Critical illness impacts on all organ systems, such as lungs, heart and gut. This last organ also includes the vast living microbial tissue of the indigenous, mainly anaerobic, flora. That enormous bacterial tissue is embedded in the mucous layer and covers the inner wall of the gut. Of all aerobic Gram-negative bacilli (AGNB), the indigenous Escherichia coli is the only one carried in the gut by healthy people. It is critical illness that converts the status of normal carriage of E. coli into carriage of abnormal AGNB, including Klebsiella, Enterobacter, Pseudomonas species and methicillin-resistant Staphylococcus aureus (MRSA) [1]. It is hypothesised that receptors for AGNB and MRSA are constitutively expressed on the mucosal lining, but are covered by a protective layer of fibronectin in the healthy mucosa. Significantly increased levels of salivary elastase have been shown to precede AGNB carriage in the oropharynx in postoperative patients and in the elderly [2, 3]. It is probable that in individuals suffering both acute and chronic underlying illness, activated macrophages release elastase into mucosal secretions, thereby denuding the protective fibronectin layer. It is thought that this possible mechanism is a deleterious consequence of the inflammatory response encountered during and after illness. This shift towards abnormal flora as a result of underlying disease is aggravated by most iatrogenic interventions in the septic patient. Gut protection using H2 antagonists raises gastric pH, thereby impairing the gastric acidity barrier [4]. © 2008 Springer-Verlag Italia.
CITATION STYLE
Van Saene, H. K. F. (2008). Gut microbiology: How to use surveillance samples for the detection of the carrier status of abnormal flora. In Selective Digestive Tract Decontamination in Intensive Care Medicine: a Practical Guide to Controlling Infection (pp. 59–71). Springer Milan. https://doi.org/10.1007/978-88-470-0653-9_4
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