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Micro Final Exam > Bailey Material > Flashcards

Bailey Material Flashcards

1
Q

Which type of Shigella is the most sever?

A

S. Dysenteriae

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2
Q

What is the inoculum size for Shigella?

A

Small inoculum required

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3
Q

How are acid resistance and other virulence factors induced in Shitella species?

A

Anerobic conditions induces these virulent factors.

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4
Q

How does Shigella enter into hot colon?

A

Through M cells

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5
Q

What cell surface is susceptible to Shigella?

A

Basolateral surface of epithelial cells

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6
Q

What is the roll of invasion plasmid antigens in Shigella?

A

Help Shigella to invade, loosens tight junctions

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7
Q

**What is the role of intracellular spread IcsA (ATPase)?

A

Causes actin polymerization and pushes Shigella through cell

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8
Q

How is an ulcer caused in Shigella?

A

When epithelial cells die and are sloughed off.

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9
Q

What leukocyte enters colonic tissue and can be seen in stool?

A

Neutrophils

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10
Q

What damage does Shigella cause?

A

Inflammatory diarrhea with leukocytes in the stool

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11
Q

Which species produces Shiga toxin?

A

Shigella dysenteriae

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12
Q

What damage does Shigella dysenteriae cause?

A

Kills intestinal epithelial cells and disrupts sodium absorption

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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

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14
Q

What do most species of Salmonella cause?

A

Gastroenteritis

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15
Q

What species of Salmonella causes typhoid fever?

A

S. typhi and S. paratyphi

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16
Q

What is the inoculum size for Salmonella?

A

Large infectious dose required

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17
Q

**What causes Salmonella to express multiple proteins on pathogenicity islands?

A

Acidic conditions (low pH)

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18
Q

What cells do Salmonella invade?

A

Apical surface of intestinal epithelial cells

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19
Q

How does invasion occur in Salmonella?

A

Invasion occurs via bacterial mediated endocytosis

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20
Q

What happens upon invasion in Salmonella?

A

Cell ruffling and signal transduction activation.

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21
Q

Where is Salmonella released?

A

Lamina propria

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22
Q

Which Salmonella species can replicate in the macrophages?

A

Salmonella typhi

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23
Q

**Where are S. typhi found during the carrier state?

A

Gall bladder

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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.

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25
Q

What similarities exist between Salmonella and Shigella?

A

Both are invasive, both cause invasive diarrhea, bloody stool, neutrophils in stool and not a lot of stool. Both respond to environmental changes

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26
Q

Which species (Salmonella or Shigella) has a larger inoculum size?

A

Salmonella

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27
Q

Which species (Salmonella or Shigella) causes bacteremia?

A

Salmonella

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28
Q

Which species (Salmonella or Shigella) causes more severe diseases?

A

Salmonella

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29
Q

Is there a vaccine for Salmonella or Shigella?

A

No Shigella vaccine

Vaccine for capsule of Salmonella typhi

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30
Q

Which vibrio species is most severe?

A

V. cholerae

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31
Q

What is the difference between the new and original El Tor strain?

A

Mutated O1 antigen, new LPS serotype, encapsulated

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32
Q

How are flagella important in Vibrio?

A

Allows motility, able to produce a protease that hydrolyzes mucous.

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33
Q

How are pili important in Vibrio?

A

Helps Vibrio to adhere to mucosal tissue.

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34
Q

What causes the expression of pili?

A

Reduced ion levels in body leads to pili expression

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35
Q

What causes expression of Cholera toxin?

A

Phage encoded (reduced ion levels)

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36
Q

**How does Cholera toxin cause diarrhea?

A

Causes transfer of ADP from NAD to activated Gs. cAMP increases Cl- loss from cell and water follows

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37
Q

What is the importance of adenylate cyclase?

A

Adenylate cyclase increases cAMP in cell

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38
Q

What is the importance of cAMP?

A

cAMP causes Cl- ions to be secreted, water follows

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39
Q

What is the inoculum size for ETEC?

A

Large inoculum size

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40
Q

WHat is ETEC known for?

A

Diarrhea in travelers to Mexico

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41
Q

Where is colonization factor antigen (CFA) found?

A

On the Fimbrae

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42
Q

Why is cfa important for virulence?

A

Help ETEC to adhere to mucosal tissue

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43
Q

What toxins does ETEC produce?

A

Heat-labile toxin (LT)

Heat stable toxin (ST)

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44
Q

Which toxin (LT or ST) activates cAMP

A

LT activates cAMP

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45
Q

Which toxin (LT or ST) activates cGMP

A

ST activates cGMP

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46
Q

Which toxin is similar to Cholerae toxin?

A

LT, both activate cAMP

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47
Q

Why is it important to rule out V. cholerae when diagnosing a non-invasive bacterial pathogen?

A

Because V. cholera can cause serious disease

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48
Q

What is the most important factor in the treatment of secretory diarrhea?

A

Oral rehydration (salt/ sugar mix)

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49
Q

What is the inoculum size of EPEC?

A

Large inoculum size required

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50
Q

Which age group is EPEC most prevalent in?

A

Newborns, especially in nurseries/ daycare

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51
Q

**How does EPEC adhere for colonization?

A

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

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52
Q

**How does EPEC induce diarrhea?

A

No toxin produced. Malabsorption due to microvilli disruptions of tight junctions. Causes accumulation of sodium in lumen.

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53
Q

How does EHEC adhere to host?

A

THrough attaching effacing lesion (same 3 steps as EPEC)

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54
Q

What toxin does EHEC produce?

A

Shiga-like toxin

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55
Q

What does Shiga-like toxin attack?

A

Attacks small blood vessels of the large intestines

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56
Q

What effect does inflammation have on the toxin?

A

Inflammation enhances the effects of the toxin (why antibiotics are controversial)

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57
Q

**Besides an inflammatory colitis what other condition can result from EHEC and what organ is affected?

A

Gastroenteritis via an attaching effacing lesion and Hemolytic uremic syndrome (HUS). Kidney is affected.

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58
Q

Why are urinary tract infections more common in females?

A

Urethra shorter in females, prostate helps in males

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59
Q

What is an uncomplicated urinary tract infection?

A

When normal defense mechanisms intact, no recent hospital visits, disease limited to lower urinary tract?

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60
Q

What is a complicated urinary tract infection?

A

When there is an abnormality in urinary tract, recent hospital visit, disease likely spread to kidneys

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61
Q

What is cystitis?

A

Inflammation of bladder from UTI

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62
Q

What is pyelonephritis?

A

Inflammation of kidneys from UTI

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63
Q

What is the most common bacterial pathogen that causes an uncomplicated UTI?

A

E. coli

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64
Q

What is the most common bacterial pathogen that causes a complicated UTI?

A

E. coli, Klebsiella, mirabilis, serratia, P. aeruginosa

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65
Q

What are natural barrier defenses found in the urinary tract?

A

Complete voidance of bladder, peristalsis, uterovesicle valves, mucous layer, normal microbiota, pH

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66
Q

What are some reasons why cystitis can progress to pyelonephritis?

A

Retrograde flow of urine, urethral catheters, urinary tract stones

67
Q

How does UPEC adhere to urinary tract tissue?

A

FImbriae attach to uroepithelial cells

68
Q

What adhesions are necessary for adhesion?

A

Fimbriae adhessions FimH and P fimbriae

69
Q

What adhesion is associated with cystitis?

A

FimH antigen

70
Q

Which adhesion is associated with pyelonephritis?

A

P fimbriae expression

71
Q

Why are aerobactin and hemolysin important?

A

Associated with pyelonephritis, hemolysin can lyse host cell aerobactin can sequester iron.

72
Q

Why are flagella important in P. mirabilis?

A

Transmission, motility, adherence

73
Q

Why is hemolysin important in P. mirabilis?

A

Lyse host cells

74
Q

Why is IgA protease important in P. mirabilis?

A

Break down IgA, avoid host detection.

75
Q

WHy is urease important in P. mirabilis?

A

Raises pH of urine, bacteria grow better, toxic to renal cells, helps form urinary stones

76
Q

How are UTI’s diagnosed?

A

Count bacteria in urine, detect alkaline urine, detect urease

77
Q

**How can Proteus mirabilis be identified/diagnosed?

A

Alkaline urine, production of urease

78
Q

**What type of pili are necessary for adhesion to urinary tract epithelium for Klebisella?

A

Type 1 pili

79
Q

What type of pili are necessary for adhesion to respiratory epithelial cells in Klebsiella?

A

Type 3

80
Q

How does Klebsiella induce watery diarrhea?

A

Enterotoxin similar to ST/LT

81
Q

Why is aerobactin important?

A

Iron sequestering protein

82
Q

Why is the capsule important in Klebsiella?

A

Antiphagocytic, in bacteria with no capsule, no pathenogenisis

83
Q

What does the phase, “H. pylori is a ‘slow’ pathogen” mean?

A

Can take months to years to affect host.

84
Q

**Where does H. pylori colonize?

A

Found in the mucous overlying mucous secreting cells of the stomach

85
Q

What diseases can H. pylori cause?

A

Erosive gastritis, Duodenal ulcer, MALT lymphoma, gastric adenocarcinoma

86
Q

**All of the above diseases are preceded by the development of what?

A

Chronic superficial (atrophic) gastritis

87
Q

**What does chronic atrophic gastritis lead to?

A

Gastric adenocarcinoma (most devastating), lymphoproliferic disease, chronic superficial gastritis, peptic ulcer disease

88
Q

Why is production of urease important?

A

H. pylori is readily killed by gastric acid, if not producing enough urease, will be killed by gastric acid

89
Q

Why is production of cytotoxin important in H. pylori?

A

Associated with peptic ulcer disease

90
Q

Why is the down-regulation of somatostatin producing D-cells important in H. pylori?

A

Somatostatin inhibits gastrin, gastrin levels are increased

91
Q

Why is an increase in gastrin producing important for the development of H. pylori mediated carcinogenesis?

A

Leads to cell proliferation and mutation

92
Q

How can enhanced inflammatory response from H. pylori infection lead to carcinogenesis?

A

Inflammation leads to increased cell proliferation, epithelial cell damage, and increased free radical production, all leading to mutation.

93
Q

What is atrophic gastritis?

A

Chronic inflammation. Leads to lower gastric acid, decreases ulcer risk but increases cancer risk

94
Q

What is the classification of Clostridia

A

Strictly anaerobic, gram positive

95
Q

What virulence factor is important in Clostridia?

A

Production of endospores, resistant to adverse conditions.

96
Q

What bacteria is the leading cause of nosocomial diarrhea?

A

Clostridia difficile

97
Q

What toxins does C. difficile produce?

A

Toxin A and Toxin B

98
Q

What is Toxin A?

A

Enterotoxin- fluid production and damage to the mucosa. Cause cells to lose cytoskeletal structure and die

99
Q

What is toxin B?

A

Cytotoxin- rounding of tissue-culture cells. Cause cells to lose cytoskeletal structure and die.

100
Q

Where is C. perfringes found?

A

In soil (every soil except Sahara desert) and intestinal tract of animals

101
Q

What conditions introduce spores to germinate?

A

Anaerobic
Compromised blood supply
Calcium ions
Availability of peptides and amino acids

102
Q

What damage do the 12 toxins of C. perfringens cause?

A

Toxins cause cellulitis which causes gas gangrene and then myonecrosis (destruction of muscle)

103
Q

What damage does Alpha-toxin in C. perfringens cause?

A

Damages cell membranes, causes gas gangrene

104
Q

What damage does phospholipase Type C in C. perfringens cause?

A

Hydrolyzes phosphatidycholine that leads to cell death.

105
Q

What is the treatment for C. perfringens?

A

Surgical removal, antibiotics, antitoxin, high oxygen concentration, return arterial supply.

106
Q

How does C. perfringens cause food poisoning?

A

Sporulating C. perfringens produce enterotoxin that results in diarrhea (self limiting)

107
Q

Where is C. botulinum found?

A

Soils and marine sediments

108
Q

How are C. botulinum spores important in their virulence?

A

They are heat resistant and can survive food processing.

109
Q

What toxin does C. botulinum produce?

A

Produces seven major neurotoxins, serotypes A-G.

110
Q

Which serotypes are the most common in humans in C. botulinum?

A

A, B, and E

111
Q

What is the size of the botulinum toxin?

A

900 kDA, toxic component 150 kDa

112
Q

**What damage does Botulinum toxin produce?

A

Prevents the release of acetylcholine neurotransmitter

113
Q

What kind of paralysis does C. botulinum produce?

A

Flaccid paralysis, cranial nerves affected, progresses until respiratory failure

114
Q

What are the three types of botulism?

A

Food-bourne, wound bourne (rare) and infant botulism

115
Q

What is the treatment for botulism?

A

Trivalent antitoxin ASAP

116
Q

What protein is responsible for all symptoms of C. tetani?

A

Tetanospasmin

117
Q

What damage does Tetanopasmin cause?

A

Inhibits GABA

118
Q

What kind of paralysis is associated with C. tetani?

A

Spastic paralysis, reflex spasms

119
Q

What is Trismus?

A

Lockjaw, spasm of masseter muscle

120
Q

What is the treatment for C. tetani?

A

DPT vaccine, human globulin, antitoxin and penicillin

121
Q

What are the characteristics of Chlamydiae?

A

Small, gram negative bacteria

122
Q

**What is unique about Chlamydiae in regards to their cell wall?

A

No murenin

123
Q

What do Chlamydiae rely on to survive?

A

Obligate intracellular pathogens, depend on host ATP

124
Q

Which species is the leading cause of preventable blindness in the world?

A

Chlamydia trachomatis

125
Q

How is Chlamydia trachomatis transmitted?

A

Droplet or direct contact

STD

126
Q

What causes damage in Chlamydia trachomatis?

A

Delayed type hypersensitivity, immune response, chlamydial heat shock protein (hsp60), chlamydial LPS

127
Q

How does Chlamydia trachomatis enter the body?

A

Extracellular Elementary body (EB)

128
Q

How is Chlamydia trachomatis internalized?

A

EB bodies disguised as nutriends and internalized by receptor-mediated endocytosis

129
Q

What effect do EB’s have on endocytic vesicles?

A

Maintain pH above 6.2, prevent vesicle from fusion with lysosome, use host components for camouflage

130
Q

What are RB’s?

A

Active organisms of EB’s, and invade nearby cells, take up nutrients

131
Q

Are RB’s or EB’s used for extracellular spread?

A

EB’s

132
Q

How many people have had “walking” pneumonia caused from Chlamydophila pneumoniae?

A

Virtually every living adult

133
Q

When humans are infected with Chlamydophila psittaci, what type of disease is this known as?

A

Zoonotic disease

134
Q

How are humans exposed to Chlamydophila psittachi?

A

Inhalation of avian fecal dust aerosols

135
Q

What damage does psittacosis cause?

A

Respiratory flu-like illness, heart valve damage

136
Q

What treatment exists for Chalmydophila psittachi?

A

Antimicrobials attacking RB forms

137
Q

What membranes would a drug have to penetrate to effect RB’s?

A

Host cell plasma membrane
Inclusion membrane
Chlamydial outer membrane
Chlamydial cytoplasmic membrane

138
Q

What are characteristics of Rickettsiae?

A

Small gram negative rods

139
Q

What are Rickettsiae dependent on making them an obligate intracellular bacteria?

A

Lack certain metabolites necessary for growth

140
Q

What is a Zoonotic disease?

A

Infections transmitted from animals to humans

141
Q

**What disease does R. rickettsii cause and how is it transmitted?

A

Rocky mountain spotted fever

Spread by ticks

142
Q

Which type of cells do Rickettsiae tagret?

A

Endothelial

143
Q

How does Rickettsiae attach to host cells?

A

Attach to vascular endothelial cells (small blood vessels)

144
Q

How do Rickettsiae spread in humans?

A

Induce endocytosis and lyse host phagosome. Replicate in cytosol

145
Q

How does R. prowazekii exit the cell?

A

Cell lysis

146
Q

How does R. rickettsii exit the cell?

A

Through local projections (filopodia) actin pushes out bacteria

147
Q

How does R. tsutsugamushi exit the cell

A

Budding through the cell membrane, remains enveloped in host cell

148
Q

What damage does lysis of the cell cause?

A

Leakage of blood which causes a rash known as hemorrhagic spots

149
Q

How is Ehrlichia spread?

A

Transmitted by Lone Star tick

150
Q

Which cells are Ehrlichia specific for?

A

Specific for leukocytes (mostly monocytes and macrophages)

151
Q

What damage does Ehrlichia cause?

A

HGE and HME, causes fever, malaise, headache, myalgia

152
Q

What are the three steps of development for Ehrlichia?

A

1) Reticulate cells (RC)

2) Dense-core cells (DC)

153
Q

Where are reticulate cells developing?

A

Host cell vacuoles

154
Q

Where are dense-core cells developing?

A

Within cytoplasmic endosomal vacuole (morula)

155
Q

**What is unique about the size of mycoplasma?

A

Smallest organ capable of growth on cell free media

156
Q

**What is required for Mycoplasma growth?

A

Requires sterol (cholesterol)

157
Q

What is unique about the cell wall of mycoplasma?

A

No murenin, not sensitive to penicillin

158
Q

What reservoirs carry M. pneumonia?

A

Only humans

159
Q

How does M. pneumonia adhere to respiratory epithelium?

A

Terminal adhesion structures, tip-mediated

160
Q

What damage does M. pneumonia cause?

A

Not highly destructive, impairs ciliary function and induce H202

161
Q

What is the newest emerging human pathogen?

A

M. genitalium

162
Q

Are mycoplasmas part of the normal human oral flora?

A

Yes

163
Q

How is mycoplasma infection diagnosed?

A

IgM cold hemagglutinins, at lower temps antibodies cause RBC’s to stick together

164
Q

How common is clinically significant hemolysis in mycoplasma?

A

Rare

Micro Final Exam (2 decks)

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