Way, Sing Sing MD*; Sidbury, Robert MD*; Dooms, Kevin MD†; Shors, Andy MD, MPH*; Qin, Xuan PhD‡; Crane, Heidi M. MD MPH§
*Department of Pediatrics, University of Washington, Seattle, WA; †Department of Pediatrics, University of Wisconsin Children's Hospital, Madison, WI; Departments of ‡Laboratory Medicine and §Medicine, University of Washington, Seattle, WA.
Supported in part by a grant from the University of Washington STD/AIDS Predoctoral and Postdoctoral Training Program National Institute of Allergy and Infectious Diseases Grant (AI-0714P) (H.M.C.), the Mentored Patient-Oriented Research Career Development Award National Institute of Allergy and Infectious Diseases Grant (AI-610320) (H.M.C.), and a Child Health and Research Center award (S.S.W.).
No authors have any affiliation with or financial involvement in any organization, matter, or materials discussed in this manuscript.
Address correspondence and reprint requests to Heidi M. Crane, MD, MPH, Center for AIDS and STDs, University of Washington, Harborview Medical Center, Box 359931, 325 9th Ave, Seattle, WA 98104. E-mail: email@example.com.
Chromobacterium violaceum is a gram-negative soil and water saprophyte with ubiquitous distribution in tropical and subtropical areas.1 Infections are associated with rapid dissemination and a high mortality rate.2 Less than 50 cases have been reported, and many have occurred in patients with underlying immune defects.2 We describe a patient without evidence of immunodeficiency who developed C. violaceum sepsis in association with unusual skin findings.
An 11-year-old boy presented with 10 days of subjective fever with associated abdominal pain and diarrhea that developed 7 days after fever onset. During this time, he noted a "red bump" on his right thigh that had enlarged and ulcerated on the day before evaluation. Review of systems was notable for a 20-lb weight loss over the previous month. Although the patient was born and lived in the Pacific Northwest, these symptoms including the weight loss developed during a month-long trip to Cambodia. There, he had contact with domesticated animals and swam in fresh water streams. He returned to the United States on day 7 of illness and presented to our emergency department 3 days later.
At the time of initial evaluation, he had a temperature of 39.5°C, blood pressure of 130/32 mm Hg, pulse rate of 132 beats per minute, respiratory rate of 48 to 60 breaths per minute, and peripheral oxygen saturation of 94% on a 55% face mask. His physical examination was significant for the following: coarse rales, diffuse abdominal tenderness, hepatosplenomegaly, lymphadenopathy (2-cm tender nodes in his right groin, left thigh, and abdomen), and a 3-cm ulcer on the right thigh with a raised border and nearby pustular lesion (Fig. 1).
Initial laboratory evaluation revealed a C-reactive protein of 28 mg/dL, an erythrocyte sedimentation rate of 100 mm/h, an elevated white blood cell count of 28,000 (60% neutrophils and 30% bands), and anemia (hematocrit level, 0.19). His platelet count was 414,000, and his alanine aminotransferase was 39 U/L. His γ-glutamyl transpeptidase was 138 IU/L; his bilirubin level was 0.2 mg/dL, and his lactate dehydrogenase was 1165 IU/L.
A chest radiograph demonstrated bilateral infiltrates. A computerized tomographic scan revealed dense bilateral lung base consolidation, hypodense 1.5-cm liver lesions suggestive of small abscesses, and an enlarged 3-cm right inguinal lymph node.
In the emergency department, he developed progressive hypotension and was transferred to the pediatric intensive care unit. Wound cultures and a biopsy specimen from the ulcer edge including some of the base were obtained. Histopathology of the biopsy revealed dense sheets of infiltrating neutrophils. Gram stain revealed polymorphonuclear leukocytes but no organisms. After overnight aerobic incubation, round and shiny colonies with characteristic purple coloration grew on sheep blood and MacConkey agar media (Fig. 2); blood cultures obtained at the same time were without growth. This appearance and subsequent biochemical characteristics were consistent with C. violaceum, which was further confirmed by bacterial 16S ribosomal DNA partial sequencing.3,4 The 2 top nucleotide sequence matches were both C. violaceum (AJ247211 and M22510) in the GenBank repository.
The susceptibility of the organism was determined by Kirby-Bauer disc diffusion. Using Pseudomonas aeruginosa breakpoints according to National Committee for Clinical Laboratory Standards M100-S12, this isolate was susceptible to cefepime, piperacillin-tazobactam, meropenem, gentamicin, ciprofloxacin, and trimethoprim/sulfamethoxazole but resistant to first- to third-generation cephalosporins. The patient was treated empirically with ceftriaxone, gentamicin, vancomycin, and metronidazole. This was changed to meropenem and gentamicin when susceptibilities became available.
The patient underwent evaluation for possible immunodeficiency. The results of oxidative burst tests (to evaluate for chronic granulomatous disease), T- and B-cell subsets, and total immunoglobulin levels were all within normal limits. He responded well to antibiotics and, after a week, was afebrile and weaned off oxygen. His inflammatory markers normalized, and liver abscesses resolved within 3 weeks on parenteral therapy. He was then discharged and given an additional 4 weeks of oral trimethoprim/sulfamethoxazole. At a follow-up visit, he was without complication or evidence of relapse.
Infections with C. violaceum are associated with a mortality rate of 50% or greater,2,5 and this increases to greater than 75% among those with bacteremia or sepsis.2,5,6 Furthermore, people with abnormal leukocyte function (such as with chronic granulomatous disease) are particularly susceptible to C. violaceum infection.5-7 Chromobacterium violaceum is a motile catalase-positive gram-negative bacillus which produces a violet pigment. Nonpigmented C. violaceum strains have been reported and likely also cause infection.8 Optimal growth for C. violaceum is at 20°C to 37°C and thus is restricted geographically between latitudes 35 degrees North and 35 degrees South. Most cases have been from Southeast Asia2,5,8,9 or the Southeast United States,6,10 but sporadic cases have also been reported from Australia, India, South America, and Africa.9,11-13 Infection typically occurs during the summer. It most often occurs after exposure to contaminated water or soil, allowing the bacterium to enter the skin through areas of minor trauma.2,6,14 In our patient, we suspect that infection occurred during exposure to contaminated water while swimming in Cambodia. This led to the ulcer and systemic symptoms and finally to sepsis.
Initial infection may resemble staphylococcal or streptococcal cellulitis. Chromobacterium violaceum infection frequently presents with sepsis4 often associated with fever, pneumonia, liver, lung, or splenic abscesses.13 In a large case series, 19 of 25 patients had disseminated infection with liver, lung, or spleen abscesses; 11 of 25 had positive blood cultures; and an additional 6 patients had cellulitis or superficial lymphadenitis without bacteremia.2 Less common presentations include orbital cellulitis, osteomyelitis, conjunctivitis,5 meningitis, or brain abscess.10 Although many C. violaceum infections are associated with a rapid fulminant course,4,5,13 slower progression, late relapses, and difficulty with eradication also occur.2,15 Cutaneous involvement is common, especially pustular lesions with surrounding erythema1,9,10,12,14; however, a large ulcer with a raised border7 as seen in our patient is unusual. This type of cutaneous involvement in a patient with sepsis would be more typical of ulceroglandular tularemia, leishmaniasis, or melioidosis.
Chromobacterium violaceum is typically susceptible to chloramphenicol, ciprofloxacin, and imipenem and resistant to penicillin in vitro, whereas susceptibilities to third-generation cephalosporins and gentamicin vary.5,8,12,14 In our patient, a 3-week course of combination parenteral antimicrobial therapy followed by an additional 4 weeks of oral trimethoprim/sulfamethoxazole was administered successfully.14
This case highlights several typical features of C. violaceum infection, including summertime exposure, sepsis, and liver abscesses that do not require surgical drainage. This case was atypical in the specific dermatologic findings; pustular lesions are more common than large ulcers with raised borders. Although C. violaceum is a rare cause of infection, it can be rapidly fatal, so it is important to consider in the differential of sepsis in nonendemic areas as worldwide travel continues to increase.
1. Tee HP, Francis AL, How SH. Chromobacterium violaceum
infection. Br J Hosp Med (Lond)
2. Sirinavin S, Techasaensiri C, Benjaponpitak S, et al. Invasive Chromobacterium violaceum
infection in children: case report and review. Pediatr Infect Dis J
3. Lee DH, Zo YG, Kim SJ. Nonradioactive method to study genetic profiles of natural bacterial communities by PCR-single-strand-conformation polymorphism. Appl Environ Microbiol
4. Grier DD, Qiu J, Rand K, et al. Pathologic quiz case: a 13-year-old boy with a 2-day history of fever, vomiting, and mental status changes. Chromobacterium violaceum
bacteremia. Arch Pathol Lab Med
5. Shao PL, Hsueh PR, Chang YC, et al. Chromobacterium violaceum
infection in children: a case of fatal septicemia with nasopharyngeal abscess and literature review. Pediatr Infect Dis J
6. Macher AM, Casale TB, Fauci AS. Chronic granulomatous disease of childhood and Chromobacterium violaceum
infections in the southeastern United States. Ann Intern Med
7. Brown KL, Stein A, Morrell DS. Ecthyma gangrenosum and septic shock syndrome secondary to Chromobacterium violaceum
. J Am Acad Dermatol
8. Lee J, Kim JS, Nahm CH, et al. Two cases of Chromobacterium violaceum
infection after injury in a subtropical region. J Clin Microbiol
9. Dromigny JA, Fall AL, Diouf S, et al. Chromobacterium violaceum
: a case of diarrhea in Senegal. Pediatr Infect Dis J
10. Moore CC, Lane JE, Stephens JL. Successful treatment of an infant with Chromobacterium violaceum
sepsis. Clin Infect Dis
11. Huffam SE, Nowotny MJ, Currie BJ. Chromobacterium violaceum
in tropical northern Australia. Med J Aust
12. Ray P, Sharma J, Marak RS, et al. Chromobacterium violaceum
septicaemia from north India. Indian J Med Res
13. Martinez R, Velludo MA, Santos VR, et al. Chromobacterium violaceum
infection in Brazil. A case report. Rev Inst Med Trop Sao Paulo
14. Ponte R, Jenkins SG. Fatal Chromobacterium violaceum
infections associated with exposure to stagnant waters. Pediatr Infect Dis J
15. Chattopadhyay A, Kumar V, Bhat N, et al. Chromobacterium violaceum
infection: a rare but frequently fatal disease. J Pediatr Surg
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