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Clinical Infection & Immunity

Case Report

Volume 1, Number 1, September 2016, pages 6-7

Enterococcal Bacteremia Caused by Enterococcus casseliflavus: A Case Report

The genus Enterococcus are Gram-positive, catalase-negative, facultative anaerobes. They are frequently isolated from polymicrobial wound infections. Enterococcus faecalis and Enterococcus faecium are the most common isolates from human infection(s) [1]. These two isolates account for more than 90% of clinical isolates. Since the 1980s vancomycin resistance among enterococcal species has become a great concern in Western Europe and the United States. Genotypes of vancomycin resistance have been described as vanA-E, G, L. VanA and vanB genotypes are associated with E. faecalis and E. faecium. This is clinically significant because these strains demonstrate inducible high level resistance to vancomycin. This resistance is transmissible with plasmids to other strains. VanC1 is specific to E. gallinarum and vanC2 to E. casseliflavus. These strains exhibit low level vancomycin resistance and susceptibility to teicoplanin. They are common normal flora inhabitants of the gastrointestinal tract of the general population [2].

Bacteremia is the third most common type of infection caused by all enterococci. Enterococcal bacteremia associated with E. faecalis and E. faecium is generally associated with a high mortality rate. Since 1989, there have been only 56 reported cases of E. casseliflavus bacteremia [1-4]. We report a similar case in a middle-aged Caucasian female who was currently undergoing chemotherapy for adenocarcinoma of the pancreas.

Risk factors associated with E. casseliflavus bacteremia include: biliary disease (most common), solid organ transplant (second most common), chronic renal failure, diabetes mellitus, hematologic malignancy, bone marrow transplant, antithrombin III deficiency, pancreatic carcinoma, chronic osteomyelitis and any immunocompromising state.[3, 4]. Polymicrobial bacteremia occurs in 45% of cases. There is incomplete evidence of increased incidence of bacteremia caused by E. casseliflavus with prior antibiotic use including vancomycin. Up to 17% of E. casseliflavus isolates demonstrate vancomycin resistance. E. casseliflavus has been reported as the causative agent in cases of endophthalmitis, spontaneous bacterial peritonitis, meningitis, pericarditis, thrombophlebitis and sepsis [4-10]. Mortality rates (1.9%) appear to be lower in those individuals who develop bacteremia from a biliary source.

A 57-year-old Caucasian female was admitted to the general medical floor with a 3-day history of nausea, vomiting and fevers. The patient was currently undergoing active chemotherapy with gemcitabine for adenocarcinoma of the pancreas. She had post-Whipple procedure 7 months prior. On admission, BP was 116/60, pulse was 102, and rectal temperature was 102.7 °F. Laboratory tests showed WBC 6,400/μL (4.0 - 11.0), hemoglobin 10.4 g/dL (12.0 - 15.4), hematocrit 31.0% (35-45%), albumin 3.1 g/dL (3.5 - 5.5), alkaline phosphatase 712 IU/L (36 - 108), SGOT/AST 288 IU/L (10 - 38), SGPT/ALT 220 IU/L (10 - 38), lipase 20 IU/L (7 - 60), total bilirubin 3.3 mg/dL (0.0 - 1.3), direct bilirubin 2.1 mg/dL (0.0 - 0.2), procalcitonin 0.16 ng/mL (< 0.10), urinalysis: 3+ bacteria, nitrate positive, 5 - 10 WBC/hpf, urine culture > 100 CFU Escherichia coli, and blood culture positive for Enterococcus casseliflavus (vancomycin resistant).

The patient was started on ceftriaxone 1 g intravenous (IV) every 24 h for a presumptive lower urinary tract infection. The patient continued to have febrile episodes (Tmax 101.4 °F) over the next 48 h. Urine culture demonstrated E. coli resistant to ampicillin. One blood culture was positive for E. casseliflavus resistant to vancomycin but sensitive to ampicillin. Ceftiraxone was continued and the patient was placed on IV ampicillin 1 g every 6 h. The patient rapidly became afebrile after the infusion of ampicillin. IV antibiotic therapy was continued for 5 days and which time the patient was discharged home on oral ampicillin 250 mg TID for 7 days.

This patient was at increased risk of development of E. casseliflavus bacteremia because of a recent biliary tract surgery, adenocarcinoma of the pancreas and active chemotherapy.

The incidence of rare enterococci as pathogens has increased over the past 25 years. The year 2015 is the 28th anniversary of the first documented report of vancomycin-resistant enterococcus (VRE) [11]. The increased use of vancomycin for the treatment of methicillin-resistant Staphalococcus aureus (MRSA) is directly related to the emergence of VRE. Seven phenotypes of vancomycin resistance have been documented. Enterococci isolates with VanA resistance are primarily E. faecium and E. faecalis. These enterococci possess a high level of resistance to vancomycin (MIC > 128 μg/mL) and teicoplanin (MIC > 16 μg/mL). VanB enterococci demonstrate variable resistance to vancomycin (MIC 4 - 1,024 μg/mL) and are susceptible to teicoplanin (MIC < 0.5 μg/mL).

Current treatment regimens for VRE include combinations of teicoplanin + amoxicillin or ampicillin + imipenem. Tigecycline and daptomycin have been used with varying success [12]. Telavancin has good activity against VanB isolates but has not been FDA approved for the treatment of VRE infections. The streptogramin combination antibiotic quinupristin-dalfropristin is available for the treatment of E. faecium infections but is ineffective against E. faecalis. Linezolid is available orally and intravenously for the treatment of VRE strains of E. faecalis and E. faecium.

Less than 10% of E. faecalis isolates from ICU patients are vancomycin resistant in contrast to greater than 70% of E. faecium isolates.

Clinical infections caused by E. casseliflavus and E. gallinarum can be serious [13]. It is important for the clinician to recognize those risk factors that put a patient at risk for the development of infections caused by these organisms. Recognizing that approximately 20% of these isolates have intrinsic vancomycin resistance helps direct appropriate antibiotic therapy in at risk individuals. In fact, enterococci with an MIC < 4 μg/mL are categorized as “susceptible to vancomycin” may not be susceptible in vivo [3].

These bacteria generally considered to be normal inhabitants of the gastrointestinal tract can become pathogenic in an immunocompromised host. Appropriate recognition and antibiotic choice can decrease morbidity and mortality in these individuals.

Conflicts of Interest

The author declares he has no conflicts of interest.

Consent

Written informed consent for the publication of any materials associated with any individual who may be a participant in this manuscript has been verified.

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