Antimicrobials Lessons | Microbiology

🧫 Antimicrobials

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💊 Antimicrobials

Beta-lactam ring binds PBP → blocks cell wall cross-linking → lysis

Beta-Lactam Antibiotics — the largest antibiotic class

The largest and most widely used antibiotic class

Penicillins: narrow (amoxicillin, ampicillin) or extended (piperacillin). Cephalosporins: generations 1–5, increasingly broad. Carbapenems (imipenem, meropenem): broadest — last resort. Beta-lactamase inhibitors (clavulanate, tazobactam): added to overcome resistance.

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🃏 💊 Antimicrobials

Beta-lactams — how do they kill bacteria?

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🃏 Answer

Beta-lactam ring binds PBP → blocks cell wall cross-linking → lysis

Beta-Lactam Antibiotics — the largest antibiotic class

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💊 Antimicrobials · Resistance

BET: Beta-lactamase · Efflux pumps · Target modification

B=Beta-lactamase (destroys beta-lactam ring) · E=Efflux pumps (export drug out) · T=Target modification (drug can't bind)

Three main ways bacteria resist antibiotics

Beta-lactamase: enzyme breaks beta-lactam ring (MRSA uses altered PBP2a instead). Efflux pumps: actively export drug from cell (tetracycline, fluoroquinolone resistance). Target modification: MRSA altered PBP; VRE altered vancomycin binding site (D-Ala-D-Lac).

Beta-lactamase — enzyme that destroys the beta-lactam ring; ESBL = extended-spectrum version

Efflux pumps — membrane proteins that actively export drug from the bacterial cell

Target modification — altered binding site so drug can't attach (MRSA: PBP2a; VRE: D-Ala-D-Lac)

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🃏 💊 Antimicrobials · Resistance

BET

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🃏 Answer

BET: Beta-lactamase · Efflux pumps · Target modification

BBeta-lactamase — enzyme that destroys the beta-lactam ring; ESBL = extended-spectrum version

EEfflux pumps — membrane proteins that actively export drug from the bacterial cell

TTarget modification — altered binding site so drug can't attach (MRSA: PBP2a; VRE: D-Ala-D-Lac)

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💊 Antimicrobials · Protein Synthesis

30S: "TAME" — Tetracyclines · Aminoglycosides. 50S: "MAC" — Macrolides · chlorAmphenicol · Clindamycin

Ribosome-Targeting Antibiotics — T=Tetracyclines · A=Aminoglycosides block 30S · M=Macrolides · A=chlorAmphenicol · C=Clindamycin block 50S

Antibiotics that block bacterial protein synthesis at 30S or 50S

30S inhibitors: tetracyclines (block tRNA entry), aminoglycosides (cause misreading — bactericidal). 50S inhibitors: macrolides (block translocation), chloramphenicol (peptidyl transferase — aplastic anemia risk), clindamycin, linezolid (MRSA/VRE). Bacteriostatic: tetracyclines, macrolides, clindamycin. Bactericidal: aminoglycosides.

Tetracyclines — block aminoacyl-tRNA from entering 30S A-site; bacteriostatic

Aminoglycosides — bind 30S, cause mRNA misreading; bactericidal; nephrotoxic/ototoxic

Macrolides — bind 50S, block translocation; bacteriostatic; azithromycin/erythromycin

chlorAmphenicol — inhibits peptidyl transferase on 50S; aplastic anemia risk

Clindamycin — blocks translocation on 50S; excellent anaerobic and Gram+ coverage

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🃏 💊 Antimicrobials · Protein Synthesis

Protein synthesis inhibitors — which act on 30S vs 50S?

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🃏 Answer

Protein synthesis inhibitors — 30S: TAME · 50S: MAC

30S: "TAME" — Tetracyclines · Aminoglycosides. 50S: "MAC" — Macrolides · chlorAmphenicol · Clindamycin

TTetracyclines — block aminoacyl-tRNA from entering 30S A-site; bacteriostatic

AAminoglycosides — bind 30S, cause mRNA misreading; bactericidal; nephrotoxic/ototoxic

MMacrolides — bind 50S, block translocation; bacteriostatic; azithromycin/erythromycin

AchlorAmphenicol — inhibits peptidyl transferase on 50S; aplastic anemia risk

CClindamycin — blocks translocation on 50S; excellent anaerobic and Gram+ coverage

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💊 Antimicrobials · Fluoroquinolones

Fluoroquinolones: "-floxacin" ending. Inhibit DNA gyrase (Gram−) and topoisomerase IV (Gram+).

Fluoroquinolone Antibiotics — DNA gyrase inhibitors with broad-spectrum coverage

Broad-spectrum DNA-targeting antibiotic class — recognize by "-floxacin"

Ciprofloxacin: excellent Gram− (Pseudomonas, E. coli, Salmonella). Levofloxacin/moxifloxacin: respiratory fluoroquinolones — add Gram+ (S. pneumoniae). Adverse effects: tendon rupture (Achilles), QT prolongation, avoid in children and pregnancy.

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🃏 💊 Antimicrobials · Fluoroquinolones

Fluoroquinolones — suffix and targets?

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🃏 Answer

Fluoroquinolones: "-floxacin" ending. Inhibit DNA gyrase (Gram−) and topoisomerase IV (Gram+).

Fluoroquinolone Antibiotics — DNA gyrase inhibitors with broad-spectrum coverage

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💊 Antimicrobials · MRSA

Vancomycin: binds D-Ala-D-Ala. MRSA drug of choice. "Red man syndrome" from fast infusion.

Vancomycin — glycopeptide that blocks cell wall synthesis by binding D-Ala-D-Ala peptidoglycan precursor

The go-to antibiotic for MRSA — and what Red Man Syndrome actually is

Mechanism: binds D-Ala-D-Ala → blocks cell wall synthesis — no beta-lactam ring, so unaffected by beta-lactamase. VRE resistance: altered target (D-Ala-D-Lac) → use linezolid or daptomycin. Red man syndrome: histamine release from rapid infusion — NOT a true allergy. Monitor renal function (nephrotoxic).

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🃏 💊 Antimicrobials · MRSA

Vancomycin — how it works, its main use, and its infusion reaction?

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🃏 Answer

Vancomycin: binds D-Ala-D-Ala. MRSA drug of choice. "Red man syndrome" from fast infusion.

Vancomycin — glycopeptide that blocks cell wall synthesis by binding D-Ala-D-Ala peptidoglycan precursor

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💊 Antimicrobials · Antifungals

Antifungal targets: Ergosterol (azoles, amphotericin B) · Cell wall glucan (echinocandins) · Nucleic acid (flucytosine)

Antifungal Drug Targets — fungi are eukaryotes, so fewer unique targets than bacteria

Why fungal infections are harder to treat than bacterial ones

Ergosterol (fungal membrane equivalent of our cholesterol): azoles (fluconazole) block ergosterol synthesis. Amphotericin B: binds ergosterol directly → pores → cell death (highly nephrotoxic). Echinocandins (caspofungin): block beta-glucan synthase → weak cell wall. Flucytosine: → 5-FU in fungi → inhibits DNA synthesis.

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🃏 💊 Antimicrobials · Antifungals

Antifungal targets — which drugs hit what?

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🃏 Answer

Antifungal targets: Ergosterol (azoles, amphotericin B) · Cell wall glucan (echinocandins) · Nucleic acid (flucytosine)

Antifungal Drug Targets — fungi are eukaryotes, so fewer unique targets than bacteria

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💊 Antimicrobials

Bacteriostatic = stops growth. Bactericidal = kills directly. Immunocompromised → must use bactericidal.

Bacteriostatic vs Bactericidal — critical distinction for immunocompromised patients who lack immune backup

Why this distinction matters most when the immune system is down

Bacteriostatic (tetracyclines, macrolides, clindamycin, TMP-SMX, chloramphenicol): halt replication — rely on immune system to finish the job. Bactericidal (beta-lactams, aminoglycosides, fluoroquinolones, vancomycin, metronidazole): kill directly. In HIV, transplant, neutropenia: no immune backup → must use bactericidal drugs.

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🃏 💊 Antimicrobials

Bacteriostatic vs bactericidal — when must you use bactericidal?

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🃏 Answer

Bacteriostatic = stops growth. Bactericidal = kills directly. Immunocompromised → must use bactericidal.

Bacteriostatic vs Bactericidal — critical distinction for immunocompromised patients who lack immune backup

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💊 Antimicrobials · Anaerobes

Metronidazole: "Metro kills what has no O₂" — anaerobes and protozoa. DNA strand breakage mechanism.

Metronidazole (Flagyl) — reduced by anaerobes to a toxic metabolite that causes DNA strand breaks

The antibiotic of choice for anaerobic bacteria and certain parasites

Coverage: anaerobes (Bacteroides fragilis, C. difficile), protozoa (Giardia, Trichomonas, Entamoeba). Uses: C. diff colitis, bacterial vaginosis, intraabdominal infections. Adverse: disulfiram-like reaction with alcohol — warn patients. Metallic taste. Bactericidal against anaerobes.

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🃏 💊 Antimicrobials · Anaerobes

Metronidazole — what organisms does it kill?

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🃏 Answer

Metronidazole: "Metro kills what has no O₂" — anaerobes and protozoa. DNA strand breakage mechanism.

Metronidazole (Flagyl) — reduced by anaerobes to a toxic metabolite that causes DNA strand breaks

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💊 Antimicrobials · Folate

TMP-SMX: "Double block" — blocks folate synthesis at 2 sequential steps. First-line for PCP and UTIs.

Trimethoprim-Sulfamethoxazole — Sulfonamide blocks PABA→dihydropteroate · Trimethoprim blocks dihydrofolate reductase

Sequential folate pathway blockade — why the combination is synergistic

Sulfonamides block PABA → dihydropteroate synthase. Trimethoprim blocks dihydrofolate reductase. Combined: sequential blockade → synergistic killing. Humans eat folate; bacteria must synthesize it → selective toxicity. Uses: UTIs, PCP prophylaxis and treatment, MRSA skin infections, Toxoplasma prophylaxis.

TMP

Trimethoprim — blocks dihydrofolate reductase (step 2 of folate synthesis)

SMX

Sulfamethoxazole — blocks PABA → dihydropteroate synthase (step 1 of folate synthesis)

Double block

Sequential inhibition of the same pathway → synergistic, prevents resistance development

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🃏 💊 Antimicrobials · Folate

TMP-SMX — the 'double block'?

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🃏 Answer

TMP-SMX: "Double block" — blocks folate synthesis at 2 sequential steps. First-line for PCP and UTIs.

TMPTrimethoprim — blocks dihydrofolate reductase (step 2 of folate synthesis)

SMXSulfamethoxazole — blocks PABA → dihydropteroate synthase (step 1 of folate synthesis)

Double blockSequential inhibition of the same pathway → synergistic, prevents resistance development

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💊 Antimicrobials · Antivirals

Acyclovir: requires viral thymidine kinase to activate — selective toxicity. Herpes/VZV only.

Acyclovir — prodrug activated by viral thymidine kinase → inhibits viral DNA polymerase

Why acyclovir only works on herpes viruses and is non-toxic to human cells

Acyclovir enters all cells, but only herpes-infected cells have viral thymidine kinase (TK) to phosphorylate it. Activated form inhibits viral DNA polymerase. Uses: HSV-1/2 (cold sores, genital herpes), VZV (chickenpox, shingles), HSV encephalitis (IV). Valacyclovir: oral prodrug of acyclovir — better bioavailability. Resistance: TK mutation in immunocompromised.

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🃏 💊 Antimicrobials · Antivirals

Acyclovir — why is it selective?

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🃏 Answer

Acyclovir: requires viral thymidine kinase to activate — selective toxicity. Herpes/VZV only.

Acyclovir — prodrug activated by viral thymidine kinase → inhibits viral DNA polymerase

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💊 Antimicrobials · HIV

ART: NRTIs + NNRTIs (reverse transcriptase) · PIs (protease) · INSTIs (integrase) · Fusion inhibitors

Antiretroviral Therapy — N=Nucleoside RT Inhibitors · N=Non-nucleoside RT Inhibitors · P=Protease Inhibitors · I=Integrase Strand Transfer Inhibitors

Four drug classes that target different steps of HIV replication

NRTIs (tenofovir, emtricitabine): chain terminators — no 3'-OH. NNRTIs (efavirenz): non-competitive RT inhibitors. Integrase inhibitors (raltegravir, dolutegravir): first-line preferred. Protease inhibitors (ritonavir): block polyprotein cleavage. Treat with 3-drug regimen (ART/HAART) to prevent resistance.

NRTI

Nucleoside RT Inhibitors — chain terminators (no 3'-OH); tenofovir, emtricitabine, abacavir

NNRTI

Non-Nucleoside RT Inhibitors — bind RT allosterically; efavirenz, nevirapine

Protease Inhibitors — block polyprotein cleavage → immature virions; ritonavir, atazanavir

INSTI

Integrase Strand Transfer Inhibitors — block viral DNA integration; dolutegravir (preferred)

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🃏 💊 Antimicrobials · HIV

Antiretroviral drug classes — what does each block?

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🃏 Answer

ART: NRTIs + NNRTIs (reverse transcriptase) · PIs (protease) · INSTIs (integrase) · Fusion inhibitors

NRTINucleoside RT Inhibitors — chain terminators (no 3'-OH); tenofovir, emtricitabine, abacavir

NNRTINon-Nucleoside RT Inhibitors — bind RT allosterically; efavirenz, nevirapine

PIProtease Inhibitors — block polyprotein cleavage → immature virions; ritonavir, atazanavir

INSTIIntegrase Strand Transfer Inhibitors — block viral DNA integration; dolutegravir (preferred)

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💊 Antimicrobials · Anti-TB

RIPE: Rifampin · Isoniazid · Pyrazinamide · Ethambutol — first 2 months of TB treatment

TB Treatment — R=Rifampin · I=Isoniazid · P=Pyrazinamide · E=Ethambutol (initial 4-drug phase)

The four-drug TB regimen — and why four drugs are required

RIPE for 2 months (intensive phase), then Rifampin + Isoniazid for 4 more months. Four drugs because M. tuberculosis mutates frequently — any two-drug combo will select for resistant mutants. Isoniazid (INH): give B6 (pyridoxine) to prevent peripheral neuropathy. Rifampin: red-orange urine/tears (warn patients), induces cytochrome P450.

Rifampin — inhibits RNA polymerase; turns body fluids red-orange; CYP450 inducer

Isoniazid (INH) — inhibits mycolic acid synthesis; add B6 (pyridoxine) to prevent neuropathy

Pyrazinamide — active in acidic environment of macrophages; causes hyperuricemia

Ethambutol — inhibits arabinoglycan synthesis; monitor for optic neuritis (color vision)

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🃏 💊 Antimicrobials · Anti-TB

RIPE

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RIPE: Rifampin · Isoniazid · Pyrazinamide · Ethambutol — first 2 months of TB treatment

RRifampin — inhibits RNA polymerase; turns body fluids red-orange; CYP450 inducer

IIsoniazid (INH) — inhibits mycolic acid synthesis; add B6 (pyridoxine) to prevent neuropathy

PPyrazinamide — active in acidic environment of macrophages; causes hyperuricemia

EEthambutol — inhibits arabinoglycan synthesis; monitor for optic neuritis (color vision)

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