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IDR > Block 2 > Flashcards

Block 2 Flashcards

1
Q

what is the function of the spleen in regards to bacterial protection

A

make IgM against encapsulated bacteria

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2
Q

what type of vaccines are given to people with splenectomy

A

protein conjugated, anti-capsular

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3
Q

what are the 3 vaccines required by healthcare providers

A

hep B
MMR
influenza

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4
Q

what types of vaccine form is given to babies after 1 year

A

live attenuated

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5
Q

what type of vaccine type are given after 1.5 years

A

killed or subunut

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6
Q

what are 2 ways in which bacteria can cause disease

A

infect a normally sterile site
disrupt our own cells

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7
Q

what are adhesins

A

proteins on the surface of bacteria that allow bacteria to enter the cell

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8
Q

what are leukocidins present on bacteria

A

proteins that kill WBC

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9
Q

why is the change of a Th1 to Th2 response not beneficially to people with bacteria evading the immune system

A

Th1 involves killing by macrophages
Th2 would only lead to an antibody production which wouldn’t be helpful to kill off the bacteria

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10
Q

virulence genes are often a result of what

A

lysogenic conversion

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11
Q

what are 3 characteristics of virulence genes

A

high CG content
upregulated by increased temperature/population density
palindromic sequences

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12
Q

adhesion on bacteria are located on pili. what are pili

A

flexible extensions through the cell envelope of gram negative bacteria

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13
Q

when a bacteria binds to the cell surface using adhesins, what are 5 options the bacteria can take

A

biofilm formation
enter cell, proliferate in endosome
enter cell, proliferate in cytoplasm
transcytosis to other side of cell
paracytosis between cells

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14
Q

what is the main function of a capsule on bacteria

A

avoid phagocytosis

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15
Q

how do capsules provide protection against adaptive immune response

A

carbohydrates that make up the capsule are poorly antigenic. IgM is made against the carbohydrates but IgM don’t make memory and are not good at opsonization

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16
Q

what is the main source of DNA transfer in encapsulated bacteria

A

natural transformation
*DNA is taken up from the environment if the bacteria has competent components on it’s capsule. RecA/recombinase is used to add the DNA into its own chromosome

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17
Q

are biofilms and capsules made by gram -, gram +, or both

A

both

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18
Q

when are biofilms produced

A

in high bacterial population density when there is a high concentration of autoinducer. The autoinducer can then bind to the autoinducer receptor, causing expression of biofilm genes, leadign to biofilm production

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19
Q

how do some bacterial work against IgA

A

they cleave IgA

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20
Q

how can bacteria affect complement

A

delete complement (C3 component) or bind to C3b preventing opsonization

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21
Q

what are undulant symptoms

A

symptoms that get better and worse without full resolution

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22
Q

what are undulant symptoms usually a result of

A

serotype switching (antigenic variation)

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23
Q

what is immune mimicry used by bacteria

A

microbes have antigens (epitopes) similar to our own, so antibodies aren’t made against them

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24
Q

what is the result of long term immune mimicry

A

production of antibodies that damage our own cells and tissues (type II and IV HSR)

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25
Q

what is the function of pore formation used by bacteria

A

create a hole in the cell membrane to cause lysis of the cell and nutrient release

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26
Q

how can you identify a pore forming microbe based on it’s name

A

ends in -lysin

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27
Q

what does “O” at the end of a microbe name indicate

A

it is oxygen liable (doesn’t do well in presence of oxygen)

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28
Q

what are 3 results of low quantities of proinflammatory cytokine release, leading to local inflammation

A

macrophage/neutrophil activation
increase cell leakiness
complement activation

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29
Q

what are 3 results of moderate quantities of proinflammatory cytokine release, leading to systemic effects

A

fever
complement components released from liver
leukocyte release from bone marrow

30
Q

what are the results of high quantities of proinflammatory cytokine release, leading to septic shock

A

increase in vessel leakiness leads to low cardiac output, increase pulse, increase respiration rate
low peripheral resistance with vessel dilation leads to low BP, low tissue oxidation
dissembled intravascular coagulopathy (capillary blood clots)
alveoli fill with fluid, capillaries fill with clots in lungs= acute respiratory distress syndrome

31
Q

what are the 2 main cytokines released into the bloodstream that cause proinflammation

A

IL-1
TNF

32
Q

what are the main class of endotoxins

A

PAMPs

33
Q

what is the effect of activity of a superantigen

A

permanently bind MHC-II and T cell receptors, resulting in continuous production of proinflammatory cytokines (IL-1 and TNF)

34
Q

in regards to symptom location, what is the importance of the B subunit of AB toxins released by bacteria

A

where B subunit binds is where the symptoms are seen

35
Q

what are the 3 possible effects of the A subunit of AB toxin release by bacteria

A
  1. stop protein synthesis by binding to EF2 in eukaryotic ribosome (kills cells, freezing them in their location, produces grey membrane)
  2. increase cAMP levels (results in pumping out NaCl which causes H2O to leave the cell)
  3. disrupt cell-cell signaling
36
Q

are staphylococcus gram + and gram -

A

gram +

37
Q

are staphylococcus motile or non-motile

A

non-motile

38
Q

are staphylococcus catalase + or -

A

+

39
Q

what is important about staphylococcus in regards to antibiotic resistance

A

most are resistant, especially to 1st generation beta-lactams

40
Q

what are 3 main ways to differential staphylococcus aureus from other staphylococcus bacteria

A

they perform beta hemolysis
ferment mannitol
clot blood plasma (make coagulase)

41
Q

how do staphylococcus aureus appear on a gram stain

A

dark purple due to thick peptidoglycan and LTA

42
Q

what virulence factors does staphylococcus aureus have

A

coagulase secretion and bound
surface bound proteins for binding (MSCRAMMS)
surface protein A for immune evasion
superantigens
alpha toxin for beta hemolysis
leukocidin for WBC killing
can survive inside neutrophils
various capsule types

43
Q

most staphylococcus aureus virulence genes are under the control of what, what is the effect

A

accessory gene regulator operon
increased expression at high population densities

44
Q

are many staphylococcus aureus infections endogenous or exogenous (PAMP)

A

endogenous (many healthy adults carry this bacteria in their nares at any time with no issues)

45
Q

what are the 2 main routes of exposure to microbes that lead to pneumonia

A

aspiration (inhalation)
hematogenous (bacterial blood infection got to lungs)

46
Q

how does tampon usage lead to toxic shock syndrome

A

the vagina is normally an anaerobic environment. tampons make the vagina an aerobic environment, allowing staphylococcus to grow. once a high population density is reached, the agr operon is turned on. toxic shock syndrome toxin crosses the vagina wall and enters the bloodstream, acting as a superantigen. there will now be continuous release of TNF and IL-1, leading to overall systemic effects including increased vessel diameter and leakiness, low BP, fever, etc.

47
Q

what virulence factor is used by staphylococcus that leads to food poisoning

A

superantigen release

48
Q

how does staphylococcus lead to food poisoning

A

in an aerobic, lipid rich environment, enterotoxins A and B are expressed, causing release of superantigens

49
Q

what is the difference between intoxication and infection in regards to food poisoning

A

intoxication- toxin was already there at the time of infection/ingestion, rapid onset of symptoms, mostly vomiting, no antibiotic use

infection- growth of bacteria in the intestines before symptom onset, >24 hrs before symptom onset, mostly diarrhea and vomiting, may be treated with antibiotics

50
Q

what bacteria is the main cause of septic arthritis in children

A

staphylococcus aureus

51
Q

what do MRSA (methicillin resistant staphylococcus aureus) have, besides beta lactamases, that allows them to be resistant to bacteria

A

mecA gene that causes a mutation in their transpeptidase gene

52
Q

what are the 2 main bacteria that cause septic endocarditis on native heart valves

A

staphylococcus aureus and staphylococcus lugdunensis

53
Q

what is the main bacteria that leads to endocarditis and joint infections in patients with prosthetic valves/joints

A

staphylococcus epidermidis

54
Q

is staphylococcus epidermidis coagulase positive or negative

A

negative

55
Q

what is the main virulence factor of staphylococcus epidermidis that allow it to adhere to prosthetic surfaces

A

biofilm production

56
Q

what bacteria is the maincause of cystitis (UTI)

A

staphylococcus saprophyticus

57
Q

staphylococcus epidermidis and saprophyticus are __ hemolytic (alpha, beta, or gamma) and coagulase ___ (positive or negative_

A

gamma
negative

58
Q

how to differentiate staphylococcus epidermidis from staphylococcus saprophyticus

A

epidermidis is killed by novobiocin
saprophyticus is resistant and urase positive

59
Q

how to differentiate staphylococcus lugdunensis from other staphylococcus (3 ways)

A

beta hemolytic
only slide coagulase positive (doesn’t make enough coagulase to clot plasma in a tube)
CAMP positive (greater beta hemolysis when grown next to another beta hemolytic)

60
Q

what are features of streptococci (6)

A

gram +
catalase negative
non-motile
usually have polysaccharide capsule
usually are capnophiles
susceptible to most antibiotics

61
Q

how to differentiate streptococcus pyrogenes (group A strep) from streptococcus agalacitae (group B strep)

A

group A- bacitracin susceptible, PYR test positive
group B- bacitracin resistant, PRY test negative

62
Q

what are the 7 virulence factors of streptococcus pyrogenes

A

hyaluronic acid capsule (immune mimicry)
M protein (immune mimicry+blocks C3)
F protein (adhesin)
DNase B (destroys neutrophils nets to escape)
streptokinase (dissolves fibrin clots to spread)
Spe A, B, and C (superantigens)
streptolysin O and S (hemolysis)

63
Q

how does M protein of streptococcus pyrogenes act as a virulence factor

A

it’s epitope is very similar to human cardiac myosin epitope so antibodies elicited against it can bind to heart tissue and lead to antibody dependent cellular cytotoxicity of heart cells

64
Q

what are 3 ways in which streptococcus pyrogenes can evade our immune system

A

contains a hyaluronic capsule–>type III HSR
M protein binding C3b and antibodies in alternate confirmations
destroying C5a leading to decrease in neutrophil activity

65
Q

in children, a sore throat is often due to infection with what bacteria

A

streptococcus pyrogenes

66
Q

with a throat swab test, what is tested for in regards to streptococcus pyrogenes

A

group A carbohydrate
streptolysin O

67
Q

what are 2 ways to confirm infection by streptococcus pyrogenes

A

throat swab
gram stain

68
Q

scarlet fever is a possible result of infection by what bacteria

A

streptococcus pyrogenes from phage-infected Spe (superantigen) producing strains

69
Q

what are the 5 main symptoms of scarlet fever

A

pastia lines
red “slapped cheek” marks
desquamation (sloughing) or digits
strawberry tongue (sloughing of skin of tongue)
erythematous patchy rash on body

70
Q

what is the relationship of evolutionary medicine to microbe activity

A

microbes evolve to become more benign so they don’t kill the host, allowing for spread

IDR (3 decks)

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