Chapter 19: Antibiotics/Chapter 20: Antibiotics Resistance

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REASONS FOR SEMISYNTHETIC:

- Expands the spectrum of the antibiotic -Narrow vs. broad spectrum -Affect both gram positive and gram-negative bacteria - Make them less toxic, fewer side effects

History of antibiotic development:

- Very first antibiotic was identified in 1940s by alexander Fleming discovering penicillin, which is a beta Lectin. - Soon after that several other classes of antibiotics were discovered - Antibiotics only apply to drugs used to treat bacterial infections - Antimicrobial agents include everything - Were originally isolated from other organisms

Selected Antifungal Agents

- more toxicity than antibacterial -Major Challenges: hard to target against fungi and not hurt ourselves 1. polyenes 2.azoles

Bacteriostatic

- prevent new cells from producing

Antibiotic Spectra

1 Narrow vs. broad spectrum 2. Spectra of natural, semisynthetic, and synthetic antibiotics: I. Patterns II. Example: b-Lactams

a) Polyenes:

1. Mechanism of action: compounds insert themselves in the plasma membrane of the fungus and create holes causing the fungus to die. - Ergosterol: compounds combine to this not cholesterol so this is why it doesn't harm our cells 2. Spectrum: broad when it comes to fungi 3. Toxicity to humans: generally high when taken internally, not as high on skin 4. Examples: amphotericin B, nystatin

b) Azoles:

1. Mechanism of action: instead of lysing the cells they insert toxic chemicals into plasma membrane of fungus and kill it without lysing 2. Spectrum: broad when it comes to fungi 3. Toxicity to humans: generally high when taken internally, not as high on skin 4. Examples: miconazole, ketoconazole

Tetracyclines

1. Mechanism of action: interfere with ribosomes, therefore disrupt translation and inhibit protein synthesis - Can be considered bacteriosital 2. Spectrum: broad spectrum 3. Toxicity to humans: low because we have different ribosomes, we have 80s vs. bacteria with 70s 4. Examples: tetracycline, doxycycline, and minocycline

Protease Inhibitors

1. Mechanism of action: interfere with the production of protease. Prevent the virus from replicating itself. Disruption of protein synthesis of virus 2. Spectrum: narrow 3. Toxicity to humans: pretty low 4. Example: indinavir

Acyclovir/Aciclovir

1. Mechanism of action: interfere with the synthesis of viral genome because the substance is a nucleotide analogue. Prevents themselves from reproducing themselves inside themselves. 2. Spectrum: very broad 3. Toxicity to humans: moderate

Sulfonamides

1. Mechanism of action: prevent the targeted bacteria from replicating their dna, bacteriostatic 2. Spectrum: broad spectrum effects 3. Toxicity to humans 4. Examples: sulfadiazine, Bactrim, pediazole

Selected Antiviral Agents

1. acyclovir/aciclovir 2. protease inhibitors

Selected Antibacterial Agents

1. beta-lactams 2. tetracyclines 3. sulfonamides 4. quinolone and fluoroquinolones

a) Anti-malarial agents

2 million people die -quinine -chloroquine -arteminisinin -many others combination therapy

Selected Anti-parasite and Anti-helminths Agents

A. Major Challenges: parasites both protozoan and animal are eukaryotic, so its hard to cause selective damage without causing harm to our own cells 1. anti-malarial agents 2. anti-protozoan agents 3. anti-helminth agents

Development of Antibiotic Resistance in Pathogens

A. Mechanisms and Reasons: one is to prevent from getting in, and other mechanism is to do something if it gets into the cell - Prevent compound from getting into cell - Push it out using efflux pumps - Destroy or neutralize the anti-microbial inside the cell - Beta Lactamase destroy beta lactame antibiotics, one way of becoming resistant

Quinolones and fluoroquinolones:

Action: similar to sulfonamides Examples: ciprofloxacin

Transpons

DNA pieces or genes that jump from one location to another

VRE: Vancomycin- resistant enterococcus:

Enterococcus faecalis: most important Enterococcus faecium - Normally doesn't cause infections, but if immune compromised can cause them

HIV infections

HAART→ Highly active anti- retroviral therapy - Use as many drugs available to prevent hiv in combination - Has become very effective with slowing down the spread and delaying it from aids stage

2. The targets:

I. Inhibition of cell wall synthesis II. Disruption of plasma membrane III. Inhibition of nucleic acid synthesis IV. Inhibition of protein synthesis/gene expression: i. Transcription ii. Translation V. Inhibition of metabolic pathways

3. Develop new of antibiotics:

I. The challenges: most antibiotics come from organisms that produced them. We are limited because there are no organisms that we know of to produce new ones II. The promises: molecular techniques that involve DNA, RNA, and protein. Hold significant promises in the future.

I. Organisms producing antibiotics II. Reasons for producing antibiotics

I. originally isolated from other organisms, come from bacteria or fungi - Penicillin was isolated from fungus - Cephisporins are isolated from different species of fungi - Most are produced from bacteria - Streptomyces are source of over 70% of antibiotics even used today

d) Anti-helminths agents:

Mebendazole: against all animal parasites, low Toxicity to humans?: toxicity varies

Other anti-protozoan agents

Metronidazole→ very commonly used against infections caused by anaerobic bacteria, also used against protozoan parasites

III. E-test

can determine mic

II. Disk diffusion method:

cant determine either

Mutation

cause an organism that is not resistant to develop resistance

ICA-MRSA:

community acquired

A. Beta-Lactams

first one isolated, and most used, all the penicillin family 1. Mechanism of action: all have ring structure. All beta lactams interfere with the synthesis of the bacterial cell wall. Prevents bacteria from reproducing (bacteriostatic) 2. Spectrum: narrow- broad. Original penicillin is narrow, synthetic broader 3. Toxicity to humans: fairly low because humans don't have cell walls 4. Examples: penicillin, ampicillin, amoxicillin

II. Synthetic antibiotics

got there start from some cell that produces then learn to modify to make them better antibiotics

HA-MRSA:

hospital/healthcare acquired

Transduction

involves a bacteriophage bringing with it the gene for resistance. When it affects the cell, it actually picks up the resistant gene from the virus.

I. Semisynthetic antibiotics

isolated anti-biotic modified to make it better. - most common

III. Arteminisinin

isolated from plant, Chinese medicine, fast acting and little toxicity

II. Chloroquine

less toxic, cheap and effective

I. Dilution method

most effective, determined mic and mbc

Selected Antiviral Agents

must be able to get into your cells to prevent virus from replicating inside your cells. Few drugs for viruses because have to get agent in cell without hurting the cell.

Vancomycin-resistant staph aureus

not a beta lactams but has the same function, interfere with cell wall in targeted organisms

I. Quinine

oldest agent, pretty toxic and several side effects

Methicillin-resistant staph aureus

one of the last beta lactams

Transformation

process by which a bacterium picks up the resistance gene from the environment

Bactericidal vs. bacteriostatic

techniqual distinction

Conjugation

the way by which bacteria exchange genetic material

Beta lactams

use lactamase to fight them off

1. Selective toxicity

when take an antibiotics, should kill pathogens without harming your own cells. Not always possible so they don't harm the patient but get rid of pathogen.


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