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| Year : 2017 | Volume
: 60
| Issue : 2 | Page : 279-281 |
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| Brevundimonas diminuta infection in a case of nephrotic syndrome |
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Abhilash Chandra1, Anupam Das2, Manodeep Sen2, Meenakshi Sharma2
1 Department of Nephrology, Dr. RMLIMS, Lucknow, Uttar Pradesh, India
2 Department of Microbiology, Dr. RMLIMS, Lucknow, Uttar Pradesh, India
Click here for correspondence address and email
| Date of Web Publication | 19-Jun-2017 |
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 Abstract | | |
Brevundimonas has rarely been isolated from clinical specimens. We here report a case of Brevundimonas diminuta infection in an 18-year-old male patient with nephrotic syndrome. B. diminuta was identified by the VITEK 2 Compact system, following isolation from his blood sample. To the best of our knowledge, B. diminuta has not been reported in patients with nephrotic syndrome. Keywords: Brevundimonas, gram negative, nephrotic syndrome
How to cite this article:
Chandra A, Das A, Sen M, Sharma M. Brevundimonas diminuta infection in a case of nephrotic syndrome. Indian J Pathol Microbiol 2017;60:279-81 |
| Introduction | |  |
Brevundimonas species are aerobic, nonfermenting Gram-negative bacilli. They are ubiquitous in the environment but are rare causes of human infection and are rarely isolated from clinical samples. Brevundimonas vesicularis and Brevundimonas diminuta, formerly classified as members of Group IV of the genus Pseudomonas, are the two most frequently isolated Brevundimonas species in human infections. These organisms are infrequently isolated in clinical microbiology laboratories. It has been isolated from sputum samples, pleural fluid, urine and blood, skin and soft-tissue infections, liver abscess, meningitis, peritonitis, septic arthritis, keratitis, and endocarditis.[1],[2],[3]
| Case Report | | |
An 18-year-old male with nephrotic syndrome with biopsy-proven focal segmental glomerulosclerosis was found to be steroid resistant. He was started on tacrolimus at a dose of 0.08 mg/kg in November 2014. In January 2015, he presented to us with sputum production, fever (100°F), and decreased appetite. On evaluation, his sputum examination was positive for acid-fast bacilli. He was started on antitubercular therapy comprising rifampicin, isoniazid, ethambutol, and pyrazinamide. Tacrolimus was subsequently stopped. His 24 h urine examination showed 800 mg of proteinuria and had a serum creatinine of 0.9 mg/dl. He again presented to us in March 2015 with complaints of high-grade fever for 10 days. Relevant laboratory findings included a white blood cell (WBC) count of 16,380/mm 3 with 88% polymorphonuclear cells, a platelet count of 157,000/mm 3, serum albumin 2.45 g/dl, serum creatinine 0.63 mg/dl, serum urea 15 mg/dl, serum sodium 132 mEq/L. Urine examination showed 3+ proteinuria with 2–3 WBCs/HPF. His blood and urine samples were sent to the Department of Microbiology for bacteriological evaluation. He was empirically started on injection ceftriaxone 1 g intravenous (iv) BD dose. Urine culture was sterile after 24 h of incubation. However, his blood culture was indicated positive by Versa Trek automated blood culture system after 48 h of incubation. Positive blood culture sample was subcultured on blood agar and MacConkey agar. Dark yellow-orange-colored colonies were grown on blood agar with 48 h incubation giving characteristic colony morphology [Figure 1] Colony morphology at 24 hours of incubation and [Figure 2] Colony morphology at 48 hours of incubation]. On MacConkey agar, there was no growth. The organism was an oxidase-positive, motile Gram-negative Bacillus. The isolate was identified as B. diminuta on the basis of the biochemical characteristics tested by the VITEK 2 automated identification system. The organism was resistant to colistin but was sensitive to the other drugs tested, namely, imipenem, meropenem, amikacin, gentamicin, fluoroquinolones, minocycline, tigecycline, cefoperazone-sulbactam, ceftazidime, cefepime, and cotrimoxazole [Table 1]. The treatment was switched to cefoperazone-sulbactam 1.5 g iv BD for 2 weeks. Patient's stay in the hospital was uneventful and subsequently was discharged in stable condition. | Figure 1: Colonies of Brevundimonas diminuta on blood agar after 24 h of incubation and positive oxidase test performed on the strain
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 | Figure 2: Colonies of Brevundimonas diminuta on blood agar after 48 h of incubation
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 | Table 1: Automated antimicrobial susceptibility profile of Brevundimonas diminuta isolated from automated blood culture obtained from the patient with nephrotic syndrome
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| Discussion | | |
Brevundimonas is an aerobic, nonsporulating and glucose nonfermenting, oxidase-positive Gram-negative Bacillus. It forms orange-pigmented colonies on blood and chocolate agar within 48 h. Most of the strains fail to grow on MacConkey agar as in this case also.
They are ubiquitous in the environment and have also been isolated in clinical settings.[4]Brevundimonas human infections are generally caused by B. vesicularis, and only a few cases of severe opportunistic infections, particularly in patients with immunocompromised status, have been reported to be caused by B. diminuta. They are primarily regarded as opportunistic organisms. B. diminuta has been mainly reported in cases of cancer, cystic fibrosis, with indwelling vascular catheter. In our case, it grew in the blood culture and is possibly the first to be reported in a case of nephrotic syndrome. Another noticeable feature of this organism is its frequent resistance to fluoroquinolones.[2] However, our case differs in the fact that it was found to be sensitive to fluoroquinolone. Susceptibility to other antibiotics such as aminoglycosides, carbapenems (mostly imipenem), and piperacillin/tazobactam is more uniform.[1],[2] Reviewing the case reports of B. diminuta, its virulence appears to be low. However, these need to be actively treated.
Brevundimonas infection in humans reported from India are presented in the [Table 2].[5],[6],[7],[8]
| Conclusion | | |
The low number of cases reported of Brevundimonas infection in humans limits the analysis of the spectrum of disease caused by this pathogen as well as the optimal line of treatment. Attribution of B. diminuta as a causative agent in human infections has prompted its antimicrobial susceptibility testing in various clinical settings. Its identification as an opportunistic organism may be an alarm for immunocompromised individuals.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | Chi CY, Fung CP, Wong WW, Liu CY. Brevundimonas bacteremia: Two case reports and literature review. Scand J Infect Dis 2004;36:59-61.  [ PUBMED] |
| 2. | Han XY, Andrade RA. Brevundimonas diminuta infections and its resistance to fluoroquinolones. J Antimicrob Chemother 2005;55:853-9. [ PUBMED] |
| 3. | Menuet M, Bittar F, Stremler N, Dubus JC, Sarles J, Raoult D, et al. First isolation of two colistin-resistant emerging pathogens, Brevundimonas diminuta and Ochrobactrum anthropi, in a woman with cystic fibrosis: A case report. J Med Case Rep 2008;2:373. [ PUBMED] |
| 4. | Lee MR, Huang YT, Liao CH, Chuang TY, Lin CK, Lee SW, et al. Bacteremia caused by Brevundimonas species at a tertiary care hospital in Taiwan, 2000-2010. Eur J Clin Microbiol Infect Dis 2011;30:1185-91. [ PUBMED] |
| 5. | Gupta PK, Appannanavar SB, Kaur H, Gupta V, Mohan B, Taneja N. Hospital acquired urinary tract infection by multidrug-resistant Brevundimonas vesicularis. Indian J Pathol Microbiol 2014;57:486-8. [ PUBMED] [Full text] |
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| 7. | Viswanathan R, Singh A, Mukherjee R, Sardar S, Dasgupta S, Mukherjee S. Brevundimonas vesicularis a new pathogen in a newborn. J Pediatr Infect Dis 2010;5:189-91. |
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Correspondence Address:
Abhilash Chandra
D2/537, Sector F, Jankipuram, Lucknow - 226 021, Uttar Pradesh
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/IJPM.IJPM_679_15
[Figure 1], [Figure 2]
[Table 1], [Table 2] |
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