Bailey Material Flashcards
1
Q
Which type of Shigella is the most sever?
A
S. Dysenteriae
2
Q
What is the inoculum size for Shigella?
A
Small inoculum required
3
Q
How are acid resistance and other virulence factors induced in Shitella species?
A
Anerobic conditions induces these virulent factors.
4
Q
How does Shigella enter into hot colon?
A
Through M cells
5
Q
What cell surface is susceptible to Shigella?
A
Basolateral surface of epithelial cells
6
Q
What is the roll of invasion plasmid antigens in Shigella?
A
Help Shigella to invade, loosens tight junctions
7
Q
**What is the role of intracellular spread IcsA (ATPase)?
A
Causes actin polymerization and pushes Shigella through cell
8
Q
How is an ulcer caused in Shigella?
A
When epithelial cells die and are sloughed off.
9
Q
What leukocyte enters colonic tissue and can be seen in stool?
A
Neutrophils
10
Q
What damage does Shigella cause?
A
Inflammatory diarrhea with leukocytes in the stool
11
Q
Which species produces Shiga toxin?
A
Shigella dysenteriae
12
Q
What damage does Shigella dysenteriae cause?
A
Kills intestinal epithelial cells and disrupts sodium absorption
13
Q
**Why is disrupted sodium absorption important?
A
Leads to an excess of fluid in the lumen and leads to diarrhea and watery stool
14
Q
What do most species of Salmonella cause?
A
Gastroenteritis
15
Q
What species of Salmonella causes typhoid fever?
A
S. typhi and S. paratyphi
16
Q
What is the inoculum size for Salmonella?
A
Large infectious dose required
17
Q
**What causes Salmonella to express multiple proteins on pathogenicity islands?
A
Acidic conditions (low pH)
18
Q
What cells do Salmonella invade?
A
Apical surface of intestinal epithelial cells
19
Q
How does invasion occur in Salmonella?
A
Invasion occurs via bacterial mediated endocytosis
20
Q
What happens upon invasion in Salmonella?
A
Cell ruffling and signal transduction activation.
21
Q
Where is Salmonella released?
A
Lamina propria
22
Q
Which Salmonella species can replicate in the macrophages?
A
Salmonella typhi
23
Q
**Where are S. typhi found during the carrier state?
A
Gall bladder
24
Q
What damage does S. typhi cause when it re-infects the intestines?
A
Inflammation and ulceration of Peyer’s patches, diarrhea, hemorrhage, perforation.
25
What similarities exist between Salmonella and Shigella?
Both are invasive, both cause invasive diarrhea, bloody stool, neutrophils in stool and not a lot of stool. Both respond to environmental changes
26
Which species (Salmonella or Shigella) has a larger inoculum size?
Salmonella
27
Which species (Salmonella or Shigella) causes bacteremia?
Salmonella
28
Which species (Salmonella or Shigella) causes more severe diseases?
Salmonella
29
Is there a vaccine for Salmonella or Shigella?
No Shigella vaccine
| Vaccine for capsule of Salmonella typhi
30
Which vibrio species is most severe?
V. cholerae
31
What is the difference between the new and original El Tor strain?
Mutated O1 antigen, new LPS serotype, encapsulated
32
How are flagella important in Vibrio?
Allows motility, able to produce a protease that hydrolyzes mucous.
33
How are pili important in Vibrio?
Helps Vibrio to adhere to mucosal tissue.
34
What causes the expression of pili?
Reduced ion levels in body leads to pili expression
35
What causes expression of Cholera toxin?
Phage encoded (reduced ion levels)
36
**How does Cholera toxin cause diarrhea?
Causes transfer of ADP from NAD to activated Gs. cAMP increases Cl- loss from cell and water follows
37
What is the importance of adenylate cyclase?
Adenylate cyclase increases cAMP in cell
38
What is the importance of cAMP?
cAMP causes Cl- ions to be secreted, water follows
39
What is the inoculum size for ETEC?
Large inoculum size
40
WHat is ETEC known for?
Diarrhea in travelers to Mexico
41
Where is colonization factor antigen (CFA) found?
On the Fimbrae
42
Why is cfa important for virulence?
Help ETEC to adhere to mucosal tissue
43
What toxins does ETEC produce?
Heat-labile toxin (LT)
| Heat stable toxin (ST)
44
Which toxin (LT or ST) activates cAMP
LT activates cAMP
45
Which toxin (LT or ST) activates cGMP
ST activates cGMP
46
Which toxin is similar to Cholerae toxin?
LT, both activate cAMP
47
Why is it important to rule out V. cholerae when diagnosing a non-invasive bacterial pathogen?
Because V. cholera can cause serious disease
48
What is the most important factor in the treatment of secretory diarrhea?
Oral rehydration (salt/ sugar mix)
49
What is the inoculum size of EPEC?
Large inoculum size required
50
Which age group is EPEC most prevalent in?
Newborns, especially in nurseries/ daycare
51
**How does EPEC adhere for colonization?
Intimate adherence pattern in 3 steps.
1) Bundle forming pilus for adherence from long distance
2) Type 3 secretion of TIr into host epithelial cell
3) Tir binds intimin to result in pedastol formation
52
**How does EPEC induce diarrhea?
No toxin produced. Malabsorption due to microvilli disruptions of tight junctions. Causes accumulation of sodium in lumen.
53
How does EHEC adhere to host?
THrough attaching effacing lesion (same 3 steps as EPEC)
54
What toxin does EHEC produce?
Shiga-like toxin
55
What does Shiga-like toxin attack?
Attacks small blood vessels of the large intestines
56
What effect does inflammation have on the toxin?
Inflammation enhances the effects of the toxin (why antibiotics are controversial)
57
**Besides an inflammatory colitis what other condition can result from EHEC and what organ is affected?
Gastroenteritis via an attaching effacing lesion and Hemolytic uremic syndrome (HUS). Kidney is affected.
58
Why are urinary tract infections more common in females?
Urethra shorter in females, prostate helps in males
59
What is an uncomplicated urinary tract infection?
When normal defense mechanisms intact, no recent hospital visits, disease limited to lower urinary tract?
60
What is a complicated urinary tract infection?
When there is an abnormality in urinary tract, recent hospital visit, disease likely spread to kidneys
61
What is cystitis?
Inflammation of bladder from UTI
62
What is pyelonephritis?
Inflammation of kidneys from UTI
63
What is the most common bacterial pathogen that causes an uncomplicated UTI?
E. coli
64
What is the most common bacterial pathogen that causes a complicated UTI?
E. coli, Klebsiella, mirabilis, serratia, P. aeruginosa
65
What are natural barrier defenses found in the urinary tract?
Complete voidance of bladder, peristalsis, uterovesicle valves, mucous layer, normal microbiota, pH
66
What are some reasons why cystitis can progress to pyelonephritis?
Retrograde flow of urine, urethral catheters, urinary tract stones
67
How does UPEC adhere to urinary tract tissue?
FImbriae attach to uroepithelial cells
68
What adhesions are necessary for adhesion?
Fimbriae adhessions FimH and P fimbriae
69
What adhesion is associated with cystitis?
FimH antigen
70
Which adhesion is associated with pyelonephritis?
P fimbriae expression
71
Why are aerobactin and hemolysin important?
Associated with pyelonephritis, hemolysin can lyse host cell aerobactin can sequester iron.
72
Why are flagella important in P. mirabilis?
Transmission, motility, adherence
73
Why is hemolysin important in P. mirabilis?
Lyse host cells
74
Why is IgA protease important in P. mirabilis?
Break down IgA, avoid host detection.
75
WHy is urease important in P. mirabilis?
Raises pH of urine, bacteria grow better, toxic to renal cells, helps form urinary stones
76
How are UTI's diagnosed?
Count bacteria in urine, detect alkaline urine, detect urease
77
**How can Proteus mirabilis be identified/diagnosed?
Alkaline urine, production of urease
78
**What type of pili are necessary for adhesion to urinary tract epithelium for Klebisella?
Type 1 pili
79
What type of pili are necessary for adhesion to respiratory epithelial cells in Klebsiella?
Type 3
80
How does Klebsiella induce watery diarrhea?
Enterotoxin similar to ST/LT
81
Why is aerobactin important?
Iron sequestering protein
82
Why is the capsule important in Klebsiella?
Antiphagocytic, in bacteria with no capsule, no pathenogenisis
83
What does the phase, "H. pylori is a 'slow' pathogen" mean?
Can take months to years to affect host.
84
**Where does H. pylori colonize?
Found in the mucous overlying mucous secreting cells of the stomach
85
What diseases can H. pylori cause?
Erosive gastritis, Duodenal ulcer, MALT lymphoma, gastric adenocarcinoma
86
**All of the above diseases are preceded by the development of what?
Chronic superficial (atrophic) gastritis
87
**What does chronic atrophic gastritis lead to?
Gastric adenocarcinoma (most devastating), lymphoproliferic disease, chronic superficial gastritis, peptic ulcer disease
88
Why is production of urease important?
H. pylori is readily killed by gastric acid, if not producing enough urease, will be killed by gastric acid
89
Why is production of cytotoxin important in H. pylori?
Associated with peptic ulcer disease
90
Why is the down-regulation of somatostatin producing D-cells important in H. pylori?
Somatostatin inhibits gastrin, gastrin levels are increased
91
Why is an increase in gastrin producing important for the development of H. pylori mediated carcinogenesis?
Leads to cell proliferation and mutation
92
How can enhanced inflammatory response from H. pylori infection lead to carcinogenesis?
Inflammation leads to increased cell proliferation, epithelial cell damage, and increased free radical production, all leading to mutation.
93
What is atrophic gastritis?
Chronic inflammation. Leads to lower gastric acid, decreases ulcer risk but increases cancer risk
94
What is the classification of Clostridia
Strictly anaerobic, gram positive
95
What virulence factor is important in Clostridia?
Production of endospores, resistant to adverse conditions.
96
What bacteria is the leading cause of nosocomial diarrhea?
Clostridia difficile
97
What toxins does C. difficile produce?
Toxin A and Toxin B
98
What is Toxin A?
Enterotoxin- fluid production and damage to the mucosa. Cause cells to lose cytoskeletal structure and die
99
What is toxin B?
Cytotoxin- rounding of tissue-culture cells. Cause cells to lose cytoskeletal structure and die.
100
Where is C. perfringes found?
In soil (every soil except Sahara desert) and intestinal tract of animals
101
What conditions introduce spores to germinate?
Anaerobic
Compromised blood supply
Calcium ions
Availability of peptides and amino acids
102
What damage do the 12 toxins of C. perfringens cause?
Toxins cause cellulitis which causes gas gangrene and then myonecrosis (destruction of muscle)
103
What damage does Alpha-toxin in C. perfringens cause?
Damages cell membranes, causes gas gangrene
104
What damage does phospholipase Type C in C. perfringens cause?
Hydrolyzes phosphatidycholine that leads to cell death.
105
What is the treatment for C. perfringens?
Surgical removal, antibiotics, antitoxin, high oxygen concentration, return arterial supply.
106
How does C. perfringens cause food poisoning?
Sporulating C. perfringens produce enterotoxin that results in diarrhea (self limiting)
107
Where is C. botulinum found?
Soils and marine sediments
108
How are C. botulinum spores important in their virulence?
They are heat resistant and can survive food processing.
109
What toxin does C. botulinum produce?
Produces seven major neurotoxins, serotypes A-G.
110
Which serotypes are the most common in humans in C. botulinum?
A, B, and E
111
What is the size of the botulinum toxin?
900 kDA, toxic component 150 kDa
112
**What damage does Botulinum toxin produce?
Prevents the release of acetylcholine neurotransmitter
113
What kind of paralysis does C. botulinum produce?
Flaccid paralysis, cranial nerves affected, progresses until respiratory failure
114
What are the three types of botulism?
Food-bourne, wound bourne (rare) and infant botulism
115
What is the treatment for botulism?
Trivalent antitoxin ASAP
116
What protein is responsible for all symptoms of C. tetani?
Tetanospasmin
117
What damage does Tetanopasmin cause?
Inhibits GABA
118
What kind of paralysis is associated with C. tetani?
Spastic paralysis, reflex spasms
119
What is Trismus?
Lockjaw, spasm of masseter muscle
120
What is the treatment for C. tetani?
DPT vaccine, human globulin, antitoxin and penicillin
121
What are the characteristics of Chlamydiae?
Small, gram negative bacteria
122
**What is unique about Chlamydiae in regards to their cell wall?
No murenin
123
What do Chlamydiae rely on to survive?
Obligate intracellular pathogens, depend on host ATP
124
Which species is the leading cause of preventable blindness in the world?
Chlamydia trachomatis
125
How is Chlamydia trachomatis transmitted?
Droplet or direct contact
| STD
126
What causes damage in Chlamydia trachomatis?
Delayed type hypersensitivity, immune response, chlamydial heat shock protein (hsp60), chlamydial LPS
127
How does Chlamydia trachomatis enter the body?
Extracellular Elementary body (EB)
128
How is Chlamydia trachomatis internalized?
EB bodies disguised as nutriends and internalized by receptor-mediated endocytosis
129
What effect do EB's have on endocytic vesicles?
Maintain pH above 6.2, prevent vesicle from fusion with lysosome, use host components for camouflage
130
What are RB's?
Active organisms of EB's, and invade nearby cells, take up nutrients
131
Are RB's or EB's used for extracellular spread?
EB's
132
How many people have had "walking" pneumonia caused from Chlamydophila pneumoniae?
Virtually every living adult
133
When humans are infected with Chlamydophila psittaci, what type of disease is this known as?
Zoonotic disease
134
How are humans exposed to Chlamydophila psittachi?
Inhalation of avian fecal dust aerosols
135
What damage does psittacosis cause?
Respiratory flu-like illness, heart valve damage
136
What treatment exists for Chalmydophila psittachi?
Antimicrobials attacking RB forms
137
What membranes would a drug have to penetrate to effect RB's?
Host cell plasma membrane
Inclusion membrane
Chlamydial outer membrane
Chlamydial cytoplasmic membrane
138
What are characteristics of Rickettsiae?
Small gram negative rods
139
What are Rickettsiae dependent on making them an obligate intracellular bacteria?
Lack certain metabolites necessary for growth
140
What is a Zoonotic disease?
Infections transmitted from animals to humans
141
**What disease does R. rickettsii cause and how is it transmitted?
Rocky mountain spotted fever
| Spread by ticks
142
Which type of cells do Rickettsiae tagret?
Endothelial
143
How does Rickettsiae attach to host cells?
Attach to vascular endothelial cells (small blood vessels)
144
How do Rickettsiae spread in humans?
Induce endocytosis and lyse host phagosome. Replicate in cytosol
145
How does R. prowazekii exit the cell?
Cell lysis
146
How does R. rickettsii exit the cell?
Through local projections (filopodia) actin pushes out bacteria
147
How does R. tsutsugamushi exit the cell
Budding through the cell membrane, remains enveloped in host cell
148
What damage does lysis of the cell cause?
Leakage of blood which causes a rash known as hemorrhagic spots
149
How is Ehrlichia spread?
Transmitted by Lone Star tick
150
Which cells are Ehrlichia specific for?
Specific for leukocytes (mostly monocytes and macrophages)
151
What damage does Ehrlichia cause?
HGE and HME, causes fever, malaise, headache, myalgia
152
What are the three steps of development for Ehrlichia?
1) Reticulate cells (RC)
| 2) Dense-core cells (DC)
153
Where are reticulate cells developing?
Host cell vacuoles
154
Where are dense-core cells developing?
Within cytoplasmic endosomal vacuole (morula)
155
**What is unique about the size of mycoplasma?
Smallest organ capable of growth on cell free media
156
**What is required for Mycoplasma growth?
Requires sterol (cholesterol)
157
What is unique about the cell wall of mycoplasma?
No murenin, not sensitive to penicillin
158
What reservoirs carry M. pneumonia?
Only humans
159
How does M. pneumonia adhere to respiratory epithelium?
Terminal adhesion structures, tip-mediated
160
What damage does M. pneumonia cause?
Not highly destructive, impairs ciliary function and induce H202
161
What is the newest emerging human pathogen?
M. genitalium
162
Are mycoplasmas part of the normal human oral flora?
Yes
163
How is mycoplasma infection diagnosed?
IgM cold hemagglutinins, at lower temps antibodies cause RBC's to stick together
164
How common is clinically significant hemolysis in mycoplasma?
Rare
