Test 3- Ch. 9, 10, 14 – Flashcards
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| Drugs (definition) |
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| Chemicals that affect physiology in any manner |
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| Chemotherapeutic agent |
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| drugs that act against diseases |
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| Antimicrobial agents |
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| drugs that treat infections (against microbes) |
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| what bacteria is the major cause of death from burns? |
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| S. pyogenes (1/2 of all deaths) |
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| What did Paul Ehrlich and Alexander Fleming discover? |
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| Penicillium inhibited growth of bacteria on agar plates |
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| What did Howard Florey and Ernest Chain contribute to Penicillin use? Who was their first patient? |
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| Discovered its use in humans and perfected the purification and solubility needed to treat. - Albert Alexander (police officer- later died) |
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| Gerhard Domagk |
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| Discovered the use of Sulfonilamide (Prontosil) which effects folic acid synthesis which is important for nucleotide synthesis. Tested on his own child who had streptococcal infection. |
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| What are the two main categories of selective toxicity for antimicrobial action? |
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| Structure and Function |
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| 6 methods of antimicrobial action |
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| 1. Inhibition of cell wall synthesis (Penicillins) 2. Inhibition of protein synthesis (Tetracyclines) 3. Disruption of cytoplasmic membrane (Polymyxins) 4. Inhibition of general metabolic pathway (Sulfonamides) 5. Inhibition of DNA or RNA synthesis (Actinomycin) 6. Inhibition of pathogen attachment or host recognition (Arildone) |
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| Penicillin- what does it target and how does it work? |
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| -Prevent bacteria from increasing amount of peptidoglycan -only effects newly reproduced bacteria -interferes with linking enzymes that connect NAM subunits. Cells eventually burst due to osmotic pressure |
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| Vancomycin and Cycloserine- what does it target and how does it work? |
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| -targets cell wall synthesis -Affects Alanine-Alanine bridges between NAM molecules |
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| Bacitracin- what does it target and how does it work? |
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| -targets cell wall synthesis -Blocks secretion of NAG and NAM from cytoplasm |
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| Isoniazid- what does it target and how does it work? |
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| disrupt arabinogalactan-mycolic acid (acid fast bacteria) in Mycobacterial species *use for long period of time since reproduction is slow. |
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| What step of protein synthesis do antibiotics usually target? |
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| Translation- Can differentiate between the 70s ribosomes of the prokaryotes and the 80s ribosomes of the eukaryotes |
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| Streptomycin and Gentamicin (Aminoglycocides)- what does it target and how does it work? |
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| -Alter 30s subunit of ribosome (protein synthesis) -mRNA is misread because it doesn't bind normally to the small subunit before translation |
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| Tetracycline- what does it target and how does it work? |
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| - blocks tRNA docking site (protein synthesis) |
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| Chloramphenicol- what does it target and how does it work? |
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| -binds between amino acids (protein synthesis) -Blocks enzymatic activity of ribosome |
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| Erythromycin (macrolide)- what does it target and how does it work? |
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| -bind to 50s, preventing mRNA from moving through ribosome (protein synthesis) |
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| Amphotericin B (polyene)- what does it target and how does it work? |
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| attaches to ergosterol which is a molecule similar to cholesterol found in fungal membranes. (disruption of cytoplasmic membranes) *Toxic to humans |
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| Polymyxin- what does it target and how does it work? |
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| -disrupts cytoplasmic membranes of G- bacteria *toxic to kidneys so used as topical |
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| Pyrazinamides- what does it target and how does it work? |
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| disrupts transport across plasma membrane (tuberculosis) -Disruption of Cytoplasmic membrane |
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| Heavy metals- what does it target and how does it work? |
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| paralyze (parasitic worms), inactivate enzymes -Metabolic antagonists (sulfonamides- Prontosil- PABA) -Interferes with the conversion of normal PABA to folic acid. This doesn't interfere with us because we obtain our folic acid from outside sources. |
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| Actinomycin- what does it target and how does it work? |
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| targets replication and transcription (binds to DNA) |
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| Nucleotide analogs- what does it target and how does it work? |
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| Block DNA replications |
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| Quinolones and fluoroquinolones- what does it target and how does it work? |
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| Inhibit DNA gyrase which coils and uncoils bacterial DNA -no effect on eukaryotes or viruses |
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| Rifampin- what does it target and how does it work? |
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| binds to RNA polymerase in bacteria (M. tuberculoses) |
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| Reverse transcriptase inhibitors |
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| HIV cocktail |
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| Amantadine & Rimantadine- what does it target and how does it work? |
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| antiviral agent -neutralize acidity of phagolysosome and prevent viral uncoating. |
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| efficacy-diffusion susceptibility test |
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| antibacterial drug on disks. Plated to see how well they inhibit growth |
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| Minimum Inhibitory Concentration (MIC) |
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| series of vials with increasing concentration of drug to identify the minimum needed to inhibit growth. |
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| Minimum Bactericidal Concentration (MBC) |
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| min concentration to kill everything Follow up test to the MIC. Plate the clear tubes solutions to see which were killed |
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| E- test |
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| strip of paper with increasing concentration of antibiotics. Used to identify the concentration needed to inhibit growth. Done on an agar plate. |
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| 4 types of antibiotic administration |
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| topical oral intramuscular IV |
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| 3 categories of antibiotic side-effects |
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| 1. toxicity (liver, kidney, pregnancy) 2. Allergies (minor --> anaphylactic shock) 3. Disrupt normal microbiota |
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| Mechanisms of Antibiotic resistance (5) |
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| 1. produce enzymes that destroy or deactivate the drug 2. slow or prevent entrance of the drug 3. alter target of drug 4. alter metabolic pathway or bypass it 5. pump the drug out |
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| cross resistance |
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| resistance to drug with same structure |
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| antibiotic combinations (synergism) |
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| 2 or more at the same time |
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| antibiotic combinations (antagonism) |
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| inhibition of one drug by other |
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| Thermal death point |
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| lowest temperature that kills all cells in broth in 10 mins |
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| Thermal death time |
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| time to sterilize volume of liquid at set temp |
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| 3 types of moist heat |
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| 1. boiling (1000 C) 2. autoclaving (1210 C) 3. Pasteurization (30 min at 63 C or 15 sec at 72 C) Ultrahigh temp sterilization (1-3 sec at 140 C) |
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| Dry Heat (2 types) |
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| Flame (15000 C) Ovens (171 C) |
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| Refrigeration and Freezing |
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| low temps slow growth but don't kill unless ice crystals form |
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| Desiccation |
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| Drying inhibits growth due to removal of water (does not kill) |
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| Lyophilization |
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| long term preservation of microbe cultures by rapid freeze and vacuum (prevent ice crystal formation) |
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| Filtration |
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| sterilization degree based on pore size. Does not kill, just removes. |
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| Osmotic Pressure |
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| prevents bacterial growth |
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| Radiation- Ionizing (1nm)- 3 types |
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| 1. electron beam- good for thin layers 2. Gamma Rays- deeper penetration (can penetrate containers) 3. X-rays-deeper penetration but low energy. No practical |
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| Radiation-Non ionizing |
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| wavelengths greater than 1nm -excites electrons to form new bonds -UV light causes thymine dimers in DNA but it does not penetrate well -used for operating beds |
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| what organisms are chemical methods most effective against? |
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| enveloped viruses vegetative cells of bacteria, fungi, and protozoa |
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| Phenol and Phenolics (examples and how it works) |
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| low level disinfectants (protein and plasma membrane) -can remain active for prolonged time -iister (carbolic acid), lysol, triclosan |
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| Alcohols (examples and how it works) |
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| intermediate disinfectants (protein and plasma membrane) -isopropanol, etoh |
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| Halogens |
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| intermediate disinfectants (damage enzymes via oxidation or denaturing) -iodine tablets, chlorine, bleach, bromine, chloramines |
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| Oxidizing Agents |
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| high level disinfectant and antiseptic -oxidation of microbial enzymes (peroxide, ozone for drinking water, peracetic acid for sporocide sterilizing equipment) -hydrogen peroxide can disinfect and sterilize surfaces (not deep wounds |
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| Soap (surfactant) |
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| hydrophilic and hydrophobic ends -good degerming agents but not antimicrobial |
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| Detergent (surfactant) |
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| positively charged organic surfactants- makes membranes soluble -Zephiran -QUATS (quaternary ammonium compounds)- colorless and tasteless- harmless to humans so used in medical and industrial applications |
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| Heavy Metals |
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| low level agents (ions alter 3-D shape of proteins) -thimerosal- preserve vaccines -Copper- algal growth in reservoirs, fish tanks, etc. (interferes with chlorophyll) -Silver Nitrate- prevent blindness caused by gonorrhea |
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| Aldehydes |
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| -compounds with terminal -CHO groups -denature proteins and inactivate nucleic acids (cross link with amino, hydroxyl, sulfhydryl and carboxyl groups) -glutaraldehyde- disinfects (short exposure) and sterilizes (long exposure) -formalin- embalming and disinfection of rooms and instruments |
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| Gaseous Agents |
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| -ethylene oxide and propylene oxide (closed chamber) denature proteins and DNE by cross linking functional groups -used in hospitals and dental offices (hazardous, explosive, poisonous, carcinogenic) |
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| use-dilution test |
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| culture metal rods with organism after 10 minutes in agent |
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| In-use test |
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| swab before and after disinfection then plate for growth |
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| Sterilization |
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| remove all microbes |
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| disinfection |
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| remove many pathogens |
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| Aseptic |
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| environment or procedure free of pathogens |
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| Antisepsis |
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| skin, tissue |
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| degerming |
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| physical removal, rubbing |
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| Sanitization |
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| disinfection in public place |
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| Pasteurizatino |
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| heat to kill pathogens |
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| -stasis/-static |
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| halt growth , not kill |
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| -cide/-cidal |
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| kill |
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| Etiology |
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| study of the cause of a disease |
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| Germ theory of disease |
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| disease caused by infections of pathogenic microorganisms |
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| Pathogenicity |
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| ability of organism to cause disease |
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| Virulence |
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| degree of pathogenicity (how they evade immune system and cause disease) |
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| Virulence factors (4) |
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| 1. adhesions 2. extracellular enzymes 3. toxins 4. anti-phagocytic factors |
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| Adhesions |
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| process by which microorganisms attach themselves to cells -specialized structures (lipoproteins or glycoproteins) -attachment proteins (viruses) -adhesins (bacteria) |
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| extracellular enzymes |
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| enzymes secreted by pathogen that help pathogen dissolve structural chemicals in the body and invade further (hyaluronidase, collagenase, coagulase, kinase) |
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| Toxins- fucntion |
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| produced by pathogen- harm tissues or trigger host response that cause damage -Toxemia- toxins in the bloodstream beyond the site of infection |
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| 2 types of toxins |
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| 1. Exotoxins- cytotoxin, neurotoxin, enterotoxin 2. Endotoxins- Lipid A |
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| Anti-Phagocyctic Factors |
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| 1. Bacterial Capsule- composed of chemicals found in the body not recognized as foreign. Can be slippery and difficult for phagocytes to engulf 2. Anti-phagocytic chemicals- prevent fusion of lysosome and phagocytic vesicles OR destroys white blood cells (leukocidins) |
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| Benefits of normal microbiota (2) |
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| 1. antagonistic protection against pathogens 2. production of certain vitamins in the body |
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| Normal sites of microbiota |
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| upper respiratory digestive tract Urinary and reproductive skin and eyes |
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| What conditions allow resident microbiota to cause disease |
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| immune suppression changes in normal flora introduction into unusual site in the body |
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| Resident Microbiota |
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| bacteria that are a part of the normal microbiota throughout life (commensalism) |
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| Transient Microbiota |
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| in/on the body hours to months before disappearing (same region as resident microbiota) |
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| How are transient microbiota removed? (3) |
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| 1. competition from other microorganisms 2. elimination by the body's defensive cells 3. chemical or physical changes in the body |
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| when do we acquire our normal microbiota? |
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| during the birthing process and are established in the first months of life |
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| Axenic |
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| womb generally free of microorganisms |
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| How do pathogens enter the body? (4) |
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| skin mucous membranes placenta parenteral route of administration (direct under the skin or mucous membrane) |
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| contamination |
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| the presence of microbes in or on the body |
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| Infection |
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| invasion and establishment by a pathogen |
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| Disease |
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| pathogen alters the normal function of the body (morbidity) |
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| 5 stages of infectious disease |
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| 1. incubation period (no signs or symptoms) 2. prodromal period (vague symptoms) 3. illness (most severe symptoms) 4. decline (declining symptoms) 5. convalescence (no signs or symptoms but still contagious) |
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| Reservoirs of infection (definition and 3 types) |
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| sites where pathogens are maintained as a source of infection 1. animal 2. human carriers 3. nonliving reservoir |
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| Zoonoses |
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| diseases that are spread from their animal reservoir to humans -direct contact with animal or waste -ingesting animals -bloodsucking arthropods |
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| Human carriers |
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| individuals who are asymptotic but infective to others |
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| Nonliving reservoirs |
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| soil, water, food (often due to contamination by feces or urine) |
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| 3 groups of disease transmission |
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| transmission from either a reservoir or portal of exit 1. contact 2. vehicle (dust, water vapors, swimming pools, food) 3. Vector (flies and insects) |
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| Methods of classification (4) |
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| 1. body system effected 2. taxonomic groups of the causative agent 3. longevity and severity 4. how they are spread to host |
