Enterococcal Peritonitis in Peritoneal Dialysis Patients: Last Name Matters

Prevention and management of peritonitis remains a challenge for nephrologists and for patients undergoing peritoneal dialysis (PD). As the incidence of peritonitis becomes a lesser—although still unresolved—problem, more attention is being focused on the prevention and management of clinically aggressive infections, which represent a fearsome source of suffering, technique failure, and mortality. Clinical presentation is closely linked to the microbes causing the infection—yeasts and enteric bacteria being the main agents producing complicated infections. The capacity of these micro-organisms to inflict severe and persistent harm is related both to the particular conditions in which they commonly appear (debilitated patients, underlying abdominal disease) and to their intrinsic aggressiveness and ability to persist under adverse conditions (taking advantage of resistance to common antibiotic regimens and of a capacity to produce biofilms and to take shelter in plastic materials, among other factors). This issue of Peritoneal Dialysis International provides relevant information on peritoneal infections caused by bacteria of the genus Enterococcus, unquestionably candidates for membership in this unpleasant club. Enterococci are gram-positive, catalase-negative, nonspore-forming facultative anaerobic bacteria belonging to the group of so-called lactic acid bacteria (1). They can be seen as isolated cocci, pairs, short chains, and even long chains. Nearly 30 different species have been identified, but 2—namely, E. faecalis and E. faecium— cause most of the human infections in which this genus is involved (2). Species identification is laborious, and with the exception of E. faecalis, quite inaccurate using standard automated or rapid biochemical methods (1). In fact, the routine of many laboratories does not include differentiation, at least beyond the 2 main species. As will be evident later, the latter may be relevant in the clinical setting, because of their distinct virulence and antibiotic susceptibility patterns. Enterococci are well adapted to survival in the gastrointestinal tract of humans, where they live in symbiosis with the immune system and other bacteria. Broad-spectrum antibacterials, particularly those with anti-anaerobic activity or biliary excretion, or both, favor proliferation of these organisms in the gut and emergence of vancomycin-resistant strains (VREs). These phenomena are a consequence of the eradication of gram-negative bacteria (mainly anaerobes), which results in downregulation of the intestinal expression of the antimicrobial peptide Reg IIIγ, the latter being essential to control the proliferation of gram-positive intestinal micro-organisms (3). Increased stomach pH also appears to favor enterococcal outgrowth (1). The foregoing factors explain why the gut is more heavily colonized by these bacteria in hospitalized patients than in the general population (4). On the other hand, the hospital environment appears to be frequently colonized by antibiotic-resistant enterococci (5), and the hands of health personnel may be a prime source of transmission of those bacteria. Risk factors for persistent colonization by VRE include debilitating conditions (immunosuppression, comorbidity), prolonged stay in a hospital or long-term care facility, proximity to other colonized patients or to their environment, invasive procedures, and as indicated earlier, previous treatment with vancomycin or widespectrum antibiotics (1). Enterococci were individualized as a genus as late as 1984. For some years, they were considered harmless to humans. They were actually used in the food industry as probiotics or starter cultures because of their capacity to produce bacteriocins (6). However, consecutive reports starting in the 1990s and multiplying since the year 2000 have clearly demonstrated that they can cause severe infections. Bacteremia, endocarditis, and urinary tract infections have received the most attention, but enterococci can also produce meningitis, COMMENTARIES