Continuous ambulatory peritoneal dialysis-associated peritonitis as a model device-related infection: phenotypic adaptation, the staphylococcal cell envelope and infection.

During the development of infection, pathogens are translocated from one body site to another and so must readily adapt to changing environmental conditions. The influence of host environment on bacterial behaviour and virulence gene expression is, however, often overlooked. Environmental signals such as temperature, pH and nutrient (especially iron) availability which inform pathogens of their living conditions thus contribute to both bacterial survival and virulence. In the context of medical device-associated infections such as peritonitis in continuous ambulatory peritoneal dialysis (CAPD) patients, the pathogenesis of infection is related to the ability of the infecting organism to multiply, to adhere to catheter polymers and host tissues and to evade host defences. Coagulase-negative staphylococci (CNS) such as Staphylococcus epidermidis are commonly responsible for CAPD-associated peritonitis. Although staphylococci cannot grow in commercial peritoneal dialysate solutions, these fluids are modified during dialysis and become enriched by a plasma ultrafiltrate which can support bacteria growth. Given that growth environment exerts considerable influence on bacterial behaviour, the physiology of CNS cultured in vitro in a model system employing pooled human peritoneal dialysate and in vivo in implanted peritoneal chambers in the rat has been investigated. Using such models marked variation in surface physicochemistry, antibiotic susceptibility and adherence to catheter polymers has been observed. This plasticity is clearly reflected in the cell envelope phenotype of CNS, the study of which has recently lead to the discovery of a staphylococcal receptor for the iron-binding serum glycoprotein, transferrin.