DISPERSAL of micro-organisms from the body surface into the air occurs mainly on particles of desquamated skin. Some people appear to have a special ability to disseminate their pathogenic flora in this way and have been termed " dispersers ". There are, however, some curious observations relating to such dispersal; males disperse more than females, healthy young males are significantly more often dispersers of Staphy Zococcus aureus than are females, and dissemination of all organisms appears to be greater from below the waist than from above it (Hill, Howell and Blowers, 1974;Mitchell and Gamble, 1974).There is no agreed definition of a disperser; Noble (1962) described as dispersers of S. aureus persons who disseminated this organism as more than 1 % of the total disseminated flora whilst undressing. According to Blowers a disperser was a person who disseminated more than 10 particles bearing this organism into a room of volume 100 cu. ft (2.83 1113) during exercise (Bethune et al., 1965). In practice the two definitions are surprisingly close. It is clear from the work of Solberg, however, that there is a complete spectrum of dispersal and that any chosen cut-off for a specific organism is arbitrary (Solberg, 1965; Solberg, Bruun and Bse, 1972). In defining as dispersers those who disseminate a potentially pathogenic micro-organism, it is easy to lose sight of the fact that all persons are dispersers or disseminators of their own normal flora. Any organism appearing on the skin will be dispersed as a result of normal desquamation. There do not appear to have been any systematic studies of dispersal in relation to quantitative assessment of the normal skin flora. This paper reports such a study and seeks to explore the origin of dispersed organisms. METHODSThe volunteers investigated were members of surgical or nursing teams (38 males and 34 females), each of whom was examined once only. They were asked to undress completely
The kinetic patterns of the phagocytosis and intracellular killing of Staphylococcus and Escherichia coli by monocytes were investigated separately to acquire more insight into the total process, i.e. from the ingestion to the death of the micro-organisms. Phagocytosis proved to be dependent on: (1) both the bacteria-to-monocyte ratio and the monocyte concentration; a concentration of at least 5 x 10(5) monocytes/ml proved necessary for the measurement of ingestion, whereas the rate of ingestion was found to be proportional to the number of extracellular bacteria until a maximum rate is reached, (2) the serum concentration in the incubation medium, which influenced both the rate of phagocytosis and the maximum number of bacteria taken up by one monocyte, and (3) the temperature, the highest rate of phagocytosis being reached at 37-41 degrees C. The intracellular killing proved to be dependent on: (1) the number of bacteria ingested; the rate of killing was proportional to the number of ingested bacteria until a maximum rate was reached; (2) the temperature, since a maximum rate of killing is only reached at 37-41 degrees C; at lower and higher temperatures the rate of killing is lower, in the latter case due to inactivation of extracellular stimuli. These separate data on the ingestion and killing processes made it possible to compute the theoretical numbers of extracellular, viable intracellular, and total intracellular bacteria for a model system consisting of 5 x 10(6) monocytes, 5 x 10(6) bacteria, and 10% serum. These calculated values are in agreement with the experimental data.
ABSTRACT. Cord blood phagocytic cells were characterized with respect to cytochemical activities, Fcy and C3b receptors, and capacity to phagocytose and kill various species of bacteria.The percentages of peroxidase-positive granulocytes and monocytes from neonates and adults were comparable; the percentage of esterase-positive cord-blood monocytes was about two-thirds of that of adults' blood monocytes. Despite improved diagnostic techniques and medical care, bacterial infections still play an important role in neonatal morbidity and mortality. A wide variety of microorganisms, including those considered to have relatively low virulence and to be susceptible to commonly used antibiotics, can lead to overwhelming septicemia in neonates. The frequency of infections in the newborn suggests a defective host defense mechanism, and various attempts have been made to investigate this point. Particular attention has been paid to the functioning of phagocytic cells. Defects in the chemotactic motility of granulocytes and monocytes (reviewed in Ref. 18) and impaired opsonization of
The interaction between povidone-iodine, phagocytic cells, and microorganisms was studied. Three preparations of povidone-iodine were investigated: commercially available povidone-iodine solution Betadine, pure high-molecularweight povidone-iodine as used in Betadine, and a low-molecular-weight povidone-iodine. Low concentrations of povidone-iodine (-0.005%) have considerable activity in vitro. The concentrations used clinically (0.1 to 20%) are toxic for granulocytes and monocytes. Leukocytes reduce the in vitro microbicidal activity of povidone-iodine. No differences of any importance were found between the three preparations of povidone-iodine.Povidone-iodine (polyvinylpyrrolidone-iodine) is a potent microbicidal drug. It is used for several purposes: prophylactically for disinfection (3), irrigation of surgical wounds (4, 8), and bladder irrigation in patients with urinary catheters (6) and therapeutically in infections of the peritoneal and pleural cavities (5, 7) and cutaneous candidiasis (9). Thus, povidone-iodine is applied not only to the surface of the body, but also in tissues and body cavities, where its interaction with phagocytic cells can be of importance because these cells are involved in the host defense against infection. Povidone-iodine can influence the function of such cells, since it is known to reduce chemotaxis (2). Since nothing was known about the effect of povidoneiodine on phagocytosis and intracellular killing or about the influence exerted by cells or tissue on the microbicidal activity of povidone-iodine, this quantitative study was performed to investigate possible interactions between povidoneiodine, leukocytes, and microorganisms. MATERIALS AND METHODSThe materials and methods used for preopsonization and the phagocytosis and intracellular killing assay have been described in detail elsewhere (10). Here, only the bactericidal agents are referred to, and the methods are briefly described.Povidone-odine. Betadine. Solutions of Betadine were made by diluting the commercially available Betadine (10o solution of the high-molecular-weight povidone-iodine PVPK30-J in water; Dagra N.V., Diemen, The Netherlands) in phosphate-buffered saline. The available iodine is about 10%6. PVPK30-J. PVPK30-J is a povidone-iodine compound prepared with the high-molecular-weight povidone PVPK30 and iodine. The available iodine in this preparation is 11.2%. Solutions were made by dissolving the substances in phosphate-buffered saline.PVPK17-J. PVPK17-J is prepared with the lowmolecular-weight povidone PVPK17 and iodine. The available iodine in this compound is 11.4%. Solutions were made by dissolving the substance in phosphatebuffered saline.Iodine. Solutions of iodine were made by diluting iodine 1% (wt/vol) in 70%o (vol/vol) ethanol in phosphate-buffered saline.Mkroorganisms. The bacteria used for the study were cultured at 37C overnight in nutrient broth no. 2 (Oxoid Ltd., London, England). Candida albicans was cultured for 5 days at 30°C in nutrient broth no. 2 containing 1% (wt/vol) glucose. After...
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