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Micro ch. 12 antibio
Ch. 12 antimicrobials
| Question | Answer |
|---|---|
| Goal of microbial drugs | to either disrupt the cell processes/structures of bacteria, fungi, and protozoa OR to inhibit virus replication. |
| Chemotherapy drugs | Most drugs used in chemotherapy interfere w/ the function of enzymes required to synthesize ore assemble macromolecules, or destroy structures already in the cell. |
| Selectively toxic | above all, drugs should kill/inhibit microbial cells without simultaneously damaging host tissues. Ex. penicillins block synthesis of bacterial cell wall. This works because human cells lack peptidoglycan and are thus unaffected by this action. |
| Selective toxicity difficulties | As characterisitics of the infectous agent become more similar to those of the host, selective toxicity becomes more difficult to achieve and adverse effects are more likely. |
| Chemotherapeutic drug | any chemical used in the treatment, relief, or prophylaxis of a disease. |
| Mechanisms of drug action | First step toward goal of chemotherapy is to identify the structural and metabolic needs of a living cell. |
| Antimicrobial drugs that affect the bacterial cell wall | Most bacterial cell walls contain peptidoglycan, so easy target |
| Antimicrobial drugs that affect the bacterial cell wall | Penicillins and cephalosporins react w/ enzymes required to complete peptidoglycan synthesis (considered bactericidal) |
| Cycloserine | inhibits the formation of the basic peptidoglycan subunits |
| Vancomycin | hinders peptidoglycan elongation |
| Penicillin and cephalosporins | binds and blocks peptidases involved in cross-linking the glycan molecules, so interrupt completion of the cell wall. |
| Broad-spectrum penicillins and cephalosporins (carbenicillin/ceftriaxone) | can access cell walls of gram-negative species. |
| Antimicrobial drugs that affect the bacterial cell wall | Most of these antibiotics are active only when cells are growing. Cell wall is weakened, leading to lysis of the cell |
| Antimicrobial drugs that affect nucleic acid synthesis | Interfere with nucleic acid synthesis by blocking synthesis of nucleotides, inhibiting replication, or stopping transcription. Effects on protein metabolism can be great since functioning DNA and RNA are required for translation. |
| Chloroquine (antimalaria drug) | binds and cross-links the double helix; Antimicrobial drugs that affect nucleic acid synthesis |
| AZT and acyclovir (antiviral drugs) | insert on viral nucleic acid and block replication; Antimicrobial drugs that affect nucleic acid synthesis |
| Antimicrobial drugs that block protein synthesis | most inhibitors react with the ribosome-mRNA complex Since ribosomes of eukaryotes different in size/structure from prokaryotes, usually have a selective action against bacteria. |
| Potential consequence of Antimicrobial drugs that block protein synthesis | eukaryotic mitochondria have same prokaryotic ribosomes, which can cause damage (30S subunit, 50S subunit) |
| Aminoglycosides | Antimicrobial drugs that block protein synthesis; insert on sites on the 30S subunit and cause misreading of mRNA making abnormal proteins. |
| Erythromycin | Antimicrobial drugs that block protein synthesis; attaches to 50S subunit and inhibits translocation of the subunit during translation |
| Tetracycline | Antimicrobial drugs that block protein synthesis; block attachment of tRNA on the A receptor site and effectively stop protein synthesis |
| Chloramphenicol | Antimicrobial drugs that block protein synthesis; attach to 50S subunit and prevents formation of peptide bonds |
| Antimicrobial drugs that disrupt cell membrane function | Cells with damage membrane dies from disruption in metabolism/lysis and does not have to be actively dividing to be destroyed; have specificity for particular microbial groups based on differences in types of lipids in their cell membranes |
| Polymyxin | Antimicrobial drugs that block protein synthesis; interact with membrane phospholipids, distort cell surface, and cause leakeage of proteins and nitrogen bases, particularly in gram-negative bacteria. |
| Amphotericin B | Antimicrobial drugs that block protein synthesis; antifungal antibiotic; form complexes with sterols on fungal membranes, which cause abnormal openings nad seepage of small ions. |
| Consequence | Antimicrobial drugs that block protein synthesis; selectivity is not exact since both microbial and animal cells have cell membranes; leads to high toxicity for humans. |
| Antimicrobial drugs that inhibit folic acid synthesis | Sulfonamides and trimethoprim; mimic normal substrate of enzyme via competitive inhibition. Supplied in high concentrations to ensure that needed enzyme constantly occupied w/ metabolic analog instead of true substrate of enzyme. |
| Sulfonamides and trimethoprim | block enzymes required for synthesis of tetrahydrofolate, which is needed by bacterial cells for folic acid synthesis and eventual production of DNA, RNA, and amino acids |
| Selective toxicity | mammals derive folic acid from their diet, so do not possess this enzyme system. Bacterial/protozoan parasites synthesize folic acid. |
| Antibacterial drugs targeting the cell wall | Penicillin and its relatives |
| Penicillin | Made by Penicillium chysogenum; can be completely synthesized in a lab, but more practical and economical to obtain natural penicillin through microbial fermentation. |
| Penicillin structure | Contain beta-lactam ring, thiazolidine ring, and variable side chain that dictates microbial activity. |
| Subgroups and uses of penicillins | Penicillin G and V most important natural forms; Penicillin considered drug of choice for infections by known senstivie, gram-positive cocci and some gram-negative bacteria. |
| Semi-synthetic—ampicillin | have broader spectra so can be sued to treat infections by gram-negative enteric rods. |
| Some bacteria produce enzymes to break down penicillin | Penicillinases (beta-lactamases) destroy beta-lactam ring of penicillins; Methicillin and nafcillin are penicillins resistant to penicillinases |
| Primary problems in penicillin therapy | allergic reactions and resistance in strains of bacteria |
| Cephalosporin group of drugs | Made by mold Cephalosporium acremonium; Currently account for majority of antibiotic administered; Similar to penicillin—have beta lactam structure; similar mode of action; Main ring is different; Two sites for R groups |
| Cephalosporin Generic names | usually have root cef, ceph, or kef. |
| Subgroups and uses of cephalosporins | versatile; broad-spectrum, resistant to most penicillinases, cause fewer allergic reactions. 4 generations. Many are administered parenterally (injection/venous) |
| 1st gen Cephalosporin | most effective against gram-postitive cocci, a few gram-negative bacteria |
| Second generation Cephalosporin | cefaclor and cefonacid for gram-neg Enterobacter, Proteus,and Haemophilus infections |
| Third generation | Keflex for beta-lactamase producers; broad-spectrum against enteric bacteria; respiratory, skin, urinary and nervous system infections |
| aminoglycoside drugs | Antibacterial drugs targeting protein synthesis; Made by Streptomyces and Micromonospora |
| Subgroups and uses of aminoglycosides | Gentamicin for Escherichia coli, Pseudomonas, and Salmonella and Shigella infections |
| Tetracycline antibiotics | Made by Streptomyces |
| Subgroups and uses of tetracyclines | Mycoplasma pneumonia and cholera |
| Erythromycin | used to treat Mycoplasma pneumoniae, legionellosis, Chlamydia, and Mycobacterium MAC |
| Clindamycin | used to treat penicillin-resistant Staphylococcus and anaerobic infections |
| Antibacterial drugs targeting folic acid synthesis | The sulfonamides, trimethoprim, and sulfones |
| Trimethoprim-sulfamethoxazole | Used to treat Pneumocystis (carinii) jirovecii pneumonia |
| Antimalarial drugs | Quinine and its relatives |
| Antiviral chemotherapeutic agents mode of action | Preventing the virus from penetrating into the host cell, Blocking transcription and translation of viral molecules; Preventing the maturation of viral particles |
| Interferons | Glycoprotein produced by human cells; Has antiviral and anticancer properties; Now made using recombinant DNA technology |
| How does drug resistance develop? | Spontaneous mutation occurs in critical chromosomes; New genes or sets of genes are acquired through transfer from another species |
| Drug inactivation mechanisms | Beta-lactamases destroy penicillins and cephalosporins; Decreased drug permeability or increased drug elimination (Multidrug resistant pumps; Change of drug receptors; Changes in metabolic patterns |
| Natural selection and drug resistance | Any large microbe population will have members already drug resistant (mutations/transfer of plasmids); If population exposed to the drug, resistant members survive & flourish, sensitive members killed; Leads to new population that is resistant overall |
| Kirby-Bauer method | uses antibiotic wafers to test for antibiotic sensitivity |
| Which antibiotics inhibit cell wall synthesis? | Penicillins, cephalosporins |
| Which antibiotics inhibit protein synthesis? | Macrolides, tetracyclines, aminoglycosides |
| Which antibiotics inhibit DNA synthesis? | Sulfa drugs, quinolones |
| Which antibiotics inhibit folic acid synthesis? | Sulfonamides (sulfa drugs), trimethroprim |
| Why is it important for a patient to finish a course of antibiotics? | Because survivor pathogenic cells can become resistant to the antibiotics. |
| In some cases a nurse will travel to a patient’s home to observe them taking antibiotics. Speculate as to why this may be the case. | To ensure protocol compliance in taking antibiotics—especially for treatment of hard-to-treat infections. |
| A bacteria is resistant to penicillin. What is the most likely mechanism of resistance? How does it work? | Penicillinase or beta-lactamase |
| How can the theory of natural selection explain the increase in antibiotic resistance seen in the world. | Application of new selection pressure against bacteria and their response to it. |
| How can lateral gene transfer contribute to antibiotic resistance? | Intermicrobial transfer of plasmids containing resistance genes (R factors) occurs by conjugation, transformation, and transduction. |
| Folic acid is required as a cofactor for the synthesis of amino acids and DNA. Why is it possible to inhibit folic acid synthesis without killing a human? | Because humans to not naturally make folic acid (it is an essential nutrient that we ingest), whereas bacteria must have folic acid to survive. |
| You are accompanying a group of explores into a deep jungle in southern Mexico. You are in charge of the group’s health. Consult table 12.3 to select the one or two drugs you will bring. | Tetracycline, penicillin, cloroquine |
| Probiotics | benign organisms that compete for space/nutrients with pathogens. |
| Prebiotic | product to encourage growth of probiotic bacteria |
| Define super infection as it applies to virology. Define super infection as it applies to antibiotic treatment. How are the uses of the term similar? | Virology- segmented genomes allow for reassortment creating new strains of the virus; Antibiotic- when gut flora have been compromised, bacterial colonization has ability to spread to areas of the body it wouldn’t normally (same pathogen, 2 places) |
| MIC | minimum inhibitory concentration; smallest concentration of drug needed to visibly control microbial growth |
| TI | therapeutic index; toxic does/MIC |
| What is the purpose of the Kerby-Bauer test and its relatives. | Determines drug effectiveness by measuring zone of inhibition. |
| What factors should be considered when choosing an antibiotic? Is there always one good answer? | Pathogen?; Complications in the patient?; Allergy, Damaged organs, Drug Interactions, Therapeutic Index and Toxicity |
Created by:
mbtrimm
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