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naturally produced substances by microorganisms that inhibit or kill other microbes

inhibit or kill other microorganisms in their environment. This allows the producing organisms to reduce competition for nutrients and space and to survive in the soil ecosystem.

bacteria: Streptomyces a genus in Class Actinobacteria, Order Actinomycetales; produces mold-like spores. Bacillus: a genus of Firmicutes; forms endospores. Molds: Penicillium Cephalosporium

Chemotherapeutic agents effective against a limited range of microorganisms

effective against wide range of microbes

drug taken before infections or symptoms start to prevent imminent infection of a person at risk

cellular target: Inhibit bacterial cell wall synthesis (peptidoglycan) pathogens targeted: bacteria (mainly G+)

cellular target: inhibit 70S ribosome therefore inhibiting protein synthesis pathogens targeted: Bacteria (gram - , some gram +)

cellular target: Bind 30S subunit of 70S ribosome, block tRNA binding → inhibit protein synthesis pathogens targeted: bacteria (broad)

cellular target: Inhibits cell wall peptidoglycan cross-linking pathogens targeted: bacteria (gram + and MRSA)

cellular target: Disrupt bacterial cell membrane, increase permeability pathogens targeted: bacteria (gram -)

cellular target: Inhibit folic acid synthesis pathogens targeted: bacteria (broad)

cellular target: Inhibits mycolic acid synthesis (cell wall of Mycobacterium) pathogens targeted: Mycobacterium tuberculosis Narrow spectrum drug

cellular target: Inhibits Plasmodium heme detoxification pathogens targeted: Protozoa (malaria)

cellular target: Inhibits ergosterol synthesis in fungal membrane pathogens targeted: fungi

Competitive inhibition: Sulfonamides mimic PABA and compete for the active site of dihydropteroate synthase (DHPS), blocking an early step in bacterial folate synthesis. Drug synergy: When combined with trimethoprim—which inhibits dihydrofolate reductase (DHFR), a later step in the same pathway—the two drugs block sequential steps, producing a far stronger, often bactericidal, effect.

ability of a drug to target and harm a pathogen (bacteria, fungi, parasites, viruses) without causing significant harm to the host.

fungi are eukaryotes like humans, so their cells are very similar. They have few unique targets, and antifungals often attack ergosterol, which is similar to human cholesterol. This makes antifungal drugs more likely to harm human cells.

it is hard to establish selective toxicity

bacitracin: target PG, narrow spectrum (G+) Neomycin: targets 70S ribosome, broad spectrum Polymyxin: target membrane, narrow spectrum (G-)

each antibiotic attacks a different bacterial target, and together they cover both Gram-positive and Gram-negative bacteria

Both drugs target the fungal cell membrane, specifically the ergosterol pathway

inhibits neuromuscular actions of the parasites, immobilize, disintegrate, paralyze, or inhibit glucose metabolism of helminths

Tamiflu → Blocks viral release by inhibiting influenza neuraminidase. Acyclovir → Blocks viral nucleic acid (DNA) synthesis by inhibiting viral DNA polymerase (a nucleoside analog). Protease inhibitors → Block viral protein processing and maturation by inhibiting viral protease (HIV)