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Severe viral pneumonia in adults: what is important for the ICU physician?

Hippocrates II of Cos referred to pneumonia as a disease namedby the ancients which was defined by the presence of acute fever, chest pain, cough, and purulent sputum [1]. Centuries later, around 1875, Prussian physician Edwin Klebs was the first one describing the presence of bacterial microorganisms in the airways of deceased patient because of respiratory disease [2]. Subsequently, further studies simultaneously performed by Louis Pasteur in France andGeorge Sternberg in the United States led to the identification in 1881 of a pathogenic diplococcus which in 1886would be named Pneumococcus, because of its propensity to cause pulmonary diseases [3]. In the following years, Pneumococcus was confirmed to be the main bacterial agent to cause pneumonia, and many other bacterial agents were identified as causative of respiratory infection. Finally, during the twentieth century, the introduction of different antibiotic molecules in the clinical practice led to the antibiotic era, and we all know which is the continuation of the tale of bacterial pneumonia. On the other hand, starting from 1892, Dmitri Ivanovskii gave the first concrete evidence for the existence of a nonbacterial infectious agent, showing that infected sap remained infectious even after filtering through finest Chamberland filters [4]. Although such a discovery was not as celebrated as other scientific achievements, it represented the beginning of a new microbiological era because it laid the basis for the discovery and understanding of virus, its interactions with humans, and the development of virus-related diseases. Coming back to contemporary medicine, viral pneumonia represents a complex medical issue because of the intrinsic nature of virus: their ability to modify their genetic information yields them a very high adaptability to different environments and systems. Moreover, it is extremely complicate to predict the virulence owned by a specific viral strain and its interaction with the host’s immune system. On one side, many families of respiratory viruses induce mild or very mild infection so they usually do not constitute a concern for intensive care unit (ICU) physician; on the other side, infection by specific viruses can lead to severe respiratory failure possibly because of an exaggerate inflammatory reaction, which is associated with severe pneumonitis and eventually acute respiratory distress syndrome (ARDS) [5,6]. This condition is usually associated with high mortality despite all treatment efforts, as was the case of pandemic H1N1/09 virus [5]. Indeed, 2009 flu pandemic raised attention and concern upon the importance of viral infection and pneumonia, worldwide. However, as ICU physician, what do we know about viral pneumonia? And, what is really important to keep in mind while assessing and treating a patient with suspect of viral pneumonia? To better address this issue, it is useful to tackle it by two different perspectives: the pathogen and the host. As per the pathogen, different families of virus are associated with different virulence. Usually, viruses associated with a high virulence spread as a breakthrough with high mortality rates; eventually, the severity of disease will decrease in the subsequent years. Examples of breakthrough caused in recent times by high virulence virus are Pandemic 2009 Influenza A (H1N1) virus (pH1N1), Influenza A (H5N1) virus, Severe Acute Respiratory Syndrome Coronavirus (SARS-CoV), and the Middle East Respiratory Syndrome Coronavirus (MERS-CoV) [5–8]. In case of coronavirus infection, either MERS-CoV or SARSCoV, it was observed that virus infection induces an excessive activation of the immune system which leads to the synthesis of several pro-inflammatory cytokines like interleukin-1beta (IL-1B), IL-6, IL-8, CXC-chemokine ligand 10 (CXCL10), CC-chemokine ligand 2 (CCL2), and interferon-γ (IFN-γ) [9–12]. This proinflammatory response will ultimately induce pulmonary circulation capillary leakage which will lead to non-cardiogenic pulmonary edema, hypoxemia, type II pneumocyte hyperplasia, and neutrophil infiltration. This stage of the disease is generally followed by increased fibroproliferation and hyaline membrane formation; depending on the patient, these gross pathological changes may progress or resolve [13]. Unfortunately, risk factors to identify patients at high risk for ARDS development are still matter of research [14]. Sometimes, depending on the type of virus responsible for the pneumonia, viral infection can extend beyond the lung tissue; it was observed that an increase of plasmatic creatine kinase in patients with pH1N1 pneumonia is associated with higher mortality, suggesting myocarditis as potential explanation for the increase of creatine kinase [15]. In recent years, many viruses were identified as a causative agent for viral infection; however, the vast majority of patient will develop mild pneumonia or simple viral bronchitis, whereas other patients with specific risk factors will develop