MCDB 132 1

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jaimevoong
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131688
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MCDB 132 1
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2012-02-03 13:18:00
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Bact path Winter 12
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Pre midterm 1
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  1. Lists 3 types of toxins
    • 1. AB toxins
    • 2. Membrane disrupting toxins
    • 3. Super Antigens
  2. Examples of AB toxins
    • Diphtheria
    • Botulism
    • Tetanus
  3. Example of Membrane disrupting toxins
    • Clostridium Perfringens
    • Gas gang green
    • food poision via CPE
  4. Example of Super Antigen
    staphlococcus Aureus ( TSS)

    Streptococcus Pyogenes ( Tss Like ) MORE DEADLY
  5. Food borne Botulism Pathogenesis
    • spres found in soil, get into food, bacteria grows
    • bacteria releases BoNT into the blood stream
    • BoNT targets the peripheral neurons ( NOT CNS)
    • Effect: Flaccid Paralysis
  6. Symptoms of Food borne Botulism
    • Similar to alcohol consumption
    • - slurred speech
    • -double vision
    • -vomiting
    • - Respiratory/ heart failure
    • ( symptoms start happening 4-6 hrs after ingestion)
  7. Botulism Overview
    • BoNT by the Gram + bacteria Clostridium Botulinium
    • - can be food borne
    • - colonization
    • a. wound botulisim
    • b. baby botulism
  8. Clostridium Botulinium
    • The bacteria that causes botulism
    • - gram +
    • - motile
    • - anerobic
    • - baccilli : rod shaped
    • - spore forming
    • - Creates an AB type exotoxin
  9. Baby Botulism Pathogensis
    • spores found in bee honey
    • when spores are ingested
    • the bacteria actually colonizes the GI tract due to low stomach acid and low natural microflora
    • BoNT is produced
    • BoNT gets into the Blood stream
    • Targets Peripheral Neurons ( NOT CNS)
    • = Flaccid Paralysis
    • same symptoms as Food borne botulism
  10. Wound Botulism Pathogenesis
    • Spores are found in the mud / dirt
    • happens during war time when soldiers are covered in mud and hurt
    • the spores get into the wound
    • since it is a wound o2 is usualy limited and runs out quickly creating an anerobic environment
    • bacteria colonizes
    • produces BoNT, it enters into the BS
    • ! same symptoms as Food borne and Baby botulism
  11. Treatment for Botulism
    • Put person on a ventilator ( due to respiratory failure)
    • Give antibiotics to prevent FURTHER damage done by the neurotoxin
  12. Tetanus Overview
    • Type B is an AB exotoxin like botulism
    • From bacteria Clostridium Tetani
    • C. Tetani produces TeNT

    • Type A is a Membrane Disrupting Toxin
    • From bacteria Clostridium Perfringens
    • C. Perfringens produces CPE ( C. Per. Enterotoxin)
  13. Clostridium Tetani
    • Gram +
    • Anerobe
    • Motile
    • Baccilli ( rods)
    • Causes Tetanus
    • Spastic Paralysis
    • TeNT: Blocks Gamma Butyric Acid ( an NT inhibitor)
  14. Enterotoxin
    An exotoxin that acts specifically on the Intestinal Mucus
  15. Pathogenesis of C. Perfringens type b
    Gas Gang green
  16. Pathogenesis of C. Perfringens Type A
    • ex. St Patty's Meat
    • Membrane disrupting toxin
    • spores get into food
    • food cools and spores germinate
    • Bugs get ingested, colonize GI tract
    • Make toxin CPE
    • 8-16 hrs after ingestion
    • Symptoms:
    • Intestingal discomfort ( gas)
    • Diarrhea
    • Cramping
  17. TSS overview
    • Toxic Shock Syndrom
    • ex Tampons
    • Super Antigen
    • caused by : Staphylococcus Aureus (toxin TSST 1) ,
    • Staph is : Aerobic, non-motile, coccus
  18. TSS-Like Overview
    • effects men and women
    • caused by Streptococcus pyogenes
    • aerobic, non motile, coccus
    • *Bugs actually live in BLOOD = more deadly 30% death rate
  19. Mechanism of Super Antigen
    • *Non specific T cell stimulation
    • SA binds directly on MHC II which then binds to a T cell receptor
    • This is an efficient binding, and will stimulate 1/5 T cells ( vs 1/ 1000)
    • *NO antigen recognition
    • T cells now release high levels if IL 2 --> cytokine storm
    • SHOCK
  20. Bacteriocidal Antibiotic
    Kills bacteria
  21. Bacteriostatic
    • Slows down bacteria
    • helps immune system combat the slowed down bacteria
  22. Targets of Antibodies
    • Cell wall
    • Protein Synthesis
    • DNA/ RNA replicaiton
    • Essential Co factors
  23. Antibody Target : Cell wall
    • *Humans don't have cell wall
    • ex. Penicillin : disrupts cell wall of a broad spectrum of bacteria ( gram +/-)
    • ex.vancomycin : inhibits cell wall synthesis in gram + ( can't get pass membrane of Gram -
  24. Antibody target : Protein Synthesis
    • *bacterial protein synthesis is different from outs, not the same enzymes
    • ex. Tetracycline :Binds to bacteria Ribosomes and prevent Translation = no proteins
    • also : Kanamycin, Azithromycin
  25. Antibody Target : DNA/ RNA Replication
    • ex Ciprofluxacin: treats anthrax , inhibits Gyrase in DNA replication
    • good for INTRAcellular pathogens
  26. Antibody Target: Essential Co-Factors
    • essential co factor : Folate
    • ex. Trimethoprim, Sulfamethoxale : inhibit steps in folate production of bacteria.
  27. Types of Antibiotic Resistance
    • Mutations
    • Enzymatic inactivation of drugs
    • Efflux
    • Modification of Drugs' Target
  28. Tetracycline
    • Binds to Bacterial Ribosomes
    • Stops translations
    • No protein synthesis
  29. Azithromyocin
    • Binds to bact Ribosomes
    • Stops transltions
    • No protein synthesis
  30. Kanamycin
    • Binds to Bact Ribosome
    • No translation
    • No protein
  31. Cirpofluxacin
    • Stops Gyrase
    • DNA/ RNA replication
    • Good for intracellular pathogens (endogenous antigen)
  32. Trimethoprim
    Disrupts Folate production
  33. Sulfamethoxale
    Disrupts Folate production in Bacter
  34. Vancomycin
    • Good for Gram positive Bacteria
    • A Cell wall synthesis
  35. Antibiotic resistance : Mutations
    • Gram - : get mutations in outer membrane so that drugs can NOT get in
    • -ex. mutations in the porforins, it would limit the drugs ability to get it
  36. Antibiotic Resistance : Enzymatic Inactivaton of Drugs
    • Bacteria produces enzymes that degrade/ inactivate the drugs
    • ex. Penicillin resistant bugs create Beta - Lactamase which cleaves the Beta -lactam part of penicillin = inactive

    ex. Kanamycin res. bugs enzymatically modifies periplasm so that it decreases drug transport
  37. Antibiotic Resistance: Efflux
    Drug functions properly, finds but, binds to target, gets inside the bug , but the bug just pumps out the toxins.
  38. Antibiotic Resistance: Modification of the target
    Bacteria modifies itself so that the drugs can NOT bind
  39. How to deal with Antibiotic Resistance
    • ex. Penicilllin res. Bact make Beta- lactamase, and so we will give penicillin + a Beta lactamase inhibitor ( complex called augmentin)
    • Clavulonic acid = beta lactamase inhibitor
  40. Diptheria Overview
    • caused corynebacterium diphtheriae
    • "the strangler"
    • Highly fatal
    • Killed George Washington
    • Iditarod Sled Dog Race
    • Serum sickness
    • Humans are the only reservoire
    • 1 molecule of toxin kils 1 cell
  41. Corynebacterium Diphtheriae
    • Bacteria that causes Diphtheria
    • Gram +
    • Facultative anerobe
    • non motile
    • Club shaped
  42. Pathogenesis of Diphtheria
    • aerosoles are inhaled from an infected person
    • bacterial colonization of the throat
    • Throat becomes necrotic
    • Toxin is AB toxin; DT toxin enhances colonization
    • Fibrin network begins in leak plasma membrane
    • Adherant membrane
  43. Symptoms of Diphtheria
    • Difficulty Breathing and swallowing
    • bacteria stays in throat
    • Heart failure due to toxin getting into the blood and targeting the peripheral nerves
  44. Diphtheria Toxin ( details)
    • AB toxin
    • A: Works by inactivating EF-II and stops translation/ cant make proteins by ADP RibosylationB: Targets the HB-EGF receptor (Heprin binding -epidermal growth factor) on MANY cells like Heart, Respiratory, + many organs
  45. ADP ribosylation: ( of host cells) transfers ADP ribose from NAD to EF II
    rxn: NAD + EF II ----> Nicatinamid + EF II-ADP riboxyl
  46. DT Vaccine
    • Now made with a Toxoid
    • - no toxin, just illicits an immune response
    • -Active part ( A) is inactivated with Formaldehyde DT-AB
    • Illicits an IgG Ab response, if you have this Ab then you will be protected from toxin
  47. Serum Sickness
    • Causes by the Anti-toxin made with Horse antibodies
    • -people were fine if given the toxin once
    • -but when given twice the horse proteins would complex with our antibodies which would cause an even more severe response by immune
  48. DTaP Vaccine
    • Diphtheria , Tetanus, P
    • Diphtheria: Corynebacterium diphtheriae
    • Tetanus: Clostridium tetani , Clostridium perfringens
    • P: whooping cough by bortatella Pertussis
  49. Tdap booster
    • More tetanus than diphtheria/ whooping
    • high school aged children in the US
  50. Efficacy of Vaccine
    • there is no 100% efficacy
    • some people might not develope Ab to the toxin, but are still protected via
    • Herd Immunity: for non-responders who don't have Ab and are safe because the responders are vaccinated and so there is noone to pass it to the non responders.
  51. AB Toxoid Carrier Vaccines
    • use Toxoid of Diphtheria and to illicit immune reaction to toxins that don't illicit immune response
    • ex. HIB vaccine against the haemophilous influenza type B
    • Haemophilous influenza causes Infant Menegitis
    • --> by Covalently linking the CHO capsule to the Diphtheria Toxoid to illicit ( MHC II and T cell response)
  52. Haemophilous Influenza type B
    • Gram NEGATIVE -, Rod, Capsular Bacteria
    • Respiratory Pathogen ( of the upper respiratory tract)
    • Causes infant menegitis
    • Pneumonia ( thats why they thought it was an influenza)
    • Highly lethal due to infants Tcell Independent

    Today:Covalently link the Diphtheria toxoid to the Haemophilous Influenza Capsule = immune system process it like a protein with ( MHC II and T cells reponse)
  53. Immuno Toxin
    Use the DT-A ( activity fragment without the toxic B fragment attach to the B fragment of the cell you want to target. Ie B frag specific for a cancer cell.

    "Magic Bullets"

    Kill Cancer cells/ Virually infected cells / w.e. certain cell type you want to kill
  54. Yersinia ( 2 types)
    • Yersinia Entercolitia : Plague like
    • Yersinia Pestis: Plague
  55. Yersinia Entercolitica
    • Gram -, rod shaped
    • Motile at 25 degree Cel, non motile at 37 degree Cel
    • YST : yersinia, heat-Stable enteroToxin
    • Plague- Like bacteria but only causes Food Poisoning = Gastroenteritis

    • Pathogenesis: Food/ water, ingested, replicates in the mesenteric lymph ( drains into the intestines)
    • Found in food/ water sources
    • Symptoms: Abdominal pain ( inflammation)

    Seems like inflammed appendix
  56. Yersinia Pestis
    • Gram NEGATIVE (-)
    • Rod shaped
    • Facultative anerobe
    • Capsular bug
    • Likes to live with RODENTS
    • Causes: Bubonic Plague, Septicimia Plague, Pneumonic Plague, Black Death
    • Principally and extracellular Pathogen
    • Virulent Plasmids : pPla, pFra + 1 non virulent pYV
  57. Stages of bubonic Plague
    • 1. bubonic Plague
    • 2. Septicimia Plague
    • 3.Pneumonic Plague
    • 4. Black death
  58. Stage 1 : bubonic plague
    • Flea bites/ direct contact with an infected rodent
    • Pathogen proliferate/ clump in the flea gut
    • Clump starves the flea, and needs to Regurgitate to feed again = ravenous fleas
    • Bites you and injects the Bacteria into your BLOOD stream, Get into your LYMPH nodes
    • Lymph nodes become, HOTswollenHemmorrhatic = Black Bubos ( swellings)
    • * swelling in the groin is very common
  59. Stage 2: Septicimia
    • Bacteria is in the Lymph nodes and now enters the Blood stream
    • Liver, spleen, lungs ( septic)
    • when in lungs , you get pnumonia and can start to exhale infectious aerosoles
  60. Stage 3: Pneumonic plague
    • after it infects your blood and gets into your lungs, the bacteria changes
    • it can now be exhaled and transfered to other humans ( Human - human aerosole transmission)
  61. Stage 4: Black Death
    • via bubonic, septicimia, or pneumonic plague
    • VERY Black Extremities
    • Hemmoratic changes in the skin ( via DIC .. causes lots of clotting and necrotic tissue proliferate and get black fingers toes etc)
    • Septic Shock
  62. Pestis Virulence Factors
    • Main two are on Plasmids
    • pPla : encodes plaminogen activator protease ( pla protease) = disrupts blood coagulation ( so that the bug can build its house and move around.
    • Enzyme works best at ~ 37 Deg Cel ( warmer like places near equator)
    • Degrades C3B and C5A, allows it to live in the BLOOD

    pFra : (fraction 1 capsule) = Antiphaocytic, phospholipase D ( promotes flea colonization)

    * two plasmids only found on yersinia pestis not yersinia entercolitica
  63. pYV
    • found in ALL Yersinia
    • pYV ( yersinia virulence)
    • pYV encodes a TYSS -3 : TYpe 3 Secretion System
    • TYSS 3 is a molecular syringe that will secrete toxin upon CONTACT
    • Toxin: YOPS ( inhibit phagocytosis, and causes macrophage apoptosis)
  64. pPla
    • from yersinia pestis
    • on a Plasmid, is a Protease
    • Cleaves blood Clots + Disrupts complement activation ( via degrades C3A and C5A)
  65. pFra ( plasmid fraction 1)
    • From Yersinia Pestis ( Black death/ plague)
    • Phospholipase D : Promotes Flea colonization
    • Anti-Phagocytic
  66. Diphtheria overview
    • Caused by corynebacterium diphtherae
    • Respiratory infection
    • Adherant pseudo-membrane
    • ADP- ribosylation of EF II( stops protein synthesis disrupt Translation)
    • Binds to HH-EGF receptor
    • AB toxin
    • Serum Sickness
    • George washington, Iditarod

    • Symptoms:
    • Swollen neck/ Bull neck
    • Hard time swallowing ( due to adherent pseudo mem)
  67. Corynebacterium diphtherae
    • Gram +
    • Aeresol infection --> bugs colonize throat
    • Facultative Anerobic ( likes aerobic)
    • causes Diphteria " strangler "

    • IMMUNOTOXIN:A portion often used to induce Immune response for other disease/ infections in cancer cells
    • Toxoid Carrier Vaccines
    • linke
    • ex. for Haemophilous infuenzae Type B: CHO bug, can't make Ab, Need the immune response of Diphteria, HIB vaccine does this, so that our body processes the CHO like a protein
  68. Classical Pathway
    • 1. Anti-bodies have already seen that pathogen ( IgG)
    • 2. Ab (Fv portion) binds to the Antigen on the Bug surface
    • 3. C1 binds to the Ab and cleaves C2 and C4
    • C2-C4 --> makes C3 convertase
  69. Alternative Pathway
    • Complement component C3B* Binds directly to the Bacterial Surface
    • C3B + BP ( blood protein) --> C5 Convertase
  70. MBL
    • Surgar binding Leptin ( mannose) binds to mannose on Bacterial surface
    • C1 binds to Leptin, C2 C4 --> C3 convertase
  71. Stopping Comlement
    • Protein factor H binds to C3B stopping C3B function because it is A KEY player
    • Then Protein Factor I Destroys C3B
  72. MAC
    • Membrane Attack complex
    • of C5B +C6-C9
    • Binds to the membranes of Gram - and KILLS them
    • ****however this is NOT the main function of Complement

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