Pseudomonas putida causing peritoneal dialysis-associated peritonitis

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Peritoneal Dialysis International, Vol. 25, pp. 503–505 Printed in Canada. All rights reserved.

0896-8608/05 $3.00 + .00 Copyright © 2005 International Society for Peritoneal Dialysis

CORRESPONDENCE

Intracorporeal Ultrafiltration with Icodextrin for the Treatment of Severe Overhydration

K. Okada* N. Maruyama O. Oikawa T. Yamazaki T. Higuchi K. Matsumoto Division of Nephrology and Endocrinology Department of Medicine Nihon University School of Medicine Tokyo, Japan *e-mail: [email protected] REFERENCES 1. Paganini EP, Fouad F, Tarazi RC, Bravo EL, Nakamato S. Hemodynamics of isolated ultrafiltration in chronic hemodialysis patients. Trans Am Soc Artif Intern Organs 1979; 25:422–5. 2. Ho-dac-Pannekeet MM, Schouten N, Langendijk MJ, Hiralall JK, de Waart DR, Struijk DG, et al. Peritoneal transport characteristics with glucose polymer based dialysate. Kidney Int 1996; 50:979–86. 3. Okada K, Urae J, Takahashi S. New prescription of peritoneal dialysis: intermittent ambulatory peritoneal dialysis. Nephron 1996; 74:459–61.

Pseudomonas putida Causing Peritoneal Dialysis-Associated Peritonitis Editor: Peritonitis is one of the most frequent and serious complications of peritoneal dialysis (PD) (1). Gram-negativeassociated peritonitis, previously less commonly seen compared to gram-positive-associated peritonitis, has become more prominent in recent years (2,3). Gramnegative organisms are thought to be associated with the gastrointestinal tract and are difficult to treat. Pseudomonas aeruginosa peritonitis requires 3 weeks of treatment 503

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Editor: The extracorporeal ultrafiltration method (ECUM) (1) has been used for treatment of severe overhydration in patients with chronic renal failure at the predialytic stage. Because the number of patients with diabetes mellitus is increasing, the number of chronic renal failure patients with nephrotic syndrome is also increasing. Nephrotic syndrome results in severe overhydration requiring periodic extracorporeal ultrafiltration. Icodextr in-based peritoneal dialysis (PD) solution was introduced to manage sustained ultrafiltration over a long dwell time (2). Because PD with icodextrin can be used to manage patients who need periodic ultrafiltration, we attempted the intracorporeal ultrafiltration method (ICUM). A 76-year-old woman with chronic renal failure and nephrotic syndrome due to diabetes mellitus was admitted to our hospital in October 2004 for severe overhydration. Her blood pressure was 170/90 mmHg and her body weight was 59.2 kg. Urinalysis and blood tests yielded the following: urinary protein excretion 5.4 g/day, urine volume 900 mL/day, serum urea nitrogen 77.2 mg/dL, serum creatinine 2.98 mg/dL, 24-hour creatinine clearance 24.6 mL/minute/1.73 m2, serum total protein 4.2 g/dL, serum albumin 2.2 g/dL. Because the patient’s body weight did not reduce with administration of diuretics, albumin, or human atrial natriuretic peptide, ECUM was started and the patient’s body weight decreased to 50.6 kg. However, in November, the patient complained of acute dyspnea. Imaging examination revealed congestive heart failure due to acute myocardial infarction. The patient’s body weight had been decreased to 39.8 kg by periodic ultrafiltration (approximately 1400 mL per time, 3 times per week). However, severe general fatigue ensued; thus, the patient and her family requested PD. We decided upon intermittent ambulatory PD (3), consisting of 1500 mL icodextrin for a single exchange overnight (10 hours), 5 times per week, with water intake restricted to 500 mL per day. Ultrafiltration volume was approximately 450 mL per time.

In the present case, ICUM with restricted water intake was performed without causing general fatigue. This approach considerably improved the patient’s quality of life.

CORRESPONDENCE

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PDI

Isolates of P. putida were not found in specimens before 1980. Pseudomonas putida was recovered from blood culture specimens between 1980 and 1985 in 15 patients with cancer (6). Sources of infection included pneumonia, phlebitis, cellulitis, and catheter related. Therapy included antibiotic and, in the cases of catheter-related infection, catheter removal. All patients recovered from their infection. In in vitro susceptibility testing, 90% of the isolates were susceptible to piperacillin, ceftazidime, imipenem, and ciprofloxacin. There is only one case of reported contamination of heparin sodium with P. putida (7). Between 1988 and 1993, P. putida infection was identified in 53 Taiwanese patients (8). Pseudomonas putida was cultured, in decreasing order of frequency, from urine, sputum, blood, wound discharge, peritoneal fluid, cerebrospinal fluid, and umbilical swab. Nosocomial infections were associated with 55% of these infections. The fatality rate was 29% in the 41 patients with clinical disease. In vitro susceptibility tests suggested that imipenem and ceftazidime were more effective than other antimicrobial agents. Pseudomonas putida was isolated from 4 patients during an infectious outbreak in Japan (9); P. putida was isolated from a sink used to prepare intravenous fluids using contaminated glass syringes. Pulsed-field gel electrophoresis, a technique to characterize antimicrobial susceptibility patterns, was used to identify the source of infection (10). Pseudomonas putida is a pathogen found in the hospital environment and results in nosocomial infections. Szeto et al. reviewed 850 consecutive PD-associated peritonitis episodes over a 5-year period (from January 1995 to December 1999) in one Hong Kong hospital and found 104 cases (12%) of pure Pseudomonas infection (11). Of these, only 3 cases (2.9%) were due to P. putida. No specific details regarding these three cases were given since the authors were reviewing the management and outcome of Pseudomonas peritonitis, with P. aeruginosa constituting 90.4% of the cases. Our patient had several risk factors resulting in P. putida peritonitis. She has a history of cancer, albeit inactive at this time, and she was seen in the PD clinic earlier that day, where the pathogen might have been present. Fortunately, no other case of P. putida peritonitis developed in our patient population. Diarrhea may have resulted in transmigration of bacteria across the bowel wall. In other patients with diarrhea preceding peritonitis, the organism is generally gram-negative. Had the patient performed her evening and night peritoneal exchanges, the washout of the peritoneal space may have removed the organism if transmigration was the means of exposure.

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with two antibiotics; if it does not respond to antibiotic therapy, it requires catheter removal (4). We report the first case of PD-associated Pseudomonas putida peritonitis diagnosed and successfully treated outside Asia. The patient is a 62-year-old Caucasian female who has had end-stage renal disease (ESRD) of unknown etiology since 1988. Due to a childhood trauma, the patient has a solitary kidney. As an adult, she experienced toxemia of pregnancy. Her ESRD treatment modalities include 7 years of renal transplantation and 9 years of PD, with shortterm hemodialysis as a bridge before and after renal transplantation. The usual ESRD comorbidities of hypertension, anemia, secondary hyperparathyroidism, and hypercholesterolemia were being treated with diet and/or standard medications. Her immune system was compromised by immunosuppressive medications during renal transplantation, breast cancer, which was diagnosed 5 years ago and treated with mastectomy and tamoxifen, and also by endometrial cancer diagnosed 2 years ago and probably associated with tamoxifen therapy. She had two peritonitis episodes (gram-positive and P. putida) over a 9-year period. An ongoing P. aeruginosa skin infection juxtaposed to the exit site and catheter tunnel but not contiguous with either one was treated with sterile ophthalmic gentamicin drops. The episode of P. putida peritonitis was preceded by daytime diarrhea. Due to intense discomfort, the patient did not perform PD exchanges for over 15 hours, that is, the evening and night exchanges. She presented the next day with cloudy peritoneal effluent and abdominal pain. There was no history of recent antibiotic treatment to put her at risk for Pseudomonas peritonitis. There was no concomitant exit-site infection at that time. She was not exposed to any new or unusual activities during the prior weeks. Initially, the patient was given empiric cefazolin and ceftazidime, 1 g each in 2 L peritoneal fluid, with a 6-hour dwell period daily. The PD effluent culture grew P. putida sensitive to amikacin, cefotaxime, ceftazidime, ceftriaxone, ciprofloxacin, gentamicin, imipenem, levofloxacin, piperacillin, ticarcillin, and tobramycin. She received 2 weeks of daily intraperitoneal ceftazidime and oral ciprofloxacin, which resulted in successfully eradicating the P. putida infection. Pseudomonas spp are aerobic, non spore-forming gram-negative rods found in water, soil, and plants. Like P. aeruginosa, P. putida produces pyoverdine, a watersoluble yellow-green or yellow-brown pigment that fluoresces under short wavelength UV light. Unlike P. aeruginosa, P. putida does not possess a distinctive colony morphology or odor. It grows at 4°C; P. aeruginosa grows at 42°C. Pseudomonas putida does not reduce nitrate or produce gas from nitrate (5).

SEPTEMBER 2005 – VOL. 25, NO. 5

PDI

SEPTEMBER 2005 – VOL. 25, NO. 5

CORRESPONDENCE

S.Q. Lew1* A. Gruia2 Division of Renal Diseases and Hypertension1 Department of Medicine George Washington University Gambro Healthcare2 Washington, DC, USA *e-mail: [email protected]

REFERENCES 1. Piraino B. Peritonitis as a complication of peritoneal dialysis. J Am Soc Nephrol 1998; 9:1956–64. 2. Piraino B, Bernardini J, Florio T, Fried L. Staphylococcus aureus prophylaxis and trends in gram-negative infections in peritoneal dialysis patients. Perit Dial Int 2003; 23: 456–9. 3. Zelenitsky S, Barns L, Findlay I, Alfa M, Ariano R, Fine A, et al. Analysis of microbiological trends in peritoneal dialysis-related peritonitis from 1991 to 1998. Am J Kidney Dis 2000; 36:1009–13. 4. Keane WF, Bailie GR, Boeschoten E, Gokal R, Golper TA, Holmes CJ, et al. Adult peritoneal dialysis-related peritonitis treatment recommendations: 2000 update [Published erratum appears in Perit Dial Int 2000; 20:828–9]. Perit Dial Int 2000; 20:396–411. 5. Kiska DL, Gilligan PH. Pseudomonas. In: Murray PR, Baron EJ, Jorgensen JH, Pfaller MA, Yolken RH, eds. Manual of Clinical Microbiology. 8th ed. Washington, DC: ASM Press; 2003: 719–28. 6. Anaissie E, Fainstein V, Miller P, Kassamali H, Pitlik S, Bodey GP, et al. Pseudomonas putida. Newly recognized pathogen in patients with cancer. Am J Med 1987; 82: 1191–4. 7. Reported contamination of heparin sodium with Pseudomonas putida. MMWR Morb Mortal Wkly Rep 1986; 35:123–4. 8. Yang CH, Young T, Peng MY, Weng MC. Clinical spectrum of Pseudomonas putida infection. J Formos Med Assoc 1996; 95:754–61. 9. Torii K, Yasunobu N, Miyazaki Y, Ohta M. An unusual outbreak of infusion-related bacteremia in a gastrointestinal disease ward. Jpn J Infect Dis 2003; 56:177–8. 10. Weng LC, Liaw GJ, Wang NY, Wang SF, Lee CM, Huang FY, et al. Investigation of an outbreak of Pseudomonas putida using antimicrobial susceptibility patterns, pulsed-field gel electrophoresis of genomic DNA and restriction fragment length polymorphism of PCR-amplified rRNA operons. J Microbiol Immunol Infect 1999; 32:187–93. 11. Szeto CC, Chow KM, Leung CB, Wong TY, Wu AK, Wang AY, et al. Clinical course of peritonitis due to Pseudomonas species complicating peritoneal dialysis: a review of 104 cases. Kidney Int 2001; 59:2309–15.

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The relationship of the juxtaposed P. aeruginosa skin infection to her exit site and tunnel to P. putida peritonitis is not clear. One wonders whether the prolonged skin infection or underlying disease processes predisposed her to other Pseudomonas infections. She was treated successfully with two antibiotics, namely cef tazidime and ciprofloxacin, for only 2 weeks. Two weeks of treatment was used because of the rapid clinical improvement and, especially, the clear PD effluent after a few days of therapy. This suggests that P. putida responds very well to medical therapy. It is of interest that the majority of case reports of P. putida infection are from Asia. It is not clear why this is so. Our patient lives in a multiethnic community, populated predominately with Asians. Neither she nor her family knowingly was exposed to anyone that had traveled to Asia recently. Likewise, no staff member from the dialysis unit who was in contact with her during her monthly visit had traveled to Asia or was exposed to anyone recently from Asia. Pseudomonas putida will probably be recognized more frequently as a pathogen. It appears in immunocompromised patients such as those with cancer or renal failure. It is found in medical facilities and may be the cause of nosocomial infections. Pseudomonas putida is generally considered less virulent than P. aeruginosa. Currently, P. putida responds remarkably well to antimicrobial therapy. Thus, the prognosis for curing P. putida infection is favorable.

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