Enterococci are
facultative anaerobic organisms, i.e., they are capable of
cellular respiration in both oxygen-rich and oxygen-poor environments.[3] Though they are not capable of forming
spores, enterococci are tolerant of a wide range of environmental conditions: extreme temperature (10–45 °C),
pH (4.6–9.9), and high
sodium chloride concentrations.[4]
Enterococci exhibit variable
hemolysis on
blood agar. Differences occur between species, and between strains of species. More
virulent organisms are more likely to exhibit alpha (partial) or beta (complete) hemolysis than less virulent specimens of Enterococcus, which frequently exhibit gamma (absent) hemolysis.[5]
History
Members of the genus Enterococcus (from
Greek έντερο, éntero 'intestine' and κοκκος, coccos 'granule') were classified as group D Streptococcus until 1984, when genomic DNA analysis indicated a separate genus classification would be appropriate.[6]
Evolution
This genus appears to have evolved 425 million years ago to 500 million years ago.[7]
Enterococcal meningitis is a rare complication of neurosurgery. It often requires treatment with intravenous or
intrathecal vancomycin, yet it is debatable as to whether its use has any impact on outcome: the removal of any neurological devices is a crucial part of the management of these infections.[12]
New epidemiological evidence has shown that enterococci are major infectious agent in chronic bacterial
prostatitis.[13] Enterococci are able to form
biofilm in the prostate gland, making their eradication difficult.[citation needed] Cases of enterococcal meningitis, in the absence of trauma or surgery, should raise suspicion of an underlying intestinal pathology (e.g., strongyloidiasis).[14]
Antibacterial resistance
From a medical standpoint, an important feature of this genus is the high level of
intrinsicantibiotic resistance. Some enterococci are intrinsically resistant to
β-lactam-based antibiotics (
penicillins,
cephalosporins,
carbapenems), as well as many
aminoglycosides.[8] In the last two decades, particularly virulent strains of Enterococcus that are resistant to vancomycin (
vancomycin-resistant Enterococcus, or VRE) have emerged in
nosocomial infections of hospitalized patients, especially in the US.[4] Other developed countries, such as the UK, have been spared this epidemic, and, in 2005, Singapore managed to halt an epidemic of VRE.[15] Although
quinupristin/
dalfopristin (Synercid) was previously indicated for treatment of VRE in the USA, the FDA approval for this indication has since been retracted.[16] The rationale for the retraction of Synercid's indication for VRE was based upon poor efficacy in E. faecalis, which is implicated in the vast majority of VRE cases.[17][18] Tigecycline has also been shown to have antienterococcal activity, as has
rifampicin.[19]
Bacillus haynesii CD223 and Advenella mimigardefordensis SM421 can inhibit the growth of Enterococcus spp. [20]
Water quality
In bodies of water, the acceptable level of contamination is very low; for example in the state of
Hawaii, and most of the United States, the limit for water off its beaches is a five-week geometric mean of 35 colony-forming units per 100 ml of water, above which the state may post warnings to stay out of the ocean.[21] In 2004, measurement of enterococci took the place of
fecal coliforms as the new American federal standard for water quality at public saltwater beaches and alongside Escherichia coli at freshwater beaches.[22] It is believed to provide a higher correlation than fecal coliform with many of the human pathogens often found in city sewage.[23]