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PubMedDate not supplied

Comparison of the binding of gram-negative bacterial endotoxin by polymyxin B sulphate, colistin sulphate and colistin sulphomethate sodium.

Polymyxins are cyclic polypeptide antibiotics. In addition to their bactericidal activity they bind lipid A and neutralize the biological effects of bacterial endotoxin. We have studied the three available polymyxin preparations: polymyxin B sulphate (PB), colistin sulphate (CS) and colistin sulphomethate sodium (CMS), and compared their endotoxin binding capacity at equivalent therapeutic dosage. Each polymyxin was bound to a column of Sepharose 4B and challenged with 5 micrograms of endotoxin from Escherichia coli O127:B8. Recovery of endotoxin in the eluate was measured by a quantitative Limulus lysate microassay. PB and CS bound 94% of the challenge dose, CMS 89% and the control column (Sepharose alone) 24%. These results suggest that parenteral CMS (the least toxic polymyxin) retains useful anti-endotoxin capacity, and that in neutropenic patients, oral polymyxin may exert both anti-endotoxin and antimicrobial effects.

Colistin↗

PubMed1976

Polyacrylic bone cement containing erythromycin and colistin. I. In vitro bacteriological activity and diffusion properties of erythromycin, colistin and erythromycin/colistin comibination.

Erythromycin and colistin demonstrate a non-antagonistic ability to inhibit the growth of a wide variety of aerobic and anaerobic bacterial isolates. When incorporated in Surgical Simplex P Radiopaque Bone Cement, fabricated cement pellets were effective in inhibiting 98% of all anaerobic and aerobic test isolates. Separate experiments indicate that each antibiotic can diffuse from polymerized cement, and that the concentration of each antibiotic is consistently above the minimum inhibitory concentration of 96% of the isolates. We conclude that erythromycin/colistin Surgical Simplex P radiopaque Bone Cement is a worthy candidate for clinical investigation.

Bone Cements↗

PubMed2026

Investigation of pmrCAB and mcr associated resistance in colistin-resistant A. baumannii isolates.

BACKGROUND & OBJECTIVES: Colistin is one of the last-resort antibiotics for multidrug-resistant Acinetobacter baumannii. Increasing resistance to colistin limits treatment options, particularly in intensive care units (ICUs). The aim of this study was to compare the expression levels of pmrC, pmrA, and pmrB, among colistin-resistant and colistin-susceptible clinical A. baumannii isolates, to investigate the presence of plasmid-mediated mcr-1-5 genes, and to determine clonal relationships among colistin-resistant isolates. METHODS: A total of 110 A. baumannii isolates recovered from ICU patients in 2020 were included. Colistin minimum inhibitory concentrations were determined using the broth microdilution method. Expression levels of pmrC, pmrA, and pmrB were analyzed by RT-qPCR and compared with the reference strain A. baumannii ATCC 19606. Colistin-resistant isolates (Group 1) were compared with 10 randomly selected colistin-susceptible isolates (Group 2). Detection of mcr-1-5 genes was performed by in-house multiplex PCR. Clonal relationships among resistant isolates were assessed by PFGE. RESULTS: Colistin resistance was detected in 15.45% (17/110) of isolates. The median relative expression levels of pmrC, pmrB, and pmrA in colistin-resistant isolates were 47.84-fold (IQR: 19.29-67.18), 14.72-fold (IQR: 10.13-16.68), and 8.57-fold (IQR: 5.17-12.82), respectively. In colistin-susceptible isolates, the corresponding median expression levels were 5.32-fold (IQR: 3.60-7.97), 3.29-fold (IQR: 0.85-5.95), and 3.31-fold (IQR: 2.58-6.55). Expression levels were significantly higher in colistin-resistant isolates for pmrC (p < 0.001), pmrB (p = 0.002), and pmrA (p = 0.024). None of the resistant isolates carried mcr-1-5 genes. PFGE analysis revealed 12 distinct genotypes among 17 resistant isolates. INTERPRETATION & CONCLUSIONS: Colistin-resistant A. baumannii isolates exhibited significantly higher expression levels of the pmrC, pmrA, and pmrB genes compared to colistin-susceptible isolates. Among the genes evaluated, pmrC showed the largest effect size and the strongest association with the colistin-resistant phenotype. No changes were found in the mcr-1-5 genes among the isolates studied. Further studies, including genomic and functional analyses, are needed to elucidate the underlying mechanisms of these expression changes and their contribution to colistin resistance.

Journal Article↗

PubMed1985

Binding and neutralization of bacterial lipopolysaccharide by colistin nonapeptide.

Polymyxin nonapeptides, proteolytic derivatives of polymyxin antibiotics, are less toxic than their parent compounds but retain some of their antibacterial activities. To confirm and expand observations that polymyxin nonapeptides have anti-endotoxin activity, we studied the ability of colistin nonapeptide to bind to bacterial lipopolysaccharide (LPS) and to inhibit the effects of LPS on Limulus amoebocyte lysate and lymphocyte mitogenicity. Colistin nonapeptide was purified by high-pressure liquid chromatography and was demonstrated to bind to LPS by equilibrium dialysis. The ability of colistin nonapeptide to render E. coli ATCC 25922 cells sensitive to erythromycin was abrogated by 50% after incubation with E. coli O18 LPS in a ratio by weight of LPS to colistin nonapeptide of 3.9:1. The presence of 4 micrograms of colistin nonapeptide or colistin per ml increased by 130- and 800-fold, respectively, the concentration of E. coli O113 LPS required to produce 50% gelation of Limulus amoebocyte lysate as measured by a spectrophotometric assay. Neutralization of LPS by colistin nonapeptide was time and concentration dependent. In contrast to the neutralization seen with LPS derived from a colistin-sensitive organism, colistin nonapeptide neutralized very little LPS extracted from a strain of Serratia marcescens that was resistant to colistin. Colistin nonapeptide also inhibited LPS-induced [3H]thymidine uptake by splenic lymphocytes, but its activity was less than 1/10 that of colistin. We conclude that colistin nonapeptide binds to LPS and possesses antiendotoxin activity. However, the anti-endotoxin activity of the nonapeptide is considerably less than that of its parent compound, colistin.

Chromatography, High Pressure Liquid↗

PubMed2025

Molecular characterization of colistin resistance in carbapenem-resistant Klebsiella pneumoniae from a tertiary hospital in China.

Colistin resistance in carbapenem-resistant Klebsiella pneumoniae (CRKP) poses a significant global health challenge, as colistin remains the last-resort antibiotic for treating multidrug-resistant K. pneumoniae infections. This study aimed to investigate the prevalence and molecular mechanisms underlying colistin resistance in CRKP (Colr-CRKP) isolates in Henan, China, from 2021 to 2024. The minimum inhibitory concentrations of colistin for 134 K. pneumoniae isolates were determined using the broth microdilution method. Whole-genome sequencing was performed using the Illumina platform to identify carbapenemase genes and sequence types (STs). Colistin resistance mechanisms were investigated, including mutations in two-component systems (pmrA/pmrB, phoP/phoQ), inactivation of the mgrB gene, and the presence of plasmid-mediated mcr genes. Most isolates were collected from intensive care units (99/134, 73.9%), with 48.5% (59/134) of patients having no documented colistin exposure history. Notably, ST11 was the predominant sequence type among Colr-CRKP isolates (113/134, 84.3%), all of which carried blaKPC-2 as the sole carbapenemase determinant. In contrast, seven non-carbapenemase-producing isolates exhibited phenotypic resistance to carbapenems. Genomic analysis revealed inactivation or loss of the mgrB gene in 53.7% (72/134) of isolates, predominantly due to insertion mutations (54/72). Although 32.8% (44/134) of isolates carried mutations in two-component systems, these alterations did not exhibit pathway-specific clustering. Intriguingly, plasmid-mediated mcr genes were detected in only 1.5% (2/134) of cases (mcr-8.2 and mcr-1.1), while 22.4% (30/134) of colistin-resistant strains lacked identifiable resistance determinants based on current detection methods. Our findings indicate that disruption of the mgrB gene is the primary mechanism of colistin resistance in ST11 CRKP clones. The emergence of resistance in 48.5% of patients without prior colistin exposure, combined with low mcr gene prevalence (1.5%) and unexplained resistance in 22.4% of isolates, suggests complex selective pressures beyond direct antimicrobial use. These findings underscore the urgent need for strengthened antimicrobial stewardship and the development of alternative therapeutic strategies to combat this high-risk pathogen.IMPORTANCEThe global rise of colistin-resistant Klebsiella pneumoniae, particularly in carbapenem-resistant Klebsiella pneumoniae (CRKP) strains, has severely restricted treatment options for multidrug-resistant infections. Our study provides the first comprehensive molecular characterization of colistin resistance in CRKP in a large tertiary hospital in central China. We identified mgrB disruption as the predominant resistance mechanism, while plasmid-mediated mcr genes were rare. Notably, nearly half of the resistant isolates occurred in patients without prior colistin exposure, suggesting alternative selective pressures driving resistance. These findings highlight the complex dynamics of colistin resistance in CRKP and underscore the need for enhanced genomic surveillance and stewardship interventions to limit further dissemination.

Colistin↗

PubMed2026

Transposon insertion sequencing of Pseudomonas aeruginosa identifies multiple intersecting pathways essential for extreme colistin resistance.

Colistin is used to treat antibiotic resistant gram-negative infections, including those caused by Pseudomonas aeruginosa (Pa). Using a diverse collection of clinical isolates, we identified BWH047, a colistin-resistant isolate with an extremely high minimum inhibitory concentration (MIC, 1280 µg/mL). To characterize the genes conditionally essential for colistin resistance in BWH047, we employed transposon insertion sequencing and identified 20 gene candidates. In-frame deletion validated 75% of the candidates and identified genes in several new pathways that contribute to colistin resistance in Pa, including algU and wapH. We also identified several candidate genes from previously reported colistin resistance pathways (e.g., arn, pmrAB). We further investigated the impact of a colistin resistance-associated inner membrane DedA-family undecaprenyl phosphate flippase, which we named DpcA (DedA of Pseudomonas necessary for colistin resistance A). Deletion of dpcA in BWH047 restored sensitivity to colistin (MIC = 0.5 µg/mL) and resulted in several unique changes to the structure of lipopolysaccharide (LPS), including production of decreased amounts of the colistin resistance-conferring 4-amino-4-deoxy-L-arabinose (L-Ara4N) modification on lipid A. This work represents a robust analysis of colistin resistance in Pa and identifies intersecting pathways that contribute to extreme phenotypic resistance.

Pseudomonas aeruginosa↗

PubMed2026

Diverse structures of mcr-10-bearing plasmids and high colistin resistance in Enterobacter cloacae complex clinical isolates from South Korea.

BACKGROUND: The emergence of mcr-mediated colistin resistance in Enterobacter cloacae complex (ECC) poses a significant threat to antimicrobial therapy. Among mcr variants, mcr-10 has been identified in various environments, but its genetic diversity, structural context, and functional role in colistin resistance remain unclear. METHODS: We investigated 183 ECC isolates and identified 60 colistin-resistant strains through minimum inhibitory concentration (MIC) testing. The presence of mcr-10 was screened using reference genomes from NCBI, and whole plasmid sequencing was conducted on mcr-10-positive isolates. The genetic environment of mcr-10 was analyzed via synteny and structural annotation. RESULTS: Whole-plasmid sequencing of eight mcr-10-positive ECC isolates identified three replicon types among the mcr-10-harboring plasmids: IncFIB (n=3), IncFII (n=3), and IncFII/IncFIB (n=2). Although all plasmids shared the xerC-mcr-10 cassette, they lacked a conserved backbone and showed diverse genetic contexts with variable insertion sequences near mcr-10, indicating marked structural heterogeneity. No additional antimicrobial resistance genes were detected on these plasmids. When introduced into E. coli DH5α, the plasmids increased colistin MICs only modestly, whereas representative plasmids transferred into colistin-susceptible E. roggenkampii and E. kobei conferred high-level resistance comparable to that of the parental mcr-10-positive isolates. Consistently, qRT-PCR showed higher mcr-10 expression in ECC transformants than in E. coli under colistin exposure, supporting a hostdependent effect on mcr-10-mediated colistin resistance. CONCLUSION: These findings highlight the diversity of mcr-10-carrying plasmids and suggest that mcr-10-mediated colistin resistance is shaped by the host genetic background. Further studies are needed to clarify the mechanisms underlying mcr-10 expression.

Colistin↗

PubMed1978

Pretreatment with colistin and Proteus sensitivity to other agents.

The effects of pretreatment with colistin (polymyxin E) on the sensitivity of Proteus mirabilis, P. vulgaris and P. morganii strains to tris and sodium deoxycholate (DOC) have been studied. Pretreatment of two P. mirabilis strains (NCTC 60 and 4199) with low concentrations (0.25 approximately 1 microgram/ml) of colistin rendered them sensitive to lysis by tris (0.05M) or DOC (250 approximately 1,000 microgram/ml) although DOC induced lysis of control (non-colistin-treated) suspensions also. In contrast, the other P. mirabilis strains, as well as the P. vulgaris and P. morganii strains were little affected by tris (0.2M) or DOC (10,000 microgram/ml) even after exposure of the cells to high colistin concentrations (up to 500 microgram/ml). Colistin-pretreated or control cells of P. mirabilis NCTC 60 rapidly lost viability when suspended in water but not when held in 0.16M sodium chloride solution. Ethylenediamine tetraacetate-pretreated cells of strains 60 and 4199 were fairly sensitive to tris, although the extent of the lysis was less than when colistin was used as pretreating agent. One strain of P. vulgaris (NCTC 4175) became sensitive to tris and to DOC following exposure of the cells to ampicillin.

Colistin↗

PubMed1988

Further studies on colistin (polymyxin E)-induced cell leakage in mycobacteria: Mg++ efflux in Mycobacterium avium and its effects on drug-susceptibility.

Action of colistin (polymyxin E) was investigated on the opportunistic pathogenic species Mycobacterium avium ATCC 15769 (resistant strain, MIC greater than 100 micrograms/ml). Mycobacterium intracellulare ATCC 13950: a colistin-susceptible strain (MIC 25 micrograms/ml), was used as a parallel control for Mg++ efflux experiments. After the addition of 100 micrograms/ml of colistin to bacteria suspended in a buffer, both loss of viability and Mg++ efflux were followed for one week. Although there was an initial Mg++ efflux in both strains, it soon attained a plateau in case of the resistant strain without any loss of viability until 48 h, whereas in case of the susceptible strain, Mg++ efflux was about 3 times higher than former, a plateau was attained only 24 h after the drug addition, and the loss of viability started only 6 h after the drug addition. Consequently, the loss of viability of M. avium with later incubation times (6 days) was not due to the action of colistin on the cytoplasmic Mg++ efflux solely, but some additional effect was implicated. The drug-susceptibility of extracellularly-growing and intracellularly-growing (in the J-774 macrophage cell line) M. avium to the antibiotics tested could not be potentiated when they were used in combination with 5 micrograms/ml of colistin (maximal obtainable serum level in man) or the polymyxin B nonapeptide (PMBN), nor in the case of bacteria pretreated with these molecules.

Amoxicillin↗

PubMed1987

Colistin inhalation therapy in cystic fibrosis patients with chronic Pseudomonas aeruginosa lung infection.

Forty patients with cystic fibrosis and chronic broncho-pulmonary Pseudomonas aeruginosa infection entered a prospective double-blind placebo-controlled study of colistin inhalation. Active treatment consisted of inhalation of colistin one million units twice daily for three months and was compared to placebo inhalations of isotonic saline. Significantly more patients in the colistin inhalation group completed the study as compared to the placebo group (18 versus 11). Colistin treatment was superior to placebo treatment in terms of a significantly better clinical symptom score, maintenance of pulmonary function and inflammatory parameters. We recommend colistin inhalation therapy for cystic fibrosis patients with chronic P. aeruginosa lung infection as a supplementary treatment to frequent courses of intravenous anti-pseudomonas chemotherapy.

Administration, Inhalation↗

PubMed1991

Toxicity of colistin in cystic fibrosis patients.

Pulmonary exacerbations of cystic fibrosis associated with strains of Pseudomonas aeruginosa that are resistant to multiple antibiotics are becoming increasingly common. The search for treatment alternatives continues and may include the reexamination of older antibiotics. Colistin sulfate is a polypeptide antibiotic with good activity against P. aeruginosa. Although its use was largely discontinued in the early 1970s because of reports of frequent renal and neurologic toxicity, intravenous colistin is often prescribed at our institution for patients with P. aeruginosa resistant to multiple-drug therapy. We prospectively monitored 19 patients during 21 courses of colistin therapy to identify the character and incidence of this agent's toxicity. Only one case of renal toxicity occurred. Six cases of neurotoxicity occurred, which were characterized by perioral paresthesia, ataxia, or both. The rate of intolerable renal adverse effects secondary to colistin therapy was appreciably lower among these patients than that reported previously for other patients. It appears that intravenous colistin can be considered for cystic fibrosis patients with strains of P. aeruginosa that are resistant to more commonly used antibiotics.

Adolescent↗

PubMed1975

Combinations of antimicrobial agents. I. The in vitro sensitivity of 100 strains of Pseudomonas aeruginosa to polymyxin B, colistin, carbenicillin, gentamicin and doxycycline and to various combinations of these antibiotics.

The MICs for 100 strains of Pseudomonas aeruginosa were determined for polymyxin B, colistin, carbenicillin, gentamicin and doxycycline and various combinations of these antibiotics. This study was carried out by means of a tube dilution method. Additive actions were observed in the combinations of polymyxin B plus carbenicillin, polymyxin B plus gentamicin, polymyxin B plus doxycycline, carbenicillin plus doxycycline and gentamicin plus doxycycline. A synergistic action was observed for the combinations of colistin plus carbenicillin, colistin plus gentamicin, colistin plus doxycycline and carbenicillin plus gentamicin. In none of the combinations was any antagonistic action encountered. Numerous reasons for using combined antibiotic treatment are listed. The results were obtained exclusively in in vitro investigations.

Carbenicillin↗

PubMed1975

Mechanism of colistin-induced neuromuscular depression.

The effect of a high concentration of the antibiotic colistin sulfate on neuromuscular transmission was examined by recording intracellularly from rat diaphragm blocked with tubocurarine chloride. The presynaptic effect of colistin was different from that of neomycin sulfate, which reduces the probability of acetylcholine release: Colistin reduced that the quantum content of the initial and the last 20 end-plate potentials of a train of 40 stimuli without altering the probability of acetylcholine release. The quantum size was reduced, while the frequency of miniature end-plate potentials was unchanged.

Animals↗

PubMed1987

Reliability of the colistin disk test in identification of Serratia marcescens and Serratia liquefaciens.

Resistance to polymycin B or E (colistin) in the disk test, which is used as a means of identification, was tested in 43 strains of Serratia marcescens and 26 of Serratia liquefaciens. While all strains had MIC values greater than 32 mg/l for colistin, false susceptibility to both polymyxins was encountered in the 24 h disk test in 9% of Serratia marcescens and 12-96% of Serratia liquefaciens strains, depending on the kind of polymyxin, temperature and duration of incubation. Using colistin disks and incubation at 25 degrees C for 48 h, the percentage of false susceptible results could be minimized.

Colistin↗

PubMed1989

Residue determination of two co-administered antibacterial agents--cephalexin and colistin--in calf tissues using high-performance liquid chromatography and microbiological methods.

Residues of two antibacterial agents, cephalexin and colistin, co-administered by intramuscular injection to calves, were quantified in four different tissues (muscle, fat, liver and kidney) by column switching HPLC and by a microbiological method. For cephalexin assay, tissue samples with cephradin as internal standard were homogenized in a 5% trichloroacetic acid solution and filtrates were injected onto a concentration precolumn filled with LiChroprep RP-18 (25-40 microns). A clean-up step was incorporated by flowing a mobile phase (methanol-0.01 M phosphate buffer (pH 3.0); 15:85, v/v) through the enrichment column before elution on a LiChrospher RP-18e (5 microns) column with a methanol-phosphate buffer (30:70, v/v) at a flow rate of 1 ml min-1. Spectrometric detection was at 260 nm. An additional "off-line" washing step of extracts with methylene chloride was operated to achieve higher selectivity in the case of liver and kidney samples. The limit for quantitative assay was 0.045 micrograms g-1 with relative standard deviations in the range 5-8% and recoveries within 70%. For microbiological assay of colistin, samples were homogenized in 0.1 M hydrochloric acid-acetonitrile mixtures (3:1, v/v, for kidney and liver; 3:2, v/v, for fat and muscle). The supernatants were assayed by the cylinder plate method after evaporation to dryness under vacuum. Bordetella bronchiseptica ATCC 4617 was chosen as test organism. After a 3-h diffusion step at room temperature, the medium was incubated at 37 degrees C for 18 h and then the diameter of the growth inhibition zones was measured. Sensitivity reached 0.10-0.15 micrograms g-1. Results from the analysed samples over a 7-28 day period after drug administration show that no cephalexin was found at concentrations higher than the quantitation limit in the four test tissues and that colistin was found in muscle (injection site only) for 15 days and in kidney for 21 days.

Adipose Tissue↗

PubMed1992

Selective oral antimicrobial prophylaxis for the prevention of infection in acute leukaemia-ciprofloxacin versus co-trimoxazole plus colistin. The EORTC-Gnotobiotic Project Group.

230 leukaemic patients were entered into a randomised, prospective, multicentre trial of either ciprofloxacin (1 g/day) or co-trimoxazole (1920 mg/day) plus colistin (800 mg/day) for the prevention of infection during granulocytopenia. Bacteraemia due to resistant gram-negative rods occurred only in the co-trimoxazole-colistin group though both regimens were effective for selective gastrointestinal tract decontamination. However, there were fewer patients without any infective complications (31% vs. 18%: P = 0.02), fewer febrile days [mean (S.D.) 5.9 (1.1) vs. 8.2 (1.4): P = 0.0242], a lower proportion of infective events (0.9 (0.16) vs. 1.2 (0.18): P = 0.005) and fever occurred later (median 19 vs. 14 days: 0.025 less than P less than 0.05) in the co-trimoxazole-colistin group. The choice of prophylactic regimen therefore appears to depend upon whether or not protection against gram-negative infection is required or better systemic prophylaxis overall.

Administration, Oral↗

PubMed1986

Action of colistin (polymyxin E) on the lytic cycle of the mycobacteriophage D29 in Mycobacterium tuberculosis.

The antibiotic colistin (polymyxin E) inhibited the lytic cycle of the mycobacteriophage D29 in the tubercle bacilli, but not the D29 adsorption. The protein and nucleic acid synthesis in D29-infected bacteria were not affected significantly. The inhibitory activity was reversed by washing off the antibiotic, and by addition of Ca++, but not in media made iso-osmotic by addition of NaCl or sucrose. Transmission electron microscopy revealed an asymmetric to symmetric transition in the staining profile of the cytoplasmic membrane. Though no mature phage particles were ever observed in colistin-treated, D29-infected tubercle bacilli, loosely arranged aggregates resembling phage proheads were occasionally found. Judging from the above data, it was concluded that colistin inhibited D29 lytic cycle by causing molecular displacements in the inner leaflet of the cytoplasmic membrane, and consequently, the binding sites for D29 structural proteins were not available.

Adsorption↗

PubMed1988

Use of colistin and sorbitol for better isolation of Serratia marcescens in clinical samples.

A comparison was made of different culture media and procedures for detection of Serratia marcescens from faecal, pharyngeal and ocular swabs collected from 213 neonates. MacConkey agar and MacConkey agar with sorbitol (1%) and/or colistin (200 i.u./ml) were used both for primary isolation and after enrichment using Mossel Enterobacteriaceae broth with colistin (200 i.u./ml). The use of MacConkey agar supplemented with colistin for primary isolation improved considerably the isolation rate of S. marcescens from faecal swabs but not from pharyngeal swabs; the number of ocular isolations were insufficient to demonstrate differences between procedures. Moreover the enrichment procedures consistently increased the number of S. marcescens isolates especially from pharyngeal and ocular swabs. Use of sorbitol made detection of S. marcescens from clinical specimens easier and time- and cost-efficient.

Colistin↗