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341 Cards in this Set
- Front
- Back
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walking pneumonia
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mycoplasma pneumoneae
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chain
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strepto
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grape like
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reandom division staphylo
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packet of 8
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sarcina
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sterols
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in bac that don't have cell wall
mycoplasma has for rigidity/adherance |
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many virulence factors
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derive from cell wall
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peptidoglycan
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cell wall structure repeadable disacharide cross linked by tetrapeptides NAms
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nag, nam
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nacetylglutamate, nacetyl muramic acid
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PG clinical relevance
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make antimicrobials, secrete lysozyme, can be attacked by cell wall inhibitors
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lysozyme
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secrections, pmn granules, degrades glycan backbone of PG even if not growin bacteria used for cell lysis
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glycan
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backbone of PG
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Cell wall inhibitor
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inhibit PG synthesis in actively growing cells
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G- layers
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Plasma Memb, periplasmic space w/PG and liipoproteins), outer membrane
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G- outer membrane inner layer
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like plasma cell membrane
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G- outer membrane outer layer contents
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LPS, trimeric porins, lipoproteins
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G- LPS makeup
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O-outer antigen
Core polysaccharide lipid Anchor |
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O antigen
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G- outer antigen,
attachment site, inhibits phagocytosis, highly variable, immunogenic. |
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Lipid A
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g- embedded in outere membrane, pro-inflammatory, toxic b-cell mitogen, cytokine
SEPSIS |
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Core polysaccharide.
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G- connects lipid A to O ntigen
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LPS clinical relevance
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LPS- lipid binding protein or SCD14 to activate compliment
LPS-cell receptor- IL1/6 TNF- septic shock. |
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Trimeric Porins
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G- outer membrane
porin channel, non specific, small H20 molecules |
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Lipoprotein
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G-, most abundant protein, anchors outer membrane to PG layer
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G- periplasmic space
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b/t outer and inner cell membrane
Thin pg Layer Can concentrate hydrolases to increase resistance |
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G+ layer
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PM, Periplasm, PG layer
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G+ PG layer
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40+, retains crystal violet
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WtA
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provide elasticity and stability- anchored to PG
Attachment site, immunogenic |
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LTA
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lipoteichoic acid anchored to PM
elasticity/stability |
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Relevance of WTA/LTA
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increase G+ virulence
Adhesins Bind receptors causes endotoxin like rxn- clot, inflammation, MAC |
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Acid fast PG thickness
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intermediate
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Acid fast layers
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PM PPS PG MA
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Mycolic acid
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acid fast, ext to P, linked w/ PG via
Arrabinogalactan (long chain fatty acid) Waxy coat, decrease dessication, antibiotic resistance, decrease phagocytosis |
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Tetrameric porins
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Acid fast in mycolic acid layer.
Small hydrophilic molecules |
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Gram Stain
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thickness of PG
- Red Safranin- thin- washed + Purple primary, violet OH is the wash |
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Acid fast stain, aka-
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Zeihl Neilson- carbol fuschin + methylen blue
AF= red not AF= bluef |
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clinically relevant acid fast s
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M. Tuberculosis
M. Lerae. M. Avium Nocardia |
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3 cell external structures
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Pili
Flagella Glycokalyx K |
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Flagell and parts
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self assemblyl, helicla structure from flagellin with a hollow core
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H- antigen
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Has Flagella, motile
flagella proteins |
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Flagella hook
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attache filament to cell surface/basal body
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basal body
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anchors flagellin in cell wall and cell membrane
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monotrichous
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one flagella at end
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lophotricus
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more than 1 at one end
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amphitricous
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one or more at either end
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Peritrochous
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flagella along entire perimeter
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Pilli
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common or sex
proteinaceous, hair like structres w/ adhesins at tips_ adhere |
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fimbriae
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pili- pilin subunits- tips have adhesion
peritrichous arrangement movement adhesion |
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pili/fimbriae clinical importance
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inhibit colonization via pillar destruction
Type I bind mannose Type P bind galactos |
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Type I pilla/fimbriae
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bind mannose
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Type P pilla/fimbriae
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bind glactose
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Sex Pilli
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gram (-)
adhere 2 cells for genetic exchange |
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sex pili clinical relevance
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rapid resistance development
|
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K antigen
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glyokalyks polysaccharide
|
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glicocalyx capsule
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ridig w/ uniform thickness
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glicocalyx slime layer
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losse, non-uniform, diffuse
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glycoalyx clinical relevance
|
mutans- teeth
some speecies not pathogenic without glycokalyx |
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Quellung reaction
|
strep pneumoniea
detect capsule in respiratory infection anticapsular antibodies- swelling |
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bacterial 5 internal cell structures
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nucleoid region, plasmid, ribosomes, inclusions, endospores
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nucleoid region
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no membrane, primarily DNA, single circular chromosome
NO introns or histones |
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Plasmid
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extrahromosomal DNA,
ancillary informatioin, increase virulence, evasion of immune response, codes for antibiotics |
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ribosomes
|
70s (30, 50)
transcription/translation are coupled |
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30s inhibitors
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aminoglycosides
tetracyclines |
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50s inhibitors
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macrolides, cloraphenocol
|
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selective toxicity
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more toxic to organisms than hose
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inclusions
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in non-unit membrane, protein/lipid
stores excess C, E, P volutin, glycogen, PHb |
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Volutin granules
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inoganic phosphate
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glycogen granules
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polymer of alpha-D glucose
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PHB granules
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chans of beta hydroxybutyric acid
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endospores
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trigger in nutrient depletion, to survive months to years
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endospore content
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1 chromosome, few proteins and ribosomes, lots of Ca via diploconic acid, keratin coat
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calcium dipicolunate
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protects endospore from heat sensitivity
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SASPs
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small acid soluble spore protiens, protect from UV and dissociation
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endospore relevant bacteria
|
bacilis, clostridum (G+)
|
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beta lactam action
|
bind to transpeptide to prohibit synthesis of PG
Seeps through porins |
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how is bac growht measured
|
OD, biomass, CFU
|
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Optical Density
|
in culture- turbidity
All Viable and non-viable more dense= more culture |
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CFU
|
colony forming unit, dilute culture and plate
only VIABLE |
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Biomass
|
wash, dry, weigh
Dry weight = viable and non-viable |
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5 stages of bacterial growth
|
Lag, Log, late log, stationary, death
|
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|
lag phase
|
increase biomass
no divisioin time in phase depends on the nutrients avaialbel |
|
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log phase
|
exponential growth
division, slope=generation time of 1 cell |
|
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when are virulence factors made in growth phase?
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Log phase
pillae, fimbriae to move to more stuff |
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late log phase
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produce secondary metabolites; antibiotics/pigments
|
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what phase is color made in colony?
|
late log phase- is secondary metabolite
|
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stationary phase
|
death=division
NO growth, change in CFU or biomass Cell death renews resources |
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Death Phase
|
determined only by CFU
exponential death |
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5 bac requirements for growth
|
E, C12, Nutrients, GF, Environment
|
|
|
What re 5 environmental factors for growth
|
Temp
pH O2 CO2 H2O |
|
|
Respiration
|
E process with ETChai
|
|
|
aerobic respiration
|
O2= ETC terminal electron receptor
|
|
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Anaerobic respiration
|
O2 is NOT ETC terminal electron receptor
|
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Fermentation
|
anaerobic substrate level phosphrylation
ETC not used |
|
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4 fermentation products
|
lactate, butyrate, poropyonic acid, mixed acids
|
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Bacterial GFs/ categores
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specific organic compounds- small quanitities, cannot be synthesized
Purines/pyrimidines AAs Vitamins for coenzymes |
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Facultative definition
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has alternatives; capable of survival in a broad range
|
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Psychrophle
|
cold 5-12 degrees
|
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Psychrotrophs
|
Refrigerator f
0-35degrees |
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Mesophiles
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most bacteria 15-43
includes body temp |
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thermophiles
|
40-80 require increased T
|
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hyperthermophiles
|
65-115
hot springs, volcanoes |
|
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Hyperthermophile use
|
heat stable enzymes for biological studies
|
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Acidophile/ neutrophile. alkalophyle
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decreased pH, neutral, increased pH
|
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human bacterial preferences
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mesophiles/ neutrophiles
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capnophiles
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requires CO2
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Halphile
|
increased salts
|
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micro-corn
|
skin,oropharynx
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osmophile
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increased osmolarity/sugar solutions
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low-temp challene
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decreased enzyme activity/ fluidity
|
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increased temp challenges
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denaturing of proteins
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obligate anaerobes lac
|
SOD, Catalase, peroxidase,
H2O2- H2O, O2 |
|
|
obligate anaerobe/aerobe
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bottom/top
|
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Facultative anaerobe
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little at top but primariliy geographic
|
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micro aerophile
|
just below the surface
|
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aerotolerant anaerobe
|
uniform thruought
|
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mackonkey agar
|
peptone, bile salts, neutral red, lactose, crystal violet
|
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mackonkey differential
|
lactose/neutral red- pH indicator
ferment=pink |
|
|
mackonkie selectivity
|
crystal violet/ bile salts/ inhbit gram +
|
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defined media
|
chemically defined,
eliminate variablity narrow range |
|
|
complex media
|
undefined, broader range
|
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enrinched
|
complex & GF
|
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What material is used to grow fastidious organisms
|
Enriched media
|
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selective media
|
against unwanted organisms
inhibition |
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Differnetial
|
differentiates b/t organisms
visible no selection use |
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|
BSL1
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No diseases
|
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BSL2
|
Ingestion, subQ, mucous membrane
Diseases |
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BSL3
|
Serious to fatal- aerosol maybe
|
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BSL4
|
Fatal, Aerosol yes or unknown
|
|
|
hemaglutanin
|
Glycoprotein
spike on H.Flu attaches virus to host |
|
|
Neuraminadase
|
enzyme on Hemaglutanin that releases the virus from the host
|
|
|
Antigenic driftt
|
V, B
Yearly vaccines Genetic mutations- H&N chage |
|
|
Antigenic shift
|
V
genome mix b/t 2 viruses Pandemics |
|
|
2 antigenic switching mechanisms
|
phase variation, gene conversion
(not drift or shift) no changes other than what is being shown on cell |
|
|
Phase variation
|
ene remains on/off
Capsule/pillaae/ flagella, LPS can be seen in urine or serum |
|
|
phase variation regulated by
|
DNA recombinase- site specific altering
Alter the mRNA stabilit |
|
|
Gene Conversion
|
function remains the same but the eptiope changes, picasso vs monet
|
|
|
VSG
|
Variable surface Glycoproteins expressed ont he surface of cells
Plasodium infects RBCs to allow to go unseen by Immune system expressed on protozoan in african seeping sickness- titse trypsanoma |
|
|
PAI
|
distinct geneome segments for virulence factors
10-200k bp, inserts into tRNA direct repeat motifs on ends %G/C change not found on non-pathogen |
|
|
Homologous recombination
|
replacement of a section
|
|
|
Non-homologous recombination
|
insert section where needed
rec proteins not needed can result in null |
|
|
3 Moile genetic elements
|
insertion sequence,
PAI composit transposon (non-homologous recombination) |
|
|
3 gene transfer mechanisms
|
tranformation, conjugation, transduction
|
|
|
transformation
|
competent cells take up DNA
insert via homologous recomb |
|
|
conjugation
|
genetic exchange b/t same genera
1-way plasmid is ssDNA |
|
|
tools for conjugation
G- G+ |
- Sex pillus (not in ecoli- just approximate)
+ adhesion molecules on the pili approximate the cells |
|
|
ss to ds DNA in conjugation
|
recipient cell's rolling circle replication changes DNA
|
|
|
conjugate plasmid
|
contains genes to direct conjugatino and make pilis, start DNA synthsis
|
|
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R plasmid
|
one that contains resistance DNA
|
|
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F plasmid
|
fertility plasmid
inserts at IS or Ta inserts non-homologous |
|
|
high probability
|
one side f' plasmid and a part of the dna
|
|
|
low probability
|
one side f' plasmid, dna, other side f' plasmid
|
|
|
HFR
|
high frequency recobinant cell
one that completely transfered |
|
|
transformation
|
competent cells take up DNA
insert via homologous recomb |
|
|
conjugation
|
genetic exchange b/t same genera
1-way plasmid is ssDNA |
|
|
tools for conjugation
G- G+ |
- Sex pillus (not in ecoli- just approximate)
+ adhesion molecules on the pili approximate the cells |
|
|
ss to ds DNA in conjugation
|
recipient cell's rolling circle replication changes DNA
|
|
|
conjugate plasmid
|
contains genes to direct conjugatino and make pilis, start DNA synthsis
|
|
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R plasmid
|
one that contains resistance DNA
|
|
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F plasmid
|
fertility plasmid
inserts at IS or Ta inserts non-homologous |
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|
high probability
|
one side f' plasmid and a part of the dna
|
|
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low probability
|
one side f' plasmid, dna, other side f' plasmid
|
|
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HFR
|
high frequency recobinant cell
one that completely transfered |
|
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transduction definition
|
pick up bDNA, use it to incorporate into cell
geneti transfer mediated by bcteriophages |
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Lytic cycle 5 steps
|
phage attaches
inject vDNA, digest bDNA rapidly replicate caspid assemble cell lysis when full |
|
|
lysogenic cycle 5 steps
|
attach
core injected non-homo integration into bacterial chromosome latent prophage, host- lysogen stress activates latent prophage |
|
|
Defectie phage
|
Lytic cycle
baspsid filled with bacterial DNA no virus transmitted (general transduction) |
|
|
Specialized transductioin
|
lysogenic cycle
bDNA and viral DNA integrated into next host via bacteriophage |
|
|
clinical- lysogenic conversion
|
prophge carries virulent gene that causes pathogenic lysogen
vibrio cholera E coli shigela clostridium botulinum dyptheria strep pyogenes- scarlet fever |
|
|
process es that pass mobile genetic elements from one cell to another
|
insertion sequence
Tn composite transposon pathogenicity island |
|
|
insertion sequence
|
uses transposase to integrate REplicon only
has inverted repeats at the ends of the coding section |
|
|
Inverted repeates
|
Inverted repeats at the end of encoding sections
Pathogenicity island and Trnasposon |
|
|
Composite transposon
class 1 |
2 insertion sequences
transposase gene and other genes coding sequence and promoter Transfers from one position to another position in both eukaryotes nad prokaryotes |
|
|
normal microbiota composition
|
phages>bacteria>fungi/protists> archaea
|
|
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Interiginous
|
infolds of skin
|
|
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colonized
|
mouth, large Intestine, Anterior Urethra, Vagina
|
|
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Transient
|
briefly established but competing
respiratory tract, bladder, uterus |
|
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UTI
|
>10^5
|
|
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sterile body parts
|
body fluids, CSF, tissues, upper urinary (kidneys)
|
|
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Germ benefits
|
Vit: K, B12, B vits from lactate bacteria, prevent pathogenesis
antagonize other bact by killing/ inhibiting stimulate tissue development: pyers patches, etc. Cross-reactive abs to prevent infection: low grade rxn |
|
|
coagulase
|
convert prothrombin to staphylothrombin
Staphylothrombin converts soluble fibrinogen to insoluble finbrinogen creates avascular area protected from immune system |
|
|
alpha hemolysis
|
verdans
partial Hgb breakdown w/o lysis |
|
|
beta hemolyssi
|
complete lysis of RBC/Hgb
white with a clear halo |
|
|
gamma hemolysis
|
no breakdown
white colonies withouth halos |
|
|
L form
|
mycoplasma bacteria
no penecillin or cephalosporins |
|
|
symbiotic relationships generally are
|
stable and predictable
unless dieseased- then they aren't |
|
|
mutualism
|
both benefit (excludes pathogens)
|
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commensalissm
|
one organism benefits and the other is not harmed
|
|
|
parasitism
|
one benefits, one harmed
|
|
|
tropism
|
preference of tissue, invariably living in one place.
b/c of GF, specific receptors |
|
|
biofilm
|
community built on tissue or another biofil
for genetic exchange same genus- one member predominates biofilms protect membranes, if removed in immune replacement will cause probs |
|
|
Coleforms
|
pollute water
|
|
|
toal colleforms
|
EECK escherichia, enterobacter, citrobacter, klebsiella
|
|
|
Fecal coliforms
|
ECK
(minus enterobacter) |
|
|
Enterics
|
E. C. PESSKY S
|
|
|
pathogenic enterics
|
vibrio sp
campylobacter jejuni heliobactor pylori |
|
|
Antibiotic
|
chemical that inhibits or kills
|
|
|
Selective toxicity
|
more harmful to bacteria than to host
|
|
|
bacteriocidal/static
|
cidal-kill
static-inhibit growth |
|
|
when not to use bacteriostatics
|
immunocompromized or to treat bacteria in immunoprivileaged sites
|
|
|
narrow spectrum/drugs
|
few organisms
peniecilliln, macrolides, vancomycin |
|
|
broad spectrum/ drugs
|
use on onknown agent or superinfection
aminoglycosides/ 2nd/ 3rd cephalosporins, synhteici penecillins, quinalogs (?) |
|
|
B lactams mech/drugs
|
inhibit transptedidation, binds transpeptidase PBPs
Penicilins natural Synthetic Cephalosporins Carbenapin monobactams |
|
|
bacitracin Mechanism
|
Wall- interferes with dephosporylization of lipid barrier- inhibits pG movement through membranes (topical only)
|
|
|
Vancomycin mechanism
|
G+, Cocci, sits on NAM
Bacteriocidal causes red-man disease w/ histamien |
|
|
Cell wall synthesis inhibitors are all
|
cidal
|
|
|
distruption of membrane drugs are all
|
cidal
Polymyxin, daptomycin |
|
|
Polymyxin
|
G-
Detergent of cell membrane |
|
|
Daptomycin
|
rapid depolarization b/c rapid efflux of K- loss of potential
|
|
|
Drugs that inhibit protein synthesis are
|
all static except Gramin, aminoglycosids
|
|
|
Inhibit 30S
|
Aminoglycosides
Tetracylcines |
|
|
Aminoblycocides
|
30s Cidal
strepto, anika, gentami, neomy mycin |
|
|
tetracyclines
|
30s cidal- Not for children or preggos
tetra, doxyamine, declo "Cycln" |
|
|
Inhibit 50s (5)
|
chloraphenacol, streptogramin, macrolides, clyndamycin, inezolid
|
|
|
chloramphenacol
|
50s
typhoid RMSF, meningococcal |
|
|
macrolides mech
|
50s blocks initiation,translocation, elongation
|
|
|
macrolide drugs
|
mycin- Erythro, clantho, azithro, teletho
|
|
|
clindamycin
|
50s MRSA, Walking Pn., topical acne
causes psueddo membrane colitis |
|
|
Streptogramin
|
Combo drugs
individual=static, combo- cidal MRSA, E faeceum |
|
|
Linezolid
|
50s Prevent initiation complex
G+ vancomycin resistant |
|
|
Inhibit nucleic acid synthesis
|
All Cidal
Rifampin/mycin, floroquinalones, metronixaodole |
|
|
rifampin/amycin
|
G+ cocci, TB
inhibit DNA dependent DNA polymerase DIRECT |
|
|
Floroquinalones
|
synthetic, G-, gyrase,
cirpofloxacidn, norfloxacin |
|
|
metronidazole
|
Neucleic acid synthsis inhibitor
Anaerobes and protozans INDIRECT |
|
|
Acts as anti-metabolite
|
Sulfonamides, trimethoprim, Dapsone, Isonazid (only cidal one)
|
|
|
trimethoprim
|
anti-metabolite
pterydine part of folic acid- doesn't make DIhydrofolate |
|
|
Sulfonamides
|
anti-metabolite
PABA mocker via direct inhibition blocks dihydropteroate NO TETRAhydrofolate |
|
|
Dopesone
|
anti-metabolite, ONLY CIDAL
PABA indirect Leprosy and PCP |
|
|
Isonozid
|
anti-metabolite
analog of nicotinamide and pyridoxane= inhibits myolic acid pair for TB with rifamptin |
|
|
Antifungals
|
Polyenes
Azoles |
|
|
Polyenes
|
antifungals
nystatin, ampotercin |
|
|
Nystatin
|
polyene antifungal
join ergosterol to cause leaks oral candiasis |
|
|
Ampotercin
|
Polyene antifungal
joins ergosterol to cause leaks TOXIC IV for systemic candiasis |
|
|
Azoles
|
Azole and terbinafine
miconazonel ,fluconazol, itraconazole |
|
|
Miconazole
|
azole antifungal
oral gel or cream G+ cocci and fungi |
|
|
Fluconazole
|
Azole antifungal
Yeasts, candida in HIV prophylaxis can take for long periods of time |
|
|
Itraconazole
|
Azole antifungal, toxic,
INhibits CYP450 synthesis of ergosterol aspergillus, fungus NOT meningitis |
|
|
Terbanifine
|
Azole antifungal
Allylamine blocks squalene epoxidase for dermatophyte topical and pill |
|
|
Echnocardia
|
antifungal
disrupts cell wall B- prohibits glucan in cell wall systemic candidaisis, aspargillus "penicillin of antifungal |
|
|
Most important step to decrease pathogens
|
wahs hands
change gloves/wash after every pt wast with >62% alcohol |
|
|
PPE
|
G
A M Eyewear |
|
|
Contact transmission precautions
|
glove, single pt room,
herpes, lice, MRSA, chickenpox |
|
|
droplet transmission precautions
|
~3ft, >5 micrometers
1pt room, may need mask/eyewear flu, pertussis, mumps, sars |
|
|
Airborne transission precautions
|
aerosols <5microns
wear respiratoryprotection, HEPA, 1pt room Mumps, sars, TB, |
|
|
standard vs universal precaution
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sttandard- protect pt and worker from infection
universal- decrease transmission of blood-borne pathogens |
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Sterilization
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destroys all mcirobial life
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Disinfection
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kills most microbes not all spores
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decontamination
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reduce microbes to a non-pathogenic level
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cleaning
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remove foreign material/debris
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Cleanliness grades
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sterilize> disinfect> decontaminate> clean
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Critical items
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Sterile tissues or vasulature
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Semi-critical items
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non-intact skin or mucus membranes
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non-critical
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no contact w/ mucous membranes or tissues
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physical microbe control
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heat, boil, pasturize, autoclave, filtration, radiation
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Boiling
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H2O- 1min
Instruments 20-30 min, 5 min kills most everything endospores not killed |
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Pasteurizing
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flash, decreases microbes, does not kill endospores
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autoclave
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heat and pressure eliminates spores
use indicators |
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filtration
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fluids that are not heat reisstant
Air-hepa removes particles andviruses |
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radiation
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UVC- 280-100nm- germicidal
penetrates packaging, sterilize gloves, syringes, food |
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Disinfectant vs antiseptic
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disinfect inanimate objects
ntiseptic-tissues |
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ideal biocide
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all good no bad
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high level disinfectant group
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all microorganisms, not all spores
critical heat-sens equipment |
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Intermediate leve disinfectant group
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kills myco, vegetative bacteria, most mycoses and fungi; Not spores
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low level disinfectant group
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kills vegitative bactera, some viruses, some fungi
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Prion tx
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standard procedures are not effectie against ryons
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Clean w/ OH
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denatures proteins
topicl does not kill spores |
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clean with aldehydes
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inactivate proteins and neucleic acids
chemical sterilization to heat sensitive equipment |
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clean with biguanides
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topical/oral antiseptics that disrupt cell membrane
doesn't kill mycobacterum or endospores |
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clean with halogens
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oxide proteins, damage DNA
Antiseptic, increased concentrations can kill pryons |
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Clean with heavy metals
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Silver nigrate
burns, infection in newborns |
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clean with oxides
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gas- chemical sterilization fo heat sensitive equipment
can explode |
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clean with peroxides
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oxide sylfhydril group, antiseptic and disinfectant
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Clean with Phenolics
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surface disinfecctant/ antiseptic, denature proteins
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Clean with quaternary amonia
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non-critical
floor cleaner, pre-moistened wipes |
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Narrow spectrum antibiotics
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older penicillins, vancomycin, macrolides
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Braod spectrum antibiotics
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aminoglycosides, secondary tertiary cephalosporins,quinalone, synthetic penicilins, tetracyclines, solfonamides
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Kills pseudomonas aruginosa
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anti-pseudomonal pinicillin
4 generation cephalosporin polymyxins |
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MRSA killers
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vancomycin, clindamycin, streptogramin
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Staph killers
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penicillinase resistant penicillins, vancomycin
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Bacteriostatics
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not for sick ppl
Tetracyclin, chloramphenoacol, macrolides, clindamycin, sulfa drugs, trimethoprim, dapsone |
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Anti malaria
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clindamycin
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TB
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rifamycins/isoniazid
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Resistant to all
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enterococcus facealis, mycobacterium tuberculosis
Psuedomonas aurginosa |
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leprosy
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dapsone
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systemic candidiasis
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amphotercin-polyene,
echinocandins |
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Aspergilluus
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Itraconaole, echinocandins
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BBB crossers
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thrid and fourth gen cephalosporins
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B lactamase resistagt
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penicliinase resistant penicillin, combination products, 3rd/4th gen cephalosporins
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Topicals
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Bacitracin, polymyxin, miconazole
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Pts allergic to B lactam antibiotics
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Vancomycin
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Vancomycin resistant bacteria
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Linezolid
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Prophylactic for HIV pts
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Fluconazole
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Daptomycin contraindications
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not for elderly, pneumonia b/c cleared by surfactnat
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Tetracycline contraindications
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no children, no preggos
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Nystatin contraindicatoins
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polyene too toxic for systemic use
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Terbenafine contraindicatiosn
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hepatotoxicity in pill form.
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Colonization
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doesn't interfere with normal body function
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infection
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invasion of tissues of host and pathogen multiplication
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disease and pathogen relationship
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pathogen doesn't always have to be present
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intoxication
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abnormal function b/c of toxin action
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toxin examples
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S-aureus food poisoning
Botox- |
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pathogenicity
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genetic ability to cause disease
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Virulence
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degree of pathology caused by pathogen
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A pathogenic organism
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has varying degrees of virulence
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Koch procedure
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isolate-
innoculate another host same disease |
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PCR
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DNA apmplification,
RNA RTPCR |
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Disease signs
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objective
observer/clincian findings |
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disease symptoms
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subjective/sensed
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disease indicator
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sign +symptom
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pre- clinical inbubation
S/S Immune Response Innoculum Contagious |
S/S: No
Immune Response: not active Innoculum: infectious dose Contagious: not infectious |
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Prodromal warning
S/S Immune Response Innoculum Contagious |
S/S: some early
Immune Response> innate Innoculum: increasing Contagious: easily |
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Acute Disease state
S/S Immune Response Innoculum Contagious |
S/S: peaking
Immune Response: acquired Innoculum: level Contagious: highly |
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Decline disease state
S/S Immune Response Innoculum Contagious |
S/S: declining
Immune Response: reduced w/ abs present Innoculum:cleared/latent Contagious: communicable if carrier |
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Convalescent
S/S Immune Response Innoculum Contagious |
S/S: none
Immune Response: none Innoculum: cleared Contagious: no |
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Incubation means
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pathogen has entered portal
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prodromal means
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warning- some early signs of infection
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Decline- Alt Innoculation means
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innoculum not cleared-> dormant-> genetic variation- > resistance
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decline- alt contagious
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communicable if re-enter prodromal (carrier)
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recurring disease
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pathogen becomes dormant and goes prodromal
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Disease carriage
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disease wont harm host, but will harm others
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opportunistic pathogen
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normal flora that establishes disease when introduced into protected sites
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Virulent bacteria/fungus/virus
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strict pathogen
always coincides w/ disease |
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tissue damaging metabolites
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acids gasses, other byproducts of growth
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Invasins
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spreading factors: proteins/ ICM properties that damage the host and facilitate spread.
Can be part of the disease/ Hyaluronidase, collagenase, neuraminadase; strepto/staphylokinase |
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haluronidase/neuroamindase
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attack CT/degrade neuraminic acid
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collagenase
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break down collagen
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strep/staphkinase
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prevents clotting
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adherence to host: adhesins
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bind receptos/ host molecules via carbohydrate moieties on hot
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antifimbral adhesins
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not fimbriae
type V secretino of proteins that mediate tissue/cell binding |
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exotoxins
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preotins toxic to ceells by direct action
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enterotoxins
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proteins toxic to cells by direct action in the enterics
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Functional toxins
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immunogenic but fatal at low concentrations
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toxoids
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denatured toxins used in vaccines
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A-B exotoxins
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B binds then A enters and attacks host cell
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membrane active exotoxins
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attack membrane, lyse and kill.
Protease: elastinase, metalloprotease; lipids: phospholipase |
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Super antigen
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antigenic toxin that non-specifically bind to MHCII of APC to TCR- activate immune response several fold (acquired)
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endotoxins
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LPS of G-, toxin associated with lipid A-> septic shock
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cause of infection in normally sterile site
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ingest, inhale, trauma, bite, sex
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circuation via blood
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causes cytotoxic effects at remote sites
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Mechanism for evasion of immune response
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capsule
catalase intracellular growth |
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purpose of encapsulation
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protect from dehydration/phagocytosis
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evasiaon via intracellular growht
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avoid inactivation, escape detection by I.S.
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Lack of Iron can:
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induce toxin production of pathogens
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Pathogenic Iron capture
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Siderophores chelate and transport into bacteria.
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