Bio 105 Lecture 7
Chemotherapy:
selective treatment of disease with drugs
Antibiotics/antibacterials:
Antimicrobial drugs used as medicines against bacteria
Antivirals
Antimicrobial drugs used against viruses
Antifungals
Antimicrobial drugs used against fungi
Antiprotozoals
Antimicrobial drugs used against protozoans
Semisynthetics
Chemically altered antibiotics that are more effective, longer lasting
Selective Toxicity
Antibiotics that are more toxic to a pathogen than its host - Easier if hosts and pathogen are very different!
Key factors for ideal antibiotics:
1. Readily available
2. Inexpensive
3. Chemically stable
4. Easily administered
5. Nontoxic, non-allergenic
6. Selectively toxic against a wide range of pathogens (broad-spectrum)
Spectrum Of Action
– Narrow-spectrum antimicrobials are effective against a few microbes
– Broad-spectrum antimicrobials are effective against many microbes
• Often too many, including normal microbiota, leading to a risk of superinfection
List Steps Of Antibiotic Use Leading to Superinfection
1. Normal Microbiota keeps Opportunistic Pathogens in Check
2. Broad-Spectrum Antibiotics kill nonresistant Cells
3. Drug-resistant Pathogens proliferate and can cause a SuperInfection
Routes of administration
– Topical application of drug for external infections
– Oral route requires no needles and is self-administered
– Intramuscular administration delivers drug via needle into muscle – Intravenous administration delivers drug directly to bloodstream
There are five major cellular drug targets, with different modes/mechanisms of action
Pg#7
1/5 Inhibitors of cell wall synthesis
Peptidoglycan is composed of chains of sugar molecules cross-linked together by short peptides
Beta-lactams like penicillin bind enzymes that cross-link cell wall sugars
– Interrupted cell wall synthesis leads to osmotic lysis: bactericidal
The mechanism of beta- lactams on penicillin-binding protein (PBP), the enzyme responsible for peptidoglycan cross-linking
– Beta-lactam antibiotics bind the active site of PBP irreversibly, breaking the enzyme permanently
Semisynthetic beta-lactams are more stable, better absorbed,
less susceptible to resistance, and have broader spectrum
2/5 Inhibitors of protein synthesis
– Prokaryotic and eukaryotic ribosomes are similar, but have slight differences that can be used as drug targets
• These drugs are usually bacteriostatic
Translationsynthesizesnewproteinsusingribosomes
– Phase 1 of translation: initiation
• A-site: aminoacyl-tRNA acceptor site • P-site: peptidyl-tRNA site
• E-site: free tRNA exit site
Ribosomal drug targets include:
– tRNA binding interference during elongation, causing incorrect protein sequences (eg. aminoglycosides)
• Often toxic to host (patient)
– A-site interference, preventing elongation (eg. tetracyclines)
– 50S interference: peptide bond disruption
(eg. chloramphenicol)
– Preventing mRNA movement (eg. macrolides)
– Initiation interference (eg. oxazolidonones)
• Newer class of antibiotics that blocks translation initiation • Used as drugs of last resort
3/5 Inhibitors of membrane function
Polyenes (eg. amphotericin B) are antifungal drugs that bind ergosterol in fungal membranes, opening holes (fungicidal)
Polymyxins disrupt gram-negative bacterial cell membrane
lipids (bactericidal), but are toxic to host kidneys and liver
4/5 Inhibitors of nucleic acid synthesis (bactericidal or
virucidal)
Many also react with host enzymes: toxic
– Quinolones inhibit prokaryotic-specific DNA gyrase (e.g. ciprofloxacin)
– Rifampin blocks mRNA transcription (preferentially in prokaryotes)
– Nucleotide analogs interfere with nucleic acid replication, especially useful for viruses (e.g. AZT or acyclovir)
5/5 Inhibitors of metabolic pathways
– Antimetabolites (analogs) that competitively inhibit pathogen enzymes
• Usually bacteriostatic
– Heavy metals inactivate pathogen enzymes with some specificity, but are generally toxic
– Sulfonamides like sulfanilamide block the synthesis of folic acid in many bacteria
• First widespread antibiotics
Antiviral drugs target unique aspects of the viral life cycle (almost always narrow-spectrum)
– Some stop virions from escaping the vesicles they are imported into the cell with (eg. amantadine)
– Various enzyme inhibitors (nucleotide analogs, integrase inhibitors, protease inhibitors) can stop viral replication at different stages
Antiviral drugs also include antagonists that interfere with
virion exit/entry (e.g. Oseltamivir/Tamiflu)
Horizontal gene transfer Conjugation
Conjugation is a one-way process: one bacterium donates a fragment of DNA to another
• The fragment can be a plasmid or chromosomal DNA
– Plasmids often contain genes for virulence or resistance
• After the transfer, the recipient is now ‘fertile’ and can pass it along!
Conjugation: transferring a plasmid from one bacterium to another
Antimicrobial Resistance
Some members of a bacterial population may be resistant to
a drug, before they’re exposed to it
• New resistances acquired beforehand by natural mutations, or
conjugation/transformation with R (resistance) plasmids
– Exposure to the drug will kill all members except the resistant
group, which will then take over
• Now all of the microbes are resistant!
Antibiotic Resistance Mechanisms Include
1. Drug inactivation by a pathogen-produced enzyme
2. Blocked penetration of the drug into pathogen
3. Efflux pump that removes drugs (cross-resistance)
4. Target modification inside pathogen (usually by mutation)
5. Enzymatic bypass to avoid inhibition by drug
Combatting Resistance Is Done By
– Common sense approach to treatments, and continued drug development
– Using antibiotics in combination: synergism to defeat resistant microbes
Synergism
in a combined antibiotic treatment resulting in a larger zone of inhibition
You Can Measure The Efficacy Of Antibiotics Using
Diffusion susceptibility test (aka. Kirby-Bauer):
• Zone of inhibition qualitatively indicates ability of antibiotics to halt
bacterial growth (bacteriostatic effect)
Diffusion susceptibility test of several antibiotic discs on a media plate
Minimum Inhibitory Concentration (MIC)
Quanitatively measures the minimum concentration of a drug necessary to inhibit growth (bacteriostatic concentration) of a standardized bacterial inoculum
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