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Micro Unit 2 Flashcards

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1
Q

Secondary Antigen-Antibody Rxns

A 
Secondary rxns (occur after primary rxns) can cause tertiary rxns
 result: pathological changes --> tissue damage
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2
Q

Most common type of transplant

A

blood transfusion!

* important to give appropriate blood type, if not, can irradiate the transfused blood to eliminate rxn

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3
Q

Transfusion reaction (“graft rejection”)

A

= type II sensitivity,
pre-formed Antibodies in host recognize and attack transfused blood
–> MAC attack and cell lysis

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4
Q

Major differences between prokaryotic and eukaryotic genetics

A
  • less genome stability in prokaryotes (mosaic, very plastic)
  • gene structure: polycystronic (mRNA has open reading frames)
  • genome packaging: prok. = haploid, anucleate
  • 20,000x faster population doubling
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5
Q

kinds of genetic mutation for bacteria

A
  1. transitions: pyrimidine - pyrimidine (or purine - purine)
  2. transversions: purine - pyrimidine (or reverse)
  3. substitutions
  4. deletions/insertions: micro or macro
  5. inversions (site specific) –> (in)activate gene expression
  6. gene conversion
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6
Q

mech. of inversion mutations

A

genetic mutation that can activate or INactivate gene expression and enable antigenic variation,

    • occur in repeated sequences
    • via site-specific recombinases
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7
Q

Transition and transversion mutations

A

transitions: pyrimidine - pyrimidine (or purine - purine) mutations
- - base analogs, alkylating agents, spontaneous errors

transversions: purine - pyrimidine (or reverse)
- -> silent, missense or non-sense mutations

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8
Q

Gene conversion mutation

A

permits synthesis of antigenically diverse surface proteins,
–> high degree antigenic variation
and prevent ability of host to generate neutralizing antibodies

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9
Q

SOS response

A

response to DNA damage to activate translesion polymerase
Goal –> to generate progeny w/ new genotypes w/ hope of survival (by replication w/ HUGE mutation rate)
1. if DNA damage, RecA cleaves LexA –> induce ApoUumDC
2. cleave and activate ApoUumDC w/ add’l damage
==> replicates chromosomes w/o concern for lesions (last resort survival attempt)

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10
Q

types of lateral gene transfer

A
  1. conjugation: exchange of plasmids/some transposons
  2. transduction: by bacteriophage
  3. transformation: uptake and maintenance of naked DNA
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11
Q

Streptococcus pneumoniae

A

aerotolerant anaerobe diplococcus,
= obligate parasite of humans, mostly serotypes 1-3;
increasing resistance, esp w/ virulence factors:
- polysaccharide capsule
- sIgA protease - pneumolysin - PspA surface protein
- biofilm formation

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12
Q

Griffith experiment

A

Experiment on mice regarding changes in genetic strains…
–> transforming factor (DNA material) in killed smooth bacteria changed the rough strain bacteria in vivo
(DNA taken up and expressed in bacteria in vivo)

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13
Q

Competence

A

term for natural transformation
(taking up of DNA by bacteria and expressing that DNA)
- regulated
- only in some bacteria (ie: strep pneumoniae, haemophillus, and Neisseria)

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14
Q

Antibiotic breakpoint

A

the concentration of antibacterial in serum that is optimal for therapy (will show inhibition in vitro (so that will have activity in vivo);
*bacterial strain = resistant when the MIC exceeds the breakpoint

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15
Q

major properties of plasmids

A

DS circular DNA (usually), self-replicating, compete w/ other plasmids;
* have toxin that will kill the host cell if plasmid not inherited
Can encode for: antibiotic resistance, toxins, cause tumor formation, degrade pollutants, coordinate conjugative transfer

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16
Q

“Tra” genes

A

genes encoded by plasmids that cause conjugative transfer via

proteins:
- pilli/adhesins: for attachment to recipients
- “Mating” channel - DNA processing and regulatory f(x)s
- entry exclusion - Male-specific phage

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17
Q

Mobilization (for plasmids)

A

conjugation-mediated transfer of DNA
* start: donor DNA includes plasmid, recipient does not…
–> part of donor DNA strand arrives incomplete in recipient cell,
==> Donor and recipient DNA recombine,
so get recipient cell w/ recombined DNA that includes the plasmid

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18
Q

R-factor vs. F-factor

A 
factors = pieces of DNA that can be transferred via plasmids
R = resistance factor (confers resistance)
F = fertility (benign factor)
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19
Q

Mechanisms of transposition

A
  1. Replicative transposition:
    copy the factor and place (non-homolgous) into recipient cell DNA
  2. “cut and paste”:
    factor moves from donor DNA to recipient cell DNA (at end: recipient w/ factor, donor: no factor)
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20
Q

where do resistance genes on transposons come from?

A

** bacteria naturally produce “antibiotic” products against neighbor bacteria –> neighbors develop mutations that make resistant to the harming product (maybe even = transferred from the original attacking bacteria??)

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21
Q

mechanism of action of diptheria toxin

A

A-B toxin in most pathogens DNA comes from phages!
B embeds in host membrane, A (released) INactivates EF-2,
–> stops protein synthesis –> cell death by necrosis
* esp. bad for humans bc = systemic!

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22
Q

generalized transduction

A

host DNA picked up by bacteriophage at random during lytic cycle

  • can occur in temperate or lytic phage (even if phage is defective)
  • can move ANY host gene (w/ low frequency)
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23
Q

general mechanisms of transmission of bacteria

A
  • aerosol - fecal:oral/food-borne
  • direct contact (w/bacteria, infected human, or animals (zoonotic)
  • sexual contact - endogenous (auto cross-contamination)
  • hospital-acquired (large percentage of cases!)
  • vertical (from mother to fetus or newborn)
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24
Q

types of red rashes

A
  • macular erythroderma (flat, like sunburn –> TSS in adults)
    • maculopapular (red and bumpy)
  • urticarial (hives)
  • petechial (small, rose-shaped spots * don’t blanch;
    = blood vessel damage from gram neg infections)
  • purpuric (more purple, larger scale petechial –> from blood leaving vessels)
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25
rashes w/ sores (fluid filled sacs)
- vesicular (small sacs w/ clear fluid) - bullous (large sacs w/ clear fluid) - pustulus (fluid filled sacs w/ yellow, white or green pus) * eschar (burn-like, starts as vesicular but form black scabs)
26
Staphylococcus aureus
gram + cocci clustered like grapes, non-motile, not spore-forming facultative anaerobes (oxidative metabolism); *catalase and coag. +, often beta-hemolysis (BUT not 100%)* can cause serious skin and soft tissue infections --> (V)MRSA, pneumonia deaths post-flu, etc.
27
most reliable identifying test for staph. aureus
mannitol salt agar: selective growth AND fermentation of mannitol (agar turns yellow due to the fermentation --> acidic)
28
Pulse field gel electrophoresis
test used to type (and separate out strains of) bacterial isolates * use "restriction fragments" (made by restriction enzymes and run along gel) to ID between. * often used to ID staph. aureus and MRSA
29
SCCmec element
the cassette transferred by plasmids that makes bacteria methicillin-resistant, but also has other genes. * encodes PBP2a (methicillin resistance gene)
30
MSCRAMM virulence factors for staph. aureus
(staph. aureus = extracellular pathogen, resistant to antibiotics...) - coagulase protein: clumping factor for fibrin - fibronectin, collagen, laminin and vitronectin binding proteins (in ECM, bind to fibrin networks) - Protein A: protein, binds to Fc of IgG & turns around (antiphagocytotic)
31
secreted virulence factors for Staph. aureus
- coagulase-protein: activates clotting cascade - hemolysins and cytolysins: form pores, release toxins... -
32
Types/subunits of hemolysins from staph. aureus
- alpha-gamma: dermonecrotic and block nerve repolarization - beta: hot:cold hemolysin, and sphingomyelinase - delta: pore former
33
pathogenicity islands (SaPI)
variable genetic traits/virulence factors of strains of Staph. aureus, (not all strains make these toxins) = phages that were trapped in the chromosome; ie: exfoliative toxin A or B, PVL, TSST-1 (for toxic shock)
34
Bacillus anthracis
gram +, spore-forming aerobe; * very large organism, and stick together end to end. - non-hemolytic and non-motile * polyglutamate capsule visible by exclusion w/ India ink stain transmission: via spores (aerosol/direct contact w/ animals, ingestion of infected animal meat)
35
bacillus cereus
Gram +, spore-forming aerobe, large organism, stick together end to end, - hemolytic and mostly non-motile (some = motile). transmission: via spore contact w/ open wounds OR ingestion of growing bacteria in starchy foods
36
Bacillus anthracis virulence factors
1. polyglutamate capsule 2. plasmid-encoded lethal toxin (AB type toxin) 3. plasmid-encoded edema toxin (AB type toxin) * A = "protective Ag" * B = lethal factor or edema factor
37
Mycobacteria characteristics
stain Gram+, but unusual wall makes resistant to desiccation - -> waxy, multiple layers of lipids (peptidoglycan, arabinoglactan, mycollic acids, LAM (toxin), outer lipids); * resist destruction w/in phagocytes*
38
mycobacteria growth patterns
most grow slowly, obligate aerobes, most = facultative intracellular pathogens of macrophages (grow w/in cells); - crenulated on solid medium - pellicle on surface of liquid (appear like mold)
39
Mycobacterium leprae
the bacteria which causes leprosy, | = obligate intracellular pathogen (only grows inside of cells)
40
Mycobacterium canetti
a bacteria that causes TB-like disease, | NOT transmitted human-->human;
41
Mycobacterium bovis
bacteria that cause TB-like disease, esp. carried in bovine animals --> can get ~TB from consuming contaminated products;
42
tuberculosis
* respiratory disease due to mycobacterial infection...often deadly. ** many multi-drug resistant strains (MDR and XDR)** Bacteria: M. tuberculosis, M. bovis, and maybe M. canetti; primary transmission: aerosol infection, infectious dose: VERY low (<10 organisms)
43
RecA protein
binds to ssDNA (fragments) from DNA damage (esp. in bacteria); starts cascade for SOS response to make highly mutated DNA replication --> in hopes of survival
44
Streptococci
Gram + cocci in chains, catalase +, aerotolerant anaerobes; Group A = beta hemolytic, grp B = non/beta-hemolytics (other grps are non/alpha/beta hemolytic) Virulence factor: polysaccharide capsule (in some) sep. into Lancefield groups (A & B = most important)
45
subclassification of Group A streptococci
* * ALL group A = bacitracin sensitive ** 1. Hemolysis on BAP - - Beta: streptolysin A -- none: Streptolysin O and S 2. presence of A antigen (rapid strep test) 3. 150 types of MSCRAMM (surface "M" proteins)
46
cell-associated Virulence factors for Group A streptococci
1. M protein (MSCRAMM): recruits H factor - -> interfere w/ complement activation 2. Fibronectin Binding proteins (Sfbl) 3. Hyaluronic Acid Capsule (polysaccharide): mimics host ECM 4. IgG Fc Binding proteins (SibA): ~protein A
47
Secreted virulence factors for Group A Streptococci
1. Streptococcal Pyrogenic Exotoxins (superAgs) 2. Streptolysin O (cytolysin): large peptide forms pore 3. Streptolysin S (cytolysin): Small peptide, pokes holes in memb. 4. Streptokinase: activates plasminogen to plasmin (clotting!) 5. C5a Peptidase: blocks PMN influx
48
Major acute illnesses caused by group A streptococci
1. pharyngitis/mild scarlet fever 2. impetigo (inflammation of skin, esp. around mouth) 3. Wound/puerperal Sepsis
49
Pharyngitis and (mild) scarlet fever
acute illness caused by infection w/ group A streptococci; -- inflammatory throat infection w/ fever, esp tonsils; can get systemic rash too. * transmission: aerosol or direct contact treatment: penicillin or azithromycin
50
Impetigo
acute illness due to infection by group A streptococci; - - inflammatory skin infection, esp. around mouth * transmission: direct contact treatment: penicillin or azithromycin
51
delayed sequelae from Grp A strep infection
1. Acute glomerulonephritis 2. acute rheumatic fever <-- reason for early antibiotic treatment 3. PANDAS (pediatric autoimmune neuropsych. disorders assoc. w/ streptococci)
52
Acute glomerulonephritis
a delayed consequence (after infection) of Grp A streptococci; - inflammation of renal blood vessels, - HTN, - Proteinuria, - hematuria * usually as skin infection (diff. w/ distinct Mprotein types)
53
Rheumatic fever
a delayed consequence after streptococci infection, - carditis (esp. mitral valve), fever, arthritis, erythema * esp. associated with M18 * * prevention of this is the major reason for early antibiotic treatment
54
Group B streptococci
Beta or non-hemolytic, ** bacitracin resistant! * 9 serotypes based on capsular polysaccharide; ** normal colonic flora and 10-40% women have vaginal colonies; (Gram +, catalase -)
55
Virulence factors for Group B streptococci
Cell surface: - antiphagocytic capsular polysaccharide (recruits factor H) - Fibronectin & ECM binding proteins Secreted: - C5a peptidase - cytolysins - some isolates have superAg
56
Diseases from Group B streptococci
1. Early onset sepsis 2. Late onset meningitis 3. TSS (toxic shock syndrome) * treatment: antibiotics and supportive care
57
illnesses caused by group C and G streptococci
can cause pharyngitis, and occasionally cause TSS
58
Group D Streptococci
alpha or non-hemolytic, --> gastrointestinal malignancy, endocarditis, UTIs, and sepsis (not as often as group A)
59
Streptococcus pneumoniae
Alpha-hemolytic, catalase -, optochin sensitive, diplococci; No lancefield group (?), Virulence factors: 85 serotypes of capsular polysaccharide, pneumolysin, and IgA1protease.
60
illnesses caused by Strep. pneumoniae | + treatment and prevention
- -> pneumonia, meningitis, otitis media transmission: droplet infection treatment: antibiotics, anti-inflammatory corticosteroids, and supportive care prevention: vaccines
61
Major causes of meningitis
in neonates: Group B streptococci and E. Coli in young children: haemophilus influenzae type B (only if not vaccinated) Older individuals: strep. pneumoniae and neisseria meningitidis
62
viridans streptococci
alpha-hemolytic (usually), part of normal flora in oral and nasopharyngeal cavities; can cause cavities in teeth and endocarditis, may predispose individuals for heart attacks!
63
common causes of endocarditis
- staphylococcus aureus (highly destructive to heart valves) - viridans streptococci - enterococcus faecalis/faecium (very resistant, esp. vancomycin) * can transfer resistance to other gram+ bacteria too!*
64
Minimum inhibitory concentration (MIC)
the minimum level of antibiotic needed to inhibit the growth of bacteria (a serum concentration value)
65
Minimum bactericidal concentration (MBC)
the minimum level of antibiotic needed to kill the bacteria | The serum concentration amt
66
Cornybacterium diptheriae
Bacteria that can contain the phage that produces diptheria toxin; Gram + rods with polar granules, Common flora of skin and nasopharynx, Rapid disease onset: bull neck and pseudomembrane (!), also fever, sore throat, malaise, etc. * non-pathogenic species have industrial uses*
67
virulence factors for tuberculosis and leprosy | mycobacteria
1. Wax D: makes + acid fast, resists drying 2. Cord factor: leukocyte toxicity, serpentine growth * needed for toxicity! 3. Tuberculin: PPD, elicits delayed hypersensitivity (type IV) 4. Mycobactin: siderophore (takes up Fe)

microbio/immunology (9 decks)

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