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M K Hayden

Publications and source records attributed to M K Hayden.

25 records · Page 2Linked to original sources

Comparison of the in vitro activity of levofloxacin and other antimicrobial agents against vancomycin-susceptible and vancomycin-resistant Enterococcus species.

The in vitro activities of levofloxacin and other antibiotics against 133 clinical isolates of vancomycin-resistant and vancomycin-susceptible enterococci were evaluated. Only 14 (39%) of the vancomycin-susceptible isolates and 11 (11%) of the vancomycin-resistant isolates were susceptible to levofloxacin. Levofloxacin exhibited a marked inoculum effect for all enterococci tested. These results suggest that levofloxacin may be of limited use in the treatment of serious enterococcal infections.

Ampicillin↗

Genotypic and phenotypic characterization of Borrelia burgdorferi isolated from ticks and small animals in Illinois.

We have characterized 33 isolates of Borrelia burgdorferi from northern Illinois (32 isolates) and Wisconsin (1 isolate) representing the largest series of midwestern isolates investigated to date. The techniques used for molecular analysis of strains included (i) genospecies typing with species-specific PCR primers, (ii) plasmid profiling by pulsed-field gel electrophoresis of total genomic DNA, (iii) large-restriction-fragment pattern (LRFP) analysis by pulsed-field gel electrophoresis of MluI-digested genomic DNA (J. Belfaiza, D. Postic, E. Bellenger, G. Baranton, and I. Saint Girons, J. Clin. Microbiol. 31:2873-2877, 1993), (iv) sodium dodecyl sulfate-polyacrylamide gel electrophoresis of total proteins, (v) microsequencing of high-performance liquid chromatography-purified peptides derived from proteins showing high levels of expression, (vi) amino acid composition analysis of proteins, and (vii) immunological analysis of proteins with a polyclonal antiserum of human origin. Five reference strains as well as two atypical tick isolates from California (DN127) and New York (25015) were included for comparison. All of the Illinois and Wisconsin isolates were typed as B. burgdorferi sensu stricto with genospecies-specific PCR primers. The isolates were found to be heterogeneous with regard to their plasmid and protein profiles. One isolate from Illinois possessed two large-molecular-size plasmids instead of the usual 49-kb plasmid. Fragment patterns resulting from MluI digestion of genomic DNA from the 33 isolates and strains DN127 and 25015 were separable into six distinct LRFPs, five of which have not previously been described. Strain 25015 and an isolate from Illinois (CT39) shared an unusual LRFP that is not typical of other B. burgdorferi sensu stricto strains, suggesting that they may represent a fifth species of B. burgdorferi sensu lato. Five of the 33 isolates and strains DN127 and 25015 showed high-level expression of proteins with molecular masses of approximately 22 kDa. Investigation of these proteins by microsequencing of individual peptides and total amino acid composition analysis indicated that the 22-kDa proteins expressed by the seven strains were polymorphic OspC proteins. By using a polyclonal serum of human origin, expression of OspC could be detected in all 33 Illinois and Wisconsin isolates.

Amino Acid Sequence↗

Bactericidal activities of antibiotics against vancomycin-resistant Enterococcus faecium blood isolates and synergistic activities of combinations.

The effects of teicoplanin (8 micrograms/ml), ampicillin (64 micrograms/ml), imipenem (32 micrograms/ml), and gentamicin (4 micrograms/ml), alone and in combination, against 13 unique blood isolates of vancomycin-resistance (MIC for 90% of isolates tested [MIC90], 512 micrograms/ml), teicoplanin-susceptible (MIC90, 2.0 micrograms/ml), ampicillin-resistant (MIC90, 128 micrograms/ml), and non-beta-lactamase-producing Enterococcus facium (vancomycin-resistant enterococci [VRE] isolates) were evaluated by time-kill studies. All 13 isolates exhibited high-level resistance to streptomycin; 7 isolates exhibited high-level gentamicin resistance (HLGR). After 24 h of incubation, ampicillin (64 micrograms/ml) combined with gentamicin (4 micrograms/ml) was bactericidal against three of the VRE isolates that did not display HLGR. Synergy between ampicillin and gentamicin was not observed against these isolates. Teicoplanin (8 micrograms/ml) alone was bactericidal at 24 h against five of six VRE isolates that lacked HLGR, but was not bactericidal against any HLGR VRE isolate at that time point. The addition of ampicillin (64 micrograms/ml) or imipenem (32 micrograms/ml) to teicoplanin did not significantly enhance the killing of HLGR VRE isolates as a group (P = 0.335). However, there was a trend toward improved killing of some HLGR VRE isolates by teicoplanin plus imipenem. Vancomycin (32 micrograms/ml) combined with ampicillin (64 micrograms/ml) was neither bactericidal nor synergistic against HLGR VRE isolates. Overall, bactericidal activity was attainable against 7 of 13 VRE isolates at 24 h.

Ampicillin↗

Confronting antibiotic resistance in enterococcal infections.

The increase in enterococcal infections, particularly nosocomial, and the resistance of many species to multiple antibiotics challenge treatment decisions. Resistance screening and synergistic combinations of antimicrobials may be effective.

Aminoglycosides↗

In vivo development of teicoplanin resistance in a VanB Enterococcus faecium isolate.

Acquired vancomycin resistance in enterococci may be associated with teicoplanin susceptibility (VanB) or teicoplanin resistance (VanA). This paper characterizes the first instance of in vivo emergence of teicoplanin resistance in an Enterococcus faecium strain of VanB phenotype. Vancomycin-resistant (MIC, 256/512 micrograms/mL) E. faecium was isolated intermittently from a patient's blood over 4 months. The MIC of teicoplanin for the first 5 isolates was 1.0 micrograms/mL; it was 64 micrograms/mL for the final 2. Analysis of plasmid and chromosomal DNA revealed the isolates to be of clonal origin. Conjugal transfer of vancomycin resistance was not obtained. A vanB DNA probe hybridized with both teicoplanin-susceptible and resistant isolates, but a vanA probe failed to hybridize with any isolate. SDS-PAGE of membrane proteins from a teicoplanin-resistant isolate revealed constitutive production of a normally inducible 41-kDa protein. These findings challenge the ultimate utility of teicoplanin for treatment of infections caused by vancomycin-resistant enterococci.

Bacterial Proteins↗

Isolation of transformation-deficient Streptococcus pneumoniae mutants defective in control of competence, using insertion-duplication mutagenesis with the erythromycin resistance determinant of pAM beta 1.

Several transformation-deficient mutants of Streptococcus pneumoniae were isolated after insertion-duplication mutagenesis. Mutagenesis was accomplished by transformation of competent cells with chimeric DNA formed by the ligation of TaqI fragments of pneumococcal DNA to the erythromycin resistance determinant of the streptococcal plasmid pAM beta 1. The two mutants described were characterized as defective in the control of competence induction, possibly due to a block in the production of the intercellular competence-inducing protein.

Chimera↗

Effects of asphyxia at birth on postnatal glucose regulation in the rat.

We have characterized the effect of a period of asphyxia at birth, followed by recovery, upon newborn rats. Asphyxiated pups were subjected to 3 to 5% (v/v) inspired oxygen during the first 20 min of life and then maintained in room air for 6 h. Control pups were maintained in room air throughout the 6-h period. Hypoxia produced severe asphyxia as reflected by a pH of 6.76 +/- 0.05, PaCO2 of 87 +/- 3 mm Hg and PaO2 of 15.4 +/- 4 mm Hg, and by a greatly increased blood lactate/pyruvate ratio. Plasma catecholamine concentrations in asphyxiated pups were elevated (epinephrine 13,866 +/- 250 pg/ml, norepinephrine 9611 +/- 1813 pg/ml) compared to control animals (epinephrine 973 +/- 234 pg/ml, norepinephrine 774 +/- 133 pg/ml) at 20 min. Asphyxia initially increased plasma glucose concentration, and then with recovery it fell below controls. Hepatic glycogen stores did not differ between asphyxiated and control pups. Plasma insulin concentrations remained elevated during asphyxia and the usual neonatal surge of plasma glucagon was significantly delayed. Neonatal asphyxia increases catecholamines, causes lactic acidemia, and alters insulin and glucagon levels. The interactions between these variables alters the normal pattern of glucose availability during the neonatal period.

Animals↗