Critical superbugs at the time of COVID-19: the same old enemy?



The spread of SARS-CoV-2, the aetiological agent of coronavirus disease 2019 (COVID-19), has impacted our approach to antimicrobial resistance in several ways. 

The first is that, during the initial peaks of the pandemic, overwhelmed hospitals may have unintentionally reduced intensity and quality of infection-control measures and antimicrobial stewardship practices, primarily due to the use of personal protective equipment (as a result of assisting different COVID-19 patients while wearing the same personal protective equipment, the potential for cross transmission of bacterial superbugs may have been overlooked). 

Another possible contributory factor may have been the redeployment of all infection-control and infectious diseases specialists to the general emergency care of COVID-19 patients. (1, 2) Another critical issue is that some pulmonary lesions due to the viral disease may resemble those of bacterial pneumonia at chest X-ray or computed tomography. This may lead physician to start useless antibacterial treatment in many patients, in turn contributing to the risk of resistance selection. (3, 4).          

In line with these theoretical scenarios, outbreaks of Klebsiella pneumoniae carbapenemase (KPC)-producing Klebsiella pneumoniae, vancomycin-resistant enterococci, and carbapenem-resistant Pseudomonas aeruginosa have been reported in critically ill hospitalised patients with COVID-19. (5-7) 

Finding an optimal solution to this novel antimicrobial resistance challenge may not be simple. In our opinion, the first essential premise to be kept in mind to be ultimately successful is that we are not fighting the same old antimicrobial resistance enemy. Both infection-control requirements and the use of antimicrobials in COVID-19 patients may be different from before the           pandemic and this implies we should pay more attention on how we prevent resistant infections. Certainly, we need to improve our ability to diagnose bacterial coinfection and superinfections in patients with moderate to severe COVID-19 through a wise and prompt use of rapid phenotypic and molecular diagnostics (for rapidly detecting both aetiological agents and resistance determinants). This would allow to identify a specific subgroup of patients that could benefit from early antibiotic treatment, in line with the principles of personalized medicine. Furthermore, rapid tests results may also allow rapid de-escalation if no resistance mechanisms are detected. Importantly, all these concepts also apply to the therapeutic approach to superinfections other than pulmonary in critically ill COVID-19 patients, e.g., bloodstream infections, that could affect as many as 50% of COVID-19 patients in intensive care units during prolonged hospitalisation. (8)

Notably, superinfections in critically ill COVID-19 patients may be difficult to recognize owing to the possible attenuation of systemic symptoms and laboratory inflammatory markers by the immunomodulatory agents used for counteracting an exaggerated host response to the viral disease. In turn, this may lead to two opposite, but not mutually exclusive perilous consequences: on the one hand, a delayed recognition of a severe bacterial infection, which implies perilous delays in antibacterial treatment that may unfavourably affect patient outcomes, and on the other hand, a widespread and inappropriate treatment with antimicrobial agents of several patients with only mild symptoms, guided by the fear of not promptly recognizing perilous systemic infectious processes. 

Fortunately, all these possible scenarios have started to be well recognized by the medical community, and dedicated countermeasures are starting to be adopted to efficiently counteract this worrisome new face of an old fastidious enemy. We should not let our guard down. 

Written by Daniele Roberto Giacobbe, Assistant Professor of Infectious Diseases (University of Genoa)




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