Micro Final - Sheet1.csv

The flashcards below were created by user Anonymous on FreezingBlue Flashcards.

  1. Antibiotics
    "Work against living things. Primary for bacteria. From soil microbes in competition with each other. Soil does not have many nutrients so the competition for them
  2. Penicillin
    Comes from the fungus Peneclium and produces penicillin. Was developed by Alexander Flemming. Good against Gram positive. Referred to as Beta-lactam. Only used on Gram positive can not be used on Gram negative because it will release Lipid A
  3. Bacteriocins
    "Small protein complexes that are excreted by bacteria to inhibit growth of other bacteria
  4. Streptomyces
    Produces streptomyocin (is the bacteriocins). Are what give soil its smell.
  5. Antibiotic resistance development
    1. Increased/overuse of antibiotics. Along with the incomplete completion of taking the medication leads to resistance. 2. Over use in agriculture (feed to livestock animals: chickens. cattle. pigs). Veterinary Markets
  6. Synergism
    "Two antibotics work together. The outcome is beneficial. The effect does not make either one work better. Same kill
  7. Potentiation
    There is an interaction between the antibiotics that actually increases the the efficacy. Efficacy is potentiated. Makes the drugs more effective.
  8. Efficacy
    How well antibiotics work.
  9. Mechanisms of antibiotics
    1. Inhibit folate synthesis (distrub metabolic pathways. sulfonamides). 2. Interfer with DNA synthesis (metronidazole. Flagyl). 3. Interfer with RNA synthesis (rifamicin). 4. Drugs which interfere with cell membrane function (polymyxin B) 5. Distrupt cell wall synthesis (penicillin. only works during active division)
  10. Antibiotic for H. pylori
    Metronidazole (Flagyl). Interferes with DNA synthesis
  11. Vancomycin
    Very strong antibiotics that is not prescribed very often. People can get VRE. Vancomycin resistant enterococci.
  12. Methicillin
    MRSA. Methicillin (very strong antibiotic. similar to vancomycin) resistant Staphylococcus aureus.
  13. Nosocomial
    Infection aquired in the hospital. Community acquired infection.
  14. Resistance mechanisms to antibiotics
    1. Capsue 2. Spores. 3. Biofilm. 4. Extracellular enzymes. (proteases) 5. Coagulse 6. Pumps to remove antibiotics 7. Intracellular enzymes 8.Change target side 9. Ramp up production of antibiotic target 10. Alter metablic pathway (go around the effected enzyme). 11. Change in Cell Wall. Cell membrane permeability
  15. Coagulase
    As S. aureus grows. It produces coagulase which turns fibrinogen to fibrin. This fibrin makes a lattice/matrix protein (mesh) of protection around the bacteria. Difficult for antibiotics to reach it.
  16. Beta-lactamases
    Intracellular Enzymes used to breakdown pencillin like antibiotics.
  17. Counter Strategies for antibiotic resistance
    1. Alter chemical structure of the antibiotics 2. Use of multiple drugs at once. 3. Patient education
  18. Drug alteration
    Ater the site which effects the bacteria. Ex. amoxicillin. has added clavulanic acid. Clavulanic acid extends the life amoxicillin and helps to resist enzyme attacks.
  19. Penicillin resistance
    On penicillin the beta-lactam ring will bind to the alanine on the amino acids that are making nag and nam. The microbe will produces beta-lactamases to break down the ring where it binds to the cell wall.
  20. Septate
    The area between a dividing cell wall. Where penicillin works attaching to alanine on the nag and nam
  21. Pateint education
    1. Tell pt. to take medication. 2. Make sure pt. follow directions for medication. Ex. take with food. the acid in the stomach will break down the food and not the antibiotic. dont take on empty stomach
  22. Surfactants
    Are used in to loosen the lipid layers on gram negative bacteria. EDTA
  23. Riboswitch
    "When a certain concentration of a protein is made the riboswitch will tell the cell to stop making it. AEC (aminoethylcysteine) is identified in the cell as cysteine. This triggers the ribose switch to stop making cysteine
  24. MIC
    Minimum inhibitory concentration. Lowest concentration that will inhibit growth. The minimum concentration that is the losest concentration that will inhibit the visible growth of a microoganism after overnight incubation.
  25. Etest
    A strip that has a varying concentration of an antibiotic. This strip is placed in the agar and the zone of inhibition is noted to help calculate MIC. Miniunum inhibitory concentration.
  26. Fungi
    "Consists of both yeasts and molds. Grow best in warm
  27. Opportunistic Systemic Mycosis
    Fungal infections. Are primarily respiratory infections. Are treated with antifungals. Antifungals will interfer with our own cell wall permeability. makes it very dangerous for our cells.
  28. Amphotericin
    Used in extreme fungal infections. Has many serious side effects that supported drugs are given. Has many CNS side effects.
  29. Petechia
    Small blood vessel leaking under skin.
  30. Fungi reproduction
    Reproduce sexual and asexually. When spores are released from the fungi and will germinate and produce a hyphea. Fungus will be haploid. Now this haploid fungus can fuse with another fungus and becomes diploid. Makes a zygote to make a new mushroom.
  31. Topical antifungals
    Used on the surface. Not to be ingested to.
  32. Systemic antifungals
    To be ingested. Amphotericin. New grizefulvin use to be just topical now can be take orally.
  33. Thrush
    Oral yeast infection. Use to be treated with crystal violet. no longer done because of presence of benzene ring.
  34. Claviceps purpurea
    Causes Ergot of Rye (infection called: ergotism). Causes seeds to turn black. Produces a neurotoxin is a derviation to LCD.
  35. Ergotomine drug
    Used to treat migraines. Are also used to for inducing labor. Are vasoconstrictors. stimulating labor. or decreasing blood flow to brain.
  36. Amanita muscaria
    Fly agaric. Is possibly the reason behind Santa Claus. Has hallucingin effect. Eaten by reindeer.
  37. Endotoxins
    "(Lipid A). G- cell well
  38. Exotoxins
    Neurotoxins.. Are produced inside mostly gram-positive bacteria as part of their growth and metabolism. They are secreted or released following lysis into the surrounding medium. Mostly gram positive
  39. Types of exotoxins
    Neurotoxins. Cytotoxins. Enterotoxins
  40. Neurotoxins
    Botulinum/Tetanus toxin (Clostridium botulinum. C. tetani)
  41. cytotoxins
    Cornynebacterium diphterial. Dip. toxin
  42. Enterotoxins
    Vibrio cholera. Cholera toxins
  43. Botulinum toxin
    Comes from Clostridium botulinum and produce subterminal spores. Seven different forms of botulism. Botulinum toxin: effects neurons (motor nerves). The toxin blocks the release Acteylcholine (neurotransmitters) at the motor end plate. This inhibits the contraction of the muscle fiber by not releasing ACh. Can be picked up from food poisoning (home canning).
  44. Irreversible Flaccid Paralysis
    The side effect of botulinum toxin. Inhibits contraction of muslce by blocking release of ACh.
  45. Medical use of botulinum toxin
    Botox (Cosmetic use). Inject into models armpits to decrease sweating (Medical use)Can be used for correcting ocular alignment.
  46. Different types of Botulism
    Wound Botulism: Specific to IV drug users. Dirty needles contains spores. Produces gases (anaerobes). Avian Botulism: Bird eats the maggots from a dead animal that had maggets. The maggets BIOACCUMLATE the botulism. Then they die from the large amount of toxins
  47. Tetanus toxin
    Compete spastic paralysis. Will interfer with the production of glycine. Glycine induces relaxation and elongation of muscle fibers. Tetani: the complete contraction of all muscles. (lockjaw). Enters cell via endocytosis Caused by clostriudium tenani
  48. Bioaccumlation
    When smaller animals eat some toxins. Then a larger animal eats more of them. This animal builds up more toxin.
  49. Cholera toxins
    Caused by Vibrio cholera (common in soil and water. gram negative). Found in countries with poor water sanitation. In the lumen of the intestine adenylcyclase helps with maintaining NaCl in gut. Cholera toxin effects adenylcyclase and causes salts to move into the lumen. Water follows the salt in the gut. this causes DIARRHEA! DIARRHEA! MASSIVE EXPLOSIVE DIARRHEA! Likes to bind to shells on seafood.
  50. Alpha toxin
    Produced by S. aureus. Binds to cell membrane of cells. Changes cell configuration and changes selective permeability. Makes large pores.
  51. Cytolysins
    Destorys cell permeability
  52. Salomonella Typi
    Causes typhoid fever. Produces cytotoxins. Produces lesions in the small intestines.
  53. hyaluronidase
    Destroys the cell glue. Enzyme that destroys Hyaluronic acid. The destruction of the tissue. Norman Cousins: Wrote a book about the Anatomy of an Illness.
  54. Hemolysins
    Destorys red blood cells. Lyses cell. Alpha and Beta. Caused by streptococcus
  55. Leucocidin
    Attack white blood cells
  56. All the extracellular toxins
    1. Streptokinase 2. Collagenase 3. Coagulase 4. Hyluronidase 5. Leukocidin 6. Proteases 7. Lipases
  57. Diptheria
    Caused by Corynebacterium diptheria. Produces a cytotoxin. Colony arranged in dismay (overlying). Destroys the back of throat and you ingest more and more spread systematically. (gray leathery appearance in the back of throat). Very intense viruence. The toxin effects reducing compounds (NAD. EF-2. ADP-ribosyl-EF-2) that leads to the blocked protein synthesis.
  58. Collagenase
    Producesd by Streptococus pyogenes. Used to destroy collagen.
  59. Types of immunity
    Specific Resistance. Non-specific resistance
  60. Non-Specficic resistance
    Does not matter on bacteria. Are mechanisms (chemical and physical means) that the body elminates bacteria or virus. Examples tears. eyelashes. eyebrows. mouth (chew). amalyases. stoamch acid. physcial digestion. bile salts. sweats. skin. stratching/itching
  61. Types of Antibodies (specific immunity)
    Natural (active and passive). and Artificial (active and passive)
  62. Natural active immunity
    Getting sick from a pathogen and body creates antibodies.
  63. Natural passive immunity
    Mother gives you at birth. Mothers immunity given at birth (short lived). Made by your mother and given to you.
  64. Artificial active immunity
    When you get the flu shot and your body begins to make antibodies against it.
  65. Artificial pass immunity
    Antibodies are made in another host and then harvested and given to you.
  66. Interferons
    (Deals with Viral infection) Small molecular weight peptides used for disaster preparedness on a molecular level (cell signal). A cell after becoming an infected with a virus produces interferon (DNA->mRNA->interferon) and they are released extraceullarly. These interferons travel to neighboring cells. The neighboring cells will have interferon receptors and when the interferons bind and notifies cells that the viral infection is coming.
  67. Pathway after interferon binding
    1. Triggers cells to produce OLIGO A SYNTHETASE. This enzyme phosphorlates endoribonucleases. This nuclease will destroy viral RNA or interfere with the production of viral components. 2 Produces INACTIVE PROTEIN KINASE. Once phosphorylated (signaled by interferon) goes on to inactivate vrial protein synthesis factor. Phosphorylates initation factor on virus and stops working on the virus and viral reproduction stops.
  68. Zoonatic Transmission
    Is contact between a human and an animal. Can be direct or indirect transmission. Direct ex. dog bites you. Indirect. flea bites dog who is infected and then bites you (vector)
  69. Plague
    Caused by Yersinia pestis. Is a gram negative rod that is short (pleomorphic. takes on many shapes) capusle former and nonmotile. Has many virulent factors. It can cause programmed cell death. Apotosis. This bacteria will go in and stimulate apotosis. Is a zoonotic disease with the primary vector is a flea. Some of the virulent factors are turned on in the pressence of fleas. Virence factors are located on the plamid (Yop) make an injectisome to inject effectors into your cell to cause aptotosis
  70. Apoptosis
    Programed cell death. Some stress on cell. Anti-progam cell proteins (on mitochondria). Pro-PCD proteins will be in competion control when signaled. The Pro-PCD will grab the anti and pull them away from the mitochondria. This makes holes in the mitochondria and cytochrome C. is released interfering with energy production. Then the capases are released and cause DNA fragmentation.
  71. Bubonic Plague vs Pneumonic Plague
    Relates to the location of the diease. In the lymphnodes/lymphatic system becomes extreemly swollen (buboes). Becomes the Pneumonic Plague when it reaches your lungs and then can be spread by droplets. Can be treated with antibiotics if treated early (streptomyocin). (Treatment and leads to endo toxic shock from lipid A release).
  72. Progession of plague
    Takes about (1-3) bubonic. Lymphnodes become extremely swollen. Then by day 5 you have flu like symptoms. Can change the permeability of cells and causes blood to leak (buboes).
  73. Cycles of Plague
    Sylvatic cycle (in wild animals) Urban cycle (domesticated animals)
  74. Mechanism of Plague
    Is injected by a vector. Must stay in your for an ample amount of time to grow. With cause apoptosis of white blood cells. Additionally it can produce a clot degrading enzyme to inhibit clot formation and becoming trapped.
  75. Virulent factors of Yersinia pestis
    Pesticin I (kills completing bacteria). Coagulase. Fibrinolysin. Simultaneous clot formation and clot break down. LPS. Capsule
  76. Treatment of Plague
    Yersinia pestis is killed by Streptomyocin. Do not use a Beta lactam becasue its gram negative adn will additionally release more lipid A. 90% death rate without treatment.Early treatment is best
  77. Hantaviruses
    Bunyvariridae RNA virus. Normally comes excrement of mice rodents (inhalation). Deer mouse around here carries it. Kills within 24 hours of illness leads to a rapid pneumonia leads to drowning in own fluid. Can be killed by lysol.
  78. Bacillus anthracis
    Causes anthrax. Non-hemolyitc. Produces a capsule. Non-motile. Gel hydrolysis -. Catalse +. Also known as woolsorters dieases. Different types of anthrax: cutaneous. systemic. and gastrointestinal. Leaves necrotic lesions on skin. Usually inhale spores (heavy spores). Vaccine for anthrax. Virulent factors: edema toxn. lethal toxins. capsular polypeptides.
  79. Streptokinases
    Dissolve clots and tissue
  80. Rabies
    Spread by bit of rabbid animal by saliva of animal. Primary effect is in the CNS. Bullet shaped virus. Moves retrograde axonal transport. Will replicate in the site near the bite. Then moves to the peripheral neurvous system. Will move from muscle to and bind to the motor end plate and move in though an endosome. Incubation 5 days to 2 years. Effects cholenesterase. Is a vaccine against it.
  81. Foot and mouth disease
    Old term (Hoof and mouth) Piconovisus (aphthovirus). Zoonotic disease. Skin begins to become necrotic and fall off. Causes lesions. Is a bioterist agent by targeting animals. Oral fecal disease
  82. Hand foot and mouth
    Is due to the coxsackie virus is short lasting conditions most often affecting young children during the summer monthss.
  83. Ringworm
    Is a zoonotic disease. is a fungus
Card Set
Micro Final - Sheet1.csv
Microfinal covering zoonotic diseases, fungi, STD's, antibiotics, exoenzymes
Show Answers