Tests of the survival of Candida spp., Aspergillus spp., a Fusarium sp., a Mucor sp., and a Paecilomyces sp. on hospital fabrics and plastics indicated that viability was variable, with most fungi surviving at least 1 day but many living for weeks. These findings reinforce the need for appropriate disinfection and conscientious contact control precautions.Fungal infections are an increasing risk, especially for patients who are immunocompromised by diseases or traumas or for patients immunosuppressed because of preparation for organ transplantation, treatment of cancers, or autoimmune diseases (3,4,5,8,10). As fungi become increasingly more resistant to the limited antifungal agents available, the physician's ability to control these infections with antifungals decreases (1, 4). An alternative or additional means of control is to decrease the exposure of the patient to these microorganisms, thereby preventing an infection from occurring. Limited data are available about the survival of fungi that commonly cause nosocomial infections in compromised patients on typical hospital materials(2, 9). As an initial step in determining if fabrics and plastics might serve as reservoirs or fomites for the transmission of fungi to patients, the ability of some medically important fungi to survive on common hospital materials, such as privacy curtains, towels, scrub suits, plastic splash aprons, and computer keyboard covers, was examined.The following were tested: two isolates each of Candida albicans, Candida tropicalis, Candida krusei, and Candida parapsilosis; three isolates each of Aspergillus flavus, Aspergillus fumigatus, Aspergillus niger, and Aspergillus terreus; and one isolate each of a Fusarium sp., a Mucor sp., and a Paecilomyces sp. With the exception of one each of the Aspergillus isolates, which were isolated from environmental surfaces in our hospital, all fungal strains used were isolated from burn patients at our hospital.All Candida species were grown overnight at 35°C in yeast extract-peptone-dextrose (1% yeast extract, 2% peptone, 2% dextrose; Difco Laboratories, Detroit, Mich.) broth and adjusted to 10 6 to 10 7 CFU per ml using a Klett-Summerson (New York, N.Y.) colorimeter. Molds were grown on Sabouraud dextrose (Becton Dickinson, Cockeysville, Md.) agar for 3 to 5 days depending upon the time needed for that genus and species to form spores. Spores were harvested by rinsing the plates, their concentration was determined by counting with a hemocytometer, and the spores were refrigerated overnight. The following day, enough spores were added to yeast extract-peptone-dextrose broth to give a concentration of 10 6 to 10 7 CFU/ml and then incubated until filaments began to form, a period of 6 to 17 h depending upon the particular fungi.Fungal survival was tested on the following materials, each of which are commonly used in our hospital: 100% smooth cotton (clothing), 100% cotton terry (towels, washcloths), 60% cotton-40% polyester blends (scrub suits, lab coats, clothes), 100% polyester (privacy curtains)...
Wound healing is the result of a dynamic balance between synthetic and degradative processes. After a burn, proteolytic activity increases at the wound site. Excised burn wounds and donor skin were examined from 20 pediatric burn patients, to determine which of two classes of neutral proteinases, serine or metalloproteinases, accounts for the majority of this proteolytic activity in these tissues; to examine messenger RNA expression of three of the principal enzymes and inhibitors of this class; and to measure enzymatic activity of two of these metalloproteinases. The majority of the increased proteolysis was due to metalloproteinases. By polymerase chain reaction assays, messenger RNAs for matrix metalloproteinase-1, -3, and -9 were strongly expressed in burn tissue and absent or weakly expressed in unburned skin. Messenger RNA for tissue inhibitor of metalloproteinase-1 and -2 was consistently present in burned and unburned skin. By zymography, there was a significant increase in matrix metalloproteinase-2 (twofold to threefold) and matrix metalloproteinase-9 (20- to 30-fold) activity in burned versus unburned skin. We suggest that postburn there is an upregulation of some matrix metalloproteinases that exceeds the level of inhibitors with the net result of an increase in proteolysis in burned tissue. This increased proteolysis may play a role in wound repair and scar formation.
In most murine models of endotoxemia, an exogenous agent is injected to increase the sensitivity of the mouse to endotoxin (lipopolysaccharide, LPS). Here, a clinically encountered event, a bum, was found to reproducibly decrease the amount of LPS required to kill half of the mice (LD50). In this more clinically relevant model, the anti-LPS agents, monophosphoryl lipid A and polymyxin B sulfate, each increased the LD50 of burned mice challenged with LPS from Klebsiella pneumoniae, while the LPS-directed monoclonal antibody E5 did not. However, E5 did protect burned mice challenged with smooth or rough LPS from Salmonella typhimurium and S. minnesota, respectively. Hence, in vivo protection was dependent upon both the anti-LPS agent and the chemical composition of the LPS used for intoxication. The differences in protection observed in this intoxication model may explain some protection discrepancies reported when these anti-LPS agents have been tested for protection against Gram negative sepsis.
In a mouse model of thermal injury, an increase in burn size produced a decrease in the ratio of Candida albicans cells adherent to the marginal zone to those adherent to the white pulp of the spleen, an increase in the number of Candida cells in the circulation and in the kidneys, and an increase in mortality.
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