Abstract
Objectives
Carbapenem resistance is a growing public health crisis with regional variability in incidence. We characterized the susceptibility of carbapenem-resistant Gram-negative rods (CR-GNRs) from the Pacific Northwest to five reserve beta-lactam agents including cefiderocol and aztreonam-avibactam.
Methods
A panel of 162 CR-GNRs from unique patients were tested against cefiderocol, aztreonam-avibactam, ceftazidime-avibactam, meropenem-vaborbactam and ceftolozane-tazobactam, with a subset of isolates derived from patients with bacteraemia (n = 55). Whole-genome sequencing (WGS) was performed on representative Stenotrophomonas maltophilia isolates displaying a range of cefiderocol MICs (n = 9).
Results
Among all isolates, the MIC50 and MIC90 to cefiderocol was 0.25 and 4 mg/L, respectively, compared with 4 and >64 mg/L for aztreonam-avibactam. Overall, 98.3% of S. maltophilia (n = 60), 91.2% of Enterobacterales (n = 34) and 88.5% of Pseudomonas aeruginosa (n = 26) isolates were susceptible to cefiderocol, while 78.6% of other non-fermenters had MICs ≤4 mg/L. Aztreonam-avibactam and cefiderocol exhibited similar activity against Enterobacterales and S. maltophilia, but aztreonam-avibactam was less active against other organisms. WGS of S. maltophilia isolates with elevated cefiderocol MICs identified disruptive mutations in PBP-encoding genes (mrcB/PBP1b and pbpC/PBP1c) that were not observed in highly susceptible isolates. The bacteraemia cohort had many comorbidities and a 29% 30 day all-cause mortality. In this cohort, cefiderocol demonstrated the highest in vitro activity as extrapolated from MICs, followed by ceftazidime-avibactam, aztreonam-avibactam, meropenem-vaborbactam and ceftolozane-tazobactam, respectively.
Conclusions
Cefiderocol exhibited the greatest in vitro activity against various CR-GNRs species in a Pacific Northwest population enriched for severely ill patients. Susceptibility to other agents was more variable among tested organisms.
Introduction
Carbapenem-resistant Gram-negative rods (CR-GNRs) represent a growing global challenge, with rates and mechanisms varying geographically and by species.1 While newer beta-lactam/beta-lactamase inhibitor combinations have increased therapeutic options, metallo-beta-lactamases (MBLs), including NDM, VIM, IMP and the L1 beta-lactamase of Stenotrophomonas maltophilia remain particularly challenging. Susceptibility data are increasingly available for carbapenem-resistant Enterobacterales but are currently limited for many non-fermenters, particularly for the newer agents.2–4
Cefiderocol and aztreonam-avibactam are active against many CR-GNRs, including MBL producers, although resistance has been described.5–7 For immunocompromised patients and those with cystic fibrosis, who have an increased risk of infections with non-fermenting organisms, understanding the in vitro activity of reserve beta-lactam agents is critical for guiding empiric therapy when CR-GNRs are suspected.8
Given regional variability in resistance, we assessed susceptibility of CR-GNRs to five reserve beta-lactams—including cefiderocol and aztreonam-avibactam—in the North American Pacific Northwest. Additionally, we described clinical outcomes for patients with CR-GNR bacteraemia and performed whole-genome sequencing (WGS) to explore genetic traits associated with cefiderocol resistance in S. maltophilia.
Methods
Selection of isolates and patients
We identified 162 unique GNR isolates based on clinical testing from 161 patients at the University of Washington Medical Center and Harborview Medical Center from 5/2008–6/2021 (Table S1, available as Supplementary data at JAC-AMR Online). Carbapenem non-susceptible inclusion criteria included the following: (i) intrinsically resistant to meropenem/imipenem (e.g. S. maltophilia) or phenotypically tested non-susceptible to meropenem (applies to 154 isolates), (ii) imipenem non-susceptible and cefepime non-susceptible (applies to 1 Achromobacter and 1 Pseudomonas), (iii) ertapenem non-susceptible and positive by the carbapenem inactivation method (applies to 4 Enterobacter and 1 Serratia) or (iv) ertapenem non-susceptible and positive by the Cepheid Xpert Carba-R test for a carbapenemase (applies to 1 E. cloacae NDM). The collection of isolates was enriched for S. maltophilia and underrepresented non-fermenters, while a subset of bacteraemia isolates was chosen for clinical review without enrichment for particular organisms. Demographic information, comorbidities and 30 day survival were extracted by chart review. The study was approved by the University of Washington Institutional Review Board (STUDY00007292).
Susceptibility testing
Cefiderocol MICs were measured by broth microdilution (BMD) using cation-adjusted iron-depleted Mueller–Hinton broth using supplied protocols and reading guidelines (Shionogi Inc. through International Health Management Associates; IHMA). Performance was assessed in 30 isolates with known reference broth dilution MICs provided by the sponsor via IHMA. Aztreonam-avibactam MICs were measured by agar dilution with performance assessed using CLSI QC ranges and inferred from isolates with known resistance.9,10 Ceftazidime-avibactam, ceftolozane-tazobactam and meropenem-vaborbactam MICs were measured by gradient strip diffusion (bioMerieux). All other MICs were performed and reported clinically prior to the initiation of this study (e.g. Table S3). Cefiderocol, ceftazidime-avibactam, ceftolozane-tazobactam and meropenem-vaborbactam MICs were interpreted per CLSI M100 35th Ed.10 Aztreonam-avibactam was interpreted per FDA breakpoints.11 For organism–agent combinations lacking established breakpoints, extrapolated susceptibility was interpreted using breakpoints from related species (Table 1).
Table 1.
Minimum inhibitory concentration (MIC) distributions
| Agent | MIC50 | MIC90 | Range | Susceptible CLSI/FDA Bp^ | Susceptible extrapolated# | |
|---|---|---|---|---|---|---|
| S. maltophilia (n = 60) | FDC | 0.06 | 0.125 | ≤0.03 to 2 | 98.3% | — |
| ATM-AVI | 2 | 4 | ≤0.03 to 8 | — | 95.0% | |
| C/T | 16 | >256 | 0.5 to >256 | — | 36.7% | |
| CZA | 16 | >256 | 0.5 to >256 | — | 46.7% | |
| MVB | >256 | >256 | 1 to >256 | — | 3.3% | |
| Enterobacterales (n = 34) | FDC | 1 | 4 | 0.03 to 32 | 91.2% | — |
| ATM-AVI | 0.25 | 1 | ≤0.03 to 64 | 91.2% | — | |
| C/T | 8 | >256 | 0.25 to >256 | 35.3% | — | |
| CZA | 1 | >256 | 0.06 to >256 | 79.4% | — | |
| MVB | 0.25 | 8 | 0.03 to >256 | 85.3% | — | |
| P. aeruginosa (n = 26) | FDC | 0.125 | 8 | 0.06 to >32 | 88.5% | — |
| ATM-AVI | 16 | 32 | ≤0.03 to >64 | — | 30.8% | |
| C/T | 4 | >256 | 0.5 to >256 | 50% | — | |
| CZA | 8 | >256 | 1 to >256 | 50% | — | |
| MVB | 16 | 64 | 1 to >256 | — | 15.4% | |
| Other non-fermenting | FDC | 1 | 16 | ≤0.03 to >32 | — | 78.6%* |
| GNRs (n = 42) | ATM-AVI | >64 | >64 | 2 to >64 | — | 2.4% |
| C/T | 4 | >256 | ≤0.016 to >256 | — | 47.6% | |
| CZA | 8 | >256 | 1 to >256 | — | 50.0% | |
| MVB | 32 | >256 | 0.25 to >256 | — | 26.2% |
MIC values reported in mg/L. Breakpoints applied: ^CLSI M100 35th Ed 2025 (FDC, C/T, CZA, MVA) or FDA (ATM-AVI). # ‘Extrapolated’ breakpoints applied: For CZA, C/T and FDC without formal interpretations, CLSI M100 35th Ed P. aeruginosa applied. For ATM-AVI without interpretations, FDA Enterobacterales breakpoints applied. For MVA, CLSI M100 35th Ed MEM applied for P. aeruginosa, Acinetobacter, Stenotrophomonas, other non-Enterobacterales or 33rd Ed MEM for Burkholderia spp. *Includes 4 Acinetobacter isolates that tested susceptible by CLSI M100 35th Ed breakpoints.
WGS of S. maltophilia
WGS library preparation, sequencing and analysis was performed on five isolates of S. maltophilia with MICs ≤0.03 mg/L and four isolates with MICs 0.12, 0.25, 0.25 and 1 mg/L as described previously,12 mapping against GenBank reference LR134324.1. Clearly inactivating mutations (stop-gain and frameshift mutations) were identified and prioritized. Sequencing data from this project are available from the NCBI SRA (Accession PRJNA1417893).
Results
Antimicrobial susceptibility
Cefiderocol BMD performance assessment of 30 reference isolates yielded 100% essential and categorical agreement with S. maltophilia (n = 7), Pseudomonas aeruginosa (n = 10) and Enterobacterales (n = 8). All four reference Acinetobacter MICs were >1-log2-fold dilution higher than MICs performed for this study, including three very major errors. Attempts at discrepancy resolution with KB supported that these were particularly challenging isolates.
For the larger epidemiological survey of 162 isolates, a total of 60 S. maltophilia, 26 P. aeruginosa, 34 Enterobacterales and 42 other non-fermenting Gram-negative organisms were included. Acinetobacter (4) were included within the other non-fermenters, given low numbers in our population. This heterogeneous group of organisms included seven Achromobacter xylosoxidans, six Chryseobacterium indologenes, four Elizabethkingia, and six Pandoraea sp., among smaller numbers of other less common species. See Table S1 for complete organism distribution.
MIC distributions for the five reserve beta-lactams are shown in Table 1. Cefiderocol was the only agent with an MIC90 within the susceptible range across all organisms. The MIC90 for S. maltophilia was 0.25 mg/L (susceptibility breakpoint ≤1 mg/L), ≤4 mg/L for Enterobacterales (susceptibility breakpoint ≤4 mg/L), 8 mg/L for P. aeruginosa (susceptibility breakpoint ≤4 mg/L) and 16 mg/L for other non-fermenting GNRs (susceptibility breakpoint ≤4 mg/L for Acinetobacter species only). Aztreonam-avibactam, the only other agent resistant to hydrolysis by both serine and MBLs, maintained similar activity against S. maltophilia and Enterobacterales. For P. aeruginosa and other non-fermenting GNRs, the cefiderocol MIC90 was lower than for any other comparator. Extrapolated susceptibility results were consistent with the MIC90 trends (Table 1). The susceptibility of cefiderocol non-susceptible isolates to the other agents was heterogeneous (Table S2).
Bacteraemia cohort
We identified 55 episodes of bacteraemia secondary to a CR-GNRs (Table S1). Thirty-day all-cause mortality was 29%. Many patients had malignancy and/or severe neutropenia (Table 2). After applying extrapolated susceptibility criteria, cefiderocol demonstrated the greatest in vitro activity (88.9% susceptible), followed by ceftazidime-avibactam (60.0%) and aztreonam-avibactam (50.9%). Seven (12.7%) cefiderocol non-susceptible isolates were identified and described in Table S3.
Table 2.
Patients with bacteraemia and chart data (n = 55)
| Demographic | Percent |
|---|---|
| Female | 38.2% |
| Male | 61.8% |
| Age | |
| 20–29 | 9.1% |
| 30–39 | 12.7% |
| 40–49 | 12.7% |
| 50–59 | 16.4% |
| 60–69 | 25.5% |
| 70–79 | 18.2% |
| 80–89 | 1.8% |
| 90–99 | 3.6% |
| 30 day all-cause mortality | 29.1% |
| Comorbidities | |
| Solid organ malignancy | 20.0% |
| Solid organ transplant | 12.7% |
| Haematopoetic malignancy | 36.4% |
| Bone marrow transplant | 21.8% |
| Cystic fibrosis | 3.6% |
| Diabetes | 20.0% |
| Heart failure | 9.1% |
| Chronic kidney disease | 14.5% |
| Neutropenia | 40.4% |
| Severe neutropenia | 34.0% |
| Extrapolated susceptibility of isolates* | |
| FDC | 88.9% |
| ATM-AVI | 50.9% |
| C/T | 41.8% |
| CZA | 60.0% |
| MVB | 45.5% |
*‘Extrapolated’ breakpoints applied: For CZA, C/T and FDC without formal interpretations, CLSI M100 35th Ed P. aeruginosa applied. For ATM-AVI without interpretations, FDA Enterobacterales breakpoints applied. For MVA, CLSI M100 35th Ed MEM applied for P. aeruginosa, Acinetobacter, Stenotrophomonas, other non-Enterobacterales or 33rd Ed MEM for Burkholderia spp.
WGS of S. maltophilia
We used WGS to screen clinical isolates for disruptive mutations in genes that were previously reported to contribute to cefiderocol resistance. One isolate with a high MIC carried a stop-gain mutation in mrcB (encoding PBP1b, c.916C>T/p.Gln306*), while two others harboured a disruptive in-frame deletion in the same gene (c.2408_2410delCTG/p.Ala804del). The fourth isolate harboured a stop-gain mutation in pbpC, encoding PBP1c (c.1859C>A/p.Ser620*). None of the highly susceptible strains carried disruptive mutations in either of these PBP-encoding genes or in other annotated PBPs present in the S. maltophilia reference genome. While several high severity mutations were noted in genes affecting iron transport (cirA-family genes), such variants were not exclusive to isolates with higher MICs.
Discussion
Relative to global surveillance projects such as SIDERO-WT6 and SENTRY5 for carbapenem non-susceptible isolates, our cefiderocol MIC90s were comparable for Enterobacterales (4 mg/L SIDERO-WT and SENTRY), higher for P. aeruginosa (8 mg/L versus 1 mg/L for SIDERO-WT) and slightly lower for S. maltophilia (0.125 versus 0.25 mg/L for SIDERO-WT and 0.5 mg/L for SENTRY). While the limited number of isolates examined here may partially explain these differences, they also highlight the importance of regional surveillance data derived from unique patient populations in characterizing expected resistance patterns.
Cefiderocol and aztreonam-avibactam were particularly active against S. maltophilia and other non-fermenting GNRs that are often implicated in cystic fibrosis and bone marrow transplant populations. The frequent avoidance of trimethoprim-sulfamethoxazole in the setting of haematologic malignancy due to marrow suppression underscores the importance of well-tolerated beta-lactam alternatives. Compared with SENTRY data, our aztreonam-avibactam MIC50 for S. maltophilia was 1-log2-dilution lower, with a comparable MIC90 suggesting efficacy in our local region.13
The optimal empiric therapy when infection with non-fermenting CR-GNRs is suspected is less clear. This uncertainty is amplified for less common genera like Achromobacter, Chryseobacterium, Cupriavidus, Elizabethkingia, Pandoraea and others for which both clinical data and interpretive breakpoints are limited.2,14,15 Pandoraea species, which harbour a chromosomal OXA-type beta-lactamase,16 were notable for four of five isolates having cefiderocol MICs >4 mg/mL. The pathogenicity of Pandoraea is unclear, however, and the organism is most frequently associated with cystic fibrosis and is often multidrug resistant.17 Importantly the isolation of two Pandoraea isolates from the bloodstream belies the allegedly reduced pathogenicity described by some authors.17
Since formal breakpoints remain unestablished for many of the organism–agent combinations considered here, we also calculated susceptibilities using ‘extrapolated breakpoints’ (Table 1). While such extrapolations cannot be used to infer clinical activity, they offer a pragmatic means for comparing in vitro activity across agents and organisms and reflect how susceptibility data are often interpreted clinically when only MICs are available. Reassuringly, our extrapolated susceptibility estimates generally aligned with the MIC50, MIC90 and established breakpoint interpretations (Table 1). While cefiderocol generally showed the highest in vitro activity, cefiderocol non-susceptible isolates exhibited variable susceptibility to the other agents tested, emphasizing both the heterogeneity in resistance mechanisms and distinctive antimicrobial spectra of the agents tested (Table S2, S3). Altogether, these data support broad reserve-agent testing when CR-GNR pathogens are isolated.
Although only a small number of clinical S. maltophilia isolates were examined, our WGS analysis identified disruptive mutations in mrcB and pbpC that were associated with higher MICs, suggesting that such mutations contribute to cefiderocol resistance. The mrcB (PBP1b) and pbpC (PBP1c) genes encode two of the seven annotated PBPs in S. maltophilia,18 and PBP mutations have been implicated as a mechanism of cefiderocol resistance,19 either directly or relating to PBP expression. Data in other species suggest that cefiderocol has the highest affinity for PBP3 (ftsI),20 but the loss of PBP3 function may be lethal in S. maltophilia.18 The relatively modest elevation in MICs seen in our isolates may reflect the lower affinity of cefiderocol for PBP1b and PBP1c relative to PBP3 in S. maltophilia, as well as the protective effect of such mutations.19 Studies involving larger numbers of clinical isolates will be necessary to verify and further explore this association.
Limitations of our study include the small number of isolates and a lack of isogenic mutants to verify WGS findings. Additionally, the clinical outcome analysis was descriptive and not designed to assess treatment efficacy. Despite these limitations, our data provide regionally relevant susceptibility data to inform antimicrobial selection when CR-GNR-related infections are suspected and provide further opportunities to explore resistance mechanisms.
Supplementary Material
Acknowledgements
We thank additional members of the University of Washington Medical Center Clinical Microbiology Laboratory for collating isolates and performing phenotypic susceptibility testing on top of their busy clinical work.
Contributor Information
Andrew Bryan, Department of Laboratory Medicine and Pathology, Mayo Clinic Arizona, Phoenix, USA.
Megan Shields-Pruiett, Laboratory Services, Samaritan Health Services, Lebanon, OR, USA.
Heather Berger, Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Ferric C Fang, Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA; Department of Microbiology, University of Washington, Seattle, WA, USA.
Kelsi Penewit, Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Adam Waalkes, Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Elizabeth A Holmes, Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Stephen J Salipante, Department of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, USA.
Brian J Werth, Department of Pharmacy, University of Washington, Seattle, WA, USA.
Funding
This study was supported by an investigator-initiated research grant from Shionogi Inc. to A.B. and B.J.W. B.J.W. and S.J.S. are supported in part by NIAID R01AI136979. S.J.S. is supported in part by NIDDK DK089507 and Cystic Fibrosis Foundation SINGH24R0.
Transparency declarations
A.B. and B.J.W. report the research grant from Shionogi Inc. that supported this work. All other authors report no potential conflicts of interest.
Author contributions
A.B., B.J.W. and S.J.S. conceived of and designed the study. H.B. and A.B. developed the aztreonam-avibactam agar dilution assay. A.B. performed chart review. M.S-P. performed phenotypic susceptibility testing. F.C.F. and the Harborview Medical Center Clinical Microbiology Laboratory contributed isolates. K.P., A.W., E.A.H. and S.J.S. performed the WGS and analysis. A.B. and B.J.W. drafted the report. All authors reviewed the data, edited the manuscript and approved the final version.
Supplementary data
Tables S1 to S3 is available as Supplementary data at JAC-AMR Online.
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