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BIOC17 Lectures > Lecture 9 > Flashcards

Lecture 9 Flashcards

1
Q

Whats techoic aicd

A

Major component found in cellgram + cell walls, not found in gram negative

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2
Q

Technolci acid consists of

A

polymers of glycerol phosphate. Varying R groups.

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3
Q

Varying R groups can lead to

A

Adherance to tissue

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4
Q

technoic acid is

A

highly immunogenic (antigenic). antibodies against indiviudals with subseuqent infection by an organism with same technoic acid

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5
Q

what makes the negative cell wall in gram postive

A

TAs

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6
Q

Whats the complement cascade in vetebrates

A

technoic acid can induce

complemt is a human blood plasma that enhances phaogcytosys

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7
Q

Whats a syndrome

A

set of symptoms characteristic of a particular disease

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8
Q

some diseases of group A strep

A

cutaneous, invasive: like strept throat
necrotizing fascilits
toxic like syndrome

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9
Q

which bacteria is part of group A strep

A

Streptoccocus pyogenes
Streptococcus pneumonia

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10
Q

Whats the toxic like symdrome

A
  1. organisms invade host via a cut
  2. the bacteria releases degrdative enzymes and other cytokines resulting in an inflammatory response.
  3. The infection enters the blood stream -> leading to damange in blood vessels, lympocytes, releasing more cytokines -> inflammatory response
  4. Tissue damange and signigicant release of cytokines -> septic sholc
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11
Q

Whats systemic repsonse

A

Whole body response to an infection rather than a local one

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12
Q

Whats septic shock

A

result in fever, tarhybia , electrolyte imblaance, multiple organ failure, death

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13
Q

What makes S pyogen infections destructive

A
  • secretion of streptokinase (wall off blood clots)
  • scercete hemolysisn that kill strpetolyisin that kill host RBC and release cytokinase

extracellular procease/nucleases
leukocykins:kill WBC
- may contain a cell wall and capsule

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14
Q

Adaptive immune resposne is also known as

A

speciifc immune respise

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15
Q
A
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16
Q

Whats another group A strep

A

Streptococcus pneumonia

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17
Q

How many types of Streptococcus pneumonia are there

A

90 serotypes dues to
antigenic capsule variants

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18
Q

Whhat are some diseases caused by group A strep, cutaneous

A

cellulitis: subcutaneous spreading infection with swelling (edema)
➢ impetigo: crusty lesions on skin (common in children)

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19
Q
A
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20
Q

Whhat are some diseases caused by group A strep, Invasive

A

strep throat: severe sore throat
pharyngitis (infection
of pharynx); tonsillitis (cause of over half the severe sore throat infections).

  • severe sore throat plus fever
  • toxic like syndrome
  • necrotizing fasciztiz
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21
Q

Important to treat Strep A rapidly and completely because can lead to:

A

possible sequelae (follow up diseases) of streptococcal diseases:
❖ glomerulonephritis : an inflammation of the kidney: in 10% of
cases can lead to kidney dialysis for life
❖ rheumatic heart disease: an autoimmune disease causing
damage to cardiac tissue
❖ scarlet fever or even toxic shock syndrome

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22
Q

Which strain can lead to toxic like syndrome

A

Streptococcus pyogenes

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23
Q

What is necrotizing fasciitis

A

caused by certain strains of S. pyogenes
▪ is the flesh eating disease,

Cellulitis is a milder form of this disease, but can become dangerous in short
order if untreated

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24
Q

What is Necrotizing Fasciitis

A

the organisms enters the soft tissues usually via a wound (scratch, cut)

organism reach fascia (membranes that surround muscle and separate muscle from fat)

fascia is relatively thin and is destroyed easily. It is destroyed as the bacteria move along

destruction of fascia detaches the skin from blood supply and the
skin dies

rate of destruction can be as fast as one inch per hour (similar to
gas gangrene)

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25
Symptomso f necrotizing fasciitis
1. flu-like symptoms (fever, chills, malaise) 2. rash, similar to scarlet fever (spreading redness, sometimes swelling, may be hot to the touch) 3. some peeling of skin (exfoliation) 4. tissue necrosis (sometimes treatable by amputation and antibiotics) 5. the person may go into shock due to drop in blood pressure, can lead to organ failure an death (septic)
26
Symptoms of necrotizing fasciitis are similar to
common in severe diabetes and leprosy, conditions which reduce the blood and nerve supply to the skin
27
What makes S. pyogenes infections so destructive
S.pyogenes as well as certain other strains of streptococci secrete a number of extracellular enzymes that damage the host tissue: + streptokinase which dissolves blood clots + hemolysins destroy RBC are considered membrane-disrupting exotoxins + extracellular proteases and nucleases also contribute to tissue damage and invasiveness + leukocydins that kill WBC including phagocytes + S. pyogenes may contain a capsule and/or cell wall components that contribute to virulence. (For example cell wall proteins F, G and M)
28
hemolysins are
membrane-disrupting exotoxins
29
streptolysin O
oxygen sensitive)
30
streptolysin S
oxygen stable
31
What are phagocytes
Monocytes, macrophages, and neutrophils are phagocytes
32
A phagocyte is a type of
white blood cell
33
What are the components of Streptococcal gram positive cell walls that contribute to virulence
cell wall proteins F, G and M
34
Whats protein F
a protein extending from the surface which increases adherence by binding to a glycoprotein found in the extracellular matrix of many mammalian cells called fibronectin, aids in binding of pathogen to eukaryotic cells
35
What is protein G
streptococcal surface protein that are Fc receptors - can bind Immunoglobulins
36
What are immunoglobulins
any of a class of proteins present in the serum and cells of the immune system, which function as antibodies.
37
How does protein G work
- These proteins bind to and immobilize the Fc region of antibo in an upside down position (some bind to both IgG and IgA) - will bind all Fc regions not just to antibodies specific to Streptococcus - when antibodies are bound in the upside down position to the Fc receptors on protein G the antibodies are unable to interact with phagocytes that could destroy the bacterial cell (block phagocytosis protecting the bacteria)
38
Does s pyogenes have a capsule
yes, and it increases virulence
39
What is protein M
Fimbriae-like, "hairy" extensions associated with virulent strains which can increase attachment and block the complement system
40
Whats fibronectin
glycoprotein found in the extracellular matrix of many mammalian cells
41
What does protein M bind to
fibrinogen, fibronectin, factor M
42
How does protein M prevent phagocytosis
it binds to serum factor H, destroying C3 convertase and preventing opsonization by C3b and hence pagocytosis
43
What are the 5 classes of immunoglbulins:
GAMDE
44
Whats IgG
the most abundant antibody found internally: high in plasma (liquid portion of blood)
45
Whats IgA
the most abundant secreted immunoglobulins (i.e. in mucous, breast milk)
46
Whats IgM
rapidly increase in new infection, expressed on surface of B cells
47
Whats IgD
found primarily on the surface of lymphocytes: helps to induce the synthesis of IgG and IgA to specific organisms
48
Whats IgE
can be secreted and is particularly active against parasites
49
What are lymphocytes
A lymphocyte is a type of white blood cell (leukocyte) in the immune system of most vertebrates. Lymphocytes include T cells B cells
50
All of the immunoglobulins function in
the adaptive (specific) immune response
51
Function of an antibody moleucle
a) recruits phagocytes to destroy the cell b) recruits specific complement proteins resulting in a complement cascade and opsonization that aids in the destruction of the bacterial cell
52
What do antibodies bind to on the surface of S. pyogenes
binds to Fc receptor on protein G on surface of S. pyogenes therefore nonfunctional antibody
53
Where do phagocytes bind to on the amtibody normally
phagocytes can bind to Fc region via Fc receptor on the phagocyte surface -> complement cascade/engulfing
54
How does the antibody become ueless
since G protein binds to Fc region the antibody is in a useless upside down position phagocytes can't bind
55
how does S. pyogenes evade the immune system of the host
inhibit phagocytic leukocytes (WBC) -> contributes to virulence
56
Whats the M protein
a family of fibrillar proteins that extend from the Steptococcal cell wall
57
How does the M protein work
functions in a manner similar to a capsule, it binds to a complement regulatory protein that inactivates C3b, interfering with complement activation and the subsequent formation of more C3b -> (i.e. results in ineffective opsonization)
58
What does M protein binding leading to
ineffective opsonization
59
How does M proteins cause an autoimmune response
It has amino acid similarity to mammalian proteins like myosin and keratin antibodies raised to M proteins can cross react with host proteins under certain conditions, antibodies can react with the mitral valve (damages heart)
60
subsequent streptococcal infections may cause further damage (sequelum of streptococcal disease)
psoriasis (recurrent inflammation of the skin/scalp often accompanied by arthritis) -> v
61
Whats the alternative pathway
C3b attaches to bacterial surfaces -> other complements protein attach -> opsinzaition -> forms an enzyme that initates the complement cascade
62
When doesnt the host cell not induce response
Host cell suface contains moleucles that bind complement regulatory protein When C3B binds to the host cell surface -> complement regulatory protein inactiates it
63
How does M protein inactivate c3b
the bacteria cell contains M protein that bidns with the complement regulatory protien. When c3b attaches -> compelement regulatory protein inactivates it. -> M protein is hijacking the host protien
64
Acquired immunity has 2 types
- Active and Passive Active: you develop your own antibodies after exposure to the infection + vaccination (artificial) + after an infection (natural) Passive: you gain your antibodies from your mother (natural) or serum medication (artificial)
65
What are some protective neutralization outcomes for host of antibody
1. Neutralization 2. Antibodies prevent attachment to host cells (attaching on flagella) 3.clumping antigens -> 1 mouthful of phagocytic ell 4. IgG antibodies have effect similar to C3b complement protein, facilitiating attachhment of phagocytic cell 5. Binding of Ab triggers complement cascade -> complement protein attaches to Fc regions triggering cascade -> leads to inflmmatory resposne and production of opson C3b 6. multiple IgG moleucles trigger descruction by natural killer cells via atachment to Fc region
65
What are the neutralization reactions via antibodies that lead to destruction of antidgens (adaptive immunity)
Usually: dimeric exotoxins produced by pathogen damange the host cell Neutralization by antiboy: binds to the exotoxins and leaves the cell undamanged Neutralization of a virus: antibodies to virus bind to the virus and leave the cell uninfected

BIOC17 Lectures (13 decks)

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