Download Recurrent Nonfatal Chromobacterium violaceum Infection in a

Recurrent Nonfatal Chromobacterium violaceum Infection
in a Nonimmunocompromised Patient
from Infections in Medicine ® October 2000
Bradley D. Bilton, MD, Lester W. Johnson, MD; Louisiana State University Health
Sciences Center, Shreveport
Abstract and Introduction
Abstract
A soft tissue infection developed in a 6-year-old boy after he sustained a traumatic injury while
playing in stagnant water. The cause of the infection was never determined. Three years later,
after exposure to the same water source, the child had an extensive soft tissue infection,
septicemia, and multiple intra-abdominal abscesses; the infectious organism was determined
to be Chromobacterium violaceum. At age 12, the child once again was hospitalized for a
febrile illness, and C violaceum was isolated from his nasopharynx. The child had no evidence
of immune deficiency and has had no further significant medical problems.
Introduction
Chromobacterium violaceum rarely causes infection in humans.[1] The organism is a
well-known inhabitant of soil and water -- particularly stagnant or slow-moving water sources -in the southeastern United States.[2,3] An underlying defect in host defense, especially that of
neutrophils, seems to predispose to infection.[2] Of the cases reported in the United States,
73% have ended in death.[3] We present the case of a child acquiring the infection while playing
in a common water source. This case appears to be the first documentation of possible
reinfection or chronic colonization with the organism.
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When this article was written, Dr Bilton was a resident in surgery at Louisiana State University
Health Sciences Center, Shreveport, where he is now a fellow in laparoscopy. Dr Johnson is
associate professor of clinical surgery, Louisiana State University Health Sciences Center,
Monroe.
Case Report
A previously healthy 6-year-old boy sustained a traumatic wound to his left fourth toe while
playing in a bayou in northeastern Louisiana. The child presented approximately 3 weeks after
this event with a slow-healing wound that had not responded to conventional outpatient
antibiotic therapy. He also had associated left proximal thigh regional lymphadenitis and
cellulitis. The wound was exquisitely tender and caused disturbance of gait. The boy's white
blood cell (WBC) count was 10,900/µL. During his hospital course, the patient received
lincomycin and clindamycin as well as operative drainage of a suppurative inguinal lymph
node. His hospital course lasted 6 days. The infectious organism was not identified, and the
patient recovered uneventfully.
Three years later, after swimming in the same water source while he had an open wound on
his right ankle, the child developed a febrile illness. He presented in September 1976 with a
necrotizing soft tissue infection of his right lower extremity (popliteal area). He underwent
extensive radical debridement of this area on admission and again 2 days later. Cultures of
urine, blood, and sputum grew C violaceum within 48 hours. Sensitivity studies indicated that
the organism was sensitive only to tetracycline and chloramphenicol. These antibiotics were
immediately initiated in the appropriate dosages.
Septicemia and subsequent multiple liver abscesses developed. The patient underwent
laparotomy and drainage/debridement of the abscesses. He continued on a septic course
despite aggressive antibiotic therapy and wound management. Abscesses formed in the
lesser sac, omentum, and spleen. Laparotomy was repeated, along with drainage/
debridement, and splenectomy was performed 4 weeks after the patient was admitted.
Cultures of the abscess fluid were positive for C violaceum. The child received antibiotic
therapy for an extended period. He survived and was discharged after another 2 weeks.
Three years later, the child again presented with a febrile illness. His WBC count was
61,900/µL. He was given the admitting diagnoses of pneumonia and sinusitis. Among other
cultures and tests, which were essentially noncontributory, was a nasal swab culture taken on
the next day that grew C violaceum. The organism was resistant to cefoxitin, ampicillin,
carbenicillin, cephalosporins, trimethoprim/sulfamethoxazole (TMP-SMX), and cefamandole. It
was sensitive to amikacin, chloramphenicol, gentamicin, nalidixic acid, nitrofurantoin,
tetracycline, and tobramycin. The patient was given tetracycline, chloromycetin, and
gentamicin for 2 weeks and doxycycline for 6 days.
Extensive testing in attempts to find reasons for an immunocompromised state (including
chronic granulomatous disease) was unsuccessful. More than 20 years after his first hospital
admission, the patient is without sequelae or significant medical problems.
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Discussion
In 1905, Wooley first described C violaceum infection in studying dead and dying water buffalo
in the Philippines. There have also been reports of the infection in other mammals, especially
gibbons, pigs, and cattle.[4] The first human infection was reported in Malaya in 1927.[3] As
stated previously, the organism is well known in the southeastern United States. [2] It is a soil
and water inhabitant, is abundant in tropical and subtropical freshwater, and is especially
prevalent in water that is stagnant or slow-moving.[2,3,5] Infections have been reported in the
southeastern and northeastern United States, Southeast Asia, and South America. Review of
the literature and communication with the CDC indicate that there have been 24 reported
cases in the United States, with a mortality rate of 73%. This case makes the 25th reported
case, reducing the mortality rate to 64%.
Underlying defects in host defenses seem to predispose to infection. However, a number of
cases have been described with no known host-factor dysfunction.[2] There has been
documentation of patients with chronic granulomatous disease and susceptibility to the
infection.[2,5] The infection is usually acquired through trauma. The resulting infection can
involve the urinary tract, GI tract, bloodstream, lung, abdominal cavity, or bone. Invasion can
occur with or without an obvious primary focus.[2]
The most common presentation is that of skin lesions and septicemia. Skin manifestations are
secondary to systemic disease and include pustular dermatitis, cellulitis, and ulcerations. [2,5]
Other dermatologic lesions include vesicles, ecchymotic maculae, maculopapular rash,
subcutaneous nodules, lymphangitis, and digital gangrene.[5]
Diagnosis is made by culture of the blood, abscess fluid, or exudate. There is no diagnostic
serologic test.[2] Gram stain may reveal a gram-negative, long bacillus that occasionally may
have a slight curve, which may result in confusing the organism with Vibrio species. The
organisms are facultatively anaerobic and grow readily in 18 to 24 hours on tryptophan
medium. Incubation at 30°C to 45°C (86°F to 113°F) is effective, although growth is enhanced
at 25°C (77°F).[1] Microbiologists may regard the culture as a contaminant when it is isolated or
may dismiss the nonpigmented form as a less virulent organism.[2] This can be a costly error.
The organism is usually susceptible in vitro to chloramphenicol, tetracycline, TMP-SMX, and
gentamicin. It is variably sensitive to penicillins and aminoglycosides but is resistant to most
cephalosporins. Erthromycin seems to be ineffective in vivo regardless of susceptibility
testing.[2] The optimal antibiotic regimen is not known.[6] Some studies advocate the use of
parenteral antibiotics for an extended period, followed by at least 4 weeks with an oral agent,
such as TMP-SMX or tetracycline, to prevent relapse.[4] Relapse has occurred more than 2
weeks after completion of therapy and apparent cure.[2] The disease is usually fatal if not
diagnosed and treated with appropriate antibiotics and debridement at the earliest possible
time. Clinicians should therefore be vigilant for the possibility of relapse or apparent reinfection,
as in the above case.
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Conclusion
It is imperative that this rare infection be considered whenever a serious infection occurs
following exposure to freshwater pathogens. Rapid definitive diagnosis as well as appropriate
antibiotic coverage and subsequent surgical intervention is of the utmost importance. Despite
aggressive therapy, the mortality rate is high.
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