susceptibility testing Antimicrobial susceptibility testing was performed using the microbroth dilution method [ 11 ]. Briefly, fresh colonies of C. striatum were subcultured onto Columbia blood agar plates and incubated at 35 °C for 24 h. Single colonies were picked and inoculated in sterile broth and adjusted to a turbidity equivalent of 1.0 McFarland standard. A 50-µL aliquot of the standardized bacterial suspension was added to antimicrobial susceptibility broth, and 100 µL of the resulting mixture was dispensed into each well of antibiotic-loaded 96-well plates (Hunan Mindray Medical Technology Co., Ltd., China), including positive control and test wells. After incubating the plates at 35 °C for 24 h, the minimum inhibitory concentrations (MICs) were determined by visual assessment of growth inhibition. Results were interpreted as susceptible, intermediate, or resistant according to the Clinical and Laboratory Standards Institute guidelines (CLSI, M45-A2) [ 15 ]. Whole-genome sequencing Genomic DNA was extracted from overnight cultures of C. striatum isolates using a commercial bacterial DNA extraction kit (Tiangen Biotech, China). Briefly, cells were lysed with lysozyme and proteinase K, followed by ethanol precipitation and column purification. DNA concentration and quality were assessed using a NanoDrop 2000c spectrophotometer (Thermo Fisher Scientific, USA). DNA samples were fragmented to 350 bp by sonication, after which fragments were end-repaired, adapter-ligated for sequencing, and subsequently PCR-amplified. Finally, PCR products were purified using AMPure XP, analyzed for library size with an Agilent 2100 Bioanalyzer, and quantified by real-time PCR. Gene sequencing was performed on an Illumina NovaSeq PE150 platform (Illumina, USA). Raw sequencing data were filtered to generate clean data, which were used for genome assembly to generate sequence files reflecting basic genomic information. After evaluating the assembly results, single-nucleotide polymorphism (SNP) analysis was performed using MUMmer (version 3.22) alignment software, insertion–deletion (InDel) detection was conducted with LASTZ software, and structural variation (SV) analysis was performed separately. Phylogenetic trees were constructed using PhyML software with the neighbor-joining (NJ) method and were modified/annotated using Evolview 2.0 software. Prediction of antibiotic resistance genes and virulence genes Antibiotic resistance genes in C. striatum were predicted using the Comprehensive Antibiotic Resistance Database (CARD) [ 16 ]. The genomic data of C. striatum were translated into protein sequences and aligned against CARD using BLASTp. with an alignment coverage of ≥ 80% and alignment identity of ≥ 80% considered as valid antibiotic resistance genes. Virulence factors were predicted using BLASTp by aligning C. striatum protein sequences against the Virulence Factor Database (VFDB) [ 17 ]. Matches with an alignment coverage of ≥ 80% and alignment identity of ≥ 60% were retained as putative virulence factors of C. striatum [ 18 ]. Biofilm formation assay Biofilm formation abilities of C. striatum clinical isolates were assessed using a qualitative Congo red agar method and a semi-quantitative crystal violet staining assay. The Congo red agar assay was performed according to the method described by Moreno et al. [ 19 ]. Inoculated plates were incubated at 35 °C for 24 h and subsequently incubated at room temperature for an additional 24 h before visual observation. Isolates identified as biofilm producers by the Congo red agar method were further evaluated using the crystal violet staining assay. For the crystal violet assay, isolates were cultured overnight at 35 °C with shaking. The cultures were adjusted to a turbidity equivalent to a 0.5 McFarland standard (approximately 1.5 × 10⁸ colony-forming units (CFU)/mL) using sterile saline and then diluted 1:100 in tryptic soy broth (TSB). Aliquots of 200 µL of the diluted bacterial suspension were added in triplicate to 96-well plates, with wells containing TSB alone serving as blank controls. Plates were incubated at 35 °C for 24 h. Then, the supernatant was removed, and wells were gently washed three times with 200 µL phosphate-buffered saline (PBS). Biofilms were fixed with 200 µL methanol for 15 min and air-dried at room temperature. Subsequently, 200 µL of crystal violet solution at a concentration of 1 mg/mL was added to each well and incubated for 20 min. Excess stain was discarded, and wells were washed three times with 200 µL PBS. The stained biofilms in each well were solubilized with 160 µL glacial acetic acid, and absorbance was measured at OD 620nm using a microplate reader (Infinite 200 Pro, Tecan, Switzerland). Isolates were categorized as non-biofilm, weak, moderate, or strong biofilm producers based on previously described criteria [ 20 , 21 ]. OD ≤ cut-off OD (ODc), ODc < OD ≤ 2ODc, 2ODc < OD ≤ 4ODc, and OD > 4ODc indicated no, weak, moderate, and strong biofilm production, respectively. The ODc denotes the OD 620nm value of the blank control group. All experiments were performed in triplicate, and mean values were calculated. Biofilm degradation assay Extracellular matrix-degrading agents used in this study included a protein-degrading enzyme (Proteinase K, catalog number RT403; 20 mg/mL, Beijing Tiangen Biotech Co., Ltd), a poly-N-acetylglucosamine (PNAG)-degrading enzyme (β-N-acetylglucosaminidase, catalog number S10237; 32.5 U/mL, Shanghai Yuanye Biotechnology Co., Ltd), and an extracellular DNA (eDNA)-degrading enzyme (deoxyribonuclease I, DNase I, catalog number D8071; 5 mg/mL, Beijing Solarbio Science & Technology Co., Ltd). Biofilms were prepared in accordance with the method described above. After 24 h of incubation, the supernatant was aspirated and discarded, and 200 µL of each degrading agent was added to the wells containing established biofilms to achieve a final concentration of 20 µg/mL for each degrading agent. Culture plates were incubated at 37 °C for 2 h. Biofilms were then stained using the crystal violet assay for visualization and quantitative analysis. To systematically evaluate the biofilm degradation effects, the following groups were established. Wells without degrading agents served as controls, whereas wells treated with individual degrading agents were designated as experimental groups [ 22 , 23 ]. Because the optimal concentration and incubation time of Dispersin B for degradation of C. striatum biofilms have not been previously defined, additional degradation assays using a time–concentration gradient of Dispersin B were performed. Based on protocols from our previous work [ 11 ] and studies involving other Gram-positive pathogens, including Cutibacterium acnes , Actinobacillus pleuropneumoniae , and Staphylococcus spp. [ 24 , 25 ], representative C. striatum isolates with stronger biofilm-forming capacity were selected to conduct this assay. Biofilms were prepared as described above and incubated for 24 h, after which the supernatant was aspirated and discarded. Wells were treated with 200 µL Dispersin B under different conditions. Specifically, incubation times of 2 and 3 h were tested at a concentration of 20 µg/mL, and concentrations of 20 and 40 µg/mL were evaluated at a fixed incubation time of 2 h. Wells without degrading agents served as blank controls. Following incubation, biofilms were stained with crystal violet as described above. All experiments were independently repeated in triplicate to ensure the reliability and reproducibility of the results. Effects of plasma proteins on biofilm formation Biofilm formation in the presence of human plasma proteins was evaluated for 60 clinical C. striatum isolates using a protocol introduced by Guimarães et al. [ 26 ]. For each isolate, three wells of a 96-well polystyrene microtiter plate were coated with 150 µL of 50 µg/mL human plasma fibronectin (Roche) or fibrinogen (Sigma-Aldrich) dissolved in 1× PBS. As negative controls, additional three wells per isolate were coated with 1× PBS alone. For each experimental condition (protein-coated and PBS-only), wells without bacterial inoculation were included as blank controls to account for background absorbance. Plates were first incubated at 37 °C for 1 h to promote initial protein adsorption to the well surfaces, followed by overnight incubation at 4 °C to ensure stable coating through temperature-dependent protein conformational changes. Then, the well contents were carefully aspirated to avoid mechanical disruption of the adsorbed protein layer, and wells were washed twice with 200 µL of 1× PBS to remove unbound proteins. This washing step was critical to minimize non-specific binding effects during subsequent biofilm assays. Biofilm formation was subsequently quantified using the crystal violet staining assay as described above. Morphological observation of biofilms produced by C. striatum isolates Experiments were performed in 6-well polystyrene microtiter plates. Each well was pre-coated with 150 µL of human plasma fibronectin (Roche) or fibrinogen (Sigma-Aldrich) at a concentration of 50 µg/mL in 1× PBS, and wells coated with 1× PBS alone served as negative controls. Plates were incubated at 37 °C for 1 h to facilitate initial protein adsorption, followed by overnight incubation at 4 °C to ensure stable immobilization of the coated layer through temperature-mediated protein conformational changes. After incubation, well contents were carefully aspirated, and wells were washed twice with 200 µL of 1× PBS. Representative C. striatum isolates in the logarithmic growth phase were suspended in TSB and inoculated into each well to achieve an initial bacterial load of 10⁷ CFU per well. Sterile plastic coverslips (Thermanox™) were placed into each well to allow biofilm formation, and plates were incubated aerobically at 35 °C for 24 h. After incubation, the culture medium was discarded, and coverslips were transferred to 0.1 mol/L sodium cacodylate buffer (pH 7.2) containing 2.5% glutaraldehyde for fixation at room temperature for 30 min. Coverslips were then post-fixed in the same buffer supplemented with 1% osmium tetroxide and 2.5 mmol/L calcium chloride at room temperature for another 30 min. The coverslips with adherent biofilms were dehydrated through a graded acetone series, dried, and sputter-coated with gold. Biofilm morphology was observed using an Apreos 2 C scanning electron microscope (SEM, Thermo Fisher Scientific, USA) [ 11 ]. Statistical analysis The OD 620nm values were analyzed using SPSS version 23.0. Continuous variables were expressed as mean ± standard deviation when normally distributed and as median values otherwise. One-way ANOVA was used to compare differences in biofilm formation among isolates treated with fibrinogen, fibronectin, or without plasma proteins. The chi-square test was used to compare the proportions of isolates with a biofilm degradation rate of ≥ 50% between Clade I and other clades, as well as the proportions of strong biofilm-producing isolates from invasive versus non-invasive infection sites and respiratory tract versus non-respiratory tract samples. Fisher’s exact test was used to compare drug resistance rates between Clade I and other clades. A p -value of < 0.05 was considered statistically significant. Results Genotypic characteristics The majority of the C. striatum isolates were isolated from lower respiratory tract specimens (56.67%), followed by secretions (16.67%, 10/60), drainage fluid (8.33%, 5/60), and blood (5.00%, 3/60). With respect to hospital wards, isolates were most frequently obtained from the Neurosurgical Intensive Care Unit (16.67%, 10/60), followed sequentially by the General Intensive Care Unit (General ICU, 11.67%, 7/60), the Rehabilitation Ward (11.67%, 7/60), and the Orthopedics Department (8.33%, 5/60). Whole-genome sequencing–based comparisons of the 60 multidrug-resistant C. striatum isolates identified 68,240 core genome SNPs, of which 17,812 informative SNPs were used for phylogenetic inference. These isolates were clustered into five distinct evolutionary clades (Clades I–V, Fig. 1 ). Clade I was predominant (45.00%, 27/60), followed by Clade III (20.00%, 12/60), Clade II (18.33%, 11/60), Clade V (11.67%, 7/60), and Clade IV (5.00%, 3/60). Clade I was mainly composed of isolates collected between 2020 and 2022 and predominantly derived from sputum samples (77.78%). In contrast, isolates belonging to the other clades were obtained from more diverse specimen types. Overall, 55.56% (15/27) of Clade I isolates were recovered from patients admitted to Intensive Care Units (ICUs). Phenotypically, analysis revealed significant differences in biofilm formation among clades. Clade I exhibited the highest proportion of strong/moderate biofilm producers (92.59%), whereas all isolates in Clades IV and V were categorized as weak biofilm producers. Fig. 1. Open in a new tab Genotyping clustering analysis of 60 C. striatum isolates based on whole-genome sequencing. CS-1 The reference isolate, CVC Central Venous Catheter, BALF Bronchoalveolar Lavage Fluid Distribution of virulence genes and antibiotic resistance genes Comparative genomic analysis identified 33 antibiotic resistance genes in the C. striatum genomes, with detailed information provided in Additional file 1. In total, 37 putative virulence genes were identified (Additional file 2), some of which showed marked heterogeneity among clades and individual isolates (Fig. 2 ). Clade I isolates exhibited the highest carriage rates of key virulence genes. The spaDEF gene cluster and whiB3 were detected in 96.30% and 100% of Clade I isolates, respectively, whereas only fagB gene was universally absent. In Clade II, 72.73% (8/11) of isolates lacked the spaD gene; however, the strong biofilm-producing isolate CS-97 retained the complete spaDEF gene cluster. Clade III isolates carried whiB3 gene at a low frequency (8.33%, 1/12). All isolates in Clade IV were weak biofilm producers and lacked both spaE and spaF . Similarly, all Clade V isolates were weak biofilm producers; 85.71% (6/7) lacked at least one gene within the spaDEF cluster, and whiB3 gene was absent in 57.14% (4/7) of isolates. Fig. 2. Open in a new tab Distribution of predicted antibiotic resistance genes and virulence genes among 60 C. striatum clinical isolates The carriage rates of predicted partial antibiotic resistance genes are shown in Fig. 2 . Overall, 96.67% (58/60) of isolates harbored two or more resistance genes. The ermX gene was detected in 95.00% (57/60) of isolates and encodes an rRNA methyltransferase conferring resistance to macrolides, lincosamides, and streptogramins. The tetW gene, which encodes a ribosomal protection protein mediating tetracycline resistance, was identified in 78.33% (47/60) of isolates. Aminoglycoside-modifying enzymes encoded by aph(6’) and aph(3’) genes were detected in 18.33% (11/60) of isolates for at least one of these genes. Significant differences in the types and numbers of resistance genes were observed among clades. All Clade I isolates carried only erm family genes, tet family genes, and otr(A) . In contrast, Clade II isolates exhibited the greatest diversity, with a total of 31 different resistance gene types identified. In this clade, the carriage rates of ermX , tetW , and aph(3’’)-Ib were 90.91%, 36.36%, and 9.09%, respectively. In Clade V, 85.71% of isolates lacked the tetW gene. Putative adhesion- or biofilm-associated genes in C. striatum include spaD , spaE , spaF , srtB , and srtC . A statistical analysis was conducted to compare the distribution of these genes among 46 C. striatum isolates, comprising 27 isolates that showed enhanced biofilm formation in the presence of 50 µg/mL fibronectin or fibrinogen and 19 isolates that did not exhibit increased biofilm production under the same conditions. No statistically significant differences were observed in the distribution of these adhesion-related genes between the two groups of C. striatum isolates ( P > 0.05). Antimicrobial susceptibility testing results Antimicrobial susceptibility testing revealed distinct phenotypic resistance profiles among the 60 C. striatum isolates analyzed in this study (Fig. 3 ). None of the isolates were resistant to vancomycin, daptomycin, or linezolid, whereas resistance rates to other antibiotics widely varied. Resistance to gentamicin was lowest (11.67%, 7/60), and resistance to cefepime was highest, reaching 95% (57/60). Relatively high resistance rates to other tested antibiotics are summarized in Additional file 3. Notably, among the 60 C. striatum isolated analyzed, only 3 isolates belonging to Clade V were not classified as MDR isolates. Of these, isolate CS-477 showed no resistance to any of the tested antimicrobial agents, whereas isolates CS-482 and CS-413 were resistant only to erythromycin and clindamycin. Fig. 3. Open in a new tab Results of antimicrobial susceptibility testing of 60 C. striatum clinical isolates. VAN Vancomycin, DAP Daptomycin, LNZ Linezolid, GEN Gentamicin, TCY Tetracycline, ERY Erythromycin, SXT Trimethoprim-Sulfamethoxazole, CLI Clarithromycin, MEM Meropenem, PEN Penicillin, CRO Ceftriaxone, FEP Cefepime, CIP Ciprofloxacin As shown in Table 1 , clear genotype-associated differences in phenotypic resistance were observed among the 60 C. striatum isolates. Clade I isolates exhibited a significantly higher resistance rate to tetracycline compared with isolates from other clades ( P < 0.05). In contrast, resistance rates to gentamicin, clarithromycin, and meropenem were significantly lower in Clade I isolates than in isolates from the other clades ( P < 0.05). Table 1. Comparison of antimicrobial susceptibility results of C. striatum isolates between those belonging to Clade I and other clades Clade Susceptibility PEN CRO FEP MEM* GEN * TCY * ERY VAN SXT CIP CLI * DAP LNZ Clade I Sensitive (S, %) 0 0 0 0 100 0 0 100 18.52 0 0 100 100 Intermediate(I, %) 0 0 0 0 0 0 25.93 0 0 0 33.33 0 0 Resistant (R, %) 100 100 100 100 0 100 74.07 0 81.48 100 66.67 0 0 Other Clades Sensitive (S, %) 0 9.09 6.06 15.15 69.70 36.36 3.03 100 21.21 9.09 3.03 100 100 Intermediate(I, %) 15.15 3.03 3.03 0 9.09 0 15.15 0 0 0 6.06 0 0 Resistant (R, %) 84.85 87.88 90.91 84.85 21.21 63.63 81.82 0 78.79 90.91 90.91 0 0 Open in a new tab PEN Penicillin, CRO Ceftriaxone, FEP Cefepime, MEM Meropenem, GEN Gentamicin, TCY Tetracycline, ERY Erythromycin, VAN Vancomycin, SXT Trimethoprim-Sulfamethoxazole, CIP Ciprofloxacin, CLI Clarithromycin, DAP Daptomycin, LNZ Linezolid. * Indicates P < 0.05 Biofilm formation capability Based on the Congo red agar assay, 57 C. striatum isolates were identified as biofilm producers, whereas 3 isolates (CS-477, CS-413, CS-217) were identified as non-biofilm producers. Crystal violet staining further demonstrated that 21.05% (12/57), 35.09% (20/57), and 43.86% (25/57) of the C. striatum isolates were classified as strong, moderate, and weak biofilm producers, respectively. The 3 isolates (CS-477, CS-413, CS-217) identified as non-biofilm producers by the Congo red agar assay exhibited low OD 620nm values and were therefore categorized as weak biofilm producers in the crystal violet assay. As shown in Fig. 4 and Additional file 4, biofilm production capacity differed significantly among 60 C. striatum isolates from different clades. Most moderate and strong biofilm producers (78.13%, 25/32) belonged to Clade I, whereas all isolates in Clades IV and V were classified as weak biofilm producers. Fig. 4. Open in a new tab Biofilm-forming capability of 60 C. striatum using crystal violet staining Biofilm degradation characteristics Biofilm degradation assay demonstrated that Proteinase K exhibited the strongest degradative activity. After treatment with Proteinase K (20 µg/mL), 63.15% (36/57) of isolates showed a biofilm degradation rate of ≥ 50%. DNase I showed intermediate activity, with 45.61% (26/57) of isolates achieving a degradation rate of ≥ 50% following treatment at 20 µg/mL. In contrast, Dispersin B (20 µg/mL) showed the weakest degradation effect, with only 15.79% (9/57) of isolates showing a biofilm degradation rate of ≥ 50% (Fig. 5 A). Mean biofilm degradation rates also followed a similar pattern: Proteinase K (53.99 ± 18.86%) > DNase I (42.47 ± 20.39%) > Dispersin B (33.32 ± 18.46%) (Fig. 5 B). These findings suggest that the EPS of C. striatum biofilms is predominantly composed of proteins, followed by eDNA and polysaccharides. After DNase I treatment (20 µg/mL), the proportion of Clade I isolates with a biofilm degradation rate of ≥ 50% was significantly higher than that of isolates from other clades ( P < 0.05). In contrast, following Dispersin B treatment (20 µg/mL), the proportion of Clade I isolates achieving a degradation rate of ≥ 50% was significantly lower than that of isolates from other clades ( P < 0.05). After Proteinase K treatment (20 µg/mL), Clade I isolates showed a higher proportion of biofilm degradation rates of ≥ 50% than isolates from other clades; however, this difference was not statistically significant ( P > 0.05) (Fig. 5 C). Fig. 5. Open in a new tab Biofilm degradation characteristics of 57 C. striatum isolates. Proportion of isolates with a biofilm degradation rate of ≥ 50% after treatment with three extracellular matrix-degrading agents. (B) Mean biofilm degradation rates of the 57 biofilm-producing C. striatum isolates following treatment with each degrading agent. (C) Proportion of isolates with a biofilm degradation rate of ≥ 50% in Clade I compared with other clades after treatment with the three degrading agents No significant differences in biofilm degradation efficacy were observed after treatment with 20 µg/mL Dispersin B for 2 and 3 h ( P > 0.05; Additional Fig. 1 ). Similarly, no significant difference was detected between treatment with 20 µg/mL and 40 µg/mL Dispersin B for 2 h ( P > 0.05; Additional Fig. 2 ). Distribution of strong biofilm-producing isolates of C. striatum by isolation site The 60 C. striatum isolates were classified into two groups, with 12 strong biofilm-producing isolates and 48 non-strong biofilm-producing isolates. Of these, 35 isolates were collected from non-invasive specimens, such as sputum and skin secretions, whereas 25 were collected from invasive specimens, including blood, catheter, etc. In addition, isolates were categorized according to specimen origin as respiratory tract samples (sputum and bronchoalveolar lavage fluid [BALF]) or non-respiratory tract samples. Statistical analysis showed that the proportion of strong biofilm-producing isolates was significantly higher among isolates from non-invasive specimens than among those from invasive samples ( P < 0.05). Additionally, the proportion of strong biofilm producers was significantly greater among isolates from respiratory tract samples compared with those from non-respiratory tract samples ( P < 0.05). Influencing effects of human plasma proteins on biofilm production in C. striatum Upon exposure to fibronectin or fibrinogen, the biofilm production capabilities of the 60 C. striatum isolates significantly varied. As shown in Additional file 5 and Fig. 6 , biofilm production capabilities of 47.37% (27/57) isolates increased significantly in the presence of fibronectin (50 µg/mL) or fibrinogen (50 µg/mL, P < 0.05). Among these, biofilm density increased significantly in 29.63% (8/27) of isolates in the presence of fibronectin (50 µg/mL) or fibrinogen (50 µg/mL), whereas increases were observed exclusively with fibronectin in 62.96% (17/27) of isolates and exclusively with fibrinogen in 7.41% (2/27) of isolates. In contrast, biofilm density decreased significantly in 19.30% (11/57) of isolates following exposure to fibronectin (50 µg/mL) or fibrinogen (50 µg/mL) ( P < 0.05), whereas no significant changes were observed in 33.33% (19/57) of isolates ( P > 0.05). Overall, fibronectin exerted a significantly stronger regulatory effect on biofilm formation than fibrinogen. Among the 27 isolates exhibiting increased biofilm production in the presence of fibronectin or fibrinogen, 9 belonged to Clade I, 7 to Clade II, 7 to Clade III, 2 to Clade IV, and 2 to Clade V. Of these, 92.59% (25/27) were classified as moderate or weak biofilm producers. Among the 11 isolates showing reduced biofilm production following plasma protein exposure, 10 belonged to Clade I and 1 to Clade II, with 72.73% (8/11) classified as strong biofilm producers. Pronounced intra-clade diversity in biofilm formation was mainly observed in Clades I and II. In the presence of plasma proteins, biofilm production increased significantly in 9 Clade I isolates and 7 Clade II isolates, whereas it decreased significantly in 10 Clade I isolates and 1 Clade II isolate. In addition, biofilm production remained unchanged in 8 Clade I isolates and 3 Clade II isolates. Fig. 6. Open in a new tab Biofilm production capabilities of 21 C. striatum isolates belonged to clades I-V isolates. * Indicates P < 0.05 Morphological changes in biofilms formed by Clade I C. striatum isolates in the presence of plasma proteins Two representative strong biofilm-forming Clade I isolates (CS-149, CS-137) were selected for SEM analysis to assess biofilm morphological changes in the presence of 50 µg/mL fibronectin or fibrinogen. The biofilm biomass of isolate CS-149 increased markedly on wells pre-coated with 50 µg/mL fibronectin compared with the control condition (Fig. 7 ). In contrast, biofilm biomass of CS-137 isolate exhibited a marked reduction in the wells pre-coated with 50 µg/mL fibronectin. The SEM observations were consistent with the results of the crystal violet staining assay and demonstrated heterogeneous alterations in biofilm production among Clade I C. striatum isolates on plasma protein-coated abiotic surfaces. Fig. 7. Open in a new tab Morphological changes in biofilms formed by Clade I C. striatum isolates in the presence of plasma proteins. Scanning electron microscopy (SEM) images of isolates CS-149 ( A – C ) and CS-137 (D–F). All images were acquired at 15,000× magnification with a scale bar of 5 μm. CS-149: (A) untreated control; (B) fibrinogen-treated; ( C ) fibronectin-treated. CS-137: ( D ) untreated control; ( E ) fibrinogen-treated; ( F ) fibronectin-treated Discussion In this study, the phenotypic and genotypic characteristics of 60 C. striatum clinical isolates collected at a tertiary teaching hospital in China were analyzed, revealing marked isolate-level and genotypic heterogeneity in antimicrobial susceptibility profiles, virulence gene distribution, and biofilm production capability. From a clinical epidemiological perspective, 60 C. striatum isolates were derived from respiratory tract specimens, which is consistent with findings from previous studies worldwide [ 5 , 27 ]. As C. striatum is a well-recognized member of human nasal mucosal microbiota, the use of multiple medical devices in susceptible patients may facilitate its colonization and subsequent infection of the lower respiratory tract. A relatively high proportion of isolates (40%) was obtained from patients admitted to ICUs, supporting previous reports that multidrug-resistant C. striatum infections are more common among critically ill patients [ 28 ]. Recent evidence indicates that C. striatum clinical isolates can invade respiratory epithelial cells, such as A549 cells, and exert significant pathogenic effects in an isolate-dependent manner [ 29 ], further underscoring the significance of isolating C. striatum from lower respiratory tract specimens. In addition, C. striatum has been increasingly recovered from normally sterile sites, including whole blood [ 30 ], highlighting its potential to cause invasive infections in susceptible patients [ 31 ]. Consistent with these observations, 28.33% (17/60) of isolates in the present study were obtained from sterile specimens, including whole blood, central venous catheters, and bile. Regarding antimicrobial resistance, the C. striatum isolates analyzed in this study exhibited extensive resistance to ciprofloxacin, cefepime, and ceftriaxone, whereas all isolates remained fully susceptible to vancomycin, daptomycin, and linezolid. Most isolates carried the ermX and tetW genes, which is consistent with the high phenotypic resistance rates to erythromycin, clarithromycin, and tetracycline. Notably, 92.31% (12/13) of isolates lacking the tetW resistance gene were susceptible to tetracycline, in agreement with the antimicrobial susceptibility testing results. Furthermore, a clear correlation between gentamicin resistance and carriage of the aph(6’) and aph(3’) genes was observed among Clade II isolates. All isolates that were resistant or intermediately susceptible to gentamicin were concentrated in Clade II, and 81.82% (9/11) of these isolates harbored aph(6’) and aph(3’) genes. This finding may explain the lower gentamicin resistance rate observed in Clade I compared with other clades. Although the overall resistance rate of these isolates to tetracycline was high (80%), it was still lower than those reported in some other regions of China [ 32 , 33 ]. Given the rapidly increasing global prevalence of multidrug-resistant C. striatum [ 27 , 31 , 34 ], enhanced surveillance of clonal transmission and further investigation into the evolutionary mechanisms underlying antimicrobial resistance are increasingly necessary. To further explore the underlying heterogeneity among C. striatum isolates, 60 C. striatum clinical isolates were genetically classified into five evolutionary clades using whole-genome sequencing, with Clade I identified as the dominant lineage. Meanwhile, 37 putative virulence genes were identified, which are involved in diverse biological processes, including adhesion and biofilm formation ( spaD , spaE , spaF , srtB , srtC ), iron uptake and metabolism ( fagA , fagB , fagC , fagD , hmuU , irp6A , irp6B ), stress responses ( sigA , sigH ), molecular chaperone activity ( groEL ), intracellular survival ( sodA ), and two-component regulatory systems ( regX3 ) [ 29 ]. Significant differences were observed in the distribution of virulence genes among clades. Overall, Clade I isolates carried the abovementioned virulence genes at higher frequencies than isolates belonging to the other clades. In particular, the distribution of whiB3 and the fagABCD gene cluster warrants special mention. WhiB3, which functions as a redox sensor and virulence regulator in Mycobacterium tuberculosis , can modulate virulence gene expression through interaction with SigA [ 35 ], and its absence results in attenuated virulence in animal models [ 36 ]. In the present study, a high carriage rate of whiB3 was observed in Clades I and II, whereas isolates from the remaining clades lacked this gene. The role of whiB3 gene in the pathogenicity of C. striatum has not yet been defined and merits further exploration. A previous study [ 29 ] has shown that biofilm formation by C. striatum is not positively correlated with invasiveness but instead displays marked heterogeneity. Specifically, strong biofilm producers tend to exhibit moderate invasiveness, whereas moderate and weak biofilm producers show enhanced invasion of host cells. This heterogeneity may be partly attributable to the presence of specific virulence determinants, such as the fagABCD gene cluster. Carriage of fagABCD was shown to strongly correlate with increased cellular invasiveness of C. striatum in vitro [ 29 ], potentially due to enhanced iron uptake capability and improved intracellular survival [ 37 ]. In contrast to previous reports, the present study found that the fagABCD gene cluster was not widely distributed among the analyzed isolates but was largely confined to a single clade, Clade III. Notably, isolates belonging to this clade predominantly exhibited weak biofilm-forming capacity. These findings are consistent with those reported by Du et al. [ 29 ] and further support a role for fagABCD gene in modulating the pathogenicity of C. striatum . As another important determinant influencing pathogenicity and resistance in multiple bacterial pathogens, biofilm production is one of the most recognized features of pathogenic C. striatum and plays a critical role in chronic and persistent infections caused by C. striatum [ 6 , 11 ]. In C. striatum , multidrug-resistant isolates belonging to dominant clones usually exhibit stronger biofilm-forming ability [ 8 , 14 ], indicating enhanced nosocomial transmission, environmental adaptability, and infection potential. Consistent with these observations, the present study demonstrated that most Clade I isolates were moderate or strong biofilm producers, whereas isolates from nondominant clades were predominantly weak biofilm producers. These results highlight a clear correlation between genotypic characteristics and biofilm-forming ability in C. striatum , implying the importance of rapid and accurate identification of biofilm-producing isolates in clinical practice. Previous studies have shown that the spaDEF gene cluster plays an important role in mediating biofilm formation in C. striatum [ 38 ]. In the present study, all isolates belonging to Clades II, IV, and V lacked the spaDEF gene cluster, whereas it was more prevalent among isolates from the dominant Clade I. Additionally, all three non-biofilm-producing isolates lacked the spaDEF gene cluster. Moreover, all Clade I isolates harbored spaD gene and were strong biofilm producers, suggesting a potential role of this virulence gene in early-stage biofilm formation. Nevertheless, exceptions were observed, such as isolates CS-139 and CS-490, which were classified as strong and weak biofilm producers, respectively, indicating that additional molecular mechanisms may also contribute to biofilm regulation in C. striatum . The adhesion proteins encoded by the spaDEF gene cluster are key determinants of biofilm formation in C. striatum and may serve as potential intervention targets for biofilm-related infections. In S. aureus , strategies targeting cell wall–anchored proteins have been shown to effectively inhibit bacterial adhesion and biofilm formation [ 39 ], providing a useful reference for the development of intervention strategies against C. striatum biofilm-associated infections. Furthermore, stronger biofilm-producing C. striatum isolates in this study were predominantly collected from lower respiratory tract specimens, suggesting enhanced colonization of respiratory epithelial surfaces and a greater potential to cause lower respiratory tract infections. Consistent with this observation, Du et al. [ 29 ] reported strong adhesive and invasive capabilities of C. striatum clinical isolates toward human airway epithelial cells, resulting in significant cellular damage. Although no significant correlation between biofilm-forming capability and invasion efficiency in the C. striatum isolates was identified in the present study, it is reasonable to speculate that strong biofilm production is closely associated with enhanced colonization of respiratory tract cells, which may promote lower respiratory infection and facilitate patient-to-patient transmission. Given that most C. striatum isolates reported in China are derived from lower respiratory tract specimens [ 40 ], more stringent infection control measures should be implemented for patients with C. striatum –associated lower respiratory tract infections, and biofilm-producing capability should be actively assessed in clinical isolates. Apart from the intrinsic bacterial genetic determinants, biofilm formation is also influenced by multiple host factors, particularly plasma proteins. For S. aureus and C. striatum , previous studies have suggested that plasma proteins (such as fibronectin and fibrinogen) mainly exert a unidirectional promoting effect on biofilm formation [ 6 , 41 ]. In the present study, we compared the distribution of putative adhesion- or biofilm-associated genes between C. striatum isolates that exhibited enhanced biofilm formation and those that showed no significant changes in the presence of plasma proteins, and no significant differences were identified between the two groups. Notably, biofilm production capabilities by C. striatum isolates on abiotic surfaces coated with plasma proteins exhibited a bimodal pattern. Biofilm production increased significantly in 47.37% of isolates, whereas it decreased markedly in 19.30% of isolates. This pattern is consistent with observations reported for Staphylococcus epidermidis . Linnes et al. [ 42 ] demonstrated that fibronectin at specific concentrations can inhibit bacterial adhesion, and that its regulatory effects do not follow a single receptor–ligand model but instead reflect a balance between specific adhesion mechanisms and non-specific adhesion processes. Coating abiotic surfaces with fibronectin may passivate the surface, thereby attenuating non-specific interactions, such as hydrophobic interactions and autoaggregation, ultimately inhibiting bacterial adhesion and biofilm formation. In contrast, Christner et al. showed that S. epidermidis expresses a specific surface protein, extracellular matrix-binding protein (Embp), which mediates adhesion of S. epidermidis to fibronectin. Strains expressing this protein exhibited markedly enhanced adhesion to fibronectin, whereas strains lacking it failed to establish effective initial adhesion, with adhesion strength correlating positively with the expression level of Embp [ 43 ]. A similar mechanism has been reported in S. aureus , which binds fibronectin via its fibronectin-binding proteins A/B (FnbpA/B), thereby enhancing its adhesive propensity [ 26 ]. For C. striatum , Souza et al. [ 6 ] hypothesized that C. striatum binding to plasma components via specific surface molecules may enhance adhesive capacity. The bidirectional response of C. striatum to fibronectin observed in the present study likely represents an extension of this mechanism. In general, C. striatum isolates expressing specific adhesion-related surface proteins may exhibit enhanced adhesion to abiotic surfaces in the presence of plasma proteins, particularly fibronectin. Conversely, isolates with low or absent expression of such proteins may display reduced adhesion and biofilm formation under the same conditions. Hence, further studies are required to identify adhesion-related surface proteins involved in this process, which would provide a stronger mechanistic basis for the prevention and control of biofilm-associated infections caused by C. striatum . Additionally, plasma protein levels are often elevated in severe infections, such as sepsis [ 44 ], which may further influence C. striatum biofilm development in vivo. Thus, both intrinsic bacterial factors and host plasma protein concentrations collectively determine the outcomes of biofilm-related infections caused by C. striatum . In clinical practice, simultaneous assessment of the biofilm-forming ability of C. striatum isolates and dynamic monitoring of plasma protein concentrations among the patients infected by C. striatum may be critical for guiding precise anti-infective therapy and optimizing treatment strategies. Conclusions This study demonstrates significant associations among virulence gene distribution, biofilm formation, and genotypic background in clinical C. striatum isolates. The potential roles of specific virulence genes in mediating C. striatum pathogenicity were highlighted, particularly fagABCD , whiB3 , and spaDEF . Notably, to the best of our knowledge, this study is the first to report the bidirectional effects of human fibronectin and fibrinogen on C. striatum biofilm production capabilities in vitro, with responses varying according to isolate genotype and baseline biofilm production capabilities. These findings provide a theoretical basis and novel insights for the development of targeted intervention strategies against biofilm-associated C. striatum infections and for the optimization of precision anti-infection therapies. Future studies should focus on elucidating the molecular mechanisms by which key virulence genes contribute to C. striatum pathogenicity and on defining the pathways underlying the diverse regulatory effects of plasma proteins on biofilm production capability of C. striatum . Supplementary Information Supplementary Material 1. (17.2KB, xlsx) Supplementary Material 2. (397.2KB, xlsx) Supplementary Material 3. (34.1KB, docx) Supplementary Material 4. (17.2KB, docx) Supplementary Material 5. (217.4KB, png) Supplementary Material 6. (217.9KB, png) Supplementary Material 7. (14KB, xlsx) Acknowledgements We thank all Lab Medicine Department staff for assisting with isolates collection, identification and storage. Abbreviations C. striatum Corynebacterium striatum BALF Bronchoalveolar Lavage Fluid Blastp Basic Local Alignment Search Tool for proteins CARD Comprehensive Antibiotic Resistance Database CLI Clarithromycin CRO Ceftriaxone CVC Central Venous Catheter CWAPs Cell-wall-anchored proteins DAP Daptomycin eDNA extracellular DNA ERY Erythromycin FEP Cefepime GEN Gentamicin General ICU General Intensive Care Unit LNZ Linezolid MEM Meropenem MDR Multi-drug resistant Mtb Mycobacterium tuberculosis NJ Neighbor-joining ODc cut-off OD PEN Penicillin PCR Polymerase chain reaction CIP Ciprofloxacin SXT Trimethoprim-Sulfamethoxazole TCY Tetracycline VAN Vancomycin CFU Colony-forming units DNase I Deoxyribonuclease I EPS Extracellular polymeric substance ICU Intensive care unit InDel Insertion–deletion MALDI-TOF MS Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry MIC Minimum inhibitory concentration OD Optical density PBS Phosphate-buffered saline PNAG Poly-N-acetylglucosamine SEM Scanning electron microscopy SNP Single-nucleotide polymorphism SV Structural variation TSB Tryptic soy broth VFDB Virulence Factor Database WGS Whole-genome sequencing Authors’ contributions Jiajia Su: Data curation, Formal analysis, Investigation, Writing original draft. Juan Wen: Data curation, Formal analysis, Investigation, Writing-original draft. Wenqi Zheng: Supervision, Writing-review & editing. Junrui Wang: Conceptualization, Funding acquisition, Methodology, Project administration, Resources, Writing-review &editing. Funding The author(s) declare that financial support was received for the research and/or publication of this article. This study is supported by National Natural Science Foundation of China (Grant no. 82260416), Science and Technology Plan Project of Inner Mongolian Autonomous Region (No. 2025YFSH0088), Zhiyuan talents project of Inner Mongolia Medical University (No. ZY20241209), and Science and Technology Program of the Joint Fund of Scientific Research for the Public Hospitals of Inner Mongolia Academy of Medical Sciences (No. 2024GLLH0302). Data availability The datasets presented in this study can be found in online repository and Supplementary material. The detailed genome sequencing data of 60 *C. striatum* clinical isolates were in the National Center for Biotechnology BioProject database (Accession number: PRJNA1298970). Declarations Ethics approval and consent to participate This study complies with the Declaration of Helsinki. The bacterial isolates used in this study were isolated from the routine biological specimens. Also, rights and health of the subjects were not under threat, and no personal identifying information was used during this study. According to the national regulation on ethical review (No. 2016–11, 12/01/2016), the requirement for the informed consent was waived by the Ethical Committee of Inner Mongolian Medical University, which belongs to the Office of Scientific Research of Inner Mongolian Medical University. Meanwhile, this study was approved by the Ethical Committee of the Inner Mongolian Medical University (Reference No. YKD202201166). Consent for publication Not applicable. 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