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The interaction of Staphylococcus epidermidis slime with human neutrophils (PMN) was examined by using isolated slime and allowing bacteria to elaborate slime and other extracellular products in situ. S. epidermidis slime was found to contain a chemoattractant. Incubation of PMN with 50 ,ug or more of slime per ml inhibited subsequent chemotaxis of the PMN to n-formyl-methionyl-leucyl-phenylalanine by 27% and to zymosanactivated serum by 44 to 67% with increasing slime concentrations. S. epidermidis slime stimulated little degranulation of untreated PMN. After pretreatment of PMN with 5 ,ug of cytochalasin b per ml, slime predominantly induced release of specific granule contents (33.8% lactoferrin release by 250 ,ug of slime per ml versus 10% myeloperoxidase release by 250 ,ug of slime per ml). By a surface phagocytosis assay, PMN uptake of radiolabeled S. epidermidis which were incubated for 18 h on a plastic surface for slime expression was less than that for S. epidermidis adhered to the plastic for 2 h or grown in unsupplemented nutrient broth. These results suggest that S. epidermidis slime interaction with PMN may be potentially detrimental to host defense and may contribute to the ability of this organism to persist on surfaces of foreign bodies in the vascular or central nervous system.

The majority of Staphylococcus aureus strains recovered in pure form from superficial skin lesions have been shown to belong to phage type 71 (1, 2). Certain unique features of this phage type have been described previously, among which are the common resistance to penicillin G (1, 2), inhibition of Corynebacterium diphtheriae on solid media (1, 3), and the production of opacity in horse serum agar, but not in egg yolk broth medium (3).In a previous communication from our laboratory (4), a bactericidal substance has been described in supernatant fluids from broth cultures of phage type 71 S. aureus. This substance was active against streptococci belonging to Groups A, C, and D, pneumococci, and corynebacteria. No inhibition of Group B streptococci or Gram-negative rods was noted, and inhibition of Group G streptococci and staphylococci was variable. The bactericidal substance has been shown to be a protein or a polypeptide. The present investigations further describe the biological properties of this bactericidal substance and indicate that it is distinct from other known staphylococcal products. Materials and MethodsMedla.--Trypdc soy broth (TSB) 1 (Difco) was used to cultivate all the staphylococcal strains. A dialysate medium of TSB was prepared as previously described (4)

In contrast to Staphylococcus aureus and coagulase-negative staphylococci, group A streptococci are infrequently present on normal human skin, except in certain populations with endemic impetigo. This has been attributed to differences in susceptibility to the bactericidal effect of skin surface lipids, particularly unsaturated fatty acids. When an M type 6 strain group A streptococcus was exposed to 500 fig of oleic acid per ml, viable counts decreased by 4 logs in 5 min. The rank order of killing was 35 > 20 > 40C. Oleic acid did not kill a strain of S. aureus, a strain of coagulase-negative staphylococcus, or a strain of Escherichia coli, but bound rapidly to these bacteria as well as to the group A streptococcus. The loss of [3H]uridine from labeled oleic acid-treated group A streptococcal cells was greater than 100 times that of controls. There was no loss of [3H]thymidine from group A streptococci or of [3H]uridine or [3H]thymidine from identically exposed coagulase-negative staphylococci. When [3H]uridine was added to group A streptococci during mid-log-phase growth, cessation of uptake occurred within 5 min of addition of 50 jtg of oleic acid per ml. Electron microscopic changes seen within 5 min included condensation of the nucleoid and distortion of the streptococcal surface by numerous clumps and blebs. Coagulase-negative staphylococci, S. aureus, and E. coli similarly exposed showed no comparable electron microscopic changes. We propose that oleic acid kills group A streptococci by altering the integrity of the cell membrane with resulting loss of ribonucleic acid but not deoxyribonucleic acid.

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