Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

EXAM 6 > Bacteria > Flashcards

Bacteria Flashcards

1
Q

defensins

A

hydrophobic, cationic

pisitive - stick to neg charged membrane in bacteria and make pores

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

gram stain

A
  1. blue stain
  2. compexing agent - make stain into larger molecules
  3. extraction agent - pull out stain, but only works on gram negative!!
  4. red stain - only sticks on gram negative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

gram positive cell membrane structure

A

peptido glycan cell wall - 1 really thick cell wall

single plasma membrane

many layers and extensive crosslinking in cell wall - gram stain cannot be washed out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Gram negative cell envelope structure

A

cytoplasmic membrane, very thin, non complex cell wall, outer cell membrane with LPS on the very outside

minimum number of layers and minimum cross linking - stain can be washed out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

LPS

A

on outside of cell envelope in gram NEGATIVE - inflammatory and parrier

gram negative ONLY - for viability and some innate antibiotic resistance (i.e. PCN doesn’t wrk against a lot of gram negative because it has to get through LPS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

peptidoglycan sructure

A

N-acetylmuramic acid, N acetylglocusamine, pentapeptide ending in D-ala, D-ala

linked and then cross linked to make cell wall

disaccharaide w pentopeptide side chain, op together for cell wall and give the bacteria shape

GM + and -

osmotic integritity and shape - strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Type 3 secretion system

A

only find in gram neg- 2 membranes

molecular syringe, inject proteins into cell - in eukaryotic cell

do bad things - paralyze or kill cell

evolutionarily related to flagella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

LPS Lipid A

A

if purify and give to someone - massive immune respoinse!

fatty acids attach and anchor LPS into outer membrane

phosphorylated glucosamine disaccharide backbone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Core polysaccharides of LPS

A

branched polysaccharide of 9-12 sugars

if gram neg - need LPS to be vaible - core and lipid A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

LPS O-specific antigen

A

repeating unit structure

long linear polysacchadie - variable, different repeating sugars

major serologic determinant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Transformation

A

bacterium takes up free DNA and adds into genome

takes up as single strand and releases soluble nts, then repairs to have 2nd strand

big receptor or small receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

neisseria antigenic variation

A

transformation!

Neisseria species can vary their surface structures, including pilli and capsule. It is clear that natural transformation plays a role in this process, allowing Neisseria to share genes encoding variations of these structures.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

PCN resistance in streptococcus pneumoniae

A

Transformation

penicillin resistance has become widespread amongst Streptococcus pneumoniae strains. In this case the penicillin resistance is due to altered penicillin-binding proteins (PBPs) which exhibit a low affinity for beta lactam antibiotics. Comparison of the nucleotide sequences encoding the PBPs in S. pneumoniae and S. mitis demonstrates that horizontal gene transfer has occurred between these two bacteria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

transduction

A

bacteriophages

viruses that attack bacteria and are specific for closely related bacterial species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

virulent phage

A

virulent phages - always cause lysis and release of phage particles - clear plaques on bacterial lawns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

temperate phage

A

may cause lysis OR may integrate stably into the bacterial host’s chromosome, generate turbind paques and persst as prophages

induced by DNA damage to excise and repliicae

all prophage genes are repressed except for a phage repressor gene

Temperate phages may establish a state of dormancy within the cell, often by integrating into the chromosomal DNA at a specific attachment site, by means of a phage-coded integrase enzyme. The dormant phage is known as a prophage and the state of dormancy is known as the lysogenic state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

intermediate phages

A

replicate stably int he host cell and continually release progeny

no lysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

lysogenic state

A

phage is in a dormant state in bacteria

integrating chromosomal DNA at a specific site

dormant phage = prophage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

lysogenic conversion

A

Certain temperate phages have incorporated bacterial genes that have nothing to do with the phage life cycle. When a bacterial cell is lysogenized by such a phage, any such incorporated gene is expressed and becomes a phenotypic trait of the bacterium. The best-known genes of this type are toxin genes, including genes for the diphtheria, tetanus, and scarlatiniform toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

generalized transduction

A

occasionally encapsulate host DNA, which is transferred to any new host upon infection

have different chromosomal segments stuffed in pacteriophage head

any bacterial gene transferred

typically only bacteria genes - no viral genes

probably accidental consequence of phage multiplication - no proven clinical relevance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

specialized transduction

A

always take same genetic info!

pecialized transduction is the process by which a restricted set of bacterial genes is transferred to another bacterium. The genes that get transferred (donor genes) depend on where the phage genome is located on the chromosome. Specialized transduction occurs when the prophage excises imprecisely from the chromosome so that bacterial genes lying adjacent to the prophage are included in the excised DNA. The excised DNA is then packaged into a new virus particle, which then delivers the DNA to a new bacterium, where the donor genes can be inserted into the recipient chromosome or remain in the cytoplasm, depending on the nature of the bacteriophage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

plasmids

A

non essential but hereditarily stable, self replicating

circular and supercoiled

medically important accessory functions

bacterial mating!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

conjugation

A

pilus - gram 0 membrane fusion - single strand into 2nd bacteria - replicate into plasmid or integrate into chromosome

plasmids spread rapidly - toxins are plsmid encoded - abx resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

transposons

A

discrete segments of DNA that encode recombination enzymes - transposases

move from one dnA location to another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

IS elements

A

The simplest transposons are DNA segments that encode only their own transposase and are known historically as insertion sequences (IS elements).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Type I transposon

A

transposase, resolution site, resolvase, short terminal inverted repeats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

conjugative transposon

A

only conjugated as a plasmid - when excised

only circular during transfer process

can reintegrate

mobility is largely theoretical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

chromosomal islands

A

chromosomal regions that contain only genes for pathogenicity, resistance, or other accessory functions

“islands” - can be visualized as genomic disparities

diff between pathogenic and non-pathogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Staph basics

A

gram positive cocci - really thick cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how to differentiate staph and strep? and what kind of staph?

A

catalase - if there is coagulation - it is staph, if no coagulation - it is strep

add coagulase to staph - if positive - s. aureus, if negative - one of the other staph

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

staphylococcus saprophyticus

A

UTIs in young women (second to e. coli)

pathogenesis: adhesins for uroepithealial cells, urination after intercourse and abx

ability to cause infection in otherwise sterile space

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

staphylococcus epidermis

A

device related - catheters, valves, joints

normal flora on the skin

form biofilms! hard to treat

abx and replacement/removal of foreign body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

MSSA, MRSA

A

methicillin sensitive (or resistant) staph aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

staphylococcus aureus

A

colonizes many people, infects a lot in hospitals and community

most infections are skin and soft tissue

MSSA, MRSA

skin and tissue infections, pneumonia, endocarditis

strain to strain variability, contact transmission

access to bloodstream, deep tissue, dissemination to all organs and tissues, attachment to ecm proteins via cell surface molecules, secrete protein for immune evasion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

s. aureus virulence factors

A

adhesions - promote attachment to tissues - switch to secreted proteins

exoproteins - made during stationary phase, promote tissue destrcution dissemination, nutrient acquisition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Protein A

A

S. aureus

binds Fc portion of IgG and inhibits ab mediated phagocytic killing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

PBP

A

penicillin binding proteins

gram positive cell wall - involved in cell wall biosynthesis

target for PCN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

mecA

A

found in MRSA

codes for PBP2 - makes bacteria resistant to all beta lactams because they can’t bind to normal PBP

s. aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

membrane damaging toxins

A

exprotien in staph aureus

pore forming toxn - targets cells - disarm host kill cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

exfoliative toxins

A

serine protease - cleaves desmoglien - scalleded skin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

superantigens

A

non specifically stimulates 20% circulating t cells

release over overwhelming amt of cytokines - severe systemic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

toxic shock syndrome toxin 1

A

TSS associated w menstration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

SEIX

A

lethality of CA_MRSA necrotitzing pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Toxin mediated diseases caused by s. aureus

A

GI (food poisoning)

TSS

scaleded skin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

necrotic diseases caused by s. aureus

A

impetigo, folliculitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Staphylococcal food poisoning

A

intoxication not an infection

eat toxin containing food

enterotoxins - heat stable - resist gastric acid hydrolysis - stimulate T cells to make cytokines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

toxic shock syndrome

A

staph

sudden onset of symptoms - high fever, rash, GI, multisymptoms

risk factors = tampons, abscesses

toxins involved

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

s. aureus abscesses

A

necrotic enter with live and dead bacteria, leukocytes, and pus

surrounded by fibrin wall and inflammatory cells

abscess promoting: dead leukocytes, secreted immune modulators and cytotoxons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

MRSA drug

A

vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

MSSA drug

A

oxacillin/nafcillin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

strep basics

A

gram positive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

beta hemolytic

A

lysis of RBC all around colonies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

alpha hemolytic

A

oxidation of Hg due to H2O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

beta hemolytic strep

A

if does not grow in presence of bacitracin - strep pyogenes

if does grow with bacitracit (resistant) - another beta hemolytic strep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

M protein

A

strep

antiphagocytic

evades phagocytic cells unless host has ab particular to that specific M protein

one you make ab, you can phagocytose the strep but that takes like 1 weeks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Streptococcus pyogenes

A

Group A strep

oropharynx of children and young adults and skin

pass person to person and through breaks in skin

can cause invasive, disseminated infection, TSS, post infections sequalae (rheumatic fever and glomerulonephritis)

skin: impetigo, erysipelas, cellulitis, scarlet fever, necrotizing fascitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

rheumatic fever

A

strep pyogenes (group A) post infections sequenli

heart inflammation - recurrent episodes can lead to rheumatic heart disease (need heart transplant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

acute post strep glomerulonephritis

A

post-infections sequeale of group a strep

inflammation

can lead to renal failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

S. Pyogenes Treatment

A

PCN

no asymptomatic carriage unless history of rheumatic fever

no vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

streptococcus agalactiae

A

Group B strem

small gram positive coccus

beta/non hemolytic

bactiracin resistant (unlike GAS)

antiphagocytic polysaccharides

normal vlora of GI - soread maternal-fetal in utero

disseminated infection, maternal and newborn infections, UTI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Group B strep treatment

A

PCR or culture

PCN suscemptible

no vaccine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

streptococcus pneumoniae

A

dipliccocus

over 90 serotypes of capsular polysaccharide (like M protein for this strain)

very common and highly adotpable

lobar pneumonia - not a lot of destruction just problem with gas exchange

middle ear infection, meningitis (survive in blood because encapsulated)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

s. pneumoniae and abx

A

resistant to beta-lactam abx

altered PBPS - reduce affinity for PCN, resistance is spread and codominant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

pneumococcal-protein conjugate vaccine

A

13 capsular polysacchardides linked to diphtheria toxoid to generate thymus dependent immunity

herd immunity

serotype replacement - keep having to add more

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

enterococcus

A

Group D

normal flora in intestine

HA infections! endocarditis on heart valves, catheters, role of biofilms, ICU

abx resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

VRE

A

vancomycin resistant enterococci

acquisition of plasmids or transposons - mediates broad resistance

when kill everything, this is what is left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Enterococci abx

A

intrinsic resistance to PCN, Cephalosporins, Clinda

beta lactams select for survival

can acquire resistance toa lot of other things

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

mechanism of vancomysin resistance

A

instaed of D-ala D-ala, becomes D-ala, D-lactate

way decreased affinity for vancomysin

get this cell wall structure from transposons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Why is there no vaccine against GAS?

A

increased variability of M protein - associated with rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Why no GBS vaccine for infants?

A

capsular polysaccharide - infants have poor response and would have to vaccinate mom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

why is s. pneumoniae vaccine incomplete

A

only covers 13 serotypes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

why no vaccine against enterococcus

A

ICU patients - hard to know who to give it to

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

e. coli basics

A

enterobacteriaceae

gram NEG

mot are lactose positive

different serotypes: O ag (LPS), H ag (Flagellum), K ag (capsule)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

ETEC

A

enterotoxigenic E Coli

mild - infant and traveler’s diarrhea

watery diarrhea (no blood, fever, vomiting)

small intestine - usually mild, self limiting

food and water, high infectious dose

shed in stool even if asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

ETEC colonization

A

pili - encoded by plasmid - binds to small bowel enterocytes (host species specificity)

strong ag - many different types (even on a single cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

ETEC Heat Labile Toxin

A

plasmid encoded

2 subunits - A1B5 - b binds and a ADP ribosylates G protein

turns on adenylate cyclease - more cAMP - phosphorylates proteins

in crypt cells: Cl- out

in absorptive cells, NaCl can’t come back in

increase ionic strength - more ions inside than outside - less water into cells, water in diarrhea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

ETEC Heat stable toxin

A

made by ETEC and other gram negative bacteria

heat stable

increased Cl- secretion from crypt and inhib NaCL absormotion

osmotic diarrhea

increases cGMP

78
Q

EPEC

A

Enteropathic E Coli

infant diarrhea - may be protracted and severe (vomiting and fever common

food and water

more developing world

generally self limiting

mult abx resistance

sheds up to 2 wks in stool

79
Q

EPEC pathogenesis

A
  1. localized adherence - pilli
  2. signal transduction (type III secretion)
  3. intimate adherence (receptor binding)

BFP binds w pillis - injects ESPs and Tir, Tir-P phosphorylated - becomes receptor, Intimin binds Tir R –> actin polymerization

80
Q

BFP

A

EPEC - pillus

mediates inital adhrence

encoded by EAF plasmid

tEPEC - has EAF plasmid

aEPEC does not have EAF plasmid

81
Q

Esp

A

EPEC -signal transduction

proteins secreted directly into host cell via T3SS

Encoded by pathogenicity island (LEE)

increased Ca2+, host protein P, microvillus effacement, actin polymerization

82
Q

Intimate Adherence

A

EPEC

Secretes Tir into cell via T3SS - it is phosphorylated - goes to surface as receptor - EPEC can inject others (like Esps) for actin polymerization

loss of microvilli –> malabsorption

Cl- ion secretion from protein kinase activation

disruption of tight junctions –> increased intestinal permeability

83
Q

EHEC

A

Enterohemorrhagic E Coli

recelntly emerged

hemorrhagic colitis

NO abx - makes it worse

Shiga toxin

food and water, low infectious dose, cattle

84
Q

EHEC pathogenesis

A

don’t know inital mech of attachment (n EAF plasmid)

has LEE pathogenicity island

Uses Intimin-Tir system but NO Tir phosphorylation

attaching and effacing histopathy

(almost exactly same as EPEC but + Shiga toxin)

85
Q

EHEC Shiga Toxins

A

Stx1, stx2 - bind Gb3 R

stx genes are on lysogenic bacteriophages - integrate (why no abx - DNA damage - virus makes mult copies of genome and leaves - will make a ton of toxin!)

A1B5 - bind receptor, A enters cell, inhibits ribosome

receptor more prevalent on absorptive villus cell tip than secretary crytp cells

destruction stays in intestine but toxin can move to kidney

86
Q

Hemolytic Uremic Sydnrome (HUS)

A

EHEC

Stx translocates to kidneys via bloodstream

Gb3 R is revalent in renal tissue - damage endothelial cells - renal failure

87
Q

EAggEC

A

Enteroaggregative E Coli

persistant diarrhea in infants- mucus and blood

biofilm and mucus, don’t know much about pathogenesis

88
Q

EAggEC Pathogenesis

A

enhances mucussecretion from intestinal mucosa

plasmid encoded pili - mediate aggregative adherence within mucoid biofim

89
Q

EIEC

A

Enterinvasive

very similar to shigella

invasion - into phagosome - escape - swims around by polarizing actin behind it, can spread from cell to cell

90
Q

UPEC

A

most common cause of UTI

colonizaton of colon may occur first (UPEC doesn’t cause intestinal disease)

ascending infections - urethra, bladder, kidneys

kidney infection can lead to sepsis

91
Q

female reasons for UTIs

A

anatomic - short distance from anus to urethra

vaginal environent supports growth

sex - mechanical action, spermicide inhibits normal flora

92
Q

Type I pili

A

UPEC

important for bladder colonization - binds mannose residues on bladder glycoproteins

differential expression

may precde invasion of bladder epithelial cells (why recurrent?

93
Q

P pili

A

UPEC

promarily on strains that cause kidney disease - bind to glycolipid on kidney cells

94
Q

Recurent UTI

A

UPEC colonization of colon - reservoir

persists in host cells in underlying bladder epithelial cells

95
Q

K1 capsular ag

A

specific interations with brain Endothelial cells

S pili mediate binding, invasions required some e coli proteins

96
Q

neisseria meningitidis

A

encapsulated

gram negative

colonizes nasopharynx, invades bloodstream and meninges, innate can usually handle

humans with complement (MAC) deficiencies are highly susceptible to invasive infections

97
Q

classical complement pathway

A

ag+IgM/IgG –> C1q, C1r, C1s, C4, C2, C3, 5, 6, 7, 8, 9 Lysis

C5-9 = MAC

C3 - also opsonizes

98
Q

alternative complement pathway

A

CHO, LPS, Sialic acid –> D, C3, P, B, C3, MAC, lysis

99
Q

Mannose-Binding Lectin Pway

A

MBL/MASP - plasma protein circulates as complex, binds to bac, recruits protease, cleaves C4, activate comlment pway –> C3, C3, MAC lysis

100
Q

Factor H

A

to limit self damage!! stops activation of C3

regulation

101
Q

Complement antimicrobial actions

A

direct lysis - MAC, C5-9

Opsonization - rec, ingest, killing by phagocytes

102
Q

C3b, C3bi

A

opsonize bacteria - rec by complement receptors on neutrophils and macrophages, lead to phagocytosis

103
Q

meningococcal defense defects

A

mannose-binding lectin defiiceincies! hets - 10% of MBL in blood - harder to activate compleent!

104
Q

GNA1870

A

meningococcal protein, resent un all strains of group B, on bacterial surface, same as fHbp!!! binds factor H and accelerates inactivation of C3b

binds Factor H - brings it to bacterial surface and inactivates C3b

also put sialic acid on the cell membrane

105
Q

meningococcal vaccine

A

immunization w polysac - poor B cell memory!

conjugate polysacc to carrier protein - provides T cell help and superior B cell/ab response

vaccine has 4 ags - not group B ag!

106
Q

Group B Meningococcus

A

polysacc is identical to human self - mimicry! no response in vaccine, don’t want people to have autoabs anyway

reverse vaccinology!

107
Q

endotoxin

A

LPS - outer layer of gram negative, not exported

cell associated

108
Q

exotoxin

A

extracellular diffusible substance (usually protein)

109
Q

toxinoses

A

toxins can cause specific diseases or can contribute genreally to pathogensis

most lethal bacterial diseases

most successful for diseases

110
Q

A-B toxins

A

one gene - single precursor cleaved into A and B, remain covalently associated

mult genes - made as separate proteins that form a non-covalent complex

B binds host receptor

A enters cytoplasm and has catalytic activity

111
Q

Pertussis Toxin (PT)

A

whopping cough - toxin affects cell signaling

AB5 - diff bunding sumunits

active = ADP-ribosyltranferase - G protein - inhibits inhibitory GPCR - increase adenylate cyclase and cAMP - increase respiratory secretions and mucus (increased ionic strength)

impaired neutrophil chemotaxis, phagocytosis and bacteriocidal activity, increased insulin production and hypoglycemia

abx work but need full recovery of ciliated epithelial cells

vaccine

112
Q

anthrax toxin

A

affects cell singlaing - edema factor is an adenylate cyclase, lethal factor inactivates MAPKK signaling molecule

PA + EF or PA + LT

PA - forms pore! gets toxin into cell - acid puts toxin into cytoplasm -

inhalation - death within days, cutaneous, GI

abx - critical

113
Q

EF

A

edema toxin

anthrax

EF = increase cAMP, upsets cellular water balance, edema

114
Q

LT

A

Lethal Toxin

anthrax

LT - deactivate MAPKK, death of cell!

115
Q

Diphtheria toxin

A

corynebacterium diphtheriae

inhibit protein synthesis

disease entirely from toxin - tox gene introlduced by lysogenic bacteriophage

B - binds GF (heart and nerve)

A- ADP-ribosylates elongation factor 2 (inactiates)

irreversible protein synthesis inhibition and cell death

respiratory and cutaneous

antitoxin and vaccine

116
Q

Immunotoxins

A

Diphtheira toxin with IL-2 on B subunit

kills all T cells with IL2 R

less efficacious against solid tumor

117
Q

Tetanus

A

spores in soil, dust, animal feces, enter body when injury

B - binds sialiac acid receptors and proteins on motor neurons

toxin transported in neuron axon to nueron soma - across synapses

blocks nt release at inhibitory synapse by cleaving synaptic vesicle protein

118
Q

neurotoxins

A

interfere w synaptic funciton

tetanus (decrease inhib NT release) and botulinum (blocks excitory NT release)

120
Q

Tetanus treatment and prevention

A

give Ig (toxin bound to nerve endings is protected from abs)

vaccine! needs boosters

121
Q

superantigens

A

antigen-independent activation of T cells

TSS

Staph. aureus

Strep. pogenes

122
Q

botulism

A

heat resistant spores in soil and water - can contaminate food (canned)

complex with other nontoxic proteins - protect in GI

B binds sialic acid and glycoproteins on motor neurons

remains at nm junction!

blocks release of Ach with vesicles - flaccid paralysis

recovery required regeneration of nerve endings

123
Q

botulism treatment and prevention

A

antitoxin

ventialtory support!

weeks or months to recover

multiple infecions are possible

botox

124
Q

mycobacterium tuberculosis

A

not gram pos or gram neg - acid fast!

slow generation time

transmitted by aerosol from person to person

any organ!

curable w drugs but resistance is worsening

125
Q

structure of mycobacterial cell wall

A

unusual - thin like gram negative, butno outermembrane

arabinogalactan (complex carb) layer

mycolic acid layer on outside ( long cahin FA)

capsules on very outside

126
Q

trehalose dimycolate

A

unique TB lipid

carb disaccharide with long FA chains

proinflamatory, rec by C-type lecitin on macrophages

127
Q

PIM and LAM

A

PIM - TLR2 agonist (proinflam)

Lam - block phagosome maturation

unique lipids to TB

128
Q

adaptive immune response to TB

A

delayed! lantent doesn’t transmit - have to be sick

129
Q

TB and macrophages

A

survives and replicates in macrophages

in immature phagosomes - don’t degrade bc phagosomes with TB do not merge with lysosomes

130
Q

EsxH

A

TB protein - targets cell ESCRT complex and inhibits phagosome maturation

so TB can live in phagosome

ESCRT - intracell trafficking

131
Q

Vitamin D and TB

A

induces macrophage expression of antimicrobial peptide

accelerates resolution of inflammation

less progress if higher vitamin D! doesn’t accelerate bacterial clearance

132
Q

Role of CD4 T cells in immunity to TB

A

secrete cytokines (IFNg, TNF)

induce death of infected cells

maintain cd8+ t cells

133
Q

TB immune evasion

A

blocks phagosome maturation

delays onset of cell immune response

minimizes rec by cd4 t cells

blocks macropahage response to ifn gamma

t cell rec - little selection pressure on bacteria!

134
Q

acid-fact bacteria

A

mycobacteria

stain

decolorize (acid and alocohol - other cells won’t hold stain but mycobacteria does!)

counterstain (to see other cells)

135
Q

new TB detection

A

culture independent, pcr based testing for presense of TB and for drug resistance (2h)

neeed electricity and to keep it cold

less false pos

136
Q

BCG

A

live attenuated TB vaccine

missing RD1 chromosomal region (needed for virulence)

137
Q

RD-1

A

important genes for virulense! protein secretion system + proteins

138
Q

PPD skin test

A

ag injected, has to be read

does not distinguish TB from BCG vaccination - ags in PPD are shared by BCG and TB

139
Q

Esx-1

A

secretes proteins to promote recruitment and infection of macrophages in vivo

spreads more efficiently

140
Q

EspB

A

secreted by Esx-1

damages host cell membrane

quantity of secretion correlates with bacterial fitness/virulence

phagosome rupture requires EspP

if cell membrane is damaged - can’t fight

141
Q

LTA4H

A

enzyme that leads to too much or too little activation!

if more inflammation - benefited a lot from antiinflammatory drugs

142
Q

HIV and TB

A

HIV - depletes CD4 t cells needed for control of TB

TB activates transciption factor NFkB –> increases HIV transcription, increases expression of CCR5

143
Q

TB drug resistant

A

does not exchange DNA with other bacteria! all drug resistance arrises by mutation, mutants can be transmitted

144
Q

Mycobacterium leprae

A

leprosy (hansen’s disease)

can’t be cultured in vivo

decaying gneome

in cool places - skin, peripheral nerve, armadillos

cutaneous lesions, nerve damage, reactional states (switch immune response)

145
Q

Tuberculoid leprosy

A

Th1 response - few bacteria

146
Q

Lepromatous leprosy

A

Th2 response, numerous bacteria

147
Q

leprosy treatment

A

multidrug! rifampin + dapsne, floroquinolose`

148
Q

mycobacterium avium

A

non specific symptoms - sytemic

associated w very low CD4 t cells (AIDS)

from environlemtal, bacterial burden can be very high

can have pulmonary disease in immunocomp pts - not transmissable human to human , can cause lung destruction

149
Q

mycobacterium marinum

A

infects fish

abcessus - subcutaneous (needles, liposuction)

resistant to many anti-TB drugs

150
Q

mycobacterium ulcerans

A

extracellular

toxin - cell necrosis - skin and soft tissue ulcers

151
Q

Salmonella basics

A

gram negative, rod shaped

highly motile, propelled by flagela

lactose negative

contaminated food or water

GI or typhoid - define by O-ag

152
Q

GI salmonella

A

s. typhimurium, s. enteritidis

high infectious dose, GI, headache

diarrhea without blood

self limiting, no abx needed

153
Q

Typhoid fever

A

s. typhi, s. paratyphi

malaise, fever, headaches, diarrhea, enlarged spleen - hemorrhage

typhoid toxin! A2B5

need abx!

can not infect mice, can infect chimps but no symptosm (enzyme modifies toxin)

154
Q

Shigella basics

A

really low infectious dose!

GI, blood, lymphocytes, mucus in stool

dysentary

contaminated water, food

survive in pH of stomach and invade epithelial cells in the gut

can invade non-phagocytic

kill/survive in macrophages

155
Q

SPI1

A

Salmonella Pthogenicity Island

most path genes in region of the chromosome

156
Q

shigella pathogenicity

A

T3ss, encoded on virulence plasmid! genes for virulence

157
Q

T3SS

A

both shigella and salmonella have - syringe spanning inner and outer membrane, injects proteins into host cell - leading to uptake of bacteria

158
Q

pyroptosis

A

how salmonella and shigella kill macrophages

apoptosis and necrosis

require T3ss for invasion

159
Q

salmonella replication

A

after invasion, replicates in vacuole of epithelial cell (moves around vacuole w flagella)

only salmonella can survive and grow in macrophages! shigella can kill but not survive

160
Q

shigella replication

A

escapes from vacuole and replicates in cytoplams,

in cytoplasm, moves around by host derived actin tains (no flagella)

161
Q

SPI2

A

another T3SS but different

prevents fusion of salmonella in vesicles w vacuoles containing anti-microbial molecules (phos, nitric oxide synthase - both will kill bac)

usually will kill bacteria, but salmonella prevents fusion with T3SS on SPI2

162
Q

Salmonella nutritional immunity

A

inflammation recruits host proteins like calprotectin and lipocalin - seqester essential metals from bacteria - salmonella has metal acquiring systems and can outcompete many bac species in the gut

163
Q

Salmonella and Shigella Pathology

A

diarrhea - tissue invasion - inflammation

kill - septic shock due to LPS

164
Q

Salmonella and shigella major similarities

A

gram neg, lactose neg

contaminated food and water

intracellular pathogens!

invade epithelial cells

require T3SS for invasion (non-phagocytic cells take up) and killing macrophages

165
Q

S and S - where invade

A

Salmonella - small intestine epithelium

Shigella - colonic epithelium

166
Q

S and S invasion genes

A

Salmonella - chromosome

Shigella - plasmid

167
Q

S and S diarrhea

A

salmonella - self limiting, blood free

shigella - severe - mucus, pus, blood

168
Q

Acinetobacteria

A

gulf war infection

gram neg, non motile

very hardy

opportunistic

abx resistance

169
Q

Klebsiella

A

gram neg, large

normal flora

usually UTIs and pneumonia in healthy people

large capsule, beta lactamase, resistance!

HMV

170
Q

Enterococcus

A

gram positive

normal intestinal fora, opportunistic

broad resistance - abx allows it to proliferate

TUI, bacteremia (endocarditis)

lots of resistance!!

171
Q

C. diff

A

gram pos, spore forming

colonizes large intestine - toxins

commensal - colonized asymptomatically

spores are widespread

abx use - removes competeing microflora, most common risk factor!

recurrent/hard to treat

fecal transplant

172
Q

pseudomonas aeruginosa

A

motile - gram neg

ubiquitous in the environment

florescent “grape like” odor

infect anywehre

acute pneumonia, UTI, CF in lungs, many more

adaptable, many virulence, abx resistance

healthy people almost never get

T2SS, T3SS

173
Q

T2SS

A

release of exotoxins, degradative enzymes, just pump out not specific

still in gram neg

secretes facors that damage tissues

174
Q

Type IV pilus

A

pseudomonas eruginosa adhesion - binds to epithelial cells! secretes subnit thatpolymerizes

175
Q

alginate polysaccharide

A

mucoid exopolysaccharide

adherence to epithelium

antiphagocytic

barrier to abx, anti-ab/comp

matrix for bioflims

synthesis is tightly reg (metabolic cost)

long term colonization of CF in the lung

176
Q

mucoid phenotype

A

constitutive alginate production

177
Q

Exotoxin A

A

secreted by T2SS

inhibits protein synthesis (inhibits elongation factor 2)

AB toxin

important virulence factor - tissue damage!

178
Q

P. aeruginosa abx resistance

A

high intrinsic (cell env, efflux pumps, beta-lactamases)

can acquire (mutation, gene transfer)

bilfim - physical barrier, gene expression

179
Q

CF and p. eruginosa

A

almost all have, can’t really be cured

inflammation and tissue distruction, leading cause of death

180
Q

biofilms

A

microbes attached to a surface and are embedded in extracelular polysaccharide matrix

on any surface - inc valves etc.

one species or mixed

slow growth, increased abx resistance and immunity resistance, can seed acute infection

181
Q

quorum sensing

A

cell-cell communication allow sensing f cell densiity

virulence,bioflims,abx production

small diffusible messenger molecules

incerased local concentration leads to affect

diffusible molecule for gram neg, secreted peptide for gram pos

control expression of community - like multicellular

invisible to host defense until enough to overwhlem

182
Q

bacillus

A

rod shaped

e. coli, shigella, salmonella, p.aeruginosa, m. tb

183
Q

coccus

A

round

staph

strep

184
Q

spirochete

A

spiral

lyme

syphillus

185
Q

catalsast test

A

is it staph or strep?

H2O2 –> 2H2O + O2

if positive (bubbles) - staph - staph has enzyme that breaks down peroxide!

if no bubbles - strep

186
Q

coagulase test

A

what kind of staph

s. aureus has coagulase enzyme - makes a clot! if clotting in plasma, it is s. aureus

187
Q

lysozyme

A

our response

kills gram positive better - can’t get across OM at all but breaks down peptidoglycan

188
Q

primary pathogens

A

cause disease in healthy

EPEC, EHEC

Salmonella

shigella

TB

Staph/strep

189
Q

opportunistic pathogen

A

p. eruginosa

enterococci

c. diff

190
Q

nosocomial pathogens

A

p aeruginosa

enterococci

191
Q

Who has T3SS

A

only in gram neg! crosses both membranes

EXAM 6 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions