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infectious diseases > Microbiology and Antibiotics > Flashcards

Microbiology and Antibiotics Flashcards

1
Q

Broad classification of bacteria:

A

Gram positive cocci:

  • Staphylococci + streptococci (including enterococci)

Gram negative cocci

  • Neisseria meningitidis + Neisseria gonorrhoeae (diplococcus), moraxella catarrhalis

Gram positive rods (bacilli)

  • Actinomyces
  • Bacillus anthracis
  • Clostridium
  • Corynebacterium diphtheriae
  • Listeria monocytogenes

Gram negative rods (bacilli)

  • Escherichia coli
  • Haemophilis influenzae
  • Pseudomonas aeruginosa
  • Salmonella
  • Shigella
  • Campylobacter jejuni
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2
Q

Classification of gram positive bacteria

A
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3
Q

Classification of gram negative bacteria

A
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4
Q

Bacteria that do not stain well on gram stain

A

These rascals may microscopically lack colour

  • Treponoma
  • Rickettsia
  • Mycobacteria
  • Mycoplasma
  • Legionella
  • Chlamydia
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5
Q

Mechanism of action common antibiotics

A
  1. Inhibitors of cell wall synthesis
  2. Inhibitors of protein synthesis
  3. Inhibitors of membrane function
  4. Anti-metabolites
  5. Inhibitors of nucleic acid synthesis
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6
Q

Notes on becteriocidal vs bacteriostatic antibiotics

A

Bacterialcidal Antibiotics

  • Kill bacteria - Very finely proficient at cell murder
  • Vancomycin
  • Fluoroquinolones
  • Penicillins
  • Aminoglycosides
  • Cephalosporins
  • Metronidazole

Bacteriostatic antibiotics

  • ECSTaTiC
  • Erythromycin
  • Clindamycin
  • Sulfamethoxazole
  • Trimethoprim
  • Tetracyclines
  • Chloramphenicol
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7
Q

Note on time dependent antibiotics

A
  • Once the concentration of the antibiotic is above MIC (typically 3-5x MIC) there is not an increased rate of killing with increased antibiotic exposure
  • E.g.s beta lactams, vancomycin, macrolides, aztreonam, carbapenams, clindamycin, tetracyclines, quinupristin/dalfopristin
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8
Q

Notes on concentration dependent antibiotics

A
  • Rate and extend of microorganism killing are a function of antimicrobial concentration
  • Fluoroquinolones, aminoglycosides
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9
Q

Examples of antibiotics that are inhibitors of cell wall synthesis

A

Beta lactams

  • Penicillins
  • Cephalosporins
  • Monobactams
  • Carbapenems

Glycopeptides

  • Vancomycin
  • Teicoplanin

Fosfomycin

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10
Q

Notes on beta lactams

A
  • Common structural beta lactam ring. Antibiotics vary by side chain attached
  • Target = PBPs in the cytoplasmic membrane
  • PBPs involved in peptidoglycan synthesis (bacteriostatic action). Also autolysin activity (bactericidal action)

Spectrum

  • GPs → no barrier to entry, PBPs on outer surface
  • Enterococcus → PBPs different to other GPs → low level of resistance to penicillins
  • GNs → many naturally resistant to penicillin G as drug can’t enter cell (LPS blocks porins)
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11
Q

Notes on penicilllins

A
  • Inhibition of bacterial cell wall synthesis via PBPs
  • Spectrum - see slide
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12
Q

Notes on cephalosporins

A
  • Enzyme drug target = PBPs
  • Cephalosporins produce persistent suppresion of bacterial growth (post-antibiotic effect) of several hours duration with GP but minimal post-antibiotic effect with GN bacteria
  • Spectrum of activity → see slide
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13
Q

Notes on ceftaroline

A
  • 5th generation cephalosporin
  • High affinity for PBP-2A (altered binding site that gives methicillin resistance)
  • Low side effect profile → case reports of eosinophilic pneumonia
  • Active against GPs and resistant Strep pneumo, some GP anaerobes, and may be avtive against VRE (faecalis, not faecium)
  • Limited activity against GNs
  • Emerging data on treatment of MRSA bacteraemia
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14
Q

Notes on carbapenems

A
  • E.g. imipenem, meropenam, ertapenem
  • Active against GP, GN, anaerobic bacteria - efficient penetration through bacterial outer membrnes
  • High affinity for multiple PBPs and stability against most beta-lactamses including class A ESBLs and class C beta lactamases (AmpCs)
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15
Q

Notes on carbapenems

A
  • E.g. ertapenem, imipenem, meropenem
  • Parenteral bactericidal beta-lactam antibiotics
  • Spectrum of activity against:
    • Haemophilus
    • Anaerobes
    • Most enterobacterales (inc. those that produce AmpC beta-lactamases and ESBL)
    • Methicillin-sensitive staphylococci and streptococci
    • Most enterococcus faecalis and pseudomonas are susceptible to imipenem, and meropenam (but resistant to ertepenam)
  • Imipenem and meropenam penetrate CSF. Meropenam used for gram-negative bacillary meningitis (imipenem not used as can cause seizures)
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16
Q

Notes on aztreonam:

A
  • Monobactam - a parenteral beta-lactam bactericidal antibiotics (aztreonam only available antibiotic in monobactam class)
  • Similar spectrum of activity to ceftazidime. Activity against:
    • Pseudomonas
    • Enterobacterales that do not produce AmpC beta-lactamase, ESBL, or klebsiella pneumoniae carbapenemase (KPC)
  • No activity against gram positive bacteria, or anaerobes
  • Cross-hypersensitivity with other beta-lactams unlikely - mainly used for severe aerobic gram-negative infections (inc. meningitis) in those with serious beta lactam allergy
  • May also have activity against bacteria which produce metallo-beta-lactamases
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17
Q

Notes on glycopeptides

A
  • E.g vancomycin and teicoplanin

Vancomycin

  • Inhibit finalcell wall stage of peptidoglycan synthesis (binds D-ALA-D-ALA)
  • All are bactericidal
  • Activity against gram positive only → MRSA, penicillin-resistant enterococcal infections, penicillin resistant Strep. pneumo, no gram negative activity
  • Adverse effects:
    • Nephrotoxicity, ototoxicity, Red Man syndrome, neutropaenia, thrombocytopaenia, rash

Teicoplanin

  • Similar to vancomycin. Equally as effective
  • Longer half life
  • Nephrotoxicity/ototoxicity relatively rare
  • Drug level monitoring not required (unless pre-existing renal impairment)
  • Less red man syndrome
  • More expensive
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18
Q

Notes on Fosfomycin

A
  • Inhibits peptidoglycan assembly by irreversibly blocking the MurA enzyme disrupting cell wall synthesis
  • Also decreases bacteria adhereance to uroepthelial cells
  • Broad spectrum: aerobic GP and GN (activity against >90% of isolates of common urinary pathogens)
  • Main use: UTI without bacteraemia, pyelonephritis or perinephric abscess (single dose for simple cystitis)
  • Primarily eliminated unchanged in kidneys with high urinary levels, efficacy reduced in renal impairment
  • Time dependent killing
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19
Q

Penicillin and cephalosporin cross-reactivity

A
  • Rate of cross-reactivity 2%
  • More likely A/W with structurally similar side chains (R1 side chain) rather than the beta lactam ring
  • Higher in older generation cephalosporins
  • Cephalexin → high cross-reactivity with penicillin, concurrent use should be avoided if history of cephalexin anaphylaxis
  • Cefazolin - minimal cross-reactivity - if history of cefazolin anaphylaxis should not preclude the use of other beta lactams
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20
Q

Antibiotics that are inhibitors of protein synthesis

A
  • Aminoglycosides
  • MLSK - Macrolides, lincosamides, streptgramins, ketolides
  • Tetracyclins
  • Glycylcyclines
  • Phenicols
  • Oxazolidinones

30S subunit ribosome = tetracyclines and aminoglycosides

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21
Q

Notes on aminoglycosides

A
  • Akikacin, gentamicin, tobramycin, streptomycin, kanamycin
  • Bind to 30S ribosomal subunit - affects all stages of protein synthesis
  • Rapid bectericidal effect
  • Broad-spectrum GN activity, synergistic activity against GPs
  • No anaerobic activity
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22
Q

Notes on macrolides and ketolides

A
  • Macrolides → azithromycin, erythromycin, clarithromycin
  • Ketolides → telithromycin (greater efficacy against S. pneumonia)
  • Inhibit 50S ribosomal subunit
  • Broad spectrum: GP (including MRSA), some GN, atypicals → legionella, chlamydia pneumonia, mycoplasma)
  • ADRs → increased peristalsis, prolonged QT, cholestatic hepatitis
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23
Q

Notes on Lincosamides → Clindamycin

A
  • 50S subunit ribosome
  • Spectrum: GPs, anaerobes (including Bacteroides fragilis)
  • Inhibits toxin production → useful in GAS and Staphylococcal toxic shock (combined with penicillin)
  • ADRs: high risk C. diff
24
Q

Notes on Streptogramins

A
  • Pristinamycin (quinupristin/dalfopristin)
    • Mixture of Pristinamycin I1 (macrolide) and pristinamycin IIA (streptogramin A) → SYNERGISTIC
  • Inhibtis 50S subunit
  • Spectrum: VRSA, VRE
25
Q

Notes on tetracyclines

A
  • Tetracycline, doxycycline, minocylcine
  • Irreversibly binds to 30S subunit
  • Broad spectrum GP, GN, intracellular organisms, protazoan parasites
  • Resistance common
  • Proteus mirabilis only GN to have intrinisic resistance
26
Q

Notes on Glycylcyclines: Tigecycline

A
  • Semi-synthetic derivative of minocycline
  • Inhibits bacterial protein synthesis by binding to 30S subunit - 5x greater affinity caompared with tetracyclines → can overcome the ribosomal protection mechanism of tetracycline resistome
  • Broad GP (including VRE, MRSA, listeria), GN, anaerobic and atypical cover
  • Eliminated via biliary tract → not useful for UTIs (and doesn’t require dse adjustment in CKD)
  • Active against GPs (VREM MRSA), GNs (ESBLs and AmpC producers), anaerobes, rapid growing mycobacteria and Nocardia, Actinetobacter, Strenotrophomonas
  • High VD → low serum concentrations, not suitable for initial treatment of bacteraemia
  • Only 25% excreted in urine - limited use in UTIs
  • Potential salvage therapy for C dif
  • Black box warning → increased mortality
27
Q

Notes on chloramphenicol

A
  • 50S subunit
  • Very active against gram positive and gram negative → clhamydia, mycoplasma, rikettsia
  • ADRs → bone marrow aplasia and other haemtological abnormalities
  • Grey baby syndrome in neonates and premies
  • Widely used in developing countries
28
Q

Notes on oxazolidinones: linezolid

A
  • 50S subunit (and 30S)
  • GP - effective for E. faecium including VRE, MRSA, and MDR S pneumonia
  • Gets into brain and bone
  • 100% oral bioavailability
  • Bacterostatic against enterococci and staphylococci, bactericidal for most streptococci
  • Gram negatives natrually resistance
  • ADRs: bone marrow suppression , serotonin syndrome, irreversible peripheral neuropathy, optic neuropathy (rare)

Tedizolid

  • Better version of linezolid
  • OD dosing (linezolid BD)
  • More potent, smaller doses possibly with less myelotoxicity
29
Q

Examples of antibiotics that are inhibitors of membrane function

A
  1. Polymyxins
  2. Cyclic lipopeptides
30
Q

Notes on Polymyxins

A
  • Target = membrane phospholipids (LPS, and lipoproteins)
  • Bind to cell membrane, alters structure and makes it more permeable, disrupting osmotic balance
  • Cell wall of GPs too thick to permit access
  • Polymyxin B
    • Narrow spectrum for GN used for UTI, blood, CSF and eye infections
  • Colistin
    • Narrow spectrum for GNs, especially P aueruginosa infections in CF patients.
    • Recent use for MDR Acinetobacter infections
31
Q

Notes on Cyclic Lipopeptides: Daptomycin

A
  • Binds to components (Ca ions) of cells membranes of susceptible organisms and causes rapid depolarisation, inhibiting intracellular synthesis of DNA, RNA, protein
  • Active against GP including those resistant to methicillin, vancomycin and linezolid
  • Gram negatives resistant
  • Inactivated by surfactant → cannot used for resp
  • Adverse effects → myopathy (serial CKs), peripheral neuropathy, eosinophilic pnuemonia
32
Q

Notes on Anti-metabolites: Co-trimoxazole

A

Sulfamethoxazole

  • Nucleotide and DNA formation requires tatrehydrofolate (TH4)
  • Bacteria make their own TH4 using PABA
  • If sulfa drug present - bacteria use this instead of PABA → inhibits production of TH4

Trimethoprim

  • TH4 gives up carbon atoms to form purines and other metabolic building blocks → TH2 and must be reduced back by dihydrofolate reductase
  • TMP looks like dihydrofolate reductase → competitively inhibits reduction → inhibits bacterial DNA formation

TMP/SMX act synergistically

Spectrum:

  • Wide GP and GN cover, no anaerobes, certain parasites (PCP, toxoplasma gondii, isosopora belli)
  • ADRs (rare in non-HIV) → rash, BM suppression, increased creatinine/K
  • Do not co-administer with methotrexate
  • TMP inhibits renal tubular secretion of creatinine affecting GFR
33
Q

Antibiotics that inhibit nucleic acid synthesis

A
  1. Fluoroquinolones (norfloxacin, ciprofloxacin, levofloxacin, ofloxacin, moxifloxacin)
  2. Ansamycins (rifampicin)
34
Q

Notes on fluoroquinolones

A
  • Target → topoisomerases e.g. DNA gyrus, regulates DNA supercoiling
  • Most potent activity against aerobic GNB (Enterobacter, P auroginosa, haemophilius)
  • Active against resp pathogens (levo and moxi more so than cipro) - strep. pneumoniae, haemophlius, moraxella, legionella, chlamydia, mycoplasma
  • Norfloxacin concentrates in urine → minimal activity outside urinary tract
  • Rapid bactericidal activity
  • ARDs: tendinopathy, unmasking MG, QTc prolongation
  • Chelation is an issue when taken with multivalent cations (Ca, Mg, Al, Fe, Zn)
35
Q

Notes on rifamipicin

A
  • Forms a stable complex with RNA polymerase → prevents DNA from being trascribed into RNA → inhibits protein synthesis
  • Bacteriostatic or bactericidal (depending on on organism and concentration)
  • Primarily GP and some GNs
  • Low barrier to resistance → must be co-administered with another antimicrobial
  • Used in combinations with other drugs → S. aureus, M. tuberculosis, and contacts of N. meningitidis
36
Q

Causes of antibiotic resistance

  • Penicillin-resistant bacteria
  • ESBL
  • Fluoroquinolone resistance
A
  • MRSA and other penicillin resistant bacteria - alteration of target- or binding site e.g. PBP the binding/target site of penicillins
  • ESBL - beta lactamases
  • Fluoroquinolones - reduced antibiotic permeability via cell wall
37
Q

Risk factors for acquisition of multidrug resistant organisms (general and specific to group)

A

General

  • Previous antimicrobial therapy
  • Prolonged hospital stays
  • Requirement for ICU/dialysis/invasive procedures, indwelling catheters/venous catheters

MRSA

  • Maori and Pacific ethnicity

ESBL and VRE

  • Rest home facilities

CRO (NDM-1)

  • Patients who have received medical care in India or Pakistan
38
Q
  • Notes on MRSA mode of resistance
A
  • Resistance conferred by mecA gene carried on a mobile genetic element - the Staphylococcal cassette chromosome - encodes and additional penicillin binding protein (PBP2a) → transpeptidase (cross-links bacterial cell wall peptidoglycan) with poor affinty for ALL beta lactam antibiotics (penicillins, cephalosporins (exception caftaroline) (I-IV), carbapenams)
  • Not enzymatic → can’t be overcome by beta-lactamse inhibitor
  • Panton-Valentine Leucocidin
    • PVL → pore forming necrotising endotoxin.
    • Initially considered important in pathogenesis of necrotising pneumonia and soft tissue infections, but not endocarditis or bacteraemia
    • Now thought to be likely an epidemiological marker of a particular strain causing more severe disease rather than the key pathogenic factor
    • More commonly seen in community MRSA than hospital
39
Q

Treatment for iMRSA infections

A

Non-severe

  • Options include: co-trimoxazole, clindamycin, erythromycin, doxycycline, rifampicin, gentamicin
  • Rifampicin or fusidic acid = rapid resistance if used as monotherapy

Severe

  • Vancomycin (glycopeptide)
  • Alternatives
  1. Daptomycin - non inferior to vanc but poor CNS penetration, inactivated by surfactant
  2. Teicoplanin - comparable efficacy to vanc, often underdosed and needs drug monitoring
  3. Ceftaroline (5th gen cephalosporin) - high affinity for PBP2a
  4. Quinupristin-dalfopristin - side effects - myalgias, infusion reactions, nausea
  5. Linezolid - good oral bioavailability and tissue penetration, bone marrow suppression and peripheral neuropathy
  6. Clindamycin - high oral bioavailability, not recommended for endovascular infections
  7. Co-trimoxazole - inferior to vanc for endovascular infections, best for skin/soft tissue
40
Q

Notes on VRSA

A
  • VRSA → acquisition of a plasmid containing the mobile transposon with the vanA gene from VRE → alters the unlinked peptidoglycan terminus
  • Rx daptomycin + another agent (Co-trim, gent, rifampicin)
  • VISA → vancomycin intermediate S. aureus (mechanism thought to be due to cell wall thickening)
  • hVISA → heterogenous VISA - isolates appear to have a susceptible MIC for vancomycin, but have a subpopulation that are VISA - population analysis profile required to detect these
41
Q

Notes on VRE (Vancomycin resistant Enterococci)

A
  • Enterococci (E. faecium, E. faecalis)
    • Typical sites of infection → UTI/catheter associated, central line, bacteraemia/endocarditis, pelvic/abdominal, wound
    • Typically treated with penicillin, amoxicillin/ampicillin or vancomycin
    • Intrinisic resistance to multiple antibiotics - cephalosporins, macrolides, glycopeptides, tetracyclines, fluroroquinolones
      • E.faecium typically resistant to amoxicillin, E. faecalis often sensitive
  • Changes enterococcal cell wall to prevent vancomycin binding. D-ALA-D-ALA → D-ALA-D-LAC
  • 5 groups of vancomycin resistance (Van A → E). VanA and VanB typically seen in E.faecium and E.faecalis
  • VanA gene cluster confers resistance to vancomycin and teicoplanin, vanB confers resistance to vancomycin only
  • Transferable resistance mechanism (plasmid) to eneterococci and other bacteria (e.g. VRSA)
  • Limited treatment options → penicillin (maybe only vanc resistant), teicoplanin (VanB, Van C), linezolid, daptomycin, tigecycline, quinupristin-dalfopristin, ceftroline (but not E. faecium)
  • Simple UTIs may be treated with nitrofurantoin or fosfomycin
42
Q

Mechanisms of beta lactam resistance in gram negative bacteria

A
  1. Altered porins
  2. Beta-lactamases - AmpC, ESCL, CRE
  3. Prevention of binding - altered PBPs
  4. Efflux pumps
43
Q

Notes on beta-lactamases

A
  • Most common mechanism of resistance in gram-negative bacteria against beta lactam drugs
  • May be called penicillinases or caphalosporinases
  • Many different enzymes now → nearly 900 identified
    • Include ESBLs KPC, NDM-1, AmpC, OXA
44
Q

Notes on AmpC beta-lactamases

A

ESCHAPPM organisms

  • Found on chromosomes in the following bacteria
    • Enterobacter
    • Serratia
    • Citrobacter ffreundii (not koseri) - freundii not your friend
    • Hafnia alvei
    • Acinetobacter and Aeromonas
    • Proteus vulgaris (not mirabilis)
    • Providencia
    • Morganella

May appear sensitive to 2nd and 3rd generation cephalosporins on initial lab testing

Resistance develops during treatment because of:

  • An inducible cephalosporinase or
  • Antibiotic therapy selects out a derepressed mutant

Cefepime is still effective against AmpC organisms

  • AmpC beta-lactamases either chromosomally mediated or plasmid mediated - plasmid mediated = infection control nightmare

Antibiotics for ESCHAPPM organisms

  • Carbapenams - empiric antibiotic of choice
  • Cefepime
  • Tazocin maybe
  • Once sensitivies known - quinolones, co-trimoxazole, aminoglycosides may be an option
45
Q

Notes on ESBLs

A
  • Resistant to all penicillins, cephalosporins (including cefepime) and aztreonam
    • May also carry genes that confer resistance to several non-beta lactam antibiotics
  • Prior hospitalisation and antibiotic therapy (particularly cephalosporins) risk factors, also travel to Asia/India
  • ESBL genes carried on plasmids and easily transferrable between bacteria
  • Most commonly found on E.coli and Klebsiella

Treatment

  • Carbapenams
  • ESBLs are inhibiteted by beta-lactamase inhibitors - clavulanate, tazobactam but some bacteria produce such large amounts of ESBL they can overwhelm the beta-lactamase inhibitor
  • OP UTI treatment options for ESBL
    • Nitrofurantoin - many ESBLs susceptible
    • Depending on susceptibilities - cipro, cotrim, boosted Augmentin, fosfomycin
46
Q

Note on carbapenem-resistant organisms

A
  • Mechanisms of resistance - efflux pumps, porin mutations, carbapenemase
  • 3 main groups:
    • Klebsiella pneumoniae carbapenemase (KPC)
    • Metallo-beta lactamases - e.g. New Delhi beta lactamases (NDM)
    • Oxacillinases (OXA 48)
  • Metallo-beta lactamases have a zinc moiety at active site, others have serine
  • Treatment with single agent = high mortality (40%). Combination therapy recommeneded
    • Colistin - effective against most, limited by nephro- and neurotoxicity
    • Tigecycline - bacteriostatic, poor tissue penetration
    • Amikacin - aminoglycoside, resistance mechanisms to the aminoglycosdes often carried on the same plasmid
    • Fosfomycin -efficacious in cystitis, data otherwise lacking
    • Ceftazidime-avibactam, ceftaroline-avibactam - efficacy against OXA and KPC groups but not NDM
    • Sometimes → high dose carbapenams
47
Q

Notes on Non-tuberculous mycobacterium following cardiac surgery

A
  • Recent case report in NZ - mycobacterium chimaera following cardiac surgery
  • Limked with use of a heater/coller device commonly used in cardiac surgery
  • Should be suspected in patients who have had cardiac surgery presenting with fatigue/fever/pain (including muscle/joint), redness, heat or puss at surgical site/night sweats/weight loss/abdominal pain, nausea/vomiting
  • Cultures will be negative and patient will not respond to conventional antibiotics
48
Q

Antibiotics that do not cross the blood brain barrier at high concentrations

A
  • Aminoglycosides
  • Erythromycin
  • Tetracyclines
  • First generation cephalosporins
49
Q

Notes on antibiotics options/indications for brain abscess or subdural empyema

A
  • Empiric → ceftriaxone and metronidazole

Specific antibiotics

  • Pencillin G → covers most mouth flora inc. aerobic and anaerobic streptococci
  • Metronidazole - readily penetrates brain abscesses. Excellent activity against anaerobes, not active against aerobic oganisms
  • Ceftriaxone → covers most aerobic, microaerophilic streptococci, and enterobacteriaceae
  • Ceftazidime → use in the setting of abscess following neurosurgical procedure, or when culture grows Pseudomonas
  • Vancomycin → should be used following penetrating head injury or craniotomy, or S. aureus bacteraemia
50
Q

Treatment of Clostridium dificile infection

A
  • Non severe - oral vancomycin or fidaxomicin (metronidazole acceptable for low-risk patients)
  • Severe or fulminant → oral vancomycin or fidaxomicin.
  • FMT for refactory cases
51
Q

Role for anaerobic cover in aspiration pneumonia

A
  • Recommend metronidazole in:
    • Putrid sputum
    • Severe peridontal disease
    • History of chronic hazardous alcohol consumption
    • Development of lung abscess, empyema, necrotising pneumonia
    • Do not respond to initial empiric therapy
52
Q

Causes of community acquired pneumonia

A

Most common down

  • Streptococcus pneumoniae
  • Mycoplasma
  • Influenza
  • Picornaviruses
  • Haemophilus
  • Legionella
  • rsv
  • Chlamydia species
  • Psuedomonas
  • Gram negative enteric bacilli
  • S. aureus
  • Moraxella catarrhalis
53
Q

Tools that identify need for ICU in CAP

A
  • SMART-COP
  • CORB
54
Q

Notes on legionella pneumonia

A
  • Common cause of CAP in spring/summer in NZ (cover Sept → March)
  • Does not respond to beta-lactams
  • Can’t distinguish from other causes of CAP
    • Suspicion raised based on time of year, exposure to potting mix, not improving on amoxicillin
  • Test if severe CAP in hospital
    • PCR of sputum
    • Urinary antigen not recommended → does not detect L. longbaechae - commonest cause in NZ (only detects L pneumophila serogroup 1)
55
Q

Notes on AMP-C inducers

A
  • HECKY → Hafnia alvei, enterobacter cloacae, citrobacter freundii, Klebsiella aerogenes, Yersinia enterocolitica (Yersinia and Hafnia less well studied)
  • initially appear to be sensitive to beta-lactams but treatment failures seen due to an inducible cephalosporin/beta-lactamase - chromosomal AmpC (Amber class c)
  • Antibiotics that are poor substrates and weak inducers of AmpC → cefepime or meropenam
56
Q

Notes on renal toxicity in vancomycin combination therapy

A

CAMERA 2 study

  • RCT comparing flucloxacillin + standard therapy vs standard therapy alone for MRSA bacteraemia (standard therapy = vancomycin)
  • Ceased early due to nephrotoxicity in fluclox + vanc group → AKI even when vancomycin in therapeutic range
  • Nephrotoxicity also observed with co-administration of Tazocin
57
Q

Notes on Pneumococcal resistance

A
  • Mechanism of resistance to penicillins and cephalosporins is via alteration of PBPs (addition of clavulanic acid will do nothing)
  • Pneumococci develop antibiotic resistance by transformation - acquisition of genetic material from other bacteria in close proximity

Macrolide resistance

  • Either via mefA gene (efflux pump) or ermB gene (alteration of binding site)
  • Macrolide resistance cannot be overcome by higher doses (penicillin often can)

infectious diseases (10 decks)

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