doctors' office equipment that is available is, of course, very attractive to the practicing physician. Do not fight it. Help manage it. Provide advice, consultation, quality control support, back-
up testing, reflex testing. OR, provide the instrument as part of a laboratory package. Broadcasting is gainful employment, but you originally went into laboratory
medicine. Adapting to changes in the ways suggested may allow you to continue in that primary role. (If not, it is always possible Dan Rather will walk off again . . . . )
toneal fluid revealed numerous leukocytes but no organisms; approximately 5 mL of fluid was inoculated into aerobic and anaerobic blood culture (Johnston Laboratories, Towson, Md.) bottles. After 3 days' incubation, a curved gram negative boullus that was subsequently identified as Campylobacter coli was recovered. The patient became moderately febrile (peak temperature of 100°F.) and died approximately 40 h after admission. Blood and stool cultures were not collected, and an autopsy was not performed. We are aware of eight previously documented cases of Campylobacter peritonitis (1-7); five occurred in CAPD patients. The organisms recovered from CAPD patients included 3 C. fetus ssp. fetus and 2 C. jejuni. Two of the three CAPD patients with C. fetus infection relapsed following antimicrobial therapy, and one of the relapses included bacteremia (2, 6, 7). Both CAPD patients with C. jejuni peritonitis had concurrent diarrhea; C. jejuni was recovered from the stool of one of these patients and from the stool of a family member of the other patient (2, 4). The isolates recovered from the three patients with spontaneous Campylobacter peritonitis included 2 C. jejuni and 1 C. coli (1, 3, 5); all three patients were bacteremic, and two of the infections were fatal. In reviewing the etiology of Campylobacter peritonitis the results of hippurate hydrolysis were not reported by any of the authors describing C. jejuni peritonitis. This is significant because this is the only routine test that distinguishes C. jejuni from C. coli, and many laboratories do not make this dis-
tinction. It is thus possible that C. coli and C. jejuni were not distinguished from one another in the references cited (2, 3, 4, 5). Campylobacter peritonitis is probably a very rare clinical entity, but it is undoubtedly underdiagnosed because, in many institutions, routine processing of peritoneal fluid may not be optimal for recovering Campylobacter spp. It is unlikely that modifying routine techniques to enhance recovery of these organisms would be cost-effective, but clinicians and microbiologists should be aware of this entity.
Case Reports
Campylobacter Peritonitis Christopher J. Papasian Ph.D. Cynthia Burdick, BSMT(ASCP)
Laboratory Service Veterans Administration Medical Center Kansas City, MO 64128
A 44-year-old man on chronic ambulatory peritoneal dialysis (CAPD) was admitted for evaluation of suspected peritonitis. He had a 12-year history of insulin-dependent diabetes mellitus, which had contributed to his renal failure and bilateral below-theknee amputations. He noted cloudy dialysis fluid on the day prior to admission and complained of diarrhea of 3 days' duration. He denied fevers, sweats, shakes, nausea, and vomiting but did experience some chills. Physical examination revealed a well-developed, well-nourished man with bilateral below-the-knee amputations and an abdominal Tencknoff catheter. He had active bowel sounds throughout, with no rebound or guarding. He was afebrile and had a pulse and blood pressure of 96/min and 90/70 mm Hg, respectively. The peripheral white blood cell count was 8.1 )< 1 0 3 / r a m 3 with 41% polymorphonuclear leukocytes, 42% band cells, 10% lymphocytes, and 7% monocytes. Other laboratory findings were indicative of an insulin-dependent diabetic with chronic renal failure. Peritoneal dialysis fluid was collected for culture, and antimicrobial therapy with gentamicin and vancomycin was initiated. The Gram stain of the peri-
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References 1. H o , H . , M. J. Z u c k e r m a n , a n d S. M.
2.
3.
4.
5.
6. 7.
Polly. 1987. Spontaneous bacterial peritonitis due to Campylobacter coli. Gastroenterology 92:2024- 2025. Kristinson, K. G., R. C. Spencer, and C. B. Brown. 1986. Campylobacter peritonitis in continuous ambulatory peritoneal dialysis. J. Infect. Dis. 13:199-204. McNeil, N. I., S. Buttoo, and G. L. Ridgway. 1984. Spontaneous bacterial peritonitis due to Campylobacterjejuni. Postgrad. Med. J. 60:487-488. Pepersack, F. et al. 1982. Campylobacter jejuni peritonitis complicating continuous ambulatory peritoneal dialysis. J. Clin. Microbiol. 16:739-741. Schrnidt, U. et al. 1980. The clinical spectrum of Campylobacterfetus infections: report of five cases and review of the literature. Q. J. Med. 196:431442. Vemont, S. E., and C. Dominguez. 1982. Campylobacter and peritoneal dialysis. Ann. Intern. Med. 96:534. Wens, R. et al. 1985. Campylobacter fetus peritonitis followed by septicaemia in a patient on continuous ambulatory peritoneal dialysis. J. Infect. Dis. 10:249-251.
Clinical Microbiology Newsletter 10:13,1988