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Epidemic enteritis in approximately 10 000 newly-imported Macaca fascicularis was common and fell into 2 distinct phases. During the 1st month of quarantine Shigella organisms, often antibiotic resistant, posed a threat to life of the animals. Later, Campylobacter jejuni/coli appeared to be the main organism in infectious enteritis. The clinical syndrome was complicated at all stages by the presence of helminths, virus infections such as measles and pathogenic protozoa, but salmonellae were not usually an important feature. Normal quarantine procedures did not guarantee freedom from either shigellae or salmonellae and serial tests were done in individual cases to ensure this. It was not possible to eradicate Campylobacter jejuni/coli from the colony.

Campylobacter jejuni was recovered from 59 of 505 (11.7 per cent) dogs with diarrhoea as compared with only two of 122 (1.6 per cent) dogs without diarrhoea. However, there was no significant difference between campylobacter isolations from 142 cats with and without diarrhoea. C jejuni infections were commonly associated with chronic diarrhoea in both species and appropriate therapy abolished clinical signs and excretion of the organism in faeces in most cases. C jejuni may be responsible for some forms of enteritis in dogs and cats and is a zoonosis in which the companion animal may be the vector.

R factors conferring high-level resistance to trimethoprim and sulphonamides were identified in bacteria causing infections in patients at three London hospitals in 1971 (Fleming, Datta & Griineberg, 1972). All were members of the W compatability group and came from the Camden area (Datta & Hedges, 1972). In April 1972 strains of Escherichia coli highly resistant to trimethoprim were isolated from calves at Frant, Kent, which is about 30 miles from the Camden area of London. The calves had been treated with large doses of a trimethoprim-sulphonamide preparation (Fleming, in preparation). The trime t hoprim-resistant strains had various patterns of multiple drug resistance (always including resistance to sulphonamides) and from them various R factors were transferred to E. coli KI2. Trimethoprim resistance was transferred with resistance to streptomycin, separately from resistance to sulphonamides or other drugs. Methods were as described previously (Fleming et al. 1972). An example of the trimethoprim-streptomycin resistance factors (R483) was studied in strains of Escherichia coli K12. Methods were as described by Datta & Hedges (1972) and by Coetzee, Datta & Hedges (1972).

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