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Molecular characterization of emergence of mobile colistin resistance 1 gene-mediated colistin resistance in clinical isolates of Escherichia coli: A concern from North India
*Corresponding author: Anita Pandey, Department of Microbiology, Subharti Medical College, Swami Vivekanand Subharti University, Meerut, Uttar Pradesh, India. anipanmicro@gmail.com
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Received: ,
Accepted: ,
How to cite this article: Singh A, Pandey A, Singh P, Jain P, Zahoor T. Molecular characterization of emergence of mobile colistin resistance 1 gene-mediated colistin resistance in clinical isolates of Escherichia coli: A concern from North India. Int J Health Sci (Qassim). 2026;20:172-8. doi: 10.25259/IJHS_242_2025
Abstract
Objectives:
Colistin is a reserved, last-resort antibiotic used to treat infections caused by multidrug-resistant Gram-negative bacilli. The mobile colistin resistance (mcr-1) gene has been identified as a key mechanism for colistin resistance. This study aimed to investigate the association between the mcr-1 gene and colistin resistance in Escherichia coli.
Methods:
A total of 1,149 clinical isolates of E. coli were collected over 1 year from various clinical specimens at a tertiary care center in North India. Initial colistin susceptibility testing was performed using the automated VITEK 2 system, followed by confirmation of resistance by the gold standard broth microdilution (BMD) method. Isolates confirmed as resistant by BMD were further screened for the mcr-1 gene by real-time polymerase chain reaction. The data were analyzed using SYSTAT software version 13.2.
Results:
Out of the total E. coli isolates, 77.5% was obtained from hospitalized patients. Colistin resistance was initially detected in 11 (0.95%) isolates, of which 9 (0.78%) were confirmed by BMD. The mcr-1 gene was detected in three (33.3%) of these nine phenotypically confirmed resistant isolates. None of the non-resistant isolates tested harbored the mcr-1 gene.
Conclusion:
The emergence of colistin-resistant E. coli is a clinically important concern because it limits treatment options. Detection of mcr-1-positive isolates supports the need for continued antimicrobial surveillance, stewardship, and infection-control vigilance.
Keywords
Broth microdilution
Colistin
Escherichia coli
mcr-1 gene
Tertiary care hospital
INTRODUCTION
Gram-negative bacilli (GNB) are major causes of human infection. Among GNBs, Escherichia coli, a member of the genus Escherichia, is a major pathogen known to cause a wide range of infections, including urinary tract infection, skin and soft tissue infection, septicemia, endotoxic shock, pneumonia, and meningitis in neonates.[1]
A well-recognized issue that frequently renders empirical therapy ineffective is multidrug resistance (MDR). Infections caused by MDR GNBs can be effectively treated with polymyxins, such as colistin. However, their clinical application is restricted by their inadequate urinary clearance and potential adverse effects, such as neurotoxicity and nephrotoxicity.[2,3] Colistin is being reconsidered as a last-resort treatment option due to the growing prevalence of MDR Gram-negative pathogens, especially those that show carbapenem resistance.[4] The use of colistin has grown as an efficient treatment option due to the increased prevalence of MDR Gram-negative infections, particularly in India.[5-8]
Colistin resistance has arisen as a result of the frequent use of colistin to treat these MDR pathogens. In accordance with the guidelines of the European Committee on Antimicrobial Susceptibility Testing and the Clinical and Laboratory Standards Institute (CLSI) Subcommittee on Antimicrobial Susceptibility Testing (AST), isolates should be reported as colistin-resistant only after confirmation by broth microdilution (BMD) using colistin sulfate, which is the reference method for colistin susceptibility testing.[9] The lack of the reference method in many laboratories, however, may result in inaccurate data and an underestimation of the true prevalence of colistin resistance among MDR GNBs.
Several mechanisms have been proposed for E. coli; the emergence of colistin resistance has been attributed to a variety of mechanisms, including genetic mechanisms. The mobile colistin resistance (mcr) gene is one of the most important ones. The most frequently linked genes to colistin resistance among the mcr variants (mcr-1 to mcr-10) is mcr-1.[3] There is currently a lack of information on the genetic characterization of colistin resistance in this geographic area. Hence, the aim of this study was to find how the mcr-1 gene is linked to E. coli strains that are resistant to colistin in North Indian tertiary care hospital.
MATERIALS & METHODS
Study design and setting
This cross-sectional hospital-based observational study was conducted in the Department of Microbiology at a tertiary care hospital over a period of 1 year, from October 2023 to September 2024. Clinical samples from patients with suspected infection were collected according to sample-collection guidelines. Samples meeting the inclusion criteria were included in the study. Data were entered into a Microsoft Excel spreadsheet after application of the inclusion and exclusion criteria.
Inclusion criteria
The clinical samples from patients of all age groups and genders showing the significant growth of E. coli on culture from both inpatient department (IPD) and outpatient department (OPD) were included in the study. In case of multiple isolations from the same patient, the E. coli isolated first was included in the study.
Exclusion criteria
The bacterial isolates other than E. coli were excluded from the study. In case of multiple isolates from the same patient, subsequent E. coli isolates were also excluded from the study. The patients with recent antibiotic exposure were excluded from the study.
The final dataset was compiled in a Microsoft Excel spreadsheet, following the inclusion and exclusion criteria.
Sample processing for isolation and identification of aerobic bacteria
The clinical specimens were processed for aerobic culture on appropriate culture media following standard bacteriological techniques.[10] The growth on solid culture media was subjected to preliminary identification based on colony characteristics and Gram staining. The final species-level identification and AST were performed by the VITEK 2 compact automated system (bioMérieux, France) using the GN test card and AST-N405 cards, respectively.
BMD method for detection of colistin resistance
Colistin resistance was confirmed by the reference BMD method performed in accordance with CLSI M07-A10 guidelines, 10th edition, 2015, using cation-adjusted Mueller– Hinton broth (CaMHB), and interpretation of minimum inhibitory concentration (MIC) was done as per CLSI M100 guidelines, 33rd edition, 2023.[11,12] Briefly, colistin sulfate (HiMedia India Pvt. Ltd., Mumbai) was used to prepare colistin concentrations by serial two-fold dilutions in CaMHB, ranging from 0.25 to 64 µg/mL.[13] A bacterial suspension was added to each well to achieve a final inoculum of 105 colony-forming units/mL. A drug-free control (growth control) and a non-inoculated control (sterility control) were included in each assay for quality control. E. coli ATCC 25922 was tested each time as a negative control (NC) with expected MIC breakpoints of 0.5–2 µg/mL. The MICs were determined after overnight incubation at 37°C. Interpretation of MIC was based on CLSI breakpoints for enterobacterales. Isolates with MIC value of ≥4 µg/mL were classified as resistant, while those with MIC ≤2 µg/mL were considered non-resistant as mentioned in CLSI M-100 guidelines 2023 (33rd Edition).[12]
Genotypic characterization of colistin resistance
The association of colistin resistance with plasmid-mediated transferable mcr genes has been reported in the literature.Out of the mcr-1 to mcr-10 variants of mcr genes studied so far, mcr-1 is the most commonly associated variant with colistin resistance. The other mcr variants, mcr-2 to mcr-10, are also associated with colistin resistance to a lesser extent only; our study was limited to finding the association of only the mcr-1 gene with colistin resistance.
Detection of the mcr-1 gene by real-time polymerase chain reaction (PCR)
All phenotypically confirmed colistin-resistant E. coli isolates, along with 1% of known colistin non-resistant isolates, were subjected to real-time PCR for detection of the mcr-1 gene for quality control.
Genomic deoxyribonucleic acid (DNA) was extracted using the GeNei Pure Bacterial DNA Purification Kit (GeNei Laboratories Pvt. Ltd., Bengaluru, India) according to the manufacturer’s instructions. Extracted DNA was stored at –20°C until use. Amplification was performed using the GeNei™ PCR kit according to the manufacturer’s guidelines.
Specific forward and reverse primers used for mcr-1 gene detection are shown in Table 1.[14]
| Primer | Primer sequences | Product bp |
|---|---|---|
| Forward primer | 5’-CGTTCAGCAGTCATT ATGCCAGTTTCTTTCGCGTGC-3’ | 956 bp |
| Reverse primer | 5’-CTTACGCATATCAGGC TTGGTTGCTTGTACCGC-3’ | 956 bp |
A: Adenine, T: Thymine, C: Cytosine, G: Guanine
The final volume for the PCR reaction was 25 µL, consisting of 3 µL of nuclease-free water, 12 µL of EvaGen™ Green quantitative PCR (qPCR) Master Mix, 2 µL of working primers at a final concentration of 5 pmoL, and 3 µL of template DNA. PCR was carried out following EvaGen™ Green qPCR guidelines (GeNei Laboratories Pvt. Ltd., Bengaluru, India). PCR cycling conditions included an initial denaturation at 95°C for 3 min, followed by 35 cycles of 95°C for 15 s, primer annealing at 58°C for 30 s, and elongation at 72°C for 1 min, with a final extension at 72°C for 15 min. Amplification was carried out using the Rotor-Gene Q system (QIAGEN, Germantown, MD, USA). DNA from colistin-susceptible E. coli ATCC 25922 served as the NC for the mcr-1 gene. A standard strain harboring the mcr-1 gene was used as the positive control.
Statistical analysis
Data generated in this study were analyzed using SYSTAT version 13.2 and the Statistical Package for the Social Sciences software 27.0 (IBM Corp., USA). Descriptive statistics, including frequency and percentage, were used to summarize the sample characteristics. Fisher’s exact test was used to calculate the p-value and the odds ratio. Fisher’s exact test was used to assess the association between hospital location and colistin resistance. Odds ratios with 95% confidence intervals were calculated to estimate the effect size. A p < 0.05 was considered statistically significant.
RESULTS
Phenotypic characterization of colistin-resistant E. coli isolates
A total of 1,149 clinical isolates of E. coli were included in the study. On antibiotic susceptibility testing, resistance to colistin was detected in 11 (0.95%) isolates by an automated method, and resistance was confirmed by the gold standard BMD method in 9 (0.78%) isolates as shown in Table 2. The microtiter plate showing the results of BMD is shown in Figure 1.
| Escherichia coli isolates | Colistin resistance by automated VITEK 2 | Colistin resistance by BMD |
|---|---|---|
| Frequency | 11 | 9 |
| Percentage | 0.95 | 0.78 |
BMD: Broth microdilution
- Broth microdilution plate used for the determination of colistin minimum inhibitory concentration in Escherichia coli isolates. SC: Sterility control, GC: Growth control, T1-T7: Test isolates, NC: Negative control, MHB: Mueller Hinton Broth.
Sample-wise and gender wise distribution of colistin resistance
As illustrated in Table 3, urine samples accounted for the majority of colistin-resistant E. coli isolates (54.5%), followed by pus samples (36.3%) and endotracheal aspirate (9.09%). Most of these isolates (72.7%) were recovered from patients admitted to the IPD and intensive care units (ICUs). With 63.3% of cases, males outnumbered females in terms of gender distribution, and the ratio of male-to-female was 1.75:1.
| Sample | Colistin-resistant isolates (Frequency) | Percentage |
|---|---|---|
| Urine | 6 | 54.5 |
| Pus | 4 | 36.4 |
| Endotracheal aspirate | 1 | 9.09 |
Genotypic characterization of colistin resistance
The presence of the mcr-1 gene was ascertained by genotypic characterization of 11 clinical isolates of E. coli, nine of which were confirmed by BMD. Only three (33.3%) E. coli isolates contained the mcr-1 gene, as shown in Table 4. The amplification curves showing positive and negative results for the mcr-1 gene are shown in Figure 2. However, the mcr-1 gene was not detected in eight phenotypically colistin-resistant isolates or in any of the colistin non-resistant E. coli isolates tested.
- Real-time amplification curves for detection of the mcr-1 gene in Escherichia coli isolates. PC: Positive control; NC: Negative control; Ct: Cycle threshold.
| Colistin-resistant isolates by BMD | Colistin-resistant isolates of Escherichia coli harboring mcr-1 gene (frequency) | Percentage |
|---|---|---|
| 9 | 3 | 33.3 |
BMD: Broth microdilution
Hospital location-wise distribution of colistin-resistant isolates
The majority of the colistin-resistant E. coli isolates were recovered from the ICU and IPD as compared to OPD. The comparative distribution of all three methods based on hospital location is shown in Table 5. The genotypically confirmed E. coli isolates harboring mcr-1 were exclusively recovered from the ICU patients. The total number of E. coli isolates and distribution of colistin-resistant E. coli isolates, along with the statistical parameters, are shown in Table 6.
| Hospital location | Automated method (n=11) | Broth microdilution (n=9) | Genotypic method (mcr-1) (n=3) |
|---|---|---|---|
| ICU | 5 | 5 | 3 |
| Other wards | 3 | 3 | 0 |
| OPD | 3 | 1 | 0 |
ICU: Intensive care unit, OPD: Outpatient department
| Hospital location | Colistin non-resistant (n=1140) | Colistin resistant (n=9) | p-value | Odds ratio with 95% CI |
|---|---|---|---|---|
| ICU | 241 | 5 | 0.012 | 4.66 (1.24–17.50) |
| Non-ICU | 899 | 4 |
ICU: Intensive care unit, CI: Confidence interval
DISCUSSION
The emergence and rising trends of antimicrobial resistance constitute a global challenge and pose a serious threat to healthcare systems worldwide, primarily due to the injudicious use and misuse of antimicrobials.[15] Colistin is often regarded as a last-resort antibiotic. It is now used to treat infections caused by bacteria that are resistant to multiple antibiotics. However, the emergence of colistin resistance in clinical isolates has become a significant therapeutic concern.[15,16]
In the present study, we observed 0.78% colistin-resistant strains of E. coli using the gold standard BMD method, which is considerably lower than the 4.2% reported in a study by Arjun et al. from South India.[17] Although the prevalence of confirmed colistin resistance in this study was low, the detection of mcr-1-positive isolates indicates the presence of plasmid-mediated resistance and supports continued surveillance.[18] Therefore, continuous surveillance is important to prevent further dissemination of resistant strains. Reliable phenotypic detection of colistin resistance before clinical use is essential using BMD, as BMD is a gold-standard, cost-effective, and reliable method for the routine detection of colistin resistance.[9]
In addition, the presence of the mcr-1 gene in 33.3% of phenotypically confirmed colistin-resistant isolates of E. coli in our study is a significant concern. Singh et al. from Himachal Pradesh reported a prevalence of the mcr-1 gene in only 5.9% of E. coli isolates that exhibited colistin resistance.[19]
The absence of the mcr-1 gene in 66.7% of phenotypically confirmed colistin-resistant E. coli isolates in our study suggests that mcr-1 is not the sole mechanism responsible for colistin resistance. Other genetic determinants or mechanisms may be contributing to resistance in these isolations. In addition, the presence of other mcr variants (mcr-2 to mcr-10) cannot be excluded. One of the major limitations of this study was that we focused solely on the detection of the mcr-1 gene, despite the existence of multiple mcr genes associated with colistin resistance.[15] These findings highlight the scope for future research to explore other resistance genes, gene-to-gene interactions, and a whole-genome sequencing approach to identify other genetic variants responsible for colistin resistance.
As the mcr-1 gene is plasmid-mediated, its potential for horizontal gene transfer raises significant concern regarding rapid dissemination, particularly within hospital settings.[2]Identification of isolates harboring plasmid-mediated mcr-1 genes is therefore crucial for understanding regional resistance trends. Horizontal gene transfer is not limited to hospital settings; environmental bacteria have also been shown to harbor the mcr-1 gene, posing a risk of transmission to other human pathogens and serving as a reservoir capable of triggering outbreaks.[6,18] Early identification of such isolates can help in preventing nosocomial outbreaks through targeted infection prevention and control measures. In this context, real-time PCR can provide rapid and accurate detection of the mcr-1 gene in comparison to conventional phenotypic methods.[20]
Limited Indian data on mcr-1 gene-based detection of colistin resistance in clinical isolates of E. coli restrict direct comparisons. However, international studies report variable prevalence of the mcr-1 gene, often higher than that observed in our study. Cannatelli et al. reported the presence of the mcr-1 gene in 88.8% of phenotypically colistin-resistant E. coli isolates in a study from Italy, while Liu et al. reported 63% prevalence of the mcr-1 gene.[6,21] In contrast, a Latin American study by Rapoport et al. documented a much lower prevalence of 10.3%.[8] These variations may be attributed to alternative resistance mechanisms, including phenotypic adaptations and genetic determinants other than mcr-1. Nevertheless, mcr-1 remains the most common and frequently reported genetic element associated with colistin resistance in E. coli, as reported by Shi et al. They reported mcr-1 in 86.1%, followed by mcr-9 in 5.7% of colistin-resistant strains of E. coli.[22]
The colistin-resistant E. coli strains were most commonly isolated from the patients admitted to ICUs, followed by other IPD settings, as compared to OPD. These trends indicate that hospital-acquired strains, especially the strains from ICUs, are more resistant than community-acquired strains. On comparing ICU and non-ICU E. coli isolates statistically, colistin resistance was significantly associated with ICU isolates as indicated by a statistically significant p = 0.012 (<0.05) and an odds ratio of 4.66, indicating that isolates from ICU patients had higher odds of colistin resistance than those from non-ICU patients.
All mcr-1-harboring colistin-resistant E. coli isolates in our study were recovered from patients admitted to ICUs. These results are consistent with the hospital antibiogram, which highlights the MDR nature of strains frequently associated with hospital-acquired infections during ICU stay. Collectively, these findings underscore the need for targeted surveillance and stringent infection prevention and control measures in high-risk healthcare settings.
Another critical concern is the under-reporting or over-reporting of colistin resistance due to the non-availability of recommended detection methods in many clinical laboratories.[6] Further studies using gold-standard phenotypic methods combined with molecular characterization of resistance mechanisms are essential to accurately determine the actual burden of colistin resistance.
In recent years, a gradual increase in colistin resistance has been observed, further exacerbated by the plasmid-mediated nature of the mcr genes, facilitating rapid horizontal gene transfer across diverse bacterial species.[4]
The emergence of colistin-resistant E. coli in North India is a trend that has substantial therapeutic and public health implications, as our study has demonstrated. Colistin resistance is conferred by genetic mechanisms, of which the mcr-1 gene is one of the most prevalent contributors. Overall,the results highlight how urgently molecular surveillance and an all-encompassing approach are needed to combat the rising threat of antibiotic resistance in India.
Limitations of the study
This study had certain limitations. First, the analysis was restricted to the detection of the mcr-1 gene only; other mcr gene variants (mcr-2 to mcr-10), as well as the plasmid characterization or genomic analysis, could not be performed due to limited resources. Second, as this was a single-center study with a few resistant isolates, the findings cannot be generalized to the broader population. Third, due to the lack of clinical outcome data, the therapeutic implications of colistin resistance could not be assessed. Fourth, due to financial constraints, only 1% of colistin non-resistant isolates were tested for the detection of the mcr-1 gene.
CONCLUSION
Colistin resistance among clinical E. coli isolates in this setting was uncommon but clinically relevant. The detection of mcr-1 in a subset of phenotypically resistant isolates highlights the importance of confirmatory susceptibility testing and ongoing molecular surveillance.
Compliance with the Strengthening of the Reporting of Observational Studies in Epidemiology (STROBE)
The authors confirm that they adhered to the STROBE reporting guidelines during the manuscript preparation.
Acknowledgment:
The authors gratefully acknowledge the technical support provided by Mr. Harimohan and Mr. Ankit Tyagi during the genotypic study.
Author contributions:
AS: Contributed to the data collection, data compilation, clinical and laboratory data analysis and interpretation, and preparation of the first draft of the manuscript; AP: Design of the study, reviewing and editing of the manuscript; PS: Review of data and manuscript editing and correction; PJ: Supervision of laboratory work; TZ: Literature search. All authors have read and agreed to the published version of the manuscript.
Ethical approval:
The research/study was approved by the Institutional Review Board at the University Ethics Committee Medical (UECM) of Swami Vivekanand Subharti University, Meerut, Uttar Pradesh with the reference number SMC/UCEM/2023/695/314, dated September 25, 2023.
Declaration of patient consent:
The authors certify that they have obtained all appropriate patient consent forms. In the form, the patient has given consent for clinical information to be reported in the journal. The patient understand that the patient’s names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Conflicts of interest:
There are no conflicts of interest.
Availability of data and material:
Subject to a reasonable request, the datasets utilized in the study may be obtained from the corresponding author.
Use of artificial intelligence (AI)-assisted technology for manuscript preparation:
The authors confirm that there was no use of artificial intelligence (AI)-assisted technology for assisting in the writing or editing of the manuscript and no images were manipulated using AI.
Financial support and sponsorship: Nil
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