The patient was an 84-year-old woman, a nursing home resident with underlying medical problems including tracheostomy for ventilator-dependent end-stage chronic obstructive pulmonary disease, chronic indwelling Foley catheter, atherosclerotic heart disease, hypertension, and congestive heart failure. The patient was referred to our hospital with complaints of fatigue for 2 to 3 months and fever on and off for least 2 to 3 weeks. On physical examination, the patient had a new loud murmur in mitral area, diffusely diminished breath sounds, and fever of 38.8°C.
A chest radiograph showed chronic emphysematous changes, and the blood work revealed 17,800/µL leukocytes (84% neutrophils and 16% lymphocytes). Blood cultures done at admission revealed gram-positive cocci in chains within 24 hours in 8 out of 8 bottles. These were later identified as Enterococcus raffinosus (BD Phoenix Automated Microbiology System) with a confidence level of 99%. Susceptibility by BD Phoenix Automated Microbiology System for minimum inhibitory concentration were: penicillin (1.0), ampicillin (1.0), moxifloxacin (0.50), daptomycin (2.0), linezolid (2.0), gentamicin-synergy (<500), and vancomycin (>16). Transthoracic echocardiography revealed normal functioning valves, without evidence of vegetation, thrombi, or pericardial effusion. Transesophageal echocardiography on hospital day 2 detected a small mobile echodensity attached to the mitral valve, consistent with a vegetation. Urine and sputum culture remained negative for bacterial growth.
The patient initially received vancomycin 1 g every 12 hours, ampicillin 2 g every 4 hours, and gentamicin 80 mg every 8 hours intravenously. Once E. raffinosus was identified on day 3, vancomycin was discontinued. Gentamicin was given for the first 2 weeks and ampicillin for a total of 6 weeks. Subsequent blood cultures during antibiotic therapy remained negative for bacterial growth. The patient had a complete recovery.
The French word enterocque was first used in 1899 by Thiercelin to describe gram-positive cocci of enteric origin that formed pairs and short chains. The genus Enterococcus includes 17 species. Although Enterococcus faecalis and Enterococcus faecium account for most clinical infections, other less common species such as Enterococcus avium and Enterococcus durans are known to cause significant disease.1-4 In 1989, a new species, E. raffinosus, was distinguished from the phenotypically similar species E. avium by the ability of the former to metabolize raffinose,1,5 a characteristic not recognized unless detailed biochemical examination is undertaken. The natural habitat of E. raffinosus is not known, but this microorganism has been identified in the oropharynx of domestic cats.6
The API 32 STREP identification system identifies only Enterococcus casseliflavus, E. durans, E. avium, Enterococcus gallinarum, and Enterococcus hirae from the recently described enterococcal species. Identification data for other enterococcal species including Enterococcus cecorum, Enterococcus dispar, Enterococcus gilvus, Enterococcus mundtii, Enterococcus pallens, and Enterococcus raffinosus are missing in the API 32 STREP system. E. raffinosus is commonly misidentified as E. avium.7,8 This misidentification may explain why E. raffinosus has been so rarely reported in humans. The BD Phoenix System, however, included E. raffinosus in its gram-positive identification database.
The first vancomycin-resistant clinical isolates of Enterococcus species were reported in Europe in 1988. Since then, vancomycin-resistant enterococci have spread with unexpected rapidity and are now encountered in hospitals in most countries. Six types of vancomycin resistance have been characterized on both a phenotypic and a genotypic basis in enterococci.9 VanA, VanB, VanD, VanE, and VanG correspond to acquired resistance. VanC is an intrinsic property of E. gallinarum and E. casseliflavus-Enterococcus flavescens. VanA-type strains display high levels of inducible resistance to both vancomycin and teicoplanin, whereas VanB-type strains have variable levels of inducible resistance to vancomycin only.10 VanD-type strains are characterized by constitutive resistance to moderate levels of the 2 glycopeptides.11 VanC-, VanE-, and VanG-type strains are resistant to low levels of vancomycin but remain susceptible to teicoplanin.12 The VanA and VanB operons are located on plasmids or in the chromosome,13 whereas the VanD,11 VanC,14 VanE,15 and VanG16 operons have, thus far, been found only in the chromosome.
A MEDLINE search of the terms "Enterococcus raffinosus" and "infection" found 33 cases of infections in humans caused by E. raffinosus, summarized in Table 1. However, detailed susceptibility patterns, treatment, andoutcome results were not available for many cases. Itseems to occur more often in elderly patients as nosocomial infections.18,19 Most of the reports describe resistance to ampicillin and penicillin and susceptibility tovancomycin.17-19 Reports of VanA7 and VanD21 types ofvancomycin resistance in E. raffinosus are available. These different results elucidate that it is difficult to provide susceptibility pattern for E. raffinosus from the few reports available so far.
Enterococcus currently is recognized as one of the most common causes of nosocomial infections and is becoming increasingly resistant to numerous antibiotics including vancomycin. This report confirms the potential of E. raffinosus to cause serious infections in humans, as described in previous reports, and emphasizes the need for further molecular-based species identification methods for enterococcal isolates that cannot be identified with certainty by traditional microbiological methods.
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