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Journal of Clinical Microbiology, April 2004, p. 1837-1839, Vol. 42, No. 4
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.4.1837-1839.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Chryseomonas luteola Identified as the Source of Serious Infections in a Moroccan University Hospital

Wafae Chihab,¹ Ahmed S. Alaoui,^1,2* and Mohamed Amar²

Laboratoire de Bactério-Sérologie et Hygiène, Hopital Ibn Sina, CHU de Rabat,¹ Laboratoire de Microbiologie et de Biologie Moléculaire, Centre National de la Recherche Scientifique et Technique, Rabat, Morocco²

Received 26 June 2003/ Returned for modification 25 August 2003/ Accepted 18 December 2003

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Chryseomonas luteola has only rarely been reported as a human bacterial pathogen. It has been shown that this organism in particular affects patients with health or indwelling disorders. Most reported cases showed septicemia, meningitis, endocarditis, or peritonitis. Two C. luteola infections observed in Morocco are described in the present study.

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Case 1. The first patient was a newborn boy, a twin, showing a respiratory failure at birth. He needed ventilator support and was intubated. Three days later he developed fever, icterus, and a bombing fontanel and was further treated in an intensive care unit. A lumbar puncture was performed, and the cerebrospinal fluid contained 200 white blood cells per mm³. The levels of albumin, chlore, and glucose were 1.25, 1.23, and 0.23 g/liter, respectively. The scanner showed a cerebral edema. Although no bacteria were found by microscopic observation, the patient was treated with ceftriaxone (100 mg/kg of body weight/day) and gentamicin (3 mg/kg/day). Unfortunately, he died the first night after admission in the intensive care unit.

In the meantime, samples from the patient were plated and showed growth of yellow-pigmented colonies. The pure culture contained gram-negative, oxydase-negative, and catalase-positive rods and was identified as Chryseomonas luteola by the API-20NE test kit (bioMérieux, La Balme-Les-Grottes, France). Antimicrobial susceptibility by agar disk diffusion methods showed that the C. luteola culture was susceptible to imipinem, colistin, ofloxacin, ciprofloxacin, amikacin, netilmicin, and doxycycline and resistant to amoxicillin, ceftazidime, cefotaxime, ceftriaxone, gentamicin, and trimethoprim-sulfamethoxazole (Table 1).

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TABLE 1. Two cases of C. luteola infections in a Morrocan hospital

Case 2. A 13-year-old boy was diagnosed with rheumatic fever associated with a degenerative mitral valve. The patient had heart surgery for replacement of the mitral valve. One month after the operation, the patient developed fever, icterus, and hematemesis. Echocardiography showed a mitral deficiency, but no vegetation was observed. The patient was treated with ampicillin (1 g/6 h) and gentamicin (80 mg/day) but without any success.

Six days after his admission to the hospital, a blood sample was plated and yielded yellow-pigmented colonies after 48 h of incubation. The culture was identified as C. luteola by API-20NE. The isolate was susceptible to imipenem, colistin, ofloxacin, ciprofloxacin, cefotaxime, ceftazidime, ceftriaxone, and doxycycline and was resistant to amoxicillin, cephalothin, and trimethoprim-sulfamethoxazole (Table 1).

After the treatment with ampicillin and gentamicin was changed to ceftriaxone treatment, the patient defervesced but remained icteric. The echocardiography was performed again and showed the presence of vegetation on the mitral prosthesis. The patient died 2 days later.

Discussion. C. luteola is a motile aerobic gram-negative rod with yellow-orange pigment. Yellow and smooth colonies are obtained after 48 h of incubation on heart infusion agar supplemented with 5% horse blood. C. luteola can be distinguished from most other motile yellow-pigmented nonfermenters by a negative oxidase reaction and from the enterobacteria by its strict aerobic growth (5). The normal habitat of C. luteola is unclear, but it is frequently found in water, soil, and other damp environments (5, 16). C. luteola was initially assigned to CDC group Ve-1 by Tatum et al. (as cited in references 7 and 14). Ve-1 is one of the biogroups of group Ve, a group of nonfermentative strains, named Chromobacterium typhiflavum by Pickett and Pedersen (13). Strains of group Ve-1 were first classified as Pseudomonas luteola by Kodama et al. (9). Holmes et al. (8) reclassified the species in the genus Chryseomonas as C. luteola, because P. luteola was a senior subjective synonym of Chryseomonas polytricha. Due to the close phylogenetic relatedness between Chryseomonas and Pseudomonas, this bacterium was reassigned to the genus Pseudomonas as Pseudomonas luteola (1). Currently, some authors still call the organism Chryseomonas luteola while others refer to it as Pseudomonas luteola (1, 6, 11, 17).

Previous studies showed that C. luteola may cause septicemia, peritonitis, and endocarditis in patients with health disorders or with indwelling devices (12). Up to now, 14 cases of C. luteola infection have been reported (2, 3, 5, 15, 17). For seven patients the organism was isolated from blood. Infections previously described include primarily septicemia (2), meningitis (10), osteomyelitis, endocarditis (12), and peritonitis (3). Also, its ability to infect critically ill patients who haveundergone surgical operations and/or had indwelling devices has been described (7). In other cases, the infection was associated with other factors, such as immunosuppressive therapy, chronic renal failure, and malignancy (14).

As far as we know, C. luteola infections in humans have never been reported in Morocco. In this work, we describe two cases in a Moroccan university hospital. The two cases reported had predisposing or associated factors: the first patient was a newborn in a transient immunosuppressive state, and the second had a mitral prosthesis.

Considering both cases, we noticed that the incubation period of the infection was different and varied from 1 day for the first case to 1 month for the second. In a previous report, a case of cerebral tumor was infected 3¹/₂ months after a surgical operation (10). Another case was reported as non-Hodgkin's lymphoma. The patient's subclavian Groshong catheter was flushed with sterile water, and the patient developed fever 1 h later (7). It seems the duration of the incubation period is unknown and may vary with the history of the infection.

It is reported that C. luteola is very resistant to trimethoprim-sulfamethoxazole, narrow- and expanded-spectrum cephalosporins, tetracycline, and ampicillin and susceptible to broad-spectrum antibiotics, such as cephalosporins, aminosids, and ciprofloxacin (4). Both isolates from the present study were susceptible to tetracycline. In the first case of the present study, the isolate was resistant to broad-spectrum cephalosporins and aminosids. For this reason the patient did not respond to treatment with ceftriaxone. With our second patient, the isolate was susceptible to ceftriaxone. However, C. luteola infections associated with foreign material are difficult to treat, and the prosthesis usually has to be removed (3, 10). With our patient, this surgical operation was not done because the physicians failed to find cardiac vegetation in the first stage of the disease.

Since these two bacteria were isolated from the same hospital, we performed molecular typing using sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The preliminary results showed significant differences between these strains and the reference strain. The two organisms isolated seemed not to be clonally related because of the differences noticed in their behavior against antibiotics, which means that the phenotypes of these isolates are different. Furthermore, the interval between the two infections was 24 months. Other molecular genotypic tools, like rep-PCR or pulsed-field gel electrophoresis, might be useful for confirmation.

Because of the dramatic outcome of both described human infections, addition of this bacterium to the expanding list of nosocomial pathogens (7) may warrant consideration.

 
* Corresponding author. Mailing address: Laboratoire de Microbiologie et de Biologie Moléculaire, Centre National de la Recherche Scientifique et Technique, 52 bd Omar Ibn Khatab, BP 8027-10102 Agdal, Rabat, Morocco. Phone: 212 61 299 065. Fax: 212 37 778 676. E-mail: alaoui.a{at}free.fr.

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Journal of Clinical Microbiology, April 2004, p. 1837-1839, Vol. 42, No. 4
0095-1137/04/$08.00+0     DOI: 10.1128/JCM.42.4.1837-1839.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Chihab, W. Articles by Amar, M. Search for Related Content PubMed PubMed Citation Articles by Chihab, W. Articles by Amar, M.