833 bances associated with pneumonia would represent use of an antimicrobial agent.
METRONIDAZOLE-RESISTANT BACTEROIDES FROM UNTREATED PATIENT has emerged as the most useful agent and prevention of anacrobic infections, 1-3 particularly those due to Bacteroides spp. Aerobes and facultative organisms are resistant to metronidazole; all anaerobes are believed to be sensitive, and sensitivity to metronidazole is accepted as confirmation that an organism is an anaerobe .4 In January, 1978, Ingham et al.5 reported the isolation of a strain of Bfragilis ss. fragilis that was resistant to metronidazole ; the minimum inhibitory concentration for their strain was 70 ug/ml and the resistance was stable throughout 16 subcultures. We have isolated a second strain belonging to the B.fragilis group which is resistant to metronidazole; the strain was an obligate anaerobe and has been identified as B.distasonis (B.fragilis ss. distasonis) by the methods of Duerden et al.6 There was no zone of inhibition around a 5 ug metronidazole disc and in agar dilution tests the strain had a consistent minimum inhibitory concentration for metronidazole of 64 µg/ml. In parallel tests the minimum inhibitory concentration of metronidazole for the control strain Bfragilis ss. fragilis NCTC 9343 was 1 fLg/ml. The strain reported by Ingham et al. was isolated from a patient with Crohn’s disease who had been treated with metronidazole for 2 years. Our strain, however, was isolated from a peritoneal swab taken at laparotomy from a 9-year-old boy with an acute suppurative perforated appendix. He had not received any antimicrobial therapy before admission and had never been given metronidazole. There is, therefore, no obvious reason why this patient should have been colonised by a metronidazole-resistant strain of Bacteroides. Metronidazole remains the drug of choice for infections with non-sporing anaerobes, but the assumption that all anaerobes are sensitive may need modification. It is, however, reassuring that, despite the widespread use of metronidazole, resistance amongst Bacteroides spp. remains so rare that the isolation of a single resistant strain is worth reporting.
Department of Infectious Diseases, Geisinger Medical Center, Danville, Pennsylvania 17821, U.S.A.
GARY R. PLOTKIN
CARCINOEMBRYONIC ANTIGEN IN LIVER DISEASE
SIR,—In view of the paper
by Hine et al.’ on serum levels carcinoembryonic antigen (C.E.A.) in liver disease, and the subsequent correspondence, we think it time that consideration be given to the underlying mechanisms which determine these levels. We agree with the spirit of Dr Hall’s comments (Jan. 13, p. 103) but would suggest that the study of C.E.A. is already a "respectable piece of physiology". C.E.A. can no longer be considered even as a tumour-associated molecule, let alone a tumour-specific one. Considerable amounts of C.E.A. can be isolated from colonic washings from healthy individuals and this "normal C.E.A." seems to be the same as that produced in malignancy;2 2-4 mg C.E.A. per day may be secreted from the colon,3and C.E.A. is found in the fasces of healthy individuals.’ of
Hall suggests measurement of C.E.A. levels in bile. We have done this: human gallbladder bile contains 460 ng/ml of C.E.A. (range 80-1300, nineteen samples). These samples gave radioimmunoassay dilution curves parallel to that found with purified C.E.A. from a metastatic colonic carcinoma. Biliary C.E.A. levels are so far above the normal plasma. level (