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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2019  |  Volume : 30  |  Issue : 3  |  Page : 738-740
A very rare pathogen in peritoneal dialysis peritonitis: Serratia liquefaciens

1 Department of Nephrology, Gazi University Faculty of Medicine, Ankara, Turkey
2 Department of Infectious Diseases, Gazi University Faculty of Medicine, Ankara, Turkey

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Date of Submission03-May-2018
Date of Decision10-Jul-2018
Date of Acceptance15-Jul-2018
Date of Web Publication26-Jun-2019


Peritoneal dialysis (PD) peritonitis has been decreasing in frequency in recent years. However, it still causes significant morbidity and mortality. Nearly 1%–6% of all peritonitis attacks result in death. Hospitalizations, loss of PD access, and intravascular catheter insertion for hemodialysis are some examples of morbidity. Approximately 15%–20% of the infectious mortality of PD patients is attributed to peritonitis. The responsible pathogens are usually Gram-positive bacteria, but unusual pathogens may be present. Prognosis is worse when Gram-negative and fungal pathogens are involved. We report a case of Serratia liquefaciens peritonitis due to defiance of hygienic practices which presented with severe abdominal pain and fever and led to loss of PD access.

How to cite this article:
Helvaci O, Hızel K, Guz G, Arinsoy T, Derici U. A very rare pathogen in peritoneal dialysis peritonitis: Serratia liquefaciens. Saudi J Kidney Dis Transpl 2019;30:738-40

How to cite this URL:
Helvaci O, Hızel K, Guz G, Arinsoy T, Derici U. A very rare pathogen in peritoneal dialysis peritonitis: Serratia liquefaciens. Saudi J Kidney Dis Transpl [serial online] 2019 [cited 2020 Sep 22];30:738-40. Available from: http://www.sjkdt.org/text.asp?2019/30/3/738/261363

   Case Report Top

A 68-year-old male patient on peritoneal dialysis (PD) for seven years presented with complaints of severe abdominal pain, nausea, and vomiting. He was compliant with his treatments. He had no history of prior peritonitis. His dialysis dose and ultrafiltration were adequate. Residual urine was around 500 mL/day. He had a fever of 39°C. Effluent was cloudy in appearance with 4900 leukocytes/mm3 (neutrophils, >90%). Gram staining of the effluent was abundant with leukocytes but with no bacteria. BACTEC ® blood culture bottle was used for culture (BACTEC, Kent, UK). Empiric treatment with intraperitoneal ceftazi-dime (20 mg/kg, rounded to 1500 mg) and intraperitoneal vancomycin (15 mg/kg) was employed. When questioned for a cause, he admitted that he had been working on the construction site of a house in a forested area. He had been doing the exchanges there and rarely washed his hands. His pain required narcotic analgesics. To exclude an unexpected pathology, plain abdominal X-rays and ultrasound were done. No specific pathology was observed. His exchanges were switched to six times a day, and dwell volume was decreased to 1500 mL. Heparin was added to each exchange. His leukocyte counts declined, and fever subsided, but a discharge problem developed and pain persisted. Due to atypical course of the case, a computed tomography scan was done which revealed findings of peritonitis but no signs of perforation or obstruction. The effluent was evaluated for acid-fast bacilli and fungi with specific stains which were negative. In addition, specific cultures for fungal, mycobacterial, and anaerobic pathogens were taken (in the end, all came back negative). On the 3rd day of treatment, Serratia liquefaciens was detected in the peritoneal fluid culture and was sensitive to all antibiotics. Because this bacterium is so rare and can be confused with other species in Serratia genus, in automated blood culture results, matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI- TOF MS) was employed which revealed that the bacterium was S. liquefaciens. Vancomycin was stopped, and ceftazidime treatment was continued. In the meantime, the patient lost his residual urine. Despite increasing the amount of heparin added to the PD exchanges, and increasing the PD cycles patient was unable to drain nearly half of the PD fluid. On the 5th day of treatment, bilateral pleural effusions developed. The patient initially refused to change the modality to hemodialysis (HD). Thoracentesis sample was compatible with leakage from the peritoneal fluid with very high glucose levels. The patient was followed up with intermittent thoracenteses. Despite 14 days of intraperitoneal antibiotic treatment and sterile PD effluent, the patient’s pain and discharge problem persisted. After extensive counseling, he agreed to convert to HD. The PD catheter was pulled out, and his pain subsided. Treatment was switched to intravenous route, and he completed 21–day course of antibiotics.

After 11 months on HD, he presented with a liver abscess and left gastric artery pseudo-aneurysm, leading to gastrointestinal bleeding complicated by sepsis, and he died after two months of intensive care admission. His relatives did not consent for autopsy. In that episode, blood, abscess, and catheter cultures were negative for S. liquefaciens.

   Discussion Top

S. liquefaciens is a Gram-negative bacterium from Serratia spp., and is a rare human pathogen, frequently found in soil, plants, and unpasteurized milk.[1],[2] S. liquefaciens is relatively similar to Serratia marcescens, most important pathogen of the Serratia family, additional laboratory evaluation is required for differentiation.[1] In our case, we used MALDI- TOF MS to differentiate S. liquefaciens.[3]

Here, we report the case of a PD patient with S. liquefaciens peritonitis. The patient presented with severe pain and fever and lost his PD access in the end. This is the second case reported in the past 30 years.

S. liquefaciens is a pathogen that can be isolated from very different clinical specimens, can produce infectious presentations with unusual courses, and can even affect immuno-competent individuals.[4] Several reports have been made on abscesses of various organs, infected aneurysms, endocarditis, septic arthritis, meningoencephalitis, urinary tract infection, hospital outbreaks, complementary medicine practices, swordfish injury, and bacte-remia. Data from retrospective studies predict that bacteria will be detected in 0.1% or less of human blood cultures.[1],[5],[6] Hospital-acquired outbreaks are due to pathogen’s ability to contaminate medical devices, due to blood bank products, and may easily occur when adequate measures of hygiene are not undertaken.[1],[7],[8],[9],[10]

S. liquefaciens has been isolated from contact lenses, endoscopes, cystoscopes, newborn nasogastric tubes, whole blood, fresh frozen plasma, blood bank preservative solutions, disinfectants, and soaps.[1] An interesting epidemic for nephrologists was an outbreak with the use of pooled erythropoietin alpha used in a dialysis unit in Colorado, USA, followed by bacterial infection in ten patients and pyro-genic reactions in six patients. All patients recovered with antimicrobial treatment. S. liquefaciens was isolated from empty vials, pooled vials, disinfectants, and antibacterial soaps. After abandoning the use of pooled erythropoietin alpha, the outbreak ceased.[11] As far as the present case is concerned, the most likely route of transmission was direct contact from soil because he unfortunately abandoned sanitary precautions while working in the construction site.

While antibiotic response is variable, hospital-acquired isolates may exhibit a wide range of antibiotic resistance.[12] In our patient, catheter was lost despite proper antibiotic treatment. Severe pain in the course of PD peritonitis is expected in complicated, neglected cases or streptococcal peritonitis.[13] PD peritonitis with S. liquefaciens has been reported only once previously.[14] Very little detail about the patient was given, but it was stated that, after a 21 -day uneventful course of oral antibiotics, the patient was cured. Because no other peritonitis has been reported with S. liquefaciens in literature, we cannot comment on whether opioid-requiring pain was related with bacterium or the patient. Abscess and pseudoaneu-rysm might be attributed to S. liquefaciens, but none of the cultures obtained were positive for the bacteria; hence, we may never know for sure if these were the sequels of peritonitis episode or not.

   References Top

Mahlen SD. Serratia infections: From military experiments to current practice. Clin Microbiol Rev 2011;24:755-91.  Back to cited text no. 1
Machado SG, da Silva FL, Bazzolli DM, Heyndrickx M, Costa PM, Vanetti MC. Pseudomonas spp. and Serratia liquefaciens as predominant spoilers in cold raw milk. J Food Sci 2015;80:M1842-9.  Back to cited text no. 2
Jang KS, Kim YH. Rapid and robust MALDI- TOF MS techniques for microbial identification: A brief overview of their diverse applications. J Microbiol 2018;56:209-16.  Back to cited text no. 3
Gutiérrez-González E, Peteiro C, Toribio J. Skin granulomatous infection caused by Serra-tia liquefaciens in an immunocompetent patient. Int J Dermatol 2014;53:e217-8.  Back to cited text no. 4
Coelho A, Lobo M, Martins V, et al. Serratia liquefaciens infection of a previously excluded popliteal artery aneurysm. EJVES Short Rep 2016;34:1-4.  Back to cited text no. 5
Choi HJ. Cervical necrotizing fasciitis resulting in acupuncture and herbal injection for submental lipoplasty. J Craniofac Surg 2014; 25:e507-9.  Back to cited text no. 6
Ikumapayi UN, Kanteh A, Manneh J, Lamin M, Mackenzie GA. An outbreak of Serratia liquefaciens at a rural health center in the Gambia. J Infect Dev Ctries 2016;10:791-8.  Back to cited text no. 7
Arı A, Ilgın Olut A, Ay B, Tosun S, Zencir M, Çayıröz MU. A small outbreak of Serratia liquefaciens bacteremia due to use of contaminated saline infusion solution for myocardial perfusion scintigraphy. Infect Dis (Lond) 2017;49:639-40.  Back to cited text no. 8
Dubouix A, Roques C, Segonds C, et al. Epidemiological investigation of a Serratia lique-faciens outbreak in a neurosurgery department. J Hosp Infect 2005;60:8-13.  Back to cited text no. 9
Roth VR, Arduino MJ, Nobiletti J, et al. Transfusion-related sepsis due to Serratia liquefa-ciens in the United States. Transfusion 2000; 40:931-5.  Back to cited text no. 10
Grohskopf LA, Roth VR, Feikin DR, et al. Serratia liquefaciens bloodstream infections from contamination of epoetin alfa at a hemodialysis center. N Engl J Med 2001;344:1491-7.  Back to cited text no. 11
Traub WH. Antibiotic susceptibility of Serratia marcescens and Serratia liquefaciens. Chemotherapy 2000;46:315-21.  Back to cited text no. 12
Li PK, Szeto CC, Piraino B, et al. Peritoneal dialysis-related infections recommendations: 2010 update. Perit Dial Int 2010;30:393-423.  Back to cited text no. 13
Rose TF, Ellis-Pegler R, Collins J, Small M. Oral pefloxacin mesylate in the treatment of continuous ambulatory peritoneal dialysis associated peritonitis: An open non-comparative study. J Antimicrob Chemother 1990;25:853-9.  Back to cited text no. 14

Correspondence Address:
Ozant Helvaci
Department of Nephrology, Gazi University Faculty of Medicine, Ankara
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DOI: 10.4103/1319-2442.261363

PMID: 31249244

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