Exam 4 Flashcards
(185 cards)
1
Q
E. coli is gram
A
negative
2
Q
e. coli is normal
A
flora in the GI tract
3
Q
E.coli diseases
A
UTI
meningitis
gastroenteritis
septicemia
4
Q
bacteria responsible for >80% of UTIs
A
e.coli
5
Q
P.pili
A
virulence factor on E.coli that helps cause UTI
6
Q
meningitis is
A
inflammation of the meninges
7
Q
most common cause of meningitis in neonates
A
e.coli from contamination from mother’s vagina during birth
8
Q
symptoms of meningitis
A
- blindness
- deafness
- severe mental retardation
9
Q
virulence factor of E.coli for meningitis
A
capsule
10
Q
gastroenteritis is
A
inflammation of the stomach and intestines
11
Q
strains of E.coli that cause gastroenteritis
A
enterotoxigenic E.coli
enterhemorrhagic E.coli
12
Q
enterotoxigenic E.coli causes
A
traveler’s diarrhea
13
Q
traveler’s diarrhea is transmitted by
A
drinking feces contaminated water or eating uncooked foods washed in this water
14
Q
traveler’s diarrhea symptoms
A
diarrhea
nausea
rarely vomiting
15
Q
traveler’s diarrhea treatment
A
is self limiting within 24-48 hrs
treat symptoms with immodium, pepto bismal
16
Q
most dangerous strain of e.coli
A
enterohemorrhagic e.coli
17
Q
enterohemorrhagic E.coli virulence factor
A
cytotoxin called virotoxin
18
Q
enterohemorrhagic E.coli symptoms
A
intestinal bleeding
copious bloody diarrhea
19
Q
transmission of enterohemorrhagic e.coli
A
undercooked ground beef
unpasteurized milk
20
Q
septicemia
A
the presence of pathogens and their toxins in the blood
21
Q
most common gram neg rod to cause septicemia is
A
e.coli
22
Q
E.coli septicemia virulence
A
lipid A endotoxin
23
Q
E.coli septicemia transmission
A
enters blood by kidney infections or intestinal wounds
24
Q
E.coli septicemia symptoms
A
fever compliment disseminated intravascular coagulation (DIC) lowered peripheral circulation shock death
25
shock
organs that receive large volumes of blood fail too
| happens in septicemia
26
rodent pathogen
Yersinia pestis
27
Yersinia pestis is transmitted by
fleas bites from rodents
| respiratory droplets
28
Yersinia pestis causes
pneumonic plague
| bubonic plague
29
bubonic plague virulence
capsule on pathogen resists phagocytosis
30
bubonic plague symptoms
moves through blood stream to lymph nodes which become hot, swollen, and hemorrhage, swelling to the size of chicken egg
if not treated moves to respiratory tract and eventually causes septicemia
31
bubonic plague mortality
50%
32
associate bobuoes with
bubonic plague
| Yersinia pestis
33
pneumonic plague symptoms
* Slimy sputum tinted with blood
* Within hours to days becomes free-flowing and bright red
* High fever
* Chills
* Headache
* Malaise
* Cough
* Purple coloring from respiratory failure and circulatory collapse
* Septicemia leading to death within 2-3 days of first symptom
34
treat Yersinia pestis with
- streptomycin
| - chloramphenicol
35
complications of Yersinia pestis infection
DIC
pneumonia
meningitis
death due to endotoxic shock
36
Yersinia pestis is gram
negative
37
salmonella is gram
negative
38
salmonella source of infection
contaminated food or water - most commonly poultry, eggs, dairy product
39
takes ___ salmonella cells to cause disease
over 1 million
40
salmonella causes
gastroenteritis
septicemia
typhoid fever
41
salmonella gastroenteritis occurs how quickly
6-28 hours after ingesting contaminated food
42
salmonella gastroenteritis symptoms
* n/v
* diarrhea
* fever
* cramps
* malaise
* headache
43
salmonella gastroenteritis treatment
self limiting within 2-7 days
44
typhoid fever transmission
ingesting human feces contaminated food or water
45
typhoid fever occurs how quickly
10-14 days after ingesting pathogen
46
typhoid fever symptoms
* fever
* malaise
* headache
* n/v, diarrhea
* fever increase over many days and can last 4 weeks if no treatment
* rash during 2nd and 3rd week – Rose spots
* spleen and intestines may burst
47
an increasing fever over 4 weeks is associated with
typhoid fever
48
rose spots are associated with
typhoid fever
49
typhoid fever grows in
macrophages
50
typhoid fever treatment
chloramphenicol
| ampicillin
51
vibrio is gram
negative
52
what is responsible for the disease cause by vibrio cholera
enterotoxins
53
mucinase
produced by virbrio chloera
| allows the cells to penetrate the mucosa where they multiply and produce enterotoxins
54
cholera is caused by
vibrio cholera
55
cholera symptoms
* first abdominal fullness
* then loose stools and vomiting
* then voluminous diarrhea - may lose more than 10L fluid/day
56
when does cholera occur
2-3 days after ingesting feces contaminated food/water
57
diarrhea from cholera can cause
o dehydration and hypokalemia that can lead to muscular, renal disorder, and heart abnormalities
o death within hours if untreated -typically from shock
58
cholera treatment
fluid and electrolyte repletion
59
source of virbrio vulnificus
coastal water
| raw oysters
60
vibrio vulnificus leads to
septicemia
61
most suscepitible to vibrio vulnificus
men
| liver disease hx
62
vibrio vulnifcus symptoms within 12 hours
malaise
fever
chills
63
vibrio vulnificus symptoms within 24 hours
n/v
hypotension
cutaneous lesions
64
vibrio vulnificus symptoms within 36 hours
50% are dead
65
vibrio vulnificus treatment
tetracycline
66
hemophilus influenza is a gram
negative rod
67
haemophilus influenza causes
infant meningitis
| acute epiglottitis
68
haemophilus influenza requires what for growth
blood
69
virulent serotype of H. influenza
type b
70
H. influenza serotypes are based on
capsule produced
71
noncapsulated h. influenza
may colonize
| do not cause disease
72
capsulated H. influenza can
invade deeper into the tissue and cause inflammation of the epiglottis and/or neck tissues
73
H. influenza virulence factors
capsule
endotoxin
IgA protease
74
IgA protease
virulence factor of H. influenza that destroys IgA antibody
75
peak incidence of H. influenza
6-18 months when infant has lost mother's immunity and do not have full set of own
76
acute epiglottitis symptoms
Sudden fever
Sore throat
Barking cough
Rapid progression to severe exhaustion within 24 hours
Inflamed epiglottis and surrounding tissue obstructing airway
77
acute epiglottitis treatment
chloramphenicol
78
Hib
H.influenza vaccine
79
bordetalla pertussis is a gram
negative coccobacillus
| strict aerobe
80
B. pertussis virulence factors
endotoxins, including lipid A
pertussis toxin
cytoxin
81
pertussis toxin
important for attachment to ciliated epithelial cells
82
pertussis cytotoxin
paralyzes the cilia and causes the loss of ciliated cells
83
pertussis stages
Catarrha
Paroxysmal coughing stage
Convalescent stage
84
catarrha stage symptoms
Nasal discharge
Low grade fever
Malaise
Sneezing
85
catarrha stage lasts
1-2 weeks
86
when is B. pertussis most communicable
catarrha stage
87
paroxysmal coughing stage
Patient has lost ciliated epithelial cells from respiratory tract
Mucus doesn’t have good water to get out of the area
Coughing seizures begin
88
paroxysmal coughing stage lasts
2-4 weeks
89
coughing seizures can
last several minutes and occur up to 50x/day
90
convalescent stage symptoms
Coughing episode diminish
| Ciliated epithelial cells begin to regenerate
91
common pertussis complications
pneumonia
| accounts for majority of deaths
92
pertussis treatment
supportive methods
watch for secondary infection
antibiotic only effective in catarrhal stage - erythromycin
93
DPT
pertussis vaccine
given at 2, 4, 6 months
can cause brain damage and convulsions in rare cases
94
staphylococcus is gram
positive
95
is staphylococcus motile
no
96
staphylococcus is aerobe/anaerobe/facultative?
facultative anaerobe
97
staphylococcus is everywhere or
ubiquitous
98
staphylococcus transmission
direct contact
fomite
respiratory droplet
99
staph aureus virulence factors
```
polysaccharide capsule
antiphagocytic capsule
protein A
antiphagocytic
lipase
penincillinase
enterotoxin
```
100
lipase
hydrolyzes lipids
101
involved in s. aureus ability to cause skin intections, boils, carbuncles
lipase
102
carbuncle
boils that extend below the skin allowing bacteria to more easily enter the blood stream and cause bacteremia
103
penicillinase
destroys penicillin
| allows more than 90% of s.aureus to be resistant to penicillin
104
s. aureus enterotoxin
causes intestinal illness
| resistant to gastric enzymes and fairly high heat
105
enterotoxin A
s. aureus
| associated with ham, pastries, potato salad, ice cream
106
enterotoxin A symptoms
vomiting
diarrhea
no fever because is intoxication not infection
107
toxic shock syndrome
toxins secreted by growing s. aureus
108
toxic shock syndrome symptoms
```
• High fever
• Hypotension
• Vomiting
• Diarrhea
• Rash
o Shedding of skin and widespread organ damage occurring
• Death within 48 hours
```
109
streptococcus is gram
positive chains
110
streptococcus is catalase
negative
111
distinguishing between strep and staph
catalase test
112
strep pneumoniae hemolysis
alpha hemolytic
partially lyses RBCs
will only grow in blood
113
has 84 serotypes
strep pneumoniae
114
strep pneumoniae capsule
allows 84 serotypes
| will maintain shape een when pathogen has left the capsule so antibodies bind the empty capsule, not the pathogen
115
strep pneumoniae disease
* Pneumonia
* Sinusitis
* Otitis media
* Meningitis
all can lead to bacteremia
116
diseases of strep pneumoniae are associated with
respiratory disease or head trauma
moves in while body fighting something else
117
strep pneumoniae treatment
penicillin
| erythromycin
118
group A strep
strep pyogenes
119
strep pyogenes virulence factors
capsule of hyaluronic acid
protein M
erythrogenic exotoxins
120
strep pyogenes capsule
our bodies will not attack because contains hyaluronic acid which is a major component of our connective tissue
121
strep pyogenes treatment
penicillin
122
Protein M is
antiphagocytic
| associated with triggering autoimmune responses
123
strep pyogenes diseases
pharyngitis
scarlet fever
strep TSS
rheumatic fever
124
strep pharyngitis transmission
respiratory
125
strep pharyngitis symptoms
Abrupt onset of sore throat
Fever
Malaise
Headache
126
scarlet fever
o Erythrogenic toxins cause cheeks and temples to turn deep red
o Pale areas around mouth and nose
o Rash beginning on upper chest and spreading to extremitites – not palms of hands or soles of feet
o Raw tongue – strawberry tongue
o Rash disappears after ~1 week
127
strawberry tongue
scarlett fever
128
rheumatic fever
o Fever
o Inflammation of the heart, joints, blood vessels, and CNS
o About 3 weeks after pharyngitis ends
o Bacteria moves from throat, into blood, and settles in heart creating autoimmune reaction with chronic, progressive damage to the heart valves
129
flesh eating bacteria
strep TSS
130
strep TSS
o Extensive soft tissue damage, high fever, hypotension, vomiting, diarrhea, rash
o Caused by specific surface protein M
131
bacillus are gram
positive rods
132
bacillus anthracis is aerobe/anaerobe
facultative anaerobe
133
bacillus can form
spores
134
virulence factors of b. anthracis
edema toxin
lethal toxin
antiphagocytic capsule
135
b. anthracis in aerobic conditions
germinate and make toxins
136
in anaerobic conditions
germinate and make toxins
| produce capsule
137
b. anthracis toxins do what
suppress neutrophil function
138
b. anthracis infects primarily
grazing animals by them ingesting the spore
| then people when they handle the infected animale
139
types of anthrax
gastrointestinal
cutaneous
pulmonary
140
cutaneous anthrax begins as
raised, itchy bumps resembling bug bites
141
cutaneous anthrax symptoms
* Within 1-2 days bumps develops into vesicle, then 1-3 cm painless ulcer
* Center of ulcer will then become necrotic
* Lymph glands in adjacent area swell
* Danger of septicemia
142
anthrax transmitted from person to person
cutaneous
143
cutaneous anthrax mortality
20% if untreated
144
woolsorters disease
pulmonary anthrax
145
pulmonary anthrax symptoms
* Begins as vague, flu-like that may improve and then turn to abrupt high fever, difficulty breathing, and chest pain
* Followed by septicemia
* Death within 24-36 hours
146
pulmonary anthrax transmission
airborne by spores
147
pulmonary anthrax fatality
90-100%
148
anthrax treatment
penicillin
149
clostridum is gram
positive rod
150
clostridium forms
spores
151
clostridium is aerobe/anaerobe
strict anaerobe
152
the spores of what are resistant to all known disinfectants and to boiling
clostridium perfringens
153
clostridium perfringens toxins
alpha
| beta
154
c. perfringens alpha toxin causes
hemolysis
bleeding
tissue destruction
155
c. perfringens beta toxin causes
paralysis
inflammation
necrosis of intestinal tissue
156
c. perfringens causes
gas gangrene
| food poisoning
157
gas gangrene description
* Spore germinates in wound after aerobes and facultative anaerobes cover the wound to create an anaerobic condition
* These new cells ferment muscle cho and produce gas which can be felt under the skin
158
gas gangrene occurs in
open lesions like compound fracture or bullet wound
159
gas gangrene is caused by
c. perfringens
160
gas gangrene symptoms
```
pain
fever
extensive bleeding
shock
death within 2 days - 100% fatal if untreated
```
161
gas gangrene treatment
penicillin
162
food poisoning
c.perfringens
163
c. perfringens food poisoning associated with
meat dishes - stews, gravies, soups
164
c. perfringens food poisoning symptoms
nausea
abdominal pain
diarrhea
no fever or vomiting
165
c. perfringens food poisoning occurs because
• Spores survive cooking of the meat and then germinate and produce toxins as the meat cools
166
symptoms of c. perfringens food poisoning vary because
of the variation of the beta toxin that may have been produced
167
rust gives these spores a place to sit
c. tetani
168
tenospasmin
produced by c. tetani
most lethal substance known to man
intestines destroy this, antibodies neutralize it
part of cell wall and release when the cell lyses
169
tetanus symptoms
* begin with spasms in masseter muscles – lockjaw
* then move along back and affect respiratory muscles and ability to swallow
* remain conscious and aware
* death due to exhaustion and respiratory failure
* 100% fatal without treatment
170
tetanus treatment
* First neutralize unbound toxins – receive large dose antitoxin by injection
* Then penicillin
* Patient sedated, provided airway, and maintained in quiet, dark environment
171
how long can tetanus toxin stick around
up to 2 years
172
c. botulinum spores are found
in moister soil like pons and lake sediments
173
c. botulinum neurotoxins do what
inhibit release of acetylcholine that tell muscle to contract leading to paralysis
174
muscle contraction
c. tetani
175
muscle paralysis
c. botulinum
176
GI tract destroys this clostridium toxin
tetani
177
this clostridium toxin is resistant to the gi tract enzymes
botulinum
178
associated with home canned, alkaline vegetable
c. botulinum
179
c. botulinum symptoms
```
• First, weak and dizzy
• Blurred vision, dry mouth, constipation
• Toxin paralyzing nerves
o First ocular
o Then pharyngeal
o Then laryngeal
o The respiratory
• 20% fatal with treatment, 100% without
```
180
c. botulinum treatment
* Large dose horse botulinum antitoxin
* Supportive measure to maintain respiration
* Can take months to 2 years
181
honey
associated with c. botulinum in infants
182
c. botulinum in infants
• Constipation, poor muscle tone, lethargy, feed problems, then death
• Same nerves but harder to catch early due to developmental stage
• Penicillin to treat to rid of the infection
- infection rather than intoxication
183
how do you tell the difference between pharyngitis and scarlet fever?
A.
Both are caused by Strep. pyogenes
B.
Pharyngitis has sore throat; Scarlet Fever might have sore throat
C.
Pharyngitis has a distinct rash; Scarlet Fever has “strawberry tongue”
D.
All of the above
Pharyngitis has sore throat; Scarlet Fever might have sore throat
184
If a person has had Rheumatic Fever in the past and then got a subsequent S. pyogenes infection, what could happen (give the best answer)?
A.
The pathogen will not be seen by our defenses
B.
The pathogen will attack our heart.
C.
Our defenses will attack our heart
D.
Our defenses will attack the pathogen and severely attack our heart
E.
Our defenses will only attack our heart
Our defenses will attack the pathogen and severely attack our heart
185
What toxin is produced and working in Gas Gangrene?(C. perfringens)
alpha
