Case Presentation: A 43-year-old male on peritoneal dialysis (PD) was admitted for nausea, vomiting, and abdominal pain. Ten days prior to admission, cloudy effluent was noted during PD, prompting initiation of empiric intraperitoneal vancomycin and ceftazidime therapy. He subsequently developed worsening symptoms leading to his presentation to the hospital.His past medical history was notable for type 1 diabetes mellitus, end-stage renal disease on PD for 2 years, and hypertension. He had been successfully treated for gram-positive cocci PD-associated peritonitis as an outpatient twice, with episodes three months ago and one year ago. Upon admission, the patient was afebrile, tachycardic, and hypertensive. Laboratory studies showed leukocytosis and peritoneal fluid cell count of 3,400 nucleated cells with 65% neutrophils, 15% lymphocytes, and 20% macrophages; no organisms were visualized. Intravenous cefepime and vancomycin were started, his PD catheter was removed, and he began hemodialysis via central venous catheter. However, his symptoms persisted.Four days into admission, the patient’s dialysate fluid grew Mycobacterium chelonae, at which time antibiotics were switched to oral azithromycin, moxifloxacin, and linezolid. His symptoms rapidly improved, and he was discharged home on 8 weeks of oral antibiotic therapy.
Discussion: Most causes of peritonitis in PD patients are directly PD-associated, wherein infection is caused by pathogenic skin bacteria contaminating the PD catheter. Coagulase-negative Staphylococcus aureus is the most common agent, causing 39% of infections (1). PD-associated peritonitis is often managed in the outpatient setting with empiric intraperitoneal antibiotic therapy consisting of both gram-positive and gram-negative coverage.However, 20-40% of cases of peritonitis are culture negative. Among culture-negative peritonitis cases, common agents include mycobacteria, fungi, Nocardia, and Legionella species. Infection with non-tuberculous mycobacteria (NTM) is a rare cause of peritonitis with symptoms indistinguishable from typical bacterial peritonitis. Specifically, M. chelonae is described as the causative organism in 14-37% of cases of NTM peritonitis (2,3). These organisms are generally found in the natural environment and may be harbored in municipal and tap water supplies. In this patient’s case, exposure to M. chelonae was likely from the well water which supplied his home. Most cases of NTM peritonitis have been observed among immunosuppressed patients (4) making this case of M. chelonae in an immunocompetent host highly unusual.Therefore, infection with NTM should be suspected and promptly treated in a patient with recurrent episodes or refractory symptoms despite empiric therapy, as morbidity and mortality is high (5). Successful treatment depends upon source control with catheter removal and appropriate antimicrobial therapy. Choice of therapy should be guided by susceptibility testing and patient response, with duration of therapy often exceeding one month (6).
Conclusions: While most cases of PD-associated peritonitis are due to infection with skin flora, NTM constitute a rare and difficult-to-diagnose cause with poor outcomes. Thus, NTM must be suspected in PD patients with refractory symptoms or poor response to traditional antibiotics, even in those who are immunocompetent. Management ideally includes PD catheter removal and selection of appropriate antimicrobial therapy and duration.