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Year : 2014  |  Volume : 16  |  Issue : 2  |  Page : 90-93

Chromobacterium violaceum causing urinary tract infection: A case report

Department of Microbiology, Government Medical College, Thiruvananthapuram, Kerala, India

Date of Web Publication14-Nov-2014

Correspondence Address:
Viji Mohan
Department of Microbiology, Government Medical College, Thiruvananthapuram, Kerala
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0972-1282.144732

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Chromobacterium violaceum is a saprophytic organism that rarely causes infection in human. Urinary tract infection by Chromobacterium violaceum is extremely rare. Here, we report the first case of urinary tract infection caused by Chromobacterium violaceum from India, in a 43-year-old diabetic female with intramural fibroid. The patient was successfully treated with Ciprofloxacin.

Keywords: Chromobacterium violaceum , pigmented, urinary tract infection

How to cite this article:
Mohan V, Rajan R, Haneefa S. Chromobacterium violaceum causing urinary tract infection: A case report. J Acad Clin Microbiol 2014;16:90-3

How to cite this URL:
Mohan V, Rajan R, Haneefa S. Chromobacterium violaceum causing urinary tract infection: A case report. J Acad Clin Microbiol [serial online] 2014 [cited 2021 Apr 22];16:90-3. Available from: https://www.jacmjournal.org/text.asp?2014/16/2/90/144732

  Introduction Top

Urinary tract infection (UTI) is one of the most common infections affecting women. The most common bacteria causing urinary tract infection in women include E. coli, Klebsiella species, Proteus species and Enterococci. However rare organisms cannot be ruled out in the context of UTI. Chromobacterium violaceum is one such bacterium that causes UTI. There are no case reports on urinary tract infections caused by this bacterium. The organism is related with high mortality when infections like abscess and septicemia occur. It is widely found in soil and water of tropical and subtropical regions. We present a case of urinary tract infection by Chromobacterium violaceum in a diabetic patient with intramural fibroid uterus having history of urinary catheterisation, which was successfully treated with Ciprofloxacin.

  Case report Top

A 43-year-old female was presented in the gynecology out-patient department (OPD) with complaints of dysuria and urinary retention for one month duration in March 2014. She was later admitted in the hospital for further evaluation. She had urinary tract infection about a month back for which she was taking Norfloxacin orally. The ultrasonogram taken, showed an intramural fibroid with post-voidal retention of urine for which she was intermittently catheterised at various local hospitals. Urine culture done at the local laboratory was reported as "no bacteriuria". The patient later on developed severe dysuria for which she sought treatment at the local hospital and subsequently was referred to this hospital. She had no fever or chills or rigors or lower abdominal pain. Patient was detected to have diabetes at this hospital and was started on human insulin. There was no history of contact of the patient with soil or stagnant water.

On examination, the patient was conscious, oriented and alert. Her vitals were normal. Pulse rate-70/minute, blood pressure-130/80 and afebrile. Systemic examination was normal. Her menstrual cycles were regular. She had no gynecological complaints like dysmenorrhea or menorrhagia. On abdominal examination, the bladder was palpable. On speculum examination, there was 2° descent of uterus and cervical erosions which bled on contact. On per vaginal examination, uterus was anteverted and size of about 14 weeks. Ultrasonogram was not repeated as the patient had done one recently at a local hospital which had reported an intramural fibroid of size 6 cm × 5 cm and post void residual urine of 100 ml. Urinary bladder and kidneys were normal. Urine was sent for bacteriological culture and sensitivity on the second day of admission.

Laboratory investigations

Haemoglobin-11.8 g/dl; total white blood cell count - 9300 cells/mm 3 , with 80% neutrophils and lymphocytes 20%; platelet count-2.2 lakh/mm 3 ; fasting blood sugar/post-prandial blood sugar-174/280 mg %, respectively; serum uric acid 3.9 mg/dl, serum creatinine-1 mg/dl; serum glutamic oxaloacetic transaminase/serum glutamic pyruvic transaminase (SGOT/SGPT) 19 IU/20 IU; HBsAg, antibodies to HIV and HCV were negative. The venereal disease research laboratory (VDRL) test was nonreactive. Routine examination of urine was within normal limits.

The patient was started on oral Ampicillin empirically on the day of admission. It was stopped next day and injection Cefotaxime was started after the urine was sent for culture.

The urine specimen was received at the lab on the second day of admission. Macroscopically, the urine appeared turbid. On wet film examination there was plenty of pus cells and bacteria. The sample was inoculated on blood agar, MacConkey agar and incubated aerobically at 37°C for 24 hours. The next day, there was significant growth of pigmented/deep violet coloured colonies on blood agar which were circular, convex and smooth about 1-2 mm in size with beta hemolysis [Figure 1]. On MacConkey agar non-lactose fermenting, pigmented, deep violet coloured colonies were seen.
Figure 1: Showing violet colored colonies with beta hemolysis in blood agar

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Another urine sample was requested on the same day. This urine sample appeared turbid on macroscopic examination. Microscopy revealed plenty of pus cells and bacteria and culture was done. The growth on blood agar and MacConkey agar were similar to that of the previous day's growth. On Mueller-Hinton agar, smooth, round, convex, violet coloured pigmented colonies were seen. Gram smear taken from the culture plate also showed gram negative bacilli.

The organism was a facultative anerobe. It was catalase positive. As the organism was pigmented, the conventional oxidase test could not be interpreted so a modification of oxidase test by Dhar and Johnson was done to demonstrate that the organism was oxidase positive. [1] Biochemically, indole was not produced. Triple sugar iron medium showed an alkaline slant and acid butt (K/A) without gas or hydrogen sulphide [H 2 S] production suggesting that the organism fermented glucose but did not ferment lactose and sucrose. Citrate was not utilized, urea was not hydrolyzed and nitrate was reduced to nitrite. In mannitol motility test, mannitol was not fermented and organism was motile. Esculin was not hydrolyzed. It fermented glucose but did not ferment lactose, sucrose or maltose. The isolate was identified as Chromobacterium violaceum based on its morphological and biochemical properties.

Antibiotic susceptibility of the organism was tested by the Kirby-Bauer disc diffusion method. The isolate was found to be sensitive to Gentamicin, Nalidixic acid, Norfloxacin, Chloramphenicol, Ciprofloxacin, Tetracycline, Cotrimoxazole, Imipenem and Amikacin [Figure 2]. It showed resistance to Ampicillin, 1 st generation cephalosporins, Cefotaxime, Cefipime and cefoxitin [Figure 3].
Figure 2: Antibiotic sensitivity pattern

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Figure 3: Antibiotic sensitivity test showing resistance pattern

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Based on the results of the antibiotic susceptibility testing, the patient was given oral Ciprofloxacin 500 mg twice daily for 14 days. With this treatment the symptoms disappeared and the patient was better. The urine examination and culture after antibiotic treatment showed no bacteriuria.

The patient had given a history of using well-water for washing her genital areas. Also there is a history of repeated catheterization performed at different hospitals which might be a possible source of introduction/entry of organism into the urinary tract.

  Discussion Top

Chromobacterium violaceum was first described by Bergonzini in 1880. The pathogenic potential of Chromobacterium violaceum was described by Wooley in 1905. [2] It was previously classified as Bacillus violaceus manilae. The first human infection was reported in Malaysia. [3] It is a saprophytic organism and is present in soil and water in tropical and subtropical countries. [4] Chromobacterium violaceum belongs to genus Chromobacterium order  Neisseria More Detailsles and family Neisseriaceae. [5] Chromobacterium violaceum species have two colony types - pigmented and non-pigmented. They rarely cause infections in humans. Infection occurs usually after contact with contaminated water or soil by the non-intact skin/exposed or damaged skin. [4] There have been about 150 cases reported worldwide including 9 from India. [6],[7] Most cases have been reported from Vietnam, Taiwan, Korea, Argentina, Brazil, Thailand, USA, Australia and India. [8]

Chromobacterium violaceum are rod shaped, gram-negative, non-spore forming bacteria which are found often in coccobacillary forms / sometimes slightly curved. They occur singly or in pairs. They are motile with a single polar flagellum and usually one or two lateral flagella. [9] They are aerobic and facultatively anerobic. They grow on ordinary media like nutrient agar, blood agar and MacConkey agar at 37°C and not at 4°C. [5] Colonies are low convex, pigmented, smooth, circular with entire edge and butyrous in consistency. They show hemolysis in blood agar. [5] On MacConkey agar, violet colonies are formed. Pigment produced is non-diffusible and violet, known as 'violacein'. It is oxidase and catalase positive. [5] Indole was not produced and urea was not hydrolyzed. Since the organism is pigmented, a modification of oxidase test by Dhar and Johnson [1] is done. Otherwise very young or anerobic cultures with no pigmentation are used for usual method. [4] Acid is produced without any gas, fermentatively from glucose, sucrose (variable) but not from lactose or mannitol. [5] It liquefies gelatine, hydrolyzes casein [5] and utilizes citrate. [5] It does not hydrolyze esculin. [5] It reduces nitrate to nitrite [5] and hydrolyzes arginine.

Chromobacterium violaceum is susceptible to Ciprofloxacin, Norfloxacin, Amikacin, Gentamicin, Imipenem Chloramphenicol, Tetracycline, [10] Doxycycline and Trimethoprim Sulphamethoxazole. It is highly resistant to Rifampicin and Vancomycin. Activity against 1 st and 2 nd generation Cepahalosporins is poor. [4] There is no definite guideline for treatment of infections by Chromobacterium violaceum.

Although Chromobacterium violaceum is known to be of low virulence it causes septicemia with pneumonia which is fatal unless treated in humans. [1] It causes pneumonia, gastrointestinal infections, osteomyelitis, meningitis, urinary tract infections, localized cutaneous infections, genitourinary infections, brain abscesses, peritonitis, respiratory distress syndrome and sepsis.

India is a tropical country and people are often exposed to contaminated water and soil. There are about nine case reports of Chromobacterium infections in India. [7] To our knowledge there has been no case report on urinary tract infection caused by this organism in India.

  Conclusion Top

Repeated catheterizations, presence of cervical erosions and immunocompromised status of patient due to diabetes posed as risk factors for infection by Chromobacterium violaceum, a saprophytic organism which is rarely infectious. Timely intervention with administration of an antibiotic to which the organism is sensitive ensured that the patient's condition was resolved completely and did not progress into fatal outcomes like septicemia. Since there are no standard guidelines for treatment of Chromobacterium violaceum, an antibiotic sensitivity testing is a must. The present case highlights the importance of early detection and prompt treatment of Chromobacterium violaceum because if untreated it can have a fatal outcome. Chromobacterium violaceum is frequently regarded as a contaminant. Chromobacterium violaceum is commonly resistant to penicillin and cephalosporin as seen in our case too which reiterates the need of appropriate antibiotic therapy for its complete cure.

  References Top

Dhar SK, Johnson R. The oxidase activity of Chromobacterium. J Clin Pathol 1973;26:304-6.  Back to cited text no. 1
Wooley PG. Bacillus violaceous manilae (a pathogenic organism). Bull Johns Hopkins Hosp 1905;16:89.  Back to cited text no. 2
Sneath PH, Whelan JP, Singh RB, Edward D. Fatal infection by Chromobacterium violaceum. Lancet 1953;265:276-7.  Back to cited text no. 3
Tille PM. Bailey and Scott′s Diagnostic Microbiology. 13 th ed. St Louis: Elsevier health sciences; 2011. p. 368.  Back to cited text no. 4
Boone DR, Castenholz RW, Garrity GM, Brenner DJ, Krieg NR, Staley JT. Bergey′s Manual of Systemic Bacteriology. 2 nd ed., Vol 2. The Proteobacteria. Georgia: Springer; 2005. p. 823.  Back to cited text no. 5
Ray P, Sharma J, Marak RS, Singhi S, Taneja N, Garg RK, et al. Chromobacterium violaceum septicaemia from north India. Indian J Med Res 2004;120:523-6.  Back to cited text no. 6
Karthik R, Pancharatnam P, Balaji V. Fatal Chromobacterium violaceum septicemia in a South Indian adult. J Infect Dev Ctries 2012;6:751-5.  Back to cited text no. 7
Steinberg JP, Del Rio C. Other gram negative and gram variable bacilli. In: Mandell GL, Bennett JE, Dolin R, editors. Mandell, Douglas and Bennett′s Principles and Practice of Infectious Diseases. 6 th ed. Philadelphia: Churchill Livingstone; 2005. p. 2751-68.  Back to cited text no. 8
In: Collee JG, Fraser AG, Marmion BP, Simmons A, editors. Mackie and McCartney Practical Medical Microbiology. 14 th ed. New Delhi: Elsevier; 2012. p. 462.  Back to cited text no. 9
Schlossberg D. Chapter miscellaneous gram negative organisms-clinical infectious diseases. 3 rd ed. New York: Cambridge university press; 2008. p. 1115.  Back to cited text no. 10


  [Figure 1], [Figure 2], [Figure 3]

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