ANTIBIOTICS

Bacterial cell wall composition

Made of peptidoglycans (protein polysaccharide structures) to withstand high internal pressure

What happens without peptidoglycans in bacteria

Cell undergoes "suicidal autolysis" → cell death

Bacterial lack of nuclear membrane meaning

Genetic material is not confined by a distinct membrane

Bacteria subcellular organelles

Contain ribosomes, enzymes, and cytoplasmic storage granules; must invade hosts for nutrients

Three ways bacteria cause pathogenic effects

1. Compete for nutrients with host cells / 2) Release toxic substances that damage human cells / 3) Trigger immune responses that damage human tissues

Beneficial roles of bacteria

Aid in food digestion, synthesize nutrients, inhibit growth of harmful microorganisms

Bactericidal definition

Destroys bacteria

Bacteriostatic definition

Inhibits bacterial growth

Broad spectrum antibiotic definition

Effective against wide range of bacteria (gram positive + gram negative)

Narrow spectrum antibiotic definition

More specific, affecting small group of bacteria

Cell wall synthesis inhibitor mechanism

Bind to penicillin binding proteins (PBPs) → disrupt peptidoglycan layer → cell loses selective barrier → suicidal autolysis

Penicillin suffix and mechanism

cillin; binds to PBPs (transpeptidase) to disrupt cell wall structure

Cephalosporin prefix and mechanism

Cef / bactericidal; inhibits PBPs → inadequate peptidoglycan production

Carbapenem suffix and mechanism

nam or nem; broader spectrum than penicillins and cephalosporins

Other cell wall synthesis inhibitors

Bacitracin, Colistin, Cycloserine, Polymyxin B, Ethambutol

Cell wall inhibitor adverse effects

Hypersensitivity (rashes, hives); severe: toxic epidermal necrosis, Stevens Johnson Syndrome (emergencies)

cell wall synthesis inhibitors list

penicilin, carbapenem, cephalosporin

Bacterial membrane disruption mechanism

Act like detergents → bind to membrane phospholipids → punch holes → osmotic imbalance → leakage → rapid cell death

Examples of membrane disruptors

Polymyxin B, Colistin, Daptomycin

poly b

COLI

DAPTO

Why membrane disruptors are limited systemically

Toxicity to human cell membranes; often limited to topical application

Protein synthesis inhibitor mechanism

Bind to ribosomal subunits (30S or 50S) → block protein chain formation OR cause misreading of mRNA → "nonsense" proteins → cell death or growth arrest

Aminoglycoside mechanism

Binds to ribosome subunits → alters ability to read mRNA code → improper protein synthesis

mRNA inability to read code

Macrolide mechanism

Binds to 50S ribosome subunit → interferes with transfer RNA (tRNA) at bacterial ribosome

Aminoglycoside suffix and examples

mycin; examples: Gentamicin, Streptomycin

GENTA, STREPTO

Macrolide suffix and examples

mycin; examples: Azithromycin, Erythromycin

AZITH

ERYTH

TH

Aminoglycoside adverse effects

Nephrotoxicity, Ototoxicity

Macrolide adverse effects

GI disturbances

Tetracycline adverse effect

Photosensitivity

Other protein synthesis inhibitors

Chloramphenicol, Clindamycin, Lincomycin, Ethionamide, Linezolid

DNA/RNA synthesis inhibitor mechanism

Bind to bacterial enzymes (DNA gyrase, topoisomerase IV, RNA polymerase) → blocks genetic replication → prevents cell division

Fluoroquinolone suffix and mechanism

floxacin; inhibits DNA gyrase (topoisomerase II) and topoisomerase IV → impairs growth and replication

Sulfonamide suffix and mechanism

Sulf / zoles; competitive inhibition of dihydropteroate synthase → blocks folic acid synthesis

Fluoroquinolone adverse effects

CNS toxicity (headache, dizziness), GI disturbances, photosensitivity, Tendinopathy (most common: Achilles tendon)

CNS/TENDON

Sulfonamide adverse effects

Photosensitivity, allergies, GI disturbances

Other DNA/RNA synthesis inhibitors

Aminosalicylic Acid, Clofazimine, Dapsone, Mupirocin, Rifamycin, Trimethoprim

Folic acid synthesis inhibitor mechanism (antimetabolites)

Mimic precursors (like PABA) or block essential enzymes (dihydrofolate reductase) → interferes with nucleic acid production → starves bacteria of DNA replication ingredients

Folic acid synthesis inhibitor examples

Sulfonamides, Trimethoprim

Antibiotic resistance definition

Bacteria change to reduce/eliminate effectiveness of drugs; property of bacteria, NOT patient

How resistance develops (3 steps)

Mutation – spontaneous change in bacterial DNA; 2) Selective pressure – antibiotic kills susceptible bacteria, resistant ones survive; 3) Misuse/overuse accelerates process

Entry prevention as resistance mechanism

Blocking antibiotic from entering the cell

Efflux pumps as resistance mechanism

Actively pumping the drug out of the cell

Enzymatic destruction as resistance mechanism

Using chemical reactions to destroy the antibiotic molecule

Vertical transfer of resistance

From parent cells to offspring during reproduction

Horizontal transfer of resistance

Sharing genetic material (via plasmids or bacteriophages) directly with other bacterial cells, including different species → major driver of resistance spread

Impact of antibiotic resistance

Superbugs" → harder/impossible to treat; treatments more costly and toxic

Antibiotic resistance prevention

Use antibiotics correctly (only when prescribed per guidelines); infection prevention measures reduce need for drugs

Isoniazid (H) mechanism

Inhibits synthesis of mycolic acids via enoyl ACP reductase → mycobacterial cell wall disruption

MYCO

Isoniazid use

Given in combination with rifampin (and pyrazinamide); for prophylaxis, used alone

Isoniazid adverse effects

Hepatotoxicity, peripheral neuropathy (numbness, tingling sensation)

hepato and neuro

Rifampicin (R) mechanism

Inhibits beta subunit of RNA polymerase → suppresses RNA synthesis; bactericidal

Rifampicin adverse effects

Hepatotoxicity, orange discoloration of bodily fluids (urine)

Pyrazinamide (Z) mechanism

Prodrug converted to pyrazinoic acid → inhibits mycobacterial cell function

Pyrazinamide adverse effects

MOST HEPATOTOXIC; inhibits urate excretion → hyperuricemia → acute gout

Ethambutol (E) mechanism

Inhibits arabinosyl transferases → disrupts arabinogalactan synthesis (essential for M. tuberculosis cell wall)

Ethambutol adverse effects

Optic neuritis

color blindness

Streptomycin mechanism

2nd line anti TB; aminoglycoside (inhibits bacterial cell membrane synthesis)

AMINOGLYCOSIDE—INHIBITS CELL MEMBRANE SYNTHESIS

Fluoroquinolones PT concern

Tendinopathy and tendon rupture; most commonly Achilles tendon; higher risk in elderly, renal failure, or those taking glucocorticoids

TENDON/ACHILLES

Action for tendon pain on fluoroquinolones

Suspend exercise programs; protect tendon from excessive stress until cause determined

Photosensitivity PT concern

Common with Penicillins, Cephalosporins, Carbapenems; if patient receives UV radiation, higher risk for severe burns

Action for photosensitivity risk

Adjust dosages; establish accurate minimal erythemal dosage before UV treatment

Hypersensitivity PT concern

Common with Penicillins, Cephalosporins, Carbapenems; range from rashes to Stevens

Action for hypersensitivity reactions

Be alert for rashes, hives, or respiratory difficulty (wheezing) during treatment sessions

Ototoxicity and nephrotoxicity PT concern

Caused by Aminoglycosides (Gentamicin, Streptomycin) and Vancomycin

Nephrotoxicity signs

Kidney damage; indicated by bloody urine

Ototoxicity signs

Dizziness, tinnitus (ringing in ears), fullness in ears; may be irreversible; affects balance and posture

Action for ototoxicity/nephrotoxicity

Monitor for hearing or balance changes; especially in elderly or those with existing liver/kidney failure

CNS toxicity PT concern

Fluoroquinolones and Carbapenems cause headache, dizziness, confusion, tremors, seizures → impairs focus and safe participation

GI distress PT concern

Nausea, vomiting, stomach cramps, diarrhea / frequent across many antibiotic classes

Action for CNS/GI disturbances

May require altering timing of therapy sessions to avoid peak bothersome periods

Infection control PT concern

Development of resistant strains (MRSA, VRE, VRSA); therapists work closely with patients and equipment → increased spread risk

Action for infection control

Maintain sterile techniques for open wounds; disinfect equipment