yersinia and strep Flashcards
(438 cards)
1
Q
Yersinia types
A
Y. enterocolitica
Y. pestis
2
Q
Bacteria in Yersinia genus
A
gram-negative bacilli
3
Q
Yersinia bacteria are
A
facultative anaerobes
4
Q
Y. enterocolitica main idea
A
causes food poisoning and mimics appendicitis
5
Q
Y. pestis main idea
A
causes plague
6
Q
Yersinia is able to divide quickly
A
at temps as low at -2 degrees C
7
Q
Yersinia is able to contaminate
A
contaminate refrigerated samples
8
Q
Yersinia bacteria are also…..
A
zoonotic
9
Q
zoonotic
A
normal hosts are other animals
10
Q
examples of host of Yersinia
A
RATS, rabbits, prairie dogs, squirrels, chipmunks
11
Q
Yersinia loves
A
iron
12
Q
since yersinia loves iron it’s classified as
A
siderophilic
13
Q
who are most succptible to Yersinia infections
A
people with hemochromatosis
14
Q
hemochromatosis
A
high iron levels
15
Q
what is the most common contaminant of blood transfusions
A
Y. enterocolitica
16
Q
how many samples of blood are contaminated with Y. enterocolitica
A
1 in 1 million
17
Q
people who receive a blood sample contaminated with Y. enterocolitica
A
quickly enter septic shock, mortality rate over 50%
18
Q
Because Y. enterocolitica is gram-negative,
A
it has endotoxin (LPS)
19
Q
prescence of LPS from Y. enterocolitica in the bloodstream causes
A
widespread inflammation, strong immune reaction
20
Q
symptoms of blood transfusion with Y. enterocolitica
A
hypotension, fever, shivering
21
Q
symptoms of blood transfusion with Y. enterocolitica set in
A
within 3 hours of transfusion
22
Q
why is food contaminated with Y. enterocolitica
A
because of urine or feces of rats
23
Q
once food contaminated with Y. enterocolitica is eaten
A
bacteria get eaten by macrophages, but cannot be destroyed
24
Q
when Y. enterocolitica can’t be destroyed by macrophages
A
macrophages unknowingly carry bacteria to Peyer’s patches of the small intestine
25
Peyer's patches
lymph-like regions of the small intestine.
26
digested material passes through the Peyer's patches
passes through them and must pass through many macrophages and dendritic cells.
27
Peyer's patches are like
surveillance system for food and drink... or a breeding ground for Y. enterocolitica
28
when macrophages carry Y. enterocolitica to Peyer's patches
Bacteria grow and “arm” themselves, then eventually pop out, ready for a bigger war
29
when macrophages carry Y. enterocolitica to Peyer's patches ........... and arm and grow and attack
causes swelling and inflammation that mimics that of appendicitis
30
Y. enterocolitica colonies produce
yst toxin
31
what does yst toxin do
binds to receptors on cells in the GI tract
32
when yst toxin binds to receptors on cells in the GI tract
causes intestines to secrete more cGMP
33
cGMP
cyclic guanosine monophosphate
34
when intestines to secrete more cGMP
channels that absorb water from the small intestine slam shut
35
Result of intestines to secrete more cGMP and channels that are responsible for absorbing water from the small intestine slam shut
extra water in the GI tract, which leads to diarrhea
36
what accompanies diarrhea when channels that absorb water from the small intestine slam shut
abdominal pain, fever and sometimes...vomiting
37
Y. enterocolitica food poisoning is also sometimes associated with
erythema nodosum
38
erythema nodosum comes from
an exaggerated and delayed immune response to a Yersinia antigen
39
erythema nodosum
splotchy patches usually confined to fatty tissue in the legs
40
Yersinia pestis has identified
as the causative agent of the european plague outbreaks
41
outbreak of Yersinia pestis often called
bubonic plague
42
3 ways Y. pestis an infect
- bubonic plaque
- pneumonic plague
- septicemic plague
43
bubonic plague
Flea bite or other vector bite permits bacterial entry to the body
44
bubonic plague death rate w/ o treatment
75%
45
pneumonic plague
bacteria are inhaled through droplets and enter lungs
46
pneumonic plague mortality rate without treatment
99%
47
septicemic plague
Y. pestis bacteria enter bloodstream, usually through open wound
48
septicemic plague mortality rate w/o treatment
99%
49
Y. pestis forms a ____ in the _______
forms a biofilm in the gut of the oriental rat flea
50
when Y. pestis forms a biofilm in the gut of the oriental rat flea
causes a small amount of bacteria to be regurgitated with each bite
51
Aside from biofilm formation Y. pestis does not
does not harm the flea
52
1894
outbreak of plague struck southern China
53
who cam to investigate outbreak of the plague in china
Shibasaburo Kitasato from JAPAN
54
who cam to investigate theh plague inchina 3 days later
Alexandre Yersin
55
what did Kitasato examine
the organs and blood of dead bodies and jndentified an unknown microbe
56
what did Kitasato do with the microbe to test it
isolated it, put it in rats, and quickly saw rats die.
57
what happened to the lymph nodes of rats with the bacteria
lymph nodes of the rats were overwhelmed with the same bacteria.
58
what did kitasato do with the bacteria he teste
took slides to london to be published.... but they WERE MESSEY
59
Kitasato messy slides were
contaminated w other bacteria
60
Yersin got access...
to cadavers for his own research >>> SHADY
61
with his cadavers Yersin was able to
produce a purer slide 6 days later >>> credited with the discovery of the bacillus>>>>YERSIN-ia.
62
black plague
- most infamous world crisis of infection
| - cutting population of europe in HALF during 1300s
63
main waves of Y. pestis
Justinian plague
Black Death
Third Wave
64
Justinian plague
600s-- killed 40% of population of Constantinople
65
Black death.
mid 1300s killed half of europe's population
66
Third Wave
late 1800s in southern china and india... killed 12 million before vaccine discovered
67
After a bit, Y. Pestis is able to grab onto _______
extracellular collagen with the help of pla protein
68
pla (PESTIS)
plasminogen activator
69
pla converts
host cell plasminogen into plasmin
70
what does plasmin do
break apart fibrin tissues in clots
71
by breaking up fibrin....... the plague
the plague is able to invade into further tissue
72
when is Yersinia killed by the body
phagocytosed by neutrophils
73
what is usallly NOT recruited to fight Yersinia
dendritic cells
74
Yersinia is NOT KILLED
not killed by macrophages
75
what happens when Yersinia is eaten by macrophage
waits inside the phagosome, using it as an “oven” to “cook” many proteins that will help it invade the human>> POPS OUT
76
when Y. pestis pops out of a macrophage
shifts gears completely
77
when Y. pestis pops out of a macrophage and shifts gears it STOPS
creating the proteins that protected it from a phagosome
78
when Y. pestis pops out of a macrophage and shifts gears it STARTS
produces different anti-phagocytic proteins so the new bacteria can't be eaten
79
what anti-phagocytic proteins does Y.pestis produce after shifting gears
yops
80
yops
Yersinia outer proteins
81
when Y. pestis shifts gears it eneters
antiphagocytic mode
82
when Y. pestis is in antiphagocytic mode
multiplies rapidly in the lymph nodes and causes the formation of a bubo or many buboes
83
buboes
hugely inflamed lymph nodes.
84
once Y. pestis is in the lymph nodes
eventually can make it into the blood
85
once Y. pestis is in the blood
secretes endotoxins that lead to the formation of many tiny blood clots
86
when Y. pestis secretes endotoxins that lead to the formation of many tiny blood clots it is called
DIC
87
DIC
disseminated intravascular coagulation
88
what does DIC do
- cuts off circulation to extremities(further away parts)
| - results in acral necrosis
89
acral necrosis
a blackening of tissue especially in fingers and toes.
90
why is black plague the name
acral necrosis
91
eventually, the tiny blood cots caused by Y. Pestis releasing endotoxins in the blood
cut circulation to organs and DEATH
92
plague is treated with
antibiotics... miniscule mortality rate if treated early
93
RED ALERT PLAGUE
Antibiotic-resistant strain of Y. pestis found in Madagascar
94
Streptococcus bacteria
gram-positive cocci
95
how many species in the Streptococcus genus
at least 37
96
how many species of Streptococcus can be pathogenic in humans
5 in immunocompetent humas
97
ALL STREP BACTERIA
obligate parasites of human mucosa
98
what does it mean to be .a obligate parasites of human mucosa
can't reproduce without finding a host
99
biggest three species Streptococcus
S. pyogenes, S. agalactiae, S. pneumoniae
100
S. pyogenes gist
strep throat and much more
101
S. agalactiae
Infant pneumonia and meningitis
102
S. penumoniae
Pneumonia, ear infection, sinus infection, meningitis
103
first tests to diminish the many gram-positive cocci
coagulase and catalase tests
104
for species that both turn up _____ on coagulase and catalase tests
both turn up negative: series of tests for surface antigens devised
105
series of tests for surface antigens of gram-positive cocci that is negative on coagulase and catalase tests DEVISED BY
Rebecca Lacefield
106
Rebecca Lancefield breaks bacteria into what groups
Lancefield groups
107
Easier to examine virulence factors of Streptococcus bacteria by
examining whole group rather than species by species
108
what Lancefield groups exist
groups A-V
109
do all strep bacteria fit into one Lancefield group
NO
110
clinically relevant Strep bacteria fall in what Lancefield group
group A or B or cannot be grouped
111
Hemolysis S. pyogenes
Beta
112
Hemolysis S. agalactiae
Beta
113
Hemolysis S. pneumoniae
Alpha
114
Lancefield group S. pyogenes
Group A
115
Lancefield group S. agalactiae
Group B
116
Lancefield group S. pneumoniae
NO GROUP
117
Disease Associated w/ group A strep
- Strep Throat (Pharyngitis)
- Impetigo
- Scarlet Fever
- Cellulitis
- Pneumonia
- Streptococcal TSS
- Necrotizing Fasciitis
- Rheumatic Fever
- PANDAS?
BRUH
118
main virulence factor in group A strep
membrane protein M protein
119
M protein extends
from the membrane beyond cell surface
120
M protein allows
S. pyogenes to avoid phagocytosis by neutrophils and macrophages
121
M protein ALSOOOO
stops antibody binding
122
M protein binds to
human fibrinogen, giving it a camouflage
123
when the M protein binds to human fibrinogen.....
only a small bit protrudes beyond this
124
how many unique M protein structures have been observed
over 100
125
to beat strep (M proteins)
body has to produce antibodies that bind to a particular strain of M protein's tip
126
many different M protein structures is an example of......
ANTIGENIC VARIATION
127
rheumatic fever
severe condition associated w/ S. pyogenes infections
128
Rhematic fever usually develops how long after the initial infection
2-4 weels
129
Regions of the M protein have...............
amino acid sequence very similar to cardiac myosin
130
because regions of M protein have amino acid sequence very similar to cardiac myosin
antibodies fighting the infection can wrongly recognize heart muscle as bad guy
131
Role of M protein in rheumatic fever first 2
- colonization of throat>> severe inflammation
| - M protein enters bloodstream and elicits antibody response
132
Role of M protein in rheumatic fever after elicitign antibody response
- antibodies-cross react with heart tissue
| - autoimmune response damages heart valves
133
more virulence factors in group A Strep
- M-like protein
- Hyaluronidase
- MSCRAMMs
- SPEs
134
M-like protein
surface protein that grabs Fc region of random antibodies and holds them
135
purpose of M-like protein
camouflage
136
Hyaluronidase
breaks down hyaluronic acid, >> increase spread of bacteria through body
137
MSCRAMMs
Promote attachment to epithelium
138
SPEs
Streptococcal pyrogenic exotoxins
139
SPEs are different ....
Different strains release different exotoxins
140
ranges of SPEs
SpeA to SpeJ
141
the TYPES OF SPEs we need to know
SpeA
| SpeB
142
SpeA
in the blood can lead to STSS (Streptococcal toxic shock syndrome)
143
STSS
Streptococcal toxic shock syndrome
144
SpeA is a ....
SUPERANTIGEN
145
SpeB
cuts many proteins like fibronectin
146
fibronectin
extracellular protein that connects collagens
147
result of SpeB cutting fibronectin
This leads to breakdown of skin in the area
148
result of SpeB cutting fibronectin >>> but the infection is superficial>>>
redness
149
result of SpeB cutting fibronectin >>> but the infection is DEEP >>>
Necrotizing fasciitis
150
Necrotizing fasciitis
s an infection of the fascia, a deeper skin layer
151
if in Necrotizing fasciitis, the infection spreads through this layer ....
BAD THINGS HAPPEN
152
what is the main species of Group B strep
S. agalactiae
153
the bacteria of group B strep
do not typically infect humans
154
the bacteria of group B strep are a member of
the normal flora in about 20% of female vaginas.
155
do group B strep cause infection in the vagina...
NO, but is a risk of inhalation of a new born during child birth
156
because infants ______ inhalation of group B strep (S. agalactiae) can cause
have a weak immune system.... can lead to pneumonia and or meningitis
157
because of the risks of group B strep to infants preg woman should
be testes and be administered antibiotics before birth
158
S. pneumoniae is commonly found
in the pharynx of humans, is harmless there
159
S. pneumoniae can do bad things when
go other places
160
S. pneumoniae can cause...... BRUH
ear infection
sinus infection
pneumonia
brain infection
161
brain infection is ie
MENINgitis
162
usually the places that S. pneumoniae infects are
protected by cilia
163
S. pneumoniae infections are often a result of
previous infection that impedes cilia function
164
what are infectious diseases caused by
viruses, bacteria, fungi , parasites
165
most bacteria is not is not dangerous
yes
166
clinically significant
bacteria that are linked to disease
167
like other species, how are bacteria named
by binomial nomenclature
168
what is binomial nomenclature
two words: genus and species
169
typically many species for
for one genus
170
binomial nomenclature should always be
italicized in print
| underlined in writing
171
first letter of genus in binomial nomenclature
capitalized
172
species name in binomial nomenclature
entirely lower case
173
there are often many species
in a genus
174
members of a species can _____ through
vary a lo through horizontal gene transfer
175
what is the genetic material of bacteria
one large circular chromosome... called plasmid
176
why are bacteria much harder to classify tan more complex species
horizontal gene transfer
177
horizontal gene transfer
passing of DNA into bacteria
178
three main ways of horizontal gene transfer
transformation
transduction
conjugation
179
transformation
"naked" DNA is absorbed by bacterium and worked into its DNA
180
transduction
DNA is injected by a bacteriophage
181
bacteriophage
bacteria-infecting virus
182
conjugation
DNA is spread from bacterium to bacterium through(cell to cell contact) sex pilus
183
horizontal gene transfers caused there to be many
many strains of any species
184
different strains of a species can be very unique.....
VERY unique
185
in most cases of bacteria; inheriting just one gene will a grant a bacterium....
- resistance to certain antibiotics
- the ability to synthesize a new nutrient
- or the ability cling to a new surface
186
metric by which bacteria are classified
- color
- morphology
- flagellation
- staining
- growth on various agars
- oxygen dependence
- other habitat preferences
- spore formation
187
how do we classify bacteria w color
bacteria secrete pigments or colored particles, they are sometimes fluorescent
188
colors can also be used to identify
microbes
189
classifying using morphology
classified with their shape
190
(rounds) a circle
cocci
191
two round circles
diplococci
192
pill shape
coccobacilli
193
rod-shaped
bacilli
194
two other shapes
curved and spiral
195
in many cases the name of the genus comes from the
shape of the bacterium
196
curved bacteria often called
vibrio
197
many bacteria have flagellation...
to help them move
198
flagellation comes in what forms
monotrichous
lophotrichous
amphitrichous
peritrichous
199
monotrichous
just one flagellum
200
lophotrichous
just one "tuft" of flagella
201
amphitrichous
having flagella on both sides
202
peritrichous
surrounded by flagella
203
flagella are made of what
flagellin
204
classifying with stain
results of gram stain
205
on a gram stain purple
is a positive result
206
what bacteria usually have a purple stain
bacteria have thick layers (usually 30-40 layers) of peptidoglycan
207
on a gram stain pink
is a negative result
208
what bacteria usually has a pink stain
bacteria usually have much thinner layers of peptidoglycan, as thin as 1-2layers
209
some bacteria don't stain with a gram stain
especially ones that grow in eukaryotic cells
210
bacteria are grown in cultures on
agar
211
agar
gel-like substance
212
agars can be packed with
various substances like antibiotics, nutrients, blood
213
classifying with agars
depending on how they grow on those plates
214
example of a special type of medium (agar)
blood agar
215
blood agar
bacteria are plated with blood to see what happens
216
things that can happen with blood agar
gamma hemolysis
alpha hemolysis
beta hemolysis
217
gamma hemolysis
means that bacteria do not break blood
218
alpha hemolysis
means that the bacteria partially break blood
219
beta hemolysis
means that the bacteria fully break blood
220
blood agar can be very
important diagnostic tool... especially for Streptococcus species
221
oxygen is required
for human cells, not all bacteria
222
when can oxygen be bad
when it forms toxic compounds such as peroxides or superoxides
223
classifying with oxygen dependence
classified by their relationship
| with oxygen
224
types of relationships with oxygen for bacteria
obligate anaerobes
obligate aerobes
facultative anaerobes
aerotolerant bacteria
225
obligate anaerobes
bacteria that can only survive if oxygen is absent
226
obligate aerobes
bacteria that can only survive if oxygen is present
227
ex obligate anaerobes
Clostridium ( cause of gangrene )
228
ex obligate aerobes
Pseudomonas
229
facultative anaerobes
bacteria that prefer to use oxygen-based respiration but can also survive in oxygen-free homes
230
ex of facultative anaerobes
Staphylococcus, Streptococcus)
231
aerotolerant bacteria
bacteria that do not use oxygen-based respiration but can survive if oxygen is present
232
classifying with other preferred living conditions
based on preferred living arrangements
233
different preferences for bacteria living conditions (temp)
thermophiles
psychrophiles
mesophiles
234
thermophiles
like it hot
235
psychrophiles
like it cold
236
mesophiles
body temp
237
different preferences for bacteria living conditions (acidity)
acidophiles
alkaliphiles
neutrophiles
238
acidophiles
like it acidic
239
alkaliphiles
like it basic
240
neutrophiles
like it neutral
241
body temp
37 degrees C
242
blood pH
7.4
243
classifying with spore formation
spores or no spores
244
special survival mechanism of some bacteria
ability to form endospore
245
bacterial cells that can form an endospore
divide and then wrap the important stuff inside a thick double-layered cell wall and lay dormant until conditions turn more favorable
246
bacteria that can form an endospore are immune to
to many things like extreme temperature and can wait years before reactivating
247
obligatory steps for infectious "bugs"
- entry or attachment to the body
- evasion of the immune system
- shedding from/exiting the host
- causing damage or disease-associated processes in the host*
248
bacterial parts that allow obligatory steps for infectious bugs are called
virulence factors
249
many bacteria enter the body through
cuts in the skin
250
for bacteria that do not enter through cuts in the skin
they need to pass through a mucus layer
251
two ways bacteria can pass through a mucus layer (Entry to the Body)
sigA proteases
| mucinases
252
the protection of mucus membranes across the body s mediated by
antibody secretory IgA (sigA)
253
sigA is found
in extremely high concentrations in the airway and GI tract
254
why would bacteria release sigA proteases
destroys human IgA antibodies
255
destruction of human IgA antibodies causes what
neutralizes host defense in those areas, allows bacteria to live there
256
mucinases
enzymes that degrade the proteins inside mucus
257
mucinases allow what for bacteria
allows them to settle on or under mucus membranes
258
many bacteria have what for attachment to body
pilli
| fimbriae
259
singular of pilli
pilus
260
singular of fimbriae
fimbria
261
fimbria and pilus can be used interchangeably
yes, for some pilus is only for conjugation
262
pili and fimbriae are what on most bacteria
peritrichous
263
peritrichous
projections all over its surface
264
pili act as
feelers for bacteria
265
when pili feel a desired surface
shorten and pull the bacterium in
266
pili are more prevalent in what
gram-negative bacteria
267
adhesive proteins that stick to other proteins
adhesins
268
membranes of many microbes have
special type of adhesins
269
what are the special adhesins that the membranes of many microbes have
MSCRAMMs
270
MSCRAMMs
```
Microbial
Surface
Components
Recognizing
Adhesive
Matrix
Molecules
```
271
roles of MSCRAMMs
target host cells and allow for tight connections between them and bacteria
272
human cells are coated in what proteins for MSCRAMMS to targe
- transport
- receptor
- adhesion
- glycoproteins
273
role of transport proteins
move things in or out of cells
274
characteristics of transport proteins
- opened and closed
| - very selective
275
role of receptor proteins
help the inside and outside of the cell communicate
276
which proteins usually work together in human cells
transport and receptor
277
example of adhesion proteins in human cells
integrins
278
role of adhesion proteins
help stick cells in place
279
characteristics of adhesion proteins
- grab onto collagen in the extracellular space
| - grab onto other integrins on other cells to hold hands
280
role of glycoproteins
stick carbon chains into the extracellular space, forming a glycocalyx around a cell (CELL ID)
281
different MSCRAMMs target
different types of host membrane proteins
282
bacteria also have their own
OWN GLYCOCALYX
283
integrin proteins connect cell to
to extracellular collagen
284
different bacteria attack the body by
colonizing different surfaces
285
bacteria choosing to live on outer epithelial layer
try to outcompete normal flora, but it is hard
286
bacteria choosing to live into deeper extracellular space
burrow way through epithelial layer to get there
287
bactiera choosing to live inside ...
inside the host cell
288
place the bacteria chooses to live...
-deeper extracellular space
-inside the host cell
outer epithelial layer
-eaten by phagocyte
289
bacteria deliberately eaten by phagocyte
so they can reproduce inside a phagosome or phagolysosome.
290
after reproducing inside a phagocyte or phagolysosome a bacteria can
pop out or keep living there
291
depending on how deep into skin a pathogen gets
the manifestation of infection varies
292
where does Y. pestis grow
inside white blood cells
293
some bacteria come with a very THICK
thick glycocalyx.. called slime layer
294
inside the slime layer there is
thinner layer of proetins called the S layer
295
proteins of S layer
highly variable between species
296
the slime layer and S layer provide the bacteria with
partial defense from phagocytes and covers some of the bacteria's PAMPs
297
example of bacteria w/ slime layer
streptococcus pneumoniae
298
what caues gonorrhoea
Neisseria gonorrhoeae
299
pili are what in Neisseria gonorrhoeae
the immunodominant structure
300
pili being the immunodominant structure in Neisseria gonorrhoeae means
predominantly N. gonorrhoeae’s pili that are recognized by antibodies.
301
different strands of N. gonnorhoeae
different structures of pilli; over1 million different pilus structures
302
N. gonnorhoeae having so many different plius structures causes
memory B cells to be useless against it, makes people prone to reinfection
303
the N. gonorrhoeae phenomenon is a tactic many other bacteria and virus use called
antigenic variation
304
bacteria that live inside a host cell need to
need to find a way to escape
305
some ways of exiting the host leave the host cell intact,
some do not
306
1 st way of exiting the host
-settle inside vacuole and drive vacuole out
307
2nd way of exiting the host
hijack cellular machine designed to secrete proteins through exocytosis
308
3rd way of exiting the host
pop a big hole in the cell's membrane, causing it to die
309
bacteria often cause collateral
damage to surrounding tissues
310
humans cells towards____ have ____
towards mucosal linings have hyaluronic acid in their membrane as a mortar
311
hyaluronic acid is very
large molecule (molecular weight in millions), largely unknown functions
312
large molecule (molecular weight in millions), largely unknown functions
largely unknown
313
some pathogenic bacteria secrete what to break down hyaluronic acid
hyaluronidase
314
why do bacteria secrete hyaluronidase
to break down hyaluronic acid to use its carbons for own processes
315
result of bacteria using hyaluronidase to break down hyaluronic acid
damage to cell membranes, cellular death
316
iron is
essential nutrient for bacteria, difficult to come across
317
iron is necessary to build
peroxidases and operate an electron transport chain
318
electron transport chains are
important for ATP production in bacteria
319
easiest place for bacterial colony to find iron in the human body
hemoglobin found in blood
320
because iron is found in the blood, bacteria secrete
hemolytic enzymes called hemolysins
321
why do bacteria secrete hemolysins
to steal the body's iron from hemoglobin
322
bacteria can also cause damage through
toxins
323
two types of toxins that bacteria have
endotoxins, exotoxins
324
endotoxin
refers to LPS in the membrane of gram-negative bacteria
325
LPS
lipopolysaccharides
326
why is LPS dangerous to humans - reason 1
-cause vast increase in secretion of cytokines cause inflammation and swelling
327
why is LPS dangerous to humans - reason 2
-leads to release of histamines.... causing vasodilation
328
why is LPS dangerous to humans - reason 3
-leads to activation of coagulation cascade
329
coagulation cascade
cascade that leads to the formation of thrombi (blood clots
330
LPS puts people at risk for
septic shock, heart attack, and stroke.
331
exotoxins
diverse class of toxins, all proteins created by a bacterium
332
1st thing that exotoxins can do
are secreted and act on surrounding issue
333
examples of exotoxins that act on surrounding tissue
hyaluronidase and hemolysin
334
2nd thing that exotoxins can do
enter cells and ribosylate host proteins
335
how does an exotoxin ribosylate a host protein
add ADP+ ribose... turns proteins on or off... often off
336
3rd thing that exotoxins can do
break turn certain proteins such as sigA
337
4th thing that exotoxins can do
other mechanisms
338
in the case of exotoxins, symptoms..
not cause y bacterium themselves but by the exotoxins secreted
339
staphylococcus genus are
gram-positive cocci
340
how long can Staphylococcus survive at 60 degree
about a half-hour
341
how long can Staphylococcus survive at 4 degrees
months
342
3 importantS Staphylococcus species
- Staphylococcus aureus
- Staphylococcus epidermidis
- Staphylococcus saprophyticus
343
each of the important species of staph are
normal flora, disease occured when misplaced or when a bad strain is aqquired
344
hemolysis S. aureus
Beta
345
hemolysis S. epidermidis
Gamma
346
hemolysis S. saprophyticus
Gamma
347
coagulas S. aureus
positive
348
coagulase S. epidermidis
negative
349
coagulase S. saprophyticus
negative
350
color S. aureus
gold/yellow
351
color S. epidermidis
white
352
color S. saprophyticus
white/yellow
353
novobiocin
antibiotic
354
is S. aureus resistant to novbiocin
no
355
is S. epidermidis resitant to novobiocin
no
356
is S. saprophyticus resistant to novobiocin
yes
357
novobiocin
is an antibiotic
358
in human blood, what waits for a signal to come from damaged tissue
prothrombin
359
when prothrombin gets a signal from damaged tissue... it is converted to
thrombin
360
what does thrombin do
convert fibrinogen into fibrin
361
what does fibrin do
weaves into a mesh, an integral part of clot formation
362
who secretes coagulase
S. aureus (few other non-staph bacteria)
363
when S. aureus and (few other non-staph bacteria) secrete coagulase
it mimics the damaged signal, but instead causes prothrombin to be converted into a special form
364
when when S. aureus and (few other non-staph bacteria) secrete coagulase it causes prothrombin to be converted into what special form
staphylothrombin
365
staphylothrombin function
converts fibrinogen to fibrin that coats the staph bacteria, protecting it from the immune system
366
in phagocytosis, dendritic cells and macrophages
hold out digested guts (antigens) for other immune cells to see
367
dendritic cells and macrophages holding out macrophages is a
delicate process- only a small subset of T cells actually res
368
why is dendritic cells and macrophages holding out macrophages is a delicate process
- only a small subset of T cells actually respond to an antigen, even if bad
369
what percentage of T cells actually respond to an antigen
0.001 %
370
superantigens are different than normal antigens because
they stimulate a large amount of T cells in an area
371
what percentage of T cells do superantigens stimulate
20% or more
372
superantigens stimulating a large amount of T cells is called
polyclonal T cell activation
373
polyclonal T cell activation leads to
excessive cytokine release
374
excessive cytokine release of polyclonal T cell activation can lead to
fatal shock or organ failure
375
some strains of what create a superantigen
S. aureus
376
superantigen created by strains of S. aureus
SEB
377
SEB
Staphylococcal enterotoxin B
378
another word for SEB, depending on wher it acts
TSST
379
TSST
toxic shock syndrome toxin
380
TSST / SEB is
a single protein created by 30-50% of strains of S. aureus
381
if an SEB-secreting strain of S. aureus makes is way to _____
to intestines, the superantigen causes widespread inflammation
382
result of SEB-secreting strain of S. aureus in intestines
- projectile vomiting
- abdominal pain
- sometimes diarrhea
383
S. aureus and its superantigen iin the intestines are a type of
food poisoning that is rapid onset
384
how long after eating food w/ S. aureus do you show symptoms of food poisoning
1-6 hours
385
is staph the only caue of food poisoning
no, but is a common one
386
other staph associated enterotoxins :
SEA - SEE, SEE - SEI, and SER - SET have been named
387
which is the only staph-associated superantigen
SEB
388
first example of S. aureus and its superantigen
Laredo TX, 1968
389
Laredo TX, 1968
1364 elementary school children fell ill, chicken salad off-sit, not refrigerated, shipped to district
390
example 2 of S. aureus and its superantigen
Spring 1989>> canned mushrooms
391
when SEB enters the blood stream
leads to toxic shock syndrome
392
toxic shock syndrome primarily associated with what 3 things
- extended use of hyperabsorbent tampons
- cosmetic surgeries
- uncleaned abrasions(rare)
393
what cosmetic surgeries usually lead to toxic shock syndrome
material packed into the nose
394
in each case of toxic shcok syndrome
S. aureus secretes SEB/TSS into the bloodstream
395
the result of of toxic syndrome is
bad.. defined by 5 plus of characteristics
396
what characteristics does toxic shock syndrome show - First 3
- body temperature over 102 degrees F
- blood pressure below 90 mmHg
- Macular Erythroderma
397
what characteristics does toxic shock syndrome show - Second 3 `
- desquamation
- involvement/failure of at least organ systems
- no positive blood results for other likely suspects
398
desquamation during toxic shock syndrome is
within 7-14 days, especially on palms and soles of feet
399
Macular Erythrodema
sunburn appearance
400
in adition to carrying superantigens, certain strains of S. aureus can carry
exfoliatins
401
what two exfoliatins can S. aureus carry
exfoliative toxin A and exfoliative toxin B
402
each of the exfoliative toxins targets
targets and cleaves protein dsg-1
403
dsg-1
desmoglein-1
404
where is desmoglein-1 found
only in the desmosomes of human skin
405
desmosomes
structure that holds cells together
406
staph (S. aureus) is more commonly the cause of
pyogenic infections
407
pyogenic infections
buildups of pus to fight the bacteria.
408
pus usually comes....
as a byproduct of the war between phagocytes and pathogens: the phagocytes eat so much that they eventually “pop”.
409
what makes more pus
bacteria also secrete substances to kill phagocytes before they start eating
410
forms that pus buildup can take
- Impetigo
- Folliculitis
- Carbuncle
- Furuncle
411
Impetigo
superficial infection
412
Folliculitis
infection of hair follicle
413
Carbuncle
abscess
414
Furuncle
boil
415
treatment of staph infections;
antibiotics , but staph infections evolving to counteract
416
MRSA
Methicillin-resistant Staphylococcus aureus
417
MRSA actually
resists many different types of antibiotics not just methicillin
418
now in order to treat MRSA doctors
give stronger antibiotic vancomyscin
419
in other regions where vancomycin was the first choice antibiotic
VRSA emerged
420
VRSA
vancomycin-resistant S. aureus
421
from horizontal gene transfer of S. aureus there is now
MVRSA >>> SUPERBUG
422
S. epidermidis is
not very scary, not have many virulence factors like S. aureus
423
scary feature of S. epidermidis
form biofilms on plastic surfaces
424
S. epidermidis forming biofilms on plastic surfaces
make it incredibly difficult for antibiotics to penetrate
425
the result of a biofilm forming is often
follow-up surgery to remove the plastic
426
biofilms of S. epidermidis often form on
- catheters
- replacement heart valves
- prosthetic joints
427
biofilms forming on catheters
response for over 50% of catheter infections
428
biofilms forming on replacement heart valves
leads to endocarditis
429
endocarditis
inflammation of heart inner lining
430
what staph species sometimes occupies the normal flora of the body
S. saprophyticus
431
when S. saprophyticus gets inside the urinary tract of a woman
(usually through sex) causes a urinary tract infection
432
symptoms of urinary tract infection
- burning sensation while urinating
- need to urinate often
- cloudy urine
433
urinary tract infections usually onsets
24-48 hours after sexual activity
434
urinary tract infections are often called
honeymoon cystitis
435
the proteins are degraded by exfoliative toxins are
in the junction between the stratum granulosum and the stratum spinosum of the epidermis
436
degradation of desmosomes between the stratum granulosum and the stratum spinosum leads to what
SSSS
437
SSSS
Staphylococcal scalded skin syndrome
438
symptoms of SSSS
skin blisters within 24-48 hours of onset, common in young children
