Enterococcus gallinarum / casseliflavus
Gram-positive cocci in pairs and short chains
Identification & Growth
Identification
- Motile (E. gallinarum) and/or yellow pigment (E. casseliflavus)
- PYR-positive, bile-esculin positive, growth in 6.5% NaCl
Growth Conditions
- Blood agar and bile-esculin agar, 35–37 °C, 24 h
Clinical Significance
- Urinary tract infection, bacteremia and intra-abdominal infection
Intrinsic Resistance
- VanC: intrinsic low-level vancomycin resistance with teicoplanin remaining susceptible
- Cephalosporins, trimethoprim-sulfamethoxazole in vivo and aminoglycosides alone have no activity
Bench Alerts
- Do not report as hospital VRE: VanC is intrinsic and does not trigger outbreak contact precautions
- Differentiate from VanA/VanB E. faecium by motility, pigment and, when available, PCR
Clinical Notes
Clinical presentations
- Causes urinary tract infections, bacteremia, and rarely endocarditis, similar to other Enterococcus species.
- Associated with polymicrobial intra-abdominal infections in hospitalized patients.
- Infection is generally less severe and less frequent than E. faecalis or E. faecium.
Specimens and collection
- Urine, blood, and rectal swab (for vancomycin resistance surveillance) are the most relevant specimens.
- Blood cultures should be drawn from two distinct sites to assess true bacteremia.
- Surveillance rectal swab should be plated on selective chromogenic media for vancomycin-resistant enterococci.
Epidemiology and at-risk populations
- Part of the normal human and animal gut microbiota.
- Possesses intrinsic low-level vancomycin resistance (vanC genes), often clinically confused with acquired VRE.
- Long-stay hospitalized and immunocompromised patients are more susceptible to invasive infections.
Resistance and therapeutic implications
- Exhibits intrinsic low-level vancomycin resistance mediated by vanC, and should not be reported as clinically transmissible VRE.
- Differentiation from acquired vanA/vanB is essential for hospital contact isolation policies.
- Ampicillin generally retains activity and is the preferred therapeutic option when susceptible.
Bench and reporting notes
- Motility and yellow pigmentation (E. casseliflavus) aid preliminary phenotypic differentiation from other species.
- Molecular confirmation of vanC genotype is recommended to clarify intrinsic versus acquired resistance mechanism.
- Report should specify species to avoid unnecessary triggering of VRE control protocols.
Sources
- CDC — Vancomycin-resistant Enterococci (VRE)
- EUCAST — Clinical breakpoints
- PubMed — Enterococcus gallinarum and casseliflavus review
Educational decision-support content. It does not replace laboratory validation, current guidelines or review by the responsible professional.
FAQ: Frequently Asked Questions
How to identify Enterococcus gallinarum / casseliflavus in the lab?
Enterococcus gallinarum / casseliflavus is identified through motile (e. gallinarum) and/or yellow pigment (e. casseliflavus), pyr-positive, bile-esculin positive, growth in 6.5% nacl.
What are the intrinsic resistances of Enterococcus gallinarum / casseliflavus?
This organism is naturally resistant to vanc: intrinsic low-level vancomycin resistance with teicoplanin remaining susceptible, cephalosporins, trimethoprim-sulfamethoxazole in vivo and aminoglycosides alone have no activity. These drugs should not be reported as susceptible.
Where is Enterococcus gallinarum / casseliflavus commonly found?
It is typically associated with urinary tract infection, bacteremia and intra-abdominal infection.
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