Enterococcal bloodstream infections in critically ill patients with COVID-19: a case series

Giacobbe, Daniele Roberto; Labate, Laura; Tutino, Stefania; Baldi, Federico; Russo, Chiara; Robba, Chiara; Ball, Lorenzo; Dettori, Silvia; Marchese, Anna; Dentone, Chiara; Magnasco, Laura; Crea, Francesca; Willison, Edward; Briano, Federica; Battaglini, Denise; Patroniti, Nicolò; Brunetti, Iole; Pelosi, Paolo; Bassetti, Matteo

doi:10.1080/07853890.2021.1988695

Cited by 31 publications

(32 citation statements)

References 28 publications

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“…Almost half of these enterococcal infections were caused by E. faecium [ 22 ]. This finding was in alignment with the results of observational studies from Italy reporting high prevalence of enterococcal bloodstream infections in critically ill COVID-19 patients [ 30 , 31 ]. The altered gut microbiota of SARS-CoV-2-positive individuals may be also a risk factor for pneumonia or other superinfections, as observed in other viral infections such as avian H7N9 influenza [ 32 ].…”

Section: Sars-cov-2 Infection and The Intestinal Barriersupporting

confidence: 89%

SARS CoV-2-Induced Viral Sepsis: The Role of Gut Barrier Dysfunction

et al. 2022

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A considerable proportion of patients with severe COVID-19 meet Sepsis-3 criteria and share common pathophysiological mechanisms of multiorgan injury with bacterial sepsis, in absence of secondary bacterial infections, a process characterized as “viral sepsis”. The intestinal barrier exerts a central role in the pathophysiological sequence of events that lead from SARS-CoV-2 infection to severe systemic complications. Accumulating evidence suggests that SARS-CoV-2 disrupts the integrity of the biological, mechanical and immunological gut barrier. Specifically, microbiota diversity and beneficial bacteria population are reduced, concurrently with overgrowth of pathogenic bacteria (dysbiosis). Enterocytes’ tight junctions (TJs) are disrupted, and the apoptotic death of intestinal epithelial cells is increased leading to increased gut permeability. In addition, mucosal CD4(+) and CD8(+) T cells, Th17 cells, neutrophils, dendritic cells and macrophages are activated, and T-regulatory cells are decreased, thus promoting an overactivated immune response, which further injures the intestinal epithelium. This dysfunctional gut barrier in SARS-CoV-2 infection permits the escape of luminal bacteria, fungi and endotoxin to normally sterile extraintestinal sites and the systemic circulation. Pre-existing gut barrier dysfunction and endotoxemia in patients with comorbidities including cardiovascular disease, obesity, diabetes and immunosuppression predisposes to aggravated endotoxemia. Bacterial and endotoxin translocation promote the systemic inflammation and immune activation, which characterize the SARS-CoV-2 induced “viral sepsis” syndrome associated with multisystemic complications of severe COVID-19.

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Section: Sars-cov-2 Infection and The Intestinal Barriersupporting

confidence: 89%

SARS CoV-2-Induced Viral Sepsis: The Role of Gut Barrier Dysfunction

et al. 2022

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“…Nasopharyngeal colonization with S. pneumoniae was associated with an impaired antiviral immune response in COVID-19 patients ( Mitsi et al, 2022 ), while we did not observe this in our subgroups. E. faecalis , more frequent among deceased patients than in COVID-19 negative subjects, is surprisingly a main agent of bacteremia among COVID-19 patients, particularly in ICU settings ( Giacobbe et al, 2021 ; Porto et al, 2022 ). Among the potentially protective species, we highlighted a decrease of A. muciniphila in deceased subjects when compared to those with a favorable outcome.…”

Section: Discussionmentioning

confidence: 99%

Profile of the Nasopharyngeal Microbiota Affecting the Clinical Course in COVID-19 Patients

et al. 2022

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While populations at risk for severe SARS-CoV-2 infections have been clearly identified, susceptibility to the infection and its clinical course remain unpredictable. As the nasopharyngeal microbiota may promote the acquisition of several respiratory infections and have an impact on the evolution of their outcome, we studied the nasopharyngeal microbiota of COVID-19 patients in association with baseline disease-related clinical features compared to that of patients tested negative. We retrospectively analyzed 120 nasopharyngeal pseudonymized samples, obtained for diagnosis, divided into groups (infected patients with a favorable outcome, asymptomatic, and deceased patients) and patients tested negative for SARS-CoV-2, by using Illumina-16S ribosomal ribonucleic acid (rRNA) sequencing and specific polymerase chain reaction (PCR) targeting pathogens. We first found a depletion of anaerobes among COVID-19 patients, irrespective of the clinical presentation of the infection (p < 0.029). We detected 9 taxa discriminating patients tested positive for SARS-CoV-2 from those that were negative including Corynebacterium propinquum/pseudodiphtericum (p ≤ 0.05), Moraxella catarrhalis (p ≤ 0.05), Bacillus massiliamazoniensis (p ≤ 0.01), Anaerobacillus alkalidiazotrophicus (p ≤ 0.05), Staphylococcus capitis subsp. capitis (p ≤ 0.001), and Afipia birgiae (p ≤ 0.001) with 16S rRNA sequencing, and Streptococcus pneumoniae (p ≤ 0.01), Klebsiella pneumoniae (p ≤ 0.01), and Enterococcus faecalis (p ≤ 0.05) using real-time PCR. By designing a specific real-time PCR, we also demonstrated that C. propinquum is decreased in asymptomatic individuals compared to other SARS-CoV 2 positive patients. These findings indicate that the nasopharyngeal microbiota as in any respiratory infection plays a role in the clinical course of the disease. Further studies are needed to elucidate the potential role in the clinical course of the disease of M. catarrhalis, Corynebacterium accolens, and more specifically Corynebacterium propinquum/diphteriticum in order to include them as predictors of the severity of COVID-19.

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“…Several studies have reported on bacteremia in patients with COVID-19 [14][15][16]; however, this is the first study to compare the incidence of bacteremia between patients with COVID-19 who were treated with tocilizumab and those who were not. According to the results, tocilizumab is not an independent factor related to bacteremia in patients with COVID-19.…”

Section: Discussionmentioning

confidence: 94%

Effect of Tocilizumab Treatment on Patients with Coronavirus Disease 2019 and Bacteremia: A Retrospective Cohort Study

et al. 2022

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Introduction: This study aimed to determine if tocilizumab treatment for coronavirus disease 2019 (COVID-19) increases bacteremia and suppresses fever and inflammatory reactants. Methods: In this single-center, retrospective, observational study, all patients with COVID-19 admitted to our emergency intensive care unit from March 2020 to August 2021 were categorized into tocilizumab-treated and tocilizumabnaı ¨ve groups, and the incidence of bacteremia and other factors between the two groups were compared. Patients with bacteremia were further classified into tocilizumab-treated and tocilizumab-naı ¨ve groups to determine if fever and inflammatory reactants were suppressed. Results: Overall, 144 patients were included in the study, 51 of whom received tocilizumab, which was administered on the day of admission. Further, of the 24 (16.7%) patients with bacteremia, 13 were in the tocilizumab-treated group. Results revealed a significant difference in the C-reactive protein level (p \ 0.001) at the onset of bacteremia between the tocilizumabtreated group [median 0.42 mg/dL (0.27-0.44 mg/dL)] and the tocilizumab-naı ¨ve group [7.48 mg/dL (4.56-13.9 mg/dL)]. The median number of days from admission to onset of bacteremia was not significantly different between the tocilizumab-treated group [10 days (9-12 days)] and the tocilizumab-naı ¨ve group [9 days (7.5-11 days)] (p = 0.48). There was no significant difference in fever between the groups. Multivariate logistic analysis showed that tocilizumab treatment did not affect the probability of bacteremia. Conclusion: Treatmentof patients with COVID-19 with tocilizumab does not increase the risk of bacteremia. Tocilizumab suppresses C-reactive protein levels but not fever. Therefore, careful monitoring of fever can reduce the risk of missed bacteremia.

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Enterococcal bloodstream infections in critically ill patients with COVID-19: a case series

Cited by 31 publications

References 28 publications

SARS CoV-2-Induced Viral Sepsis: The Role of Gut Barrier Dysfunction

SARS CoV-2-Induced Viral Sepsis: The Role of Gut Barrier Dysfunction

Profile of the Nasopharyngeal Microbiota Affecting the Clinical Course in COVID-19 Patients

Effect of Tocilizumab Treatment on Patients with Coronavirus Disease 2019 and Bacteremia: A Retrospective Cohort Study

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