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54 Cards in this Set
- Front
- Back
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Moist Heat
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• 60-135 degrees C
• denature proteins and destroy membranes • methods: boiling, autoclaving (), pasteurization, and ultra high temperature sterilization |
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. Boiling
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Kills veg. bacteria; and fungi, prpotozoa trophozoites, and most viruses. Length of boiling one time is critical. (not cysts, spores and some viruses)
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autoclaving
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uses steam under pressure. Boiling temp increases, increases pressure; can sterilize
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Pasteurization
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liquids that we don’t want to change the consistency (milk, ice cream, apple cider, fruit juice) NOT sterilization and if are heat tolerant will survive. Time and heat can vary. Heat short time 60-73 degrees
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Ultra high temp sterilization
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140 degrees X 1 sex, rapid cool, stored at room temperature
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Dry Heat
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• Higher temperature= 160- several thousands
• Used when moist heat methods don’t work • Results in: burning of cells, cell damage and dehydration/incineration • Need higher temperature for longer times than in moist heat (ULTIMATE TECHNIQUE) |
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Cold
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refrigeration and freezing
• Decreases microbial metabolism, growth and reproduction • At freezing liquid water is not available, refrigeration (happens very slowly) • Psychrophils are exception |
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Desiccation
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• Desiccant= something that can remove water
• Drying inhibits the growth of the microbes because of the removal of water; metabolism can’t take place |
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Osmotic Pressure
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increase salt or sugar in foods, inhibits growth, cells lose H20
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Radiation
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energy emitted from atomic activities and dispersed @ high velocity through matter or space
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Ionization Radiation
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radiation ejects E- from atom, causing ion to form breaks of DNA or protein damage (leading to cell death)
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Nonionizing radiation
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excites atoms to higher energy state, but doesn’t cause ions to form→ when electrons excited → cause damage, make new covalent bonds (when they should not be doing it—weird covalent bonds) + alter the 3-D structure of proteins and NA’s.
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UV light (nonionizing)
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messes up the DNA in skin cells, too many mutations= cancer (doesn’t penetrate well)
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Filtration
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physical removal by a filter to remove particles/ microbes
• Filter pore size is important |
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Chemical Method of Control
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Phenol and Phenolic compounds, Alcohols
Halogens, Oxidizing agents, Surfactants,Heavy Metals, Aldehyde |
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Phenol and Phenolic compounds
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o Intermediate disinfectant
o Denature proteins of organic matter o Active for long time |
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Alcohols
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o Intermediate disinfectant
o Ethyl alcohol o Isopropyl alcohol o Denature proteins and disrupt membranes of microbes o Works better than just soap |
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Halogens
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o Fl, Cl, I, BR
o Intermediate o Damage enzymes (determines inhibition/death) o Used in hospitals, water supply, bleach |
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Oxidizing agents
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o H2O2→ can disinfect and sterilize surfaces
o O3 (treat drinking H20) o kill by disrupting (oxidizing) enzymes o high levels of disinfectants + antiseptics |
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Surfactants
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o Lower surface tension of water → disrupts membranes (soaps, detergents—pure surfactants vs better working by decrease ST, disrupts proteins in the membrane by the positive charged ends of detergent interacting with negative charged ends of bacterial surface—almost pulling apart the cell)
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. Heavy Metals
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o Heavy metals can turn into heavy metal ions→ denature proteins (can be toxic to humans)
o Thimerosal in vaccines (mercury compound to preserve) |
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Aldehyde
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o Compounds contain CHO @end
o Crosslink proteins (knocking out activity of proteins) o Inactivate nucleic acids o Ex. gluteraldehyde • Diluted it can disinfect and sterilize o Formaldehyde (formalin) • Used in embalming/disinfectant |
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Chemo
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therapeutic drug= chemical used in treatment, relief or prophylaxis of disease
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When given for infection
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antimicrobial
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Antibiotics
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o =chemicals that are derived from bacteria or molds
o inhibits/destroy other microbes o synthetic= made in lab o semisynthetic= come from bacteria and mold where lab tweaks them |
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Antimicrobial
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most generic = all antimicrobes, doesn’t matter origin
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Scope of Activity
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o Narrow spectrum→ effective against limited microbes
o Broad spectrum→ much greater variety, active against a wider range of different microbes o KEY= want to destroy microbe without harming the host! |
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History of Discovery of Antimicrobial drugs--Paul Ehrlich (1800’s)
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o first antimicrobial
o specific dyes stain certain microbes and not animal tissues o ? maybe drugs can selectively kill microbes, not human tissue o tested theory by treating syphilis, started playing with arsenic 606th try with salvarsan—used therapeutically for few years |
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Alexander Flemming 1928
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o plate of S. aureus (plate got contaminated with mold)
o Mold= penicillium noatatum (isolated “penicillin”) (bactericidal) |
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Domagk (1935)
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o working with dye and bacteria
o used red dye (protonsil—active against certain bacterias and infection in animals) o same microbes in test tube (nothing happened/dye not effective) o Drug was altered to be “active in body”→ changed protonsil to sulfonamide → first sulfa drug |
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Classes of Antimicrobials
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Drugs that effect the bacteria cell wall—Gram positive= more succeptible and gramp-negative less succeptible b/c OM, so drugs can’t get in
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Beta Lactams (have lactam ring= square double bonded to O)
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• Inhibit crosslink of peptidoglycan; between lines of NAM-NAG-NAM-NAG
• Penicillin= bactericidal; natural and synthetic forms (lyse, rupture and blow up) • Cephalosporin= semi-synthetic |
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Vancomycin
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• Inhibits early cell wall synthesis, disrupts polysaccharide back bone, for life threatening infections; Staphylococcus infection, neurotoxic, last line of defense/ BIG GUNS. Microbes are becoming resistant
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Bacitracin
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• In Neosporin
• Disrupts polysaccharide back bone • For streptococci + staphylococci • For Gram + (works really well) |
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Isoniazid (INH) & Ethambutol
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• Used to treat TB
• TB caused by microbe called mycobacterium tuberculosis • Has waxy coating → cell wall is composed of mycolic acid • Isoniazed inhibit mycolic acid synthesis (leaky cell wall) (first line of defense for TB) • Secondary treatment= Ethambutol → given separately to avoid resistance • Inhibits incorporation of the mycolic acid into cell wall (explodes) |
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Affect Nucleic acid synthesis--Fluoroquinolones
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inhibits DNA girase of prokaryotes (which is important in unwinding DNA, without they can’t replicate) Potent, broad spectrum
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Rifampin
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inhibits RNA polymerase—blocks RNA synthesis, leprosy/TB, hepatoxic, resistant microbes
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Inhibitors of Metabolic pathways
1. Sulfonamides |
inhibits DNA girase of prokaryotes (which is important in unwinding DNA, without they can’t replicate) Potent, broad spectrum
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2. Rifampin
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inhibits RNA polymerase—blocks RNA synthesis, leprosy/TB, hepatoxic, resistant microbes
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Inhibitors of Metabolic pathways
1. Sulfonamides |
• broad spectrum
• block the enzymes that make purines and pyrimidine—competitive inhibitors of KABA, which is a substrate for the enzyme that converts PABA (enzyme blocked by sulfonamide) to DHFA (enzyme) to THF (enzyme) to purine & pyramidines→ DNA & RNA |
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Thrimethoprim
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• PABA→ DHFA (blocked by thrimethoprim)—THF—DNA
• Binds to enzyme that converts DHFA to THF |
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Quinolones
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• Quinine drugs
• Extracted from bark of cinchona tree • Now synthetic—chloroquine • For plasmodium to cause malaria, drug inhibits enzyme and changes heme (in RBC) to nontoxic form, then heme is toxic to |
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Drugs that inhibit protein synthesis
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prokaryotic ribosomes diff’t ours
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Chloramphenicol
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• Broad spectrum
• Bind 50S (large) ribosomal subunit Prevents peptide bond formation so incoming AA can’t bind |
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tetracycline
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• interferes with attachment of tRNA to mRNA (on ribosomes)
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Erythromycin
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• (group = macroliders)
• bind 50S • prevent movement of the ribosome along the MRNA |
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Aminoglycoside
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• change shape of 30S
• so codons read improperly • ex. streptomycin |
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Affect cell membrane
1. Polymixins |
• disrupt membrane of Gram – bacteria (outermost membrane/outer membrane)
• cationic detergents, disrupt bilayer, lead to burst • nephrotoxic/renal toxic/neuromuscular toxic , effect the kidney’s nephron |
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2. Amphotericin B & nystatin
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• antifungal
• binds to ergosterol (like the cholesterol in our cell membranes)→ loss of selective permeability • Human side effects→ may be somewhat susceptible because similar to cholesterol |
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3. Synthetic Azoles
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• inhibit the enzymes that makes ergosterol
• mostly topical medications • ex. ketoconazole, miconazole |
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Antiviral Drgus
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o Interfere with viral replication by: blocking entry to cell, preventing assembly, inactivate replication
o Many antiviral are nucleotide analogs which inactivate replication when they are incorporated into the viral nucleic acids |
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1. Acyclovir
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• analog of guanine (G of DNA) gets put in every time a G is supposed to go in and therefore the fake G makes it impossible to replicate later on
• treat herpes viruses herpes simplex virus (cold sore/genital herpes) varicella foster—causes chicken pox/shingles |
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Drug Resistance
How do microbes become resistant? Through: |
o Random chromosomal mutations (can help survive)
o Transfer of plasmids from one resistant strain to non-resistant strain |
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Mechanisms of drug resistance
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1. Enzyme made that inactivate the drug
2. Decrease the permeability and therefore drug uptake/absorption 3. Change in the affinity or # of receptors 4. Modification of essential metabolic pathways |