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Micro 3010 > Unit 7 - Pathologic Consequences of Infection > Flashcards

Unit 7 - Pathologic Consequences of Infection Flashcards

1
Q

What 2 types of pathology can result directly from the microbe?

A

1) Directly cause cell damage. Multiplication within host cell and usually causes tissue damage by causing host cell to rupture
2) Dormant viruses bud out without killing (Pt will show no signs or symptoms)

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2
Q

Describe endotoxins

A
  • Can cause serious tissue damage
  • Secreted proteins
  • Can be encoded on plasmids/phages
  • Can be part of a vaccine (toxoid)
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3
Q

Explain how endotoxins can be part of a vaccine (toxoid)

A

1) Chemically inactivated toxin (formaldehyde) ex. diphtheria
2) Effective, highly conserved ex. scarlet fever (Streptococcal erythrotoxin)

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4
Q

List the modes of action of endotoxins

A

1) Hemolysins
2) Alteration of metabolic machinery
3) Interference with nerve-muscle transmission
4) Botulinum

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5
Q

Describe Hemolysins (A mode of action of endotoxins)

A
  • Many cells affected beyond RBC
  • Enzymatic lysis
  • Pore formation
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6
Q

Describe enzymatic lysis

A

Clostridium perfringenes

  • an alpha toxin (PLC) hydrolyses phophorylchlorine in cell membrane
  • causes lysis of cell membrane and death of cell
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7
Q

Describe pore formation

A

Staphylococcus aureus

  • an alpha toxin forms a pore and causes K+ to leak out of the cell membrane
  • pore formation causes loss of nutrients and leads to cell death
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8
Q

Describe Alternation of metabolic machinery (A mode of action of endotoxins)

A 
-A and B subunits
A = active
B = binding
ex. Diphtheria toxin 
blocks protein synthesis

-Cholera toxin
5 B subunits
1 A subunit

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9
Q

Describe “inhibition of protein synthesis”

A

C. diphtheriae

  • B binds to the membrane
  • A enters the cell through the membrane
  • Inactivates elongation factor-2
  • Prevents protein synthesis by ribosome
  • Causes cell death
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10
Q

Describe “hyper activation”

A

V. cholera

  • 5 B subunits
  • A1 and A2 subunit
  • Attach to ganglioside receptor

A1 and A2 enter through the cell membrane

  • Cause increased adenylate cyclase activity
  • Increase cAMP
  • Loss of cell nutrients through cell membrane (Na, H2O, Cl, K, Bicarbonate)
  • Causes diarrhea
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11
Q

Describe Interference with nerve-muscle transmission (A mode of action of endotoxins)

A

Ex. tetanus and botulinum toxins

  • Extremely potent
  • A-B toxins
  • B subunit binds to ganglioside receptors on nerve cells
  • Tetanus
  • B-unit binds to nerve cell receptor, A-subunit internalized area ?
  • X synaptic transmission and neurotransmitter release
  • Continuous stimulation of motor neurons, spastic paralysis

Effects on nerve-muscle transmission:

  • Cl. tetani
  • Tetanospasmin blocks inhibitory transmitter release
  • Results in continuous stimulation by excitatory transmitter
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12
Q

Describe botulinum (A mode of action of endotoxins)

A
  • Via intestine
  • Peripheral nerve endings at neuromuscular junction
  • X acetylcholine release - flaccid paralysis

Cl. botulinum

  • toxin blocks release of Each from vesicles
  • excitatory stimulation blocked
  • plastic surgery
  • people who sweat a lot
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13
Q

List some points about diarrhea

A
  • Invariable result of intestinal infections
  • Allows host to get rid of infecting organism
  • Allows parasite spread to fresh hosts
  • Toxin/microbial invasion
  • Results in loss of fluid that can be very bad
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14
Q

Immune response is very ______ with respect to distinguishing self vs. foreign

A

controlled

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15
Q

Immune response is not so well controlled with respect to degree of immune response and ____-______

A

over-activation

*this can cause host tissue damage

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16
Q

Endotoxins are produced by gram-_____ organisms. They are not secreted, always attached to pathogen

A

negative

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17
Q

Describe endotoxins

A
  • Integral parts of microbial cell wall
  • Released when cells die
  • Lipopolysaccharides
    • Lipid A
    • Core oligosaccharide
    • O-polysaccharide - variable
  • Fever and shock
    • Fever causes a release of cytokines by macrophage (IL-1 and TNF effect hypothalamus)
  • Other microbial molecules stimulate cytokines
    • TSST-1 (T cells release cytokines)
18
Q

T or F: LPS can activate both the alternative (polysaccharide) and classical (lipid A) C pathways

A

True

19
Q

Gram ____ organisms (ex. septicemia) leads to “toxic amount of endotoxin”

A

negative

20
Q

Allergic responses 1, 2, and 3 are ____ mediated

A

antibody

B cells

21
Q

Allergic response 4 is ___ mediated

A

cell

T cells

22
Q

Describe allergic response Type 1

A
  • Most common (runny nose, eyes, itchy skin)
  • Reaction to an allergen (Ag in the environment)
  • Symptoms
    • Location of the effector cells (cells which respond to presence of allergen)
    • May be unrelated to the actual point of entry of the allergen (ex. hives from ingesting strawberries)
  • Individuals with multiple allergies or severe allergies
    • Genetic disorders
    • Overproduction of IL-4 selects for IgE production over IgG, increased IL-4 receptors on B cells, or even certain types of MHC-2
23
Q

List the 6 steps involved in Type 1 Allergic Response

A

1) Initial exposure to the allergen
2) IgE formation following the primary Ab-mediated immune response
3) IgE binds via the Fc portion to specific receptors of basophils (in blood) and mast cells (in tissues), both cells types contain histamine granules
4) Second and subsequent exposure to the same allergen. Allergen binds to V region of the Fab and crosslinks two adjacent IgE’s on mast cell/basophil surface
5) Crosslinking triggers degranulation and release of histamine and other mediators
6) Immediate response (minutes after exposure)

**May not show sins of symptoms in first encounter.

24
Q

List some symptoms of a Type 1 Allergic Response

A
  • Hay fever (allergic rhinitis): Watery eyes, runny nose from vascular permeability and edema
  • Swelling and itchiness: Nasal congestion, hives, and edema
  • Anaphylaxis: Bronchoconstriction, shock, edema
  • Asthma: smooth muscle contraction
25
Q

List the 2 Key mediators of Type 1 Allergic Responses

A

1) Histamine

2) SRS-A (slow reaction substance of anaphylaxis)

26
Q

Describe the role of histamine as a key mediator in Type 1 Allergic Responses

A
  • Preformed molecules in granules (present in granules in mast cells at all times)
  • Binds receptors on target cells (lungs, skin, blood vessels)
  • Vasodilation, capillary permeability, smooth muscle contraction
  • Antihistamines block histamine receptors (prevents binding)
27
Q

Describe the role of SRS-A (slow reacting substance of anaphylaxis) as a key mediator in Type 1 Allergic Responses

A
  • Produced after exposure to allergen, not preformed
  • Slow release and lag time
  • Bronchoconstrictor implicated in asthma (asthma rxn mediated by SRS-A)
28
Q

What do you need to treat in Type 1 Allergic Responses?

A

1) Chronic allergies
2) Acute allergies (anaphylactic shock)
3) Hyposensitization

29
Q

How do you treat chronic allergies?

A

Antihistamines - block histamine receptors on target cells

Corticosteroids - block degranulation of mast cells (using corticosteroids long term can suppress immune system and make you more prone to infections)

30
Q

How do you treat acute allergies (anaphylactic shock)?

A

Epinephrine (EpiPen)

  • Inject directly, increases cAMP levels which decreases mediator release
  • Immediate, short effect (20 min)
  • Results in an increase in blood pressure and prevent/counteracts shock
  • Followed by IV antihistamines
31
Q

How do you treat hyposensitization?

A
  • Reducing sensitivity to particular antigen

- Long term treatment option has to be done in controlled setting

32
Q

Describe Type 2 Cytotoxic Hypersensitivity

A
  • Ab-mediated response is made of non-self cells/autoantibodies
  • IgG produced binds to non-self cell surface and activates the classical complement pathway (MAC attack)
33
Q

Give some examples of IgG produced binds to non-self cell surface and activates the classical complement pathway (MAC attack)

A
  • ABO blood transfusion reactions, Rh incompatibility
  • Blood stage malaria (Parasite Ag picked up by red cells)
  • Antimyocardial antibody of GAS (Group A streptococci) infection (cross-reacting carbohydrate antigen)
34
Q

Describe Type 3 Immune Complex Hypersensitivity

A
  • Large Ag-Ab complexes precipitate and induce inflammation
  • Activation of complement, attraction of phagocytes, general tissue damage
  • Lungs, kidneys, joints
    • Arthus Reaction
    • Serum sickness
35
Q

Describe Arthus Reaction

A

“Farmer’s lung”

Microbial antigens that enter the tissues (ex. fungal particles in the lung) encounter antibody and form immune complexes. These activate complement and initiate chemotaxis of polymorphonuclear leukocytes (PMNs) and degranulation of these and tissue mast cells. The resulting inflammatory response is further potentiated by damage induced by PMN-derived lysosomal enzymes.

36
Q

Describe serum sickness

A
  • Repeated doses of passive immunization
  • Circulating complexes
  • Deposition in kidneys, skin and joints (Glomerulonephritis, rheumatoid arthritis)
37
Q

Describe how glomerulonephritis occurs

A

-Glomerulonephritis is caused by immune complex-mediated tissue damage. Type 3 hypersensitivity results in the deposition of immune complexes in the blood vessels walls, particularly at sites of high pressure, filtration of turbulence such as the kidney. Large complexes deposit on the glomerular basement membrane, while small ones pass through the basement membrane and then deposit on the epithelial side of the glomerulus.

38
Q

Describe Type 4 Delayed of Cell-mediated Hypersensitivity

A
  • No Ab involvement
  • Th and Tc cell-mediated
  • Delayed as starts hour/days after contact and can last for days
39
Q

What is The Hygiene Hypothesis?

A
  • Allergic reaction more common than previously
  • Microbial exposure deficiency syndrome (expose young children to antigens early on, eat dirt)
  • C-section vs. vaginal birth (more chance of asthma in c-section because they are not exposed to antigens that they would be in vaginal birth)
  • Pets (grow up with pets, less likely to form a reaction)

Basically, need to be exposed to antigens when you are young, so that the initial reaction is small and can form immunity. Versus if they were exposed when older and used to a clean environment, the antigen response is much bigger.

40
Q

What bacteria is linked with stomach cancer?

A

Helicobacter pylori

41
Q

How can infectious agents cause tissue damage in various ways?

A
  • Direct destruction of cells
  • Toxin production
  • Overstimulation of immune system

Micro 3010 (20 decks)

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