Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
50 Cards in this Set
- Front
- Back
|
what should you do if you have a positive blood culture
|
repeat to make sure there was no contamination
|
|
|
normal protozoan flora
|
Enatmoeba coli
|
|
|
Benefits of normal flora
|
produce needed nutrients, vitamins
benefit digestion compete for resources with pathogens antibacterial effect stimulate immune system |
|
|
disadvantages of normal flora
|
can increase infection risk
can be opportunists transform chemicals into carcinogens (cyclamate --> cyclohexamine) bladder carcinogen |
|
|
primary bacteremia
|
minor trauma such as toothbrushing and defecation
|
|
|
secondary bacteremia
|
localized infection shedding organism into the blood
|
|
|
when is sepsis considered
|
when there is evidence of inflammation - systemic inflammatory response syndrome (SIRS)
|
|
|
potent virulence factor that causes inflammation in low numbers
|
lipopolysaccharide
|
|
|
tropism
|
predilection an organism has for a particular tissue
|
|
|
primary tropism
|
specific receptors or mechanisms that allow a microbe to actively invade a specific tissue
|
|
|
secondary tropism
|
ability of an organism to infect a given tissue by happenstance when environmental factors are present: temperature, oxygen saturation, nutritional microrequirements
|
|
|
examples of secondary tropism and locations
|
tuberculosis - upper lobe
kingella - epiphysial plate |
|
|
what causes many of the symptoms of shock
|
immune response
|
|
|
what is needed for CD14 to be able to bind LPS
|
LPS binding protein
|
|
|
what is the strongest activator of TLR 4
|
hexacyl lipid A
|
|
|
what competes with LPS binding protein and CD14
|
bacterial permeability-increasing protein
|
|
|
the relative concentration between what two proteins control the magnitude of the inflammatory response
|
LPS binding protien
bacterial permeability-increasing protein |
|
|
what does gram positive peptidoglycan bind to
|
soluble form of CD14 and TLR2
|
|
|
cytokines responsible for uncontrolled inflammation leading to septic shock
|
TNF-a, IL-1, 2, 6
|
|
|
which cytokines are responsible for underactive immune response
|
IL-4, 10, 13
|
|
|
what happens eventually with an underactive immune response
|
usually leads to superinfections within a few days
|
|
|
organisms responsible for sepsis in adults
|
neisseria meningitidis
strep pneumoniae staph aureus |
|
|
organisms responsible for sepsis in asplenism
|
strep pneumoniae
haemonphilus influenzae neisseria meningitidis |
|
|
organisms responsible for sepsis in the elderly
|
strep pneumoniae
haemophilus influenza listeria monocytogenes |
|
|
organisms responsible for sepsis in neonates
|
E. Coli
Group B strep Listeria monocytogenes |
|
|
organisms responsible for sepsis in infants prior to immunization and after immunization
|
prior - strep pneumoniae and haemophilus influenzae
after - neisseria meningitis |
|
|
toxic shock
|
shock that is mediated by toxins stimulating the immune response often without bacteremia present
|
|
|
organisms responsible for toxic shock
|
staph aureus
strep pyogenes |
|
|
3 exotoxins that are superantigens from staph aureus
|
TSST-1
Staphylococcal entertoxins B and C |
|
|
2 exotoxins secreted by streptococcus pyogenes
|
streptococcal pyogenic exotoxins A and C
|
|
|
what must you have to get toxic shock syndrome
|
staph aureus colonization with a superantigen gene containing a strain that you do not make antibodies to
|
|
|
causitive agent for toxic shock syndrome
|
staph aureus
|
|
|
what increases the risk for the exotoxin from staph aureus to be expressed
|
increased oxygen
decreased magnesium |
|
|
what three ways can tampon usage increase the risk that TSST-1 gene be expressed
|
using tampons for longer than 8 hours
superabsorbent tampons Magnesium sequestering tampons |
|
|
what is the mechanism of superantigens
|
non-specifically activates T cells without antigen being present
|
|
|
what is the result of superantigen T cell activation
|
massive cytokine release: fever, vomiting, rash, shock, renal failure, DIC, ARDS
|
|
|
do you have protective antigens produce from superantigen activation
|
NO, normal antigen presentation and blast cell activation is dysfunctional, patients are at risk of repeat infections
|
|
|
what happens to most of the T cells from superantigen activation
|
anergy - die
|
|
|
causitive agent for streptococcal toxic-shock-like syndrome
|
strep pyogenes
strep pnuemoniae if no spleen |
|
|
two organisms responsible for pneumoniae presenting with shock
|
strep pyogenes
strep pneumoniae (no spleen) |
|
|
source of streptococcal toxic shock like syndrome
|
pneumoniae or deep seated infection
|
|
|
what is the different between TSS and STSS
|
STSS has rash less commonly, usually results in bacteremia, and strep pyogenes or pneumoniae cause the shock
|
|
|
inhibits protein production used against superantigens
|
clindamycin and erythromycin
|
|
|
how do clindamycin and erythromycin work
|
block ribosome protein production
|
|
|
when should clindamycin be given before other antibiotics
|
20 minutes, because don't want to release more exotoxin when break cell wall with other antibiotics
|
|
|
antibiotic used for gram negative sepsis
|
cephalosporin
|
|
|
what produces 50% of needed vitamin K
|
gram negative enterics in the gut - such as E. coli
|
|
|
what is somewhat protective against strep pneumoniae
|
antibodies against normal skin flora - strep mitis and sanguis
|
|
|
two examples of infections that almost always cause bacteremia
|
endocarditis
osteomyelitis |
|
|
examples of organisms without hexacyl lipid A
|
Yersinia
Francisella Vibrio Pseudomonas |
