Lecture 5 -2nd half Flashcards
(41 cards)
slide 38
review at end
slide 39
review at end
What to know to select correct treatment:
-identify organism
-susceptibility of organisms to a give mobile agent
-client factors (regnanct, allergies, breastfeeding)
-safety of drugs
-cost of drug
Gram negative:
-thin peptidoglycan layer
-has outer lipid layer that has LPS: harder for antibiotics to penetrate LPS layer
-gram stain pink
Gram Positive:
-thick layer of peptidoglycan
-no outer lipid layer
-gram stain purple
Gram variable Bacteria:
-not clearly pink or purple gram stain (both)
-mobiluncus spp, and gardnerella vaginalis which are typical associated with bacterial vaginosis are gram variable
-it’s likely BV if not yeast
slide 44 labelling gram + vs -
mobiluncus and gerdnerella
mobiluncus = gram - with thin peptidoglycan cell wall and an outer membrane
gernerella = gram + with thick cell wall and absence of external membrane
antibiotic resistance
-antibiotic resistance rapidly increased (superbugs, MRSA as examples)
-how to avoid:
1.Use antibiotics properly and avoid when possible
2.Start with narrow-spectrum (narrow treats single group of microbes, extended/medium treat more globally, broad spectrum is a wide range)
3.Culture and sensitivity tests (helpful with drug allergies)
4.Counsel clients appropriately (complete entire course of treatment)
-**slide 47 = white circles are different antibiotics, yellow is bacteria. Circles with big green circles are effective antibiotics for that specific bacteria
Antibiotic Resistance causes:
-occurs when antibiotics that have historically killed a given strain of bacteria no longer work
-arises from alteration sin bacterial DNA (mutations or takes on DNA from another strain)
Antibiotic Resistance Mechanisms:
-microbes can become antibiotic resistant by take DNA from another drug resistant strain (horizontal gene transfer)
-drug resistance genes often coded on plasmid dna
horizontal gene transfer occurs in 3 ways:
- transformation
-pieces of dna are taken up from the external environment - conjugation
-transfer of plasmid dna via direct cell to cell contact (via a pilus) - transduction
-a bacteriophage (virus that infects bacteria) performs the gene transfer
slide 50 antibiotic resistance mechanisms
Antibiotic Resistance Types
- Enzymatic inactivation of antibiotic
-most common mechanism
-bacteria make enzymes that metabolize antibiotics
-ex beta-lactamases - Decreased antibiotic uptake
-gram - organisms can be resistant to some antibitoics as drug cannot pentrate outer cell membrane
-decrease number of porins/protein channels
-ex cephalopsporins - increased antibiotic efflux
-energy dependent pumps transport the drug out of cells
-ex quinolones - modification of antibiotic targets
-receptors for drugs, target molecules, enzymes are modified
-ex. s. aureus became resistant to methicillin because the penicllin-binding protein changed shape
slide 52 antibiotic resistance - types
Antibiotics:
-anti life - inhibit growth of bacteria without hammering host
-bacteriocidal = kill directly, ex penicillins make holes in bacteria, bacteria die, immune system clears up the cellular fragments
-bacteriostatic = stop growth or division of bacteria
-need an actively fighting immune system to resolve the infection
slide 54 modes of antibiotic action
cell wall synthesis inhibitors
-peptidoglycan cell wall is in bacteria is made of a carbohydrate backbone linked together by amino acid side chains and cross bridges
-the beta-lactam antibtioics (ex peniciilins and cephalosporins) inhibit the formaion of the peptide cross-bridges
-the peptidoglycan cell wall is thus incomplete and weakened, and the cell may undergo autolysis
slide 56 cell wall synthesis inhibitors
slide 57 protein synthesis inhibitors
yt video
Protein synthesis inhibitors - 50s subunit
50s subunit
-clindamycin
-macrolide class - azithromycin and erythromycin
Protein synthesis inhibitors - 30s subunit
30s subunit:
-aminoglycoside class - gentamicin
-tetracycline class - doxycycline
-trna interference:
-mupirocin (part of apno)
dna synthesis inhibitors
fluroquinolones inhbit dna synthesis:
-most common is cirprofloxacin
-gets inside bacteria via porins and inhibits DNA gyrase
-dna gyrase is the enzyme responsible for relaxing/uncoilin DNA so it can be replicated
nitrofurantoin is a prodrug:
-activated by susceptible bacteria when excreted into urine
-reactive intermediates have many functions, including inhibit bacterial DNA synthesis but also:
inhibit protein synthesis, inhibit aerobic energy metabolism, inhibit RNA synthesis, inhibit cell wall synthesis
