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OBJECTIVE: To examine the role of total parenteral nutrition (TPN) in predisposing infants to infection caused by coagulase-negative staphylococci. SUMMARY BACKGROUND DATA: Total parenteral nutrition is an important means of providing essential nutrients to newborn infants. However, its use has been associated with complications, particularly infection caused by coagulase-negative staphylococci. Recent data suggest that TPN may modulate immune function; however, reports directly indicating impaired immunity against coagulase-negative staphylococci 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 TPN and 11 were receiving a normal enteral diet. An in vitro whole blood model was used to measure the host bactericidal activity against coagulase-negative staphylococci. Bacterial killing and phagocytosis were measured after a 45-minute challenge with viable coagulase-negative staphylococci. In study 2, whole blood killing and intracellular killing of coagulase-negative staphylococci were measured in five newborn infants (younger than 2 months) who were receiving long-term TPN (>10 days), five control infants receiving a normal enteral diet, 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-negative staphylococci phagocytosis and killing. There were significant negative linear correlations between the duration of TPN and killing of coagulase-negative staphylococci and phagocytosis of coagulase-negative staphylococci. In study 2, infants receiving long-term TPN had lower whole blood killing and intracellular killing than infants receiving a normal enteral diet and healthy adult volunteers. These data seem to indicate a neutrophil dysfunction mediated by TPN in infancy. CONCLUSIONS: Host defense mechanisms, including phagocytosis and killing of coagulase-negative staphylococci, are impaired during long-term TPN. The impaired bactericidal 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.
Twelve strains of Staphylococcus aureus isolated from patients and two collection strains were grown on membranes placed on agar containing subminimal inhibitory concentrations of oxacillin. Clusters of staphylococci held together by thick cross walls resulted. These organisms, as well as the same strains grown in the same way on drug-free medium (control), were eluted from the membranes and were incubated with human polymorphonuclear leukocytes (PMNs) from various donors. Phagocytosis was comparable for both staphylococci exposed to oxacillin and control staphylococci, but the killing effect was different. The staphylococci grown on membranes in the presence of oxacillin were less susceptible to killing than the control staphylococci, but the killing effect was different. The staphylococci grown on membranes in the presence of oxacillin were less susceptible to killing than the control staphylococci. After 0.5 and 1 h of incubation with PMNs, the killing rates for oxacillin-grown versus control staphylococci were 52 and 70% and 65 and 85%, respectively (P < 0.01). After 2 and 3 h of incubation, the killing was similar. Most clusters of staphylococci contain a few individual cells that are located in the center of the cluster and are surrounded by other staphylococci; therefore, they are protected from adverse agents in the environment. This could explain why the phagocytized clusters are less susceptible than control staphylococci to the killing effect of PMNs during the first hour of incubation. Oxacillin does not penetrate into PMNs and in the absence of the drug the cross walls lyse, liberating the constituent staphylococci. This coincides with the increase in the percentage of cluster killing by PMNs after 2 and 3 h of incubation.
Attempts were made to identify 900 species of staphylococci or micrococci recovered from samples of bovine milk examined for mastitis pathogens. The presence and identity of haemolysins was recorded together with results of disc diffusion antibiotic sensitivity tests. The occurrence of clinical mastitis was also noted and somatic cell counts (SCC) were performed on milk samples which were normal in appearance. Eight hundred and thirty-one coagulase positive staphylococci were obtained, of which 810 were S. aureus and 21 were S. intermedius. Of 65 coagulase negative staphylococci the species of 19 could not be determined by the identification systems used. The remainder were identified as S. hyicus sub sp. hyicus (1), S. hyicus sub sp. chromogenes (19), S. haemolyticus (17), S. hominis (3), S. epidermidis (4), S. capitis (1) and either S. hominis or S. warneri (1). Four other isolates could not clearly be assigned to the genus Staphylococcus or Micrococcus and were designated irregular strains. No micrococci were identified. The presence of alpha, beta, or delta haemolysins occurring singly or in various combinations was identified in 98.3% of coagulase positive staphylococci and in 60% of coagulase negative staphylococci. Epsilon haemolysin was detected in 47.6% of the coagulase negative staphylococci and in 9.5% of S. intermedius. All staphylococci were sensitive to tetracycline (30 microg), novobiocin (1.6 microg), nafcillin (30 microg), methicillin (10 microg) and cephalothin (30 microg) and variable numbers of each species were sensitive to penicillin (2 iu) and streptomycin (10 microg). One non-identified species of coagulase negative staphylococcus was sensitive to erythromycin (0.4 microg) the remaining staphylococci were resistant. Each of the four irregular strains was sensitive to erythromycin and novobiocin. Clinical mastitis was associated with 30.6% of coagulase positive staphylococci, 15.3% of coagulase negative staphylococci, and two of the four irregular strains (50%). Subclinical mastitis as determined by SCC of 500 x 10(3) or greater was associated with 92.7% of coagulase positive and 37.5% of coagulase negative staphylococci.