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Test Two MicroBiology 2300 Guide

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by: Kazendi Simon

Test Two MicroBiology 2300 Guide BIOL 2300

Marketplace > Georgia State University > Biology > BIOL 2300 > Test Two MicroBiology 2300 Guide
Kazendi Simon
GPA 3.8

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About this Document

Detailed overview of Test Questions. Main topics coverage.
Hanan Lea El-Mayas (P)
Study Guide
50 ?




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This 9 page Study Guide was uploaded by Kazendi Simon on Tuesday January 26, 2016. The Study Guide belongs to BIOL 2300 at Georgia State University taught by Hanan Lea El-Mayas (P) in Fall 2015. Since its upload, it has received 250 views. For similar materials see MICROBIOLOGY & PUBLIC HEALTH in Biology at Georgia State University.


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Date Created: 01/26/16
Chapter 5 Controlling Microbial Growth Key Terms (If needed create Flash Cards)    Bactericidal: Various agents that kill bacteria. o Disinfectant: A chemical used to destroy many microorganisms and virus. o Disinfection: A process that eliminates most or all disease­causing  microorganisms and virus on or in a product. o Fungicide: Kills Fungi o Germicide: Kills microorganisms and inactivates virus. o Terilant: A chemical used to destroy all microorganisms and viruses in a product  rendering it sterile. o Sterile: Completely free of all microorganisms and viruses; an absolute term.  o Sterilization: The process of destroying or removing all microorganisms and  virus. o Viricide: Inactivates viruses    Bacteriostatic: Various agents that inhibit growth. (Slow down) o Antiseptic: A disinfectant that is non­toxic enough to be used on skin.  o Decontamination: Treatment used to reduce the number of disease­causing  microbes to a level that is considered safe to handle o Degerm: Treatment used to decrease the number of microbes in an area o Pasteurization: A brief heat treatment used to reduce the number of spoilage  organisms and to kill disease­causing microbes. o Preservation: The process of inhibiting growth of microorganisms in products to  delay spoilage.    Decimal reduction time o D value: time required to kill 90% of a population.    Time to kill suspension of M. tuberculosis: with Sodium Hypochlorite o at 50o C 150 sec o at 55o C  55 sec    Heat to Control Microorganisms o Boiling: Fast, reliable, and inexpensive method to destroy most microbes. Can’t  kill endospores easily. o Pressurized Steam: Achieves temperatures above 100*C, which is necessary to  destroy endospores. Utilized for sterilizing surgical items and create canned  foods. o Dry Heat: A flame used to sterilize bacteriological loops. HTLT (High  temperatures for long Lengths of time.)  Oven (160­170*C) (320­340*F) o HTST Method: High temp. Short time.  72*C(162*F) for 15 sec (for milk) then rapidly cooled  82*C (180*F) for 20 sec (ice cream) o UHT: Ultra high temp.  Cream and milk juices in boxes :  Heat 140­150* C (284­302*F) o Autoclave: typically uses an operating temperature of 121*C (250*F) at 18 psi;  for 15 minutes.   At this temperature, bacterial endospores have a D value = 4 ­ 5 min,  whereas vegetative cells have a D value= 0.1 to 0.5 min.      Filtration o Air filtration: HEPA (high­efficiency particulate air) 0.3mm.   Laminar flow hoods to prevent spread of air­borne pathogens o Membrane filters: Made chemically inert material such as cellulose acetate or  cellulose nitrate.    Filter pores = 0.2­ 0.45 mm. Some can filter smallest viruses.  Microorganisms are trapped on the surface of the filter. o Depth filters: Made with paper or glass fibers, consist of many layers of  overlapping fibers.    Microorganisms are trapped by electrostatic charges on the walls of the  filter.     Radiation o UV Radiation: Does not penetrate solid, opaque or light absorbing materials  useful for disinfecting surfaces, air and liquids that do not absorb the UV waves.  Kills microorganisms by damaging DNA: create thymine dimers that lead  to insertion of a wrong base pair causing mutation.  Does not kill endospores.     Chemicals Used in Sterilization and Disinfection, and Preservation: o Alcohols: Disinfectant and antiseptics for surface sterilization; limitation  evaporates quickly. o Aldehydes: Strong disinfectants (formaldehyde, glutaraldehyde) inactivates  proteins and Nucleic acids irritating to skin eyes and respiration suspected to be  carcinogenic.  Glutaraldehyde: liquid chemical sterilant and used for disinfecting  medical instruments.  Formaldehyde: (at 37% = formalin) is used in inactivating viruses and  bacteria to use in vaccine preparation. o Ethylene oxide gas: gaseous sterilizing agent: Penetrates hard to reach places;  kills endospores; sterilize disposable Petri dishes and pipettes.  o Quaternary ammonia compounds (QAC): e.g. benzocalium chloride: disinfectants and antiseptics. Non­toxic. Used on inanimate objects and surfaces; preserves  non­food substances.    Classification of General Methods for Controlling Microbial Growth o Bactericidal Physical  Disinfectants (Kills Most)  Microwaves  UV Waves  Boiling  Pasteurization  Sterilants (Kills All)  Autoclave  Gamma Rays o Bactericidal Chemical  Disinfectants (Kills Most)  Ozone  Phenolic   Alcohols (60% ­ 80%)   Hydrogen Peroxide  Quaternary Ammonium Compounds  Sterilants (Kills All)  Aldehydes  Ethylene Oxide Gas  Antiseptics (Safe on Skin)  Iodine  Alcohols  Hydrogen Peroxide [Catalase H O2] 2 o Bacteriostatic  Detergent  Mycells  Refrigerating/Freezing  Drying Food Chapter 21 Antimicrobial Medications {Fused with Rene’ Notes}    Antimicrobial Drugs: Chemically synthesized drugs that inhibit growth or kill  microorganisms. o Antibiotics have been altered chemically to give new derivatives with new  properties e.g.: family of Penicillin.    The common core portion of Penicillin G called 6­amino­penicillanic acid  (6­ APA).  Drug Synergy (Combination Power) o Synergistic: the activity of the drug in combination is GREATER than the sum of  their independent activity. o Antagonistic: the activity of the drug in combination is LESS than the sum of  their independent activity. o Addictive: the activity of the drug in combination is EQUAL than the sum of their independent activity.  Understanding Toxicity: o Antimicrobials selective toxicity: drug cause more harm to microorganisms than  to humans by interfering with biological structures and biochemical processes in  microorganisms and not in humans. (This means that anti­bacterial drugs must  target specific structure in the bacterial cell that do not exist in our body)  Common Targets: The peptidoglycan cell wall, protein synthesis in  ribosomes, nucleic acid (DNA or RNA) synthesis, a metabolic process  that bacteria have (not us), etc. o Therapeutic index: Toxicity of a given drug is expressed as a therapeutic index.   High therapeutic index is less toxic to the patient.   Higher selective toxicity of the antibiotic the bacteria  the higher  therapeutic index of the antibiotic to us.  Penicillin which selectively targets a PBP (enzyme responsible for  building the peptide inter­bridge in the peptidoglycan layer).  Penicillin G: acting on cell wall synthesis has high therapeutic index.  Polymixin B: which targets the phospholipid in the bacterial cell  membrane has a low therapeutic index since we too have phospholipids in  our cell, membrane.  Spectrum of Activity: o Broad­spectrum antimicrobials: affect wide range of bacteria (Ampicillin,    chloramphenicol, tetracyclines)  Advantage: for treatment of live threatening diseases when there is no  time to culture and identify the disease causing agent.   Disadvantage: kill normal flora that keeps pathogens away. (Can cause  yeast infections when looking at females.) o Narrow­spectrum antimicrobials: have limited use requires identification of the  pathogens and cause less disruption to the normal flora.     Half­life and Dosage of an Antibacterial Drug o Antimicrobial rate of elimination is expressed as the half live; is the time it takes  for the body to eliminate one half of the original dosages in the serum.   The longer the half­life of a drug the less is the frequency of doses that are required to maintain an effective level in the body.  Amoxicillin has a longer generation time than Ampicillin and therefore, it  requires less dosage.   This helps when trying to get kids to take their medicine easier.     Length of treatment: Depends on the generation time of the bacteria o The longer the generation time for a bacteria (the slower it metabolizes) the  longer time is the treatment   E coli: has a generation time of 18 min treatment with amoxicillin would  last for 5­7 days for a UTI.  Mycobacterium tuberculosis: has a G time of 12­24 hours treatment of a  patient with antibiotics would last 1­3 years.     Adverse side effects: o Allergies: For some Penicillin cause fever, rash or anaphylactic shock (sudden  drop in blood pressure caused by Ig E). o Toxicity: Some drugs may have high concentrations.  Streptomycin: cause kidney damage, irreversible deafness  Chloramphenicol: in rare cases causes aplastic anemia i.e. inability to  make red and white blood cells. o Some broad spectrum activity antibiotics may cause:  Suppression of the normal flora: can lead to antibiotic associated pseudo­ membranous colitis a severe intestinal infection leading to bleeding and  loss of chunks of epithelial layer and pus in stools.  Caused by toxic secreting Clostridium difficile.  o Yeast infections: caused by Candida albicans which grow when antibiotics  treatment destroy normal bacterial flora that normally keeps the healthy vagina's  pH =4; when these are killed pH turns 7.     Targets of Antibiotic Families o Inhibition of cell wall synthesis o Inhibition of protein synthesis o Inhibition of nucleic acid synthesis o Inhibition of metabolic pathways o Inhibition of cell membrane integrity     Inhibition of cell wall synthesis:  o Beta­Lactams Drugs: inhibit the enzymes PBBs from synthesizing peptide chains  and penicillin­binding proteins.   Include penicillin family and Cephalosporin family.  Inhibits PBPs which are enzymes involved in the formation of  peptide bridges between adjacent strands of peptidoglycan; this  cause cell wall lysis. o Natural Penicillin: branches off into Penicillin (G and V)  Ampicillin and amoxicillin: broad spectrum even active against gram neg.  Methicillin & Dicloxicillin: is penicillinase resistant (useful against S.  aureus)  Cephalosporins: also destroy PBP especially in gram negative.  o Vancomycin: blocks synthesis of peptide side chains by binding to an amino acid,  a side chain of NAM molecules, therefore blocking the formation of the tetra  peptide.   Used only as last resort against gram positive some S. aureus developed  resistance against it. Strongest form of penicillin.  o Bacitracin: interferes with the transport of peptidoglycan precursors across the   cytoplasmic membrane.  For topical application only. Poorly absorbed, cause kidney damage.  Efficient on gram positive     Inhibition of protein synthesis: o Aminoglycosides: Blocks the initation of translation and causes the misreading of  mRNA.  Effective against gram neg.  Binds to 30S subunit.  Streptomycin  Neomycin: for intestine infections and eye infections o Tetracycline: Blocks attachment of tRNA to the ribosome  Selective toxicity against some gram pos., gram neg., and obligate  intracellular pathogens Chlamydia and Rickettsia.  Binds to 30S subunit  Bacteriostatic o Macrolides: Prevents the continuation of protein synthesis (Stops process  midway.)  Binds to the 50S subunit  Effective against walking pneumonia  Erythromycin: Given to patients allergic to Penicillin  Azithromycin: effective against gram neg. o Chloramphenicol: Prevents peptide bonds from being formed (Stops at first cycle)  Wide spectrum   Binds to 50S subunit.  Used only in emergency can cause aplastic anemia o Lincosamides: Prevents the continuation of protein synthesis  Binds to 50S subunit o Oxazolidinones: Thought to interfere with the initiation of protein synthesis  Binds to 50S subunit     Inhibition of nucleic acid synthesis: o It is very important that you understand that these drugs inhibit the enzymes involved in the  synthesis of nucleic acids, and do not target directly the   nucleic acids,  because we also have the same nucleic acid o Fluoroquinolones: Target gyrase that maintain the supercoiling of closed circular  DNA. We do not have gyrase.  Novobiocin  Ciprofloxacin (against anthrax) o Rifamycins: targets bacterial RNA polymerase enzyme for DNA transcription into mRNA. Which is different in its structure than our RNA polymerases  Used synergistically with other antibiotics against tuberculosis.     Inhibition of metabolic pathways: o Sulfanilamide: (sulfa drug) inhibits the metabolic pathway that leads to the  synthesis of Folic acid (vitamin B12).   In other words sulfa drug act as a competitive inhibitor to PABA and  block the synthesis of folic acid in E. coli.  PABA sits on the active site of Enzyme 1 and this will lead to the product, folic acid.  We do not synthesize (make) folic acid. o Trimethoprim: deprive them of dihydrofolate coenzymes; by inhibiting the  enzyme catalyzes.  Used in combination with a sulfa drug for a synergistic effect  Sits on the active site of Enzyme 3     Inhibition of cell membrane integrity: o Polymixin B: interfere with bacterial cell membrane, more efficient on gram  negative.  Very toxic; Low therapeutic index     Anti TB. Drugs: o Interfere with processes essential to mycobacterium tuberculosis  Isoniasid: inhibits synthesis of mycolic acid, which is used to help form  the mycobacterial cell wall.  Etambutol: inhibits the synthesis of a component of mycobacterial cell  wall.  These are usually prescribed in combination with rifamycin.  Pyrazinamide: role unknown  General Classification of Antibiotic Drug Families o Bacteriostatic  Tetracyclines  Glycocyclines  Chloramphenicol  Macrolides  Sulfa Drugs  Trimethoprim  o Bactericidal   B­ Lactam   Bacitracin  Vancomycin  Aminoglycoside  Polymyxin B  Metroniclazole  Ethambutol  Iozinazid  Pyrazinamide  Daptomycin      Resistance to antibiotics o Selective advantage: Bacteria from one species have a variation in their genes.  Some may be killed by antibiotics and some have plasmids for resisting  antibiotics.   When you treat a bacterial disease with an antibiotic A, the selective one  would die and the resistant one will survive and will reproduce, therefore  generating a new strain that resist antibiotic A.      Mechanisms of resistance  o Drug­inactivating enzymes: E.g. penicillinase or beta lactamase will destroy  penicillin or a Beta lactam drug. o Alteration in the target molecule: E.g. alteration in the PBPs prevent penicillin or  other beta lactam drugs from binding to them. o Decreasing uptake of the drug: Alteration in the porin protein on the outer  membrane of the gram neg.   Bacteria can alter their permeability and prevent some drug from entering  the cell. o Increased elimination of the drug: Efflux pumps excrete detrimental compounds  out of the cell.   Alteration of these pumps can increase their activity enabling the  organisms to resist high concentration of the drug.   Allows organisms to be resistant to various drugs at the same time. o Pseudomonas spp: has efficient efflux pump.     Resistance to antibacterial drugs: o Innate resistance: intrinsic resistance  E.g. Mycoplasma: lacking a cell wall is resistant to Penicillin.  In Gram negative bacteria, outer membrane of cell wall gives intrinsic  resistance to certain drug.   o Acquired resistance: Heavy uses of antibiotics  E.g.  Penicillin: progressively eliminated sensitive strains of e.g. S.aureus.  Today 90% of present strains are now resistant to the same drug. o Spontaneous mutation: leading to acquisition of resistance  Vertical evolution: because it is passed on to daughter cells of the same  strain o Gene transfer via conjugation of R­plasmid: can occur even between unrelated  organisms.   Horizontal evolution: R plasmids can carry many different Resistance  genes.   Allowing cells to be resistance to many drugs at the same time.  E.g. Resistant E coli: that has resistance to carbapenem can pass that  carbapenem resistant plasmid to any other gram negative bacteria.


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