Saudi Journal of Kidney Diseases and Transplantation

LETTER TO THE EDITOR
Year
: 2013  |  Volume : 24  |  Issue : 5  |  Page : 1003--1004

Mycobacterium fortuitum peritonitis in a patient receiving continuous ambulatory peritoneal dialysis


Dwarakanathan Ranganathan, Robert Fassett, George T John 
 Department of Renal Medicine, Royal Brisbane and Women's Hospitals, Herston, Brisbane, Australia

Correspondence Address:
Dwarakanathan Ranganathan
Department of Renal Medicine, Royal Brisbane and Women«SQ»s Hospitals, Herston, Brisbane
Australia




How to cite this article:
Ranganathan D, Fassett R, John GT. Mycobacterium fortuitum peritonitis in a patient receiving continuous ambulatory peritoneal dialysis.Saudi J Kidney Dis Transpl 2013;24:1003-1004


How to cite this URL:
Ranganathan D, Fassett R, John GT. Mycobacterium fortuitum peritonitis in a patient receiving continuous ambulatory peritoneal dialysis. Saudi J Kidney Dis Transpl [serial online] 2013 [cited 2020 Dec 6 ];24:1003-1004
Available from: https://www.sjkdt.org/text.asp?2013/24/5/1003/118073


Full Text

To the Editor,

Mycobacterial infections are a rare cause of peritonitis in patients on continuous ambulatory peritoneal dialysis (CAPD), but pose special diagnostic and therapeutic challenges. Mycobacterial infections could be caused by Mycobacterium tuberculosis or atypical mycobacteriae (AMB). In Australia, during the year 2000, infections with AMB atypical mycobacteriae occurred at a rate of 1.8 cases per 100,000 population. [1] Of the AMB, M. fortuitum is the most common pathogen causing peritonitis. [2] We report a case of peritonitis with M. fortuitum in a patient on peritoneal dialysis (PD).

A 62-year-old man with end-stage renal disease secondary to diabetic nephropathy on CAPD for nine months presented with nausea, vomiting and generalized abdominal pain of three days' duration. The PD fluid was noted to be cloudy and examination showed a white cell count (WCC) of 93/μL with 12% polymorphs and 88% mononuclear cells. The patient was discharged as he was asymptomatic and the repeat WCC remained at 84/μL, with 88% mononuclear cells. Two days later, he was admitted electively when the PD culture showed a rapidly growing mycobacterium. At that stage, the dialysate WCC was 780/μL, with 62% polymorphs and 38% mononuclear cells. The organism was identified as M. fortuitum sensitive to clarithromycin, ciprofloxacin, cefoxitin, imipenem and amikacin. He received intravenous cefoxitin and intraperitoneal amikacin. The Tenckhoff catheter was removed the next day. There was no growth from the exit site swabs or granulation tissue at the catheter site following removal. The Quantiferon-TB Gold assay for M. tuberculosis was negative. The patient completed five days of intravenous cefoxitin and weeks of oral clarithromycin, and was transferred to hemodialysis for two months. PD was recommenced without recurrence of peritonitis. Three months after completing the treatment of peritonitis, the PD adequacy tests were satisfactory: A weekly creatinine clearance: 66, Kt/V 2.09 and protein catabolic rate: 1.03.

AMB colonizations as well as infections are not uncommon in Australia. In 2000, 1447 AMB isolates and 341 (23%) infections were identified, suggesting the ubiquitous nature of these organisms. There was a difference in geographical distribution: Infections were highest in the Northern Territory (4.1 per 100,000 population), followed by Queensland (3.8), and lowest in New South Wales (0.78). The main sites of the infections were the respiratory tract, soft tissue and the lymphatics. Almost all the isolates from lymph node (99.84%) and soft tissue (91.0%) were associated with disease compared with 9.5% of the pulmonary isolates that were thought to be pathogenic. Rapidly growing mycobacteriae, predominantly M. fortuitum, M. abcessus and M. chelonae, caused soft tissue infections, whereas the M. avium complex caused lung lesions.

Soft tissue infections due to M. fortuitum were more prevalent in Queensland, suggesting a significant environmental presence.

A literature review showed there were 23 cases of M. fortuitum PD-related exit site infection or peritonitis worldwide, but none of the cases were reported from Australia. [3] The organism sensitivity to antibiotics and resistance to antitubercular drugs was similar to the antibiogram reported from the Netherlands as well. [4] The PD catheter is often removed in patients with M. fortuitum peritonitis. Treatment for our patient included early microbiological identification, catheter removal, appropriate antibiotics and a prolonged course of oral antibiotics to avoid the potential toxicity of amikacin. [3],[4] It is possible to restart PD with preserved membrane characteristics as in this patient.

References

1Haverkort F; Australian Mycobacterium Reference Laboratory Network; Special Interest Group in Mycobacteria within the Australian Society for Microbiology.. National atypical mycobacteria survey, 2000. Commun Dis Intell. Q Rep 2003;27:180-9.
2White R, Abreo K, Flanagan R, et al. Non-tuberculous mycobacterial infections in continuous ambulatory peritoneal dialysis patients. Am J Kidney Dis 1993;22:581-7.
3Hod T, Kushnir R, Paitan Y, Korzets Z.. Mycobacterium fortuitum infection in continuous ambulatory peritoneal dialysis. Clin Nephrol 2008;70:546-53.
4van Ingen J, van der Laan T, Dekhuijzen R, Boeree M, van Soolingen D. In vitro drug susceptibility of 2275 clinical non-tuberculous Mycobacterium isolates of 49 species in The Netherlands. Int J Antimicrob Agents 2010;35: 169-73.