TY - JOUR

T1 - SARS-CoV-2 Interacts with Mucosal Dysbiosis to Cause the Wide Range of Disease Seen in Covid-19

AU - Morris, James

AU - Shepherd, Rebecca

AU - Wray, Marisa

AU - Diep, P.-T.

AU - Rigby, Rachael

PY - 2022/3/26

Y1 - 2022/3/26

N2 - Hypothesis: SARS-CoV-2 amplifies pre-existing dysbiosis induced mucosalinflammation and this can cause a severe systemic inflammatory disease. Themicrobial flora perturbation can persist long after the virus has been eliminatedleading to a wide range of long Covid symptoms.Evidence: Dysbiosis induced mucosal inflammation increases with age andis strongly associated with the metabolic syndrome (obesity, type 2 diabetesmellitus, ischaemic heart disease, hypertension, and depression). These arerisk factors for the conversion of mild to severe Covid-19. Certain commonstrains of Staphylococcus aureus, which is commonly carried in pharyngealmucosa, can trigger a cytokine cascade as seen in severe Covid-19. Bloodgroup A and vitamin D deficiency, which are risk factors for hospitalisation inCovid-19 are also associated with increased S. aureus pharyngeal carriagerates. Multi-inflammatory syndrome in children is a post Covid condition whichresembles toxic shock syndrome and Kawasaki disease (the former is knownto be caused by staphylococcal pyrogenic toxins). A number of studies haveshown dysbiosis of the oral mucosa and rectal mucosa in patients who progressto severe Covid-19. The wide range of pathology seen during and followingSARS-CoV-2 infection is more in keeping with dysbiosis induced inflammation(multiple pathogenic bacteria at multiple sites) than with an otherwise simpleviral induced respiratory tract infection.Implication: Optimization of the microbial flora, prior to encountering thevirus, could have reduced the severity of the pandemic. The consumptionof fermented foods, especially yoghurt, holds the most promise for reducingdysbiosis induced mucosal inflammation and preventing a wide range ofcomplications. Reduced mucosal inflammation brings not only health but alsohappiness in which oxytocin has a key role.

AB - Hypothesis: SARS-CoV-2 amplifies pre-existing dysbiosis induced mucosalinflammation and this can cause a severe systemic inflammatory disease. Themicrobial flora perturbation can persist long after the virus has been eliminatedleading to a wide range of long Covid symptoms.Evidence: Dysbiosis induced mucosal inflammation increases with age andis strongly associated with the metabolic syndrome (obesity, type 2 diabetesmellitus, ischaemic heart disease, hypertension, and depression). These arerisk factors for the conversion of mild to severe Covid-19. Certain commonstrains of Staphylococcus aureus, which is commonly carried in pharyngealmucosa, can trigger a cytokine cascade as seen in severe Covid-19. Bloodgroup A and vitamin D deficiency, which are risk factors for hospitalisation inCovid-19 are also associated with increased S. aureus pharyngeal carriagerates. Multi-inflammatory syndrome in children is a post Covid condition whichresembles toxic shock syndrome and Kawasaki disease (the former is knownto be caused by staphylococcal pyrogenic toxins). A number of studies haveshown dysbiosis of the oral mucosa and rectal mucosa in patients who progressto severe Covid-19. The wide range of pathology seen during and followingSARS-CoV-2 infection is more in keeping with dysbiosis induced inflammation(multiple pathogenic bacteria at multiple sites) than with an otherwise simpleviral induced respiratory tract infection.Implication: Optimization of the microbial flora, prior to encountering thevirus, could have reduced the severity of the pandemic. The consumptionof fermented foods, especially yoghurt, holds the most promise for reducingdysbiosis induced mucosal inflammation and preventing a wide range ofcomplications. Reduced mucosal inflammation brings not only health but alsohappiness in which oxytocin has a key role.

KW - SARS-CoV-2; Covid-19; Dysbiosis induced mucosal inflammation; Staphylococcal pyrogenic toxaemia; Periodontitis; Yoghurt

M3 - Review article

VL - 9

JO - Austin Journal of Pulmonary and Respiratory Medicine

JF - Austin Journal of Pulmonary and Respiratory Medicine

SN - 2381-9022

IS - 1

M1 - 1086

ER -