No abstract

No abstract

No abstract

No abstract

No abstract

Summary. Seven (27 %) of 26 gentamicin-resistant human clinical isolates of Escherichia coli were resistant to the veterinary aminoglycoside antibiotic apramycin. A gentamicin-resistant Klebsiella pneumoniae isolate from a patient infected with gentamicin/apramycin-resistant E. coli was also resistant to apramycin. DNA hybridisation studies showed that all gentamkin/ apramycin-resistant isolates contained a gene encoding the enzyme 3-N-aminoglycoside acetyltransferase type IV (AAC[3]IV) that mediates resistance to gentamicin and apramycin in bacteria isolated from animals. Seven of the eight gentamicin/apramycin-resistant isolates were also resistant to the veterinary antihelminthic agent hygromycin B, a phenomenon observed previously in gentamicin/apramycin-resistant Enterobacteriaceae isolated from animals. Resistance to gentamicin/apramycin and hygromycin B was cotransferable in six of the isolates. Restriction enzyme analysis of plasmids in apramycinresistant transconjugants derived from E. coli and K. pneumoniae isolates from the same patient were virtually identical, suggesting that inter-generic transfer of plasmids encoding apramycin resistance had occurred in vivo. These findings support the view that resistance to gentamicin and apramycin in clinical isolates of E. coli results from the spread of resistant organisms from animals to man, with subsequent inter-strain or inter-species spread, or both, of resistance genes on transferable plasmids.

No abstract

The Lough Neagh catchment area covers about one‐third of the land area of Northern Ireland. This report documents NO2− concentrations in the major rivers entering Lough Neagh, which are frequently in the range of 100 to 150 μg N L−1 and exceed the European Community (EC) water quality guide values. The contribution of land drainage to NO2− loads carried by these rivers was estimated to be about 40%. The remaining 60% of NO2− appears to originate from N transformations at the sediment‐water interface of the river system. The available evidence suggests that NH+4 originating from agricultural pollution provides the N substrate for nitrification by Nitrosomonas to NO2−. What is anomalous is why this NO2− is not further oxidized rapidly to NO−3 by Nitrobacter. A possible mechanism is that the Nitrobacter is retarded by the presence of free ammonia concentrations that can be predicted to be present in the range of 65 to 76 μg N L−1.