Block 3 (Bacteria, Spores, Viruses) Flashcards

Question 1

Q

Bacterial genetics

Answer

A

Thymine & Adenine = 2 Hydrogen bonds
Guanine & Cytosine = 1 Hydrogen Bond
Same as eukaryotic cells
Chromosome-single circular highly coiled ^{(Replication requires uncoiling)}
- _{Haploid (one set of chromosome)}
- _{Double stranded DNA}
- _{No introns/NO nuclear membrane}
Antibiotics flouroquinolones ^{(e.g. norfloxacin)} bind to DNA gyrase, inhibit restoration of supercoiling
Islands OR Virulence cassettes:
Unique area in the chromosome where several genes are clustered = ^{Co-inheritance}
- _{May contain virulence gene (cause disease in host)}
- _{Antibiotic resistance}

Question 2

Q

Bacterial Genetics Contd…

Answer

A

Plasmids (small DNA mol):
Extra chromosomal circular DNA
One or more in a cell (^{lost or gained})
Replicate independent of main chromosome
Integrate into main chromosome
Carry gene for specialized function BUT NOT essential for survival
R-plasmid gives resistace to antibiotics
Bacteriophage genes: Prophage (integrated into bacterial chromosome) virus infects & replicates in bacteria
Transposons: Jumping genes

Question 3

Q

DNA replication Prokaryotic

Answer

A

Enzymes & proteins required for bacterial replication SIMILAR to eukaryotic BUT different to be targets for ANTIBIOTICS
Replication = Uncoiling & recoiling of SUPERcoiled DNA
DNA information stored in continous DNA segment ^{(circular)}
mRNA directly sythesize corresponding protein
There is NO capping ^{(early transcription)}, NO poly-A tail, NO splicing mRNA ^{(splicesomes mature RNA)}
Bacterial genes organized into:
Operons (clusters of co-reg gene)
Inducible or repressible
Sigma factor
Quorum sensing

Question 4

Q

Bacterial Operon

Answer

A

Clusters of co-reg genes ^{(Turn on/off together)}
Grouping ^{(clusters)} common control mechs allow for bacteria RAPIDLY change to enviroment
Single promoter & operator
Inducible system:
repressor binds to the operator unless it is bound by an inducer
molecule at the start of the metabolic pathway governed by the enzymes encoded by the operon genes
Repressible system:
repressor ONLY binds to the operator if it binds to a co-repressor
end product of the metabolic pathway governed by enzymes encoded by operon genes.

Question 5

Q

Bacterial Quorum Sensing

Answer

A

Some genes are turned on in the presence of HIGH amounts of bacteria
QS detects presence of _autoinducers: _measure cell density
- _{specific peptides(gram positive bacteria)}
- _{homoserine lactones(gram-negative bacteria)}
Autoinducers diffuse freely across membranes ^{(conc same inside & outside)}
As accumulation of auto-inducers increases (MORE bacteria) turns on Transcription
Cross cell membranes-activate products:
toxins
enzymes
surfactants

Question 6

Q

Bacterial transcription Sigma

Answer

A

P=Promoter binds to RNA poly+sigma factor - Transcription started sigma falls off
O=Operator decides if genes are activated
Lac 1=Codes for Repressor genes
DNA-Dependent RNA poly (SIGMA):
Requires specific sigma factors
Accuracy & affinity of binding to promoter
turn on & off genes
**initation of RNA synthesis **
Inserted into plasma membrane for adaptive immunity “sensing enviroment”
NEW sigma factors = NEW phenotypic expressions
MONO or POLYcistronic mRNA messages

Question 7

Q

Translation of Bacterial cells

Answer

A

Unique initiation, elongation, & termination factors
1st AA= N-formyl methionine (fMet):
- ^{Soluble PAMP=recognized by innate immunity as foreign}
Translation: Target for antimicrobal agents ^{(tetracyclines, erythromycins)}
Most control if done through transcription of gene into mRNA

Question 8

Q

Bacterial Genetic change (adaption)

Answer

A

Highly adaptable due to:
Change their genetic information ^{FAST}
Mutation: due fast repro = probability of mutation is HIGH
Spontaneous mutation: polymerase enzyme errors
Induced mutations: caused by mutagens _{(CHEMS/RADIATION)}
Due to haploid state bacterial mutations are expressed FAST ^{(NO RECESSIVE OR DOMINANT)}
Gene transfer between bacterial cells MORE COMMON
Change most common is change on MEMBRANE of Ag receptors

Question 9

Q

Bacterial Gene Transfer (adaption)-Transformation

Answer

A

Transfer of “naked” DNA through homologous recombonation
Most common in GRAM + bacteria (strep)
DNA is taken up by enviroment ^{(dead bacteria genetic info) }& incorporated in reciept’s chromsome
_Competence of recipient: _
So bacteria can take up DNA naturally ONLY when they produce protein ^{(COMP FACTOR)}
Comp factor can be induced in-vitro w/CaCL2
Leads to increased virulence ^{(penetrance of infection to HOST)}
Widely used in recombinant DNA technology

Question 10

Q

Bacterial Gene Transfer (adaption)-Conjugation

Answer

A

Mediated by F-factor (Fertility)
Plasmid contains TRA operons ^{(GENES FOR SIX PILI & OTHER FERTILITY FACTORS)}
Found in Gram (-)
Requires direct cell to cell contact
F+ with TRA operons to F-
F- will become F+ after conj
NO external pressure to maintain plasmid = Lost over time - CURE or treatment of bacteria
Antibiotic resistance ^(R-plasmids):
Plasmid carry multiple resistance genes
Rapid spread
Process takes less then 2 hours
Virulence genes ^{(HOW LIKELY TO INFECT HOST)}:
Pili genes mediate adherance to epithelial cells
Exotoxin genes

Question 11

Q

Bacterial Gene Transfer (adaption)-HfR conj

Answer

A

HfR = high frequency plasmid are integrated partial integration of plasmid into donor chromosome (F+)
Hfr male (donor) conj ^{(Sex Pilus)} w/F- reciepent
Transferred donor DNA ^{(Portion NOT Whole)} in F- reciepent cytoplasm then INSERTED into nucleoid
Even with the portional transfer to F- plasmid still remains ^{F NEGATIVE}
Requires homologous recombonation

Question 12

Q

Bacterial Gene Transfer (adaption) Transduction

Answer

A

Transfer of genetic info using bacteriophage ^{(VIRUS REPLICATES IN BACTERIA)}
Bacteriophage = dsDNA protected by protein coat ^{(phage-Protected from nucleases in envrioment)}
Phage w/wide host range = **transfer between speicies **
Phage effeciency in transduction = Life cycle
Virulent or Lytic Phage
Temperate or Lysogenic phage
Temperate can also go through lytic

Question 13

Q

Bacterial Gene Transfer (adaption) Transduction Types

Answer

A

Generalized: Transfer of any bacterial gene from disrupted cell
Ex.Lyctic cycle- Adherance, penetration, replication, assembly, release = LYSIS_^{(VIRULENT PHAGE)}_
Specialized: Transfer of specific genes AFTER integration of phage into bacterial chromosome
Ex.Lysogenic cycle- Adherance, penetration, integration, ^{(PROPHAGE FORMATION)}-Lysogenic state ^{(TEMPERATE PHAGE)-} NO LYSES

Question 14

Q

Generalized Transduction

Answer

A

Any bacterial gene from donor CAN be transferred to reciepent
Phages involved breakdown **HOST DNA & pack it into PHAGE **
RANDOMLY during assembly Host DNA is integrated into PHAGE coat ^{(bacterial DNA)}
In reciepent gen recombo homologous event occurs WHICH subs donor DNA w/reciepent DNA
Lysis of cells in necessary for spread of viral agents to other cells

Question 15

Q

Specialized Transduction

Answer

A

Transfer on CERTAIN donor genes given to reciepent
Mediated by Temperate phage - Genes transferred depends on where PROPHAGE has inserted on chromosome
Excision happens when repressor is damaged ^{(UV light, Chems)} = Induction**
During excision of prophage error=Induction Phage DNA saves itself and excises itself = Lytic cycle
Excision error repressor damaged=Lysogenic (phage) conversion is source of VIRULENT strains of bacteria
Size limitation on amount of genetic material that can be packaged into CASPID ^{(LEAVING ORIGINAL GENOME)}

Question 16

Q

Transposons

Answer

A

Small segments of DNA that hold genes for their OWN replication & others
Able to inegrate/excise and take their genes to another place while leaving itself behind
Move to and from any DNA-phage or Plasmid ^{(MOVE KEY GENES LIKE ANTIMICROBIAL RESISTANCE)}
Smallest ones have self genes ONLY=^{INSERTION SEQUENCES}
Responsible for bacterial strains w/multiple drug resistance

Question 17

Q

Transposition

Answer

A

Insertion sequence-minimal genetic info required for transport
Can carry addtional information ^{(REPLICATIVE & NON-REPLICATIVE)}
Consequence of integration:
Disruption of normal gene sequence
Insertion of NEW genetic info
Pathogenicity Islands (PAIs):
Modified TRANSPOSONs-carry many genes under control on SINGLE promoter
Gene products = Toxins, adhesins, Antibiotic resistance

Question 18

Q

Recombonation

Answer

A

Integration of donor DNA to recipient chromosome
Stabilizes genetic info AFTER gene transfer = new combos of genes or genetic info on choromosomes involved
Homologous recombo: DsDNA break-Single strand degeneration-Single strand integrates itself ^{(D-LOOP FORMATION}^{)}
Gene repair synthesis fills in gap-Ligation = _{BRANCH MIGRATION & RESOLUTION}
Requires = Long region of homology & series of recombo enzymes (recA/recB)
_Site-specific recombo: _
NO homology
Needs restriction endonucleases & sutes for endonucleases on ^{BOTH DNA}
DNA can circular or linear
Product = exsisting genome + integrated DNA (combo of 2)

Question 19

Q

Phase variation (Conversion)

Answer

A

Also programmed gene rearrangement
Switch genes on/off = phenotypes switching FASTER than mutation rate
NOT a mutation:
NO gene change
ONLY change in direction of promoter or Pos of gene
This can be done through recombonation or in-situ (Lab)
Inversion of promoter changes what will be expressed
Ex. Neisseria gonorrheae (able to change antigenic determinants-_^{WHERE Ab will bind}_)

Question 20

Q

Bacterial growth

Answer

A

Bacterial growth in number = Pop growth
Pop size increases by cell division:
- _{Divide by BINARY FISSION}
- ^{SINGLE CELL DIVIDES into 2 ID daughter cells}
- 1-2-4-8-16-32
- ^{Number of cells in pop size=2n (n=GENERATION #)=EXPONENTIAL growth}
Regulated by surface to volume ratio
1. Lag phase, 2. Exponenetial phase, 3.Stationary phase, 4. Decline=^{Spores are formed here }
Phases In closed system

Question 21

Q

Phases of Bacterial Growth

Answer

A

Lag Phase: Bacteria adpats to enviroment, synthesis of RNA & enzymes ^{(Maturing NOT YET READY TO DIVIDE)}
Log Phase: exponential growth, Cell doubling, plateus due to lack of nutrition
Stationary Phase: Growth limiting factor ^{(DEPLETION of nutrients)} growth/death rate are equal-Antibiotics are produced @ this point due to maxed out space
Death Phase: Bacteria death^{ (spore formation)}

Question 22

Q

Nutritional requirement (growth)

Answer

A

Cultivating, propagating, growing microbes requires proper enviromental cond.
Physical factors:
Temp- COLD loving = ^psychrophils / Moderate temp = ^Mesophils / High Temp=^{Thermophils}
PH = 6.5-7.5
Ostmotic pressure: Physiological=saline
Chem factors:
Gas - O2
Source elements - N, P, S trace
GF-Vitamins & AAs
Source of energy-Organic matter/Carbs

Question 23

Q

O2 & Growth

Answer

A

Obligate aerobes: Require O2 & grow best @ atomospheric conc of O2
Microaerophiles: Require O2 @ lower conc than atomspheric conc
Facultative anaerobes: Grow in O2 or absence of O2
Aerotolerant anaerobes: do NOT use O2 BUT can grow in O2
Obligate anaerobes: Inhibited by O2
Can use O2 make end products-Hydrogen peroxide, singlet O2, hydroxyl radical
Generally lack or def in catalases & superoxide dismutase (peroxidases)
Reactive O2 species accum & suicide occurs

Question 24

Q

Types of culture Media

Answer

A

Selective Media: Allows growth of ^{ONLY DESIRED} microbes = inhibit growth of unwanted organisms
Diff media: Used to distinguish among diff organisms
Enriched media: Has additional substances found in blood or extracts from animal tissue =^{ Encourage GROWTH}
Blood agar: Sheep’s blood = enriched&diff
Eosin methylene Blue agar (EMB):
Selective & diff = ONLY gram - grow & Diff between lactose fermenter or NON
Mannitol Salt agar:
Selective_^{ (HIGH osmotic)}_ - 7.5 Saline
Diff - Mannitol fermenters ONLY ^{(Staph aureus)}

Question 25

Q

Disinfection & Sterilization Terms

Answer

A

Microbal Death=Irreversible Loss of ability to reproduce
Sterilization=Inactive of microbal life in terms of repro
Disinfection=Elimination of disease producing organisms on inanimate objects
Septic=appearance of micro in tissue
Antiseptic=inhibits growth of micro applied on tissue
Bacteriostatic=Property of inhibiting multiplication of bacteria-RESUMES when removed
Bactericidal=Property of killing bacteria
Antibiotics=PRODUCTS of microbes inhibit other microbes

Question 26

Q

Physical agents of Killing bacteria (heat)

Answer

A

Heat = DENATURE PROTEINS
Dry Heat:
Incineration
Direct flaming-sterilize heat resistant materials for immediate use (Inoculating loop)
Dry HOT AIR-180 C for 2 hours (use as sterilize heat resistant glass ware)
Moist heat:
Boiling @ atomosph pressure kill everything BUT spores ^{(not sterilization)}
Tyndallization intermittent boiling CAN sterilize
Autoclaving: Boiling-Steam under pressure 121 C kills all
Pasteurization kill pathogenic bacteria in milk & canned food ^{(low heat, rapid cooling, HIGH heat)}

Question 27

Q

Physical agents of Killing bacteria (radiation)

Answer

A

Ionizing- Xrays & gamma rays
higher energy & greater penetrating power
Create O2 & H radicals from water
Denature proteins & DNA
Sterilize gloves & syringes
NON-ionizing UV light (Mutations in DNA)
Destroy DNA by forming thymine bonds
Lethal waves 240-280nm
Poorly penetrate = Sterilize air, OR, Surfaces & TREATMENT of water

Question 28

Q

Physical agents of Killing bacteria (chem.)

Answer

A

Rate of killing by chems depends on:
Conc of chem BUT exceptions exsist (Alcohol 70% more effective than 95%)
Time of exposure
physiological cond of microbe
Presence of organic matter
POP size
Mode of action=Disrupts cell membrane, denature proteins, breaking DNA

Question 29

Q

Physical agents of Killing bacteria (Chem)

Answer

A

Phenol-Carbolic acid
1st disinfactant replaced by phenol
Dissolves lipid solvents-Cell membranes
Alcohols-Ethanol & isopropanol
Dissolve lipids & denature proteins
Bacteridical BUT NOT against spores & non-enveloped virus
More effective in presence of water
Halogens-Denature proteins
Chloirine: purification of water & disinfectant on inanimate objects
Iodine: Tincture or iodophors used as antiseptics ^{(before surgery)}
Heavy metals(denature proteins)
Silver nitrate-Used to prevent eye infection in new borns (blindness from ghonerhia)

Question 30

Q

Physical agents of Killing bacteria (Chem)

Answer

A

Ehtylene oxide-Gas
Bactericidal against ^{SPORES}
GREAT penetrating power=GAS
Sterilize medical materials
Detergents-Quaternary ammonium salts
Surfactants (disrupt cell membrane)
Composed of long chain lipid sol ^{(hydrophobic end & hydrophilic end)}
Effective against Gram (-) cell & enveloped viruses
Used as SKIN antiseptics

Question 31

Q

Koch’s postulates

Answer

A

Used to establish relationship w/microorganism & disease
Organism must be isolated from diseased host & grown in culture
Disease must be reproduced when pure culture of organism is introduced in healthy host
Problems with postulate:
NOT all microorganims are cultivable (mycobacterium, trepanema)
Some diseases are synergistic etiology of 2 or MORE agents
Some pathogens are found as normal flora
Amendments to postulate:
Serology - detection of Ab or Ag specific to pathogen in question
Molecular tech - detection of nucleic acid specific to pathogen in question

Question 32

Q

Determinants of bacterial pathogenesis

Answer

A

Transmissions: Ability of pathogen to find next host
Adherence to host cells
Ability to invade, spread & cause inflammation
Toxin production-Toxins may NOT kill the host cells BUT alter physiology (normal fnx)
Opportunistic pathogens: cause disease in immun-ocompromised pts or when normal flora enter body site other than normal site or overgrowth of normal flora
Surviving host defesnses-
Immunopathogenesis: Collateral damage due to host immune response or immune complication

Question 33

Q

Chain of infection-Transmission

Answer

A

Mode of transmission:
3 I’s - Ingestion, inhalation, Injection
Addition vertical transmission Mother-Fetus/baby
Means of entry
Host susceptibility
Pathogenic mech
_Reservoir: _
- **Exogenous **(humans internal enviroment)
- Living rese-person carrying pathogen w/o showing symptoms (passive carrier)
- Non-living rese-water (legionella), soil (spore)
Means of escape

Question 34

Q

Chain of infection-Adhesion

Answer

A

Binding between specific mols on BOTH host & pathogen
Determines tissue/host specificity

Pili, capsule, biofilm
Cell wall-lipoteicoic acid
Proteins on cell wall
ex. E-coli UTI has P fimbriae binds to GAL-GAL dimer on P Ag on uroepithelial cells
ex. F protein found on cell wall of Strep BINDS to fibronectin

Question 35

Q

Infection-Invasion or spreading factors

Answer

A

Exoenzymes-Act on Extracell matrix
Tissue degrading enzymes ^{(PROTEASES, PHOSOLIPASES, HYALURONIDASE, COLLAGENASE, STREPTOKINASE)}
To penetrate cell
Inhibition of phagocytosis & spread w/o exiting cell - Ex. Shigella & Listeria

Question 36

Q

Bacterial Exotoxins (A-B)

Answer

A

Proteins secreted by Many bacteria ^{(GRAM+ & -) }:teichoic and lipoteichoic acid, peptidoglycan of gram positive = Endotoxic like fever & acute phase response
A-B toxin:
Most common
A unit translocated through membrane after B binds to it
B binds to host cell receptor ^{(determines host cell specificity of toxin)}
After entering cell the A unit cleaves OR modifies target mol w/in cell

Question 37

Q

Bacterial Exotoxins (A-B) Mode of action

Answer

A

Once inside cell A comp:
Catalyzes ADP-ribosylation of target protein ^{(INACTIVATION/HYPOACTIVATION)}
ADP is removed from NAD & convalently attached to host cell target protein=Inactive
Causes the following to be inactive:
Protein synthesis = Elongation factor 2 ^{(DIPHITHERIA TOXIN)}
Protein synthesis = Cleaves Host cell rRNA ^{(SHIGELLA)}
Reg factor = Control of CAMP ^{(CHOLERA)}
Proteolytic activity = Control nerve transmission ^{(TETANI)}

Question 38

Q

Bacterial Exotoxins (A-B)-ADP ribosylation

Answer

A

inactivation of EF-2 by ADP ribosylation ^{(INHIBITION OF PROTEIN SYNTHESIS)}
Diphertheria:
Upper resp tract pathogen=Cell death
Toxin can enter circulation affect-Heart, Kidney, nerves
Carried by temperate phage (lysogenic)
Pseudomonas aeruginosa:
Exotoxin A
Common in CF pts

Question 39

Q

Bacterial Exotoxins (A-B)-Increase cAMP

Answer

A

Activation of G-protein by ADP-ribosylation=^{INCREASE in cAMP}
Cholerae & E-coli:
Small intestine
Watery diarrhea & secretory
Bordetella pertussis “whooping cough”:
Resp epithelium pathogen
HIGH lvls of cAMP = INCREASE resp secretions & mucous production = INCREASE coughinng

Question 40

Q

Bacterial Exotoxins (A-B)-Cleavage of rRNA

Answer

A

Inhibition of protein synthesis by removing adenine from sites on 28s rRNA of 60s
Shiga/Vero toxin: enterohemorrhigc (resembles toxin) of Ecoli & shigells
Intestines - BLOODY diarrhea
If it enters blood = Hemolytic uremic syndrome (HUS)-Premature killing of RBCs MOST common in children

Question 41

Q

Bacterial Exotoxins (A-B)-Neurotoxins

Answer

A

Clostridium Botulinum:
Toxin blocks Ach release by working on SNAP anchoring proteins
Flaccid paralysis
Clostridium tetani:
Toxin tetanospasmin - blocks release of Glycine & GABA ^{(inhibitory) }@ Ant. Horn of spinal cord
Causing spastic paralysis = Tetanus

Question 42

Q

Bacterial Exotoxins-Membrane Disrupting

Answer

A

Cytolysins/Cytolytic:
Promote leakage of water & ions disrupting cell fnx or lysis
2 modes of actions:

Pore (channel) formation-Streptolysin O (Streptococcus pyogenese)
Destruction of phosolipid bilayer (Lechtinase-Alpha toxin made by Clostridium)

Can be called hemolysins or Leukocidins
RTX = have repeats of amino acid sequence
CDC = cholesterol dependent cytolysins

Question 43

Q

Bacterial Exotoxins-SuperAgs

Answer

A

Make bridges between MHC 2 of macrophages or APCs AND receptors on T-cells
Present in high lvls of cytokines in circulation ^{(CYTOKINE STORM)} = Toxic shock syndrome
Ex. Staph aureus & Strep pyogenes

Question 44

Q

Bacterial Exotoxins-Secretion systems

Answer

A

Classified Type 1-6
Released through special apparatus depending on Type #
Type 1,3,5 = transport toxins directly in extracellular space
Type 3-Ex. Pseudomonas, Shigella, Salmonella
Type 2, 4, 6 = Inject toxin directly into target host cell “molecular syringe”-^Injectosomes(Ecoli & salmonella)

Question 45

Q

Bacterial Endotoxins (LPS)

Answer

A

Lipid A comp-Attached to cell wall of Gram(-)
O Ag-exposed to exterior of cell
Mode of action:
Acts as PAMP-activates macrophages, PMN, mast cells, endothelial cells, platelets
Activates Comp-Alternative pathway (C3B-Factor B/D)
B cell polyclonal activation (IgM made)
Low conc signal inflammation for clearing it
HIGH conc = Endotoxic shock
Also known as SIRS-
Fever ^{(IL-1)}
hypotension ^{(TNF increase perm)}
DIC ^{(platelets)}
inflammation
multiorgan failure

Question 46

Q

Additional Defenses

Answer

A

Interference-
Capsule = ANTI-phagocytic
Biofilm:
Prevents complement & Ab/Anti-biotics
Inhibition of phagosome fnx or escape into cytoplasm
Killing of phagocytic cell by producing toxins
Avoiding Ig Mediated opsonization:
Protein A of Staph & M of Strep
Cleavage of Ab/Comp:
IgA proteases, C5a cleavage
Camouflage:
Mol mimicry - Antigenic similar w/host
Hiding w/in cell - Intracell growth (virus)
Antigenic variation:
Exiting in multiple sites
Antigenic/Phase variation - NO mutation

Question 47

Q

Immunopathogenesis

Answer

A

Excessive immune response - Innate, specific & inflammatory response (NK & CTls - Cell death)
Activated neutrophils & macrophages-Bystander damage
Comp activation-Anaphylatoxins
Granuloma formation
Induction of Autoimmune disease-Mol mimicry- Ex. Strep, M-protein to heart=Rheumatic fever
Immune complex deposition: Poststrep glomerulonephritis

Question 48

Q

Pathogenicity Islands

Answer

A

Pathogenic bacteria assemble several virulence genes into ONE or more DNA sequences
Commonly a transposon inserted into chromosome or plasmid
Coordinated expression of several genes-turned on by single stim
Ex. Salmonella-25 genes turned on by change in pH in phagocytic vesicle w/in Macrophages

Question 49

Q

Antibiotic Resistance (intrinsic)

Answer

A

_Bacteria lacking the target: _
Cell wall less (mycoplasma & Ureaplasma)
Cell wall w/o peptidoglycan: Chlamydia, Chlamydophila, orientia, Ehlichia, Anaplasma
Antimicrobal cannot enter the bacterium-
Gram negative due to OUTER membrane

Question 50

Q

Mechanisms of Antibiotic Resistance

Answer

A

Inactivation ^{(cleavage)} of antibiotics by ENZYMES
Mod of antibiotic ^{(transfer of acetyl group)}
Decrease in cell perm of cell
Active Efflux of drugs by membrane-bound drug resistant ^{(MDR)} pumps
Alteration of cell drug target through mutation or post-translational mods
Hyper-production of target
Formation of biofilm

Question 51

Q

Antimicrobal susceptibility Testing (Kirby-Bauer)

Answer

A

Used to make best drug of choice to treat infections
Diffusion (Kirby-Bauer):
Paper discs w/known conc. of antibiotics on Smear of culture on agar
Measure_^{ ZONE of INHIBITION}_ in mm
E-Test: Strip of paper w/decreasing conc mini inhibitory conc ^{(MIC + Kirby-Bauer)}
Dilution test: Can measure-
MIC ^{(minimal inhibitory conc)} -Used to see minimum effect of antibiotics
MBC ^{(minimal bactericidal conc)} - Lowest Conc kill 99% of all bacteria-using MIC 1st ^{(IMMUNOCOMPRIMISED Pts)}
Spot test: phenotype test/Rapid colorimetric assays
beta lactamases^{ (ESBL)}
Optochin Sensitivity-^{TESTING ANTIBIOTICS}

Question 52

Q

Variations in Microscope

Answer

A

Bright field-^{Most widely used}
Specimen is darker than surrounding fields
Live & preserved stained specimens
Dark fields-
Brightly illuminated specimens surround by dark fields
Live & unstained specimens ^{(SPIROCHETS)}
UV/Fluorescent:
Uses UV light & fluorescent compounds
Staining DFA-direct fluorescent Ab ^{(FAST DIAGNOSIS-Test presence of Ag)}
Electron Microscope: Beams of electrons
Used for Viruses

Question 53

Q

Types of staining

Answer

A

Negative staining ^{(Halo Appearance)}:
Stain background NOT the object of interest^{ (APPEAR TRANSPARENT AGAINST COLORED BACKGROUND)}
Capsule staining
Simple stains:
One dye used-REVEALS shape, size, & arrangement
Differential stains:
Primary stain & conterstain
Distinguish **cell types or parts **
Ex. Gram-stain, acid-fast stain, endospore stain

Question 54

Q

Differential Staining-Gram

Answer

A

Pts sample dried & fixed using heat:

Staining w/Cyrstal Violet ^{(BOTH GRAM +/-)}
Fixation w/iodine stabilizes crystal violet ^{(Both Gram +/- STAY Violet or Blue)}
Decoloization w/alcohol gram (-) reacts BUT NOT gram (+) <THIS step can effect overall STAINING if left here to long>
Counterstaining w/Safranin=Gram + remain voilet while Gram(-) Stain Pink

Question 55

Q

Differential Staining-Acid Fast

Answer

A

Also called ziehl-neelsen stain
Used on acid fast bacteria ^{(Long-chain Fatty acids giving it a waxy outermembrane)}

Heat specimen of carbol fuchsin
Decolorizer with acid alcohol sol
Use secondary dye methylene blue ^{(non-acid will stain blue & ACID will not)}

Question 56

Q

Biochemical Tests

Answer

A

_Biotyping-_Presence or absence of biochem markers
Formation of distinct bio-chem end products ^{(CARB FERMENTATION)}
Presence of certain bacterial enzymes & or toxins (^{catalase, oxidase, hemolysins)}
Use of specific nutrients-E.coli acetate as sole carbon source
Information from selective & differential media ^{(LACTOSE FERMENTATION)}
Catalase test = Using Hydrogen peroxide (H20 + O2)
Oxidase test = Measure of complete electron transport system (aerobes) using ^{CYTOCHROME C}
Carb fermentation tubes-Red neutral & Yellow is acidic ^{(FERMENTATION)}

Question 57

Q

Immuno Methods-In Vitro

Answer

A

Measuring Specific Ab levels against particular pathogan:
IgM=Current infection
**IgG w/4x increase = Acute **
IgG in a single serum sample = Compare with upper limits of normal for particular pathogen = Chronic
Detection of Ag specific to particular pathogen in clinical sample ^{(IFT or ELISA)}

Question 58

Q

Mol methods

Answer

A

Nucleic acid Based tests-
Highly specific, sensitive, safe & fast
USED for pathogens difficult to culture & highly contagious (RAPID DIAGNOSIS)
Amplification: Polymerase chain rxn (PCR)-Require primers
Hybridization: Detection & localization (Radio or Enzyme Labelled probes)
Sequence analysis: 16s RNA sub unit used to ID bacteria

Question 59

Q

Fungal cell structure

Answer

A

Eukaryotic cells ^{(unicellular or multicellular)}
membrane bound organelles
nuclear membrane
cytoskeleton
Fungal cell membrane:
Phospholipid bilayer ^{(mammalian cells)}
Differs in sterol structure = ^{ERGOSTEROL}
Amphotericin B & Azole work on Ergosterol
Beta-glucans: part of fungi cell wall linear unbranched polysacs of Beta-D glucose ^{(CELLUOSE)}

Question 60

Q

Fungal cell wall

Answer

A

Made of:
Chitin-Polymer of N-acetylglucosamine adds to rigidity of cell wall ^{(ALSO FOUND IN BACTERIAL CELL WALL)}
GLucan-polymer of D-glucose ^{(PROVIDES ADDITIONAL STRENGTH)}
Mannan + Proteins = polymer of sugar mannose linked to **surface proteins **
Add to serologic specificity when classifying diff fungi
Antigenic - activates compliment system ^{(PAMP)}
Act as adhesion factor for fungi invading mucus membranes

Question 61

Q

Fungal Structures (Types)

Answer

A

Yeast:
Oval & unicellular
Reproduce by budding ^{(Pseudoyphae)}
Mold form:
Thread-like hypahe
Colonies have Cotton or velvet like appearance
Intertwining mass of hypahe(web)=MYCELIUM
Dimorphismic ^{(CAN EXSIST IN 2 FORMS)}:
Interconversion between yeast & mold
Influenced by temp ^{(THERMAL DIMORPHISM)}
Non-septate or COENOCYTIC: No seperation of cells-Multinucleated
Septate: Cells sep by cell wall
Pseudohyphae are elongated yeast cells, ^{NOT TRUE hyphae}

Question 62

Q

Fungal Growth

Answer

A

Most are aerobic or Facultative (both)
Heterotrophic - require organic matter to grow
Fungi Grow best @:
Room temp - 20-40C
Slightly acid media, drier, higher osmotic pressure
BACTERIA DO NOT ^{(alkaline PH, wetter, Lower osmotic pressure)}
Common culture - Sabouraud’s dextrose medium ^{(HIGHER OSMOTIC PRESSURE)}
Antibacterial may be incorporated into med.^{(CHLORAMPHENICOL=SELECTIVE MED)}
Cycloheximide-in media inhibits non-path fungi BUT can favor growth of pathogenic

Question 63

Q

Fungal colonies

Answer

A

Yeast colony:
Opaque
compact
mucoid bacteria like
ALCOHOL ORDER
Grows well @ RT 24hrs
Mold colony:
Hairy, cotton like, velvet
Vegetative hyphae: Extend into growth med-_^{NEEDS NUTRITION}_
Aerial (repro) hyphae: Extend from agar surface & often HAVE SPORES ^{(ID MOLD)}

Question 64

Q

Fungal reproduction

Answer

A

Vegetative Repro (ASEXUAL):
Budding (YEAST)
Fragmentation of hyphae
Asexual spores (ANAMORPH):
Shape, color and arrangement of spores used for ID of fungi
Sporangia = Contained in sac like structure
Conidia = NO sac, naked spores, MOST COMMON
Sexual spores (TELEOMORPH):
Bases for taxonomic classification of fungi^{(NOT RELEVANT FOR ID PATHOGENS)}

Answer 65

A

Blastospores: Budding by constrictions cells DO NOT seperate & form pseudohyphae (stalk like)
Asexual spores (CONIDIA):
Chlamydoconidia-Become larger than hypha^{ (round thick walled) }made on terminal end or along side hyphae
Arhroconidia-Formed by fragmentation@ tip of hyphae ^{(filament structure)}
Conidiophore-Stalk like structires (Flower)
Microconidia-Single celled in chains
Macroconida-Multinucleated have diff shapes
Sporangia-Formed in sac ^{(sporangium) }easily broken to free sporongiospores

Answer 66

A

Only a FEW are associated with disease
True/PRIMARY pathogens:
Cause disease in healthy individual
Oppurtunistic pathogens:
Fungi w/weak nonexistent virulence or invasiveness cause disease in immunocomprimised pts
Increase incidence in hospitals
Source:
Exogenous-Enviromental exposure (SPORE or HYPHAL FORM)
Endogenous-Overgrowth of normal flora
Route of entry: Resp, cutaneous, or mucus membranes

Answer 67

A

Virulence Factors ^{(ALLOW FOR GROWTH)}:
Cell wall comp are inflammatory stim
Adhesion
Capsules ^{(anti-phagocytic)}
Survival in macrophages ^{(due to melanin secretion)}
Hydrolytic enzymes ^{(proteases, phosopholipases)}
Thermal dimorphism-Ability to grow @ 37C
Mycotoxins-Produced in envrioment assoc w/Mycotoxicosis

Answer 68

A

Superficial: Limited to outermost layers of skin & hair ^{(NO INFLAMMATION)}
Cutaneous: May extend into epidermis ^{(INVASIVE HAIR & NAILS)}
Subcutenous: Dermis, subcutanous tissues, muscles, fascia ^{(REQUIRES TRAUMATIC IMPLANTATION)}
Systemic: TRUE & OPPUTUNISTIC Start off localized ex. lung & spreads to skin or other organs ^{(USUALLY INHALED)}
Oppurtunistic Fungi: ususally normal flora take adavatage of immunocomprimised ^{(ANTIBIOTICS, HIV, DIABETES)}

Answer 69

A

Hypersensitivity: Airborne spores-Hyphael fragments
Mycotoxicoses(exotoxin mediated): interrupt physio functions
Ergot Alkaloids (ergotism): Mold growing in grains outbreak bread from rye infected w/claviceps purperea ^{(NEURO EFFECTS MADNESS)}
Aflatoxin-produced by Apergillus Sp. ^{(FOUND IN MOLDY GRAINS & PEANUTS)}
Carcigenic toxin induce mutation on p53 ^{(GROWTH SUPRESSOR GENE)}
Causes liver cancer
Mushrooms: Toxin resistant to ^{HEATING }can cause severe/fatal liver&kidneyfailure

Answer 70

A

Direct LM exam: Sputum, lung biopsy, Skin scraping
Treat w/10% KOH to clear debris
Wet mount or stained smears:
Gram stain-Candida may stain as G+
Calcoflour white stain-Fluorescent binds to chitin
Hematoxylin & eosin: Silver stain
Indian ink = Negative staining ^{(HALO)}
Determine-YEAST or MOLD ^{(hyphal structure-asexual spore structure)}

Answer 71

A

Sabourand’s dextrose sugar:
Slightly acidic-may contain Antibacterial drugs
2 cultures = @ 25 C & 37 C detect dimorphism
Takes 4 weeks
Microscopic exam: Hyphal & spore structures
Serology: systemic mycosis (inhaled)
Dermal hypersens testing^{ (TB)}
Detection of Ab ^{(4X increase of paired)}
Detection of fungal Ag in pts sample
DNA probes:
Clinical sample-Amplification of fungal DNA or detection of fungal DNA in tissue biopsy
Culture: use of DNA probes of ID fungal culture

Answer 72

A

Acellular-Inert ^{(NOT LIVING)} incapable of self-replication
Obligate intracellular parasites ^{(encode required processes NOT provided by host cell)}
Replicate by assembly of individual comp w/in host cell
Complete virus=Virion
- ^{Genome+capsid=Nucleocaspid}
Genome ^{(nucleic acid)}
RNA or DNA ^{(NOT BOTH)-}Can be SS or dS
ssRNA(+) = mRNA
ssRNA(-) = RNA-dep RNA poly
Capsid ^{(protect nucleic acid from envrioment)}
Made up of repeated subunits capsomeres
Arrangement of capsomeres make shape of virus
Targets for immune reponse

Answer 73

A

Envelope: Lipid bi-layer frm host cell & viral glycoproteins ^{(LACK of = NAKED virus)}
All helical viruses of animals are enveloped=^{Flexible w/helix coiled w/in}
Envelope gives rough spherical shape
Matrix proteins: Mediates attachment of caspid w/envelope ^{(host cell or nuclear membrane)}
Packaged enzymes: Help w/initial replication
ex.polymerases, proteases = cut proteins
Can be located in nucleocaspid or in SPACE between caspid/envelope ^{(TEGUMENT)}
Structural proteins (mature virus)-Non-structural (part of host cell)

Answer 74

A

Peplomers/Spikes: Viral glycoprotein-bind to host cell
Attachment of virus to host cell-Viral attachment proteins ^{(determines tissue/host specificity)}
Some have enzymatic activity=entry or exit of virus
Ag target them, can be classified based on
Hemagglutination (mix w/RBCs)

Answer 75

A

Naked Icosahedral-Capsomeres arranged in 20 triangles that make symmetric figure ^{(Polyhedral)}
- Polio
- Adeno
- Hep A
Naked Helical-Capsomeres arranged in a hollow coil looks like ^{ROD}
- Tabacco mosaic Virus
- No human viruses
_Enveloped isoahedral _
- Herp
- Yellow Fever
- Rubella
Enveloped Helical-Rabies, influen, Parainfluen, Mumps, Measles
Complex-Various prop. (Poxvirus-^{Bricklike} & Rabies-^{Bulletlike }& Bacterophage)

Answer 76

A

12 vetices & 20 triangular faces (Soccerball)
Each face one or more capsomers
Peplomer(fibers)-Projections/Spikes
Penton-Base of peplomer ^{(involved in pathology)}
Nucleic genome located in empty space created by Rigid structure
Naturally forming

Answer 77

A

Helical:
Rabies Virus
Bullet shaped (-)ssRNA = requires RNA-dep/RNA poly
G-glycoprotein = Spike
Nucleoprotein N (inside)
Paramyxovirus-Non-segmented(-)RNA
Peplomers/Spike-
F(fusion) mediate cell entry by fusion of envelope & cell membrane
HN-H, G - Viral attachment proteins^{(some have both or one)}
Hemmagglutinin=Binds and agglucant RBC (ex. Influenza)
Neuraminadase=Enzymes that cleave Sialic acid groups from glycoproteins for virus replication ^{(ex. influenza-segmented RNA)}

Answer 78

A

Complex:Smallpox (Variola)
DsDNA
Brick-like external & complex internal
Complex due to more than 1 membrane
HIV:
2 ID (+) RNA strands
Surface glcoproteins are for:
Adhesion & Entry of packed enzymes-
Reverse transcriptase
Integrase^{ (how above becomes integrated into host DNA)}
Proteases

Answer 79

A

Enveloped:
Enviromentally Liable
To spread-
Must stay wet
secretions
Blood & organ transplants
Enter cell by fusion w/cytoplasmic membrane
Released by budding through cell membrane ^{(NO CELL DEATH RIGHT AWAY)}
Cell to Cell spread by SYNCYTIA (merge & create giant cells)
Naked:
Enviromentall stable
Easily spread
Enter cell through receptor mediated ^{(endocytosis)}
Exit cell by lysis=Death of cell

Answer 80

A

Based on Genome, Capsid structure, Mode of Replication
Genome:
DNA-
dsDNA (circular), Gapped DNA, ssDNA
RNA-
dsRNA, (+)ssRNA, (-)ssRNA
(+)ssRNA w/iDNA=intermidiate requires reverse transcriptase
Capsid-Helical, Icosahedral, complex OR enveloped or NOT

Answer 81

A

7 Families
Genome =
Ds/Linear
Ds/Circular
Partially Ds/Circular- Only in Hepadnavirus (Gap)
Single stranded linear = Parvovirus
All replicate in host cell NUCLEUS except for POX ^{(unloads in cytoplasm by cell membrane endocytosis)}
ALL have neoplatic protential due to intranuclar mech & might damage host DNA
May cause latent infection

Answer 82

A

7 families (HHAPPPP (y))
Icosahedral-
Enveloped DS:
Herpes
Hepada
Non-Enveloped (naked) SS:
Parvo
Non-Enveloped DS:
Polyoma
Papilloma
Adeno
Complex
Env DS:
Pox (cytoplasm)

Answer 83

A

20 families of RNA
ALL RNA replicate in host cell cytoplasm EXCEPT influenza (nucleus)
RNA structure:
SS (either + or -)
DS
Segmented
Ambisense ^{(both +,- can be translated)}
All (-) RNA are enveloped & carry RNA-dependent/RNA-polymerase-have to mRNA in host then make protein
All (+) RNA=mRNA can immidiately start making proteins
Arthropod Borne come from RNA ^{(Yellow Fever, dengue - Ticks or Mosquitos)}

Answer 84

A

Absorption/Attachment-binding of virus to specific mol on host cell (spikes/receptors)
Entry/Penetration-Virus enters host cell
Uncoating-Viral nucleic acid released from capsid
Macromol synthesis-Viral comp are produced
Assembly-New viral particles are made
Release-Assembled viruses released by budding (enveloped) or Cell lysis (naked)

Answer 85

A

Mediated by Mol integration between virus & target cell
Viral attachment structures:
On caspid or envelope-VAP, peplomers, Spikes
These determine nost/tissue specificity
High mutation rate in VAP can result in change of host specificity
Ex. Hemaglutinin on Influenza
120 gp on HIV
Receptors on Host cells:
Proteins or carb on glycoproteins/Glycolipids
Ex CD4/5 (chemokine receptor) on T-helper & macrophage link to HIV
ICAM-1 on epi cells for rhinovirus
Sialic acid on epi cells for influenza
Permissiveness=Entry + Replication

Answer 86

A

Penetrations:
Fusion ^{(enveloped virus fuses w/membrane)}
@ neutral PH fusion/release of genome on surface ^{(HIV):}
- VAP ^{(GP120)} bind to CD4 complex binds to CCR-5
@ acid PH whole virus engulfed/released takes place in cytoplasm (INFLUENZA)
Endocytosis- Naked Virus taken up by receptor mediated phagocytosis
Viropexis- Direct penetration of genome
Naked virus binds to receptor sites on membrane-^{INJECT }nucleic acid
Ex.* picornaviruses and papovaviruses*
Uncoating-Caspid digested or opened up & nucleic acid released

Answer 87

A

Immediate early & Late mRNA
Early Transcripts/Synthesis of regulatory proteins & enzymes needed for replication
Replication of genome = intiation trancription of Late mRNA synthesis
Late mRNA synthesis = encode for structural proteins of virus
Nucleic Replication comes BEFORE transcription of late genes

Inclusion bodies are created by viral material intracytoplasmic or intranuclear ^{(DIAGNOSTIC IMPORTANCE)}

Answer 88

A

Based on replication strategy:
1 = DsDNA-same as for eukaryotic DNA make mRNA from dsDNA
- Use host DNAdep-DNApoly & DNA dependent RNA polymerase
- Papo, Herpes
2 = ssDNA-replication passes through dsDNA then to mRNA (ex.Parvovirus)
- Use host DNAdep-DNApoly & DNA dependent RNA poly
- Parvovirus

Answer 89

A

7 = Partially dsDNA-pass w/RNA intermediate
Uses host DNA-dep RNA poly to repair gap
mRNA makes proteins
Viral RNAdep-DNApoly (Reverse transcriptase)
New copies of genome
Ex. Hep B & D

Answer 90

A

3 =dsRNA-one strand of mRNA, requires viral RNAdep-RNApoly
Ex. ^{Reovirus-}GI/Resp & ^{Rotavirus}-Diaherrea
4 =ss+ve RNA-Pass through a (-) strand RNA to mRNA requires **viral RNAdep-RNA poly **
^{Picornavirus & Rhinovirus} “common cold”
5 =ss (-)ve RNA-Require viral RNAdep-RNA poly make mRNA
^{Influenza or Orthomyxovirus}
6 =ss +ve RNA-Pass through a DNA inter, have their own RNAdep-DNApoly (reverse transcriptase)
Use host DNAdep-DNApoly & RNApoly to make mRNA
Ex. HIV

Answer 91

A

SS (+) RNA (HIV):
RNA dep/DNA poly ^{(REVERSE TRANSCRIPTASE)} - Copies (+) RNA strand
Makes SS (-) DNA & Reverse transcriptase is carried into cell w/virus
HOST DNA-dep/DNA-Poly makes dsDNA from SS(-)DNA
HOST DNA-dep/RNA poly transcription copies (-)DNA strand from dsDNA
(-) DNA strand = (+) RNA viral mRNA-Translation Viral proteins ^{(RIBOSOMES)}& ss(+) RNA Viral genome

Answer 92

A

Site & mechanism of assembly depends:
Site of replication of genome & whether virus is naked or enveloped
Can be in nucleus or cytoplasm
Nucleocaspid assembly:
Procaspid formation (Empty caspid proteins assemble first THEN filled w/genome)
Capsid proteins assemble around genome
Naked Virus: Released by lysis or exocytosis = Cell death
**Enveloped virus: **
Proteins delivered to cell membranes ^{by Golgi}-Viral glycoproteins inserted on host membrane
Nucleocaspid moves underneath the membranes
Viral proteins leave by budding

Answer 93

A

Lytic (Naked) = Adherance, penetration, replication, assembly, release-Cell death
Budding (ability to be presistant)= Adherance, penetration, replication, assembly, release-Intact host cell
Transforming (Tumor/cancer)=Adherance, penetration, integration

Answer 94

A

New viral strains w/properties different from parent or wild type can arise
Error in duplication:
Mutations rate in viruses is high due to poor fidelity or viral polymerases
This defective virus can still alter metabolism of infected cell (Measles)
Different types of mutations:
Lethal mutant
Defective mutant-deletion/mutations of genes
Host range mutant-Change of host/tissue specific
Attenuated mutant-Causes less serious disease (vaccines)
Conditional mutant-ex. influenza temp sensitive multiply @ lower temp

Answer 95

A

2 viruses infect cell @ one time & genomes become mixed by BREAKAGE or RECOMBO
Reassortment: 2 segmented viruses simultaneously present & segments mixed in progeny caspid (ex. Influenza vaccine)
RNA virus only & useful in lab experiments
Transcapsidation/Pheotypic mixing: dual infection mistakely places capsid on “other” virus
Complementation: Defective virus aided in replication by complete virus OR other defective virus
carries mutated gene in other defective virus
Activates cell processes needed for both viruses
Ex. Hep D requires presence of Hep B

Answer 96

A

2 different viruses infect 1 host cell
Viral Shedding or Progency may contain coat comp from both parents = PHENOTYPIC MIXING
_Involves NO alteration to genetic material _
This mixing can happen in related viruses or complely different viruses
Pheotypic mixing form pseudotype:
Coat is completely different = Pseudotype
This helps with giving a wider range of host range/tissue variety

Answer 97

A

Inhibition of protein synthesis
Inhibtion & degradation of cell DNA
Cytophatic effect (CPE)-
Alteration of cell structure that can lead to cell death
Syncytia formation-Fusion of host cells by enveloped virus
Disruption of cytoskeletion
Inclusion bodies-
Found in cytoplasm & nucleus help with ID of virus
By products of replicated virus
ex. Negri body RABIES virus in cytoplasm of neural cells
ex. Multi-nucleated Syncytial cells ofetn results of infections by enveloped virus=Cell fusion ^{(Syncytia)}

Answer 98

A

Abortive: infects a cell w/o reproducing into more cells
Apparent: little to no damage or RAPID resolution ex cytomegalovirus-Herpes
Acute/Lytic: Infects cells & multiplies=Host cell death, ex. Adenovirus
Persistant (chronic): Starts with acute phase
Productive-nonlytic viruses (Hep B)
Latent/Non-productive-limited macromol BUT no virus synthesis (Varicella-zoster or Slow replicator HIV)
Can become productive or Reactivate after Latent time
Transforming-Immortalization (oncogenesis) ex. Papillomavirus

Answer 99

A

Innate:
Interferons a/b first secreted by ^{Infected cell}
IL-12, TNF-alpha produce chemokines attract & activate NK & DCs
Viral recognition mol (PAMPs)-dsDNA & ssDNA are sought out by TLR4 & TLR7-8 BOTH found on NKs
Adaptive:
_Cell med: CD4 Th1 & CD8 _
Kill infected cells by targeting intracellular phase of virus
Humoral: Targets extracell phase
Ab against viral attachement proteins
Neutralize & oponize C-activation of Virus by Ab
Elimination via ADCC & NK cells
Prevents spread by blocking extracell virus particles

Answer 100

A

Interferon receptor linked to cytoplasm signaling mol ^{(JAK-STAT) }to nuclus to turn gene expression to STOP viral replication

Oligoahenylate Synthetase: Rnasel degrades viral RNA
PRK kinase: Serine threonine kinase inactivated elf-2 (elongation factor)=Protein synthesis inhibition
MX protein-BLOCK viral transcription

This all happens before NKs recruitment

Answer 101

A

Antigenic variation-Influenza
Latency-wait until immune reponse weakens
Infection of immuno-privileged site w/in body ^{HSV in sensory ganglia CNS}
Interfere w/Ag presentation:
- Down reg MHC 1 expression (adenovirus)
- Down reg LFA-3 & ICAM-1 (EBV)
- Inihibit TAP proteins-^{Transporter assoc w/Ag processing}
Interfere w/KAL & KAR-NK recognition & killing (CMV-cytomegalovirus)
Direct infection of cell in the immune system (HIV)

Answer 102

A

Direct microscope:
Light microscopy-^{Cytopathic effect (CPE)}
UV microscopy-Fluorescent Ab staining
Electron microscopy-immunoelectron
Culture: cell culture
ID-CPE, hemadsorption (RBCs sticking to other cells), serology
Quanification^(VACCINES)-Viral titer/Plaque assay
Direct detection of viral Ag:
ELISA, Immunofluorescence-clinical specimen or ID of virus in culture
Mol analysis of genetic material:
PCR, in-situ hybridization-Clinical specimen or ID of virus in culture
Serological analysis: Ab detection/titer:
ELISA, hemagglutinin, inhibition assay
Neutralization test (block cytopathic effect)
Western blot

Answer 103

A

Tissue culture-monolayer procedure is prepared from host
Virus is inoculated into system and replication follows
The tissue changes are defined as CPE
Morphological change-Change in shape (rounding of cell, aggreation, degeneration)
Loss of attachment of culture dish-Loss of contact with monollayer
Histo changes:
Syncytia formation ^{(multinucleated cells)}
Inclusion bodies-Aggregation of viral proteins cytoplasm or nucleus
Haemadsorption-cells ability to stick to RBCs by expressing Vrial hemmagglutin

Answer 104

A

Formed by ENVELOPED viruses
Infected host cell’s plasma membranes have been altered by insertion of Virus glycoprotein FUSE
Ex. Measles virus
Chromosomal aberration & degradations=Owl’s eye ^{(chromatin ring in nuclear membrane)}
Owl’s eye ex. Herpes, Tzanck smear, cowdry type 1

Answer 105

A

Virus induced changes in the membrane or chromosomal structure
Site of viral replication or accumulation of viral capsids
Negri bodies-pink cytoplasmic inclusions found in Rabies (Found in neuro cells)
Typical Owl’s eye-Intranuclear inclusions of cytomegalovirus (Herpes):
Basophilic inclusion fills entire nucleus

Answer 106

A

Fluorescent Ab staining-Detection & ID of viruses
- DEAFF (Detection of early antigen fluorescent foci)
- Good for early detection (24hrs)
- Used for CMV (herpes) immunocomprimised
Electron microscopy-Using viral specific Ab to ID virus
- Used when there are sufficient viral particles present
- Fluorescent Ab staining is combined to help further ID

Answer 107

A

Chicken eggs (influenza vaccine)
Animals
Cell culture: 3 types all monolayer growth

Primary cells-ex. Monkey kidney. Normal cells obtained from freshly killed animal. Cells have limited shelf life (once or twice)
Semi-continuous cells-(dipolid cell line) ex. Human embryonic kidney & skin fibroblasts. Can be sub-cultured up to 50 times.
Continuous cells-HeLa, Vero, Hep2, LLC-MK2, BGM are immortalized cells
ex. tumor cell line and can be subcultured indefinitely

Answer 108

A

Used to determine Titers ^{(measurement or conc in a sol.)} of viral infections on plaque assay
Step 1 - Attachment viral titer stable in this stage virus is still infectous
Step 2 - Disassembly (dip in graph) transcription, translation, genome replication
Step 3 - Replication (Bottoms out)
Eclipse uncoating begins this stage and no intact virons can be detected.
During replication and AFTER uncoating Virus is NOT infectious.
Eclipse interval is made up of disassembly & replication
Step 4 - Assembly (steady rise) increase in vrial titer progency fully INFECTIOUS

Answer 109

A

Quantification of viral particles, ex Titration
Determine viral titer (count)
Each complete plaque assay is the result of ONE virus infecting ONE host cell
Use of several liquid assays to observe viral infection (turns liqiud to semi-solid)
Plaques form due to viral particle infecting cell, replicates, & kills that cell (infection spreads to surronding cells)
Cells are stained w/dye ONLY stains LIVING cells

Answer 110

A

Used on viruses w/oncogenic potential

Tissue is treated w/enzymes to sep cells
Cells are suspended in culture medium
Normal cells ^{(primary cells)} grow in monolayer ACROSS (line) & Transformed cells ^{(continuous)} clump and do NOT grow in a monolayer formation.

Answer 111

A

Cells infected with an enveloped virus containing a hemagglutinin ^{(viral peplomers)} in its envelope to adsorb red blood cells
These hemagglutins are inserted on infected host cell membrane
These sites of insertion will be where the viral progeny (replication) & maturation begin
RBCs will interact with Hemagglutin-peplomer of infected cells ^{(showing clumping on cell surface)}
Useful for detecting infection by viruses that cause LITTLE cytopathic effect ^{(DAMAGE TO HOST CELLS)}

Answer 112

A

Used for enveloped viruses that express hemaglutinins on surface
Hemaglutinins-bind to sialic acid receptors on cells BUT can also bind to RBCs forming a **lattice **
2 fold serial dilution of virus prepared
Mixed w/specific amount of RBCs ^{(1:4, 1:8, 1:16,etc..)}
RBCs added to wells of plastic tray
RBCs NOT bound sink to bottom of tray=Button formation ^{(red dot)}
RBCs that bind (lattice) and coats well like ELISA but for Viral detection
Ex. influenza, parainfluenza, adenoviruses, rubella, alphaviruses, bunyaviruses, flaviviruses

Answer 113

A

Definitive Host: haboring the adult sexually mature stage parasite
Intermidiate host: Development of parasite occurs BUT not adulthood is NOT reached
Reservoir Host: an organism that harbors a species of parasite can be transmitted or infect
Zoonosis: disease involving a parasite for the normal host animal and humans can also be infected
Carrier Host: harbors a parasite but exhibits NO clinical signs
Vetor: Living carrier transports a pathogenic organism
Passive transport ^{(mech.vector)} or an essential host in life cycle ^{(Biologic vector)}

Answer 114

A

Cell & tissue damage
Hydrolytic enzymes, cytolytic enzymes
Mechanical damage-
- ^{Blockage, pressure, migration of larva}
*Immunopathology: *
- ^{IgE mediated hypersens-Mast cells & eosionophils degranulation (Bystander tissue damage)}
- ^{Type 2 & 3-Tissue damage, inflammation & scarring (immuno-complex deposits)}
- ^{Type 4-cell mediated & granuloma}
Competition for nutrition: malnutrition & loss of blood

Answer 115

A

Antigenic variation: depending on life stage
Ig/complement proteases: Can produce DAF like mols = destabilize C3b & formation of MAC
Encystation: Uses HOST response to wall itself
Masking: Uses discarded host Ags by pasting them to their surface
Immunosupression-^{Diversion of effective immune response}
^{Extracellular developmental stage secretes chems down regulate humoral (Th2)response}
^{Intracellular developmental stage secretes chems down regulate cell mediated (Th1)}
^{Others suppress producing antioxidant – interfere with macrophage killing}

Answer 116

A

Microscopic exam:
Blood, CSF, biopsy
Serologic exam:
- Ab response
- Ag detection
Increased eosinophils=parasitic infection
Nucleic acid hybridization
- PCR
- Detection-in situ
Animal inoculation
Xenodiagnosis^{ (lyme disease)}
Culture
imaging-Detect presence of parasite in tissue

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Block 3 (Bacteria, Spores, Viruses) Flashcards

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