In a Tunisian hospital 27 babies, including 12 who were premature, in a single intensive care unit suffered acute gastroenteritis in the period from January to May 1988. The mean age at the onset of gastroenteritis was 8.4 days; nine babies died. Salmonella wien was isolated from stools (all babies) and blood (4 babies). It was also isolated from the stools of one nurse and from a mattress. Twelve of the babies had received cefotaxime, which was successfully replaced by oral colimycin. The outbreak was stopped by the implementation of infection control measures. All isolates of Salmonella wien were of the same biotype, and had the same antibiotic resistance pattern (third generation cephalosporins, monobactams, aminoglycosides, chloramphenicol, trimethoprim and sulphonamides) and plasmid DNA restriction pattern. The isolates were all susceptible to a combination of cefotaxime and clavulanic acid (a beta-lactamase inhibitor), which displayed synergy, suggesting the presence of a beta-lactamase (geometric mean MICs 11.24 micrograms/ml for cefotaxime alone and 0.24 micrograms/ml in combination with 0.1 micrograms/ml potassium clavulanate). All isolates produced TEM-1 and SHV-2 beta-lactamase which was not transferable to Escherichia coli by conjugation. The presence of the SHV-2 enzyme in Salmonella wien may allow it to adapt to newer beta-lactams which is a cause for concern in this hospital.