Mycobacterium chlorophenolicum: An uncommon cause of peritonitis in a peritoneal dialysis patient

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We report the first case of Mycobacterium chlorophenolicum peritonitis in a 48‐year‐old woman on peritoneal dialysis (PD). She had end‐stage renal failure due to IgA nephropathy and also suffered from rheumatoid arthritis, receiving low dose prednisolone (5 mg alternate days). She presented with mild abdominal pain associated with cloudy PD effluent (total cell count (TCC) 150/cm3), without any evidence of tenckhoff catheter exit‐site infection. As per regional protocol, empirical intraperitoneal (IP) cefazolin and amikacin was commenced with rapid subsidence of symptoms. Direct Gram stain and bacterial culture were unrevealing. After 2 weeks of treatment, the peritonitis had resolved and the TCC came down to 12/cm3. However, a week later, the PD effluent became cloudy again with a TCC rebounding to 204/cm3. Treated as a case of relapse, IP cefazolin and amikacin were reinstituted but subsequently switched to IP vancomycin and amikacin in view of poor response. Thereafter, TCC descended but lingered between 50‐75/cm3. Repeated Gram smears, bacterial and fungal cultures were all persistently negative. Eventually, the initial PD effluent had grown acid‐fast bacilli after an interval period of 7 weeks. While awaiting the full identity of the isolate, she was empirically initiated on isoniazid, rifampicin, levofloxacin and pyrazinamide for suspected Mycobacterium tuberculosis peritonitis. In the end, M. chlorophenolicum was isolated and sensitivity testing demonstrated susceptibility to amikacin, ciprofloxacin and clarithromycin but resistance to cefoxitin. In view of the prolonged course of IP amikacin given, with the potential for resistance development, the patient was started on ciprofloxacin and clarithromycin. The patient was maintained on ciprofloxacin and clarithromycin for a total of 6 months, resulting in total resolution.
Mycobacterium chlorophenolicum is a rapidly growing acid‐fast bacillus that was initially misclassified as Rhodococcus chlorophenolicus.1 Usually, it grows within 7 days at an optimal temperature of 28–30 °C on a solid medium. Despite being a rapidly growing organism, the time to positive culture may take longer, when the microbial load in the testing specimen is initially low. In our illustrated case, the isolate required 2 months for growth and identification, resulting in diagnostic confusion with slow growing M. tuberculosis. Currently, molecular techniques are available to hasten identification and commonly used PCR targets with high specificity include 16 s rRNA, heat shock protein‐65, and rpoB genes.3
The mode bacterial transmission into the peritoneal cavity is likely to be via touch contamination of the catheter during peritoneal fluid exchange as isolates are generally found in soil. To our knowledge, this environmental pathogen has never been reported to cause any clinical disease. In this particular case, the possible predisposing factors rendering our patient susceptible include renal failure and long‐term corticosteroid therapy.
The optimal duration of treatment is unclear but a prolonged course of therapy was given due to unknown pathogenicity of M. chlorophenolicum. Our experience suggests that M. chlorophenolicum peritonitis can be successfully eradicated without recurrence using appropriate antibiotics. Furthermore, tenckhoff catheter removal was unnecessary. Importantly, his PD exchange technique was re‐educated to prevent further episodes of peritonitis resulting from touch contamination.
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