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Year : 2003  |  Volume : 21  |  Issue : 4  |  Page : 284-286

Ralstonia mannitolilytica infection in renal transplant recipient: First report

Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh, India

Correspondence Address:
Department of Microbiology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow - 226 014, Uttar Pradesh, India

 ~ Abstract 

Ralstonia mannitolilytica is being increasingly identified as an opportunist pathogen in immunocompromised patients. We report the first case of post renal transplant infection by R. mannitolilytica, in a 14-year-old recipient. The graft and the patient were saved with prompt microbiological identification, sensitivity testing and subsequent administration of appropriate antibiotic.

How to cite this article:
Mukhopadhyay C, Bhargava A, Ayyagari A. Ralstonia mannitolilytica infection in renal transplant recipient: First report. Indian J Med Microbiol 2003;21:284-6

How to cite this URL:
Mukhopadhyay C, Bhargava A, Ayyagari A. Ralstonia mannitolilytica infection in renal transplant recipient: First report. Indian J Med Microbiol [serial online] 2003 [cited 2021 Feb 25];21:284-6. Available from:

The novel genus Ralstonia includes three main pathogenic species: R. pickettii,  R.gilardii  , R.basiliensis.[1] Ralstonia pickettii biovar 3/thomassii was recently shown to represent a separate species, R.mannitolilytica.[2] It is widely distributed in nature, being a frequent contaminant in water supplies. It is increasingly identified as an opportunistic pathogen in nosocomial infections,[3],[4] especially among immunosuppressed patients.[5] It has also been implicated in common source nosocomial infection outbreaks due to the addition of contaminated water to parenteral fluid[6] and to medical equipment presumed to be sterile.[7] We are reporting the first case of R.mannitolilytica, isolated from the drain fluid of a child with renal transplant.

 ~ Case Report Top

A 14-year male child first presented in June 1999 with complaints of swelling feet and face for last one year with gradual increase in the frequency of micturition. Previous investigation shows he had proteinuria (urine albumin 4+) and microscopic haematuria (4-6 RBCs/HPF). He subsequently developed swelling all over body along with fever, anorexia and vomiting. He was hypertensive and had moderate renal failure with serum creatinine of 3.9 mg/dL. An ultrasound revealed unequal sized kidneys. A probable diagnosis of acute on chronic renal failure was made and the patient was kept on conservative management that included initial intermittent hemodialysis at weekly interval and later was put on continuous ambulatory peritoneal dialysis. Over a period of 25 months, his glomerular filtration rate (GFR) fluctuated from 24 to 14 to 20 mL/min. and the serum creatinine from 3.4 to 7.2 to 5.6 mg/dL. Meanwhile, his mother was identified as the prospective donor and a live related renal transplant was done in October 2001.
Two days post transplant, patient became febrile and his blood, urine and drain fluid were sent to the microbiology department for culture and sensitivity. On examination, there was no tenderness or any visible evidence of intraabdominal sepsis. There were however signs of inflammation at drain site. There was leukocytosis (TLC=19,800/mm3) with high neutrophil count (DLC=N86L13M1E0) and ESR 64mm/hr. Chest X-ray was within normal limits. Ultrasound abdomen did not reveal any abnormality. On microscopy, drain fluid showed gram-negative bacilli with plenty (9-10/HPF) of pus cells. Culture grew non-lactose fermenting, non- pigmented colonies of gram-negative rods that were catalase and oxidase positive, and motile. Acid was oxidatively produced from glucose, L-arabinose, lactose, maltose and mannitol. Alkalization occurred on minimal mineral agar with acetate, serine, malonate, -alanine, succinate, fumarate, butyrate, formate, malate, citrate and lactate, but not with acetamide, allantoin, L-arginine, L-ornithine, maleate and tartarate. They were resistant to desferrioxamine and colistine. No acid was produced from ethylene glycol. Urease, pyrrolidonyl arrylamidase, Tween esterase and phenylalanine deaminase were positive. The nitrate and nitrite reduction tests were negative. The isolate was identified as R.mannitolilytica after being differentiated biochemically from Pseudomonas fluorescens and P. aeruginosa and also from the other Ralstonia species. A commercially available standardized microtitre plate with 95 biochemical tests, Biolog GN Microplate (Biolog, Hayward, California, USA) was used to type the Ralstonia species. Blood and urine cultures collected simultaneously were sterile.
The isolate was found to be sensitive by modified Stokes method to ampicillin (10g), ampicillin-sulbactum (10/10g), amoxycillin (20g), amoxycillin-clavulanic acid (20/10g) and cefaperazone-sulbactum (75/10g), moderately sensitive to piperacillin (100g), cefuroxime (30g), ceftriaxone (30g), and cefotaxime (30g) and resistant to cephalexin (30g), ceftazidime (30g), ciprofloxacin (5g), amikacin (30g) and gentamicin (10g).
Ciprofloxacin and amikacin were started empirically and later it was changed to cefaperazone-sulbactum third day onwards, patient then responded clinically. TLC decreased to 15,400/cmm and ESR to 43mm/hr. The drain fluid sent on fourth day contained the same isolate, although in less number. On sixth day, the patient became afebrile and the drain fluid became sterile. TLC became 9,200/cmm with neutrophil 57% and ESR 37mm/hr. The antibiotic course was however continued for 14 days. No other foci of infection were found anywhere else in the body. The allograft was healthy.
Environmental samples were collected from the antiseptic solutions used, hands of nursing staff and doctors, bed of the patient, dressing tray and drain tube and clamp. None of these samples grew R.mannitolilytica. The samples from the haemodialysis machine and catheters used during previous hospitalization could not be obtained.

 ~ Discussion Top

A limited number of cases of hospital outbreaks with  R.pickettii   biovar 3/thomasii i.e., R.mannitolilytica isolates have been reported in the literature. The first report[8] dealt with bacteremia and bacteremia due to parenteral fluids prepared with deionized water contaminated with P.thomasii. An epidemic of R.pickettii involving 24 patients caused by contaminated saline solution was reported.[9] Although no serious infections related to outbreak have been reported so far, the clinical importance of R.mannitolilytica may have been overlooked, possibly due to misidentification. Most of these isolates are usually misdiagnosed as  P.aeruginosa  . In our case, the organism isolated was unlikely to be a contaminant since it was isolated thrice on three consecutive days from the patient having the same antibiotic sensitivity pattern. Moreover the patient responded dramatically when he was treated with the appropriate antibiotic in accordance with the sensitivity pattern. Patient's leucocyte count gradually diminished and the culture became sterile from sixth day onwards.
Two possibilities can be hypothesized regarding the probable source of infection and the portal of entry for R.mannitolilytica in this patient. One potential portal of entry could be the hemodialysis machines and catheters used to dialyze him every week or the peritoneal dialysis catheter used later on. The patient may have been infected during the previous hospitalization for hemodialysis or by aseptically tampering the peritoneal dialysis catheter. This patient's situation was complicated by the underlying uraemia and corticosteroid therapy. This immune suppression and the trauma of surgery may have facilitated the aggressive course of infection in the post-renal transplant patient. The other possibility could be the postoperative introduction of the pathogen through drain site from skin due to contaminated chlorhexidine gluconate (0.5% alcoholic solution) skin cleansing solution as was reported in a previous study.[4] This could not be confirmed as the solution could however not be traced. There are however reports where no source could be identified.[10] The isolate fortunately was sensitive to a battery of drugs and did not cause any serious damage to the patient or the graft. We believe that it may have caused greater damage, had the correct identification and antibiotic sensitivity of the organism not been done promptly.
This case shows that R.mannitolilytica may be a more virulent pathogen than previously believed. Although no serious non-outbreak related infections have been described thus far, the clinical importance of R.mannitolilytica may have been overlooked, possibly due to misidentification as  P.fluorescens  , Burkholderia multivorans and/or R.pickettii, which are most often treated as contaminant. Therefore, correct identification of this organism is of great importance, especially so in post renal transplant patients. Misdiagnosis of infection in post renal transplant cases is unaffordable since it could lead to graft rejection and even death of the patient, thus demanding strict microbiological vigilance.  

 ~ References Top

1.Yabuuchi E, KosakoY, Yano I, Hotta H, Nishiuchi Y. Transfer of two Burkholderia and an Alcaligenes spp., to Ralstonia gen. Nov.: Proposal of Ralstonia pickettii (Ralston, Palleroni and Doudoroff, 1973) comb. Nov., Ralstonia solanacearum (Smith 1896) comb. Nov. and Ralstonia eutropha (Davis 1969) comb. Nov. Microbiol Immunol 1995;39:897-904.  Back to cited text no. 1    
2.De Baere T, Steyaert S, Wauters G, Des Vos P, Goris J, Coenye T, Suyama T, Verschraegen G, Vaneechoutte M. Classification of Ralstonia pickettii biovar 3/ "thomasii" strains (Pickett, 1994) and of new isolates related to nosocomial recurrent meningitis as Ralstonia mannitolyticus sp. Int J Syst Evol Microbiol 2001;51:547-558.  Back to cited text no. 2    
3.Chomarat M, Lepape A, Riou JY, Flandrois JP. Septicemia a Pseudomonas pickettii. Pathol Biol 1985;33:55-56.  Back to cited text no. 3    
4.Fass RJ, Barnishan J. Acute meningitis due to a Pseudomonas like group Va-1 bacillus. Ann Intern Med 1976;84:51-52.  Back to cited text no. 4    
5.Lacey S, Want SV. Pseudomonas pickettii infections in a paediatric oncology unit. J Hosp Infect 1991;17:45-51.  Back to cited text no. 5  [PUBMED]  
6.Gardner S, Shulman ST. A nosocomial commensal ourbreak caused by Pseudomonas pickettii. Pediatr Infect Dis 1984;3:420-422.  Back to cited text no. 6    
7.Kahan A, Philippon A, Paul G, Weber S, Richard C, Hazebroucq G, Degeorges M. Nosocomial infections by chlorhexidine solution contaminated with Pseudomonas pickettii (biovar Va-1). J Infect 1983;7:256-263.  Back to cited text no. 7    
8.Phillips I, Eykyn S, Laker M. Outbreak of hospital infection caused by contaminated autoclaved fluids. Lancet 1972;i:1258-1260.  Back to cited text no. 8    
9.Pan HJ, Teng LJ, Tzeng MS, Chang SC, Ho SW, Luh KT, Hsieh WC. Identification and typing of Pseudomonas pickettii during an episode of nosocomial outbreak. Zhonghua Min Guo Wei Sheng Wu Ji Mian Yi Xue Za Zhi 1992;25:115-123.   Back to cited text no. 9    
10.Raveh D, Simhon A, Gimmon Z, Sacks T, Shapiro M. Infections caused by Pseudomonas pickettii in association with permanent indwelling intravenous devices: Four cases and a review. Clin Infect Dis 1993;17:877-880.  Back to cited text no. 10    
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