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Micro > T1 > Flashcards

T1 Flashcards

1
Q

Genera of Gram + bacteria

A 
Actinomyces
Bacillus
Bifidobacterium
Clostridium
Corynebacterium, Propionibacterium (& other diphtheroids)
Enterococcus
Gardnerella
Lactobacillus
Listeria
Mobiluncus
Peptostreptococcus
Staphylococcus
Streptococcus
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2
Q

med-important G+ cocci

A

Strep
Staph
Enterococcus

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3
Q

general of bacterial endospore-formers

A

Clostridium

Bacillus

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4
Q

Genera of acid-fast + pink bacteria

A

Mycobacteria

Nocardia (usually)

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5
Q

cell shaped determined by

A

murein sacculus and cytoskeleton

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6
Q

cocci arrangements

A 
diplococcus (pairs) 
     G- :  (kidney bean)
     G+:  (lancet)
chains (strep)
clusters (staph)
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7
Q

bacillus/rod

A 
v. short: G-
short, thin: G-
short, thin, needle-like: fusiforms, G-
long, thick: G+
short, thick:  G+
clubbed-shaped:  G+
     -thin, branching filamentous rods w. club ends
*arranged as single cells, pairs (doublet) or chains
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8
Q

helicoidal

A

curved, comma: (G-)
curved, comma: (G+)
spirochetes
*arranged as single cells, pairs, chains

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9
Q

pleomorphic

A

can vary in size/shape:

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10
Q

flagella

A

H-Ag, protein composition
plain: extend out from cell surface
endoflagella: internal structure (spirochetes)
motility, sensory system (chemotactic), surface translocation, aids in identification, virulence factor (chemotactic)

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11
Q

Pili (Fimbriae)

A

protein composition
normal (I-IV) and sex pili extend out into environment
adherence (virulence factor), antiphagocytic, surface translocation (v.f.)
sex pilus: conjugation

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12
Q

capsule

A

glycocalyx, exopolysaccharides (EPS)
mucoid-like coat around cell, slime layer
polysacch. polymers: K-Ags: single, complex, D-glutamic acid repeating units OR O-Ag: LPS (G-)

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13
Q

biofilms

A

communal, protected, complex, 3-D structure (bac/yeast)
in exopolysacch. film, sometimes protein amyloid fibers
CDC: 50% human bac inf. involved biofilms
phenotypic changes: become sessile in biofilm, MDR, quorum sensing–>activation?
can revert to normal/planktonic form–>recurrent inf.
D-A.A. can disrupt amyloid protein connections–>release bad
*are a capsule

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14
Q

clin sig of EPS/biofilms

A

adherence, anti-phagocytic, anti-antibiotic, anti-dessication, Ag used to ID some human pathogen

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15
Q

HKO Ag

A 
H: flagella
K: capsular
O: LPS (acts as capsule)
G+: capsule or no capsule
G-: O+K-, O+K+, O+,K- (again)
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16
Q

S-layers

A

A- or T-layers, (glyco)protein composed, 10-20% cell mass
present on some human normal flora AND pathogens
on cell wall, rigid layer w. pores of fixed diameter
virulence factors: anti-complement (C3b), anti-phago(PMN)

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17
Q

translocation

A

thru human cells to new site

paracellular, sliding motility (biofilms)

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18
Q

cell membrane contains no sterols except

A

Mycoplasma
Helicobacter
Ehrlichia
Anaplasma spp.

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19
Q

Type III secretion system

A

injectosome; conserved multiprotein system used by G- bac to insert protein toxins into human cells

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20
Q

cell membrane contains respiratory system

A

ETC, ATP synthase, PMF/ion current

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21
Q

cell membrane systems

A

perm/transport, respiration, cell wall synthesis components, cellular replication components, osmoreg/sensory (chemotactic) mechanisms (hypertonic to ext. environ.)

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22
Q

G+ or G-: polysacchs are covalently linked to peptidoglycan layer in cell wall and lipoteichoic acid polymers are anchored in cell membrane

A

G+

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23
Q

G+ or G-: contains an outer membrane with LPS, peptidoglycan layer located in periplasm

A

G-

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24
Q

cell wall functions

A

sieve, prevents bursting, mech. strength, vir/tox factors, Ag-comps, rec. for Abs, sex pilus, bacteriophages; anchors external bac structures (flag, pili, caps)

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25
Q

peptidoglycan layer

A

“fabric” of crosslinking, covalently bound threads: N-acetylmuramic acid (NAM) and N-actelyglucosamine (NAG)

  • cleavage by lysozyme (human tears/saliva)–>bac lysis
  • all peptide stems possess some D-a.a.s (i.e. D-alanine)
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26
Q

lytic transglycosylases

A

cell wall enzyme, causes cell wall turnover during exponential phase growth
product recognized by TLRs–>SIRS!

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27
Q

pathogenic bacteria WITHOUT peptidoglycan

A

Mycoplasma
Rickettsia
Ehrlichia
Anaplasma

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28
Q

G+ or G-: contain periplasm and an outer membrane

A

G- (thin pep. layer)

*confers resistance to dyes, hydrolytic enzymes, detergents

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29
Q

periplasm functions

A

osmotic protection (for thin pep. layer), nutrient uptake from OM–>CM, chemotactic sens. mech, degradative enzyms, osmoreg

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30
Q

OM functions

A

bac-environ interaction site, vir/tox factors, Ag-comps, ref for Abs, sex pilus, bacteriaphages, anchors ext. structures of bac, shield against dyes, hydrolytic enzymes, detergents

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31
Q

OM comp

A

lipopolysacc, phoslip, proteins (OMP)

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32
Q

OM structure

A 
lipid bilayer (NOT phoslip bilayer)
LPS as outer leaflet, phoslip inner
porins: OMP, allows hydrophilics to pass thru
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33
Q

LPS

A

aka: endotoxin, exogenous pyrogen

Lipid A + core + O-Ag

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34
Q

Lipid A

A

disacch, phos grps, fatty acids, toxic factor

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35
Q

Core oligosacch of LPS

A

sugars, aminosugars, sugar acids, or sugar alcohols

-ketodeoxyoctulonate (KDO): common Ag in enteric bac

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36
Q

terminal polysacch.

A

aka O-Ag, repeating unit, contains sugars (like core), highly specific btw genera AND species

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37
Q

Lipooligiosaccharide (LOS)

A

lipid A + extended core, NO O-Ag

syn. instead of LPS, assoc. w/ Neisseria meningitidis and N. gonorrhoeae; Haemophilus influenza and H. ducreyi

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38
Q

props of LPS/LOS

A

part of OM, chromosome encoded, broad sp.(effects many org sys in susc. host) i.e. induction of IL-1 (endo. pyro), also acts directly on hypothalamus itself (exogenous pyrogen)
act. alt compl pathway, activator of Hageman factor (XII), induction release of endo mediators, heat stable, does not form toxoids

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39
Q

endogenous mediators induced/released by LPS/LOS

A

TNF-a, IL-1, IL-6

arch acid metals, bradykinin, histamine, NO, free radicals

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40
Q

only ways to disrupt primary structure of LPS/LOS

A

burning, oxidation –>detoxifies the endotoxin

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41
Q

Endotoxin/LPS/Lipid A is a potent immunomodulatory substance

A

SIRS–>distributive shock (DS) (G-)

systemic w. macros, PMNs, endothelial cells

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42
Q

SIRS activated by

A

50%: infection (usually G- (contain LPS))

50%: non-inf. etiology

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43
Q

initiation of SIRS

A

LPS binds LBP–>LPS-LBP complex interacts with mem-bound CD14 rec on PMS, macros/monos–>LPS-CD14 binds TLR–>signal transduction–>cytoplasm–>nucleus
–>induction/release of endogenous mediators
soluble CD14 rec in serum–>binds ECs–>dysfunction/leakiness>hypotension/vascular leak syndrome (ARDS: feature of DS, not SIRS)

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44
Q

why endotoxin (LPS) is not a true toxin

A

human response to presence is what causes fatality, not toxin itself

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45
Q

SIRS classification

A

2+:
temp >38 or =90 bpm
tachypnea >=20
leukocytosis: >12000 or

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46
Q

3 pathophys processes of sepsis etc.

A

systemic inflammation (“hyperinflammatory state”)
coagulation activation
fibrinolysis inhibition

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47
Q

Disseminated Intravascular Coagulation (DIC)

A

LPS activates Hageman factor (XII)–>activation of coag (fibrin deposition)–>fibrinolysis activated by this but inhibited by plasminogen activator inhibitor–>accumulation of undiss. thrombin in microcirculation
DIC–>MOF +/- purpura fulminans

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48
Q

if survived hyperinflammatory state of sepsis, pt enters

A

“immunoparalysis”; hypoinflammatory state:
loss of type IV hypersn, failure to clear primary infection, dev. of new secondary infections, dormant viruses may “awaken” (HSV-1, EBV, CMV, HHV-7)

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49
Q

sepsis classification

A

2+ of SIRS criteria PLUS proven infection: i.e. pneumonia, UTI, bacteremia

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50
Q

severe sepsis

A

sepsis criteria PLUS organ failure (OD, MOD, MOF) most: heart, lungs, liver, kidneys

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51
Q

septic shock

A

severe sepsis criteria PLUS refractory hypotension

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52
Q

shock

A

inadequate profusion of tissues; 3 forms:

cardiogenic, vascular obstructiv, hypovolemic (DS)

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53
Q

distributive shock (DS)

A

“warm shock” (dilation)

  • EC dysfunction/leakiness–>loss of plasma into tissues–>hypotension
  • loss of vasc resistance–>hypotension
  • coagulopathy–>DIC
  • septic cardiomyopathy: rev., does not damage heart structure–>reduces CO (LPS, C5A, IL-1B, TNF-a, IL-6)
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54
Q

clinical manifestations of DS

A 
fever or hypothermia, chills, 
leukopenia/cytosis
tachy x2
DIC
hypotnsn, shock, DIC-->OD, MOD, MOF
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55
Q

Early Goal-Directed Therapy (EGDT) for SIRS/DS

A
  • sepsis resuscitation bundle: measure serum lactate, obtain blood spec for culture, admin broad spec Ab, if hypotnsv: admin fluids: iconic crystalloid or iso-onccotic colloid (4% albumin) or vasopressin, achieve O2 sat goals
  • sepsis management bundle: corticosteroids, tight glycemic control
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56
Q

failed SIRS/DS tx

A

eritoran tetrasodium: anti-TLR-4 compound

Drotecogin alfa: act. recombinant protein C, approved, no proof of benefit

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57
Q

detection of LPS in pharm industry

A

Limulus Amebocyte lysate test and/or monoclonal Abs (MoAb) against LPS (detects nanogram amounts of endotoxin)

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58
Q

G+ peptidoglycan layer

A

larger (50% cell wall) and more cross linked than G-
can induce TNF-a, IL-6
can lead to SIRS/shock/DS (not as much as LPS)

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59
Q

Lipoteichoic acid structure

A

polymer of glycerol-PO4 or ribitol-PO4, covalently bound to glycolipid, integrated/NON-COVALENTLY bonded into outer leaflet of CM, extends thru cell wall/pep layer into environ
*adhesion of Strep. pyogenes to fibronectin on surface of pharyngeal epithelial cells

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60
Q

Teichoic acids (and other polymers)

A

polymer of glycerol-PO4 or ribitol-PO4, covalently bound to peptidoglycan, extends thru cell wall/pep layer into environ

  • peptidoglycan + teichoic acids–>can produce endotoxin-like shock in pts with Staph aureus infections
  • interacts with CRP–>activates alternative comp pathway–>inflammatory response
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61
Q

PAMPs (pathogen assoc. molecular patterns)

A

on pathogen, recognized by PARs/PRRs–>can initiate release of endogenous mediators that cause SIRS/DIC/DS
*caused DIC/DS to occur in absence of endotoxin: G+ bac inf., fungal inf., viral inf.

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62
Q

PARs (PRRs)

A

NOD1/2: internal/cytoplasmic *NOD2 def. related to Crohn’s
TLR rec: extracellular, 11 total, bind to sp. PAMPs: peptidoglycan, teichoic acid polymers, N-f-met-leu-phe, CpG nucs, LPS

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63
Q

bacterial spores

A

-most bac do not form spores, help survive adverse conditions, forms inside mother cell (dies), complete but inactive cell in protective shell, germination when conditions are favorable

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64
Q

bacterial endospores have increased

A

longevity, resistances to heat/temp, desiccation, chem agents *req special disinfectants/sterilization

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65
Q

medically important spore-forming bacteria

A

Bacillus

Clostridium

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66
Q

small colony variants (SCV)

A

growth-def variants, form colonies 1/10 normal size
enhanced resistance to Ab (*aminoglycosides)
formed by both G+/G-: Staph aureus, Pseudomonas aeruginosa, E.coli, UTIs
phenotype switching: able to revert to normal size

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67
Q

SCVs are associated with chronic, recurrent infections of

A

bones, heart, lungs, urinary tract

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68
Q

bac are good metabolizers b/c

A

large surface:volume ratio, close contact w. environ, accumulate nutrients quickly, grow rapidly

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69
Q

autotrophs

A

“fix CO2”, cell energy from redox of inorganic ions (chemoautotroph) OR harvesting light energy (photoautotroph)

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70
Q

heterotrophs

A

oxidize organic molecules for cellular energy

*all bac which cause disease in humans

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71
Q

heterotrophs utilize..

A

carbs, proteins, then lipids

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72
Q

fastidious bacteria

A

will not grow on blood agar (complex growth req)

non-fastidious do

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73
Q

optimal growth occurs at temps..

A

closer to maximum
min determine primarily by reduced enzyme activity and red. mem fluidity
max: protein denaturation

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74
Q

mesophile growth occurs btw

A

20-50 degrees C

*most pathogens are mesophiles: 35-36 C

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75
Q

thermophiles

A

(obl. or fac) >55 C

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76
Q

psychrophiles/cryophiles

A

(obl, fac)

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77
Q

microaerophilic organisms

A

grow in presence of red. O2 conc.

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78
Q

facultative anaerobe

A

*most pathogens
aerobic respiration when O2, otherwise fermentation
-early on use aerobic, consume all O2, switch to anerobic

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79
Q

aerotolerant anaerobe

A

grow best in absence of O2 (only fermentation) but can grow in O2

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80
Q

obligate anaerobe

A

only grow in absence of O2 (only fermentation)

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81
Q

bacteria become O2 tolerant when..

A

they produce enzymes (SOD, catalase) to detoxify the byproducts of O2 metab (O2-, H2O2, respectively)

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82
Q

if bac are O2 intolerant

A

they lack nec. enzymes, so toxic agents (O2-, H2O2) kill them

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83
Q

special ionic requirements

A 
non-halophile vs halophiles (need Na+)
eg:
low Fe+++: C. diph-->produces diphtheria toxin
low Ca++: plague bac-->produces exotoxin
low Mg++: S. aureus strains-->TSST-1
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84
Q

glycolysis

A

catabolic pathway; partially oxidizes organic matter–>end products are substrates for other pathways; phosphorylation generates ATP

  • additional energy if end-products enter:
  • TCA(gen red power (NADH2)–>respiration (gen ATP, recyc. NADH2)
  • fermentation pathways
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85
Q

TCA

A

completes oxidization of organic carbon into CO2
gen. intermed. for anabolic pathways
gen. reducing power (NADH2) for ana/catabolic pathways
FADH2 and/or NADH2 is recycled in resp/anabolism

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86
Q

fermentation pathways

A

produce shorter C chain-org comps +/-CO2
recycle NADH2 for ana/catabolic pathways
may gen ATP via substrate level phosphorylation* sole source energy

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87
Q

respiration must occur

A

in mem vesicle/sack, generates energy: ion current (PMF) for ATP synthesis, occurs during recycling of NADH2–>NAD+(oxidized) *Abs exist that collapse the gradient

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88
Q

1st part of respiration: ETC..

A

transfers e-s and H+ from NADH2 to TEA–>generates both PMF and reduced TEA

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89
Q

oxidase test

A

determines presence of ETC comp (cytochrome C) in some bac that can oxidize derivatives of P-phenylenediamine to a colored product
-used by lab to ID bac: enterobacteria (oxidase -)
other G- rods (oxidase +)

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90
Q

2nd part or respiration: ATP synthetase…

A

uses PMF to synthesize ATP from ADP and inorg. phos

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91
Q

aerobic respiration

A

(oxidative phosphorylation)
TEA is O2–>red. to H2O by ETS
*common pathway among pathogens and humans

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92
Q

anaerobic respiration

A

TEAs are inorganic comps
med sig:
-methemoglobinemia (MetHb) happens when elevated levels of NO3 are in drinking water
-GI tract NF convert NO3–>NO2–>if absorbed in blood–>MetHb (risk esp to fetus)

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93
Q

fermentation

A

simpler than respiration, incomplete oxidation of C substrate, utilizes substrates less efficiently (NO respiration), but still allows growth, occurs in cytosol (NOT vesicle), does NOT directly produce PMF

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94
Q

fermentation substrates are..

A

partially oxidized to 1-4 C compounds and some CO2, these serve as TEA (accept e- from NADH2, H+) during recycling of NADH2–>NAD+
–>then excreted from cell (pyruvate–>ethanol +CO2)

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95
Q

microbial end products of fermentation cause..

A

dental caries; end prod. is lactic acid from homolactic fermentation (like hum. musc.)

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96
Q

microbial end products of fermentation lead to…

A

acidic pH of vagina and skin (lactic acid, again, and propionic acid, acetic acid, CO2)

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97
Q

microbial end products of fermentation cause abscesses..

A

that are acidic and anaerobic

  • many Abs not effective at low pH
  • many Abs bind free NAs and render them unavailable
  • low pH kills surrounding viable human cells –>rel. compounds that bac req for growth (para-aminobenzoid acid) –>Abs like sulfas are ineffective
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98
Q

microbial end products of fermentation help..

A

ID bac

  • mixed acids: lactic, acetic, formic, succinic, etOH, CO2, H2
  • typical of enteric bac of human gut (coliforms)
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99
Q

certain bac can only grow fermentatively

A
  • lack cytochrome/ETC OR cannot use it for energy prod.

- do not use NAD+ or NADP+ as e- and H+ ion carrier, rather ferredoxin is used–>must be recycled to oxidized form

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100
Q

aerotolerant anaerobes

A

(Strep and Lactobacillus)
-produce lactic acid and H2O2 (from ferredoxin recycle)
H2O2 detoxed by human host’s peroxidase (otherwise can’t grow)

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101
Q

fermentation by Clostridium

A

end products include H2, CO2 and 4 C compounds; recycling of ferredoxin catalyzed by hydrogen lyase (not aerotolerant?) –>H2 byproduct

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102
Q

H2 gas produced by Clostridium’s fermentation can cause..

A

Gas gangrene! (myonecrosis)
H2 is insoluble in tissues, tracks along fascial planes (sep muscles, collapses blood vessels, impeding perfusion (anaerobic)

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103
Q

alkaline end products are NOT

A

fermentative or oxidative phosphorylation end products
i.e. Proteus spp. (cause UTIs, kidney stones) rel. urease–>hydrolyzes urea in urine–>ammonia and CO2–>raises pH to above 7, allows Proteus to grow–>Ca++ and NH4+ ions form salts, precip. at alkaline pH–>renal calculi

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104
Q

renal calculi are composed of

A

triphosphate: Struvite: Mg ammon phos)and poorly crystalline form of apatite (hydroxylated Ca phos (some repl by carbonated)

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105
Q

H. pylori cause..

A

type b and duodenal ulcers

produce urease–>cleaves urea to CO2, NH4+–>raises microenvironment pH (stomach mucous lining) so bac can grow

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106
Q

primase

A

synthesizes short ssRNA primers for DNA synthesis

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107
Q

DNA gyrase (topoisomerase II)

A

negatively supercoils bac genome and plasmid DNA

relieves torsional stress cause by helicase: “unwinding”

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108
Q

topoisomerase IV

A

required for decatenation (separation of 2 daughter chromosomes (rings))
*both topo. II and IV are essential for bac DNA sun

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109
Q

DNA synthesis originates..

A 
at one origin of replication in prokaryotes
is bidirectional (as is eukaryotic)
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110
Q

DNA synthesis must be primed with..

A

RNA

primes synthesizes primers

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111
Q

partitioning of daughter strands

A
  • in prok: req membrane attachment

- in euk: utilize spindle fibers and centromere to sep. each chromosome

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112
Q

DNA synthesis occurs when

A

prok: lag and exponential phase
euk: S-phase

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113
Q

RNA synthesis produces

A

mRNA, tRNA, rRNA

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114
Q

why antimicrobial protein synthesis inhibitors are so effective

A

mRNA in bac has a v. short 1/2 life

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115
Q

some gene transcription req. DNA gyrase

A

to neg. supercoil DNA

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116
Q

protein synthesis occurs in the

A

cytoplasm

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117
Q

bac ribosomes

A

free, 70S (30S + 50S)

rRNA + proteins + accessory comps

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118
Q

charged tRNAs accomplished by

A

aminoacyl-tRNA synthetase: covalently bond sp. aa’s to appropriate tRNA (mRNA is template)
mRNA is codon, tRNA is anticodon (base-pair)

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119
Q

what catalyzes peptide bond formation during which ATP is consumed

A

rRNA (not proteins)

–>polypeptides are product

120
Q

protein turnover is v. short, so

A

Abs that inhib port sun are effective

121
Q

biosynthesis of peptidoglycan(PTG) backbone of cell wall:

1. synthesis of amino sugars/PTG subunits

A

uracil diphosphate (UDP) is tag for directed synthesis of amino sugars/PTG subunits
NAG and NAM syn. occurs while cov. bonded to UDP
peptide side chain of NAM syn. by ind. enzymes

122
Q

biosynthesis of peptidoglycan backbone of cell wall:

2. assembly and translocation of PTG subunit thru CM

A

PTG subunit formed by transfer of NAM and then NAG from UDP–>bactoprenol (Lipid P (carrier)) w/ release of UMPs
PTG subunit then shuttled thru CM to growing end of PTG chain

123
Q

addition of subunit to PTG chain occurs via..

A

transglycolase enzyme (transglycosylation)

124
Q

biosynthesis of PTG backbone of cell wall:

final cross linking (transpeptidation)

A

done by transpeptidases (penicillin binding proteins (PBPs)

2 aa subunits from each peptide side chain covalently bonded–>”fabric shell”: mech. strength and rigidity to PTG

125
Q

G+ bacteria use unique enzymatic pathway to make heme

A

HemQ, used in final step
MRSA, enterococcus, listeria, Mtb
*selective toxicity

126
Q

lag phase

A

cell volume and mass increase, chromosome replication (DNA syn) begins
*NO cell division/change in #

127
Q

exponential/log phase

A

balanced growth occurs

cell number, mass, volume, and cell comp. amounts increase by same exponential factor

128
Q

exp./log phase expressed as

A

generation (doubling/replication) time (GT): time req for one bacterium to divide into 2 cells (replicate)

129
Q

stationary phase

A

no net increase in cell numbers occur

130
Q

death phase

A

cell death occurs at logarithmic rate

most bac autolyse (everything is gone)

131
Q

rapidly growing organism produces

A 
acute disease (fulminant) -in general 
short mean GT
high Ag dose, strong IR
anti-infective tx usually 8-10 days
132
Q

slow growing organism produces

A 
chronic disease (insidious) -in general
long mean GT
low Ag dose, weak IR
anti-infective tx prolonged
133
Q

chemotherapy that inhibits protein and/or PTG synthesis is most effective against

A

fast growing organisms

134
Q

what DOES NOT determine GT/growth rate

A

Gram stain, metabolism, ext. cell structures, spore production

135
Q

genome

A

chromosomes PLUS any extrachromosomal elements (plasmids) deemed crucial to the organism
-in bac: sing or doub stranded, covalently closed, circular

136
Q

replicon

A

DNA or RNA molecule that controls its own replication, can self-duplicate

137
Q

extra chromosomal elements (ECE)

A

replicons in cell, except host DNA

138
Q

genomic islands are

A

horizontally transferred?…

139
Q

plasmids

A

typ. ds, much smaller, code for ancillary genes, replicons

control their own DNA replication and copy number

140
Q

plasmids DO NOT code for

A

housekeeping genes (req for viability)

141
Q

plasmids replicate in ..

A

the cytoplasm, utilize host bacterial cell DNA replication machinery

142
Q

conjugative plasmids

A

encode for mech to transfer a copy of itself from donor cell to recipient cell

143
Q

resistance plasmids

A

possess Ab resistance determinants

144
Q

plasmids can be..

A

acquired or lost from bac cells (non essential info) and are a metabolic burden on the host

145
Q

bacteriophage

A 
virus replicons (DNA, RNA) which infect bac cells
*can exist latently in bac cells as a prophage
146
Q

prophage can be..

A
  1. a plasmid in bac cytoplasm (ECE)
  2. integrated into bac cell chromosome
  3. can encode genes that confer a new phenotype to their host bac
    * most abundant bio entity on earth!
147
Q

recombination

A

exchange of recipient DNA w/ donor DNA

  • breakage and joining of replicon DNA molecules to form hybrid, recombinant molecules
  • can only occur in cell
148
Q

homologous/legitimant recombination (prok)

A
  • donor DNA integrated into rec. chrom. and excised rec. DNA fragment is degraded
  • allows gene transfer/exchange, esp. w/ transformation or abortive transduction
149
Q

homologous/legitimant recombination requires

A

RecA, an enzyme which func. when donor and rec. DNA segments share sig. homologous sequences

150
Q

site-specific/DNA seq specific

AKA illegitimate/non-homologous recombination

A

insertion of or replication of genetic elements in DNA w/ recombination restricted to identical sites at 2 locations on one replicon or at identical locations on 2 replicons

151
Q

site-specific/DNA seq specific does NOT require

152
Q

several types of site-sp recombination mediated by mobile genetic elements

A

insertion sequences

transposons

153
Q

since genetic elements cannot move themselves from donor to recipient in site-sp recombination, this must occur

A

Horizontal gene transfer (HGT) w. genetic element carried on transferred DNA

154
Q

genetic apparatus of bacteria

A

chromosome: structure, size, number
ECEs: bacteriophages (prophages in bac cells), plasmids

155
Q

phenotypic variation

A

an event in which all cells in a population respond to environmental stimulus in the same what which produces a new/altered phenotype via gene expression, without change in genotype**no genotypic variation is involved!

156
Q

the total potential phenotype is limited by

A

the organism’s genotype
*expressed phenotype is usually LESS than the full genotype potential (genotype can encode for more traits then the phenotypic traits currently express)

157
Q

phenotypic variation occurs b/c

A

microorgs are exposed to radically diff environments, req different phenotypes

158
Q

microorg does not express its entire phenotype at one time b/c

A

it would require enormous energy expenditure and cell mass (would be out-competed by more reserving, environ-appropriate cells)
i.e. fungus switches from minimal capsule–>max capsule when in human host–>cause meningoencephalitis

159
Q

phenotypic variation occurs via

A

-reg proteins controlling transcr/translation of sp. operons
-2 component signal transduction via sensor kinase and response regulator
-quorum sensing
-Ag variation
(and other)

160
Q

genotypic variation

A

event in which genome of 1+ cells in population is altered

acquire new genetic information

161
Q

2 mechanisms of genotypic variation

A

-internal by mutation (NO foreign/donated DNA involved)
or
-external: trasformation, conjugation, transduction
–>transduction: generalized/abortive or lysogenic conver

162
Q

mutation (internal alteration of genotype)

A

-internal alteration of genotype

rare, but happens due to so many bacteria

163
Q

mutations create new genes, but do not transfer them; require this mechanism to transfer

A

Horizontal gene transfer

dynamic duo!

164
Q

horizontal gene transfer

A

transformation, transduction, conjugation

165
Q

transformation

A

DNA fragments released by donor cell autolysis and accumulated by recipient cell (donor dies!)

166
Q

transduction

A

abortive phages carrying donor cell chromosomal fragments transfer their DNA to the recipient cell

167
Q

conjugation

A

donor cell plasmid encodes for mechanism to transfer a self-copy of itself to recipient cell which lacks the plasmid

168
Q

genetic info is either..

A 
carried/contained:
  -plasmid: conjugation, transformation
  -gen/abortive bacteriophage: transduction
  -lysogenic bacteriophage: transduction
OR "naked" :transformation
169
Q

external genetic information exchanged when..

A
  • highly homologous genes form donor replace (recomb) the corresp. chromosomal or plasmid genes in the rec cell
  • plasmid carrying new/altered genes makes a home in the rec. cell
  • latent bacteriophage/prophage (carrying new/altered genes) makes a home in the rec cell by 2 mechanism..
170
Q

2 ways a latent bacteriophage/prophage can make a home in the rec cell

A
  • integrating into rec cell’s chromosome

- functioning as a plasmid in the rec. cell’s cytoplasm

171
Q

clin sig of HGT

A

can transfer Ab resistance

-Acinetobacter baumannii: major cause of hops-acq inf

172
Q

transformation

A

uptake of “naked” EC DNA (fragment) by rec cell by mech encoded by rec cell’s chromosomal genes

  • donor cell autolyses
  • can be accomplished in vitro (HSSN) and imp. to certain genera: Strep
173
Q

only what types of cells can acquire “naked” extracellular DNA

A

competent:

  • naturally competent: chromosome of rec. bac cell contains genes that encode for acquisition of extracellular DNA
  • “forced” competent: chem/phys tx which “force”/induce bac cell to acquire EC DNA by unknown mech*
  • used in recomb DNA technology (G- enteric bac E. coli)
174
Q

transformation part 1

A

rec accumulates EC DNA of any origin (bac chromosome or plasmid)

175
Q

transformation part 2

A

integration of acquired DNA requires RecA (i.e. mediates homologous recombination)
any accum. DNA fragments not integrated into host (rec) cell replicon (host genome/plasmid) cannot replicate and is degraded and consumed for carbon and energy

176
Q

HGT mechs that DO require RecA

A

transformation

generalized/abortive transduction (SOMETIMES-if homolog.)

177
Q

HGT mechs that do NOT require RecA

A

conjugation
generalized/abortive transduction (SOMETIMES)
lysogenic conversion

178
Q

conjugation

A

donor cell plasmid encodes for mechanism to transfer copy of itself (the plasmids) to rec cell

  • incidental transfer of donor cell chrom DNA v. rare, may not be possible
  • involves ECE (plasmid)
179
Q

1st mechanism of conjugation: in G- bac

A

ex: transfer of resistance (R-factors)
- “mating”: cell to cell contact is essential- sex pili functions to make contact in some, not all conditions
- ssDNA copy of R factor transferred through mem pore from donor to recipient cell during replication of R factor
- transferred DNA made double stranded in rec cell
- NO RecA OR site sp. recombination involved

180
Q

limitation of conjugation

A

limited bacterial host range

181
Q

limitation of transformation

A

not all bac cells are naturally competent

182
Q

transduction

A

horizontal transfer of information (chromosomal, plasmid DNA, latent virus bearing a particular gene) btw bacteria mediated by bacteriophage

183
Q

lytic phage

A

infects bacterial host cell to generate a productive infection(new virions) by binding to a sp. comp. on cell surface–>penetration of phage NA (DNA, RNA) into cytoplasm–>replication of NA–>transcription & translation of phage core and coat genes–>phage components self-assemble into infectious particles–>host cell releases new inf. particles (virus)

184
Q

new infectious particles produced in lytic phage transduction are release into medium via

A

virus encoded cell wall hydrolase(PTG hydrolase)->cell lysis

OR slow release without lysis

185
Q

temperate phage

A

infects host cell by binding to sp comp on cell surface–>penetration of phage NA into cytoplasm–> then 2 options for phage..

186
Q

temperate phage after penetration

A
  1. phage can undergo normal lytic cycle as above OR

2. phage can become latent

187
Q

latency

A

involves repression of phage genes which code for lytic (productive) cycle of phage replication–>will reside as plasmid or is integrated into host cell DNA–>replicates in synchrony with host cell DNA & passed on to daughter cells–>are now “lysogenized”–>latency ends when phage genes become productive again: replicate and lyse host cell

188
Q

lysogenized

A

bac strains with prophage DNA

189
Q

2 options for temperate bacteriophage replication (again):

A
  1. lytic cycle will result in a productive viral infection with lysis of host cell
  2. temperate cycle viral reproduction habbpens via replication of lysogenic virus genome and distribution to each daughter cell
190
Q

mechanisms of transduction (HGT)

A

generalized/abortive transduction

lysogenic conversion

191
Q

which form of transduction occurs is determined by

A

the vector (bacteriophage)

192
Q

generalized (abortive) transduction

A

occurs with defective phage particles of both lytic and temperate phages and may require RecA

193
Q

gen (abort) transduction: during viral lytic replication cycle..

A

the donor genome is sheared into fragments–>v. rarely; the DNA or intact plasmid is randomly “packaged” into virus particles: pseudovirions/abortive phages–>function as normal infectious virion: attach to rec on uninf. rec cell–>pkgd DNA is introduced into the rec cell cytoplasm–>any DNA frag not integrated or unable to replicate is degraded and consumed

194
Q

in generalized transduction, the pseudovirion/abortive phage DOES NOT

A

carry viral genome, so no lytic or temperate life cycle can occur in rec cell
*NO viral reproduction can occur!

195
Q

unlike a typical virus, the packaged DNA of a pseudovirion is a..

A
  • plasmid that can replicate in rec cell
  • chromosomal fragment that shares homology with a portion of the recipient chromosome and is integrated into that chromosome via RecA
  • plasmid fragment that shares homology w. portion of rec plasmid and is integrated via RecA
  • no site sp. recombination is involved!
196
Q

lysogenic conversion is mediated ONLY by

A

a temperate bacteriophage (rec. is inf by temperate virus)

197
Q

lysogenic conversion

A

when rec cell possess a new phenotype/trait due to acquisition of a prophage (latent temp. phage) which encodes for the new phenotype can be expressed without activation of the temp. virus genome!

198
Q

does lysogenic require RecA

199
Q

lysogenic conversion process

A

temp. phage encodes for an exotoxin gene- not req for viral replication or any part of viral infectious cycle

200
Q

the exotoxin gene

A

is reg sep&ind of the viral genes
can be expressed without altering repression of the phages genes which code for the lytic cycle (does not affect latency)
-changes the cell phenotype from exotoxin negative to exotoxin positive

201
Q

clin sig of transduction

A

transfer of drug resistance

lysogenic conversion: prophages can carry genes for toxin production

202
Q

bacterial genomes consists of a conserved core gene pool

A

most encode “housekeeping” proteins

exhibit homogen. G+C contents/codon usage

203
Q

bacterial genomes also consist of flexible gene pools

204
Q

the functional (flexible) gene pool consists of

A 
genomic islands (GEIs, >10kb) related to mobile genetic elements
genomic islets (
205
Q

genomic islands (aka fitness islands) traits

A

presence of:
-residual material from mobile genetic elements
-flanking direct repeats
-genes that aid in an org’s adaptation (put/virulence funcs)
carry fragments (transfer genes) of other mobile elements (phages, plasmids)
large: >10Kb up to 100Kb

206
Q

genomic islands are inserted in

A

the vicinity of tRNA sequences or other small RNA genes, which leads to instability, risk for excisement

207
Q

genomic islands can be differentiated from native genome

A

has evidence of horizontal/lateral origins:

-abnormal %GC index, dinuc frequency diff, codon usage bias

208
Q

GEIs help an org survive a certain ecological niche, i.e.

A

PAIs: pathogenicity islands carry type 3 and 4 sec sys

Ab resistance islands

209
Q

DNA polymorphism answers

A

what/whom is the SOURCE of the infection, does NOT identify the agent present
ex: plasmid analysis (GE), RFLP/ribotyping, PFGE

210
Q

in plasmid analysis, plasmid DNA is

A

isolated, purified, and may be treated with restriction endonucleases

211
Q

gel electrophoresis

A

separates plasmid DNA/fragments by size–>stain, take pic

*bac must possess plasmids!

212
Q

restriction fragment length polymorphism (RFLP) and Ribotyping

A

bac chromosome (DNA) is isolated to fragments and purified–>treated with restriction endonucleases to fragment (again?)–>gel e-phoresis used to sep DNA fragments–>compare genomes (not used for banding patterns-too many!)

213
Q

RFLPs and Ribotyping uses this as detection

A

Southern or Northern blots–>labeled probe is hybridized to sep. DNA fragments–>detection

214
Q

in RFLP analysis, the probe detects

A

a particular sequence

*used for cellular life-forms: prok and euk

215
Q

in ribotyping, the probe detects

A

DNA encoding for rRNA; which is unique for each genera/spp

*used only for cellular life-forms: bacteria

216
Q

pulse field gel electrophoresis

A

variation of RFLP BUT inf. agent’s cells are gently lysed to rel. their chrome. DNA INTACT (vs. fragments)–>dig w/ rester endonuclease reg rare sites so large DNA frags–>sep by special agarose GE where the e- field orientation is changed often (“pulsing”)

217
Q

PFGE produces restriction fragments profile of

A

5–>20 bands, 10–>800kb, visualized by staining

*restricted to cellular life forms: prok and euk

218
Q

clin sig of DNA polymorph technologies

A

epidemiological; compare strains of partic pathogens

  • typically multiple strains for one infectious agent in a host population
  • determine if there is a common source
219
Q

detection of etiologic agents in human specimens:

detection of target NA AND amplification of target NA genome answer..

A

what AGENT is making the patient ill?

NOT used to answer what/whom is the source (DNA polymorphisms)

220
Q

detection of target DNA

A

Southern blot

221
Q

detection of target RNA

A

Northern blot

222
Q

to detect target, use

A

a single probe for each nat. occurring in vivo target, labeled with either radioactive or non radioactive marker

223
Q

tissue sample prep (w/ target NA)

A

in situ prep: specimen treated so NA is single stranded and accessible to probe

224
Q

blotting

A

NA extracted–>dig by restriction endonuclease–>electrophoresed–>transferred to support (blotted to membrane)–>denatured (made ss)
*may or may not occur

225
Q

RNA is often chosen as target NA b/c

A 
1000x more (r)RNA than DNA in bac cells
possess unique signature of sequences sp. for genus/spp
226
Q

hybridization

A

ss, labeled (DNA/RNA) prob anneals w/ ss NA in sample

wash off non-spec. bound probe

227
Q

detection

A

label probe–>anneals to target NA–>detection!

228
Q

since target DNA may be rare in certain human infections this helps detection

A

amplification: signal or target

229
Q

signal amplification

A

produces multiple signals vs. one signal per in vivo target

  • mult. non-radioactive marker bind to each target so SIGNAL not target is amplified
  • ->developed so no need to employ heat stable DNA polymerase/PCR, save $
230
Q

PCR

A

on form of in vitro or in situ amplification of target DNA or RNA
amplifies NA sequences unable to be detect. by N/S blots directly (10-100x more sensitive, more in vitro targets!)

231
Q

PCR: 3 step cycling process

A

(if RNA, amp then converted to DNA (cDNA) by reverse transcriptase)
1. denature (heat) ds–>ss DNA
2. anneal primers to ss DNA (cDNA) after cooling
3. extension of primer: amp w/ heat stable DNA polymerase
then detect with Northern or Southern blot

232
Q

PCR clinical applications:

A
  • screen blood

- detect viruses, bac, genetic defect, genetic marker (neoplasm), infectious agent (not successfully cultured)

233
Q

other amplification techniques

A

LCR: ligase chain reaction
TMA: transcription mediated amplification
*do NOT employ heat stable DNA polymerase

234
Q

do viruses require living cells

A

YES (some bacteria do not)

235
Q

do viruses divide by binary fission

A

NO (bac do)

236
Q

do viruses have both DNA and RNA

A

NO (bac do)

237
Q

are viruses susceptible to Ab

A

NO (bac are)

238
Q

exception: mimivirus and CMV

A

contain BOTH RNA and DNA

239
Q

viruses are

A

submicroscopic entities
obligate intracellular parasites
infect specific living cells and reproduce in said cells
consist of DNA OR RNA and protein, often an envelope
have a definite structure

240
Q

although relatively simple replicons, viruses..

A

can take over host cell, utilize for own replication and self-assembly, do not always kill the host they infect

241
Q

viruses are small

A

15–>300 nm, observed by e- microscope not light

242
Q

virion

A

complete viral particle, able to infect another host cell and repeat the replicative cycle

243
Q

for any one virus, each infectious virion possess the same NA..

A
  • dsDNA (w/ ss regions)
    • ssDNA:
    • +ssRNA (positive sense polarity)
    • -ssRNA (negative) (seg/nonseg genome)
    • dsRNA: 2 identical or complimentary strands
244
Q

the NA genome is either…

A

linear or circular

usually condensed by histones or histone-like proteins

245
Q

protomer

A

protein subunit of capsid, repetitive polypep subunits arranged in symm patterns, either:

  1. protomers–>capsomers–>capsid (i.e. icosahedral capsid)
  2. protomers–>capsid (i.e. helical capsid)
246
Q

capsomers

A

oligomeric clusters of protomers
form the capsid
(in orgs w/ icosahedral symmetry)

247
Q

capsid

A

protein shell or coat of protomers that self-assemble by non covalent bonds to enclose the core of NA genome + associated proteins

248
Q

3 architectural structures of capsids

A

complex, cubic/icosahedral, helical

249
Q

complex symmetry

A

viruses w/ unresolved structures b/c too complex

250
Q

cubic symmetry of all animal viruses is icosahedral which

A

consists of 20 faces, each an equilat triangle, in most protomers are arranged into capsomers

251
Q

helical symmetry

A

capsid consists of multiple copies of single species of protomer that bind to each other and ssRNA genome

252
Q

helical structure of non-enveloped virus

A

individual protomers assembled in helical structure around NA genome of virus–>forming the nucleocapsid

  • RNA genome extends the entire length
  • the core is hollow
  • each helical virus has sp diameter/length
253
Q

nucleocapsid

A

capsid + NA genome + associated proteins

*stable structure; resistant to drying, mild acids, detergents

254
Q

some virus consist solely of a..

A

nucleocapsid

255
Q

envelope

A

viral membrane that covers/encloses the nucleocapsid (not always present)

256
Q

envelop composition

A

virus-encoded proteins

host-derived lipids and carbs

257
Q

2 important proteins in viral envelope:

A

peplomer= spikes: viral glycoproteins, play a role in virion-rec attachment
layer btw envelope and nucleocapsid that mediates interaction btw capsid and envelope:
-tegument: amorphous layer, complex funds
-matrix protein: structure-providing lattice

258
Q

viral membrane derived from

A

nuclear membrane, sub-cellular organelle membranes, cytoplasmic membrane
-obtained from host during “budding” of some viruses

259
Q

enveloped viruses are…

A

inherently fragile, sn/inac by drying, detergents

the NUCLEOCAPSID is more stable

260
Q

disruption of envelope of enveloped virus leads to

A

virus inactivation, no longer infectious

261
Q

nearly all enveloped viruses are transmitted via

A

arthropods
respiratory droplets
bodily fluids: semen, saliva, secretions
*non-env. viruses may also be transmitted these ways

262
Q

how to classify animal viruses

A

type of nucleic acid with polarity
type of capsid symmetry
+/- envelope
quantitative: # of capsomeres for icosahedrals, diameter of helix for helicals

263
Q

clade

A

group containing all descendants from a given common ancestor, grouped based on seq similarity among members and seq diversity w.in total viral population

  • NOT a serotype
  • *the clinical importance is immune evasion
264
Q

serotypes are based on

A

antigenic diversity

265
Q

all human viruses that successfully replicate in humans result in ? infections but only some also produce ? infections

A

productive

persistent

266
Q

non-productive

A

no infectious virions:

  • abortive (lack infectious viral synthesis post-absorption?)
  • interference: virus interferes w. growth of other viruses in same cell
267
Q

productive infections comprised of..

A
  1. non-lethal alteration of cell & functions
  2. cell damage/death: lytic infections: via viral replication
  3. persistent infection without cell death
268
Q

persistent infections without cell death..

A

may persist for years

  • latent: intermittent acute episodes of disease, periods of NO infectious particles (HSV, varicella-zoster)
  • chronic: continued viral presence, disease may be absent (CMV, HHV, HBV) or is assoc. with late immunopathologic disease: HBV–>cirrhosis of liver or primary hepatocellular cancer
  • slow: long incubation period, slowly progressive, lethal (SSPE, measles) no infectious virion may be detected!
269
Q

the most common outcome of viral infection is

A

asymptomatic infection with seroconversion

270
Q

mechanisms which cause injury in viral infections

A
  • immunopathology
  • autoimmune induction
  • cell damage/death (lytic infections)
271
Q

lytic infections cause cell death

A

viral replication modifies and damages host cell:

  • inhibits/shuts down macromolecular sun
  • cytopathic effect (CPR); toxic
  • inclusion bodies and cell fusion (syncytia formation-multinuc giant cells)
  • induce apoptosis
  • chromosomal alterations–>oncogenesis
272
Q

characteristics of tumors

A
  • transformation to unrestricted cell growth
  • loss of contact inhibition/senescence (unreg growth)
  • appearance of new Ags (tumor sp Ags)
  • other changes: metabolic, genetic
273
Q

viral agents assoc with malig neoplasms

A

RNA tumor viruses HTLV

DNA tumor viruses: HPV, EBV, HBV

274
Q

viral agents of benign neoplasms

A

(somewhat organized growth, does not invade)
human wart viruses: verruca lesions, condyloma acuminatum
poxvirus: molluscum contagiosum

275
Q

6 stages of replication

A

attachement–>penetration–>uncoating–>macromolecular synthesis–>viral genome replication–>translation of viral transcripts–>synthesis of other/non-protein comps

276
Q

virus-rec interactions are major determinant of

A

infectivity
-specificity determined by:
host range (low affinity rec)
tissue tropism (high affinity rec)

277
Q

HIV therapy target (Fusion inhibitors)

A

inhibit HIV virion fusion w/ human cell surface receptors–>prevent infection of individual cells

278
Q

penetration

A

direct
surface eclipse
rec-mediated endocytosis

279
Q

direct penetration

A

non-env. viruses, nucleocapsid attaches cell surface–>release viral NA genome into host cytoplasm

280
Q

surface eclipse penetration

A

pH-independent cell entry
enveloped virus membrane fuses with cell membrane releasing viral genome into cytoplasm (*penetration and uncoating happen in 1 mechanism)

281
Q

rec-mediated endocytosis

A

viroplexis: pH-DEPENDENT cell entry
attachment of enveloped virion to cell rec–>endocytosis of virion–>enclosed in endosome–>acidification–>virus env. fuses with vesicle membrane–>releasing viral genome into cytoplasm

282
Q

uncoating

A

removal of protective coats with release of NA

  • infectivity lost here!!*
  • some virus AND host encoded mechanism to uncoat
  • target of antiviral therapy
283
Q

macromolecular synthesis

A

need to make more genome and more viral proteins:
1. DNA viruses replicate in nuc and RNA in cytoplasm
-exp. pox (DNA) virus in cytoplasm, influenze (RNA) in
nuc
2. +ssRNA, -ssRNA, and dsRNA virions all must encode for an RNA-dep RNA polymerase (RNA POL)
-exp. retroviruses: reverse transcriptase: RNA
dependent-DNA polymerase
3. both -ssRNA and dsRNA infectious virus must also carry function RNA POL (the protein) to make the mRNA along with possessing the gene
-+ssRNA viruses DON’T carry RNA POL

284
Q

DNA viruses replicate genome utilizing

A

host cell DNA replication machinery

285
Q

RNA viruses

A

+ sense or - sense RNA genome replication produces many new viral genomes and produces RI (req. RNA POL, virus encoded)

286
Q

retroviruses are the exception

A

-encode for reverse transcriptase (RT; RNA dep-DNA POL)

transcribes +ssRNA–>DNA–>incorp. into host genome–>viral DNA transcribed into mRNa

287
Q

RT is target for many anti-HIV drugs

A

-nucleoside analogue RT inhibitors
-non-nucleoside RT inhibitors
integrase enzyme also target (integrate inhibitor prevents insertion of HIV DNA genome into human genome)

288
Q

primary replication

A

site or sites in host where 1st replication occurs
-is it near the portal of entry? (POE), related to incubation
period

289
Q

secondary replication

A

where replication occurs after spread from primary site (not present in all viruses)

290
Q

some not all viruses spread from

A

the POE, primary site

291
Q

local spread

A

always occurs

292
Q

when does spread occur?

A

before, during, after entry, or only local

before, during or after primary replication

293
Q

spread/replication within host

A

cell to cell within tissues
in bloodstream/lymphatics
in nerves: peripheral–>CNS
transplacentally

294
Q

tissue tropism

A

specificity of a virus for a particular host tissue

*major determinant of infectivity!

295
Q

signs and symptoms may only occur..

A

during the primary and/or secondary replication

296
Q

immune response to viral infection

A

outcome related to capacity of virus to damage host and disrupt host defense mechs

Micro (61 decks)

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