Micro 16

  1. immunocompromised
    refers to individuals that have weaknesses or defects in innate or adaptive defenses that leave them vulnerable to infection
  2. symbiosis
    means living together
  3. Types of relationships bwtn microorganism and human host
    • Mutualism 
    • Commensalism
    • Parasitism
  4. Mutualism
    • An association in which both partners benefit
    • Ex: In large intestine, some bacteria synthesize vit K and certain B vit.
    • Nutrients made available for host, and bacteria residing are supplied with warth & variety of different energy sources
  5. Commensalism
    • association in which one partner benefits but the other remains unharmed
    • Ex: microbes living on skin are neither harmful nor helpful to human host, but they obtain food and other necessities from host
  6. Parasitism
    • association in which one organism, the parasite, benefits at the expense of the other
    • All pathogens are parasites
  7. What bacteria is in nose
    Staph & corn

    • Staphylococcus
    • Corynebacterium
  8. What bacteria in throat
    • *My Hell Nelly, More strep & corn?
    • Streptococcus
    • Moraxella
    • Corynebacterium
    • Haemophilus
    • Neisseria
    • Mycoplasm
  9. Bacteria in mouth
    • *Strep from Vanilla Licorice anyone?
    • Strep
    • Fusobacterium
    • Actinomyces
    • Leptotrichia
    • Veillonella
  10. Bacteria in Urethra
    • *Bitch, my Strep's everywhere
    • Streptococcus
    • Mycobacterium
    • Escherichia
    • Bacteroides
  11. Bacteria in vagina
    • *Because you are lacking sex
    • Lactobacillus
  12. hygiene hypothesis
    proposes that insufficient exposure to microbes can lead to allergies
  13. colonization
    refers to a microbe establishing itself and multiplying on a body surface
  14. subclinical
    • refers to infection
    • meaning that symptoms either do not appear or are mild enough to go unnoticed
  15. infectious disease
    an infection that results in disease - a noticeable impairment of body function
  16. primary vs secondary infection
    • primary is the initial infection
    • If an additional infection occurs as a result of the primary, referred to as secondary
  17. primary pathogen
    • or simply a pathogen
    • A microbe or virus that causes disease in otherwise healthy individuals
    • Ex: plague, malaria, measles, flu, tetanus, TB
  18. Opportunistic pathogen
    • or opportunist
    • causes disease only when body's innate or adaptive defenses are compromised, or when introduced into an unusual location
    • can be members of normal microbiota or common in environment
  19. virulence
    • refers to degree of pathogenicity of an organism
    • An organism described as highly virulent is more likely to cause disease, particularly severe disease, than might otherwise be expected
  20. Virulence factors
    • traits of microorganism that specifically allow it to cause disease
    • genes encoding these traits can sometimes be transferred horizontally
  21. communicable diseases
    • also called contagious
    • infectious diseases that spread from one hose to another
    • some are transmitted easily, like cold and measles
  22. infectious dose
    the number of microbes necessary to establish an infection
  23. ID50
    • an experimentally derived figure that indicates the number of microbial cells administered that resulted in disease in 50% of the population
    • Generally the infectious dose is expressed as this
  24. incubation period
    • time btwn introduction of microbe to susceptible host and onset of illness
    • varies considerably, from only a few days to several weeks
  25. illness
    • follows incubation - duh
    • person will experience s/s
    • in some cases onset it heralded by prodromal phase
  26. prodromal phase
    the early, vague symptoms such as malaise and headache
  27. convalescence
    • occurs after the illness subsides
    • stage of recuperation and recovery from disease
  28. carriers
    those individuals that harbor an infectious agent for months or years and continue to spread hte pathogen, even though they show no s/s
  29. Acute infection
    • characterized by symptoms that develop quickly but last only short time
    • Ex: strep throat
  30. Chronic infections
    • develop slowly and last for months or years
    • Ex: TB
  31. Latent infections
    • never completely eliminated
    • Microbe continues to exist in host tissues, often within host cells, w/o causing s/s
    • If decrease in immunity, latent infection may be reactivated and become symptomatic
  32. localized infection
    • the microbe is limited to small area
    • Ex: boil
  33. systemic infection
    infectious agent is disseminated (spread) thoughout body
  34. bacteremia
    • bacteria circulating in bloodstream
    • does not necessarily imply disease state, person can become transiently bacteremic after vigorous tooth brushing
    • *recall "-emia" means "in the blood"
  35. Toxemia
    indicates toxins are cirulating in bloodstream
  36. viremia
    viral particles are circulating in bloodstream
  37. Koch's postulates
    • criteria that Koch used to establish Bacillus anthracis causes anthrax
    • Provide a foundation for establishing that a given microbe causes a specific infectious disease:
    • 1. microbe must be present in every case of disease
    • 2. microbe must be grown in pure culture from disease hosts
    • 3. same disease must be produced when pure culture of microbe is introduced into susceptible hosts
    • 4. Microbe must be recovered from experimentally infected hosts
  38. Molecular Koch's postulates
    • Rely on molecular techniques to study microbe's virulence factors
    • 1. virulence factor gene or it's product should be found in pathogenic strains of organism
    • 2. Mutating the virulence gene to disrupt its function should reduce the virulence of pathogen
    • 3. Reversion of mutated virulence gene or replacement with wild type version should restore virulence to strain
  39. Mechanisms of pathogens
    • Production of toxins that are then ingested - foodborne intoxication
    • Colonization of mucous membranes of the host, followed by toxin production - adheres to mucous membranes & multiplies
    • Invasion of host tissues - penetrate first line defenses & then multiplies
    • Invasion of host tissues, followed by toxin production -
  40. balanced pathogenicity
    the pathogen becomes less virulent while the host becomes less susceptible
  41. Establishing infection
    • To cause disease, most pathogens must first adhere to body surface and then multipy:
    • Adherence
    • Colonization
  42. Adhesins
    • what bacteria use to attach to host cells
    • often located at tips of pili
    • can also be component of other surface structures such as capsules or various cell wall structures
    • attaches to receptors
  43. siderophores
    • iron-binding molecules produced by some pathogens
    • defense against body's defense of limiting iron to limit growth of microbes
  44. IgA proteases
    enzymes that cleave IgA

    Along with rapid turnover of pili, and antigenic variation, these are mechanisms pathogens have evolved to avoid secretory IgA antibodies on mucosal surfaces
  45. type III secretion system
    • also called injectisome
    • Way to deliver effector proteins to host cell
    • syringe like structure that injects proteins into eukaryotic cells
    • injected proteins, referred to as effector proteins, induce changes such as altering cells cytoskeleton structure
    • Other types direct host cell to engulf bacterial cell
  46. 2 mechanisms used for invasion of mucous membranes
    • Directed uptake by cells
    • Exploiting antigen-sampling processes
  47. Directed uptake by cells
    • Some pathogens induce non-phagocytic cells to engulf them
    • Pathogen first attaches to cell, then triggers endocytosis
  48. membrane ruffling
    • characteristic membrane ruffling on cells surface
    • Used by pathogens to induce endocytosis from non-phagocytic cells
    • ruffles enclose the bacterial cells, bringing them into the intestinal cell
  49. Exploiting antigen-sampling process
    • Recall MALT (mucosa-associated lymphoid tissue) samples material from mucosal surface. Some pathogens hitch a ride
    • Pathogens use M cells to cross intestinal barrier
  50. Ways to avoid host defenses
    • Hiding within host cell
    • Avoiding killing by complement system proteins
    • Avoiding destruction by phagocytes
  51. What effects to MACs have on gram neg & gram pos
    Gram neg are susceptible as outer membrane serves as target

    MACs have little effect on gram pos
  52. serum resistant
    refers to bacteria that use mechanisms to avoid killing by complement proteins
  53. How do some pathogens prevent encounters with phagocytes & avoid destruction
    • They avoid macrophages and neutrophils altogether:
    • C5a peptidase - enzyme degrades complement system C5a, which is a chemoattractant that recruits phagocytic cells
    • Membrane-damaging toxins - these kill phagocytes and other cells, often forming pores in their membranes
  54. How do some pathogens avoid recognition and attachment
    • Capsules - have ability to interfere with opsonization
    • Some also bind host's complement regulatory proteins
    • M protein - for strep pyogenes, this component in cell wall binds with complement regulatory protein that inactivates C3b
    • Fc receptors - bind to Fc region of antibodies, interfering with function as opsonins
  55. Howe do some pathogens Survive with phagocytes
    • Escape from phagosome before it fuses with lysosome, then multiply in cytoplams
    • Preventing phagosome-lysosome fusion, avoiding the otherwise inevitable exposure to lysosomes
    • Surviving within phagolysosome (Cox can) somehow delays fusion with lysosome, allowing time to equip self for growth
  56. How do some pathogens avoid antibodies
    • IgA protease 
    • Antigenic variation
    • Mimicking host molecules by covering themselves with molecules similar to those normally found in hose
  57. exotoxins
    • proteins that have very specific damaging effects
    • cause major damage in host
    • both gram neg and gram pos
  58. E. coli O157:H7
    • Is an enterotoxin
    • Causes bloody diarrhea, hemolytic uremic syndrome, shiga toxin
    • Diarrhea may be bloody, can cause kidney damage
  59. Shigella dysenteriae
    • Enterotoxin
    • Causes dysentery, hemolytic uremic syndrome, shiga toxin
    • Diarrhea that contains blood, pus, and mucus; can also cause kidney damage
  60. toxoids
    • vaccines which are inactivated
    • Ex: tetanus and diphtheria
  61. Cytotoxins
    damage a variety of different cell types, either by interfering with essential cellular mechanisms or by lysing cell
  62. A-B toxins
    • consist of 2 parts: 
    • A subunit is toxic (active) portion and B subunit binds to a specific surface molecule on cells
    • In other words:
    • A subunit, usually enzyme, responsible for effect, where B dictates type of cell to which toxin is delivered
  63. Membrane-damaging toxins
    cytotoxins that disrupt plasma membranes, causing cell to lyse
  64. hemolysins
    • refers to many membrane damaging toxins
    • as many lyse red blood cells, causing hemolysis that can be observed when organisms are grown on blood agar
  65. Phospholipases
    hydroyze phospholipids in plasma membrane
  66. Superantigens
    • override specificity of helper T cell response, causing toxic effects due to massive release of cytokines by TH cells
    • include toxic shock syndrome
  67. exfoliatin
    • toxin that destroys material that binds together the layers of skin, causing the outer layer to separate
    • Causes scalded skin syndrome
  68. Endotoxin
    • In both gram pos and gram neg species
    • Synthesized in cytoplasm, may or may not be secreted
    • Is a protein
    • Can generally form a toxoid
    • Inactivated by heat
    • Distinct toxic mechanism for each type
    • Generally very potent, some are among most potent toxins known
  69. Endotoxin
    • Involves Gram neg ONLY
    • Component of outer membrane of gram neg wall
    • Is a Lipopolysaccharide (the lipid A component)
    • Cant form toxoid
    • Heat stable (due to fat)
    • Innate immune response, systemic response leads to fever, dramatic drop on BP
    • Small amts in localized area lead to approp immune response that helps clear infection, but systemic can be deadly
  70. septic shock
    • State in which inflammation occurs throughout the body:
    • extensive leakage of fluids from permeable blood vessels and widespread activation of coagulation cascade
    • Overwhelming systemic repsonse causes dramatic drop in BP, disseminated intravascular coagulation and fever
  71. Damage associated with adaptive immunity
    • Immune complexes - antibodies bind to antigens, complexes can settle in kidneys and joints where they activate complement system, causing destructive inflammation
    • Cross-reactive antibodies - certain antibodies produced in response to an infection bind to body's own tissues, promoting autoimmune response
  72. Avoiding immune responses
    • some viruses can avoid effects of interferon
    • some can regulate apoptosis of host cell
    • To subvert the role of antibodies, some viruses transfer directly from cell to cell
    • surface antigens of some viruses change quickly, outpacing production of antibodies
Card Set
Micro 16
micro ch 16