Bacteria Flashcards
1
Q
defensins
A
hydrophobic, cationic
pisitive - stick to neg charged membrane in bacteria and make pores
2
Q
gram stain
A
- blue stain
- compexing agent - make stain into larger molecules
- extraction agent - pull out stain, but only works on gram negative!!
- red stain - only sticks on gram negative
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
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
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)
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
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
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
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
10
Q
LPS O-specific antigen
A
repeating unit structure
long linear polysacchadie - variable, different repeating sugars
major serologic determinant
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
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.
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.
14
Q
transduction
A
bacteriophages
viruses that attack bacteria and are specific for closely related bacterial species
15
Q
virulent phage
A
virulent phages - always cause lysis and release of phage particles - clear plaques on bacterial lawns
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
17
Q
intermediate phages
A
replicate stably int he host cell and continually release progeny
no lysis
18
Q
lysogenic state
A
phage is in a dormant state in bacteria
integrating chromosomal DNA at a specific site
dormant phage = prophage
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
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
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.
22
Q
plasmids
A
non essential but hereditarily stable, self replicating
circular and supercoiled
medically important accessory functions
bacterial mating!
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
24
Q
transposons
A
discrete segments of DNA that encode recombination enzymes - transposases
move from one dnA location to another
25
IS elements
The simplest transposons are DNA segments that encode only their own transposase and are known historically as insertion sequences (IS elements).
26
Type I transposon
transposase, resolution site, resolvase, short terminal inverted repeats
27
conjugative transposon
only conjugated as a plasmid - when excised
only circular during transfer process
can reintegrate
mobility is largely theoretical
28
chromosomal islands
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
29
Staph basics
gram positive cocci - really thick cell wall
30
how to differentiate staph and strep? and what kind of staph?
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
31
staphylococcus saprophyticus
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
32
staphylococcus epidermis
device related - catheters, valves, joints
normal flora on the skin
form biofilms! hard to treat
abx and replacement/removal of foreign body
33
MSSA, MRSA
methicillin sensitive (or resistant) staph aureus
34
staphylococcus aureus
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
35
s. aureus virulence factors
adhesions - promote attachment to tissues - switch to secreted proteins
exoproteins - made during stationary phase, promote tissue destrcution dissemination, nutrient acquisition
36
Protein A
S. aureus
binds Fc portion of IgG and inhibits ab mediated phagocytic killing
37
PBP
penicillin binding proteins
gram positive cell wall - involved in cell wall biosynthesis
target for PCN
38
mecA
found in MRSA
codes for PBP2 - makes bacteria resistant to all beta lactams because they can't bind to normal PBP
s. aureus
39
membrane damaging toxins
exprotien in staph aureus
pore forming toxn - targets cells - disarm host kill cells
40
exfoliative toxins
serine protease - cleaves desmoglien - scalleded skin syndrome
41
superantigens
non specifically stimulates 20% circulating t cells
release over overwhelming amt of cytokines - severe systemic reactions
42
toxic shock syndrome toxin 1
TSS associated w menstration
43
SEIX
lethality of CA\_MRSA necrotitzing pneumonia
44
Toxin mediated diseases caused by s. aureus
GI (food poisoning)
TSS
scaleded skin syndrome
45
necrotic diseases caused by s. aureus
impetigo, folliculitis
46
Staphylococcal food poisoning
intoxication not an infection
eat toxin containing food
enterotoxins - heat stable - resist gastric acid hydrolysis - stimulate T cells to make cytokines
47
toxic shock syndrome
staph
sudden onset of symptoms - high fever, rash, GI, multisymptoms
risk factors = tampons, abscesses
toxins involved
48
s. aureus abscesses
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
49
MRSA drug
vancomycin
50
MSSA drug
oxacillin/nafcillin
51
strep basics
gram positive
52
beta hemolytic
lysis of RBC all around colonies
53
alpha hemolytic
oxidation of Hg due to H2O2
54
beta hemolytic strep
if does not grow in presence of bacitracin - strep pyogenes
if does grow with bacitracit (resistant) - another beta hemolytic strep
55
M protein
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
56
Streptococcus pyogenes
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
57
rheumatic fever
strep pyogenes (group A) post infections sequenli
heart inflammation - recurrent episodes can lead to rheumatic heart disease (need heart transplant
58
acute post strep glomerulonephritis
post-infections sequeale of group a strep
inflammation
can lead to renal failure
59
S. Pyogenes Treatment
PCN
no asymptomatic carriage unless history of rheumatic fever
no vaccine
60
streptococcus agalactiae
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
61
Group B strep treatment
PCR or culture
PCN suscemptible
no vaccine
62
streptococcus pneumoniae
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)
63
s. pneumoniae and abx
resistant to beta-lactam abx
altered PBPS - reduce affinity for PCN, resistance is spread and codominant
64
pneumococcal-protein conjugate vaccine
13 capsular polysacchardides linked to diphtheria toxoid to generate thymus dependent immunity
herd immunity
serotype replacement - keep having to add more
65
enterococcus
Group D
normal flora in intestine
HA infections! endocarditis on heart valves, catheters, role of biofilms, ICU
abx resistance
66
VRE
vancomycin resistant enterococci
acquisition of plasmids or transposons - mediates broad resistance
when kill everything, this is what is left
67
Enterococci abx
intrinsic resistance to PCN, Cephalosporins, Clinda
beta lactams select for survival
can acquire resistance toa lot of other things
68
mechanism of vancomysin resistance
instaed of D-ala D-ala, becomes D-ala, D-lactate
way decreased affinity for vancomysin
get this cell wall structure from transposons
69
Why is there no vaccine against GAS?
increased variability of M protein - associated with rheumatic fever
70
Why no GBS vaccine for infants?
capsular polysaccharide - infants have poor response and would have to vaccinate mom
71
why is s. pneumoniae vaccine incomplete
only covers 13 serotypes
72
why no vaccine against enterococcus
ICU patients - hard to know who to give it to
73
e. coli basics
enterobacteriaceae
gram NEG
mot are lactose positive
different serotypes: O ag (LPS), H ag (Flagellum), K ag (capsule)
74
ETEC
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
75
ETEC colonization
pili - encoded by plasmid - binds to small bowel enterocytes (host species specificity)
strong ag - many different types (even on a single cell)
76
ETEC Heat Labile Toxin
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
77
ETEC Heat stable toxin
made by ETEC and other gram negative bacteria
heat stable
increased Cl- secretion from crypt and inhib NaCL absormotion
osmotic diarrhea
increases cGMP
78
EPEC
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
EPEC pathogenesis
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
BFP
EPEC - pillus
mediates inital adhrence
encoded by EAF plasmid
tEPEC - has EAF plasmid
aEPEC does not have EAF plasmid
81
Esp
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
Intimate Adherence
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
EHEC
Enterohemorrhagic E Coli
recelntly emerged
hemorrhagic colitis
NO abx - makes it worse
Shiga toxin
food and water, low infectious dose, cattle
84
EHEC pathogenesis
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
EHEC Shiga Toxins
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
Hemolytic Uremic Sydnrome (HUS)
EHEC
Stx translocates to kidneys via bloodstream
Gb3 R is revalent in renal tissue - damage endothelial cells - renal failure
87
EAggEC
Enteroaggregative E Coli
persistant diarrhea in infants- mucus and blood
biofilm and mucus, don't know much about pathogenesis
88
EAggEC Pathogenesis
enhances mucussecretion from intestinal mucosa
plasmid encoded pili - mediate aggregative adherence within mucoid biofim
89
EIEC
Enterinvasive
very similar to shigella
invasion - into phagosome - escape - swims around by polarizing actin behind it, can spread from cell to cell
90
UPEC
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
female reasons for UTIs
anatomic - short distance from anus to urethra
vaginal environent supports growth
sex - mechanical action, spermicide inhibits normal flora
92
Type I pili
UPEC
important for bladder colonization - binds mannose residues on bladder glycoproteins
differential expression
may precde invasion of bladder epithelial cells (why recurrent?
93
P pili
UPEC
promarily on strains that cause kidney disease - bind to glycolipid on kidney cells
94
Recurent UTI
UPEC colonization of colon - reservoir
persists in host cells in underlying bladder epithelial cells
95
K1 capsular ag
specific interations with brain Endothelial cells
S pili mediate binding, invasions required some e coli proteins
96
neisseria meningitidis
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
classical complement pathway
ag+IgM/IgG --\> C1q, C1r, C1s, C4, C2, C3, 5, 6, 7, 8, 9 Lysis
C5-9 = MAC
C3 - also opsonizes
98
alternative complement pathway
CHO, LPS, **Sialic acid** --\> D, C3, P, B, C3, MAC, lysis
99
Mannose-Binding Lectin Pway
MBL/MASP - plasma protein circulates as complex, binds to bac, recruits protease, cleaves C4, activate comlment pway --\> C3, C3, MAC lysis
100
Factor H
to limit self damage!! stops activation of C3
regulation
101
Complement antimicrobial actions
direct lysis - MAC, C5-9
Opsonization - rec, ingest, killing by phagocytes
102
C3b, C3bi
opsonize bacteria - rec by complement receptors on neutrophils and macrophages, lead to phagocytosis
103
meningococcal defense defects
mannose-binding lectin defiiceincies! hets - 10% of MBL in blood - harder to activate compleent!
104
GNA1870
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
meningococcal vaccine
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
Group B Meningococcus
polysacc is identical to human self - mimicry! no response in vaccine, don't want people to have autoabs anyway
reverse vaccinology!
107
endotoxin
LPS - outer layer of gram negative, not exported
cell associated
108
exotoxin
extracellular diffusible substance (usually protein)
109
toxinoses
toxins can cause specific diseases or can contribute genreally to pathogensis
most lethal bacterial diseases
most successful for diseases
110
A-B toxins
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
Pertussis Toxin (PT)
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
anthrax toxin
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
EF
edema toxin
anthrax
EF = increase cAMP, upsets cellular water balance, edema
114
LT
Lethal Toxin
## Footnote
anthrax
LT - deactivate MAPKK, death of cell!
115
Diphtheria toxin
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
Immunotoxins
Diphtheira toxin with IL-2 on B subunit
kills all T cells with IL2 R
less efficacious against solid tumor
117
Tetanus
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
neurotoxins
interfere w synaptic funciton
tetanus (decrease inhib NT release) and botulinum (blocks excitory NT release)
120
Tetanus treatment and prevention
give Ig (toxin bound to nerve endings is protected from abs)
vaccine! needs boosters
121
superantigens
antigen-independent activation of T cells
TSS
Staph. aureus
Strep. pogenes
122
botulism
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
botulism treatment and prevention
antitoxin
ventialtory support!
weeks or months to recover
multiple infecions are possible
botox
124
mycobacterium tuberculosis
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
structure of mycobacterial cell wall
unusual - thin like gram negative, butno outermembrane
arabinogalactan (complex carb) layer
mycolic acid layer on outside ( long cahin FA)
capsules on very outside
126
trehalose dimycolate
unique TB lipid
carb disaccharide with long FA chains
proinflamatory, rec by C-type lecitin on macrophages
127
PIM and LAM
PIM - TLR2 agonist (proinflam)
Lam - block phagosome maturation
unique lipids to TB
128
adaptive immune response to TB
delayed! lantent doesn't transmit - have to be sick
129
TB and macrophages
survives and replicates in macrophages
in immature phagosomes - don't degrade bc phagosomes with TB do not merge with lysosomes
130
EsxH
TB protein - targets cell ESCRT complex and inhibits phagosome maturation
so TB can live in phagosome
ESCRT - intracell trafficking
131
Vitamin D and TB
induces macrophage expression of antimicrobial peptide
accelerates resolution of inflammation
less progress if higher vitamin D! doesn't accelerate bacterial clearance
132
Role of CD4 T cells in immunity to TB
secrete cytokines (IFNg, TNF)
induce death of infected cells
maintain cd8+ t cells
133
TB immune evasion
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
acid-fact bacteria
mycobacteria
stain
decolorize (acid and alocohol - other cells won't hold stain but mycobacteria does!)
counterstain (to see other cells)
135
new TB detection
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
BCG
live attenuated TB vaccine
missing RD1 chromosomal region (needed for virulence)
137
RD-1
important genes for virulense! protein secretion system + proteins
138
PPD skin test
ag injected, has to be read
does not distinguish TB from BCG vaccination - ags in PPD are shared by BCG and TB
139
Esx-1
secretes proteins to promote recruitment and infection of macrophages in vivo
spreads more efficiently
140
EspB
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
LTA4H
enzyme that leads to too much or too little activation!
if more inflammation - benefited a lot from antiinflammatory drugs
142
HIV and TB
HIV - depletes CD4 t cells needed for control of TB
TB activates transciption factor NFkB --\> increases HIV transcription, increases expression of CCR5
143
TB drug resistant
does not exchange DNA with other bacteria! all drug resistance arrises by mutation, mutants can be transmitted
144
Mycobacterium leprae
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
Tuberculoid leprosy
Th1 response - few bacteria
146
Lepromatous leprosy
Th2 response, numerous bacteria
147
leprosy treatment
multidrug! rifampin + dapsne, floroquinolose`
148
mycobacterium avium
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
mycobacterium marinum
infects fish
abcessus - subcutaneous (needles, liposuction)
resistant to many anti-TB drugs
150
mycobacterium ulcerans
extracellular
toxin - cell necrosis - skin and soft tissue ulcers
151
Salmonella basics
gram negative, rod shaped
highly motile, propelled by flagela
lactose negative
contaminated food or water
GI or typhoid - define by O-ag
152
GI salmonella
s. typhimurium, s. enteritidis
high infectious dose, GI, headache
diarrhea without blood
self limiting, no abx needed
153
Typhoid fever
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
Shigella basics
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
SPI1
Salmonella Pthogenicity Island
most path genes in region of the chromosome
156
shigella pathogenicity
T3ss, encoded on virulence plasmid! genes for virulence
157
T3SS
both shigella and salmonella have - syringe spanning inner and outer membrane, injects proteins into host cell - leading to uptake of bacteria
158
pyroptosis
how salmonella and shigella kill macrophages
apoptosis and necrosis
require T3ss for invasion
159
salmonella replication
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
shigella replication
escapes from vacuole and replicates in cytoplams,
in cytoplasm, moves around by host derived actin tains (no flagella)
161
SPI2
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
Salmonella nutritional immunity
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
Salmonella and Shigella Pathology
diarrhea - tissue invasion - inflammation
kill - septic shock due to LPS
164
Salmonella and shigella major similarities
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
S and S - where invade
Salmonella - small intestine epithelium
Shigella - colonic epithelium
166
S and S invasion genes
Salmonella - chromosome
Shigella - plasmid
167
S and S diarrhea
salmonella - self limiting, blood free
shigella - severe - mucus, pus, blood
168
Acinetobacteria
gulf war infection
gram neg, non motile
very hardy
opportunistic
abx resistance
169
Klebsiella
gram neg, large
normal flora
usually UTIs and pneumonia in healthy people
large capsule, beta lactamase, resistance!
HMV
170
Enterococcus
gram positive
normal intestinal fora, opportunistic
broad resistance - abx allows it to proliferate
TUI, bacteremia (endocarditis)
lots of resistance!!
171
C. diff
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
pseudomonas aeruginosa
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
T2SS
release of exotoxins, degradative enzymes, just pump out not specific
still in gram neg
secretes facors that damage tissues
174
Type IV pilus
pseudomonas eruginosa adhesion - binds to epithelial cells! secretes subnit thatpolymerizes
175
alginate polysaccharide
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
mucoid phenotype
constitutive alginate production
177
Exotoxin A
secreted by T2SS
inhibits protein synthesis (inhibits elongation factor 2)
AB toxin
important virulence factor - tissue damage!
178
P. aeruginosa abx resistance
high intrinsic (cell env, efflux pumps, beta-lactamases)
can acquire (mutation, gene transfer)
bilfim - physical barrier, gene expression
179
CF and p. eruginosa
almost all have, can't really be cured
inflammation and tissue distruction, leading cause of death
180
biofilms
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
quorum sensing
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
bacillus
rod shaped
e. coli, shigella, salmonella, p.aeruginosa, m. tb
183
coccus
round
staph
strep
184
spirochete
spiral
lyme
syphillus
185
catalsast test
is it staph or strep?
H2O2 --\> 2H2O + O2
if positive (bubbles) - staph - staph has enzyme that breaks down peroxide!
if no bubbles - strep
186
coagulase test
what kind of staph
s. aureus has coagulase enzyme - makes a clot! if clotting in plasma, it is s. aureus
187
lysozyme
our response
kills gram positive better - can't get across OM at all but breaks down peptidoglycan
188
primary pathogens
cause disease in healthy
EPEC, EHEC
Salmonella
shigella
TB
Staph/strep
189
opportunistic pathogen
p. eruginosa
enterococci
c. diff
190
nosocomial pathogens
p aeruginosa
enterococci
191
Who has T3SS
only in gram neg! crosses both membranes
