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Important resistant bacteria Flashcards

1
Q

Why do we have antibiotic resistant bacteria?

A

•Poor antibiotic stewardship (see antibiotic stewardship lecture)
- over prescribing in the community and hospital
- lack of knowledge on correct dosing & drug spectrum
- poor access to diagnostic facilities
•Non compliance i.e. not completing course
•Overuse in agriculture
•Bacteria are very good at adapting to develop resistance i.e. through mutation or genetic exchange processes (conjugation, transformation, transposition, transduction)

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2
Q

what is the impact of antibiotic resistance?

A

• Increased microbial fitness
- bacteria less susceptible to treatments
• Increased morbidity and risk of mortality
- Empiric treatment failures
- Use of broad spectrum antibiotics as empiric treatment
- common infections once easily treated with antibiotics are now more difficult
- patients more susceptible to complications of infection e.g. sepsis
- poorer outcomes
• Increased costs associated with patient care
- longer hospital stays
- use of more expensive medications

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3
Q

what are the multidrug-resistant G-negative bacteria?

A

Gram negative bacteria that demonstrate resistance to at least three of the four main antibiotic classes consisting of broadband penicillins, cephalosporins (groups 3 and 4), carbapenems, and fluoroquinolones. Antibiotics that are principally regarded as a combination partner (e.g., aminoglycosides) or a reserve antibiotic (e.g., glycylcycline) are not part of this definition.

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4
Q

what are the key antibiotic-resistant bacteria

A
  1. Penicillin-resistant Streptococcus pneumoniae
  2. Meticillin resistant Staphylococcus aureus (MRSA)
  3. Vancomycin-resistant enterococci (VRE)
  4. Resistant Enterobacteriaceae:
    - Extended spectrum β lactamase (ESBL) producers
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5
Q

what is the VRE?

A

Definition: bacterial strains of the genus Enterococcus that are resistant to the antibiotic vancomycin (e.g., E. faecalis , E. faecium)
Resistance: acquisition of van genes ( through the transposition of plasmid-encoded genes.) → alteration of peptidoglycan synthesis pathway → inhibits binding of vancomycin to peptidoglycan

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6
Q

how does vancomycin work?

A

Vancomycin binds to the d-alanine-d-alanine amino acid sequence of peptidoglycan precursors, thereby inhibiting cell wall synthesis of gram-positive bacteria.

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7
Q

what is the MRSA?

A

Resistance: developed by forming a modified penicillin-binding protein (PBP) that inhibits binding to beta-lactam antibiotics, thereby decreasing their bactericidal effect
Occurrence: asymptomatic colonization of the nasal mucosa estimated at 0.5–5% of the population
Measures to curb MRSA
Hygiene measures: hand disinfection, protective clothing (gown, mask) , disinfection of patient rooms
Patient isolation, if necessary cohort isolation
MRSA eradication in asymptomatic carriers
Mupirocin nasal ointment, antiseptic solution for skin/hair contamination (e.g., chlorhexidine)

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8
Q

the resistance of MRSA to beta-lactams is due to beta-lactamases. True/False

A

False
The resistance mechanism of MRSA is caused by modified PBPs, not the formation of beta-lactamase! Every detected case of MRSA (symptomatic or asymptomatic) requires treatment!

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9
Q

define penicillin-resistant pneumococci

A

he resistance mechanism of MRSA is caused by modified PBPs, not the formation of beta-lactamase! Every detected case of MRSA (symptomatic or asymptomatic) requires treatment!

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10
Q

define penicillin-resistant pneumococci

A
  • mainly in the community and largely in children.
    • Resistance through the modification of the structure of penicillin-binding proteins in cell-wall synthesis.
    • associated with community-acquired pneumonia and bloodstream infections
    • meningitis in children and the elderly
    • Cross-resistance to other penicillins is common - as is resistance to other antibiotics such as cephalosporins, clarithromycin (a macrolide), tetracyclines and co-trimoxazole.
    • Resistance arises from the acquisition of a gene cassette or transposon encoding resistance to multiple antibiotics.
      • To date, no resistance to vancomycin has been reported!
    • The 23-valent pneumococcal polysaccharide vaccine (PPSV23) is now recommended for adults and high-risk children.
    • It is an effective prevention against both the penicillin-susceptible and resistant pneumococci.
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11
Q

how pneumococci became resistant to penicillin?

A

Resistance through the modification of the structure of penicillin-binding proteins in cell-wall synthesis.

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12
Q

how pneumococci acquire resistance to penicillin

A

Resistance arises from the acquisition of a gene cassette or transposon encoding resistance to multiple antibiotics.

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13
Q

pneumococci are resistant to vancomycin.

True/False

A

False

To date, no resistance to vancomycin has been reported!

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14
Q

what is the PPSV23?

A

PPSV23 is a vaccine that protects against 23 serotypes of S. pneumoniae. It is recommended in the elderly and individuals > 2 years of age with high-risk factors, including functional or anatomic asplenia, immunosuppresion, chronic heart or lung disease, cochlear implants, and cerebrospinal fluid leaks.

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15
Q

what is included in the empirical therapy of bacterial meningitis?

A

1) IV antibiotics for different patient groups
- -< 1 month: ampicillin PLUS aminoglycoside (e.g., gentamicin) PLUS third-generation cephalosporin (e.g., cefotaxime or ceftriaxone )
- -> 1 month to < 50 years: vancomycin PLUS third-generation cephalosporin (e.g., cefotaxime or ceftriaxone)
- -> 50 years: vancomycin PLUS ampicillin PLUS third-generation cephalosporin (e.g., cefotaxime or ceftriaxone)
- -Immunocompromised: vancomycin PLUS ampicillin PLUS cefepime OR meropenem
- -Hospital-acquired: vancomycin PLUS ceftazidime OR cefepime OR meropenem
2) Possibly dexamethasone: only beneficial in some cases
- -In adults: when pneumococcal meningitis is strongly suspected or confirmed
- -In children: for suspected or confirmed HiB meningitis
3) Doxycycline (during a tick-bite season in endemic areas only!)

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16
Q

when ampicillin is included in the empirical therapy of bacterial meningitis?

A

Ampicillin is added if patients are at risk of Listeria infection (e.g., newborns, pregnant women, elderly or immunocompromised patients) because cephalosporins are ineffective against Listeria.

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17
Q

when do you need to change antibiotics after empirical therapy?

A

when susceptibility results will be available

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18
Q

what kind of infections causes MRSA?

A

• Mainly associated with hospital and other healthcare environments e.g. Long term care facilities
- in recent years found in community (community-acquired MRSA).
• MRSA causes a similar spectrum of infections as methicillin susceptible S. aureus (MSSA) and is associated with numerous health-care associated infections
- surgical site (wound) infections
- device-related infections involving biofilms e.g. central lines
- blood stream infections

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19
Q

In the laboratory, MRSA is characterized by…

A
  • Gram-positive coccus in clusters
  • Coagulase-positive, catalase-positive
  • Ferments mannitol (colour change from pink to yellow)
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20
Q

how MRSA become resistant to beta-lactams?

A
  • Resistance is due to target site modification of the S. aureus penicillin binding protein which results in a lower affinity to β-lactam antibiotics.
  • Methicillin resistance is associated with the chromosomally located mecA gene.
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21
Q

MRSA can often display resistance also to

A

erythromycin, gentamicin and ciprofloxacin.

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22
Q

what antibiotics are used to treat MRSA?

A

• Alternative antibiotics used in treatment include glycopeptides (vancomycin and teicoplanin) linezolid, daptomycin and tigecycline.
• Care should be taken when prescribing these antibiotics and they should always be only used appropriately or when indicated.
- e.g. Linezolid often on restricted use &tigecycline should not be used to treat blood stream infections.
• Resistance to vancomycin is emerging

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23
Q

what is the linezolid?

A

–An antibiotic commonly used to treat infection caused by gram-positive bacteria resistant to other antibiotics, e.g., methicillin-resistant staphylococci and vancomycin-resistant enterococci.
Mechanism of action:
–Inhibition of bacterial protein synthesis by binding at the 50S subunit of the bacterial ribosome

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24
Q

what is the tigecycline?

A

A bacteriostatic, broad-spectrum antibiotic that binds to the 30S subunit of the bacterial ribosome, which blocks peptidyl transferase and inhibits protein synthesis. Used to treat anaerobic, gram-positive, gram-negative, and multidrug-resistant organisms (e.g., MRSA, VRE).

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25
Q

how MRSA is prevented?

A

MRSA is best prevented by standard precautions (including hand hygiene), antibiotic stewardship, the isolation of colonised patients with contact precautions and decolonisation of colonised individuals.

  • -Hygiene measures: hand disinfection, protective clothing (gown, mask) , disinfection of patient rooms
  • -Patient isolation, if necessary cohort isolation
  • -MRSA eradication in asymptomatic carriers
  • -Mupirocin nasal ointment, antiseptic solution for skin/hair contamination (e.g., chlorhexidine)
26
Q

what are the side effects of vancomycin?

A
  • -Nephrotoxicity
  • -Ototoxicity/vestibular toxicity
  • -Rapid infusions are associated with anaphylactoid reactions (“red man syndrome” or “red neck syndrome”)
  • -Thrombophlebitis
  • -Neutropenia
27
Q

what is the red man syndrome of vancomycin?

A

Diffuse flushing of the skin, hypotension, and dyspnea due to the rapid release of histamine following nonspecific mast cell degranulation; Red man syndrome can be prevented by slowing the rate of infusion and possibly pretreating with antihistamines.

28
Q

what are the side effects of linezolid?

A

Bone marrow suppression (especially thrombocytopenia)
Peripheral neuropathy
GI upset
Serotonin syndrome (Linezolid inhibits monoamine oxidase activity. Therefore, its use with other monoamine oxidase inhibitors (MAOI) and selective serotonin reuptake inhibitors (SSRIs) is contraindicated.)

29
Q

what antimicrobial agent is used in a patient with MRSA colonization?

A

mupirocin

30
Q

what is the mupirocin?

A

An antibiotic that is primarily effective against gram-positive bacteria. Used topically for treatment of skin infections (e.g., impetigo, folliculitis) and MRSA decolonization (when applied to the anterior nares).

31
Q

linezolid drug is licensed for maximum use of…

A

4 weeks

32
Q

what parameters should be monitored in the case of linezolid use?

A
  • Weekly full blood counts- myelosuppression has been reported (including anemia, leucopenia, pancytopenia, and thrombocytopenia)
  • There are potential interactions with the Selective Serotonin Reuptake Inhibitors and a tricyclic group of antidepressants. Unless close observation and blood pressure monitoring are possible, linezolid is contraindicated for patients taking these drugs.
  • Peripheral neuropathy and optic neuropathy have been reported – Patients should be advised to report symptoms of visual impairment or any numbness or tingling felt in the extremities or worsening of pre-existing neuropathy.
  • Linezolid can increase the patient’s blood pressure when taken with food/beverages that contain high tyramine content (cheese, beer, and yeast or soya bean products) and patients should be advised to avoid these.
  • Metabolic acidosis i.e. increase in plasma acidity has been reported with linezolid
33
Q

VRE is found in?

A

enteric tract or vagina

34
Q

VRE is prevalent in?

A

Prevalent in most countries within the community but mostly in the healthcare setting.

35
Q

VRE always cause only infection

A

Not always associated with infection i.e. individuals may be colonized

36
Q

what kind of infections cause VRE?

A

UTIs, bloodstream, infections, central line infections (usually long term devices become colonised), peritonitis and surgical site (wound) infections.

37
Q

what are the microbiological characteristics of VRE?

A

Gram-positive cocci in short chains that have variable haemolytic growth patterns on Columbia blood agar. They can grow on MacConkey agar where they appear as small magenta-coloured colonies.

38
Q

how VRE acquires resistance?

A

• There are six different mechanisms of resistance in VRE depending on what resistance genes have been acquired.

  • -vanA+ = resistant to both vancomycin and teicoplanin,
  • -vanB+ = isolates or strains are resistant vancomycin but still susceptible to teicoplanin.

Resistance is due to the alteration of the amino acid side-chains of the peptidoglycan cell wall.

39
Q

administration of which antibiotics are associated with VRE acquisition?

A

Prior administration of cephalosporins, macrolides, and fluoroquinolones is associated with VRE acquisition.

40
Q

does VRE colonization require treatment?

A

Individuals may become colonised with VRE and these patients do not require treatment.

41
Q

VRE cause infectious diarrhea. True/False

A

False

but colonised individuals may shed the organisms during a bowel movement.

42
Q

how VRE is spread?

A

VRE can be easily spread through the hands of healthcare workers and can often be found in the environment.
- Correct hygiene and infection prevention measures are necessary to stop the spread of the antibiotic resistant organism in the healthcare environment.

43
Q

what are the ESBL producing bacteria?

A

Include Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis and Enterobacter cloacae (bowel organisms)
A group of bacteria that produce beta-lactamases capable of inactivating penicillins, cephalosporins, and carbapenems in isolated cases.

44
Q

how ESBLproducing organisms are diagnosed?

A

routinely cultured on MacConkey agar and they can be non-lactose (P. mirabilis) or lactose fermenters (E. coli and K. pneumoniae).

45
Q

ESBLs cause what type of infections?

A

ESBLs are common causes of UTIs in the hospital, in nursing homes and in the community.
- also often the cause healthcare-associated infections such as intra-abdominal infections and surgical site (wound) infections.

46
Q

how ESBLs acquire antibiotic resistance genes?

A

The genes encoding ESBL enzymes are often acquired on plasmids.

47
Q

what is the mechanism of resistance to antibiotics of ESBL’s?

A

– The enzymes are capable of hydrolyzing and inactivating a wide variety of β-lactams, including penicillins and third cephalosporins e.g. cefotaxime and ceftazidime.
– The plasmids may carry additional genes that confer resistance to other antibiotics, such as aminoglycosides and fluoroquinolones.

48
Q

what antibiotics are used to treat ESBLs?

A
  • Meropenem (carbapenem) can be suitable in patients with severe infection or those that are critically ill but it should only be prescribed on advice from a clinical microbiologist & pharmacist!
  • Even though they can be highly resistant, nitrofurantoin may be useful in patients with an uncomplicated cystitis
  • Gentamicin, amikacin (both aminoglycosides), and ciprofloxacin (a fluoroquinolone) may be useful where indicated but only if the organism is susceptible to MIC testing.
  • ESBLs are a significant cause of morbidity and mortality within the healthcare environment
49
Q

what risk factors predispose to infection with ESBL?

A

prolonged previous exposure ot broad spectrum antibiotics, living in care facility

50
Q

how ESBL acquires enzymes for resistance?

A

on a plasmid,

51
Q

what is the most likely source of ESBL?

A

own gut flora,

52
Q

what are ‘carbapenems’?

A

class of broad-spectrum, β-lactam antibiotics that are resistant to β-lactamase. Administered intravenously due to poor enteric absorption. Examples include imipenem, meropenem, ertapenem, and doripenem.
Gram-negative activity (including ESBLs), anaerobes (Bacteroidesfragilis), Gram-positive bacteria (Enterococcus spp. &Listeria spp.)
• Treatment of an ESBL infection with a carbapenem is associated with a more favourable outcome and clearance of infection
- Meropenem indicated for intraabdominal infections, meningitis and UTIs
- Imipenem indicated for use as above but requires co-administration with cilastatin to prevent inactivation in renal tubule (not indicated for meningitis due to CNS toxicity e.g. altered mental state, seizures)
• Resistance already emerging

53
Q

why imipenem is administered with cilastatin?

A

Cilastatin inhibits human dehydropeptidase I, a renal tubular enzyme that breaks down imipenem.

54
Q

which carbapenem is toxic to CNS?

A

imipenem

55
Q

what is the colistin (Polymyxin E)

A

A cationic detergent molecule disrupts cellular membranes and causes cell death due to leakage of intracellular contents. Used to treat infections caused by gram-negative bacilli (particularly Pseudomonas aeruginosa) that are resistant to other antibacterial drugs.
• Is the polymyxin (E) antibiotic with a narrow spectrum of activity (Gram-negative infections)
• A bactericidal drug that binds to lipopolysaccharides and phospholipids in the outer cell membrane of Gram-negative bacteria.
- It competitively displaces divalent cations from the phosphate groups of membrane lipids, which leads to disruption of the outer cell membrane
• Indicated for use in hospital-acquired infections and in cystic fibrosis lung infections
- these infections often involve multi-drug resistant bacteria e.g. Acinetobacter sp.
• Can be administered intramuscularly or given in a nebulized form
• Can be nephrotoxic, neurotoxic and interact with other medicines e.g.cephalothin (1st generation cephalosporin)

56
Q

what are the carbapenemase-producing Enterobacteriaceae?

A

A group of gram-negative bacteria, including Klebsiella and E. coli, that can produce enzymes capable of inactivating antibiotics of the carbapenem class (e.g., meropenem). cause numerous healthcare-associated infections such as bloodstream infections, pneumonia, and surgical site (wound) infections.
• Causing much concern as treatment options are extremely limited.
- produce enzymes (carbapenemases) that hydrolyze broad spectrum β-lactams, including third-generation cephalosporins.
- also resistant carbapenems such as meropenem.
- Cross-resistance is also common and CRE isolates and strains can be resistant to common fluoroquinolones and aminoglycosides.

57
Q

what is the treatment of carbapenemase-producing Enterobacteriaceae?

A
  • Effective treatments would include tigecycline, colistin or fosfomycin
58
Q

does glycopeptide resistantS. aureus is common?

A

• Vancomycin resistance is still uncommon but glycopeptide resistance has been recorded especially in the United States.
- Resistance has emerged from the transfer of van genes from VRE to MRSA.
• The degree of resistance varies and is determined by laboratory MIC testing. Breakpoints usually between 0.5-2 μg/ml for S. aureus
- isolates are classified as being VISA (intermediate resistance) or VRSA (fully resistant).
- VISA isolates have vancomycin MICs of between 4-8
- VRSA isolates have vancomycin MICs of > 16 μg/ml.
• VISA and VRSA have the potential to cause healthcare associated infections such as central line infections, bloodstream infections, ventilator associated pneumonia and surgical site (wound) infections.

59
Q

what are the treatment options for VISA and VRSA?

A

linezolid

60
Q

list other important resistant organisms

A
  • Other bacteria you should be aware of are MDR Pseudomonas aeruginosa and the emergence of quinolone resistance in Nesseria gonorrhoeae.
  • In the tropics, ciprofloxacin resistance has been recorded in Salmonella Typhi and antibiotic resistance is also emerging in Shigellaspp. and Vibrio spp.
  • Resistance to components of highly active antiretroviral therapy (HAART) has been documented in HIV.
  • Aciclovir resistance is has emerged in Herpes simplex,
  • Oseltamivir resistance has been found in influenza.
  • In fungi, azole resistance has been noted in Candida spp.
  • In parasites chloroquine resistance has also been seen in Plasmodium falciparum.

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