Chapter 10. Antimicrobials. PowerPoint Lecture Slides for MICROBIOLOGY ROBERT W. BAUMAN
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1 PowerPoint Lecture Slides for MICROBIOLOGY ROBERT W. BAUMAN Chapter 10 Antimicrobials
2 Antimicrobial Drugs Chemotherapy - The use of drugs to treat a disease Antimicrobial drugs - Interfere with the growth of microbes within a host Antibiotic - Substance produced by a microbe that, in small amounts, inhibits another microbe Selective toxicity - A drug that kills harmful microbes without damaging the host
3 Table 20.1
4 The Action of Antimicrobial Drugs Broad-spectrum Narrow-spectrum Superinfection Bactericidal Bacteriostatic
5 The History of Antimicrobial Agents Paul Ehrlich Magic Bullets Arsenic compounds for syphilis patients killed trypanosomes and another that worked against treponemes 600 derivative compounds tried
6 The History of Antimicrobial Agents Alexander Fleming discovered penicillin, produced by Penicillium. Zone of inhibition 1940 Howard Florey and Ernst Chain performed first clinical trials of penicillin. Figure 20.1
7 The History of Antimicrobial Agents Gerhard Domagk Nobel Prize for Sulfa Drugs - Sulfanilamide Red dye Prontosil converts to sulfanilamide First antimicrobial agent used to treat wide array of infections Semisynthetics and synthetics
8 Mechanisms of Antimicrobial Action 1. Inhibition of cell wall synthesis 2. Inhibition of protein synthesis 3. Disruption of cell membrane 4. Inhibition of a metabolic pathway 5. Inhibition of DNA or RNA synthesis 6. Inhibition of pathogen attachment
9 The Action of Antimicrobial Drugs Figure 20.2
10 1. Inhibition of Cell Wall Synthesis Figure 10.3a
11 Inhibitors of Cell Wall Synthesis Penicillin Natural penicillins Semisynthetic penicillins
12 Inhibition of Cell Wall Synthesis Most common agents act by preventing cross-linkage of NAM subunits Most prominent in this group beta-lactams; functional groups are beta-lactam rings Beta-lactams bind to enzymes that cross-link NAM subunits Bacteria have weakened cell walls and eventually lyse
13 Penicillins Figure 20.6
14 Inhibitors of Cell Wall Synthesis Penicillin resistant bacteria produce the enzyme Penicillinase Figure 20.8
15 Inhibition of Cell Wall Synthesis Figure 10.3b
16 Inhibition of Cell Wall Synthesis Simplest beta-lactams effective only against aerobic Gram-positive organisms Figure 10.3d
17 Inhibition of Cell Wall Synthesis Figure 10.3e
18 Inhibition of Cell Wall Synthesis Semisynthetic derivatives of beta-lactams More stable in acidic environments More readily absorbed Less susceptible to deactivation More active against more types of bacteria
19 Inhibition of Cell Wall Synthesis Figure 10.3c
20 Inhibitors of Cell Wall Synthesis Cephalosporins 2 nd, 3 rd, and 4 th generations more effective against gram-negatives Figure 20.9
21 Inhibition of Cell Wall Synthesis Vancomycin and cycloserine interfere with bridges that link NAM subunits in many Gram-positives Bacitracin blocks secretion of NAG and NAM from cytoplasm Isoniazid and ethambutol disrupt formation of mycolic acid in mycobacterial species
22 Inhibition of Cell Wall Synthesis Prevent bacteria from increasing amount of peptidoglycan Have no effect on existing peptidoglycan layer Effective only for growing cells No effect on plant or animal cells; no peptidoglycan
23 2. Inhibition of Protein Synthesis Prokaryotic ribosomes are 70S (30S and 50S) Eukaryotic ribosomes are 80S (40S and 60S) Drugs can selectively target translation Mitochondria of animals and humans contain 70S ribosomes; can be harmful
24 The Action of Antimicrobial Drugs Figure 20.4
25 Inhibitors of Protein Synthesis Chloramphenicol Broad spectrum Binds 50S subunit, inhibits peptide bond formation Aminoglycosides Streptomycin, neomycin, gentamycin Broad spectrum Changes shape of 30S subunit
26 Inhibitors of Protein Synthesis Tetracyclines Broad spectrum Interferes with trna attachment Macrolides & Erythromycin Gram-positives Binds 50S, prevents translocation
27 Inhibition of Protein Synthesis streptomycin erythromycin Figure 10.4
28 3. Disruption of Cytoplasmic Membranes Some drugs become incorporated into cytoplasmic membrane and damage its integrity Polymyxin disrupts cytoplasmic membranes of Gram-negatives; toxic to human kidneys Amphotericin B (polyene) attaches to ergosterol found in fungal membranes Humans somewhat susceptible because cholesterol similar to ergosterol Bacteria lack sterols; not susceptible
29 Disruption of Cytoplasmic Membranes Figure 10.5
30 4. Inhibition of Metabolic Pathways When differences exist between metabolic processes of pathogen and host, anti-metabolic agents can be effective Metabolic antagonists
31 Inhibition of Metabolic Pathways Figure 10.6
32 Competitive Inhibitors Sulfonamides (Sulfa drugs) Inhibit folic acid synthesis Broad spectrum Figure 5.7
33 Figure 20.13
34 Inhibition of Metabolic Pathways Trimethoprim - binds to enzyme involved in conversion of dihydrofolic acid to THF Humans obtain folic acid from diet; metabolism unaffected Antiviral agents can target unique aspects of viral metabolism Amantadine, rimantadine, and weak organic bases neutralize acidity of phagolysosome and prevent viral uncoating
35 5. Inhibition of Nucleic Acid Synthesis Several drugs function by blocking DNA replication or mrna transcription Only slight differences between prokaryotic and eukaryotic DNA; drugs often affect both types of cells Not normally used to treat infections; used in research and perhaps to slow cancer cell replication
36 Inhibition of Nucleic Acid Synthesis Compounds can interfere with function of nucleic acids (nucleotide analogs) Distort shapes of nucleic acid molecules and prevent further replication, transcription, or translation Most often used against viruses; viral DNA polymerases more likely to incorporate viral nucleic acid synthesis more rapid than that in host cells Also effective against rapidly dividing cancer cells
37 Inhibition of Nucleic Acid Synthesis Figure 10.7
38 Inhibition of Nucleic Acid Synthesis Rifamycin Inhibits RNA synthesis (RNA polymerase) Antituberculosis Quinolones and fluoroquinolones Ciprofloxacin Inhibits prokaryotic DNA Urinary Tract Infections
39 6. Inhibition of Pathogen Attachment Prevention of Virus Attachment Attachment can be blocked by peptide and sugar analogs of attachment or receptor proteins (attachment antagonists) Still in developmental stage
40 Mechanisms of Antimicrobial Action Figure 10.2
41 Ideal Antimicrobial Agent Readily available Inexpensive Chemically stable Easily administered Nontoxic and nonallergenic Selectively toxic against wide range of pathogens
42 Evaluation of Antimicrobial Spectrum of action Efficacy Dosages required to be effective Routes of administration Overall safety Side effects
43 Spectrum of Action Figure 10.8
44 Diffusion Susceptibility Test Figure 10.9
45 Routes of Immunization Figure 10.13
46 Routes of Immunization Topical - if infection is external Oral simplest lower drug concentrations in blood no reliance on health care provider patients do not always follow prescribing information Intramuscular requires needle for administration concentration never as high as IV administration Intravenous requires needle or catheter drug concentration diminishes as liver and kidneys remove drug from circulation Must know how antimicrobial agent will be distributed to infected tissues
47 Safety and Side Effects Three main categories of side effects Toxicity Allergies Disruption of normal microbiota
48 The Development of Resistant Organisms in Populations Some organisms are naturally, partially, or completely resistant Resistance by bacteria acquired in 2 ways New mutations of chromosomal genes Acquisition of R-plasmids via transformation, transduction, and conjugation
49 The Development of Resistant Organisms in Populations Figure 10.15
50 Multiple Resistance and Cross Resistance Pathogen can acquire resistance to more than one drug at a time Common when R-plasmids exchanged Develop in hospitals and nursing homes; constant use of drugs eliminates sensitive cells Superbugs Cross resistance
51 Retarding Resistance High concentrations of drug maintained in patient for long enough time to kill all sensitive cells and inhibit others long enough for immune system to destroy Use antimicrobial agents in combination synergism vs. antagonism Limit use of antimicrobials to necessary cases Development of new variations of existing drugs (novel side chains added to original molecule) Second-generation drugs Third-generation drugs
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