ID and LC Flashcards
describe the mneumonic for live attenuated vaccines
Music and lYRICSS are best enjoyed Live
M= MMR
Y= Yellow fever
R= Rotavirus
I= Influenza nasal
C= Chickpox (VZV)
S= Smallpox
S= Sabin polio virus
what does catalase distinguish between
catalase = positive makes bubbles in the presence of hydrogen peroxide
staph= catalase +
and
strep= catalase -
describe the mneumonic for oxidase + organisms
oxidase positive = changes the paper color (turns blue or pink with that black dot)
spell punch with a “v”
PVNCH
P= Pseudomonas
V= Vibrio
N= neisseria
C= Campylobacter
H= H pylori
what is the treatment for neisseria gonorrhea
ceftriaxone= 3rd generation cephalosporin = because theyre great for serious gram negative infections and neisseria is a gram negatvie diplococci
also give a macrolide or tetracycline =azithromycin or doxycycline for possible chlamydial coinfections
what does coagulase test distinguish between
coagulase positive test causes clumps/clots
different strains of staph
staph aureus is coag + (golden hemolytic… clumping factor= turns fibrinogen into fibrin to make a clump that is protective from phagocytosis)
the rest are coag -
(more than >90% of the time its a contaminant… but be wary if there is metal or plastic in the body… staph epidermidis)… coag neg= 31 + staph species, white, non hemolytic
describe alpha and beta hemolysis
alpha= partial hemoglobin reduction causes a green brown color without clearing
(strep pnu [optochin sens] and strep viridans [optochin resistant])
beta= complete lysis of RBCs causes a clearing around bacteria
(staph aureus [cat +], strep pyogens GAS [bacitracin sens], strep agalactia GBS [bacitracin resistant])
both are gram + cocci
gamma hemolysis is no hemolysis
what is the “danger hypothesis”
that our bodies recognize pathogens because they cause damage to us
PAMPs are now MAMPs (Microorganism) and DAMPs (Damage/Danger)
example- innate immune response to mitochondrial DNA or uric acid s/p trauma
what is the 5th sign of infection
- tumor
- rubor
- dolor
- calor
- loss of function (functio laesa)
Describe what grows and what you will see with different bacteria on McConkey agar
McConkey agar= lactose fermenters turn pink (ex- ecoli) non fermenters are colorless - contains bile salts - inhibits growth of gram + bugs
what is protein A
a virulence factor on staph aureus cell wall which binds Fc of IgG and prevents compliment activation
what are the two superantigens that cause shock
toxic shock syndrome toxin (TSST 1) = staph aureus
binds to MHC2 and TCR and causes an overwhelming release of IL1 and IL2… (presents as fever, rash, shock)
what are the toxins of staph aureus
Toxic shock syndrome toxin (TSST 1)= fever, rash, shock
exofoliative toxin A or B= scalded skin syndrome (proteases digest desmosome in the skin causing separation at the granular layer… causes bullae and sloughing, no scarring)… also called Ritter’s disease of the newborn or staph scarlet fever in older kids… bullous impetigo (most common bacterial skin infection in kids) is the localized version of scalded skin syndrome
heat stable enterotoxin = food poisoning
what is important about the MEC-A gene
it confers resistance to penicillins
it codes for PBP2A which decreases beta lactam’s ability to bind cell wall and inhibit formation
seen in MRSA
what is a positive D-test
when erythromycin is placed next to clindamycin and the clearing around clindamycin is blunted from the erythromycin
what happens is “erythromycin induced resistance to clindamycin”
due to the plasmid gene erm
thus you do not give a patient clindamycin if there was a positive D test
what is a furuncle
a boil
commonly caused by staph aureus
what is osteomyelitis
a bone abscess
what is chronic granulomatous disease
aka Bridges Good Syndrome or Quie Syndrome
x linked recessive inherited neutrophil defect
cells have problems making reactive oxygen species for killing (hydrogen peroxide)
what is Job’s syndrome
Hyper IgE, recurrent colds, rash
defect in neutrophil chemotaxis
AD (STAT3 mut…. affects JAK STAT pathway)
mneumonic: FATED F= Facies (coarse) A= cold Abscesses T= Teeth (primary teeth retained) E= increased IgE D= Dermatologic problems
Describe Toxic shock syndrome
macular erythema (widespread red rash that looks like a sunburn... later it peels on the palms and soles) acute high fever organ failure (kidneys and liver) confusion diarrhea low blood pressure muscle aches nausea and vomiting redness of facial mucosa seizures
TSST1 enterotoxin of staph aureus
genetically predisposed with no pre existing ab to the toxin
what are lancefield (A-U) groups
ways to identify different beta hemolytic strains of strep (complete lysis)
GAS pyogens [virulence factor is M proteins which has a neg charge to repel phagocytes)
Group B
Group C and G
Group D= now enterococci
what is the spreading patterns of staph vs strep
staph likes to localize (and build fibrin walls)
strep likes to spread out (they break down fibrin)
Describe the eagle effect
In cases of extremely high bacterial burden (such as with Group A Strep), bacteria may be in the stationary phase of growth. In this instance since no bacteria are actively replicating (presumably due to nutrient restriction) penicillin has no activity. This is why adding an antibiotic like clindamycin, which acts ribosomally, kills some of the bacterial and returns them to the log phase of growth
what are some ways to differentiate viral from bacterial sore throat
viral (2/3rd) =
cough
runny nose
bacterial=
tender lymph nodes
close contact
(biopsy = tonsillar #1, second best is posterior wall of pharynx… neg rapid test then do culture)
what are complications of strep pharyngitis
scarlet fever
toxic shock syndrome
ARF (3-6 weeks later, JONES criteria)
reactive arthritis (assume its a less severe ARF in high prevalence areas)
PSGN (glomerulonephritis) 2-4 weeks after
PANDAS (pediatric autoimmune neuropsychiatric disorders associated with strep)
if you suspect ARF or PSGN you can do strep serology (ASO or ADB- anti Dnase B)
