Bactericidal activity against coagulase-negative staphylococci is impairedin infants receiving long-term parenteral nutrition

Objective To examine the role of total parenteral nutrition (TPN) in predisposing inf ants to infection caused by coagulase-negative staphylococci. Summary Background Data Total parenteral nutrition is an important means of providing essential nut rients to newborn infants. However, its use has been associated with compli cations, particularly infection caused by coagulase-negative staphylococci. Recent data suggest that TPN may modulate immune function; however, report s directly indicating impaired immunity against coagulase-negative staphylo cocci during TPN are limited. Methods Study 1 involved 31 infants younger than 4 months who had undergone surgery and were not receiving antibiotics; 20 were receiving IPN and 11 were rece iving a normal enteral diet. An in vitro whole blood model was used to meas ure the host bactericidal activity against coagulase-negative staphylococci . Bacterial killing and phagocytosis were measured after a 45-minute challe nge with viable coagulase-negative staphylococci. In study 2, whole blood k illing and intracellular killing of coagulase-negative staphylococci were m easured in five newborn infants (younger than 2 months) who were receiving long-term TPN (>10 days), five control infants receiving a normal enteral d iet, and five healthy adults. Results In study 1, infants receiving a normal enteral diet showed a high capacity to ingest and kill coagulase-negative staphylococci. In contrast, the blood of infants receiving long-term TPN showed a reduction in coagulase-negativ e staphylococci phagocytosis and killing. There were significant negative l inear correlations between the duration of TPN and killing of coagulase-neg ative staphylococci and phagocytosis of coagulase-negative staphylococci. I n study 2, infants receiving long-term TPN had lower whole blood killing an d intracellular killing than infants receiving a normal enteral diet and he althy adult volunteers. These data seem to indicate a neutrophil dysfunctio n mediated by TPN in infancy. Conclusions Host defense mechanisms, including phagocytosis and killing of coagulase-ne gative staphylococci, are impaired during long-term TPN. The impaired bacte ricidal activity seems to be related to defective intracellular killing in neutrophils. These findings may explain the high rate of septicemia caused by coagulase-negative staphylococci in infants receiving TPN.