MID Ia Flashcards
what percent of bugs can be cultured?
1.00%
DNA hybridization (species), 16S rRNA sequencing (for PCR primers, builds phylogenetic trees)
genotyping/phylogenetic
pulsed field gel electrophoresis, restriction fragment length polymorphism
molecular subtyping
thick peptidoglycan layer, purple
Gram +
thin peptidoglycan layer, red
Gram -
intracellular bacteria, won’t stain
chlamydia, rickettsia
really small, won’t stain
mycoplasma, legionella, helicobacter
acid fast (mycolic acid repels CV+ crystal violet ions) won’t stain
mycobacteria (TB) nocardia
have no outer membrane, make spores
gram positive
have outer membrane with LPS, no spores
gram negative
precursor made in cytoplasm, transferred to membrane pivot lipid (bactoprenol) via nylcoetide, chains crosslinked via transpepsidases
peptidoglycan synthesis
blood, bladder, CNS, lower respiratory tract, sinuses
normally sterile
typical exogenous bacteria: in water
legionella, cholera
typical exogenous bacteria: air/fomites
TB, anthrax
typical exogenous bacteria: food
salmonella, e. coli
typical exogenous bacteria: insects/animals
borrelia, rickettsia
do bacteria have recessive traits?
no, they are haploid
conjugation is mostly performed by
gram positives
F+ containing plasmid that only
sends unidirectionally
CTX phage, cholerae toxin gene product, cholera
vibrio cholerae bacteria
lamba phage, shigalike toxin gene product, hemorrhagic diarrhea
E. coli bacteria
clostridial phage, botulinum toxin, botulism food poisoning
clostridium botulinum
corynephage beta, diphtheria toxin, diphtheria
corynebacterium diphtheria
T12 phage, erythrogenic toxins, scarlet fever
strep pyogenes
direct binder of TLR-5 and cmacrophages on outside, inflammasome on the inside. Increases virulence
flagella. Can be modified to not bind TLR
cleaves pro-caspase 1, leading to inflammation, and (perhaps) apoptosis
inflammasome
upregulates Nf-kB via TLR-4, different TLR-4 polymorphisms lead to different degrees of response
LPS
cause rho/ras GTPase cascades that alter membrane permeability and allow invasion
type III secretory system (injectosome)
close binding of many bacteria and laying down extracellular matrix
biofilm
common biofilm on catheters
pseudomonas
common biofilm on heart valves
s.epidermidis
staph is gram
positive cocci in clusters
staph grows in this shape
in clusters
this virulence factor in staph binds Fc-IgG, inhibiting complement activation and phagocytosis
protein A
staph commonly colonizes
the nose
causes inflammatory disease: skin infection, organ abscesses, pneumona (after influenza virus) endocarditis, osteomyelitis
staph
TSS, scalded skin syndrome, rapid onset food poisoning
Toxin-mediated disease from staph
resistant to methicillin and nafcillin because of altered penicillin binding protein
MRSA
due to superantigen that binds MHCII and T-cell receptor, results in polyclonal T cell activation: fever, vomiting, desquamation, shock, organ failure
TSS
due to ingestion of pre-formed toxin, short incubation (2-6 hours), enterotoxin in heat stable, not destroyed by cooking
S. aureus food poisoning
all staph makes ____, bad staph (aureus) makes ____as well
catalase, coagulase and toxins
infects prosethetic devices and IV catheters with biofilm, contaminates cultures
s. epidermidis
s. epidermidis is sensitive to
novobiocin
second most common cause of uncomplicated UTI in women
s. saphrophyticus