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Block 2 Flashcards

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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
what is the function of pore formation used by bacteria
create a hole in the cell membrane to cause lysis of the cell and nutrient release
26
how can you identify a pore forming microbe based on it's name
ends in -lysin
27
what does "O" at the end of a microbe name indicate
it is oxygen liable (doesn't do well in presence of oxygen)
28
what are 3 results of low quantities of proinflammatory cytokine release, leading to local inflammation
macrophage/neutrophil activation increase cell leakiness complement activation
29
what are 3 results of moderate quantities of proinflammatory cytokine release, leading to systemic effects
fever complement components released from liver leukocyte release from bone marrow
30
what are the results of high quantities of proinflammatory cytokine release, leading to septic shock
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
what are the 2 main cytokines released into the bloodstream that cause proinflammation
IL-1 TNF
32
what are the main class of endotoxins
PAMPs
33
what is the effect of activity of a superantigen
permanently bind MHC-II and T cell receptors, resulting in continuous production of proinflammatory cytokines (IL-1 and TNF)
34
in regards to symptom location, what is the importance of the B subunit of AB toxins released by bacteria
where B subunit binds is where the symptoms are seen
35
what are the 3 possible effects of the A subunit of AB toxin release by bacteria
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
are staphylococcus gram + and gram -
gram +
37
are staphylococcus motile or non-motile
non-motile
38
are staphylococcus catalase + or -
+
39
what is important about staphylococcus in regards to antibiotic resistance
most are resistant, especially to 1st generation beta-lactams
40
what are 3 main ways to differential staphylococcus aureus from other staphylococcus bacteria
they perform beta hemolysis ferment mannitol clot blood plasma (make coagulase)
41
how do staphylococcus aureus appear on a gram stain
dark purple due to thick peptidoglycan and LTA
42
what virulence factors does staphylococcus aureus have
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
most staphylococcus aureus virulence genes are under the control of what, what is the effect
accessory gene regulator operon increased expression at high population densities
44
are many staphylococcus aureus infections endogenous or exogenous (PAMP)
endogenous (many healthy adults carry this bacteria in their nares at any time with no issues)
45
what are the 2 main routes of exposure to microbes that lead to pneumonia
aspiration (inhalation) hematogenous (bacterial blood infection got to lungs)
46
how does tampon usage lead to toxic shock syndrome
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
what virulence factor is used by staphylococcus that leads to food poisoning
superantigen release
48
how does staphylococcus lead to food poisoning
in an aerobic, lipid rich environment, enterotoxins A and B are expressed, causing release of superantigens
49
what is the difference between intoxication and infection in regards to food poisoning
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
what bacteria is the main cause of septic arthritis in children
staphylococcus aureus
51
what do MRSA (methicillin resistant staphylococcus aureus) have, besides beta lactamases, that allows them to be resistant to bacteria
mecA gene that causes a mutation in their transpeptidase gene
52
what are the 2 main bacteria that cause septic endocarditis on native heart valves
staphylococcus aureus and staphylococcus lugdunensis
53
what is the main bacteria that leads to endocarditis and joint infections in patients with prosthetic valves/joints
staphylococcus epidermidis
54
is staphylococcus epidermidis coagulase positive or negative
negative
55
what is the main virulence factor of staphylococcus epidermidis that allow it to adhere to prosthetic surfaces
biofilm production
56
what bacteria is the maincause of cystitis (UTI)
staphylococcus saprophyticus
57
staphylococcus epidermidis and saprophyticus are __ hemolytic (alpha, beta, or gamma) and coagulase ___ (positive or negative_
gamma negative
58
how to differentiate staphylococcus epidermidis from staphylococcus saprophyticus
epidermidis is killed by novobiocin saprophyticus is resistant and urase positive
59
how to differentiate staphylococcus lugdunensis from other staphylococcus (3 ways)
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
what are features of streptococci (6)
gram + catalase negative non-motile usually have polysaccharide capsule usually are capnophiles susceptible to most antibiotics
61
how to differentiate streptococcus pyrogenes (group A strep) from streptococcus agalacitae (group B strep)
group A- bacitracin susceptible, PYR test positive group B- bacitracin resistant, PRY test negative
62
what are the 7 virulence factors of streptococcus pyrogenes
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
how does M protein of streptococcus pyrogenes act as a virulence factor
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
what are 3 ways in which streptococcus pyrogenes can evade our immune system
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
in children, a sore throat is often due to infection with what bacteria
streptococcus pyrogenes
66
with a throat swab test, what is tested for in regards to streptococcus pyrogenes
group A carbohydrate streptolysin O
67
what are 2 ways to confirm infection by streptococcus pyrogenes
throat swab gram stain
68
scarlet fever is a possible result of infection by what bacteria
streptococcus pyrogenes from phage-infected Spe (superantigen) producing strains
69
what are the 5 main symptoms of scarlet fever
pastia lines red "slapped cheek" marks desquamation (sloughing) or digits strawberry tongue (sloughing of skin of tongue) erythematous patchy rash on body
70
what is the relationship of evolutionary medicine to microbe activity
microbes evolve to become more benign so they don't kill the host, allowing for spread

IDR (3 decks)

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