Sepsis from SARS-COV2 Infection (COVID-19): Pathophysiology and Clinic of SARS-COV2 Infection and Sepsis

In December 2019, a new epidemic infectious disease made its appearance in Wuhan fish market in China. The disease was characterized by an upper airway infection that rapidly evolved into bilateral pneumonia and rapidly complicated into acute respiratory failure and other organ failures (WHO, Novel coronavirus—China, 2020). The aetiologic agent was a novel coronavirus that was named SARS-COV2, and the SARS-COV2 infection was named COVID-19 (Lu et al., Lancet 395:565–574, 2020). The infection expanded very quickly from its original core in Wuhan throughout Hubei Province, and by March 11, 2020, the World Health Organization declared the infection and its spread around the world as a pandemic infection. From the very beginning of the pandemic, clinicians and researchers understood that COVID-19 infection, in its full expression, evolved in three phases: the first phase manifested with cough, most often dry, fever, wheezing, muscle fatigue, headache, dyspnoea, and sometimes diarrhoea, all symptoms that led back to an upper respiratory tract infection. The second phase was manifested by the rapid onset of bilateral pneumonia, infiltrates accompanied by a variable degree of hypoxaemia, and possible passage of some patients into the third phase characterized by the development of severe respiratory failure (ARDS) and other organ failure and high incidence of mortality (Mason, Eur Respir J 55:2000607, 2020). About 80% of those infected with SARS-COV2 were asymptomatic or developed mild or moderate infection, mostly limited to the upper airways and bronchial tract. The other 20% developed a symptomatic infection requiring hospitalization, and 5% developed severe respiratory failure with the need for ventilatory support and admission to the intensive care unit or high-dependency care unit (Wu and McGoogan, JAMA 323:1239–1242, 2020). The clinical stages of this viral infection well reflect the pathogenetic events that begin with the virus gaining its access into the lungs from the external environment. The clinical manifestations and pathogenetic events of any infectious disease, and thus also of COVID-19 infection, should be critically revisited in the light of a new interpretive model of host-pathogen interaction: the Damage Response Framework (DRF) in which variable factors and forces can tip the scales on the side of the host or the side of the pathogen (Pirofski and Casadevall, J Infect Dis 218:S7–S11, 2018).