Identities of
            <i>Microbacterium</i>
            spp. Encountered in Human Clinical Specimens

Gneiding, Kathrina; Frodl, Reinhard; Funke, Guido

doi:10.1128/jcm.01202-08

Cited by 108 publications

(77 citation statements)

References 20 publications

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“…There are more than 35 members of the genus Microbacterium, some of which are human pathogens (7). The C. elegans pathogen M. nematophilum adheres to the rectal and anal region of the nematode, causing a distinct swelling in the region and surrounding tissues (8).…”

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confidence: 99%

The Caenorhabditis elegansbus-2 Mutant Reveals a New Class of O-Glycans Affecting Bacterial Resistance

Palaima

Leymarie

Stroud

et al. 2010

Journal of Biological Chemistry

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Microbacterium nematophilum causes a deleterious infection of the C. elegans hindgut initiated by adhesion to rectal and anal cuticle. C. elegans bus-2 mutants, which are resistant to M. nematophilum and also to the formation of surface biofilms by Yersinia sp., carry genetic lesions in a putative glycosyltransferase containing conserved domains of core-1 ␤1,3-galactosyltransferases. bus-2 is predicted to act in the synthesis of core-1 type O-glycans. This observation implies that the infection requires the presence of host core-1 O-glycoconjugates and is therefore carbohydrate-dependent. Chemical analysis reported here reveals that bus-2 is indeed deficient in core-1 O-glycans. These mutants also exhibit a new subclass of O-glycans whose structures were determined by high performance tandem mass spectrometry; these are highly fucosylated and have a novel core that contains internally linked GlcA. Lectin studies showed that core-1 glycans and this novel class of O-glycans are both expressed in the tissue that is infected in the wild type worms. In worms having the bus-2 genetic background, core-1 glycans are decreased, whereas the novel fucosyl O-glycans are increased in abundance in this region. Expression analysis using a red fluorescent protein marker showed that bus-2 is expressed in the posterior gut, cuticle seam cells, and spermatheca, the first two of which are likely to be involved in secreting the carbohydraterich surface coat of the cuticle. Therefore, in the bus-2 background of reduced core-1 O-glycans, the novel fucosyl glycans likely replace or mask remaining core-1 ligands, leading to the resistance phenotype. There are more than 35 Microbacterium species, some of which are pathogenic in man. This study is the first to analyze the biochemistry of adhesion to a host tissue by a Microbacterium species.

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confidence: 99%

The Caenorhabditis elegansbus-2 Mutant Reveals a New Class of O-Glycans Affecting Bacterial Resistance

Palaima

Leymarie

Stroud

et al. 2010

Journal of Biological Chemistry

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“…Prior to validation of the species name, Gneiding et al described isolation of M. binotii in Germany from a superficial wound on a 5-year-old male and from a bone infection of a 23-year-old male with no further clinical details published. In that study, 50 strains of yellow-pigmented, Gram-positive rods isolated from human specimens over the course of 5 years were differentiated to the species level with two isolates (4%) characterized as M. binotii (20). Moreover, Clermont et al initially described the species of M. binotii using two strains originally isolated from human blood in France (5).…”

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confidence: 99%

“…Due to difficulty in identification, Microbacterium species have been described as diphtheroids, Corynebacterium spp., or CDC group A-4 or A-5 bacteria in previous reports (22). Additionally, Microbacterium species have been misidentified using the API Coryne system (bioMérieux) (13,20,23) and the RapID CB Plus system (Remel) as noted in this study, rendering these systems of limited utility for identification of yellow-pigmented, Gram-positive rods. The utility of using the 16S rRNA gene target along with phenotypic methods for identification was shown in this study.…”

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confidence: 99%

“…Reported infections caused by Microbacterium species include endophthalmitis caused by a Microbacterium species that most closely resembled Microbacterium laevaniformans (11), catheter-related bacteremias caused by a motile Microbacterium sp., (12), isolates that most closely resembled M. oxydans and Microbacterium trichothecenolyticum (13), Microbacterium paraoxydans (14,15), and an undefined Microbacterium species (16), interstitial pulmonary inflammation caused by M. hydrocarbonoxydans (17), skin and soft tissue infections caused by an undefined Microbacterium species (16), and peritonitis caused by an undefined Microbacterium species (18) and M. paraoxydans (19). Microbacterium binotii has been isolated from human clinical material at least 4 times previously (5,20). Prior to validation of the species name, Gneiding et al described isolation of M. binotii in Germany from a superficial wound on a 5-year-old male and from a bone infection of a 23-year-old male with no further clinical details published.…”

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confidence: 99%

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Bacteremia Caused by Microbacterium binotii in a Patient with Sickle Cell Anemia

Buss

Starlin²,

Iwen

2014

J Clin Microbiol

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cMicrobacterium species are non-spore-forming, Gram-positive rods rarely associated with human disease. In this report, we describe the first case of bacteremia caused by Microbacterium binotii in a patient with sickle cell anemia. The utility of using 16S rRNA gene sequence analysis along with phenotypic methods for identification is shown. CASE REPORTA 28-year-old male presented to the emergency department (ED) complaining of fever, fatigue, nausea, and nasal congestion. The patient had a history of sickle cell anemia with recurrent pain crises and narcotic dependence. He reported no other localizing symptoms of infections, admitted no exposures to others who were ill, and had no indwelling lines or hardware.On physical exam, the patient was febrile (38.4°C/101.2°F) with no other signs of sepsis. Hematological testing revealed leukocytosis, microcytic anemia, and mild thrombocytosis, which were relatively unchanged from prior labs. A urinalysis and chest X-ray were unremarkable. Two sets of blood cultures (BD Bactec; Becton, Dickinson and Co., Sparks, MD) were collected peripherally, and the patient was discharged from the ED with a presumed viral illness. Subsequently, both aerobic blood culture bottles grew small, Gram-positive rods after 43 h of incubation. The patient was asked to return to the hospital for a follow-up evaluation and treatment.Upon readmission, the patient appeared nontoxic with a lowgrade fever (38.0°C/100.4°F). Again, no localizing signs of infection were found, and repeat labs revealed near resolution of leukocytosis. Two sets of additional blood cultures were drawn prior to empirical administration of intravenous (i.v.) piperacillin-tazobactam (4,500 mg, once) and vancomycin (15 mg/kg of body weight, then 1,000 mg every 8 h). The patient rapidly defervesced following antibiotic therapy, with one repeat aerobic blood culture bottle growing Gram-positive rods after 67 h of incubation.All three positive blood culture bottles produced nonhemolytic colonies about 1 mm in size after subculture to 5% sheep blood agar and overnight incubation at 37°C in ambient air. The isolates were catalase positive and oxidase negative and developed a light-yellow pigment that became more intense over time. Using the RapID CB Plus system (Remel, Lenexa, KS), the isolates produced a microcode of 3755513, which yielded a probability of 99.66% for Oerskovia spp. and 0.34% for Microbacterium spp. Consequently, the isolates were reported as "most closely resembles Oerskovia species." Antimicrobial MICs were determined using Etest strips (bioMérieux, Durham, NC) and Mueller-Hinton agar containing 5% sheep blood (Remel, Lenexa, KS). Interpretations were based on the criteria for coryneform bacteria found in the CLSI document M45-A2 (1). The isolate was susceptible to linezolid (0.5 g/ml) and vancomycin (0.5 g/ml) and nonsusceptible to daptomycin (8.0 g/ml) (using Etest strips that contain a standard Ca 2ϩ overlay equivalent to 40 g/ml). Vancomycin was continued for 2 weeks, with repeat blood cultures drawn on day ...

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“…strain 4N2-2, was isolated from wastewater (16). Some strains of this genus have been isolated from human clinical specimens, and the majority of them have shown fluoroquinolone resistance (17). Microbacterium sp.…”

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confidence: 99%

Identification of the Enzyme Responsible forN-Acetylation of Norfloxacin by Microbacterium sp. Strain 4N2-2

Kim

Feng

Chen

et al. 2013

Appl Environ Microbiol

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bMicrobacterium sp. 4N2-2, isolated from a wastewater treatment plant, converts the antibacterial fluoroquinolone norfloxacin to N-acetylnorfloxacin and three other metabolites. Because N-acetylation results in loss of antibacterial activity, identification of the enzyme responsible is important for understanding fluoroquinolone resistance. The enzyme was identified as glutamine synthetase (GS); N-acetylnorfloxacin was produced only under conditions associated with GS expression. The GS gene (glnA) was cloned, and the protein (53 kDa) was heterologously expressed and isolated. Optimal conditions and biochemical properties (K m and V max ) of purified GS were characterized; the purified enzyme was inhibited by Mn 2؉ , Mg 2؉ , ATP, and ADP. The contribution of GS to norfloxacin resistance was shown by using a norfloxacin-sensitive Escherichia coli strain carrying glnA derived from Microbacterium sp. 4N2-2. The GS of Microbacterium sp. 4N2-2 was shown to act as an N-acetyltransferase for norfloxacin, which produced low-level norfloxacin resistance. Structural and docking analysis identified potential binding sites for norfloxacin at the ADP binding site and for acetyl coenzyme A (acetyl-CoA) at a cleft in GS. The results suggest that environmental bacteria whose enzymes modify fluoroquinolones may be able to survive in the presence of low fluoroquinolone concentrations. Fluoroquinolones are widely used as human and veterinary antimicrobial agents (1). Because their persistence in the environment (2) may act as a selective pressure for naïve strains to acquire resistance (3), an understanding of the fate of these drugs should help to prevent drug resistance. The principal resistance mechanisms for fluoroquinolones include the following: (i) mutation of genes for the drug targets (GyrA, GyrB, and ParC) (4-6), (ii) mimicking the drug targets (QnrA, QnrB, and QnrS) (7-9), (iii) reduction of drug accumulation in the cells (AcrAB-TolC and QepA) (4, 10, 11), and (iv) enzymatic modification of the drug [N-acetylation by AAC(6=)-Ib-cr] (12-14).In some strains of Escherichia coli, a mutated aminoglycoside acetyltransferase, AAC(6=)-Ib-cr, acetylates fluoroquinolones at the N-terminal of the piperazine ring (12-14) and enhances bacterial resistance to these drugs (14). Production of N-acetylnorfloxacin and N-nitrosonorfloxacin by environmental Mycobacterium sp. strains has also been found, but the enzymes responsible for modifications are unknown (15) and the aac(6=)-Ib-cr variant gene has not been detected in these strains (12).A norfloxacin-modifying bacterium, Microbacterium sp. strain 4N2-2, was isolated from wastewater (16). Some strains of this genus have been isolated from human clinical specimens, and the majority of them have shown fluoroquinolone resistance (17). Microbacterium sp. 4N2-2 transforms norfloxacin into four different metabolites, including N-acetylnorfloxacin, and cell extracts of this strain catalyze the N-acetylation of norfloxacin (16). NAcetylation is enhanced by Casamino Acids and inhibited by ammo...

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Identities of Microbacterium spp. Encountered in Human Clinical Specimens

Cited by 108 publications

References 20 publications

The Caenorhabditis elegansbus-2 Mutant Reveals a New Class of O-Glycans Affecting Bacterial Resistance

The Caenorhabditis elegansbus-2 Mutant Reveals a New Class of O-Glycans Affecting Bacterial Resistance

Bacteremia Caused by Microbacterium binotii in a Patient with Sickle Cell Anemia

Identification of the Enzyme Responsible forN-Acetylation of Norfloxacin by Microbacterium sp. Strain 4N2-2

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