Block 2 quiz prep Flashcards
Staphylococcus aureus “GP’S CHange Fates”
Gram-positive & COPS (coagulase positive via protein A binding IgG),
Halotolerant (~9%NaCl) & tolerant to desiccation (low H2O meaning it can survive on fomites at ~50degrees celsius)
Catalase positive (Beta hemolysis)
Fasciculus (needs iron via RBC hemolysis)
enterotoxin/gastroenteritis (food poisoning)
Food= via s.aureus released enterotoxin (heat tolerant) acts as a superantigen stimulating macrophages & it causes non-bloody watery diarrhea and severe vomiting
Toxic shock syndrome toxin (TSST) “HOly Fucked DReaMs”
TSST= via STAPHYLOCOCCAL TOXIC SHOCK TOXIN TYPE 1 from s. aureus can be caused by prolonged tampon use or wound packing. TSST gets into the blood and acts as a superantigen which stimulates macrophages and helper t-cells to release cytokines (IL-1,2, & TNF)
TSST won’t show on a blood culture
Look for Hypotension, organ failure (3+), fever, diffuse macular rash
Scalded Skin Syndrome/Ritters/pemphigus neonatorum
S.aureus exotoxin acts as a protease and cleaves the desmoglein of desmosomes to separate the epithelium from the granular cell layer, causing blisters and large areas of skin to slough off
Look for; fever, serous fluid discharge, & large areas of sloughed-off skin
Impetigo
large bullae (fluid-filled blisters
Yellow/honey-crusted lesions caused by s. aureus (the color comes from the carotenoid pigment staphyloxathin s. aureus makes)
Folliculitis
Multiple small pustules on the chin and neck due to s. aureus
What drug helps differentiate s. epidermis & s. saprophyticus?
Novobiocin
s. epi = sensitive
s. sapro = resistant
Endocarditis
right-sided endo, subacute endo,
native valve endo, prostatic valve
& symptoms
aureus= Common in IV drug users, causing Right-sided endocarditis (COPS)
S.epi= makes biofilms that cause prostatic valve endocarditis (CONS)
1st s. pyogenes & 2nd s. aureus = native valve endo
Viridians Strepto (mutans) = usually from dental procedure/injury, where the bacteria feed on detrains/glucans (plaque/tartar), then seep into the blood and affect the heart
Look for; Osler’s nodes (tender lesions on fingers), Janeway lesions (non-tender lesions on palms), Splinter hemorrhages, hemorrhagic roth spots in eyes, glomerulonephritis, splenomegaly, and neurological symptoms, clubbing (long-term), & petechiae (embolic or vasculitis)
Necrotizing pneumonia
Due to s. aureus releasing leukocidins which form pores causing leukocytes to spill their cytokines
Causes; necrosis of lung tissue & inflamed fluid-filled lungs
Metastatic infections:
Hematogenous Osteomyelitis & Bacteremia
Osteo= 1st choice salmonella typhi (those with sickle cell anemia are predisposed with higher risk) 2nd choice s. aureus
Bacteremia= infection has moved to blood (usually manifests as a rash on skin)
How to diff Strep vs Staph TSST
Gram staining
gram + cocci in chains =strep
gram + cocci in clusters = staph
next use catalase
how to collect specimens based on conditions
osteomyelitis + endocarditis
Lesions/blisters/sore throat
food poisoning/enterotoxin
pneumonia
meningitis
OE= Blood
LBST= Sterile swab
FP= Vomitus, stool, the food
P= Broncho alveolar lavage (1st choice) or sputum (2nd choice)
A phage typing test (+) means
The isolate is susceptible and more related to the original organism
Penicillin resistance in S. aureus =________
Methicillin (MRSA) & Nafcillin (NRSA) resistant S. aureus = __________
VRSA resistant S. aureus =________
B-lactamase (treat with B-lactamase resistant B-lactone antibiotics ex. nafcillin, cloxacillin, cephalosporins, or vancomycin)
Altered PBP (penicillin-binding proteins) via mutated mecA gene making it produce PPP2A
(treat with vancomycin)
Bacterial
Transformation “TED” vs conjugation “CSF” vs Transduction “
Trans= bacterial takes up DNA material exogenously & incorporates it into its DNA (needs to be a close homolog)
Conju= (aka bacteria sex) an F+ plasmid with a sex pilus (male) attaches to an F- plasmid (female) to transfer DNA
Hfr= High-frequency replication conjugation is essentially the same thing, but DNA is being passed from chromosome to plasmid
Transduc= done via bacteriophages
general (Random + large DNA strands/plasmids)
specialized (specific + small DNA strands)
temperate phages (don’t lyse the host + specific restriction sites on chromosome)
virulent phage (do lyse the host)
S. aureus “My FASHIOn Sense”
Gram + in clusters
halotolerant & desiccation (low H2O) tolerant
Mannitol fermenting (diff mannitol-salt agar)
Causes: Impetigo, Scalded skin syndrome, Osteomyelitis (1st choice salmonella typhi + sickle cell anemia) (2nd choice s. aureus)
Transduction of C. diphtheria
yields lysogenic conversion to confer virulence to the bacteria via prophages & b-phages
Endocarditis symptoms “Ew GROSS Cum & Jizz”
& types:
Natural valve
Subacute
Right-sided + IV user
Prostatic valve
symptoms: Glomerular nephritis, roth spots in eyes, Osler’s lesions (tender fingers), Janeway’s lesions (non-tender palms), cardiac signs, splenomegaly, & splinter hemorrhage
NV= strep (75%) or staph (25%)
Right-sided/IV user = S. aureus
prostatic valve= S. epidermis
Subacute = viridian’s strep
Pseudomonas aeruginosa
grams report=
“GBP in ARe pOCket”
2 pigments & type of secretion =
Virulence factors
fomites (where its found x4)
conditions cause “FOOlS TEnd to Cry & BEG Pitifully”
Gram positive motile bacilli, Catalase +, Oxidase +,
Obligate/strict aerobe
2p=
pyocyanin (blue pus + grape smell) increases the ROS in cells to increase oxidative damage.
pyoverdine (green/fluorescein) acts as an iron chelator to bind and bring iron into p. aeruginosa & it indicates skin infections in burn patients under UV light.
VF=
Capsules + biofilm
Exotoxin A (tissue necrosis)
Endotoxin (causes sepsis and it targets ADP ribosylation of EF2 to stop DNA transcription & kill host cells)
Fomites:
water, surfaces, hands, catheters, ventilators (can survive anywhere, but it loves warmth & humidity)
Conditions:
Folliculitis ((Hot Tub folliculitis i.e. inf from water (self-limiting aka no treatment needed))
Ostitis externa (infected outer ear canal/aureus)
Osteochondritis/osteomyelitis from a puncture wound (usually in the foot & especially in diabetic mellitus type 2 patients)
Sepsis
Tricuspid valve Endocarditis (usually from IV drug abusers)
Conjunctivitis (contact lens wearers)
Ecthyma gangrenosum (infects burn/deep wounds and causes necrotizing fasciitis esp. in diabetics or immune compromised patients)
pneumoniae in patients with cystic fibrosis (have a glycocalyx/slime layer)
Which organism can survive harsh antiseptics like hexachlorophene?
What diagnostic tools are used to ID it?
How do you prevent it?
psuedomonas aeruginosa
A nutrient enriched Agar shows blue and green colouration
MacKonkeys shows colourless colonies (because they don’t ferment lactose)
TSI (Triple sugar iron) =shows a metallic sheen
Preventing it:
keeping their neutrophils above 500mew/liter
hand washing
taking extra care with burn patients
removing indwelling catheters
what’s the 1st choice of treatment for a pseudomonas aeruginosa infection?
“APPointment AGendA”
antipseudomonal penicillin (piperacillin/ticarcillin) + aminoglycoside (gentamycin/antimycin)
Aeromonas hydrophila:
grams report
what does it cause in general patients vs. immunocompromised?
describe its colony morphology on:
- MacConkey’s
- Sheep blood agar
- Oxidase
- Indole
What is the differential test to determine a. hydrophila vs vibrio? and which is S & R?
What is the selective media for A. hydrophila (CIN)
Gram negative bacilli
GP= cellulitis & necrotizing fasciitis
AID’s= Myonecrosis & eczema
McConkeys= red colonies that ferment lactose
SBA= Beta hemolysis (partial hemolysis)
Oxidase & Indole positive
Disc 0129 is the differential test: A. hydrophila is susceptible & vibrio is resistant
The selective media is cefsulodin, irgasan, & novobiocin)
plesiomonas shigelloides (tropical water + soil)
grams report
causes what condition in general patients? & what additional conditions in AID’s patients?
what is the differential test/tool for this species?
Gram negative motile bacilli &
oxidase positive, glucose fermenting, facultative anaerobes
in the general population it causes gastroenteritis (usually from eating bad oysters/shrimp)
In AID’s patients it also causes bacteremia & meningitidis
0129= susceptible/sensitive
Burkholderia pseudomallei (also called pseudomonas pseudomallei)
Grams report
what does it cause?
what’s the selective media used for this organism?
what are the virulence factors?
Where is it endemic?
gram negative, non-fastidious, motile, & aerobic bacilli that ferments sugars without acid
It causes: melioidosis
acute = 8-9 incubation period with fever, pain, cough + pleuritic chest pain (similar to pneumonia), sepsis, arthritis, cellulitis, osteomyelitis
Chronic= symptoms persist for ~2 months (and it seems a lot like TB)
VF= it makes exo & endo toxins
It’s endemic to Thailand & North Australia
