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181 Cards in this Set

  • Front
  • Back
Gram Neg Staining
lipid layer is dissolved using decolorizer which leaches the primary dye
Gram Pos Staining
decolorizer dehydrates bacteria and the wall shrinks, retaining color
gram staining
based on ability of cell wall to retain crystal violet treatment
safranin red
counter stain, gives gram neg. bacteria color
coccus
round
bacills
rod
strepto
chains
staphylo
cluster
flagella
H-antigens, composed of flagellin, evade phagocytosis, immunogenic
long conjucation pili
f or sex pili, produced by bacteria w/ f-plasmid. RAPID SPREAD OF ANTIBIOTIC RESISTANT GENES
short attachment pili
aka fimbriae, promote adhesion to human cells, result in blod clot formation, hemagglutination
Capsule
k-antigen, prevents phagocytosis, hydrophobic arrier, polysaccharide
pili
mostly gram neg bacteria
Gram Pos
Thick peptidoglycan, teichoic acid, lipoteichoic acid, complex polysaccharides, no outer envelope
Gram Neg
thin peptidoglycan, no techoic acids or complex polysaccharides, outer membrane present
acid-fast bacteria
presence mycolic acids forms a waxy layer resistant to stain, resistant to environ, insults, look pink
weak staining bacteria
legionella
thin cell walled-bacteria
treponema and leptospira
no cell walled-bacteria
mycoplasma
Peptidoglycan backbone
n-acteyl glucosamine and n-acetyl muramic acid linked by beta 1,4
lysozyme
degrate beta 1,4 linkages in peptidoglycan backbone
transpeptidase
catalyzes cross-linking of peptide chains in peptidoglycan, PBP
carboxypeptidases
remove unreacted d-alanines to limit crosslinking of peptidoglycan, PBP
Virulence of Peptidoglycan
Muramyldipeptide (NAM +2aa) is adjuvant, pyrogen (fever) somnogen (sleep) and blocks macrophages
Teichoic Acids and virulence
surface antigens, limit autolysis to promote growth, addherence, techoic acid in blood induces shock, fever
lipoteichoic acid and virulence
dermal necrosis (schwartzmans rxn), cell mitosis, adhesion, complement, anaphylaxis
polysaccharides and virulence
polysaccharides linked to the peptidoglycan cause inflammatory arthritic joint disease, granulomatous liver disease, hemopoetic stem cell production, Crohn's disease
Periplasmic space
between cytoplasmic membrane and outer membrane, contains peptidoglycan and enzymes
LPS
O-antigen, core, lipid A
Cell envelope and virulence
barrier to enviro. conditions, prevents antibiotics, absorption for bacteriophages,
LPS and virulence
O antigen induces immune response, lipid A induces IL1-> fever, blood clotting, shock, TNF- clotting and necrosis
Endospore
ONLY gram positive, high conc. of calcium bound to dipicolinic acid, most resistant life forms
spore forming bacteria
bacillus anthracis, acillus cereus, clostridium botulinm, clostridium perfringens, clostridium tetani
binary fission
segregation of chromosomes, septum formation, cell division-
Growth curve
log of turidity versus time
Lag phase
initial pd of adaptation, accumulate metabolites, suceptibility to phys/chem agents
Log phase
bacteria multiply rapidly, double at constant rate, susceptible to certain antibiotics- beta lactams
generation time
time required for bacterial mass to double, longer is advantageous, g=t/n
stationary phase
induction of immune response, dcreased growth rate but no death yet, spores form here, less susceptible to antibiotics
death phase
decrease in number of live bacteria
Phototroph
use light as main source of energy
chemotroph
use redox of chem. compounds as energy
autotroph
require inorganic chemiclas (CO2) for carbon source to synthesize organic molecules
heterotroph
utilize organic form of carbon for growth
chemoheterotrophs
most pathogenic bacteria- use organic compounds as both their energy and carbon source
enriched media
allow nonselective grown of any bacteria in a sample, sterile body fluids
selective media
only permit certain growth, for samples where there is a lot of bacteria-> stool, sputum, ex- macconkey
siderophores
sequster available iron for cytochromes- necessary for energy of bacteria
obligate aerobes
aerobic respiration, contain superoxide dismutase and catalase
facultative anaerobes
aerobic untill O2 runs out, contain superoxide dismutase and catalase
obligate anaerobe
anaerobic respiration, no catalse or superoxide dismutase
mesophiles
bacteria that grow at body temp- all human pathogens and opportunists
psychrophiles
bacteria that grow at freezing temps
thermophiles
bacteria that grow at boilng temps
aerobic respiration
uses O2 as terminal electrion receptor, glycolysis, TCA cycle and ETS, NAD is converted to NADH, ATP and water produced
anaerobic respiration
used other inorganic compoud as final electron receptor- for facultative anaerobes and anaerobes
fermentation
fermentable substrate like sugars yeild reducible intermediates like lactic acid, absense of oxygen
Targets of antimicrobials
protein synthesis, cell wall synthesis, cell membrane synthesis, and ncleic acid synthesis
sulfonamides
prevent PABA incorporation into folic acid, used with trimethoprim to inhibit nucleic acid synthesis in bacteria
trimethoprim
inhibits dihydrofolate reductase - used along with sulfonamides to inhibit nucleic acid synthesis in bacteria
Quinolones
inhibit DNA gyrase and topoisomerase- inhibit bacteria DNA replication
Metronidazole
fragments bacterial DNA which inhibits replication
Rifampicin
binds to RNA-Pol to inhibit RNA synthesis
Tetracyclines
bind to A site to prevent protein synthesis in bacteria
Aminoglycosides
bind to small subunit of ribosome and also cause misreading of mRNA
Macrolides
bind to large subunit of ribosome and inhibit bacterial protein synth
cholarmpnicol lincomycin, chlindamycin
bind to lg subunit, inhibit peptidyl transferase activity in protein synth of bacteria
bactroprenol
carrier of NAM and NAG in the cell membrane of peptidoglycan for cell wall synth
Cycloserine
inhibits cell wall synthesis by blocking addition of terminal alanine residues
Bacitracin
prevents recycling of pyrophosophobactoprenol so NAG-NAM can't attach to peptidoglycan chain
glycopeptides
bind to terminal D-alad-ala residues interfere with peptidoglycan chains
beta-lactams
interefere with PBPS which prevents crosslinking of peptidoglycan
episome
plasmid integrates into bacterial genome
opeon
group of functionally related genes
negative control
repressor binds to promotor and represses transcription, inducer can bind to repressor to start transcription again
Positive Control
both lactose and CAP-cAMP must be present in order for transcription to occur
regulon
one regulator protein that controls the expression of several proteins- ex-> CAP
quorum sensing
bacteria turn on expression of virulence genes bbased on sensing the conc. of bacteria around
direct DNA repair
for pyrimidine dimers and alkylated bases from UV radiation, photoreactivation reverses damage
excision repair
removes segment of damaged DNA and synthesizes a new one.
recombination
for damage to both strands
SOS response
network to detect aned repair damage- can bypass it by mutagenesis
error-prone repair
last ditch effort
homologous recombination
exchange of DNA when there is a region of homology a nd recombination enzymes/factors like recA
site specific recombination
one DNA molecule integrates into another- no homology besides a small portion- ex-> f-plasmid to Hfr. requires restriction endo and exonucleases
Plasmids
carry R-factors, toxins, bacteriocins and virulence determinants
r-factors
antibiotic resistance genes
bacteriocins-
antibacterial agents to similar bacterial strains
bacteriophages
viruses that infect bacteria
lytic phages
take over host replication- eventually cell lyses
temperage phages
integrate into host DNA, go to quiescent stage and eventually environment stimulus pushes them into lytic phase
prophage
virus integrated into bacterial DNA
lysogen
a bacteria carrying a prophage
Insertion Sequences
small, only encode proteins for transposition, flanked by short inverted repeats
Simple Transposon
flanked y inverted repeats, carry one or more protein-coding regions unlike ISs, Tn3-> beta lactam resistance
composite transposon
flanked by identical IS elements, carry 1+ resistance genes -> Tn5
Pathogenicity Islands
carry groups of coordinately regulated virulence genes, mvmt of island within chromosome or to other bacteria
Integrons
capture genes, mostly antibiotic resistance genes. NO terminal repeats, contains integrase,
Tramsformation
uptake of naked DNA, Gram pos- Bacillus, Strep pneumo, gram neg- neisseria, haemophilus influenza, e.coli. , VERY susceptible to antibiotics
generalized transduction
phage DNA injected into host, cells are eventually lysed, phages released
specialized transduction
temperate phages are intedgrated into host DNA, small part of baterial gene is transduced into next cell
conjugation
form bridge by F plasmid
F+ x F-
2 F+
F' X F-
2 F'
Hfr X F-
Hfr and F-, recipient cell doesn't bcome Hfr
common hospital infections
surgical wounds, resp tract infections, UTI (most common),
Most common causes of infection in hospitals
staphylocci and e. coli
Sterilization
total destruction of all microorganisms
moist heat
for sterlization, autoclavin, kills bacteria and spores, used on all heat and moisture resistant items
dry heat
for sterilization- kills spores, denatures proteins, causes single strand breaks in DNA, for glass wear and other things that cdan be damaged by steam
Ethylene oxide gas
for sterilization- toxic alkylating agent, toxinc byproducts have to dissipate first, for things like bandages
UV radiation
for sterilization- for things that can't be heated
disinfection
most organisms are destroyed, mycobacteria, viruses, fungi and spores may survive
high level disinfectants
for things that cant' be sterilized, endoscopes and plastic instruments, moist heat, glutaraldhyde, hydrogyn peroxide
intermediate level disinfectants
alcohol, iodophor, phenolic, for instruments unlikely to be contaminated with spores- don't come in contact with skin like speculum, endoscope
low level disinfection
quaternary ammounium compounds, for non-critical instruments like stethoscopes
antisepsis
disinfectants to lower numer of microorganisms on skin
alcohols
most effective with water, don't kill spores, clean skin before immunization,
phenolic compounds
rarely used today- penol coefficient is the rating of activity of a compound compared to phenol
What are 6 examples of acts that would be conversion?
[1] Theft,

[2] wrongful transfer,

[3] wrongful detention,

[4] substantially changing,

[5] severely damaging, or

[6] misusing a chattel.
chlorine
hypochoorites are the most widely used chlorine disinfectants
pastuerization
heating liquids to destroy harmful organisms- reduced number so they don't cause disease
antibiotics
antimicrobial agents made by living organisms
antimicrobials
synthetic drugs with antimicrobial properties
Disc-diffusion/ Kirby-Bauer test
small disks with antibiotic added to the causitive agent- leaves halos= zone of inhibition
Minimal Inhibitory concentration
lowest concentration of the antimicrobial agent which inhibits visible growth
bacteriocidal
kills bacteria- used with life-threatning infections and when the immune system is low
bacteriostatic
inhibits bacterial growth but doens't kill- used when host defense kills bacteria, so won't work with immunosupprsed patients
Antibiotic Resistance pathways
hydrolysis, chemical modification, mutations, altered permeability
Beta lactams
inhibit cell wall synthesis- main drug = penicillins, mostly against gram positive like neisseria meningitidis
Cephalosporins
cell wall inhibitors, first gen-4th gen by increasining activity against resistant and gram neg bacteria
Tetracyclines
inhiit protein synthesis- block A site, used against cholera
aminoglycosides
inhibit protein synthesis- block small ribosomal subunit
macrolides
inhibit protein synthesis, blocks large ribosomal subunit. erythromycin and azalides are most important drugs. WALKING PNEUMONIA
What is the Intent necessary for

[1] Trespass to Chattels; and

[2] Conversion?
[1] The intent necessary for Trespass to Chattels is intent to do the act that brings about the interference;

[2] The intent necessary for Conversion is the intent to do the act that brings about the interference
Koch's Postulates
organism required- grown in vitro and inoculated. disease must result. how to identify bacteria that cause disease
Molecular Koch's Postulates
Presence of a virulence gene, replacement with wildtype should reverse pathogenicity
molecular guidelines for establishing microbial disease causation
pathogen associated sequence, don't need organism
Things that allow bacteria to evade host's immune sys
capsule, antigenic mimcry, antigenic masking, production of IgA proteases
Exotoxins Intoxication
the toxin in the cause of all of the persons disease, colstridium botulinum, usually consumed, antimicrobials won't work
exotoxin colonization with toxin production
bacteria have to be present to produced toxin, cholera and tetans, antibiotics are effective
exotoxin infection and localized tissue damage
localized growth of bacteria in a wound, damage to host tissue. clostridium perfringens
A-B Exotoxins
diptheria, cholera, tetanus, botulism
membrane disrupting toxins
toxins can cause: small pores, large pores, transient pores, membrane perturbing toxins, enzymatic damage to membrane. E. coli, clostridium perfringens
superantigens
bridge class II MHC, massive T-cell activation and cytokine release. Staph aureus
helical capsid
one subunit, likea spring
icosahedral capsids
made of regularly repeating patterns, closed structures
complex capsids
modification of icosahedral
syncytia
multinucleated cell from multiple fusions with virally infected cells
Types of viral entry
direct fusion and recepter mediated uptake
viral DNA replications mechanisms
encode their own replication machinery, or push infected cells into the host's cell cycle so it's available
Two ways viruses egress
Budding and lysis
tropism
range of cell types that support infection and replication of a particular virus- hep b replicates readily in livr cells
host immune response to viruses
first- innate response of interferons. NK cells, CTLs antibodys prevent binding of virus to recepter and opsonize them
Plaque Assay
detection of cytopathic effect- the more plaque, the more virus
ELISA
detection of proteins and antibodys
western blot
protein antigen detection
yeast reproduction
budding
dimorphic
fungi that can grow as both yeast and mold
mold sexual reproduction
spores
mold asexual reproduction
conidia
Host response to fungi
cell mediated immunity- neutrohils, macrophages. no antibodys. in dimorphic fungi- t-cells and IFN gamma
Polyenes
class of antifungal drugs, bind to ergostarol, AMMPHOTERICIN B is main drug
Azoles, allyamines, morpholines, thicarbomates
inhibit ergostarol synthesis
Potassium Hydroxide preparation
best procedure to identify fungi- leaves ehind rigid cell wall, for hair nails skin
Chlorazol black and calcofluor white st ain
id fungi by revealing cell wall
india ink stain
identify fungi with capsules- cryptococcus neoformans- fungal meningitis
germ tube test
id's candida albicans
definitive ost
a host where the parasite reaches sexual maturity or adulthood
intermediate host
hosst that harbors asexual stages of paraside
classes of protozoa
ameba, flagellate, sporozoa, ciliates- first three cause the majority of infections in man- all but sporozoa reproduce by binary fission
sporozan reproduction
asexually- schizogony
sexually- sporogeny
protozoa
single celled eukaryotes, metabolically active stage is called the trophozoite
helminthes
multicellular eukaryotes
classes of helminthes
nematodes- roundworms
cestodes (tapeworms) and trematodes(flukes)- flat worms
*tapeworms are only segmented
Mechanical damage of a parasite
caused by physical presence or movement w/in host. RBC lysis, obstruction of intestine,
damage caused by parasite products
hydrolytic enzymes, - produce persistant infections
immune response to protozoa
neutralizing antibody, complement, opsonization, macrophates, CTLs
immune response to helminthes
IgE and Eosinophils. Eosinophillia is a hallmark of helminthic infections
Parasitic evasion of immune defense
size, anatomical location, cyst, antigenic variation, antigenic masking, immunosupression
treatment of parasites
target metabolic differences of differencesi n susceptibility betwen parasite and host