# The Resistance Paradox in COVID-19 Ventilator-Associated Pneumonia: A Retrospective Study on Rapid Molecular Stewardship

**Authors:** Andrei Mihai Bălan, Tudor-Mihai Magdaș, Andrada Elena Urda-Cîmpean, Constantin Bodolea, Andrada Nemeș, Lucreția Avram, Dana Crișan, Sebastian Trancă

PMC · DOI: 10.3390/antibiotics15030236 · Antibiotics · 2026-02-24

## TL;DR

This study found that ventilator-associated pneumonia in COVID-19 patients shows higher antibiotic resistance and benefits from faster molecular testing.

## Contribution

The study identifies a distinct antimicrobial resistance profile in VAP-COVID and evaluates rapid molecular diagnostics for faster results.

## Key findings

- VAP-COVID patients had higher resistance to carbapenems and fluoroquinolones compared to non-COVID-VAP patients.
- POC-PCR significantly reduced diagnostic turnaround time compared to standard culture methods.
- VAP-COVID patients had lower pleural effusion and higher neutrophil-to-lymphocyte ratios.

## Abstract

Background/Objectives: The COVID-19 pandemic complicated the diagnosis of Ventilator-Associated Pneumonia (VAP), leading to empiric antibiotic overuse due to the difficulty in distinguishing viral progression from bacterial superinfection. However, it remains unclear whether COVID-19-associated VAP displays a distinct antimicrobial resistance profile compared to classical VAP. Methods: This monocentric, retrospective cohort study primarily investigated differences in clinical phenotypes and antibiotic resistance profiles between patients with VAP-COVID (n = 26) and non-COVID-VAP (n = 26). Logistic regression was used to identify factors associated with the COVID-19 phenotype and predictors of antimicrobial resistance. As a secondary objective, we evaluated the diagnostic efficacy of a multiplex Point-of-Care PCR (POC-PCR) system (n = 22) compared to standard culture (n = 26) regarding turnaround time and resistance detection. Results: Patients with VAP-COVID exhibited significantly higher resistance rates to carbapenems (76.9% vs. 50%, p = 0.04) and fluoroquinolones (88.5% vs. 61.5%, p = 0.02) despite fewer traditional risk factors at admission. The clinical profile of the VAP-COVID group was distinguished by a significantly lower incidence of parapneumonic pleural effusion (19.2% vs. 84.6%, p < 0.001) and a higher median Neutrophil-to-Lymphocyte Ratio (41.36 vs. 9.63, p < 0.001). Regarding diagnostic speed, POC-PCR significantly reduced the time to result validation compared to standard culture (~1 h vs. ~62.5 h, p < 0.001). Conclusions: VAP in COVID-19 patients presents a distinct microbiological profile characterized by higher antimicrobial resistance. In this context, the integration of rapid molecular diagnostics may support earlier microbiological guidance compared to standard methods.

## Linked entities

- **Diseases:** COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}
- **Diseases:** immune dysregulation (OMIM:614878), fever (MESH:D005334), Infectious Diseases (MESH:D003141), pleural effusion (MESH:D010996), COVID (MESH:D000086382), ischemic heart disease (MESH:D017202), immunothrombosis (MESH:D000090882), acute respiratory failure (MESH:D012131), colonization (MESH:D003108), MDR (MESH:D018088), inflammation (MESH:D007249), co-infections (MESH:D060085), vascular disease (MESH:D014652), Failure (MESH:D051437), lymphopenia (MESH:D008231), viral infection (MESH:D014777), organ failure (MESH:D009102), pulmonary infarction (MESH:D054060), hypoxemia (MESH:D000860), gastric suppression (MESH:D013272), bacterial pneumonia (MESH:D018410), leukopenia (MESH:D007970), critically ill (MESH:D016638), infiltrates (MESH:D017254), Associated (MESH:D018886), XDR (MESH:D054908), lung damage (MESH:D008171), Diabetes Mellitus (MESH:D003920), VAP (MESH:D053717), invasive (MESH:D009361), purulent (MESH:D003234), GERD (MESH:D005764), infection (MESH:D007239), hypochlorhydria (MESH:D000126), bacterial superinfection (MESH:D015163), injury to (MESH:D014947), Septic shock (MESH:D012772), Pulmonary Infection (MESH:D012141), leukocytosis (MESH:D007964), fungal (MESH:D009181), Comorbidity (MESH:D004194), bacterial (MESH:D001424), Pneumonia (MESH:D011014), death (MESH:D003643)
- **Chemicals:** gentamicin (MESH:D005839), Linezolid (MESH:D000069349), Doxycycline (MESH:D004318), Vancomycin (MESH:D014640), Fluoroquinolone (MESH:D024841), Ceftriaxone (MESH:D002443), dexamethasone (MESH:D003907), Carbapenem (MESH:D015780), tocilizumab (MESH:C502936), azithromycin (MESH:D017963)
- **Species:** Escherichia coli (E. coli, species) [taxon 562], Klebsiella pneumoniae (species) [taxon 573], Cytomegalovirus (genus) [taxon 10358], Pseudomonas aeruginosa (species) [taxon 287], Acinetobacter baumannii (species) [taxon 470], Candida [taxon 1535326], Homo sapiens (human, species) [taxon 9606], Staphylococcus aureus (species) [taxon 1280], Bacteria Latreille et al. 1825 (Bacteria stick insect, genus) [taxon 629395]

## Full text

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## Figures

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## References

77 references — full list in the complete paper: https://tomesphere.com/paper/PMC13024024/full.md

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Source: https://tomesphere.com/paper/PMC13024024