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Lectures 28-31 MMG 301

SomeCreativeName MMG 301 English 61 cards

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  1. 1Two major groups of animals based on gut anatomyForegut Fermenters - carnivorous animals / complex stomachs
    Hindgut Fermenters - herbivores and single chamber stomachs
  2. 2RumenContains an anaerobic microbial community that breaks down plant fibers
  3. 34 Steps to food digestion in ruminants1. Food enters rumen & begins digestion
    2. Mixture goes to omasum & is concentrated by water adsorption
    3. Mixture goes to abomasum (true stomach) - acid kills and digests food & mictobes
    4. Food + Microbes go to small intestine
  4. 4Volatile Fatty AcidsProduced in rumen - provide 70% of a ruminants energy supply
  5. 5dysbiosisSudden dietary changes that produce significant changes in the makeup of a microbial community
  6. 6acidosisA buildup of acid that damages the rumen and acidifys blood
  7. 7Human Microbiome/Human Microbiome Project1. All the microbes on the site of the body, outnumber human cells 10:1
    2. An ongoing study to document microbe populations, diversity and changes at anatomical sites using 16S rRNA gene sequencing
  8. 8Changes as food goes though the upper&lower gastrointestinal tractspH - low in stomach, increases to neutral through the tracts
    Oxygen - decreases through the tracts
  9. 9Positive effects of intestinal microbesVitamin Synth.,Glycosidase activity, Steroid Metabolism, Stimulation of immune system, antagonism of pathogens
  10. 10Transmission of Symbionts 1. Horizontal 2. Vertical1. Symbiont comes from environment
    2. (aka heritable) Symbiotic is passed down from parent
  11. 11BacterioicytesInsect host cells for heritable symbionts- i.e. Buchnera bacteria w/ Pea Aphids
  12. 12Termite source of energyIn the hindgut there are symbiots that digest wood fibers, providing nutrients
  13. 13Hawaiian Bobtail SquidLight emitting bacteria in a specialized light organ that emit light in response to quorum sensing
  14. 14Rifta Tubeendosymbiotic chemolithotropic bacteria in a sponge-like tissue known as a trophosome
  15. 15Colonization ( and location)-The growth of microbes found at any anatomical site
    -Commonly occurs on the mucus membrane, outer layer of epithelial cells that are on the surface of many tissues
  16. 16Skin CommunitiesContaining sebaceous glands (hair growth gland)
    -skin communities have many examples of bacterial interference - preventing pathogens from colonizing/growing
  17. 17Anti-Bacterial Enzymes in mouth (2)Lactoperoxidase - Makes a ROS that kills bacteria
    Lysozyme- enzyme that cleaves peptidoglycan
  18. 18Oral Microbal Communities-many pollysaccaride-producing bacterial colonies that form a biofilm on the tooth surface & in the gingival crevice
  19. 19Steps of biofilm formation in dental diseases1. layer of glycoprotein on clean tooth
    2. Colonization of bacteria that form a biofilm
    3. Continued growth results in a thicker layer = plaque
    4. Plaque calcifys, becomes tartar
    +Facilitated by surcorse that is used to synth. dextran
  20. 20Dental Caries Gingivitis1. anaerobic microbes in an oral biofilm ferment diatary sugars& acids = demineralize tooth enamel
    2. Gingivitis - infection of gingival crevice
  21. 21Heliobacter pylori- often colonized stomach & is associated w/ 80% of stomach ulcers
    - not an acidophile (urea/blood->Heliobacter->NH4+(alkaline))
  22. 22Upper Respiratory Tract-normal microfloura antagonize pathogens from growing
    -in some, pathogenic bacteria are present but do not cause symptons -> hosts are carriers
  23. 23Lower Respiratory TractSterile in healthy individuals
  24. 24Urogenital Tract-bladder is sterile
    - in the vagina bacteria like Lactobacillus acidophilus ferment glycogen & produce acid, preventing bacteria growth
  25. 25PathogenicityThe ability of a microorganism to cause disease
  26. 26Oppertunistic PathogenCan cause disease in an already weakened host
  27. 27Invasion & InfectionInvasion is the entry of a pathogen through epithelium layers, and an infection is growth of a pathogen at an anatomical site
  28. 28ID50 & LD50ID50 is the amount needed of a pathogen to infect 50% of hosts, LD50 is the amount of a pathogen that kills 50% of hosts
  29. 29Adherence-Aided by adherence factors
    -is usually specific - tissue trophism
  30. 30Adherence FactorsGlycocalyx - polymers that aid in biofilm formation (often are slime layers of capsules)
    Adherence proteins- found on fimbrae and pili
  31. 31Bacteremia-Bacteria in blood, allows for easy transport to other tissues and organs. Sometimes leads to sepsis in the event of bacteria in the blood or lymph system
  32. 32Virulence factor- A pathogen-produced substance (protein,enzyme,adherence factor, or toxin) that promotes the establishment & pathogenisis of a disease
  33. 33Examples of Virulence FactorsHyaluronidase - breaks down polymer that holds cells together
    Collagenase - breaks down collagen in connecitve tissue
    Streptokinase - destorys fibrins of blood clots
    Coagulase - creates a fibrin later around the cell that prevents the immune system from detecting the bacteria
  34. 34ExotoxinProteins that are excreted by bacteria and are toxic to host cells
    -If they affect the small intestine they are known as enterotoxins
  35. 35Types of Exotoxins1. Cytotoxins - damage to cell membrance causing host cell lysis and death
    2. AB toxins - two subunits; B binds to the surface and A acts as an enzyme to produce host cell damage
    3. Superantigens - cause a hyper-stimulated immune response resulting in excessive inflamation and tissue tamage
  36. 36hemolysins- cytolytic exotozins that can lyse red blood cells
    -some are phospholipases (break down phospholipids)
    - others can cause holes in host cell membranes (i.e. Staphylococcas a-toxin)
  37. 37Diptheria toxin1 toxin mollecule kills one host cell
    produced by Corynebacterium Diphtheriae (a URT bacteria)
    -is an AB toxin, B binds to host cell receptors, A is an enzyme that blocks tRNA from entering the ribosome
  38. 38Tetanus & Botulism (AB toxins)-similar toxins that elicit opposite effects
    -block neurotransmitter release from nerve cells that signal muscles
    -produced by the spore-forming anaerobe Clostridium
  39. 39Botulism Toxin7 types, Type A has medical use (Botox)
    -Results in flaccid paralysis by blocking the release of Acetylcholine which is responsible for muscle contraction
  40. 40Tetanus toxinResults in spastic paralysis, prevention of an inhibitory interneuron from preventing acetylcholine release
  41. 41Cholera - Vibrio cholerae-Colonizes small intestinal wall and produces cholera toxin
    - AB toxin, A acts as an enzyme to stimulate formation of cAMP
    -increased cAMP alters regulation of ion movment across the epithelium, and osmosis results in large fluid loss (diarrhea)
  42. 42Effects of endotoxins on humans and animals- Fever - host stimulates to release more endogenous pyrogens which regulate temp
    -Diarrhea
    -Inflamaition
    -Generally less toxic than exotoxins
    From G- Bacteria lypopollysaccarides
  43. 43Assay for endotoxins-Limulus amoebocyte assay (LAL) - generates color, uses the cells of Limulus as they are extremely sensitive to endotoxins and lyse easily
  44. 44Innate Resistance-Physical Barriers ( cilla in nasopharynx, mucus in trachea, etc.)
    -Chemical Barriers (pH of stomach, etc.)
    -Normal microfloura (compete with pathogens for colonization & can prevent growth)
  45. 45Risk Factors for Infections-Age, stress, and overall health
    - a compromised host is one that is weakened by - Injury, Illness from another pathogens, or being immunocompromised
  46. 46Innate ImmunityA preexisting ability to recognize and destroy pathogens/toxins
    -carried out by cells known as phagocytes (Specialized blood cells that engulf and kill pathogens)
  47. 47Adaptive ImmunityRelies on previous exposure to a pathogen
    3 Main functions
    -Recognise a pathogen and their toxins
    -Discriminate for pathogens vs normal cells
    -Eliminate pathogen/toxin
  48. 48AntigenAny molecule or portion of a molecule that stimulates a response in immune system; i.e. proteins and pollysaccarides
  49. 49Phagocyte-Specialized blood cells that engulf and kill pathogens
  50. 50Macrophage-1st line of defence
    -Recognize pathogen-associated molecular patterns - structures found on common pathogens
    -Recognition occurs via pattern recognition receptors on phagocyte
    -after contact with PAMP, pathogen is destroyed and and pieces of the pathogen are presented on the cells surface
  51. 51Two Parts of Adaptive Immunity1.Antibody-Mediated
    2.Cell-Mediated
  52. 52T-CellsT-Cell receptors recognize a specific antigen produced by a phagocyte after pathogen destruction
    -called the Major histocompatibility complex
  53. 53T-Cell SubtypesTc cytotoxic cells - kill host cells infected with virus
    Th Helper cells (2 types)
    -T1H - release cytokines to induce inflammation
    T2H - stimulate antigen-reactive B cells to proliferate and produce antibodies
  54. 54B cellsAntibody Production via. B Cells
    1. Antigen-recognizing B cells ingest and degrate antigen
    2. Antigen is presented to a T2H cell
    3. If the T2H cell recognized the antigen the B cell is stimulated to produce antibodies
    -Some serve as receptors on B cell surface, some are released to target pathogen for destruction (produced by plasma cells)
    -Some differentiate into memory B cells for long term protection
  55. 55Antibodies (immunoglobulins)- 5 major classes based on physical and immunological properties - IgG, IgA, IgM, IgD, IgE
    -IgG composed of
    -2 light chains & two heavy chains (Y shape)
  56. 56epitopes/antigenic determinantsThe small region of a molecule recognized by T-cells and antibodies
  57. 57Superantigenbacterial exotoxins that interact indirectly w/ hoest T helper cells and antigen presenting cells,
    -bing outside the MHC t-Cell receptor binding site
    -result in the activation of a large number of T-cells and production of cytokines, producing excessive inflammation and tissue damage
  58. 58Natural Active ImmunityAfter an infection, immunity to a pathogen develops
  59. 59Artificial Passive ImmunityNo immune system response involved - individual receives antibodies
    -i.e. injection of antiserum (antibodies vs. a specific pathogen or toxin) for someone recently exposed to a toxin (i.e. snake bite)
  60. 60Artificial Active Immunity-uses vaccination to produce response that provides immunity
    - in some cases boosters are provided for longer immunity
  61. 61Vaccine Types1. Toxoid - exotoxin that has been chemically inactivated but is still antigenic
    2. Inactivated Pathogen - pathogens are killed w/ reaction of a chemical compound or heat
    3. Live attenuated pathogen - a mutated version of the pathogen is used ( can't cause disease but will still allow the immune system to produce immunity)

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