Secondary Bacterial Infections in Patients With Viral Pneumonia

Abstract

Pulmonary diseases of viral origin are often followed by the manifestation of secondary infections, leading to further clinical complications and negative disease outcomes. Thus, research on secondary infections is essential. Here, we review clinical data of secondary bacterial infections developed after the onset of pulmonary viral infections. We review the most recent clinical data and current knowledge of secondary bacterial infections and their treatment in SARS-CoV-2 positive patients; case reports from SARS-CoV, MERS-CoV, SARS-CoV2 and the best-studied respiratory virus, influenza, are described. We outline treatments used or prophylactic measures employed for secondary bacterial infections. This evaluation includes recent clinical reports of pulmonary viral infections, including those by COVID-19, that reference secondary infections. Where data was provided for COVID-19 patients, a mortality rate of 15.2% due to secondary bacterial infections was observed for patients with pneumonia (41 of 268). Most clinicians treated patients with SARS-CoV-2 infections with prophylactic antibiotics (63.7%, n = 1,901), compared to 73.5% ( n = 3,072) in all clinical reports of viral pneumonia included in this review. For all cases of viral pneumonia, a mortality rate of 10.9% due to secondary infections was observed (53 of 482). Most commonly, quinolones, cephalosporins and macrolides were administered, but also the glycopeptide vancomycin. Several bacterial pathogens appear to be prevalent as causative agents of secondary infections, including antibiotic-resistant strains of Staphylococcus aureus and Klebsiella pneumoniae .

Repurposing carrimycin as an antiviral agent against human coronaviruses, including the currently pandemic SARS-CoV-2

“…Pneumonia caused by viral infections usually has secondary bacterial infection 22 . COVID-19 may also be associated with secondary bacterial infections 23 , 24 .…”

The interrelationships between antimicrobial resistance, COVID-19, past, and future pandemics

“…This included the occurrence of ventilator-associated pneumonia and MRSA transmission associated with remarkable increases in antimicrobial administered in the intensive care unit [ [71] , [72] , [73] ]. Besides, during the Middle East respiratory syndrome (MERS) CoV outbreak in Saudi Arabia, the most common bacteria reported among infected patients were MRSA, among others such as carbapenem-resistant Acinetobacter baumannii , Vancomycin-Resistant Enterococci and Streptococcus pneumoniae [ 74 ]. Research suggests that about half of the deaths of patients hospitalized with COVID-19 are attributable to bacterial and fungal infections some of which are resistant to antibiotics and antifungals [ 68 ].…”

COVID-19 in a Patient with Liver Cirrhosis

“…Thus, the treatment initiated for infection (dexamethasone 6 mg/day) was based on the RECOVERY study in which this drug reduced deaths by one-third in patients who received invasive mechanical ventilation and in one-fifth of patients who received auxiliary oxygen without invasive mechanical ventilation [ 8 ]. Regarding bacterial infection, in previous pandemics, it was concluded that the co-infections, secondary infections, or “superinfections” are common during viral pandemics [ 9 ]. The 1918 Spanish Flu pandemic saw around 50 million deaths ascribed to bacterial co-infections, and during the 2009 H1N1 Influenza pandemic up to 34% of all deaths were a result of bacterial co-infections [ 9 ].…”

“…Regarding bacterial infection, in previous pandemics, it was concluded that the co-infections, secondary infections, or “superinfections” are common during viral pandemics [ 9 ]. The 1918 Spanish Flu pandemic saw around 50 million deaths ascribed to bacterial co-infections, and during the 2009 H1N1 Influenza pandemic up to 34% of all deaths were a result of bacterial co-infections [ 9 ]. While the precise mechanism for susceptibility to secondary infections is unclear, it is likely that virus-mediated immunosuppression of the host innate immune enables opportunistic bacteria to colonize the host [ 9 ].…”