Staphylococci: Colonizers and Pathogens of Human Skin

Rosanna Coates; Josephine Moran; Malcolm J Horsburgh

Disclosures

Future Microbiol. 2014;9(1):75-91. 

In This Article

Arginine Catabolic Mobile Element & Skin Survival

The arginine catabolic mobile element (ACME) encoding arginine deiminase activity is found in various species of staphylococci. Its evolutionary origins are speculated to have been in the CoNS, possibly S. epidermidis.[119] The gene clusters best characterized on the ACME are the oligopeptide permease operon (opp) and the arc operon, recognized as bacterial virulence genes.[119] The enzymes encoded by the arc operon form a metabolic pathway, whereby L-arginine is transported into the cell (ArcD) and is converted by ArcA to NH3 and citrulline, which is then converted by ArcB to ornithine (exported by ArcD) and carbamoyl phosphate, and is finally converted by ArcC to CO2 and NH3, with the production of ATP. The presence of ACME in S. epidermidis did not alter its pathogenicity or host inflammatory responses.[120] The appearance of ACME within the hypervirulent USA300 lineage of community-acquired methicillin-resistant S. aureus[119] duplicates activity. However, the arginine deiminase operon of ACME is constitutively transcribed with markedly increased transcript abundance, compared with the anaerobiosis-induced, core genome operon.[121] Diep et al. first proposed that ACME carriage and its expressed arginine metabolism might allow commensal bacteria, such as S. epidermidis and S. haemolyticus, to survive more easily in an acidic environment.[119] The ACME element promotes acid tolerance in USA300 and when plasmid-borne in strain Newman.[121] Arginine deiminase activity is proposed to counteract acidity from lactic acid in sweat[121] and may similarly contribute to AFA defense, as attributed to the core genome-encoded arc operon.[106] ACME-driven arginine metabolism results in elevated host polyamines, which are integral to host healing and clearance of S. aureus. As a result, the presence of speG is required to offset the increased polyamine levels caused by the constitutive arginine metabolism of ACME.[121] Increased survival of USA300 from skin antimicrobial barriers identifies both a skin survival mechanism and the potential for increased transmission. Biofilm formation of ACME-positive S. epidermidis isolates is reduced compared with ACME-negative isolates.[120] Similarly, S. epidermidis commensal isolates have a lower carriage rate of the ica locus (involved in biofilm formation) than disease isolates.[122] Increased transmission might explain why the ability to form a biofilm is sacrificed in favor of skin survival.

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