Chapter 10 study Quis

What are chemotherapeutic agents?

Drugs used to treat diseases.

What are antimicrobial agents?

Chemotherapeutic agents used to treat infections.

Who proposed chemotherapy and the idea of "magic bullets"?

Paul Ehrlich.

What did Alexander Fleming discover?

Penicillin, released from Penicillium chrysogenum.

What did Gerhard Domagk discover?

Sulfanilamide—the first widely used antimicrobial.

Who coined the term "antibiotics" and discovered streptomycin?

Selman Waksman.

What are semisynthetics?

Chemically modified antibiotics that are more effective, stable, or easier to use.

What are synthetics?

Drugs synthesized entirely in a lab.

What is selective toxicity?

The ability of a drug to target microbial structures without harming the host.

Why are there fewer antifungal, antiprotozoan, and antiviral drugs?

Because these organisms are more similar to humans than bacteria.

What do beta-lactams do?

Inhibit cell wall synthesis by preventing cross-linking of NAM subunits.

What are examples of beta-lactams?

Penicillin, cephalosporins, carbapenems.

What do vancomycin and cycloserine do?

Interfere with bridges between NAM subunits in Gram-positive bacteria.

What does bacitracin do?

Blocks transport of NAG and NAM across the cytoplasmic membrane.

What do isoniazid and ethambutol target?

Mycolic acid synthesis in mycobacterial species.

Are cell wall inhibitors effective against dormant cells?

No—they work only on growing cells.

What do echinocandins target?

Fungal cell wall synthesis by inhibiting glucan synthesis.

What type of ribosomes do prokaryotes and eukaryotes have?

Prokaryotes: 70S; Eukaryotes: 80S.

Why can protein synthesis inhibitors affect human mitochondria?

Because mitochondria have 70S ribosomes.

How does mupirocin work?

Inhibits isoleucyl-tRNA synthetase in Gram-positive bacteria.

What do nystatin and amphotericin B target?

Ergosterol in fungal membranes.

How do azoles and allylamines work?

Inhibit synthesis of ergosterol in fungi.

What does polymyxin target?

Disrupts cytoplasmic membranes of Gram-negative bacteria; toxic to kidneys.

How do antimetabolic agents work?

Interfere with enzymatic pathways unique to pathogens.

What does atovaquone inhibit?

Electron transport in protozoa and fungi.

What do sulfonamides and trimethoprim target?

Folic acid synthesis, which is necessary for nucleotide production.

What are protease inhibitors used for?

Inhibit HIV protease, blocking replication.

What do quinolones and fluoroquinolones do?

Inhibit bacterial DNA gyrase, affecting DNA replication.

How do nucleotide analogs work?

Distort nucleic acid shapes, blocking replication and transcription.

What do reverse transcriptase inhibitors target?

Enzymes used by retroviruses like HIV.

How do attachment antagonists work?

Block viral entry by preventing receptor binding (e.g., pleconaril).

What does arildone do?

Prevents viral uncoating after entry into host cells.

What characteristics define an ideal antimicrobial drug?

Cheap, stable, easy to administer, non-toxic, non-allergenic, and broad-spectrum.

What is a broad-spectrum drug?

Effective against many pathogens.

What is a narrow-spectrum drug?

Effective against a few pathogens.

What is a superinfection?

Secondary infection from overgrowth of normal flora suppressed by broad-spectrum antibiotics.

How is drug effectiveness tested?

Kirby-Bauer (diffusion), MIC test, MBC test.

What is MIC?

Minimum Inhibitory Concentration—the lowest drug concentration that prevents visible growth.

What is MBC?

Minimum Bactericidal Concentration—the lowest concentration that kills 99.9% of bacteria.

What is an E-test?

A test combining MIC and diffusion to assess drug potency.

What are the main drug administration routes?

Topical, oral, intramuscular (IM), intravenous (IV).

How does route affect drug concentration in blood?

IV delivers fastest/highest concentration; oral and IM slower.

What is therapeutic index (TI)?

Ratio of toxic dose to effective dose; higher is safer.

What are side effects of antimicrobial drugs?

Toxicity (e.g., kidney, liver, nerve), allergies, and disruption of microbiota.

What is a superinfection?

Overgrowth of normal flora due to disruption by antibiotics.

How do bacteria develop resistance?

Through mutations or acquisition of resistance (R) plasmids.

What are common resistance mechanisms?

Enzyme production (e.g., beta-lactamase), altered drug targets, efflux pumps, biofilms.

What is beta-lactamase?

An enzyme that inactivates beta-lactam antibiotics like penicillin.

What is cross resistance?

Resistance to multiple drugs of the same class or similar structure.

What are multidrug-resistant pathogens (MDRs)?

Resistant to at least three antimicrobial agents.

Where do MDR pathogens commonly develop?

In hospitals and nursing homes with frequent drug use.

What is synergism?

Two drugs working better together than alone.

What is antagonism?

Drugs interfering with each other’s effects.

How can resistance be slowed?

Maintain high drug levels, use combinations, limit unnecessary use, develop new drugs.

What are second- and third-generation drugs?

Modified versions of existing drugs with improved properties.

What are bacteriocins?

Proteins produced by bacteria to inhibit other bacteria—potential drug candidates.

How might future drugs be designed?

To fit specific microbial protein shapes and block function.