Salmonella typhimurium strains resistant to most beta-lactams, co-trimoxazole, tobramycin and gentamicin were isolated from patients in two hospitals in Buenos Aires, Argentina, beginning in August 1990. The patients were suffering from meningitis, septicaemia or enteritis. Therapy including ampicillin, ceftriaxone and gentamicin failed. The strains produced a plasmidic (pMVP-4) extended broad-spectrum beta-lactamase which is more active against cefotaxime than against ceftazidime (Vmax for cefotaxime 350 times higher than for ceftazidime). This cefotaximase demonstrates similarity to the previously described CTX-ase-M-1 from Escherichia coli, but it is distinctly different from CTX-ase-M-1 by its isoelectric point (7.9 for CTX-ase-M-2 in comparison with 8.9 for CTX-ase-M-1) as well as in its lower susceptibility to the beta-lactamase inhibitors sulbactam, clavulanic acid, tazobactam and BRL 42715. Thus, the beta-lactamase produced by S. typhimurium strains from Argentina appears to represent a new member (CTX-ase-M-2) of a novel group of plasmidic extended broad-spectrum beta-lactamases designated as cefotaximases.

Argentina↗

PubMedDate not supplied

[Effect of chloroquine on polyanions].

Chloroquine forms complexes with polyanions as does the metachromatic dye pseudoisocyanine. This phenomenon can be used to show chloroquine binding to polyanions. It is shown spectrophotometrically that glycosaminoglycans form complexes with chloroquine more readily than with pseudoisocyanine. Moreover chloroquine abolishes fluorescence of glycosaminoglycan inclusion bodies in leucocytes of mucopolysaccharidosis patients. A woman of 34 suffering from mucopolysaccharidosis type I-S had such inclusion bodies in 19 out of 200 leucocytes examined before and in only two after a month of chloroquine treatment. In heparinized blood chloroquine induces clotting faster than does saline in control samples. This finding suggests inactivation of polyanions by chloroquine binding.

Anions↗