2. INTRODUCTION
• Enterococci are gram-positive cocci which often occur in pairs
(diplococci).
•Occur almost everywhere, including soil, food, water, plants, animals,
birds, and insects
•they inhabit in humans and other animal's gastrointestinal tract and the
female genital tract
• In humans, Concentrations of enterococci in Stool are up to 108 CFU
per gram.
• When the bacteria seeds elsewhere it will cause infections including
urinary tract, blood, and wound infections.
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3. VRE
• Vancomycin-antibiotic used to treat the infections caused by enterococci.
• In some cases the bacteria has become resistant to this antibiotic.
• They call this resistant bacteria vre (vancomycin-resistant enterococci).
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4. TRANSMISSION OF VRE
• Direct contact with stool, urine or blood containing VRE.
• Indirectly: spread via the hands or on contaminated environmental
surfaces.
• VRE usually is not spread through casual contact such as touching or
hugging.
• Not spread through the air by coughing or sneezing
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6. RISK FACTORS
• Enterococci growing (colonizing) in body (mostly intestines)
• Contact with infected person or contaminated fomite
• Previous treatment with vancomycin or another antibiotic for a long time
• Being hospitalized (e.g. ICU, etc.) Or long term care facility
• Weak immune system
• Treated with corticosteroids, parenteral feeding, chemotherapy
• Having chest or abdominal surgery
• Having urinary catheter
• Undergoing dialysis
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7. MECHANISM OF ACTION
MOA: inhibits cell wall synthesis.
Mechanism of resistance:
• Mediated by van genes- alters the target site for vancomycin present in cell wall.
• Vancomycin and teicoplanin inhibit cell wall synthesis by forming complexes
with peptidyl-d-alanyl-d-alanine termini.
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8. Genotypes of van gene
• Van A to van G.
• Strains for van A gene: has high level resistance to both vancomycin (va) and
teicoplanin (tei).
• Van B strains: low level resistance to vancomycin , sensitive to teicoplanin
• Van C strains: intrinsic resistance to both va and tei.
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9. • Van G and E: low level resistance to va, sensitive to tei.
• Van A and van B resistance phenotypes are associated with the
acquisition of gene clusters that lead to the production of peptidoglycan
ending in d-alanyl-d-lactate or d-alanyl-d-serine
• Altered side chains have less affinity for binding to vancomycin
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10. CLINICAL MANIFESTATIONS
• Prominent nosocomial cause.
• Urinary tract infection (UTI)-most common
• Intra-abdominal and pelvic infection (also common)
• Surgical wound infection
• Bacteraemia- bacteria in the blood
•Endocarditis - infectionof the inner surface of the heart muscles and valves
•Neonatal sepsis -bacteria in the blood, occurring in infants
• Meningitis -infection of the membranes that surround the brain and spinal
cord
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12. SAMPLE COLLECTION
• sample of the infected tissue is taken.
• wound infection- a swab is rubbed over the surface to get infected material.
• Blood is drawn and cultured to detect sepsis or endocarditis.
• Urine samples are taken to identify urinary infections
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13. CULTURE
• On BA: non-haemolytic, translucent colonies.
• Grow in presence of bile hydrolyse the esculin; and liberate aesculetin.
• Aesculetin combines with ferric chloride brown/black coloured complexes.
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14. • Pyrrolidinyl-beta-naphthylamide (PYR) test: positive
• Chromogenic medium for the detection of vancomycin resistant enterococcus
(VRE) E. Faecalis and E. Faecium.
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15. ANTIBIOTIC SUSCEPTIBILITY TESTING (AST)
• Susceptibility to vancomycin by kirby- bauer disc diffusion Method on mueller
hinton agar ( M H A )
• By using 30µg vancomycin disc .
• Resistance also determined by vancomycin agar screen method using 6µg/ml of
vancomycin incorporated in brain heart infusion (BHI) agar.
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16. MINIMUM INHIBITORY CONCENTRATION (MIC)
• Def: the lowest concentration of antimicrobial agent that will inhibit the growth of
a microorganism after overnight incubation.
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18. MOLECULAR METHODS
• By polymerase chain reaction (PCR).
• Useful in epidemiologic studies.
• PCR cant be performed directly on clinical specimens.
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20. PREVENTION AND CONTROL
• Limiting use of certain broad spectrum reduce rate of VRE colonization and
infection.
• Reduction of third-Generation cephalosporins (3GP)
• Substitute with piperacillin/tazobactam reduce the incidence of VRE in
intensive care unit setting.
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21. SUGGESTIONS OF PREVENTION
• Isolate patient
• Contact precaution sign on door of room
• Equipment used for patient remains in same room
• Kill germs by frequent hand hygiene especially after using toilet
• Avoid touching open sores
• Any gross contamination of body fluids should be cleaned up ASAP.
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