Chromobacterium violaceum is widely distributed in natural aquatic environments and is temperature sensitive. Usually it produces an antioxidant pigment called violacein which is responsible for the purple color.1 At 30 °C to 45 °C, it grows on Nutrient agar, Blood agar and Mac Conkey agar media producing distinctive smooth low convex colonies with a dark violet metallic sheen in the typical pigmented strain.2 It is an emerging pathogen and only few cases of osteomyelitis were reported yet.3
A seven day old baby boy was referred to our Hospital with history of fever and excessive crying for two days. The baby was term, average gestational age and delivered by LSCS. On fourth day of delivery, baby developed fever and treatment was taken from local hospital. On current admission, the patient was febrile and was in shock. On examination pain while moving left lower limb was noted. X-ray revealed a fracture and periosteal reaction on fibula of left lower limb. Ultrasound scan was suggestive of acute osteomyelitis. CRP was 53 and total count was elevated. The baby was ventillated for 3 days and started on Cefoperazone –Sulbactam and Neomycin. But fever was persisting. Provisional diagnosis of osteomyelitis left lower end of fibula was made.
Incision and drainage was done and the pus aspirate was sent for culture and sensitivity. Blood culture was also done by BacT Alert. Gram stain from the aspirated sample showed plenty of pus cells and gram negative bacilli. Sample was inoculated into Blood Agar and Mac Conkey Agar. After 24 hours of incubation, heavy growth of smooth, convex, round, violet coloured beta haemolytic colonies on Blood agar and Mac Conkey Agar was grown. The organism was motile, gram-negative rod. It was catalase and oxidase positive. Biochemically, indole, methyl red, and Voges-Proskauer test were negative. The organism fermented glucose (producing acid but no gas) but did not ferment lactose or mannitol. Triple sugar iron medium showed an alkaline slant and acid butt (K/A) without gas and H2S production. Citrate was utilized and nitrate was reduced. Arginine was decarboxylated but not lysine and ornithine. Sensitivity test done in Meuller Hinton agar showed that the organism was sensitive to Piperacillin/Tazobactam, Amikacin and Ciprofloxacin and was resistant to Ceftazidime, Cefepime and Cefoperazone /Sulbactam. Vitek 2 (Biomereaux) also identified as Chromobacterium violaceum. As per our report the antibiotic was changed to Piperacillin -Tazobactam and Amikacin and was continued for 28 days. Patient responded well on antibiotics. Patient was investigated for immunodeficiency .But no evidence of immunocompromised diseases were found. Fortunately blood culture was sterile and the patient was improved on follow up visit.
Chromobacterium violaceum is a facultative anaerobic, motile, oxidase positive gram negative bacillus.1 Only a few case reports are available in the literature even though the organism is ubiquitous in distribution. Typically the disease starts with a localized skin infection or localized lymphadenitis following contact with stagnant water or soil and later it progresses to fulminating septicemia, with necrotizing metastatic lesions and multiple abscesses in the liver, lung, spleen, skin, lymph nodes, and brain, leading to fatal multiorgan failure.4 Chromobacterium violaceum infection presenting as chronic granulomatosis, osteomyelitis, cellulitis, and periorbital and ocular infections are also reported in literature. A characteristic feature of Chromobacterium infection is rapid progression to sepsis and multi organ dysfunction. Of the total infections caused by Chromobacterium violaceum, it has been seen as localized abscess was found in more than 50 %.5
The entry of the bacilli to the body is mainly through minor skin trauma or through ingestion of contaminated water and seafood. Unusual routes of exposure include infection after scuba-diving or near drowning.6 In the present case, the baby probably had a fracture in fibula leading to osteomyelitis. The exact source could not be found. Importance of early diagnosis and proper antimicrobial therapy can never be neglected to avoid progression to sepsis. Quick diagnosis, accurate bacterial identification, and specific treatment is very important because C violaceum may cause serious infection in healthy people. The major complications of the cases with fatal outcome seem to be sepsis, multiple liver abscesses, and diffuse pustular dermatitis. Some studies have reported instances of untreated C violaceum causing brain abscess and diarrhea.7 Prolonged antimicrobial treatment is recommended in Chromobacterium infection, as relapse of the disease has been documented and postulated to be due to the presence of internal organ abscesses.8 Our patient did not develop any complications due to the institution of early and proper antibiotic regimen.
C. violaceum is considered as an emerging pathogen in view of the recent climatic changes. Increasing reported cases with Chrombacterium violaceum infection has been noticed in recent decades. It has a propensity to develop into fatal septicemia unless appropriately treated. Thus it is required that the clinician must be aware of the sensitivity pattern and duration of treatment required for this infection.