skin / hair / nail bacterial / fungal / parasitic infection → topical antimicrobial selection by organism + site — via site + organism + resistance pattern guide choice. Topical anti-infective choice is driven by organism and site: superficial bacterial, fungal, and parasitic infections each have preferred agents, and penetration differs by tissue (nail and hair are hard to reach). Matching drug class to pathogen and location is the core clinical logic this pathway maps.
mupirocin + isoleucyl-tRNA synthetase → bacterial protein synthesis block — via staphylococci + streptococci; MRSA decolonization. Mupirocin inhibits bacterial isoleucyl-tRNA synthetase, blocking incorporation of isoleucine and halting protein synthesis. Its unique target (not shared with systemic antibiotics) and poor systemic absorption make it ideal topically against staphylococci/streptococci, including nasal MRSA decolonization.
clindamycin-topical + 50S ribosomal subunit → bacterial protein synthesis block — via C. acnes + anaerobes; acne mainstay. Topical clindamycin binds the 50S ribosomal subunit to block bacterial protein synthesis — used in acne for activity against Cutibacterium acnes plus an anti-inflammatory effect. It is combined with benzoyl peroxide to curb the resistance that monotherapy readily selects.
azole + CYP51 (lanosterol 14α-demethylase) → ergosterol biosynthesis block — via fungal membrane defect; dermatophytes + Candida + Malassezia. Azole antifungals inhibit CYP51 (lanosterol 14α-demethylase), blocking conversion of lanosterol to ergosterol — the fungal-specific membrane sterol. Depleting ergosterol (and accumulating toxic precursors) disrupts the membrane; targeting a fungal sterol pathway is what gives selectivity over human cells.
terbinafine + squalene epoxidase → squalene accumulation + ergosterol depletion — via fungicidal; onychomycosis 1st-line. Terbinafine inhibits squalene epoxidase, acting earlier in the same ergosterol pathway — both starving the cell of ergosterol and causing toxic squalene accumulation, making it fungicidal. Its keratin affinity and persistence make it first-line for dermatophyte nail and hair infections.
permethrin + voltage-gated Na channel (insect) → persistent depolarization → paralysis — via scabies + lice; selective for arthropod over mammalian Na channels. Permethrin (a pyrethroid) binds insect voltage-gated sodium channels, holding them open to cause persistent depolarization and paralysis of lice and scabies mites. Selective toxicity comes from insects’ channel sensitivity and humans’ rapid metabolism, giving a wide safety margin.
ivermectin + glutamate-gated Cl channel (parasite) → parasite paralysis — via topical for rosacea + scabies; oral systemic use as well. Ivermectin activates invertebrate glutamate-gated chloride channels, hyperpolarizing and paralyzing parasites (mites, lice, helminths). These channels are absent in mammals, and the drug is normally excluded from the CNS by P-glycoprotein — the basis of its selective antiparasitic action.