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In order to reveal the mineral filling sequence and fluid action process in the dissolution pores of the bedded siliceous rocks in the Dongrong Formation of the Sanjiang Basin, the petrological characteristics, geochemical analysis and testing methods were comprehensively applied to research, and the databases of major amount and rare earth elements of siliceous rocks were established, and the sedimentary environment, origin and source of siliceous materials were systematically judged again. The results show that the siliceous rocks of the Nadanhada terrane exposed in the Sanjiang Basin are biogenic. On the basis of early metasomatic microbial dolomite, the layered siliceous rocks have experienced six stages (three fluid properties) of fluid filling, including magnesium rich hydrothermal fluid, siliceous hydrothermal fluid, asphalt and siliceous hydrothermal fluid. Siliceous rock cavity filling material is the product of fluid rock coupling under different temperatures, concentrations and reaction systems under the control of different tectonic movements and hydrocarbon maturation.

Through field geological survey and drilling exploration in Sanjiang Basin, combined with geochemical analysis, the tectonic thermal evolution history of intrusive rocks is studied. The results show that the Early Mesozoic siliceous rocks in Qianjin Depression of Sanjiang Basin are widely distributed. The siliceous rocks are of post diagenetic hydrothermal metasomatic origin, and the hydrocarbon source rock indicators are good, which is expected to be a new formation for oil and gas exploration in Sanjiang area. The time temperature thermal history simulation of fission track shows that there have been two rapid cooling events (late Early Cretaceous Late Cretaceous and Paleocene Eocene) in the Nadanhadaling area since the Mesozoic era, with cooling rates of 3.42~4.81 ℃/Ma and 1.43~1.83 ℃/Ma, respectively. The two rapid cooling processes were caused by the subduction of the Pacific plate. The rapid cooling during the Early Cretaceous to the Late Cretaceous was caused by the change of the subduction direction of the Pacific plate and the collision and superposition of the Okot Motsk block and the East Asian continental margin; The rapid cooling from Paleocene to Eocene was mainly caused by the subduction and retreat of the Pacific plate, which made the East Asian continental margin in an extensional environment and caused denudation and cooling in most parts of Northeast China.

Objective To characterize the evolutionary pathways of tigecycline (TGC) resistance and alterations in the biological characteristics of hospital-derived Staphylococcus aureus isolates under selective pressure. Methods Three clinical S. aureus strains and one standard S. aureus strain, ATCC 29213, were used for the in vitro selection of TGC-resistant S. aureus variants with gradient concentrations of TGC. Changes in drug resistance and genetic alterations in resistance-related genes (operon mepRAB and rpsJ) in mutant strains were determined. The efflux inhibitor assay for MepA and the fitness cost, determined by comparing the growth and virulence of parental and mutant strains, were also investigated. Results Mutants induced in vitro showed a 64- to 128-fold increase in the minimum inhibitory concentration (MIC) of TGC. Substitution mutations were detected in the transcriptional repressor mepR and the efflux pump gene mepA. A K57M amino acid substitution occurred in the ribosomal S10 protein-encoding gene rpsJ. The MICs of TGC in the final mutants were significantly decreased in the presence of efflux pump inhibitors. It was worth noting that growth was unaffected by TGC resistance selection in vitro, with the exception of one strain, and the MICs of other antibiotics and virulence were also unaffected. Conclusions The evolution of TGC resistance in S. aureus in vitro is associated with a loss-of-function mutation in the efflux pump transcriptional repressor mepR and a missense mutation in the efflux pump-encoding gene mepA. Our work further validated the resistance mechanisms of S. aureus to TGC and reported previously undiscovered mutations.

In this study, we report a clinical isolate of a carbapenem-, colistin-, and fosfomycin-resistant Escherichia coli isolate DC-3737 co-harboring blaNDM-1, mcr-1, and fosA3 from an inpatient in China. Antimicrobial susceptibility testing, polymerase chain reaction, multi-locus sequence typing, conjugation experiment, and Southern blot hybridization were performed on E. coli DC-3737 isolated from the wound. Plasmid analysis is presented and the locations of blaNDM-1, mcr-1, fosA3, and other resistance genes were identified as well. E. coli DC-3737 was resistant to ampicillin, ceftriaxone, ceftazidime, ciprofloxacin, levofloxacin, gentamicin, tobramycin, trimethoprim-sulfamethoxazole, imipenem, meropenem, ertapenem, fosfomycin and colistin, and with intermediate susceptibility to amikacin. It was typed as sequence type 27. The isolate possessed blaNDM-1, mcr-1, fosA3, blaCTX-M-9, blaTEM-1, aac (6')-Ib-cr and sul1 simultaneously. In addition, the mutations in quinolone resistance-determinant regions (QRDRs) such as Ser83Leu and Asp87Asn in gyrA, and Ser80Ile in parC were detected. Conjugation assays revealed that blaNDM-1, fosA3, sul1, mcr-1, and blaCTX-M-9 genes could successfully transfer their resistance phenotype to E. coli strain J53. Plasmid analysis and Southern hybridization showed that DC-3737 possessed Z-type self-transmissible plasmid bearing blaNDM-1, fosA3, and sul1. Moreover, mcr-1, blaCTX-M-9, and blaTEM-1 were located on a ~60-kb IncFIB type self-transmissible plasmid. This is the first report of blaNDM-1, mcr-1 and fosA3 co-harboring in E. coli in China. Moreover, it is also the first description of the co-harboring of blaNDM and fosA3 in a single Z plasmid in Enterobacteriaceae species. The identification of E. coli DC-3737 co-harboring blaNDM-1, mcr-1, and fosA3 in this study highlights the need to increase epidemiologic surveillance and the need for new classes of antibiotics to address multidrug-resistant bacteria.

Background The emergence and spread of carbapenem-resistant Escherichia coli (E. coli) pose a serious threat to human health worldwide. This study aimed to investigate the molecular mechanisms underlying carbapenem resistance and their prevalence among E. coli in China. Methods A collection of 5796 E. coli clinical isolates were collected from the First Affiliated Hospital of Wenzhou Medical University from 2002 to 2017. Sensitivity to antibiotics was determined using the agar dilution method. The detection of carbapenemases production and the prevalence of resistance-associated genes were investigated through modified carbapenem inactivation method (mCIM), PCR and sequencing. The mutations in outer membrane porins genes (ompC and ompF) were also analyzed by PCR and sequencing assays. The effect of efflux pump mechanism on carbapenem resistance was also tested. E. coli were typed by pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing (MLST). Results A total of 58 strains (1.0%) of carbapenem-resistant E. coli were identified. The strains carrying bla KPC-2 and bla NDM accounted for 22.4% (13/58) and 51.7% (30/58), respectively. Among bla NDM- positive strains, 27 bla NDM genes were assigned to bla NDM-5, while the remaining three strains were bla NDM-1, whereas bla VIM, bla IMP, bla OXA-48, and bla SHV were not found. The CTX-M-type β-lactamase genes accounted for 96.6% (56/58). In addition, bla TEM-1 genes were identified in 58.6% of tested strains. In carbapenem-resistant isolates, mutations in OmpC (the majority of mutated sites were D192G and Q104_F141del, accounting for 54.5%) and OmpF (large deletions S75_V127del, W83_D135del and Q88_D135del) were detected. Of note, the antibiotic resistance was not associated with overexpression of efflux pump. Moreover, MLST categorized the 58 carbapenem-resistant isolates into 19 different sequence types. PFGE analysis revealed that homology among the carbapenem-resistant isolates was low and sporadic. Conclusion The bla NDM was the principal resistance mechanism of carbapenem-resistant E. coli in the hospital. bla NDM-5 is becoming a new threat to public health and the alteration of outer membrane porins might help further increase the MIC of carbapenem.

Background Colistin resistance is considered a serious problem due to a lack of alternative antibiotics. The Rapid ResaPolymyxin Acinetobacter/Pseudomonas NP test is a resazurin reduction-based technique that relies on the visual detection of bacterial growth in the presence of a defined concentration of colistin. The aim of this study was to evaluate the performance of the Rapid ResaPolymyxin Acinetobacter/Pseudomonas NP test in the detection of colistin susceptibility in common clinical Gram-negative bacteria. Results A total of 253 clinical isolates from a teaching hospital, including Acinetobacter baumanii (n = 58, 8 colistin-resistant), Pseudomonas aeruginosa (n = 61, 11 colistin-resistant), Klebsiella pneumoniae (n = 70, 20 colistin-resistant) and Escherichia coli (n = 64, 14 colistin-resistant) were tested in this study. The sensitivity and specificity of the Rapid ResaPolymyxin Acinetobacter/Pseudomonas NP test compared to Broth microdilution method was 100 and 99%, respectively. Conclusions Our results suggest that Rapid ResaPolymyxin Acinetobacter/Pseudomonas NP test could be used as an accurate detection method for colistin resistance.

Chinese dragon’s blood (CDB), a characteristic red resin, is an important traditional Chinese medicine (TCM), and empiric therapy of infected wounds with CDB is performed in clinical settings. For the first time, we herein report the antibacterial and anti-biofilm efficacy of CDB against Staphylococcus aureus (S. aureus). Antimicrobial susceptibility testing, growth curve assay, time-kill curve assay, crystal violet biofilm assay, scanning electron microscope (SEM) analysis, cell membrane tests, and quantitative real-time polymerase chain reaction (qRT-PCR) were used for this purpose. The results suggested that the minimum inhibitory concentration (MIC) values of CDB against S. aureus ranged from 32 to 128 μg/mL. Growth curves and time-kill curves confirmed that CDB could inhibit the growth of S. aureus. The biofilm formation ability and the expression levels of saeR, saeS, and hla of S. aureus in the presence and absence of CDB were statistically significant (P < 0.01). The results of SEM analysis and cell membrane tests revealed that exposure to CDB had some destructive effects on S. aureus cells. In conclusion, CDB exhibits positive antibacterial activity against S. aureus. Moreover, CDB could reduce the biofilm formation and the virulence factors of S. aureus by downregulating the expression levels of saeR, saeS, and hla genes. These findings indicated that CDB has immense potential to serve as a viable alternative for the treatment of infected wounds caused by S. aureus in clinical settings.

Background We aimed to determine the evolutionary pathways of rifampicin resistance in Staphylococcus aureus, and the impact of resistance mutations in the rpoB gene on fitness. Methods Three clinical strains and one reference strain were used to select for rifampicin-resistant S. aureus variants. The mutations responsible for rifampicin resistance in all of the selected isolates in vitro were investigated by polymerase chain reaction (PCR) and DNA sequencing. To compare the fitness cost of rpoB mutations against their corresponding original isolates, we performed bacterial growth curve assays, static biofilm assays, in vitro competition experiments and an infection model of Galleria mellonella larvae. Results We obtained four rifampicin-resistant S. aureus isolates that showed high levels of resistance to rifampicin with a minimal inhibitory concentration (MIC) of 128 mg/L, and all isolates had a mutation at position 481 (H481F/Y) in RpoB. A broth microdilution assay indicated that mutation of H481F/Y did not affect susceptibility to common antibacterial drugs but slightly increased the vancomycin MIC. To identify the pathways involved in the development of rifampicin resistance, 32 variants (eight mutants for each strain) and four original isolates were selected for gene sequencing. Different generations of isolates were found to harbor various mutations sites. Compared with the corresponding original isolates, an in vitro fitness assay of the variant isolates showed that growth and virulence were reduced, with a statistically significantly decreased fitness, whereas the capacity for biofilm formation was elevated. Conclusions Our findings suggested that the acquisition of rifampicin resistance in S. aureus was dynamic and was associated with a significant fitness cost.

Xiangkuo Zheng,1,* Renchi Fang,2,* Chong Wang,3 Xuebin Tian,4 Jie Lin,1 Weiliang Zeng,4 Tieli Zhou,1 Chunquan Xu1 1Department of Clinical Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325035, People’s Republic of China; 2Department of Laboratory Medicine, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, 310003, People’s Republic of China; 3Department of Laboratory Medicine, Qingdao Municipal Hospital, Qingdao, 266000, People’s Republic of China; 4School of Laboratory Medicine and Life Sciences, Wenzhou Medical University, Wenzhou, 325035, People’s Republic of China*These authors contributed equally to this workCorrespondence: Chunquan Xu; Tieli ZhouDepartment of Clinical Laboratory, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, 325000, People’s Republic of ChinaTel +86-577-5557-9725; +86-577-8668-9885Email 417242374@qq.com; wyztli@163.comBackground: Staphylococcus aureus (S. aureus) is a major contributor to nosocomial and community-acquired infections. S. aureus small colony variants (SCVs) which changed in relevant phenotype have made more limited and difficult for therapeutic options against S. aureus infections increasingly. Rifampicin is considered as the “last-resort” antibiotic against S. aureus. Our study investigated resistance profiles and biological characteristics of rifampicin-resistant S. aureus SCVs.Methods: We collected S. aureus SCVs that were selected from 41 rifampicin-resistant clinical isolates. Then, biological characteristics, resistance spectrum, and rifampicin resistance mechanisms of tested S. aureus SCVs and corresponding parental strains were investigated by classic microbiological methods, agar dilution method, polymerase chain reaction (PCR). Moreover, the fitness cost of S. aureus SCVs, including growth, biofilm formation ability, and virulence profile, was also determined by bacterial growth curve assay, biofilm formation assay, and Galleria mellonella infection model.Results: There were three S. aureus SCVs (JP310 SCVs, JP1450 SCVs, JP1486 SCVs) that were selected from 41 rifampicin-resistant S. aureus. S. aureus SCVs colonies were tiny, with decreased pigmentation, and the hemolysis circle was not obvious compared with corresponding parental strains. And SCVs could not be restored to normal-colony phenotype after hemin, menaquinone, or thymidine supplementation. Different rpoB mutations occurred in JP1486 SCVs. Antimicrobial susceptibility testing revealed MICs of SCVs were higher than corresponding parental strains. Besides, the growth ability and virulence of SCVs were lower, and biofilm formation ability of which increased compared with parental strains.Conclusion: S. aureus SCVs share the rifampicin resistance mechanisms with parental strains, although there were some differences in the position of rpoB mutations. Moreover, we found that the biological characteristics of SCVs were significantly different from corresponding parental strains. In contrast, decreased susceptibility to other antibiotics of SCVs was observed during phenotype switch. Furthermore, SCVs incur the fitness cost.Keywords: Staphylococcus aureus, small-colony variant, rifampicin resistance, resistance profile, biological characteristic

Background Staphylococcus aureus (S. aureus) is a major contributor to nosocomial and community-acquired infections. S. aureus small colony variants (SCVs) which changed in relevant phenotype have made more limited and difficult for therapeutic options against S. aureus infections increasingly. Rifampicin is considered as the “last-resort” antibiotic against S. aureus. Our study investigated resistance profiles and biological characteristics of rifampicin-resistant S. aureus SCVs. Methods We collected S. aureus SCVs that were selected from 41 rifampicin-resistant clinical isolates. Then, biological characteristics, resistance spectrum, and rifampicin resistance mechanisms of tested S. aureus SCVs and corresponding parental strains were investigated by classic microbiological methods, agar dilution method, polymerase chain reaction (PCR). Moreover, the fitness cost of S. aureus SCVs, including growth, biofilm formation ability, and virulence profile, was also determined by bacterial growth curve assay, biofilm formation assay, and Galleria mellonella infection model. Results There were three S. aureus SCVs (JP310 SCVs, JP1450 SCVs, JP1486 SCVs) that were selected from 41 rifampicin-resistant S. aureus. S. aureus SCVs colonies were tiny, with decreased pigmentation, and the hemolysis circle was not obvious compared with corresponding parental strains. And SCVs could not be restored to normal-colony phenotype after hemin, menaquinone, or thymidine supplementation. Different rpoB mutations occurred in JP1486 SCVs. Antimicrobial susceptibility testing revealed MICs of SCVs were higher than corresponding parental strains. Besides, the growth ability and virulence of SCVs were lower, and biofilm formation ability of which increased compared with parental strains. Conclusion S. aureus SCVs share the rifampicin resistance mechanisms with parental strains, although there were some differences in the position of rpoB mutations. Moreover, we found that the biological characteristics of SCVs were significantly different from corresponding parental strains. In contrast, decreased susceptibility to other antibiotics of SCVs was observed during phenotype switch. Furthermore, SCVs incur the fitness cost.

Background The emergence of carbapenem-resistant Klebsiella pneumoniae (CRKP) poses a looming threat to human health. Although there are numerous studies regarding porin alteration in association with the production of ESBLs and/or AmpC β-lactamase, a systematic study on the treatment-emergence of porins alteration in antibiotic resistance does not yet exist. The aim of this study was to investigate the underlying mechanism of resistance of K. pneumoniae during carbapenem treatment. Results Here, we report three strains (FK-2624, FK-2723 and FK-2820) isolated from one patient before and after imipenem treatment during hospitalization. Antibiotic susceptibility testing indicated that that the first isolate, FK-2624, was susceptible to almost all tested antimicrobials, being resistant only to fosfomycin. The subsequent isolates FK-2723 and FK-2820 were multidrug resistant (MDR). After imipenem therapy, FK-2820 was found to be carbapenem-resistant. PCR and Genome Sequencing analysis indicated that oqxA, and fosA5, were identified in all three strains. In addition, FK-2624 also harbored blaSHV-187 and blaTEM-116. The blaSHV-187 and blaTEM-116 genes were not detected in FK-2723 and FK-2820. blaDHA-1, qnrB4, aac (6′)-IIc, and blaSHV-12, EreA2, CatA2, SulI, and tetD, were identified in both FK-2723 and FK-2820. Moreover, the genes blaDHA-1, qnrB4, aac (6′)-IIc were co-harbored on a plasmid. Of the virulence factors found in this study, ybtA, ICEKp6, mrkD, entB, iroN, rmpA2–6, wzi16 and capsular serotype K57 were found in the three isolates. The results of pairwise comparisons, multi-locus sequencing typing (MLST) and pulsed-field gel electrophoresis (PFGE) revealed high homology among the isolates. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) results showed that isolate FK-2820 lacked OmpK36, with genome sequence data validating that there was a premature stop codon in the ompK36 gene and real-time RT-PCR suggesting high turnover of the ompK36 non-sense transcript in FK-2820, with the steady-state mRNA level 0.007 relative to the initial isolate. Conclusion This study in China highlight that the alteration of outer membrane porins due to the 14-day use of imipenem play a potential role in leading to clinical presentation of carbapenem-resistance. This is the first description of increased resistance developing from a carbapenem-susceptible K. pneumoniae with imipenem treatment driven by outer membrane remodeling.

Additional file 1: Table S1.Klebsiella pneumoniae isolated during hospitalization. Table S2. Genomic DNA comparison between the tested strains, SNPs and (% identity). Table S3. MICs of Pseudomonas aeruginosa.Table S4. The allelic profile of ST 660. Table S5. Genomic DNA assigned to plasmids.

The siliceous shale oil and gas in Nadanhada terrane has been studied through field geological survey, geochemistry and sedimentary petrology. The results show that the area belongs to a good shale reservoir, and the siliceous rock is brittle and suitable for exploitation. The abundance of organic matter is relatively high. From west to east and from south to north, the abundance of organic matter increases and the maturity of organic matter decreases. From west to east and from south to north, the dynamic metamorphism and thermal contact metamorphism of the siliceous rocks in the Nadanhada terrane are gradually weakened, and the folds and magmatic intrusion of the strata are alleviated.

The Nadanhada terrane is basically a large tectonic sedimentary hybrid, which is an accretionary complex belt formed by the subduction of the Pacific plate to the Eurasian plate. Through field geological survey, paleomagnetic analysis, paleontological analysis and microscopic observation of core slices, its structural and petrological characteristics were studied. The results show that the accretionary complex is mainly composed of 7 parts, including undeformed sedimentary rocks, shear deformed sedimentary rocks, shear deformed volcanic rocks, turbidites, deformed siliceous rocks, limestone blocks and basic ultrabasic rocks. Shear deformation structures of deformed sedimentary rocks and volcanic rocks are developed. The sediment grain size of the Lower Cretaceous reservoirs in each basin in the northern region is relatively coarse, the sorting is moderately deviated, and the rounding is poor, mainly secondary to angular. The grain size of the lower Cretaceous sediments of each basin in the southern region is relatively fine, with coarse, medium and fine sandstones, but mainly medium fine sandstones, with medium sorting preference and sub angular to sub round roundness.

The emergence of carbapenem-resistant Kelbsiella pneumoniae (CRKP) posed threats to human health. Although there are numerous studies regarding porin alteration in association with the production of ESBLs and/or AmpC β-lactamase, a systematic research about the treatment-emergence of porins alteration in antibiotic resistance does not exist yet. The aim of this study was to investigate the underlying mechanism and evolution of resistance of K. pneumoniae during carbapenem treatment. Here, we reported three strains (FK-2624, FK-2723 and FK-2820) isolated from one patient before and after imipenem treatment during hospitalization. Antibiotic susceptibility testing indicated that FK-2624 was susceptible to almost antimicrobials but fosfomycin; FK-2723 and FK-2820 were MDR. After imipenem therapy, FK-2820 was evolved to carbapenem-resistant. PCR and Whole-Genome sequencing ( WGS) indicated that resistance genes bla SHV , oqxA and fosA5 were detected in FK-2624, in addition, FK-2723 and FK-2820 harbored bla DHA , qnrB , aac (6’)-Ib . Virulence factors K57, ybtA, mrkD, entB and iroN were detected simultaneously in all of three strains. The results of pairwise comparisons , multi-locus sequencing typing (MLST) and pulsed-field gel electrophoresis (PFGE) revealed high homology among the isolates. Sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) results showed that isolate FK-2820 lacked OmpK 36 as there was a premature stop codon of the outer membrane porin encoding gene ompk36 confirmed by sequencing. Real-time RT-PCR revealed that the expression of ompK36 in FK-2820 was 0.093 times the control isolate ATCC 13883. Our study highlighted that the alteration of outer membrane porins due to the 14-day use of imipenem clinically play a potential role in leading to the carbapenems-resistance of FK-2820.

Table S2. The details of biofilm formation ability of all strains derived in this study, quantified by measuring the absorbance at 595â nm, and the data for each strain represented average values taken from four replicate wells performed in two independent experiments. (DOCX 20 kb)

Table S4. The details of infection model of Galleria mellonella larvae, larvae were injected with 5 × 108 CFU of bacterial suspension and their survival was monitored, at 96 h post-infection, the mortality of larvae was lower for RIF-R S. aureus isolates compared with the corresponding RIF-S strains. (DOCX 17 kb)

Table S3. The details of in vitro competition index (CI) results of all strains derived in this study, CI was defined as the ratio between the CFU of the rifampicin-resistant strain and the rifampicin-susceptible strain. (DOCX 18 kb)

Table S1. The details of bacterial growth curves for all strains derived in this study, the optical density of the bacterial culture at 595â nm was measured after 0 to 24â h of incubation. Experiments were performed in duplicate, and the averages were used for estimating growth parameters. (DOCX 41 kb)

Object To analyze the difference in biofilm formation between carbapenem-resistant and carbapenem-sensitive Klebsiella pneumoniae based on analysis of mrkH distribution and to further explore the function of mrkH for biofilm formation from the perspective of gene regulation. Methods 40 imipenem-resistant strains and 40 imipenem-sensitive strains were selected to conduct experiments. Carbapenem (imipenem) susceptibility test was performed by the agar-dilution method. blaKPC resistance gene, type 3 fimbriae-related coding genes (mrkA and mrkD) and regulation gene (mrkH) were screened by PCR. Biofilm formation assay was performed using crystal violet staining method in MHB. The relative expression of genes that critically involved in biofilm formation (mrkA, luxS, pgaA) and carbapenem resistance (ompk35, ompk36, acrB) were measured by quantitative real-time PCR (qRT-PCR). Furthermore, the mrkH cassette was cloned into pGEM-T Easy plasmid to yield pGEM:pmrkH and expressed in Escherichia coli DH5α and K. pneumoniae FK1911, and the biofilm formation assay after transformation was further tested. Results The MICs of imipenem were all more than 16 μg/mL in 40 imipenem-resistant strains and ranged from 0.125 μg/mL to 0.5 μg/mL in 40 imipenem-sensitive strains. Moreover, the blaKPC was identified in the 40 imipenem-resistant K. pneumoniae strains. All 80 K. pneumoniae strains were found to carry mrkA and mrkD genes. Interestingly, the mrkH gene was detected in 43 strains, of which 32 were carbapenem-sensitive strains. The biofilm formation capacity of strains carried mrkH cassette was significantly higher than other 37 strains in MHB media. The relative expression of mrkA in K. pneumoniae carrying mrkH gene was significantly up-regulated. Importantly, the biofilm formation ability of FK1911-pGEM:pmrkH strain was more higher than the strain of FK1911 in MHB medium. Conclusions Our data demonstrated that MrkH played a crucial role in the regulation of biofilm formation by K. pneumoniae. In contrast to carbapenem-sensitive K. pneumoniae, carbapenem-resistant K. pneumoniae was less likely to have strong biofilm-forming capacity because it does not carry the mrkH gene.