Block 2 Flashcards
what is the function of the spleen in regards to bacterial protection
make IgM against encapsulated bacteria
what type of vaccines are given to people with splenectomy
protein conjugated, anti-capsular
what are the 3 vaccines required by healthcare providers
hep B
MMR
influenza
what types of vaccine form is given to babies after 1 year
live attenuated
what type of vaccine type are given after 1.5 years
killed or subunut
what are 2 ways in which bacteria can cause disease
infect a normally sterile site
disrupt our own cells
what are adhesins
proteins on the surface of bacteria that allow bacteria to enter the cell
what are leukocidins present on bacteria
proteins that kill WBC
why is the change of a Th1 to Th2 response not beneficially to people with bacteria evading the immune system
Th1 involves killing by macrophages
Th2 would only lead to an antibody production which wouldn’t be helpful to kill off the bacteria
virulence genes are often a result of what
lysogenic conversion
what are 3 characteristics of virulence genes
high CG content
upregulated by increased temperature/population density
palindromic sequences
adhesion on bacteria are located on pili. what are pili
flexible extensions through the cell envelope of gram negative bacteria
when a bacteria binds to the cell surface using adhesins, what are 5 options the bacteria can take
biofilm formation
enter cell, proliferate in endosome
enter cell, proliferate in cytoplasm
transcytosis to other side of cell
paracytosis between cells
what is the main function of a capsule on bacteria
avoid phagocytosis
how do capsules provide protection against adaptive immune response
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
what is the main source of DNA transfer in encapsulated bacteria
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
are biofilms and capsules made by gram -, gram +, or both
both
when are biofilms produced
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
how do some bacterial work against IgA
they cleave IgA
how can bacteria affect complement
delete complement (C3 component) or bind to C3b preventing opsonization
what are undulant symptoms
symptoms that get better and worse without full resolution
what are undulant symptoms usually a result of
serotype switching (antigenic variation)
what is immune mimicry used by bacteria
microbes have antigens (epitopes) similar to our own, so antibodies aren’t made against them
what is the result of long term immune mimicry
production of antibodies that damage our own cells and tissues (type II and IV HSR)
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
how can you identify a pore forming microbe based on it’s name
ends in -lysin
what does “O” at the end of a microbe name indicate
it is oxygen liable (doesn’t do well in presence of oxygen)
what are 3 results of low quantities of proinflammatory cytokine release, leading to local inflammation
macrophage/neutrophil activation
increase cell leakiness
complement activation
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
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
what are the 2 main cytokines released into the bloodstream that cause proinflammation
IL-1
TNF
what are the main class of endotoxins
PAMPs
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)
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
what are the 3 possible effects of the A subunit of AB toxin release by bacteria
- stop protein synthesis by binding to EF2 in eukaryotic ribosome (kills cells, freezing them in their location, produces grey membrane)
- increase cAMP levels (results in pumping out NaCl which causes H2O to leave the cell)
- disrupt cell-cell signaling
are staphylococcus gram + and gram -
gram +
are staphylococcus motile or non-motile
non-motile
are staphylococcus catalase + or -
+
what is important about staphylococcus in regards to antibiotic resistance
most are resistant, especially to 1st generation beta-lactams
what are 3 main ways to differential staphylococcus aureus from other staphylococcus bacteria
they perform beta hemolysis
ferment mannitol
clot blood plasma (make coagulase)
how do staphylococcus aureus appear on a gram stain
dark purple due to thick peptidoglycan and LTA
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
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
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)
what are the 2 main routes of exposure to microbes that lead to pneumonia
aspiration (inhalation)
hematogenous (bacterial blood infection got to lungs)
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.
what virulence factor is used by staphylococcus that leads to food poisoning
superantigen release
how does staphylococcus lead to food poisoning
in an aerobic, lipid rich environment, enterotoxins A and B are expressed, causing release of superantigens
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
what bacteria is the main cause of septic arthritis in children
staphylococcus aureus
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
what are the 2 main bacteria that cause septic endocarditis on native heart valves
staphylococcus aureus and staphylococcus lugdunensis
what is the main bacteria that leads to endocarditis and joint infections in patients with prosthetic valves/joints
staphylococcus epidermidis
is staphylococcus epidermidis coagulase positive or negative
negative
what is the main virulence factor of staphylococcus epidermidis that allow it to adhere to prosthetic surfaces
biofilm production
what bacteria is the maincause of cystitis (UTI)
staphylococcus saprophyticus
staphylococcus epidermidis and saprophyticus are __ hemolytic (alpha, beta, or gamma) and coagulase ___ (positive or negative_
gamma
negative
how to differentiate staphylococcus epidermidis from staphylococcus saprophyticus
epidermidis is killed by novobiocin
saprophyticus is resistant and urase positive
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)
what are features of streptococci (6)
gram +
catalase negative
non-motile
usually have polysaccharide capsule
usually are capnophiles
susceptible to most antibiotics
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
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)
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
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
in children, a sore throat is often due to infection with what bacteria
streptococcus pyrogenes
with a throat swab test, what is tested for in regards to streptococcus pyrogenes
group A carbohydrate
streptolysin O
what are 2 ways to confirm infection by streptococcus pyrogenes
throat swab
gram stain
scarlet fever is a possible result of infection by what bacteria
streptococcus pyrogenes from phage-infected Spe (superantigen) producing strains
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
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
