This study conducted a retrospective review of clinical data from patients diagnosed with CRKP infection disease at the 940th Hospital of the Joint Logistics Support Force of the People’s Liberation Army. Statistical analyses were performed on factors such as antimicrobial therapy (Ceftazidime-Avibactam), enzyme type, infection site, underlying diseases, and in-hospital mortality.

The study was approved by the Ethics Committee of the 940th Hospital of the Joint Logistics Support Force of the People’s Liberation Army. The committee waived the need for informed consent. The study adhered to the ethical standards outlined in the Declaration of Helsinki (1975) and its amendments.

This study carefully selected participants from 2018 to 2025, ultimately including 148 eligible patients who were followed for 12 months. A detailed flowchart illustrates participant eligibility and reasons for exclusion (Figure 1).

Demographic and clinical characteristics were analyzed as exposure variables. These included age, sex, KPC-Producing K. pneumoniae Infections, antimicrobial therapy (Ceftazidime -Avibactam, sensitive for antimicrobial sensitivity test), infection site, ICU admission, median hospital time (20 day), Pathogen source.

The primary endpoint was in-hospital mortality among CRKP inpatients for 12 month.

All the subjects recorded episodes who were hospitalized and suspected of BSIs (Bloodstream infection) between January 2018 and January 2025, blood cultures were obtained using BacT/ALERT blood culture bottles (bio-Mérieux, Inc., Durham, NC) or BD FA and SN blood culture bottles and incubated in the BacT/ALERT 3D (bioMérieux, Inc.) or BD FX 400 automatic monitoring system for a week in the clinical microbiology laboratory of the hospital. When Bottles flagged as positive after Gram-negative Bacillus, report the critical value and switch to blood culture onto blood tablet and Chinese blue agar plates and incubated at 35°C CO₂ for 24 h. BALF and qualified sputum specimens were also inoculated onto blood tablet and Chinese blue agar plates and incubated at 35°C CO₂ for 24 h. It is clinically significant that the count value of urine colonies Midstream urine culture is ≥ 1 × 105 cfu/mL, so colony identification and antimicrobial susceptibility test should be carried out. After colony formation, microbial identification was performed using the corresponding GN card on the VITEK Compact-II automatic microorganism identification system or MALDI-TOF MS. Antimicrobial susceptibility test was used GN 335 card in VITEK 2 system (bioMérieux, Inc., Durham, NC). A strain is classified as CRKP if its minimum inhibitory concentration (MIC) for carbapenem antibiotics—such as imipenem or meropenem—exceeds the specified resistance breakpoint (e.g., MIC >4 mg/L for imipenem or meropenem).

Modified Carbapenem Inactivation Methods (mCIM): For each isolate, emulsify a 1-μL loopful (K. pneumoniae) from a blood agar plate into 2 mL TSB. Vortex 10–15 s, add a 10-μg meropenem disk, ensuring full immersion. Incubate at 35°C ± 2°C for 4 h ± 15 min. Concurrently, prepare a 0.5 McFarland E. coli ATCC^® 25922 suspension in broth/saline. Inoculate an MHA plate per CLSI M024 (6), completing suspension prep and plate inoculation within 15 min. Dry plates 3–10 min. Post-incubation, remove meropenem disks from TSB using a 10-μL loop: press the loop’s flat side against the disk edge, leveraging surface tension to lift it. Drain excess liquid by dragging the loop against the tube’s inner edge, then transfer the disk to the inoculated MHA plate (max 4 disks/100-mm plate; 8/150-mm plate). Invert and incubate plates at 35°C ± 2 C for 18–24 h. Measure inhibition zones per CLSI M024, Carbapenemase positive: Zone diameter of 6–15 mm or presence of pinpoint colonies within a 16–18-mm zone. Metallo-β-lactamase positive: ≥5-mm increase in zone diameter for eCIM vs. zone diameter for mCIM (e.g., mCIM = 6 mm; eCIM = 15 mm; zone diameter difference = 9 mm) (6). Ensure timing alignment: E. coli suspension prep and plate inoculation must occur ≤15 min before/after TSB-disk incubation completion. Maintain aseptic technique throughout. Colloidal gold method for determination of CRKP: Pick the pure cultured colony of K. pneumoniae, add the lysate and shake it evenly, and drop the lysate into the sample adding hole of colloidal gold test strip (Jinshanchuan, Beijing). Observe the results within 10–15 min, and the T line and the quality control line (C line) are positive at the same time (specific enzyme type: KPC, NDM, IPM, VIM, and OXA-48), Only C-ray was negative.

Laboratory-confirmed CRKP, report to the clinical department immediately as a critical value and enzyme type, communicated by telephone. Implement single-room isolation and dedicated care. If associated with an indwelling venous or catheter device, remove and replace the device promptly.

Statistical analyses were performed using SPSS 22.0. A paired t-test revealed significantly higher overall drug resistance in the KPC group compared to non-KPC isolates. Multivariate regression identified the following independent predictors of mortality: KPC-Kp infection, ICU admission, bloodstream infection, specific antimicrobial therapy, nosocomial acquisition, and prolonged hospitalization (≥20 days). The log-rank test showed significantly lower 28-day survival in KPC-Kp patients versus non-KPC groups, particularly between Ceftazidime-Avibactam and non-Ceftazidime-Avibactam subgroups. Kaplan–Meier survival curves were constructed with the time of first etiological diagnosis as the starting point, death as the event of interest, and discharge as censoring. Factors associated with in-hospital mortality were visualized using a forest plot (p < 0.01). The significance threshold was set at p < 0.05 for all analyses.

A cohort of 100 patients with KPC-producing K. pneumoniae (KPC-Kp) infections was analyzed, representing 67.6% of all CRKP isolates (KPC: 100 cases; NDM, VIM, OXA-48: 48 cases). The mean patient age was 62.3 ± 20.2 years, with a male-to-female ratio of 1.8:1. KPC-producing Klebsiella pneumoniae represented 1.16% of all K. pneumoniae infections (100/8647). Twenty-eight percent of patients had hospital stays exceeding 14 days, with a median duration of 58 days (IQR 30–165). The predominant infection sites were lung (58%), bloodstream (22%), and urinary tract (11%). Pathogen sources were primarily nosocomial (86%), with 14% with 14% transfer from outside hospital, colonization rate 13.5% (20/148). Major comorbidities included cerebrovascular disease/cerebral infarction (23%), pulmonary disease (16%), hematological malignancies (12%), and viral pneumonia (12%) (Table 1).

Analysis of 148 CRKP isolates revealed KPC-producing K. pneumoniae (67.6%, n = 100) as the predominant strain, followed by NDM (23.6%, n = 35), VIM (3.4%, n = 5), and OXA-48 (5.4%, n = 8). KPC producers exhibited >90% resistance to cefazolin, ceftriaxone, cefepime, cefoxitin, piperacillin/tazobactam, cefoperazone/sulbactam, levofloxacin, ciprofloxacin, aztreonam, imipenem, and meropenem, while demonstrating markedly lower resistance to tigecycline (5.1%) and ceftazidime-avibactam (4.3%). In contrast, non-KPC strains (NDM/VIM/OXA-48) showed <50% resistance to cefepime, cefoxitin, piperacillin/tazobactam, cefoperazone/sulbactam, levofloxacin, ciprofloxacin, and aztreonam, with near-zero resistance to tigecycline (0%) and ceftazidime-avibactam (1.0%). Paired t-test confirmed significantly higher overall resistance in KPC versus non-KPC groups (t = 7.617, p < 0.001) (Figure 2).

Among 100 patients with KPC-Kp infections, the in-hospital mortality rate was 46.0%—significantly higher than the 10.4% mortality in non-KPC carbapenemase producers (NDM/VIM/OXA-48; p < 0.001), with nearly half (48%) of KPC-Kp deaths occurring within 7 days of infection. Survival analysis demonstrated substantially lower 28-day survival in KPC-Kp patients (0.609 ± 0.054) versus non-KPC groups (0.839 ± 0.069; log-rank χ² = 17.732, p < 0.001), with KPC-Kp 90-day survival at 0.514 ± 0.061. Within the KPC-Kp cohort, 28-day survival did not significantly differ between patients receiving ceftazidime-avibactam (0.450 ± 0.132) and those not receiving this agent (0.573 ± 0.076; χ² = 1.001, p = 0.317) (Figures 3A,B). KPC vs. NDM, VIM, OXA-48 28 days survival rate 0.609 ± 0.054 vs. 0.839 ± 0.069, χ = 17.732, p < 0.001, KPC-Kp infections demonstrated 5-day and 90-day survival rates of 0.769 ± 0.042 and 0.514 ± 0.061, respectively. In KPC-Producing K. pneumoniae infections patients, the usage rate of Ceftazidime-Avibactam vs. Non- Ceftazidime-Avibactam 28 days survival rate 0.450 ± 0.132 vs. 0.573 ± 0.076, χ = 1.001, p = 0.317.

Univariate analysis identified KPC-KP infection, ICU admission, infection site (particularly bloodstream), antimicrobial therapy, nosocomial acquisition, and prolonged hospitalization (median ≥20 days) as mortality-associated factors. Multivariate regression confirmed independent mortality predictors: KPC infection (OR 5.96, 95%CI 2.33–15.29, p < 0.001), bloodstream infection (OR 8.57, 95%CI 3.08–23.85, p = 0.006), ICU admission (OR 3.39, 95%CI 1.38–8.33, p = 0.006), Susceptibility-guided antimicrobial therapy (ceftazidime/avibactam, tigecycline or polymyxin B; OR 5.00, 95%CI 1.74–14.37, p < 0.001) (Figures 3, 4 and Table 2).