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Antibiotic Pharmacology Cheat Sheet by

antibiotics cheat sheet including prescriptions for Ontario chiropodists

Gram Positive Bacteria

- Plasma membrane covered by thick peptid­oglycan (murein) cell wall
-Certain abx inhibit synthesis of the petido­glycan cell wall: penici­llins, cephal­osp­orins, bacitr­acin, vancom­ycin, monoba­ctams and carbap­enems
-Blue purple stain
-most common aerobic gram + bacteria w/ podiatric compli­cat­ions: staphy­loc­occus (grm += staph aureus, grm - = staph epider­midis), strept­ococcus - penicillin sensit­ive­/no­n-p­eni­cil­linase producing, methic­illin resistant staph aureus, methic­illin sensit­ive­/pe­nic­ill­inase producing, vancomycin resistant staph a and coryne­bac­terium
Group A strep common in superf­icial skin infections (erysi­pelas)
Group B strep very common in diabetic foot infections
Group A and B strep sensitive to: penici­llins, cephal­osp­orins, clinda­mycin, erythr­omycin
Cornye­bac­terium minuti­ssimum is implicated in erythrasma (treat with erythr­omycin)
*If C&S reports MRSA or group D strep (enter­oco­cci), consider infectious disease consult

Gram Negative Bacteria

-Plasma membrane covered by a thinner peptid­oglycan cell wall which is then covered w/ an outer lipopo­lys­acc­haride membrane
-prohibits entry of most penici­llins and cephal­osp­orins
- resists the uptake of blue dye so stains pink
-Aerobic gram - pathogens: enterics like salmon­ella, klebsi­ella, proteus, etc, pseudo­monas, etc
some broad spectrum synthetic penici­llins and 3rd gen cephal­osp­orins (IV) may allow some entry through outer membrane. However, space b/ cell wall and outer membrane is high in B-lact­amases which is a penici­lli­n-d­est­roying enzymes
The addition of B-lact­amase inhibitor (clavu­lanic acid) to a broad spectrum penicillin may increase its spectrum of activity to include some gram - coverage
*possible to have a mixed gram + and gram - bacteria (ie diabetic foot that has been exposed)


-infec­tions often composed of mixed gm+ and gm- bacteria
produce foul smelling gas and frequently encased in abscess wall
common anaerobes: clostr­idium which respond well to penici­llin, clinda­mycin and tetrac­yline. infection may be aggressive and may need iV therapy and surgical interv­ention
Bacteroids are also a common anaerobe which is a gm- bacillus. They are common in diabetic foot infect­ions. Abx therapy include PO clinda­mycine, amoxi clav.

inhibitors of Cell Wall Synthesis - B-Lactams

The final step in bacterial cell wall synthesis is cross linking of adjacent peptid­oglycan strands. B-lactams bind to transp­ept­idase (penic­illin binding proteins) prevents crossl­inking of peptid­oglycan strands in cell wall during wall synthesis leading to weakened cell wall and eventually cell death
Natural PCNs
Penici­llinase Resistant PCNs (Cloxa­cillin) - good for strep, penici­llinase producing staph, anaerobes except bacter­oides
Aminop­eni­cillins (Amoxi­cillin) - good for strep, gm- organisms, non penici­llinase producing staph, anaerobes other than bacteroids
Penici­lli­n/B­-La­ctamase Inhibitor (Amoxi­cillin clavul­anate)- good for strep, increase in gm - (not pseudo­monas), penici­llinase producing staph, anaerobes including bacter­oides. Beta-l­act­amase inhibitors are a class of medicine that block the activity of beta-l­act­amase enzymes (also called beta-l­act­ama­ses), preventing the degrad­ation of beta-l­actam antibi­otics ie amoxic­illin which can be restored and widened with clavul­anate
Most PCNs are excreted unchanged via renal tubular mechanism, therefore dosages must be adjusted in pts w/depr­essed renal function
PCNs are bacter­iocidal
Side effects: anaphy­laxis, 5-15% cross sensit­ivity w/ cephs, rash/d­erm­atitis, nephritis, diarrhea, entero­colitis
1st Gen- Cephal­exin, Cefadr­oxil. Good for gm+ staph (penic­ill­inase & non-pe­nic­ill­inase producing except MRSA), & strep, okay against gm- and anaerobes other than bacteroids
Most cephal­osp­orins are excreted unchanged via renal tubular mechanisms (secre­tion). need to adjust dosage in pts w/ reduced renal function
Bacter­iocidal activity
Side effects: same as penici­llins

Cell Wall Synthesis inhibitor- Glycop­eptides

MOA: glycop­eptide that inhibits cell wall synthesis by preventing transport of cell wall precursors
Activity against gm+ and some gm-. However pseudo­monas is resistant
side effects: nephro­toxic, neurotoxic and toxic to bone marrow if used system­ically therefore only used topically

Folate Antago­nists

Synergists -> produces a greater effect when used together
MOA: Bacteria synthesize folate from pteridine & PABA, whereas humans require dietary folate b/c humans don't have the enzymes seen in this bacterial pathway, these abx are relatively free of adverse effects. Prevents formation of folate at step and ultima­tely, the synthesis of bacterial purines and DNA, resulting in a bacter­ios­tatic effect.
Metabo­lized in liver
effective against Gm+ organisms & some strains of MRSA, excellent coverage of Gm-, except pseudo­monas
Bacter­ios­tatic, renal clearance
Side effects: allergic reactions in 30% population (poten­tially fatal), diarrhea, N/V, compete w/bili­rubin for binding sites on serum albumin -> kernic­terus in newborns (increase bilirubin levels) , hemolytic anemia in pts w. G6PD defici­ency, renal clearance

Folate Antago­nists- Quinolones

Inhibit DNA synthesis through a specific action on DNA gyrase or topois­omerase IV. Topois­ome­rases (DNA gyrase or topois­omerase IV) bind to DNA -> transient cleave complexes (double stranded breaks). In presence of quinol­ones, levels of cleavage increase dramat­ically. After traversal by replic­ation complexes, these breaks become permanent double stranded fractures -> cell death
Excellent activity against all Gm- organisms, including pseudo­monas. Marginal activity against staph A, including some strains of MRSA, minimal activity against strep or anaerobes
100% bioava­ila­bility, renal and hepatic clearance, bacter­iocidal
Best bet for highly suspected Gm- or pseudo­monas bacteria
Side effects: N/v, contra­ind­icated in children with open growth plates due to to possible cartilage degene­ration, tendon degene­ration, peripheral neurop­athy, mental health side effects and blood sugar distur­bances (hypog­lyc­aemic coma), concom­itant NSAID use may increase risk of CNS stimul­ation and convul­sions, aortic aneurysm, highest risk of causing coloni­zation w/MRSA and C.difficle

Antibiotic Mechanism of Action

Inhibitors of Protein Synthesis- 30S Subunit

MOA: bind reversibly to the 30S ribosomal subunit at a position that blocks the binding of the aminoa­cyl­-tRNA to the acceptor site on the mRNA-r­ibosome complex. Protein synthesis is ultimately inhibited, leading to a bacter­ios­tatic effect
effective against gm+ except MRSA, few gm- and some anaerobes (no bacter­oides)
Bacter­ios­tatic, renal clearance
Side effects: possible allergic rxn, diarrhea+ N/V, thromb­oph­leb­itis, photos­ens­iti­vity, kidney toxicity, intera­ction w/calcium, need to be taken on empty stomach
Aminog­lyc­osides (Genta­myc­in,etc)
Effective against aerobic gm- and pseudo­monas, not effective against anaerobes
Topica­l/IV, bacter­ioc­idal, renal clearance
Side effects: possible allergic rxn, diarrhea, n/v, nephro­tox­icity, ototox­icity, neurom­uscular block, photos­ens­itivity
Prokar­yotes have 70s ribosomes, consisting of a 30s and 50s subunit

Inhibitors of Protein Synthesis- 50S Subunit

Bind reversibly to the 50S ribosomal subunit at a position that blocks the binding of the aminoa­cyl­-tRNA to the acceptor site on the mRNA-r­ibosome complex. Protein synthesis is ultimately inhibited, leading to a bacter­ios­tatic effect
Erythr­omycin (Macro­lides)
Effective against gm+ except MRSA, few gm- and some anaerobes (no bacter­oides)
Bacter­ios­tatic and hepatic clearance
Side effects: possible allergic rxn, diarrhea, n/v, thromb­oph­leb­itis, hepato­tox­icty, metabo­lites can inhibit certain cp450 isoenzymes in the liver & thereby increase conc. of drugs also metabo­lized by liver enzymes (eg increase in levels of calcium channel blockers)
Clinda­mycin (Linco­sam­ides)
Effective against gm+ including some MRSA, and most anaerobes, including bacter­oides; however not effective against c.diff­icile
Bacter­ios­tatic (very close to bacter­ioc­idal), hepatic clearance
good penetr­ation of most tissues, including bone
Side effects: Diarrhea

Cell Wall Synthesis Inhibitors

Cloxac­illin Penici­llinase resistant penici­llins
250 or 500 mg, mitte: X tablet­s,sig: 1 PO every 6h for x days
Amoxic­illin Aminop­eni­cillins
250 or 500mg, mitte: X tablets, sig: 1 Po every 6-8 hours for x days
Amoxic­ill­in/­cla­vul­anate Penici­llin/ B/lact­amase inhibitor
250,50­0,8­75mg, mitte: x capsules. sig: 1 PO every 8-12h (12 for 875mg)
Cephalexin Cephal­osporin
250 or 500mg, mitte: X tablets, sig: 1 PO every 6h for X days
Cefadroxil Cephal­osp­orins
500mg, mite: x capsules, sig: 1 PO every 12h for x days

Protein Synthesis Inhibitor

Clinda­mycin Lincos­amides
150 or 300mg, mitte: X capsules, sig: one PO every 6-8 hours for X days
Erythr­omycin Macrolides
250 or 500mg, mitte: X tablets, sig: 1 PO every 6h for X days
Azithr­omycin Macrolides
250mg, mitte: 6 tablets, sig: day 1- 2 tablets once PO, days 2-5: 1 tablet PO daily
Tetrac­yclines (30S subunit)
250 or 500mg, mitte: X tablets, sig: 1 PO every 6h for X days

Folate Antago­nists

Sulfam­eth­oxa­zol­e/t­rim­eth­oprim Sulfon­ami­des­/tr­ime­thoprim
800/160mg tablets, mitte: X tablets, sig: 1 PO every 12h for X days
Ciprof­loxacin Quinolones
250,50­0,750mg mitte: X tablets, sig: 1 PO every 12H


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