Decoupling the role of stress and corrosion in the intergranular cracking of noble-metal alloys.

Intergranular stress-corrosion cracking (IGSCC) is a form of environmentally induced crack propagation causing premature failure of elemental metals and alloys. It is believed to require the simultaneous presence of tensile stress and corrosion; however, the exact nature of this synergy has eluded experimental identification. For noble metal alloys such as Ag-Au, IGSCC is a consequence of dealloying corrosion, forming a nanoporous gold layer that is believed to have the ability to transmit cracks into grain boundaries in un-dealloyed parent phase via a pure mechanical process. Here using atomic-scale techniques and statistical characterizations for this alloy system, we show that the separate roles of stress and anodic dissolution can be decoupled and that the apparent synergy exists owing to rapid time-dependent morphology changes at the dealloyed layer/parent phase interface. We discuss the applicability of our findings to the IGSCC of important engineering Fe- and Ni-based alloys in critical applications.

Apparent inverse Gibbs-Thomson effect in dealloyed nanoporous nanoparticles.

The Gibbs-Thomson effect (the reduction of local chemical potential due to nanoscale curvature) predicts that nanoparticles of radius r dissolve at lower electrochemical potentials than bulk materials, decreasing as 1/r. However, we show here that if the particle is an alloy--susceptible to selective dissolution (dealloying) and nanoporosity evolution--then complete selective electrochemical dissolution and porosity evolution require a higher electrochemical potential than the comparable bulk planar material, increasing empirically as 1/r. This is a kinetic effect, which we demonstrate via kinetic Monte Carlo simulation. Our model shows that in the initial stages of dissolution, the less noble particle component is easily stripped from the nanoparticle surface, but owing to an increased mobility of the more noble atoms, the surface of the particle quickly passivates. At a fixed electrochemical potential, porosity and complete dealloying can only evolve if fluctuations in the surface passivation layer are sufficiently long-lived to allow dissolution from percolating networks of the less-noble component that penetrate through the bulk of the particle.

In situ scanning tunneling microscopy of corrosion of silver-gold alloys.

An in situ scanning tunneling microscope (STM) was used to observe the morphological changes accompanying the selective dissolution of Ag from low-Ag content Ag-Au alloys in dilute perchloric acid. This study was undertaken to explore the role of surface diffusion in alloy corrosion processes. These results are interpreted within the framework of the kink-ledge-terrace model of a crystal surface and a recent model of alloy corrosion based on a variant of percolation theory. The corrosion process leads to roughening of the surface by dissolution of Ag atoms from terrace sites. Annealing or smoothening of the surface occurs by vacancy migration through clusters and the subsequent annihilation of clusters at terrace ledges.

Suppression of glycopeptide resistance in a highly teicoplanin-resistant mutant of Staphylococcus aureus by transposon inactivation of genes involved in cell wall synthesis.

The teicoplanin-resistant laboratory mutant TNM of Staphylococcus aureus strain COL (minimal inhibitory concentration for teicoplanin increased from 3 to 200 microg/ml) produced an abnormal peptidoglycan in which the proportion of cross-linked oligomeric muropeptides (pentameric and higher than pentameric species), representing approximately 60% of all muropeptide species in the parental strain, was reduced to approximately 17% in the mutant. In parallel, there was an increase in the representation of the monomeric muropeptides from 4% (in the parent) to 20% in the resistant strain. The mutant cell wall showed greatly increased porosity for the detergent extraction of cytoplasmic proteins, and this property was abolished in a Tn551 insertional derivative of TNM, which was selected for reduced (parental level) teicoplanin resistance. Transposon inactivation of the global regulatory genes Sigma-B and sar, and several genes involved in early steps of staphylococcal peptidoglycan synthesis, all caused extensive reduction of teicoplanin resistance in mutant TNM, in some cases to levels close to or below the MIC value of the parental strain.

Inactivation of the methicillin resistance gene mecA in vancomycin-resistant Staphylococcus aureus.

Acquisition of high-level resistance to vancomycin in the laboratory mutant VM50 (vancomycin MIC increased from 1.5 to 100 microg/ml) was accompanied by the appearance of a heterogeneous phenotype and a virtual loss in methicillin resistance: in most cells of cultures of VM50 the methicillin MIC of the parental strain was reduced from 800 to 1.5 microg/ml with only a subpopulation (10(-5)) retaining methicillin resistance at near the parental level (MIC of 400 microg/ml). Interestingly, the vancomycin MIC of this subpopulation was less (25 microg/ml) than that of VM50 (100 microg/ml). A similar antagonism between methicillin and vancomycin resistance levels was observed upon introduction of an intact mecA into VM50 on a plasmid vector: methicillin resistance of the majority of cells increased from 1.5 to 100 microg/ml while the vancomycin MIC declined from 100 to 12/25 microg/ml. Membrane preparations from mutant VM50 showed no detectable penicillin-binding protein (PBP) 2A by the fluorographic assay. Sequencing of the mecA gene resident in mutant VM50 indicated the presence of a 19-bp duplication between nucleotide residues 280-298, leading to the generation of a stop codon TAA starting at nucleotide position 286.

Penicillin-resistant and multidrug-resistant Streptococcus pneumoniae in a pediatric hospital in Zagreb, Croatia.

Sixty-four penicillin-resistant Streptococcus pneumoniae isolates [benzylpenicillin minimal inhibitory concentrations (MICs) between 0.05 and 1.6 micrograms/ml] recovered at the Pediatric Hospital "Dr. Fran Mihaljevic" in Zagreb, Croatia between October 1990 and March 1993 were analyzed for serotype, antibiotic susceptibility patterns, and chromosomal relatedness using pulsed-field gel electrophoretic (PFGE) analysis of chromosomal DNA fragmented by digestion with the SmaI endonuclease. Hospital "Dr. Fran Mihaljevic" services the capital of Croatia and its vicinity. Most of the isolates were from nasopharyngeal carriage, but several isolates were from otitis media, sinusitis, and meningitis. Most isolates belonged to either serotype 23F (36/64) or 19F (12/64); the rest, including three 15C isolates, were in 11 additional distinct serotypes. The overwhelming majority (25/36) of the serotype 23F isolates had penicillin MIC values of 1-2 micrograms/ml and shared variants of a common PFGE pattern, closely related to the PFGE identified in multiresistant pneumococci of the same serotype with wide geographic spread to Spain, Portugal, France, and the United States. This group of bacteria was also resistant to tetracycline, chloramphenicol, and sulfamethoxazole/trimethoprim. In contrast to the relative genetic and phenotypic homogeneity of the more highly penicillin resistant isolates, pneumococci with penicillin MICs between 0.5 and 0.4 microgram/ml (29/64) were distributed in 13 different serotypes and as many as 20 distinct PFGE patterns.

A highly vancomycin-resistant laboratory mutant of Staphylococcus aureus.

A resistant mutant with vancomycin MIC of 100 micrograms/ml was isolated relatively easily through step pressure in the laboratory from a Staphylococcus aureus strain with initial MIC of 1.5 micrograms/ml for the antibiotic. Upon addition of vancomycin (50 micrograms/ml) to the growth medium mass increase of the culture and peptidoglycan synthesis continued but cell division (daughter cell separation), cell wall turnover and autolysis were inhibited, resulting in the production of multicellular clumps of bacteria. Parallel with the increase of culture density, the concentration of vancomycin measured both by biological activity and by HPLC gradually declined in the culture medium. Cell division and wall turnover of the culture resumed with the production of cells of normal morphology at the time when the concentration of the drug in the medium decreased below 0.5-1.0 micrograms/ml. There was no detectable change in the antibiotic concentration in the culture medium during growth of a vancomycin-resistant (vanA-positive) strain of Enterococcus faecium and an intrinsically vancomycin-resistant strain of Leuconostoc. The vancomycin-resistant staphylococcal mutant gave no signal with the vanA or vanB DNA probes and contained no detectable D-lactate terminating cell wall precursors. The biochemical mechanism and clinical significance of such glycopeptide-resistant mutants remained to be established.