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Where both the exposure to antibiotics and the anthropic pressure are minimal, acquired antibiotic resistance traits are not normally found in bacteria from wildlife, even if the ecological landscape is highly favourable to bacterial circulation among animals.
Even a modest deficiency in vitamin A is now known to exacerbate measles severity, and postmeasles bacterial pneumonias appear to be much more common in situations of poverty, crowding, and high bacterial circulation.
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This evidence shows the translocation of oral bacterial into systemic circulation.
Measuring microbial translocation requires accurate measurement of microbial constituents such as LPS or bacterial DNA in circulation.
Consumption of an energy-rich high-fat diet may result in increased levels of gut-derived bacterial endotoxins in circulation.
Mice pre-conditioned with super-low dose LPS experienced severe tissue damage, inflammation, increased bacterial load in circulation, and elevated mortality when they were subjected to cecal-ligation and puncture (CLP).
Also, roughly one third of patients with advanced cirrhosis and culture-negative ascites exhibit bacterial DNA in circulation, which is closely correlated to the presence of intrahepatic and systemic endothelial dysfunction [ 47, 48].
Thus, a substantial breach of the anatomo-functional GI barrier occurs, with progressive failure of mucosal immunity and leakage into the systemic circulation of bacterial by-products, such as lipopolysaccharide (LPS) and bacterial DNA fragments, which contribute to systemic immune activation [1] [4], [5], [6].
This possibility is clinically important because bacteremia and/or circulating bacterial products, such as LPS, are present in the circulation of critically ill humans [ 13- 16].
By contrast, extensive bacteremia, when it is associated with the release of bacterial toxins into the circulation (septicemia; see also sepsis), can be a serious medical emergency leading to bacteremic shock and eventual vascular collapse.
It has been known for many years that platelets localize and adhere to sites of bacterial lesions in the circulation, for example in endocarditis [80].
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