Silver Sulfadiazine: Effect on the Ultrastructure of
            <i>Pseudomonas aeruginosa</i>

Coward, Joe E.; Carr, Howard S.; Rosenkranz, Herbert S.

doi:10.1128/aac.3.5.621

Cited by 57 publications

(40 citation statements)

References 12 publications

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“…Although it has been suggested that binding to DNA is the mode of action in vivo [18], other workers suggest that Ag 2 binds preferentially to external cell structures and that only small amounts are bound to DNA [24]. Cells of S. aureus treated with AgSD were enlarged, some retraction of the cytoplasmic membrane from the cell wall was seen and division planes between bacteria became indistinct, supporting the view that the effect is on external cell structures [26]. Studies have shown that subinhibitory levels of sulphadiazine affect membrane permeability [27].…”

Section: Introductionsupporting

confidence: 54%

Effects of silver sulphadiazine on the production of exoproteins by Staphylococcus aureus

Edwards-Jones¹,

Foster

2002

Journal of Medical Microbiology

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The effects of subinhibitory concentrations of silver sulphadiazine (AgSD) on exoprotein production in Staphylococcus aureus strains T1, T4, RN4282 and RN 4282agr were studied. AgSD markedly increased levels of toxic shock syndrome toxin (TSST)-1 in strains T4 and RN4282. This effect was independent of agr and AgSD restored TSST-1 production to the wild-type level in RN 4282agr. AgSD had no effect on enterotoxin A or coagulase activity in strains T1 or T4. Strain T4 produced enterotoxin C at high levels and no effect was observed with AgSD. AgSD repressed metalloprotease production in strain T4 but the overall protease activity remained the same. No change in proteolytic activities was seen in strain T1 with AgSD. Molecular mechanisms for these observations are discussed.

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Section: Introductionsupporting

confidence: 54%

Effects of silver sulphadiazine on the production of exoproteins by Staphylococcus aureus

Edwards-Jones¹,

Foster

2002

Journal of Medical Microbiology

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“…Rosenkranz and Carr found that most silver was associated with the cell membrane (and proteins), and some with the cell wall (43). They further examined AgSu treated bacteria by electron microscopy, and observed them to be distorted in shape, with surface blebs (45). A strain resistant to AgSu did not display surface blebs.…”

Section: Water Sterilizationmentioning

confidence: 99%

Antibacterial Silver

1994

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The antibacterial activity of silver has long been known and has found a variety of applications because its toxicity to human cells is considerably lower than to bacteria. The most widely documented uses are prophylactic treatment of burns and water disinfection. However, the mechanisms by which silver kills cells are not known. Information on resistance mechanisms is apparently contradictory and even the chemistry of Ag + in such systems is poorly understood. Silver binds to many cellular components, with membrane components probably being more important than nucleic acids. It is difficult to know whether strong binding reflects toxicity or detoxification: some sensitive bacterial strains have been reported as accumulating more silver than the corresponding resistant strain, in others the reverse apparently occurs. In several cases resistance has been shown to be plasmid mediated. The plasmids are reported as difficult to transfer, and can also be difficult to maintain, as we too have found. Attempts to find biochemical differences between resistant and sensitive strains have met with limited success: differences are subtle, such as increased cell surface hydrophobicity in a resistant Escherichia coli. Some of the problems are due to defining conditions in which resistance can be observed. Silver(I) has been shown to bind to components of cell culture media, and the presence of chloride is necessary to demonstrate resistance. The form of silver used must also be considered. This is usually water soluble AgNO 3 , which readily precipitates as AgCl. The clinically preferred compound is the highly insoluble silver sulfadiazine, which does not cause hypochloraemia in burns. It has been suggested that resistant bacteria are those unable to bind Ag + more tightly than does chloride. It may be that certain forms of insoluble silver are taken up by cells, as has been found for nickel. Under our experimental conditions, silver complexed by certain ligands is more cytotoxic than AgNO 3 , yet with related ligands is considerably less toxic. There is evidently a subtle interplay of solubility and stability which should reward further investigation.

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“…AgSu has a broad spectrum of action, and most microorganisms capable of infecting burns and wounds are susceptible to the antimicrobial action of the drug at levels which are readily obtainable topically (2,19). The mechanism of action of AgSu was studied mainly in Pseudomonas aeruginosa where it affects primarily the external cell structure (3,12,14 (Ag/ml) CB synthetic medium (medium HA, ref. 13).…”

mentioning

confidence: 99%

Properties of Silver Sulfadiazine-Resistant Enterobacter cloacae

Rosenkranz

Coward

Wlodkowski

et al. 1974

Antimicrob Agents Chemother

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Two silver sulfadiazine-resistant isolates of Enterobacter cloacae obtained in a burns unit where the drug was in use were studied. These strains were resistant to elevated levels of the drug, and they were cross-resistant to silver benzoate, but not to silver nitrate. Growth of the strains in nutritionally poor defined media sensitized them to the inhibitory action of the drug. Exposure of the bacteria to penicillins rendered them susceptible to silver sulfadiazine. The resistant bacteria harbored episomes for resistance to carbenicillin and kanamycin; however, resistance to silver sulfadiazine could not be transferred by these episomes. Twenty-three strains of E. cloacae isolated in a general hospital were sensitive to much lower levels of the drug (≤50 μg/ml).

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Silver Sulfadiazine: Effect on the Ultrastructure of Pseudomonas aeruginosa

Cited by 57 publications

References 12 publications

Effects of silver sulphadiazine on the production of exoproteins by Staphylococcus aureus

Effects of silver sulphadiazine on the production of exoproteins by Staphylococcus aureus

Antibacterial Silver

Properties of Silver Sulfadiazine-Resistant Enterobacter cloacae

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