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Biomedical subjects

L Gutmann

Publications and source records attributed to L Gutmann.

296 records · Page 17Linked to original sources

Acquired versus familial demyelinative neuropathies in children.

The electrophysiologic differences between chronic acquired demyelinative neuropathy and the demyelinative form of Charcot-Marie-Tooth disease have recently been reported. The present report extends these observations to include the genetically determined demyelinating neuropathies seen in metachromatic leukodystrophy, Krabbe's leukodystrophy, and Cockayne's syndrome. The electrophysiologic features of metachromatic leukodystrophy (five patients), Krabbe's (four patients), and Cockayne's syndrome (three patients) were all similar. There was uniform slowing of conduction (both in different nerves and in different nerve segments), and conduction block was not seen. These findings are consistent with a uniform degree of demyelination in multiple nerves and throughout the entire length of individual axons. Thus, uniform slowing of nerve conduction constitutes strong evidence for a familial demyelinative neuropathy, as opposed to the multifocal slowing seen in acute and chronic acquired demyelinative neuropathy.

Adolescent↗

Mechanisms and spread of fluoroquinolone resistance in Streptococcus pneumoniae.

The development of fluoroquinolones (FQs) with enhanced activity against Streptococcus pneumoniae is a potential advance in the treatment of pneumococcal infections, particularly those due to beta-lactam-resistant pneumococci. However, FQ-resistant clinical isolates selected by the older FQs have already been reported, with mutation(s) in both FQ targets conferring cross-resistance to newer FQs. It is likely that recombinational events between topoisomerase genes from related species of streptococci contribute to the spread of FQ resistance in S. pneumoniae. A scenario resembling that of the worldwide spread of resistance to beta lactams should be anticipated.

Anti-Infective Agents↗

Plasmid-mediated beta-lactamase (TEM-7) involved in resistance to ceftazidime and aztreonam.

TEM-7, a novel TEM-type beta-lactamase (pI 5.41) encoded on a plasmid of approximately 85 kilobases, was found in a clinical isolate of Citrobacter freundii. Strains containing this enzyme exhibited decreased susceptibility to ceftazidime (64-fold) and aztreonam (16-fold) but not to other third-generation cephalosporins. Addition of a beta-lactamase inhibitor--clavulanic acid, sulbactam, or YTR 830--restored normal susceptibility to associated compounds such as ampicillin, piperacillin, ceftazidime, and aztreonam. DNA-DNA hybridization of an intragenic probe of TEM-1 occurred with a 19-kilobase EcoRI fragment of the plasmid encoding TEM-7. A TEM-2 derivative, TEM-201, with characteristics similar to those of TEM-7 was selected spontaneously in the presence of ceftazidime in vitro.

Aztreonam↗

Some properties of Serratia marcescens, Salmonella paratyphi A, and Enterobacter cloacae with non-enzyme-dependent multiple resistance to beta-lactam antibiotics, aminoglycosides, and quinolones.

Non-enzyme-dependent multiple-drug resistance occurs preferentially in some genera of Enterobacteriaceae, such as Serratia, Klebsiella, Enterobacter, and Salmonella. Susceptibility to beta-lactam antibiotics, aminoglycosides, quinolones, trimethoprim, and chloramphenicol may be affected in various combinations in different mutants. Proteins from the outer and inner membranes and lipopolysaccharides may be altered concomitantly. Although porin alterations have been observed in all resistant mutants studied, these modifications alone do not seem sufficient to explain the various cross-resistance phenotypes.

4-Quinolones↗

[Kingella kingae osteomyelitis].

A case of Kingella kingae osteomyelitis characterized by an early onset of cellulitis, positive blood culture and negative bone scintigraphy is reported. Exclusive of vertebral involvement, eleven cases have been described in the pediatric literature. The bacterial nature of this disorder may prove hard to demonstrate since fever, leucocytosis, and increased CRP levels are inconstant. The difficulties of isolation and growth of Kingella kingae as well as its likely resistance to antistaphylococcal agents constitute the main features of this type of infection.

Bacterial Infections↗

In vivo and in vitro emergence of simultaneous resistance to both beta-lactam and aminoglycoside antibiotics in a strain of Serratia marcescens.

In a patient with Serratia marcescens bacteraemia, a variant resistant to cefotaxime and amikacin was isolated in a blood culture under combined treatment with cefotaxime and amikacin. In addition, in vitro selection on cefotaxime and/or amikacin yielded resistant mutants from the sensitive parent strain. These mutants displayed the same type of cross-resistance as the clinical strain to all beta-lactam and aminoglycoside antibiotics. The mechanism for this resistance was a decrease in the permeability of the cell. To our knowledge, the isolation of such strains from blood cultures and the mechanism responsible for this "broad-spectrum resistance" have not been previously described.

Aminoglycosides↗