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181 Cards in this Set
- Front
- Back
Gram Neg Staining
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lipid layer is dissolved using decolorizer which leaches the primary dye
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Gram Pos Staining
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decolorizer dehydrates bacteria and the wall shrinks, retaining color
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gram staining
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based on ability of cell wall to retain crystal violet treatment
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safranin red
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counter stain, gives gram neg. bacteria color
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coccus
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round
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bacills
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rod
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strepto
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chains
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staphylo
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cluster
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flagella
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H-antigens, composed of flagellin, evade phagocytosis, immunogenic
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long conjucation pili
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f or sex pili, produced by bacteria w/ f-plasmid. RAPID SPREAD OF ANTIBIOTIC RESISTANT GENES
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short attachment pili
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aka fimbriae, promote adhesion to human cells, result in blod clot formation, hemagglutination
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Capsule
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k-antigen, prevents phagocytosis, hydrophobic arrier, polysaccharide
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pili
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mostly gram neg bacteria
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Gram Pos
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Thick peptidoglycan, teichoic acid, lipoteichoic acid, complex polysaccharides, no outer envelope
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Gram Neg
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thin peptidoglycan, no techoic acids or complex polysaccharides, outer membrane present
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acid-fast bacteria
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presence mycolic acids forms a waxy layer resistant to stain, resistant to environ, insults, look pink
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weak staining bacteria
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legionella
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thin cell walled-bacteria
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treponema and leptospira
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no cell walled-bacteria
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mycoplasma
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Peptidoglycan backbone
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n-acteyl glucosamine and n-acetyl muramic acid linked by beta 1,4
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lysozyme
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degrate beta 1,4 linkages in peptidoglycan backbone
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transpeptidase
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catalyzes cross-linking of peptide chains in peptidoglycan, PBP
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carboxypeptidases
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remove unreacted d-alanines to limit crosslinking of peptidoglycan, PBP
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Virulence of Peptidoglycan
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Muramyldipeptide (NAM +2aa) is adjuvant, pyrogen (fever) somnogen (sleep) and blocks macrophages
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Teichoic Acids and virulence
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surface antigens, limit autolysis to promote growth, addherence, techoic acid in blood induces shock, fever
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lipoteichoic acid and virulence
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dermal necrosis (schwartzmans rxn), cell mitosis, adhesion, complement, anaphylaxis
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polysaccharides and virulence
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polysaccharides linked to the peptidoglycan cause inflammatory arthritic joint disease, granulomatous liver disease, hemopoetic stem cell production, Crohn's disease
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Periplasmic space
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between cytoplasmic membrane and outer membrane, contains peptidoglycan and enzymes
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LPS
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O-antigen, core, lipid A
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Cell envelope and virulence
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barrier to enviro. conditions, prevents antibiotics, absorption for bacteriophages,
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LPS and virulence
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O antigen induces immune response, lipid A induces IL1-> fever, blood clotting, shock, TNF- clotting and necrosis
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Endospore
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ONLY gram positive, high conc. of calcium bound to dipicolinic acid, most resistant life forms
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spore forming bacteria
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bacillus anthracis, acillus cereus, clostridium botulinm, clostridium perfringens, clostridium tetani
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binary fission
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segregation of chromosomes, septum formation, cell division-
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Growth curve
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log of turidity versus time
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Lag phase
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initial pd of adaptation, accumulate metabolites, suceptibility to phys/chem agents
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Log phase
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bacteria multiply rapidly, double at constant rate, susceptible to certain antibiotics- beta lactams
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generation time
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time required for bacterial mass to double, longer is advantageous, g=t/n
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stationary phase
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induction of immune response, dcreased growth rate but no death yet, spores form here, less susceptible to antibiotics
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death phase
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decrease in number of live bacteria
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Phototroph
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use light as main source of energy
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chemotroph
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use redox of chem. compounds as energy
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autotroph
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require inorganic chemiclas (CO2) for carbon source to synthesize organic molecules
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heterotroph
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utilize organic form of carbon for growth
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chemoheterotrophs
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most pathogenic bacteria- use organic compounds as both their energy and carbon source
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enriched media
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allow nonselective grown of any bacteria in a sample, sterile body fluids
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selective media
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only permit certain growth, for samples where there is a lot of bacteria-> stool, sputum, ex- macconkey
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siderophores
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sequster available iron for cytochromes- necessary for energy of bacteria
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obligate aerobes
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aerobic respiration, contain superoxide dismutase and catalase
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facultative anaerobes
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aerobic untill O2 runs out, contain superoxide dismutase and catalase
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obligate anaerobe
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anaerobic respiration, no catalse or superoxide dismutase
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mesophiles
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bacteria that grow at body temp- all human pathogens and opportunists
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psychrophiles
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bacteria that grow at freezing temps
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thermophiles
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bacteria that grow at boilng temps
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aerobic respiration
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uses O2 as terminal electrion receptor, glycolysis, TCA cycle and ETS, NAD is converted to NADH, ATP and water produced
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anaerobic respiration
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used other inorganic compoud as final electron receptor- for facultative anaerobes and anaerobes
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fermentation
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fermentable substrate like sugars yeild reducible intermediates like lactic acid, absense of oxygen
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Targets of antimicrobials
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protein synthesis, cell wall synthesis, cell membrane synthesis, and ncleic acid synthesis
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sulfonamides
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prevent PABA incorporation into folic acid, used with trimethoprim to inhibit nucleic acid synthesis in bacteria
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trimethoprim
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inhibits dihydrofolate reductase - used along with sulfonamides to inhibit nucleic acid synthesis in bacteria
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Quinolones
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inhibit DNA gyrase and topoisomerase- inhibit bacteria DNA replication
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Metronidazole
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fragments bacterial DNA which inhibits replication
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Rifampicin
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binds to RNA-Pol to inhibit RNA synthesis
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Tetracyclines
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bind to A site to prevent protein synthesis in bacteria
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Aminoglycosides
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bind to small subunit of ribosome and also cause misreading of mRNA
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Macrolides
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bind to large subunit of ribosome and inhibit bacterial protein synth
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cholarmpnicol lincomycin, chlindamycin
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bind to lg subunit, inhibit peptidyl transferase activity in protein synth of bacteria
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bactroprenol
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carrier of NAM and NAG in the cell membrane of peptidoglycan for cell wall synth
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Cycloserine
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inhibits cell wall synthesis by blocking addition of terminal alanine residues
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Bacitracin
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prevents recycling of pyrophosophobactoprenol so NAG-NAM can't attach to peptidoglycan chain
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glycopeptides
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bind to terminal D-alad-ala residues interfere with peptidoglycan chains
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beta-lactams
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interefere with PBPS which prevents crosslinking of peptidoglycan
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episome
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plasmid integrates into bacterial genome
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opeon
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group of functionally related genes
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negative control
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repressor binds to promotor and represses transcription, inducer can bind to repressor to start transcription again
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Positive Control
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both lactose and CAP-cAMP must be present in order for transcription to occur
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regulon
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one regulator protein that controls the expression of several proteins- ex-> CAP
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quorum sensing
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bacteria turn on expression of virulence genes bbased on sensing the conc. of bacteria around
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direct DNA repair
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for pyrimidine dimers and alkylated bases from UV radiation, photoreactivation reverses damage
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excision repair
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removes segment of damaged DNA and synthesizes a new one.
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recombination
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for damage to both strands
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SOS response
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network to detect aned repair damage- can bypass it by mutagenesis
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error-prone repair
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last ditch effort
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homologous recombination
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exchange of DNA when there is a region of homology a nd recombination enzymes/factors like recA
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site specific recombination
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one DNA molecule integrates into another- no homology besides a small portion- ex-> f-plasmid to Hfr. requires restriction endo and exonucleases
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Plasmids
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carry R-factors, toxins, bacteriocins and virulence determinants
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r-factors
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antibiotic resistance genes
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bacteriocins-
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antibacterial agents to similar bacterial strains
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bacteriophages
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viruses that infect bacteria
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lytic phages
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take over host replication- eventually cell lyses
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temperage phages
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integrate into host DNA, go to quiescent stage and eventually environment stimulus pushes them into lytic phase
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prophage
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virus integrated into bacterial DNA
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lysogen
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a bacteria carrying a prophage
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Insertion Sequences
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small, only encode proteins for transposition, flanked by short inverted repeats
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Simple Transposon
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flanked y inverted repeats, carry one or more protein-coding regions unlike ISs, Tn3-> beta lactam resistance
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composite transposon
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flanked by identical IS elements, carry 1+ resistance genes -> Tn5
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Pathogenicity Islands
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carry groups of coordinately regulated virulence genes, mvmt of island within chromosome or to other bacteria
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Integrons
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capture genes, mostly antibiotic resistance genes. NO terminal repeats, contains integrase,
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Tramsformation
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uptake of naked DNA, Gram pos- Bacillus, Strep pneumo, gram neg- neisseria, haemophilus influenza, e.coli. , VERY susceptible to antibiotics
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generalized transduction
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phage DNA injected into host, cells are eventually lysed, phages released
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specialized transduction
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temperate phages are intedgrated into host DNA, small part of baterial gene is transduced into next cell
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conjugation
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form bridge by F plasmid
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F+ x F-
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2 F+
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F' X F-
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2 F'
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Hfr X F-
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Hfr and F-, recipient cell doesn't bcome Hfr
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common hospital infections
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surgical wounds, resp tract infections, UTI (most common),
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Most common causes of infection in hospitals
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staphylocci and e. coli
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Sterilization
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total destruction of all microorganisms
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moist heat
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for sterlization, autoclavin, kills bacteria and spores, used on all heat and moisture resistant items
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dry heat
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for sterilization- kills spores, denatures proteins, causes single strand breaks in DNA, for glass wear and other things that cdan be damaged by steam
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Ethylene oxide gas
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for sterilization- toxic alkylating agent, toxinc byproducts have to dissipate first, for things like bandages
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UV radiation
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for sterilization- for things that can't be heated
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disinfection
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most organisms are destroyed, mycobacteria, viruses, fungi and spores may survive
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high level disinfectants
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for things that cant' be sterilized, endoscopes and plastic instruments, moist heat, glutaraldhyde, hydrogyn peroxide
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intermediate level disinfectants
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alcohol, iodophor, phenolic, for instruments unlikely to be contaminated with spores- don't come in contact with skin like speculum, endoscope
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low level disinfection
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quaternary ammounium compounds, for non-critical instruments like stethoscopes
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antisepsis
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disinfectants to lower numer of microorganisms on skin
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alcohols
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most effective with water, don't kill spores, clean skin before immunization,
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phenolic compounds
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rarely used today- penol coefficient is the rating of activity of a compound compared to phenol
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What are 6 examples of acts that would be conversion?
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[1] Theft,
[2] wrongful transfer, [3] wrongful detention, [4] substantially changing, [5] severely damaging, or [6] misusing a chattel. |
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chlorine
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hypochoorites are the most widely used chlorine disinfectants
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pastuerization
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heating liquids to destroy harmful organisms- reduced number so they don't cause disease
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antibiotics
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antimicrobial agents made by living organisms
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antimicrobials
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synthetic drugs with antimicrobial properties
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Disc-diffusion/ Kirby-Bauer test
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small disks with antibiotic added to the causitive agent- leaves halos= zone of inhibition
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Minimal Inhibitory concentration
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lowest concentration of the antimicrobial agent which inhibits visible growth
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bacteriocidal
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kills bacteria- used with life-threatning infections and when the immune system is low
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bacteriostatic
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inhibits bacterial growth but doens't kill- used when host defense kills bacteria, so won't work with immunosupprsed patients
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Antibiotic Resistance pathways
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hydrolysis, chemical modification, mutations, altered permeability
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Beta lactams
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inhibit cell wall synthesis- main drug = penicillins, mostly against gram positive like neisseria meningitidis
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Cephalosporins
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cell wall inhibitors, first gen-4th gen by increasining activity against resistant and gram neg bacteria
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Tetracyclines
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inhiit protein synthesis- block A site, used against cholera
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aminoglycosides
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inhibit protein synthesis- block small ribosomal subunit
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macrolides
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inhibit protein synthesis, blocks large ribosomal subunit. erythromycin and azalides are most important drugs. WALKING PNEUMONIA
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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 |
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Koch's Postulates
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organism required- grown in vitro and inoculated. disease must result. how to identify bacteria that cause disease
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Molecular Koch's Postulates
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Presence of a virulence gene, replacement with wildtype should reverse pathogenicity
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molecular guidelines for establishing microbial disease causation
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pathogen associated sequence, don't need organism
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Things that allow bacteria to evade host's immune sys
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capsule, antigenic mimcry, antigenic masking, production of IgA proteases
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Exotoxins Intoxication
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the toxin in the cause of all of the persons disease, colstridium botulinum, usually consumed, antimicrobials won't work
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exotoxin colonization with toxin production
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bacteria have to be present to produced toxin, cholera and tetans, antibiotics are effective
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exotoxin infection and localized tissue damage
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localized growth of bacteria in a wound, damage to host tissue. clostridium perfringens
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A-B Exotoxins
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diptheria, cholera, tetanus, botulism
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membrane disrupting toxins
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toxins can cause: small pores, large pores, transient pores, membrane perturbing toxins, enzymatic damage to membrane. E. coli, clostridium perfringens
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superantigens
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bridge class II MHC, massive T-cell activation and cytokine release. Staph aureus
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helical capsid
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one subunit, likea spring
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icosahedral capsids
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made of regularly repeating patterns, closed structures
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complex capsids
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modification of icosahedral
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syncytia
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multinucleated cell from multiple fusions with virally infected cells
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Types of viral entry
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direct fusion and recepter mediated uptake
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viral DNA replications mechanisms
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encode their own replication machinery, or push infected cells into the host's cell cycle so it's available
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Two ways viruses egress
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Budding and lysis
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tropism
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range of cell types that support infection and replication of a particular virus- hep b replicates readily in livr cells
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host immune response to viruses
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first- innate response of interferons. NK cells, CTLs antibodys prevent binding of virus to recepter and opsonize them
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Plaque Assay
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detection of cytopathic effect- the more plaque, the more virus
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ELISA
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detection of proteins and antibodys
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western blot
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protein antigen detection
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yeast reproduction
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budding
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dimorphic
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fungi that can grow as both yeast and mold
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mold sexual reproduction
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spores
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mold asexual reproduction
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conidia
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Host response to fungi
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cell mediated immunity- neutrohils, macrophages. no antibodys. in dimorphic fungi- t-cells and IFN gamma
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Polyenes
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class of antifungal drugs, bind to ergostarol, AMMPHOTERICIN B is main drug
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Azoles, allyamines, morpholines, thicarbomates
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inhibit ergostarol synthesis
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Potassium Hydroxide preparation
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best procedure to identify fungi- leaves ehind rigid cell wall, for hair nails skin
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Chlorazol black and calcofluor white st ain
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id fungi by revealing cell wall
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india ink stain
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identify fungi with capsules- cryptococcus neoformans- fungal meningitis
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germ tube test
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id's candida albicans
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definitive ost
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a host where the parasite reaches sexual maturity or adulthood
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intermediate host
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hosst that harbors asexual stages of paraside
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classes of protozoa
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ameba, flagellate, sporozoa, ciliates- first three cause the majority of infections in man- all but sporozoa reproduce by binary fission
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sporozan reproduction
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asexually- schizogony
sexually- sporogeny |
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protozoa
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single celled eukaryotes, metabolically active stage is called the trophozoite
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helminthes
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multicellular eukaryotes
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classes of helminthes
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nematodes- roundworms
cestodes (tapeworms) and trematodes(flukes)- flat worms *tapeworms are only segmented |
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Mechanical damage of a parasite
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caused by physical presence or movement w/in host. RBC lysis, obstruction of intestine,
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damage caused by parasite products
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hydrolytic enzymes, - produce persistant infections
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immune response to protozoa
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neutralizing antibody, complement, opsonization, macrophates, CTLs
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immune response to helminthes
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IgE and Eosinophils. Eosinophillia is a hallmark of helminthic infections
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Parasitic evasion of immune defense
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size, anatomical location, cyst, antigenic variation, antigenic masking, immunosupression
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treatment of parasites
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target metabolic differences of differencesi n susceptibility betwen parasite and host
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