GoConqr hat ein neues Design! Sag uns, wie es dir gefällt.

Karteikarten

Micro part 2

Melanie Horne Englisch 200 Karten

Karten in diesem Stapel (200)

  1. 1What are chemotherapeutic agents?Drugs that act against diseases
  2. 2What are antimicrobial agents?Drugs that treat infections
  3. 3What are antibiotics?Antimicrobial agents produced by microorganisms that kill or inhibit the growth of other microbes
  4. 4Who was Paul Ehrlich?Convinced there were chemicals that would harm the infecting agent without harming the host ("magic bullets")
  5. 5Who was Alexander Fleming?Discovered that penicillin released from penicillin fungus inhibited the growth of Staphylococci
  6. 6What is the difference between smisynthetics and synthetics?Semisynthetics are produced by organisms, and then altered by chemists. Synthetics are produced by chemists
  7. 7What is a common genus that produce antibiotics?Streptomyces - a gram-positive genus of soil dwelling bacteria
  8. 8What are five major mode of action of antimicrobials?1) Inhibition of cell wall synthesis
    2) inhibition of protein synthesis
    3) Disruption of cytoplasmic membranes
    4) Inhibition of metabolic pathways
    5) Inhibition of nucleic acid synthesis
  9. 9Which antibiotics inhibit cell wall synthesis?Vanomycin
    Bacitracin
    Penicillins
    Cephalosporins
    Monobactams
    Carbapenems
    (most are beta-lactams)
  10. 10Whuch antibiotics act on RNA polymerase?Rifampin (Works on prokaryotic but not eukaryotic RNA polymerase)
  11. 11Which antibiotics act on protein synthesis?Erythromycin
    Chloramphenicol
    Clindamycin
    Tetracyclines
    Streptomycin
    Gentamicin
    Kanamycin
  12. 12Which antibiotics act on folic acid metabolism?Trimrthroprim
    Sulfonamides
    (Inhibit different steps of metabolism, when used together they work much better, since some bugs are resistant)
  13. 13Which antibiotics act on cytoplasmic membrane structure?Polymyxins
    Amphotericin B (polyene)
  14. 14Which antibiotics act on DNA gyrae>Quinolones (such as Ciprofloxacin)
    (acts on the prokaryotic form, has little effect on eukaryotic form)
  15. 15Which antibiotics act on cytoplasmic membrane structure?Polymixins
  16. 16How do cell wall inhibitors work?-Prevent cross-linkage of NAM subunits (leads to weak cell wall, lyses)
  17. 17how to vanomycin and cyclcoserine work to inhibit cell wall synthesis?I/nterfere with particular alanine-alanine bridges that link GAM subunits
  18. 18How does Bactiracin work to inhibit cell wall synthesis?Blocks secretion of NAG and NAM from cytoplasm
  19. 19How do Isoniazid and ethambutol work to inhibit cell wall synthesis?Disrupt the formation of arabinogalactan-mycolic acid in mycobacterial species
  20. 20Can animals are humans be harmed by antibiotics that inhibit protein synthesis?Yes because mitochondria of animals, humans and chloroplasts of plants contain 70S ribosomes
  21. 21How does tetracycline work to block protein synthesis?Blocks docking site of the tRNA
  22. 22How does Chloramphenicol work to block protein synthesis?Chloramphenicol blocks peptide bond formation
  23. 23How do macrolides work to inhibit protein synthesis?Bond to 50S subunit blocking proper mRNA movement through ribosome
  24. 24How does oxazolindinone work to block protein synthesis?It blocks initiation
  25. 25Which antimicrobials are used most commonly against viruses?Nucleoside analogs (drugs that inhibit nucleic acid synthesis)
    (Azidothemidinne, ribavarin, acyclovir)
  26. 26What are some characterics of an ideal antimicrobial?-Cost-effective
    -Readily available
    -Chemically stable
    -Easily administered
    -Nontoxic
    -Selectively toxic against wide range of pathogens
  27. 27What can result from the use of broad-spectrum antimicrobials?-May kill normal microbial flora in the body
    -May allow for secondary or superinfections to occur
  28. 28What is the diffusion suseptibility test? (Kirby-Bauer)Streak an entire plate of the organism you want to kill, but plpace disks of antibibotics. Measure the zone of inhibition around the anitmicrobial and look it up on a chart to see if it is susceptible
  29. 29What is the minimum inhibitory concentration test? (MIC)The lowest amount of the drug that will inhibit growth.
    -In test tubes, grow culture in increasingly higher amounts of the drug
  30. 30What is the E test?Impregnate filter paper strips with differing concentrations of the antimicrobial. When it is placed on a plate with a lawn of the organism, you can see where the growth intersects with the concentration on the disk
  31. 31What is the minimum bactericidal concentration test?Plate some of the tubes from the MIC test that shows no growth and plate them. Look for the first plate that shows NO GROWTH
  32. 32What are some toxicity side effects of anitmicrobials?Kidneys, liver, nerves
    -Allergies (rare, but life threatening)
    -Disruption of normal microbiota
  33. 33What are the most commonly used antibiotics?Cephalorsporins
  34. 34What are the two ways that bacteria can acquire resistance?1) New mutations in chromosomal genes
    2) Acquisitions of R-plasmids through transformation, transduction, and conjucation
  35. 35How can we combat resistance?1) High concentrations of drug for long duration
    2) Multiple antimicrobials used synergistically
    3) Limit use to necessary cases only
    4) Second and third generation drug development
  36. 36What must occur in order for a pathogen to attack a host?The correct chemical receptors for those pathogens must be present
    -The environnment of the cell must be correct
  37. 37What are the nonspecific defenses?1st line (skin, mucous membranes, chemicals)
    2nd line (Phagocytosis, complement inferon, inflammation, fever)
  38. 38What is are the specific defense systems, and what are they also known as?3rd line: lymphocytes, antibodies
    Also called aquired immunity
  39. 39How does skin prevent pathogen infection?-Its dry and nutrient poor
    -Shedding of skin also sheds pathogens
    -Epidermal dendritic cells recognize and process invaders
  40. 40What are the rolls of sweat and sebum against pathogens?Salt: inhibits growth of pathogen by drawing water from their cells
    -Sebum keeps skin pliable, many fatty acids are toxic to bacteria
  41. 41How do the body's microbes make it hard for pathogens to compete?-Secrete antimicrobials
    -Competition of nutrients
    -Create unfavourable env for other pathogens (changing pH)
    -Stimulate body's second line of defense
    -Promote overall health by getting vitamins to host
  42. 42What is plasma?Mostly water containing electorlytes, dissolved gases, nutrients and proteins
  43. 43What is blood serum?It is what is left of the blood plasma when you remove clotting flactors
  44. 44Serum =Serum = Plasma - Fibrinogen factors
  45. 45What is the role of platelets?Blood clotting and inflammation
  46. 46What is the role of leukocytes?Defend against invaders.
  47. 47What are the two types of leukocytes?Granulocytes
    Agranulocytes
  48. 48What is the shape of the nuclei of basophil, eosinophils and neutrophils?Basophils and Eosinophils have a bi-lobed nuclues
    Neutrophils have a many-lobed nucleus
  49. 49What are the distribution of granulocytes?Neutrophils: 50-70% of circulating WBCs (acute inflammation)
    Eosinophils: 1-3% (parasite defense)
    Basophils: 0.5-1% of WBC (contain histamine)
  50. 50What are the two types of agranulocytes?Lymphocytes: 20-40% (specific immunity)
    Monocytes: 1-6% WBC (mature into macrophages)
  51. 51What is diapedesis?The outward passage of blood cells through intact wall
  52. 52What can a leukocyte count signal about health?Increased eosinophils = parasitic worm or allergies
    Increased neutrophils = Bacterial infection
    Increased lymphocytes = viral infection
  53. 53What components of secondary defense?Phagocytosis, extraccellular killing by leukocytes, nonspecific chemical defenses, inflammation, fever
  54. 54Which twp cells perform most phagocytosis?Neutrophils and the macrophages
  55. 55How does phagocytosis work?Phagocytes have receptors for components on the surface of bacteria, viruses, etc
  56. 56What are opsonins?Opsonins are substance that enhance phagocytosis (provide a handle for the phagocyte)
  57. 57What do eosinophils primarily target?-Attack helminths by grabbing on and secreting substances to lkill helminth
  58. 58What are the role of natural killer NK cells?-Target virally-infected cells and tumor cells
  59. 59What are toll-like receptors?They bind to pathogen-associated molecular patterns
  60. 60What are NOD proteins?Nod proteins are intracellular receptors for sub-components of bacterial peptidoglycan
  61. 61What are interferons?Interferons are protein molecules released by host cells to nonspecifically inhibit the spread of viral infections
    (3 classes: alpha, beta and gamma)
  62. 62What is the role of alpha and beta inteterferon?Alpha and beta are also known as type 1: produced early in the infection
  63. 63What is a complement pathways system?Set of serum proteins designs to be activated in sequence
    -Results in lysis of foreign cell
  64. 64What are the three complement pathways?Classical
    Alternative
    Lactin
  65. 65What is the classical pathway?Bonding of two antibodies
    (unless we have an immune response, we cannot have the classical pathway)
  66. 66What is the alternative pathway?e
  67. 67What is the lectin pathway?Binds to sugars like mannose that are found on the surface of some bacterial cells, but not found on human cells
  68. 68What is the resutof the complement cascade?Membrane attack complex: large pores are formed in the membrane which causes cell lysis
  69. 69What effector in the complement cascade is a strong neutrophil attractant?C5a
  70. 70What are the functions of complements pathways?Induce inflammation (C3a, C5a)
    Opsonization (C3b)
    Chemotaxis of phagocytes (C3a, C5a)
    Lysis of foreign cells (MAC - mostly C9)
  71. 71What are Defensins?Small peptides that function nonspecifically to protect against a broad range of pathogens
  72. 72How do defensins work?-Rupture membranes
    -Interfere with internal signalling
    -Interfere with protein shapes
  73. 73Where would you find a lot of defensins?-Eyes
    -Small intestine
  74. 74What is inflammation?A nonspecific response to tissue damage resulting from various causes
    -Characterized by redness (rubor), heat (calor), swelling (tumor), and pain (dolor)
  75. 75What are some characteristics of actue inflammation?-Quick and short lived
    -Usually beneficial
    -Dilation and increased permeability of blood vessels
    -Migration of phagocytes
    -Tissue repair
  76. 76What are some characteristics of chronic inflammation?-DEvelops slowly, last long
    -Can cause damage to tissues
  77. 77How does fever result?Pyrogens trigger the hypothalamus to increase the body's core temperature
    -Speeds up immune response, prevents some bacteria from growing
  78. 78What are the five attributes of adaptive immunity?1) Specificity
    2) Induceibility
    3) Clonalilty
    4) Unresponsive to self
    5) memory
  79. 79What triggers specific immune responses?Antigens
  80. 80What are primary lymphoid organs??Places that produce T and B cells
  81. 81What are secondary lymphoid organs?Where an immune response takaes place
  82. 82Where are B-cells produced?Bone marrow
  83. 83where are T-cells produced?Thymus gland
  84. 84What are lymph nodes?House lymphocytes
    -Attack invaders in lymph fluid
    -Drain lymph into efferent lymphatic vessels
  85. 85What is the function of the spleen?Filters bacteria, viruses, toxins, etc from the blood
  86. 86What is the function of the tonsilts?Trap foreign particles and microbes that are ingested or inhaled
  87. 87What are epitopes?Antigenic determinants
    -There may be more than one epitope per antigen
  88. 88Where are MHC class 1 antigens found?They are glycoproteins found in the membranes of most all nucleated cell of vertebrate animals
    -hold a peptide fragment from an intracellular protein
  89. 89Where are MHC class II antigens found?Found only on APCs
    -Function to hold a peptide fragment from an extracellular protein
  90. 90How many different MHC class I molecules are expressed on the cells of a norml human?6
  91. 91Where do the antigen binding cites of T-cells emerge?In the thymus through random genetic shuffling
  92. 92What are Th1 cells?Activated macrophages
    + Killer T -cells
  93. 93What are Th2 cells?Mucosal and barrier immunity; includes many T folicular helper cells
    (helps a B cell generate an antibody response)
  94. 94What are Tr cells?Regulatory cells: suppress immune responses
  95. 95What do helper T cells do?-Help regulate activities of B cells and cytotoxic T cells during an immune response
    -Secrete cytokines (which determine which immune response will be activated)
    -Bosses: tell everyone what to do and when to do it
  96. 96What do Interleukines do?Interleukins = type of cytokines
    -signal among laurkocytes
  97. 97What are interferons?Antiviral proteins that may act as cytokines
  98. 98What are growth factors?Proteins that stimulate stem cells to divide, maintaining adequate supply of leukocytes
  99. 99What are tumor necrosis factors?-Secreted by macrophages and T ells
    -Kill tumor cells
    -Regulate immune responses and inflammation
  100. 100What are Chemokines?Chemokines are signal leukocytes
    -Stimulate arrival of other leukocytes at infection sites
  101. 101What happens to T cells in the Thymus?Positive and negative selection
  102. 102What is positive selection?-Selects thymocytes bearing receptors capable of binding self-MHC molecules
  103. 103What is negative selection?Selects against thymocytes bearing high-affinity receptors for self-MHC/peptides complexes, resulting in self tolerance.
  104. 104How many thymocytes are killed in the thymus?95%
    (ensures T cells can recognize self and foreign proteins)
  105. 105What are the role of B Lyphocytes?Differentiate into plasma cells which secrete antibodies
  106. 106What is true of B cell receptors?-They are just membrane-bound immunoglobulin
    -Each BCR is complementary to only one antigenic determinant
  107. 107What is immunoglobulin called when secreted?Antibody
  108. 108How do we get diversity for B cell receptors?It randomly combines 3 segments of DNA: V, D and giving millions of possibilites
  109. 109What do antibodies do?Secreted by plasma cells, they bind antigens
  110. 110What is the basic structure of an antibody?2 heavy chains and two light chains
    -2 antigen binding pockets
    -Fab: antigen binding fragments
  111. 111Which type of bonds occur between epitopes and antigen binding sites?Strong noncovalent bonds
    -h bonds, ionic attractions, and hydrophobic interactions
  112. 112What are the functions of antibodies?1) Neutralization
    2) Opsonization
    3) Agglutination
    4) Activation of complement
    5) Target a cell for destruction nu other cells
  113. 113What differs between classes of antibodies?The type of heavy chain, the function of the antibody, the location in the body it acts upon
  114. 114Which class of antibody is made in largest abundance throughout the day?IgA
  115. 115How many epitopes can react with a singl molecule of IgM10
    (pentamer, each has 2 sites)
  116. 116What is a cell-mediated immmunne response used for?Responds to INTRAcellular pathogens and abnormal body cells
  117. 117What is a major component of cell-mediated immune response?-Cytotoxic T cells
    -Directly kill certain cells
  118. 118What is the Humoral immune response?-Responses against exogenous pathogens (pathogens outside the cell)
    -B cell activation and clonal selection
    -memory B cells and the establishment of immunological memory
  119. 119What are Memory B cells?-produced from B cell proliferation
    -Have BCR complimentary to specific antigenic determinant
    -Long-lived
    -Initiate antibody production more rapidly if the same antigen is encountered again
  120. 120What is the difference between naturally acquired and artificially acquired imunity?Naturally: immune response against antigens encountered in daily life
    Artificially acquired: response to medical intervention
  121. 121What is the difference between active and passive immunity?Active = antibodies you make yourself
    PAssive = Someone else's antibodies
  122. 122What is the primary role of Basophils and what is their stain colour??Stains Blue
    Contain Histamine (respond to allergies)
  123. 123What is the main role of Eosinophils and what colour do they staian?Stain Red
    Parasite defense
  124. 124What is the role of Neutrophils and what colour granules do they have?Stain Lilac
    Major phagocytes
    Respond to acute inflammation
  125. 125This is the first antibody produced to a new antigen; it is usually found as a pentamerIgM
  126. 126This is the most common class of antibody in the blood; it can cross the placenta.IgG
  127. 127This is the only class which is not secreted; it is found only on the surface of B cells.IgD
  128. 128This binds avidly to mast cells and basophils; it is involved in allergies.IgE
  129. 129This is the major immunoglobulin in secretions; it is usually found as a dimer.IgA
  130. 130Which ancient civilizations knew of vaccines?-Ancient chinese
    -Collected scabs of smallpox survivors, ground them and snorted them (variolation)
  131. 131What did Edward Jenner notice?-Noticed milkmaids never got smallpox, they got cow pox
    -He innoculated someone with cowpox and it protected them against smallpox
  132. 132What did Louis Pasteur develop?A vaccine against Pasteurella multocida
  133. 133What are the 5 types of vaccines?1) Attenuated live (weakened)
    2) Inactivated (killed) (no capacity to replicate)
    3) Toxoids
    4) Conjugate (polysaccharide conjugated to a protein)
    5) Combinations
  134. 134What are two toxoid vaccines?Diptheria
    Tetanus
  135. 135What is attenuation?Attenuation is the process of reducing virulence
    -Raised in tissue culture for which they aren't adapted until they lose the ability to produce disease
    -Or genetically mutated to be attenuated
  136. 136What do viral vaccines trigger?A cell0mediated immune response dominated by Th1 and cytotoxic t cells
  137. 137What are some problems with attenuated vaccines?-May cause disease in immunosuppressed individuals
    -Pregnant women should not receive, risk of modified pathogen crossing placenta
    -Modified viruses can revert to wild type (or mutate to a virulent form)
  138. 138What are inactivated vaccines?Could be an entire organism deactivated, fragments or microbes
    -Safer than live vaccines
  139. 139What type of response do inactivated vaccines produce in the body?-Stimulate a Th2 response that promotes antibody-mediated immunity
  140. 140Problems with inactivated vaccines-No herd immunity
    -May stimulate inflammatory response
    -Weak immunogenicity (no strong immune response
    -May have to include an adjuvant
  141. 141What are common adjuvants?Aluminum, Saponin, Mineral oil, Freund's complete adjuvant
  142. 142What are toxoid vaccines?Chemically or thermally modified toxins are no longer physiologically active
  143. 143What modern technology allows us to make better vaccines?Recombinant DNA technology
    (think Hep B vaccines)
  144. 144What is a concern with vaccine safety?-Mild toxicity
    -Pain at injection site
    -High fever, seizures in rare cases
    -Allergies/anaphylactic shock
    -Residual virulence
  145. 145What is passive immunity?-used when protection against a recent infection or an ongoing disease is needed quickly
    -Serum is used from human or animal donors with antibodies
  146. 146What are limitations of antisera?-Contain many antibodies, not just target
    -Allergic reactions
    -May be contaminated with viruses
    -Antibodies degraded quickly
  147. 147What is Serology?The study and diagnostic use of antigen-antibody interactions
  148. 148What is a precipitation test?Soluble antigens and soluble antibody mixed in proper proportions form large macromolecular complexe called precipitates
  149. 149What is immunodiffusion (ouchterlong technique)Antigen well and antibody well. If they are in optimal proportions, they form a line in the gel. Called the zone of optimal precipitation
  150. 150What is radial immunodiffusion?Pre-formed antibodies used to show the concentration of an antibody in a serum
    -Calibration curve relates size of ring to concentration of serum
    -Quantitative test
  151. 151What is immunoelectrophoresis?-Separate proteins and blood serum out
    -Separates out proteins based on charge
    -Can identify many antigens (>30) that are present and determine if there are deficiencies
  152. 152What is an agglutination test?-Agglutination is the clumping of insoluble particle
    -blood type is an example
  153. 153What are neutralization tests?-Antibodies can bind and neutralize toxic effects of many antibodies
    -2 neutralization tests: viral neutralization and viral hemagglutination inhibition test
  154. 154What is a viral neutralization test?-When a virus is mixed with antibodies against it, the ability for the virus to kill the culture cells is neutralized
    -If we apply the virus to a cell culture and we dont see any negative effects
  155. 155What is a viral hemagglutination inhibition test?-Ability of some viral surface proteins to clump red blood cells
    -Serum from inv. will stop hemagglutination if the serum contains antibodies against the specific virus
  156. 156What is the labeled antibody test?-We can link a chemical label to an antibody and follow where it binds
    (fluorescent, ELISA, immunoblots)
  157. 157What is the fluorescent antibody test?-Uses fluorescent dyes as labels
    -Glows when exposed to light
    -Fluorescin commonly used
  158. 158What is a direct flurorescent antibody tests?d
  159. 159What is an indirect fluorescent antibody test?d
  160. 160What is an ELISA test?Enzyme-linked immunosorbent assay
    -Uses an enzymes as the label
    -Reaction of enzyme and substrate produces a coloured process indicative of antibody presence
    -Most commonly used to detect presence of antibodies in serum
  161. 161What is a modification of ELISA?The antibody sandwich ELISA
    -Commonly used to detect antigen
  162. 162What are advantages of ELISA?-Can detect either antibody or antigen
    -Quantitative
    -Easy
    -Inexpensive
    -Can be stored
    -Sensitive
  163. 163What is immunoblotting ? (western blotting)-Detects antibodies against multiple antigens in a complex mixture
    -Separates out proteins based on size, using bands
  164. 164What is hypersensitivity?Any immune response directed against a foreign antigen that is exaggerated beyond the norm
  165. 165What is a Type 1 hypersensitivity?Also called immediate
    -IgE-mediated
    -Localized or systemic reaction that result from the release of inflammatory molecules in response to an antigen
    "allergies" antigens called allergens
  166. 166What is the function of IgE?Mast cells and basophils have a high-affinty receptor for IgE
  167. 167What are mast cells?-Found close to body surfaces
    -Cytoplasm with large granules
    -Granules contain inflammatory chemicals like histamine
  168. 168What chemicals are released from masst cells?Proteases, Kinins and Histamine
    Later: Leukotrienes and Prostoglandins
  169. 169What are clinical signs of systemic allergic reactions?Degranulation of many mast cells at once - anaphylactic shock
  170. 170What are clinical signs of anaphylactic shock?-Bronchial contraction
    -Leakage of fluid from blood vessels swelling in larynx and tissues
    -Contraction of smooth muscle in intestines and bladder
  171. 171How do wetreat Type I hypersensitivity?-Drugs that counteract the niflammatory mediators released by degranulation
    (antihistamines)
    -Epiephrine (life threatening, emergencies)
  172. 172What is type II hypersensitvity?Results in cells being destroyed by an immune response (combined activities of complement and IgM and IgG)
    -Component of many autoimmune diseases
  173. 173What are two exammples of Type II cytotoxic hypersensitivity?1) Destruction of blood cells following an incompatible blood transfusion
    2)
  174. 174What antigens and antibodies do bloud group A have?Antigens: A
    Serum antibodies: Anti-B
  175. 175What antigens and antibodies do group B have?Antigens: B
    Antibodies: Anti-A
  176. 176What antigens and antibodies do AB have?Antigens: A and B
    Antibodies: none
  177. 177What antigens and antibodies do blood group O have?Antigens: None
    Antibodies: Anti-A and Anti-B
  178. 178Why do we have antibodies present?These antigens are present everywhere, we are constantly exposed to them. Our body will form antibodies to everything that is foreign,
  179. 179What is the Rh system?Rh antigen: common on RBCs of humans, 15% do not have the antigen
    -Transports anions and glucose across the membrane
  180. 180When is there a risk of hemolitic disease of the newborn?When mother is - and fetus is +
  181. 181How do we prevent hemolytic disease of the newborn?Administer anti-Rh serum called Rhogam to all Rh- pregnant women
    -Destroys any fetal RBCs that may have entered the mody
    -Sensitization of the mother does not occur
  182. 182w/hat is Type III (immune-complex mediated) hypersensitivity?-Formation of antigen-antibody complexes
    -Can cause systemic or localized reactions
    -Localized or systemic
  183. 183What is hypersensitivity pneumonitis?Individuals become sensitized when antigens are inhaled deep into the lungs, stimulating the production of antibodies
  184. 184What is glomerulonephritis?Immune complexes circulating in the bloodstream a re deposited on the walls of the glomeruli (small BVs in the kidneys)
    -Leads to kidney failure and death
  185. 185What is Systemic Lupus Erythematosus? (SLE)-Autoantibodies against DNA result in formation of immune complexes
    -Joints (arthritis)
    -Issues with glomeruli
  186. 186What is Rheumatoid arthritis?B cells produce autoantibodies against antibodies and against a variety of nuclear antigens or collagen
    -Joints become distorted and lose range of motion
  187. 187Most of the damage in type III hypersensitivity is caused by?Destructive products released from neutrophils
  188. 188Most of the damage in type IV hypersensitivity is caused byTc cells and macrophages
  189. 189Most of the damage in type II hypersensitivity is caused byComplement-mediated lysis
  190. 190Most of the damage in type I hypersensitivty is caused byHistamine release from mast cells
  191. 191What is type IV hypersensitivity?-Only type not mediated by antibodies
    -Inflammation occurs 24+ hours after exposure, results from interactions of antigens, antigen-presenting cells and T cells
  192. 192What is the tuberculin response?Inject tuberculin
    -no response = never been exposed
    -red hard swelling - have been exposed
  193. 193What are some immunoprivledged sites?Brain, cornea, eyes, testes,
  194. 194Which two groups are gram-positive pathogens categorized into?Low G + c vs High G + C
  195. 195What do staphylococcus look like?Purple, spherical (coccus)
  196. 196What are some characteristics of Staphy?Facultative aerobes
    -Can tolerate high salt and low water
    -Coagulase negative
  197. 197What is the most common organism on the skin surface?S. epidermidis
    (mostly opportunistic)
  198. 198What are some characteristics of Staph aureus?-30-50% carry it
    -Coagulase positive
    -Form large, golden-coloured colonies
  199. 199What causes Staph infection?-Evade phagocytosis
    -Produce ezymes
    -Produce toxins
  200. 200How does staph evade phagocytosis?Protein A coats cell surface (innhibits complement)
    -Bound coagulase
    -Slime layer

Informationen

Beschreibung
Karteikarten am Micro part 2, erstellt von Melanie Horne am 08/07/2018.
Erstellt von
Melanie Horne
Aufrufe
0
Bewertung

Feedback

Worum geht es?

Wie gefällt dir das neue Design?

Dein Eindruck