Submitted Successfully!
To reward your contribution, here is a gift for you: A free trial for our video production service.
Thank you for your contribution! You can also upload a video entry or images related to this topic.
Version Summary Created by Modification Content Size Created at Operation
1 -- 1228 2022-11-27 09:10:10 |
2 layout Meta information modification 1228 2022-11-28 04:00:39 |

Video Upload Options

We provide professional Video Production Services to translate complex research into visually appealing presentations. Would you like to try it?

Confirm

Are you sure to Delete?
Cite
If you have any further questions, please contact Encyclopedia Editorial Office.
Boulos, M.;  Bassal, T.;  Layyous, A.;  Basheer, M.;  Assy, N. Inflammation in COVID-19. Encyclopedia. Available online: https://encyclopedia.pub/entry/36660 (accessed on 30 December 2024).
Boulos M,  Bassal T,  Layyous A,  Basheer M,  Assy N. Inflammation in COVID-19. Encyclopedia. Available at: https://encyclopedia.pub/entry/36660. Accessed December 30, 2024.
Boulos, Mariana, Tamara Bassal, Asad Layyous, Maamoun Basheer, Nimer Assy. "Inflammation in COVID-19" Encyclopedia, https://encyclopedia.pub/entry/36660 (accessed December 30, 2024).
Boulos, M.,  Bassal, T.,  Layyous, A.,  Basheer, M., & Assy, N. (2022, November 27). Inflammation in COVID-19. In Encyclopedia. https://encyclopedia.pub/entry/36660
Boulos, Mariana, et al. "Inflammation in COVID-19." Encyclopedia. Web. 27 November, 2022.
Inflammation in COVID-19
Edit

SARS-CoV-2 is an enveloped and positive-sense single stranded RNA (+ssRNA) virus. It belongs to the betacoronavirus family, one of the four groups of the coronoviridae, which also includes two highly pathogenic viruses, Severe Acute Respiratory Syndrome Human Coronavirus (SARS-CoV) and the Middle Eastern Respiratory Syndrome Coronavirus (MERS-Cov).

corona virus disease 19 (COVID-19) respiratory syndrome coronavirus-2 (SARS-CoV2) intensive care units (ICU)

1. Introduction

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was medically challenging to health systems worldwide [1][2][3][4]. Due to respiratory complications, some patients needed to be hospitalized, and in more severe cases required mechanical ventilation in intensive care units [5][6]. High rates of mortality were observed, mainly in the elderly or in adults with serious comorbidities [7].
During outbreaks of respiratory infection, treatment usually focuses on the viral infection itself and its complications, but there always remains risk of secondary infections [8]. Viral respiratory infections predispose patients to bacterial infections that worsen outcomes of the original viral infection [9]. One such example documented in microbiological studies suggests that most deaths associated with the influenza pandemic of 1918–1919 were due to secondary infections [10][11][12]. Bacterial, viral, and fungal infections are common complications that have also been reported in other influenza virus pandemics [13][14][15][16]. As with other viral outbreaks, questions began to be asked about whether this novel coronavirus is associated with super pathogens or co-pathogens [17][18]. However, with thousands of cases diagnosed in a short period of time, many clinical decisions were made without scientific evidence. One such decision was the use of antibiotics. Although COVID-19 is a viral disease, 70% of ICU patients received antibiotics in addition to immunomodulatory drugs [19][20][21][22]. Coinfections describe simultaneous viral infection, while secondary infections typically refer to bacterial secondary infection, and both have been described in COVID-19 patients [23][24]. It is believed that the high mortality rates in severely ill COVID-19 patients are due to superinfections and viral replication, leading to severe lung injury and acute respiratory distress syndrome (ARDS) [25][26][27][28][29][30][31][32]. However, there is a lack of data regarding the frequency of superinfections in COVID-19 patients. As the diagnosis and treatment approaches for superinfections are not clear, some clinicians have argued for the use of empirical antibiotics while others have called for sampling severely ill patients for early detection and treatment [33].

2. The Virus: Classification and Possible Origin

SARS-CoV-2 is an enveloped and positive-sense single stranded RNA (+ssRNA) virus [34]. It belongs to the betacoronavirus family, one of the four groups of the coronoviridae [35], which also includes two highly pathogenic viruses, Severe Acute Respiratory Syndrome Human Coronavirus (SARS-CoV) and the Middle Eastern Respiratory Syndrome Coronavirus (MERS-Cov) [34]. SARS-CoV-2 is a novel human-infecting betacoronavirus, genetically different from but related to SARS-CoV and MERS-CoV. Another study found a very close relation (96.2% genome identity) with the bat coronavirus BaTCoV RaTG13 detected in rhinolofus affinis. This almost identical genome suggests bats as a possible origin of the virus [35].

3. SARS-CoV-2 Transmission and Immune Response

SARS-CoV-2 is transmitted mainly by the person-to-person route, which was confirmed by infected clusters of medical staff and family members, in addition to the animal-to-human transmission route which was seen early in the epidemic [36]. Once infected, the spike protein which covers the SARS-CoV-2 surface binds to the host cell’s angiotensin converting enzyme-2 (ACE2) receptor, mediating viral entry [37]. The next challenge for the virus is to encounter the innate immune response. Unfortunately, it is still unknown how SARS-CoV2 evades the immune response and drives its pathogenesis [28].
The inflammation and cellular anti-viral activity caused by the immune response is critical in inhibiting the viral replication. However, an exaggerated response affects the host, resulting in severe pneumonia which can rapidly deteriorate to acute respiratory distress syndrome (ARDS) [38].
When the immune reaction does not resolve after completing its mission, it becomes chronic or hyperinflammed, which can result in organ failure and tissue damage. COVID-19 is manifested by uncontrolled production of inflammatory cytokines such as IL-6, G-CSF, IP10 (Interferon gamma-induced protein 10), MCP-1 (Monocyte chemoattractant protein-1), MIP-1α (Macrophage inflammatory protein-1 alpha), TNF-α, IL-10, IL-7, and IL-2 [39][40]. In addition, in ICU patients, GSCF, MCP, and TNF-a values are significantly higher than in non-ICU patients, suggesting that the cytokine storm is closely related to the severity and mortality of the disease [38].
Depletion of CD4+ T cells in COVID-19 patients has been shown to reduce pulmonary lymphocyte recruitment and production of cytokines and antibodies, processes that lead to severe pneumonitis and delayed clearance of the virus [41]. One study demonstrated that the viral replication in lungs continues for 10 days post-infection. However, lung inflammation was more intense after clearance of the virus, peaking at 14 days and remaining until day 28, suggesting that the early inflammation phase is dependent on viral replication, but the later stages are viral independent and are caused by the hyperinflammatory response [42].

4. Clinical Features: Mortality and Morbidity

The incubation period in every case defined as COVID-19 is 14 days [43]. Viral infection was mostly seen in adult males with median ages of 32–72 [44]. Those most affected by the virus were the immunocompromised and the vulnerable, such as those with cardiovascular or cerebrovascular diseases [45][46]. Clinically, the virus has a wide spectrum of symptoms ranging from asymptomatic infections to patients suffering from cytokine storms. Mild disease is defined as presenting various symptoms of COVID-19, such as fever, cough, sore throat, malaise, headache, and muscle pain, with no pneumonia or dyspnoea. Moderately ill patients have evidence of clinical and radiologic pneumonia or lower respiratory disease, but O2 saturation is preserved above 93% in room air. Severely ill patients are those who have one of the following: Spo2 < 94% in room air, a respiratory rate above 30 breaths per minute, or PaO2/FiO2 < 300 mmHg. Critically ill patients have one of the following: respiratory failure, septic shock, or multiple organ dysfunction and failure [47][48][49][50][51][52][53].

5. Complications

The hospitalization and mortality rate for COVID-19 in China was up to 10% in adults, with men being more likely to develop severe complications [54]. Complications reported included increased coagulopathy, necrotizing pneumonia with staphylococcus aureus that was usually fatal cardiovascular complications (pericarditis, left ventricular dysfunction, myocardial infarction, arrythmias), ARDS (approximately 5% of COVID-19 patients) ventilation associated pneumonia, massive pulmonary embolism with right heart failure, sepsis, septic shock with multiple organ failure, and higher mortality risk especially with severe hyperglycaemic disease, heart failure, or the use of high doses of corticosteroids [55][56][57][58].

6. Diagnosis and Definitions of Superinfections

Superinfection can be diagnosed when a patient exhibits clinical symptoms and signs of bacteraemia or pneumonia, with a positive culture from blood samples or lower respiratory tract samples taken at least 48 h following admission [59]. One new and potential future first-line method for detecting superinfection and helping to decide the use of antimicrobials is metagenomic sequencing, as reported by Qing Miao et al. [60]. A gold standard is yet to be attained for diagnosis of ventilator-acquired pneumonia (pneumonia developing in a person on a ventilator), but reasonable criteria to diagnose VAP would be new or progressive radiographic consolidation or infiltration, with at least two of the following: temperature >38 °C, leucocytosis > 12,000 cells/mm3, leukopenia < 4000 cells/mm3, and the presence of purulent secretions [61]. Sepsis and septic shock are defined based on the Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). Sepsis is also represented by an increase in sequential organ failure assessment (SOFA) score of two or more. Septic shock is identified by maintaining mean arterial pressure (MAP) of 65 mmHg or more with vasopressors or serum lactate greater than 2 mmol/L in the absence of hypovolemia [62]. Catheter-associated UTI is defined as a new appearance of bacteriuria or funguria with more than 103 CFU/mL.

References

  1. Zhou, F.; Yu, T.; Du, R.; Fan, G.; Liu, Y.; Liu, Z.; Xiang, J.; Wang, Y.; Song, B.; Gu, X.; et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: A retrospective cohort study. Lancet 2020, 395, 1054–1062.
  2. Guan, W.; Ni, Z.; Hu, Y.; Liang, W.; Ou, C.; He, J. Clinical characteristics of coronavirus disease 2019 in China. N. Engl. J. Med. 2020, 382, 1708–1720.
  3. Lupia, T.; Scabini, S.; Pinna, S.M.; Di Perri, G.; De Rosa, F.G.; Corcione, S. 2019 novel coronavirus (2019-nCoV) outbreak: A new challenge. J. Glob. Antimicrob. Resist. 2020, 21, 22–27.
  4. Wu, Z.; McGoogan, J.M. Characteristics of and important lessons from the coronavirus disease 2019 (COVID-19) outbreak in China: Summary of a report of 72314 cases from the Chinese Center for Disease Control and Prevention. JAMA 2020, 323, 1239–1242.
  5. Zu, Z.; Jiang, M.; Xu, P.; Chen, W.; Ni, Q.; Lu, G.; Zhang, L. Coronavirus disease 2019 (COVID-19): A perspective from China. Radiology 2020, 296, E15–E25.
  6. Möhlenkamp, S.; Thiele, H. Ventilation of COVID-19 patients in intensive care units. Herz 2020, 45, 329–331.
  7. Velavan, T.; Meyer, C. The COVID-19 epidemic. Trop. Med. Int. Health 2020, 25, 278–280.
  8. Del Pozo, J.L. Respiratory co-and superinfections in COVID-19. Rev. Esp. Quimioter. 2021, 34 (Suppl. 1), 69–71.
  9. Arnold, F.W.; Fuqua, J.L. Viral respiratory infections: A cause of communityacquired pneumonia or a predisposing factor? Curr. Opin. Pulm. Med. 2020, 26, 208–214.
  10. Brundage, J.F.; Shanks, G.D. Deaths from Bacterial Pneumonia during 1918–19 Influenza Pandemic. Emerg. Infect. Dis. 2008, 14, 1193–1199.
  11. Morris, D.E.; Cleary, D.W.; Clarke, S.C. Secondary Bacterial Infections Associated with Influenza Pandemics. Front. Microbiol. 2017, 8, 1041.
  12. Morens, D.M.; Taubenberger, J.K.; Fauci, A.S. Predominant Role of Bacterial Pneumonia as a Cause of Death in Pandemic Influenza: Implications for Pandemic Influenza Preparedness. J. Infect. Dis. 2008, 198, 962–970.
  13. Burrell, A.; Huckson, S.; Pilcher, D.V. ICU Admissions for Sepsis or Pneumonia in Australia and New Zealand in 2017. N. Engl. J. Med. 2018, 378, 2138–2139.
  14. Abelenda-Alonso, G.; Rombauts, A.; Gudiol, C.; Meije, Y.; Ortega, L.; Clemente, M.; Ardanuy, C.; Niubó, J.; Carratala, J. Influenza and Bacterial Coinfection in Adults With Community-Acquired Pneumonia Admitted to Conventional Wards: Risk Factors, Clinical Features, and Outcomes. Open Forum Infect. Dis. 2020, 7, ofaa066.
  15. Voiriot, G.; Visseaux, B.; Cohen, J.; Nguyen, L.B.L.; Neuville, M.; Morbieu, C.; Burdet, C.; Radjou, A.; Lescure, F.-X.; Smonig, R.; et al. Viral-bacterial coinfection affects the presentation and alters the prognosis of severe community-acquired pneumonia. Crit. Care 2016, 20, 375.
  16. Martin-Loeches, I.; Schultz, M.J.; Vincent, J.L.; Alvarez-Lerma, F.; Bos, L.D.; Solé-Violán, J.; Torres, A.; Rodriguez, A. Increased incidence of co-infection in critically ill patients with influenza. Intensive Care Med. 2017, 43, 48–58.
  17. Bengoechea, J.A.; Bamford, C.G.G. SARS-CoV-2, bacterial co-infections, and AMR: The deadly trio in COVID-19? EMBO Mol. Med. 2020, 12, e12560.
  18. Chen, J. COVID-19 Scientific Advisory Group Rapid Response Report 2020. Available online: https://www.albertahealthservices.ca/assets/info/ppih/if-ppih-Covid-19-sag-anti-microbial-use-forsecondary-infections-rapid-review.pdf (accessed on 6 May 2020).
  19. Zhu, N.; Zhang, D.; Wang, W.; Li, X.; Yang, B.; Song, J.; Zhao, X.; Huang, B.; Shi, W.; Lu, R.; et al. China Novel Coronavirus Investigating and Research Team. A novel coronavirus from patients with pneumoniain China, 2019. N. Engl. J. Med. 2020, 382, 727–733.
  20. Wu, C.; Chen, X.; Cai, Y.; Xia, J.; Zhou, X.; Xu, S.; Huang, H.; Zhang, L.; Zhou, X.; Du, C.; et al. Risk Factors Associated With Acute Respiratory Distress Syndrome and Death in Patients With Coronavirus Disease 2019 Pneumonia in Wuhan, China. JAMA Intern. Med. 2020, 180, 934–943.
  21. Bendala Estrada, A.D.; Calderon Parra, J.; Fernandez Carracedo, E.; Muino Miguez, A.; Ramos Martinez, A.; Munez Rubio, E.; Rubio-Rivas, M.; Agudo, P.; Arnalich Fernandez, F.; Estrada Perez, V.; et al. Inadequate use of antibiotics in the COVID-19 era: Effectiveness of antibiotic therapy. BMC Infect. Dis. 2021, 21, 1144.
  22. Schouten, J.; De Waele, J.; Lanckohr, C.; Koulenti, D.; Haddad, N.; Rizk, N.; Sjövall, F.; Kanj, S.S.; Alliance for the Prudent Use of Antibiotics. Antimicrobial stewardship in the ICU in COVID-19 times: The known unknowns. Int. J. Antimicrob. Agents 2021, 58, 106409.
  23. Kreitmann, L.; Monard, C.; Dauwalder, O.; Simon, M.; Argaud, L. Early bacterial co-infection in ARDS related to COVID-19. Intensive Care Med. 2020, 46, 1787–1789.
  24. Rawson, T.M.; Moore, L.S.P.; Zhu, N.; Ranganathan, N.; Skolimowska, K.; Gilchrist, M.; Satta, G.; Cooke, G.; Holmes, A.H. Bacterial and Fungal Coinfection in Individuals With Coronavirus: A Rapid Review To Support COVID-19 Antimicrobial Prescribing. Clin. Infect. Dis. 2020, 71, 2459–2468.
  25. Toloui, A.; Moshrefiaraghi, D.; Madani Neishaboori, A.; Yousefifard, M.; Haji Aghajani, M. Cardiac Complications and Pertaining Mortality Rate in COVID-19 Patients; a Systematic Review and Meta-Analysis. Arch. Acad. Emerg. Med. 2021, 9, e18.
  26. Lalani, K.; Seshadri, S.; Samanth, J.; Thomas, J.J.; Rao, M.S.; Kotian, N.; Satheesh, J.; Nayak, K. Cardiovascular complications and predictors of mortality in hospitalized patients with COVID-19: A cross-sectional study from the Indian subcontinent. Trop. Med. Health 2022, 50, 55.
  27. Yang, X.; Yu, Y.; Xu, J.; Shu, H.; Xia, J.; Liu, H.; Wu, Y.; Zhang, L.; Yu, Z.; Fang, M.; et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: A single-centered, retrospective, observational study. Lancet Respir. Med. 2020, 8, 475–481.
  28. Chen, N.; Zhou, M.; Dong, X.; Qu, J.; Gong, F.; Han, Y.; Qiu, Y.; Wang, J.; Liu, Y.; Wei, Y.; et al. Epidemiological and clinical characteristics of 99 cases of 2019 novel coronavirus pneumonia in Wuhan, China: A descriptive study. Lancet 2020, 395, 507–513.
  29. Zhang, J.; Zhou, L.; Yang, Y.; Peng, W.; Wang, W.; Chen, X. Therapeutic and triage strategies for 2019 novel coronavirus disease in fever clinics. Lancet Respir. Med. 2020, 8, e11–e12.
  30. Ruan, Q.; Yang, K.; Wang, W.; Jiang, L.; Song, J. Clinical predictors of mortality due to COVID-19 based on an analysis of data of 150 patients from Wuhan, China. Intensive Care Med. 2020, 46, 846–848.
  31. He, Y.; Li, W.; Wang, Z.; Chen, H.; Tian, L.; Liu, D. Nosocomial infection among patients with COVID-19: A retrospective data analysis of 918 cases from a single center in Wuhan, China. Infect. Control Hosp. Epidemiol. 2020, 41, 982–983.
  32. Cox, M.J.; Loman, N.; Bogaert, D.; O’Grady, J. Co-infections: Potentially lethal and unexplored in COVID-19. Lancet Microbe 2020, 1, e11.
  33. Daria, S.; Islam, M.R. Indiscriminate Use of Antibiotics for COVID-19 Treatment in South Asian Countries is a Threat for Future Pandemics Due to Antibiotic Resistance. Clin. Pathol. 2022, 15, 2632010X221099889.
  34. Lu, R.; Zhao, X.; Li, J.; Niu, P.; Yang, B.; Wu, H.; Wang, W.; Song, H.; Huang, B.; Zhu, N.; et al. Genomic characterisation and epidemiology of 2019 novel coronavirus: Implications for virus origins andreceptor binding. Lancet 2020, 395, 565–574.
  35. Guo, Y.R.; Cao, Q.D.; Hong, Z.S.; Tan, Y.Y.; Chen, S.D.; Jin, H.J.; Tan, K.S.; Wang, D.Y.; Yan, Y. The origin, transmission and clinical therapies on coronavirus disease 2019 (COVID-19) outbreak—An update on the status. Mil. Med. Res. 2020, 7, 11.
  36. Letko, M.; Marzi, A.; Munster, V. Functional assessment of cell entry and receptor usage for SARS-CoV-2 and other lineage B betacoronaviruses. Nat. Microbiol. 2020, 5, 562–569.
  37. Shang, J.; Wan, Y.; Luo, C.; Ye, G.; Geng, Q.; Auerbach, A.; Li, F. Cell entry mechanisms of SARS-CoV-2. Proc. Natl. Acad. Sci. USA 2020, 117, 11727–11734.
  38. Vaninov, N. In the eye of the COVID-19 cytokine storm. Nat. Rev. Immunol. 2020, 20, 277.
  39. Chousterman, B.G.; Swirski, F.K.; Weber, G.F. Cytokine storm and sepsis disease pathogenesis. Semin. Immunopathol. 2017, 39, 517–528.
  40. Chen, J.; Lau, Y.F.; Lamirande, E.W.; Paddock, C.D.; Bartlett, J.H.; Zaki, S.R.; Subbarao, K. Cellular Immune Responses to Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV) Infection in Senescent BALB/c Mice: CD4+ T Cells Are Important in Control of SARS-CoV Infection. J. Virol. 2010, 84, 1289–1301.
  41. Clay, C.; Donart, N.; Fomukong, N.; Knight, J.B.; Lei, W.; Price, L.; Hahn, F.; Van Westrienen, J.; Harrod, K.S. Primary Severe Acute Respiratory Syndrome Coronavirus Infection Limits Replication but Not Lung Inflammation upon Homologous Rechallenge. J. Virol. 2012, 86, 4234–4244.
  42. WHO. Global Surveillance for Human Infection with Novel Coronavirus (2019-nCoV); World Health Organization: Geneva, Switzerland, 2020.
  43. Wu, Y.; Kang, L.; Guo, Z.; Liu, J.; Liu, M.; Liang, W. Incubation Period of COVID-19 Caused by Unique SARS-CoV-2 Strains: A Systematic Review and Meta-analysis. JAMA Netw. Open 2022, 5, e2228008.
  44. Fu, L.; Wang, B.; Yuan, T.; Chen, X.; Ao, Y.; Fitzpatrick, T.; Li, P.; Zhou, Y.; Lin, Y.-F.; Duan, Q.; et al. Clinical characteristics of coronavirus disease 2019 (COVID-19) in China: A systematic review and meta-analysis. J. Infect. 2020, 80, 656–665.
  45. Wang, D.; Hu, B.; Hu, C.; Zhu, F.; Liu, X.; Zhang, J.; Wang, B.; Xiang, H.; Cheng, Z.; Xiong, Y.; et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus—Infected Pneumonia in Wuhan, China. JAMA 2020, 323, 1061–1069.
  46. Basheer, M.; Saad, E.; Shlezinger, D.; Assy, N. Convalescent Plasma Reduces Mortality and Decreases Hospitalization Stay in Patients with Moderate COVID-19 Pneumonia. Metabolites 2021, 11, 761.
  47. Duan, K.; Liu, B.; Li, C.; Zhang, H.; Yu, T.; Qu, J.; Zhou, M.; Chen, L.; Meng, S.; Hu, Y.; et al. Effectiveness of convalescent plasma therapy in severe COVID-19 patients. Proc. Natl. Acad. Sci. USA 2020, 117, 9490–9496.
  48. Panel, C.T.G. Coronavirus disease 2019 (COVID-19) Treatment Guidelines. Available online: https://Covid-19treatmentguidelines.nih.gov/introduction/ (accessed on 18 August 2021).
  49. Wong, J.P.; Viswanathan, S.; Wang, M.; Sun, L.-Q.; Clark, G.C.; D’Elia, R.V. Current and future developments in the treatment of virus-induced hypercytokinemia. Future Med. Chem. 2017, 9, 169–178.
  50. Mustafa, M.I.; Abdelmoneim, A.H.; Mahmoud, E.M.; Makhawi, A.M. Cytokine Storm in COVID-19 Patients, Its Impact on Organs and Potential Treatment by QTY Code-Designed Detergent-Free Chemokine Receptors. Mediat. Inflamm. 2020, 2020, 8198963.
  51. Tisoncik, J.R.; Korth, M.J.; Simmons, C.P.; Farrar, J.; Martin, T.R.; Katze, M.G. Into the eye of the cytokine storm. Microbiol. Mol. Biol. Rev. 2012, 76, 16–32.
  52. Xu, Z.; Shi, L.; Wang, Y.; Zhang, J.; Huang, L.; Zhang, C.; Liu, S.; Zhao, P.; Liu, H.; Zhu, L.; et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome. Lancet Respir. Med. 2020, 8, 420–422.
  53. Du, F.; Liu, B.; Zhang, S. COVID-19: The role of excessive cytokine release and potential ACE2 down-regulation in promoting hypercoagulable state associated with severe illness. J. Thromb. Thrombolysis 2021, 51, 313–329.
  54. Azer, S. COVID-19: Pathophysiology, diagnosis, complications and investigational therapeutics. New Microbes New Infect. 2020, 37, 100738.
  55. Duployez, C.; Le Guern, R.; Tinez, C.; Lejeune, A.-L.; Robriquet, L.; Six, S.; Loïez, C.; Wallet, F. Panton-Valentine Leukocidin-Secreting Staphylococcus aureus Pneumonia Complicating COVID-19. Emerg. Infect. Dis. 2020, 26, 1939–1941.
  56. Kluge, S.; Janssens, U.; Welte, T.; Weber-Carstens, S.; Marx, G.; Karagiannidis, C. German recommendations for critically ill patients with COVID-19. Med. Klin.-Intensiv. Notfallmedizin 2020, 115, 111–114.
  57. Ullah, W.; Saeed, R.; Sarwar, U.; Patel, R.; Fischman, D.L. COVID-19 Complicated by Acute Pulmonary Embolism and Right-Sided Heart Failure. JACC Case Rep. 2020, 2, 1379–1382.
  58. Li, X.; Xu, S.; Yu, M.; Wang, K.; Tao, Y.; Zhou, Y. Risk factors for severity and mortality in adult COVID-19 inpatients in Wuhan. J. Allergy Clin. Immunol. 2020, 146, 110–118.
  59. Huang, C.; Wang, Y.; Li, X.; Ren, L.; Zhao, J.; Hu, Y.; Zhang, L.; Fan, G.; Xu, J.; Gu, X.; et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet 2020, 395, 497–506.
  60. Miao, Q.; Ma, Y.; Ling, Y.; Jin, W.; Su, Y.; Wang, Q.; Pan, J.; Zhang, Y.; Chen, H.; Yuan, J.; et al. Evaluation of superinfection, antimicrobial usage, and airway microbiome with metagenomic sequencing in COVID-19 patients: A cohort study in Shanghai. J. Microbiol. Immunol. Infect. 2021, 54, 808–815.
  61. Kalanuria, A.A.; Zai, W.; Mirski, M. Ventilator-associated pneumonia in the ICU. Crit. Care 2014, 18, 208.
  62. Singer, M.; Deutschman, C.S.; Seymour, C.W.; Shankar-Hari, M.; Annane, D.; Bauer, M.; Bellomo, R.; Bernard, G.R.; Chiche, J.-D.; Coopersmith, C.M.; et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 2016, 315, 801–810.
More
Information
Contributors MDPI registered users' name will be linked to their SciProfiles pages. To register with us, please refer to https://encyclopedia.pub/register : , , , ,
View Times: 656
Revisions: 2 times (View History)
Update Date: 28 Nov 2022
1000/1000
Video Production Service