A four-year-old HIV negative male presented at the Hospital for Tropical Diseases in Ho Chi Minh City with a puncture wound on his right ankle. He was admitted and had a three-day history of fever, fatigue, vomiting and anorexia. He had previously been diagnosed with pulmonary Tuberculosis when three years old and had previously been taking a combination of rifampicin, 4-aminosalicylic acid and ethambutol for eight months. He had no other underlying diseases. On admission he had a pulse rate of 180 beats/minute, low blood pressure, a respiration rate of 57 breaths/minute, crackling chest sounds and pale sclera. The cervical lymph nodes were swollen, measuring 2 cm in diameter. He had displayed evidence of hepatomegaly, but was not jaundiced and had two small blisters on the abdomen.
The initial clinical diagnosis was acute sepsis. An antimicrobial regime of 200 mg/day of amikacin, 150 mg/day of vancomycin and 1.25 g/day of ceftriaxone was initiated immediately. On admission, the hematology results showed a normal white blood cell count with low hemoglobin (Table  1). The blood chemistry was also unremarkable (Table  2), apart from a C reactive protein concentration of 312 mg/l (normal range 0-5 mg/l), indicating severe sepsis. Radiography showed new pulmonary infiltrations, yet this was deemed not to be consistent with a progression of tuberculosis, a sputum smear was negative and further smears from a stomach aspirate and bronchial fluids were also negative. A blood sample was taken and inoculated into a Peds Plus/F BACTEC bottle and incubated at 37 C in an automated BACTEC 9240 machine (Becton Dickinson, United Kingdom). After 24 hours a positive result was recorded, and a Gram-negative bacilli was identified. Subcultures were performed on blood agar and nutrient agar plates and incubated aerobically at 35 C. After overnight incubation the agar plates demonstrated numerous small colonies with a dark violet metallic pigmentation. This pigmentation is unique to Chromobacterium violaceum, differentiating the organism from other tropical, soil dwelling organisms, and is due to the production of a chemical called violacein . Identification of Chromobacterium violaceum was confirmed by a positive mannitol test and API 20NE . The bacterial isolate was tested for susceptibility to a range of antimicrobials (cefapine, ciprofloxacin, amikacin, ofloxacin, imipenem, ceftriaxone, ceftazidime and piperacillin/tazobactam) on Mueller-Hinton agar, and interpreted according to the CLSI guidelines for non-Enterobaceriaceae Gram-negatives . The phenomenon of intrinsic antimicrobial resistance in Chromobacterium violaceum is well described . However, this isolate did not exhibit comprehensive resistant to any of the tested antimicrobials. On day three the antimicrobial therapy was changed to 330 mg/8 hours of meropenem, 150 mg/8 hours of ciprofloxacin and 150 mg/6 hours of vancomycin. This antimicrobial regime was continued for 23 days until the patient was afebrile and had no symptoms synonymous with bacteremia, additional blood cultures were not performed. The child made a complete recovery without complications.