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BIO 315 > Module 12 - Bacterial Pathogenesis > Flashcards

Module 12 - Bacterial Pathogenesis Flashcards

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1
Q

In what two groups can bacteria be divided into?

A

Pathogenic and nonpathogenic

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2
Q

What is pathogenesis?

A

Processes used by pathogens to produce disease

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3
Q

What are the key aspects of bacterial pathogenesis?

A

Attachment to host tissue to gain access, avoid host defense, damage host tissues to get nutrients and replicate

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4
Q

What is a principle feature in pathogen evolution?

A

Genetic mobility

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5
Q

What are virulence factors?

A

Pathogen products that enhance the ability to cause disease

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6
Q

In what common ways do virulence factors act?

A

They can gain access to tissue, overcome host defense, and get nutrients (by damaging cells or stealing from the host)

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7
Q

What diseases does Neisseria gonorrhoeae lead to?

A

STIs such as gonorrhea

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8
Q

What virulence factors are produced by Neisseria gonorrhoeae?

A

Fimbriae, IgA protease, and LOS

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9
Q

What does Neisseria gonorrhoeae do with its fimbriae?

A

Attaches to host cell and invades underlying tissues

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10
Q

What does Neisseria gonorrhoeae do with LOS?

A

It invokes an intense inflammatory response in the host

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11
Q

Why would a pathogenic bacteria want to induce inflammation?

A

It damages host tissue, which facilitates invasion and provides nutrients

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12
Q

How come pathogenic bacteria want to stop the host immune system?

A

The host defense system can stop entry and growth of pathogenic bacteria

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13
Q

What does Neisseria gonorrhoeae do with IgA protease?

A

It uses it to avoid the host defense system

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14
Q

How can pathogenic bacteria avoid the host defense system?

A

By changing surface antigens, or by producing IgA protease

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15
Q

What disease does Bordetella pertussis lead to?

A

Whooping cough

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16
Q

What disease does Escherichia coli O157:H7 lead to?

A

Hemorrhagic colitis and kidney failure

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17
Q

What disease does Helicobacter pylori lead to?

A

Gastritis, ulcers

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18
Q

What disease does Streptococcus pneumoniae lead to?

A

Pneumonia, meningitis

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19
Q

What disease does Streptococcus pyogenes lead to?

A

Various skin, throat, and systemic infections

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20
Q

What do the symptoms of Neisseria gonorrhoeae depend on?

A

The site of infection

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21
Q

What do nonpathogenic bacteria do (when growing)?

A

They colonizes and do not directly attach to host cell

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22
Q

What are some common attachment factors used by pathogenic bacteria?

A

Fibronectin binding proteins, fimbriae, outer membrane molecules, and other specialized proteins for attachment

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23
Q

What are adhesions?

A

Molecules that allow bacteria to bind to host tissues

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24
Q

In which bacteria are fibronectin binding proteins best studied in?

A

Streptococcus pyogenes, Staphylococcus aureus, and E. coli

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25
Q

What is fibronectin?

A

A plasma glycoprotein in plasma and as fibers in extracellular matrix

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26
Q

How come fibronectin is a prime target for pathogen binding?

A

It is present everywhere

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27
Q

What disease does Corynebacterium diphtheria lead to?

A

Diptheria

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28
Q

What disease does Clostridium difficile lead to?

A

Colitis

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29
Q

What disease does Clostridium perfringens lead to?

A

Gas gangrene

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30
Q

What disease does Mycobacterium tuberculosis lead to?

A

Tuberculosis

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31
Q

What disease does Staphylococcus aureus lead to?

A

Various skin and invasive diseases

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32
Q

What disease does Streptococcus pyogenes lead to?

A

Various invasive and toxic diseases

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33
Q

What disease does Treponema pallidum lead to?

A

Syphilis

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34
Q

What disease does Borrelia burgdorferi lead to?

A

Lyme disease

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35
Q

What disease does Porphyromonas gingivalis lead to?

A

Gum disease

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36
Q

What do fimbriae do?

A

They are used for attachment to host tissues and nonbiological surfaces (medical implants)

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37
Q

What is a fimbriae?

A

A specialized pili with an adhesive tip?

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38
Q

How come fimbriae are used to aid in adhesion?

A

It can help span the distance of repulsion

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39
Q

What repulsion is there when bacteria try to bind to host tissues?

A

Cell surfaces have net negative charge that causes electrostatic repulsion

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40
Q

What is found at the end of a fimbriae strand?

A

A specific adhesive tip composed of a tip protein

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41
Q

What does the adhesive tip of a fimbriae do?

A

It is used for attachment by targeting oligosaccharides

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42
Q

True or false: several different types of fimbriae can be produced by a single bacterium

A

True: they are frequently modified

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43
Q

Why are fimbriae modified?

A

To respond to environmental conditions

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44
Q

How does Neisseria gonorrhaea use its fimbriae?

A

It is needed for attachment to epithelial cells of urethra and cervix

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45
Q

What happens once infection has been established (in terms of fimbriae)?

A

Fimbriae expression can be turned on or off

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46
Q

How can fimbriae avoid host immune system?

A

By undergoing an amino acid change through genetic combination

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47
Q

What is the consequence of fimbriae undergoing amino acid change?

A

By the time one specific antibody is made, another fimbriae is produced

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48
Q

How do E. coli cells form lesions to obtain nurtients?

A

Through interactions of intimate virulence factors

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49
Q

What special adherence proteins are used by E. coli?

A

Intimin and Tir

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50
Q

Where is Tir found?

A

It is produced by E. coli, and translocated to intestinal cells

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51
Q

Where is Intimin found?

A

It is produced by E. coli

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52
Q

When do intestinal cells express Tir?

A

When E. coli insert it through a type III secretion pathway

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53
Q

What happens once Tir is inserted into intestinal cells?

A

It can interact with Intimin found on the E. coli cell

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54
Q

What happens when Tir interacts with Intimim?

A

A pedestal is formed for the E. coli cell

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55
Q

What is a capsule?

A

A well organized polysaccharide layer that surrounds some bacterial cells

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56
Q

What is another name for a capsule?

A

The glycocalyx

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57
Q

What are capsules composed of?

A

Usually polysaccharides, but sometimes polypeptides

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58
Q

True or false: capsules can help adhere to surfaces

A

True: they can bind to receptors to help adhere to surfaces

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59
Q

What is the primary role of capsules for pathogens?

A

To protect the bacterium from early immune defenses (phagocytosis and lyse from complement)

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60
Q

What happens to nonencapsulated bacteria (in terms of early immune defenses)?

A

They are opsonized and are regularly phagocytosed by phagocytes

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61
Q

What happens to encapsulated bacteria (in terms of early immune defenses)?

A

The antibody must move through the capsule to attach to the cell surface, so it will not be available for phagocyte binding

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62
Q

What is needed for phagocytosis of encapsulated bacteria to occur?

A

An antibody specific to the capsule

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63
Q

What is the result of constructing a capsule from host self molecules?

A

It prevents stimulation of the host immune response

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64
Q

What is the purpose of capsules containing water?

A

It protects the bacteria against desiccation

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65
Q

What do capsules exclude?

A

Bacterial viruses

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66
Q

True or false: immunity to one type of capsule is sufficient

A

False: immunity to one capsule type does not result in immunity to other types

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67
Q

What is the capsule of Bacillus anthracis made out of?

A

Poly-D-glutamic acid

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68
Q

What is the capsule of Streptococcus pyogenes made out of?

A

Hyaluronic acid

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69
Q

What is the capsule of Haemophilus influenzae made out of?

A

There are six different capsule types

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70
Q

What is the capsule of Neisseria meningitidis made out of?

A

Sialic acid

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71
Q

What is the capsule of Pseudomonas aeruginosa made out of?

A

Alginate (biofilm formation)

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72
Q

How do bacteria release toxins or virulence factors?

A

Either through their lysis, secretion to extracellular environment, or injection directly into a host cell

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73
Q

What are major virulence factors in gram negative bacteria?

A

Type III and Type IV secretion systems

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74
Q

What are some examples of gram negative bacteria that use Type III secretion systems?

A

E. coli, Shigella sonnei, Klebsiella pneumoniae, Nesseria gonorrhoeae, Salmonella Typhimurium

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75
Q

What are Type III secretion systems?

A

Injection assemblies that deliver virulence factors directly into the target cell

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76
Q

How do Type III secretion systems work?

A

They form a channel that passes through plasma membrane and outer membrane of pathogen and host cell membrane

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77
Q

Which is more common: Type III or Type IV secretion systems?

A

Type III secretion systems

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78
Q

How do Type IV secretion systems work?

A

They deliver molecules across the plasma membrane to inject virulence factors

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79
Q

What are Type III and IV secretion systems often encoded with?

A

The gene products that they will inject

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80
Q

Why is iron a limiting nutrient for the pathogen?

A

It is kept tightly bound by host iron binding proteins

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81
Q

What are the 4 strategies pathogens can use to obtain iron from the host?

A

Siderophores, transport proteins, low pH, and hemolysin

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82
Q

What are siderophores?

A

Bacterial iron binding proteins

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83
Q

How do siderophores obtain iron?

A

They compete with host iron binding proteins for iron

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84
Q

How are transport proteins used to obtain iron?

A

They can transport host iron binding proteins into the bacterial cell

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85
Q

How can low pH be used to obtain iron?

A

It reduces the ability of host iron binding proteins to bind to iron

86
Q

What do hemolysins do?

A

Lyse red blood cells

87
Q

How can hemolysins be used to obtain iron?

A

They can lyse red blood cells to release intracellular iron and other nutrients

88
Q

Why do bacteria use toxins?

A

To gain nutrients from the host

89
Q

What is a toxin?

A

A poisonous substance produced by an organism

90
Q

What are the two categories of toxins?

A

Endotoxins and exotoxins

91
Q

What are endotoxins, and what do they do?

A

They are part of the cell wall structure, and induce inflammatory responses

92
Q

What are some examples of endotoxins?

A

LPS and LTA

93
Q

What type of bacteria use LPS?

A

Gram-negative bacteria

94
Q

What type of bacteria use LTA?

A

Gram-positive bacteria

95
Q

What does LPS stand for?

A

Lipopolysaccharide

96
Q

What does LTA stand for?

A

Lipoteichoic acid

97
Q

What are exotoxins?

A

Soluble proteins released outside of the producing cell, or passively released upon bacterial lysis

98
Q

What are some examples of exotoxins?

A

AB toxins, cytolysins, and super antigens

99
Q

What are AB toxins?

A

Exotoxins with two subunits (A and B)

100
Q

What does the A subunit do in an AB toxin?

A

It has toxic enzymatic activity

101
Q

What does the B subunit do in an AB toxin?

A

It binds to the host cell receptor

102
Q

Generally, what is a cytotoxin?

A

A substance toxic to cells

103
Q

What are cytolysins?

A

Bacterial cytotoxins that act on the plasma membrane

104
Q

What are super antigens and what do they do?

A

Exotoxins that can non specifically stimulate T cells to secrete cytokines

105
Q

What does LOS stand for?

A

Lipooligosaccharide

106
Q

What is the structure of LOS?

A

Lipid A and a core polysaccharide

107
Q

What is the structure of LPS?

A

Lipid A, a core polysaccharide, and an O antigen

108
Q

How was LPS discovered?

A

Scientists isolated a heat stable element from gram negative bacteria that was responsible for many toxic effects of systemic diseases

109
Q

Where is LPS found?

A

In the outer membrane of gram-negative bacteria

110
Q

What is the most common type of endotoxin?

A

LPS

111
Q

What is the composition of the O antigen?

A

Repeating units of polysaccharide

112
Q

What does the O antigen do?

A

It is strain specific, and the target of the immune response

113
Q

What is used for serotyping?

A

The O antigen

114
Q

What is the composition of the core polysaccharide?

A

Various sugars with side chains that are genus or species specific

115
Q

What is the innermost component of LPS?

A

Lipid A

116
Q

What does Lipid A do?

A

It anchors LPS to outer membrane, and causes inflammation

117
Q

What is the composition of Lipid A?

A

Unusual fatty acids

118
Q

What is the toxic portion of LPS?

A

Lipid A

119
Q

What does Neisseria meningitis cause?

A

Inflammation of meninges

120
Q

What are meninges?

A

Lining that surrounds the brain and spinal cord

121
Q

What was shown to be responsible for the toxic properties of Neisseria meningitis?

A

Lipid A

122
Q

What does endotoxin do in low concentration?

A

It stimulates immune system response that can prevent disease

123
Q

True or false: systemic production of endotoxin is deadly

A

True: this can overwork the immune system

124
Q

Where is LTA found?

A

Anchored to the plasma membrane in most gram positive pathogens

125
Q

What is LTA?

A

A cell wall molecule

126
Q

True or false: LTA is recognized by TLRs?

A

True: like LPA, LTA is recognized by TLRs

127
Q

What does LTA do?

A

It induces inflammation

128
Q

True or false: LTA is useful in small quantities

A

True: the endotoxin produces septic shock only when there are large amounts of bacteria present

129
Q

What is the protective activity of a fever?

A

Inhibition of pathogen replication, increase in immune cell activities

130
Q

What is the protective activity of complement activation?

A

Lysis by MAC formation, induction of inflammation

131
Q

What is the protective activity of inflammation?

A

Transport of immune cells and molecules to site of infection

132
Q

What is the protective activity of B-cell proliferation?

A

Antibody production

133
Q

What is the protective activity of IFN-gamma expression from T cells

A

Activation of macrophages and NK cells

134
Q

What is the protective activity of stimulation of the clotting cascade?

A

Prevention of pathogen spread

135
Q

How are exotoxins grouped?

A

By structure (AB toxins), molecular activity (super antigens), or cellular activity (cytotoxins)

136
Q

Which bacteria have an AB toxin with one B subunit?

A

Diptheria, tetanus, and botulinum

137
Q

Which bacteria have an AB toxin with multiple of the same B subunit?

A

Cholera and Shiga

138
Q

Which bacteria have an AB toxin with multiple different B subunits?

A

Pertussis

139
Q

How does Corynebacterium diphtheria AB toxin spread?

A

It is absorbed in the circulatory system, where it is distributed to other organs (heart, kidney, liver, and spleen)

140
Q

What does Corynebacterium diphtheria AB toxin do?

A

It prevents protein synthesis

141
Q

How does Corynebacterium diphtheria AB toxin enter the host cell?

A

Through receptor mediated endocytosis

142
Q

What happens when the AB toxin is in the endosome?

A

Acidification causes a conformational change, forming a channel

143
Q

What happens once the B subunit forms a channel in the endosome?

A

The A subunit can inactivate EF2 to stop protein synthesis

144
Q

What does EF2 do?

A

It is a translation factor needed for protein synthesis

145
Q

What does EF2 stand for?

A

Elongation factor 2

146
Q

Which bacteria produces Shiga toxin?

A

E. coli O157:H7

147
Q

How come cattle, pigs, sheep, and deer can be a reservoir of infection for Shiga toxin?

A

These animals do not have the Shiga receptors, but these receptors are enriched in human kidney cells

148
Q

What do Shiga toxins do?

A

They cleave ribosomal RNA to prevent protein synthesis

149
Q

How does Diphtheria toxin inactivate EF2?

A

By adding an ADP ribose to EF2

150
Q

What is ADP-ribosylation?

A

The process of adding an ADP ribose to a protein

151
Q

How does EF2 work?

A

It is needed for movement of ribosomes along mRNA in eukaryotes

152
Q

How does Pertussis toxin work?

A

It adds an ADP ribose to Gi to activate adenylyl cyclase

153
Q

How does Cholera toxin work?

A

It adds an ADP ribose to Gs to activate adenylyl cyclase

154
Q

What is the effect of increased activation of adenylyl cyclase?

A

Disruption of ion and water balance

155
Q

What are two examples of AB toxins that cleave host proteins?

A

Botulinum toxin and tetanus toxin

156
Q

What do botulinum toxin and tetanus toxin have in common?

A

They are both neural toxins, similar in structure and function, and act on SNARE proteins

157
Q

What does SNARE protein stand for?

A

Snap receptor

158
Q

What do SNARE proteins do?

A

They are required to release neurotransmitters

159
Q

What are SNARE proteins?

A

A large protein super family, consisting of more than 60 members in yeast and mammalian cells

160
Q

What happens when neurotoxins cleave SNARE proteins?

A

They prevent neurotransmitter release

161
Q

What does acetylcholine do?

A

Causes muscle contraction

162
Q

What does botulinum toxin lead to?

A

Flaccid paralysis (botulism)

163
Q

What is flaccid paralysis?

A

Weakness of muscle and loss of muscle tone (limp and cannot contract)

164
Q

How does botulinum toxin lead to flaccid paralysis?

A

It prevents release of acetylcholine

165
Q

How can flaccid paralysis be fatal?

A

If it affects respiratory muscles (suffocation)

166
Q

What is one possible cause of sudden infant death syndrome?

A

Infant botulism

167
Q

What does tetanus toxin lead to?

A

Spastic paralysis (tetanus)

168
Q

What is spastic paralysis?

A

Unusual tightness or stiffness of muscles (persistent contraction)

169
Q

How does tetanus toxin lead to spastic paralysis?

A

It prevents release of glycine and GABA, which leads to continuous secretion of acetylcholine

170
Q

What does GABA stand for?

A

Gamma aminobutyric acid

171
Q

How do patients usually die in botulism or tetanus?

A

Respiratory failure

172
Q

What is needed to release neurotransmitters in vesicles?

A

The vesicles must fuse with the neuronal plasma membrane

173
Q

Which SNARE proteins help with membrane fusion?

A

Synaptobrevin, SNAP-25, and syntaxin

174
Q

Where is synaptobrevin found?

A

Inserted in the vesicle membrane

175
Q

Where is syntaxin found?

A

Inserted in the neuronal membrane

176
Q

What does SNAP-25 do?

A

It binds to synaptobrevin and syntaxin to form a complex that allows the membranes to fuse

177
Q

What is the primary role of SNARE proteins?

A

To mediate fusion of vesicle with target membrane bound compartments

178
Q

What is needed for normal muscular contraction?

A

Release of acetylcholine neurotransmitter from vesicles in the terminals of motor neurons

179
Q

What does botulinum toxin type A do?

A

It cleaves SNAP-25 to prevent muscular contraction

180
Q

How toxic is botulinum toxin?

A

300,000x more toxic than snake venom

181
Q

What is one of the most important toxins discovered?

A

Botulinum toxin

182
Q

What toxins attack synaptobrevin?

A

Tetanus toxin, botulinum toxin type B, D, F, G

183
Q

What toxins attack SNAP-25?

A

Botulinum toxin type A, C, E

184
Q

What toxins attack syntaxin?

A

Botulinum toxin type C

185
Q

How is muscular contraction halted?

A

By the release of neuroinhibitory neurotransmitters glycine and GABA

186
Q

How does tetanus toxin move through the body?

A

It is taken up by motor neurons, transported to the central nervous system, and then to the inhibitory neurons

187
Q

What does tetanus toxin do?

A

It cleaves synaptobrevin in inhibitory neurons

188
Q

How do glycine and GABA work?

A

They act on motor neurons to block acetylcholine release, ending contraction

189
Q

How does tetanus toxin lead to continuous muscle contraction?

A

It allows acetylcholine to be continually released from stimulated neurons

190
Q

True or false: cytolysins can destruct membranes without creating lysis

A

True: they do not have to cause lysis

191
Q

What does MDT stand for?

A

Membrane damaging toxin

192
Q

How much of bacterial protein toxins are cytolysins?

A

1/3

193
Q

How many cytolysins have been studied and published?

A

70

194
Q

How are cytolysins named?

A

According to the cells that they can destroy

195
Q

What do hemolysins do?

A

Lyse red blood cells

196
Q

What is the result of hemolysis?

A

A zone of clearing surrounding the bacteria

197
Q

What are hemolysis patterns used for?

A

Identifying streptococcus species (characteristic patterns)

198
Q

What are the three different types of hemolysis?

A

Alpha, beta, and gamma

199
Q

What is alpha hemolysis?

A

Partial hemolysis

200
Q

What is beta hemolysis?

A

Complete hemolysis

201
Q

What is gamma hemolysis?

A

No hemolysis

202
Q

What type of hemolysis do streppygenes bacteria that cause strep throat cause?

A

Beta hemolysis

203
Q

What type of hemolysis do strep pneumonia bacteria cause?

A

Alpha hemolysis

204
Q

What type of hemolysis do Entercoccus faecalis cause?

A

Gamma hemolysis

205
Q

What causes the green color in alpha hemolysis?

A

Partially decomposed hemoglobin

206
Q

What categories can cytolysins be grouped into?

A

Pore-forming toxins and membrane degrading toxins

207
Q

How do pore forming cytolysins work?

A

They are produced as monomers that polymerize in the membrane to form a circular pore

208
Q

What is an example of a pore forming cytolysin?

A

Alpha toxin from Staphylococcus aureus, and perfringolysin from Clostridium perfringens

209
Q

What do pore forming cytolysins do at high concentrations?

A

They form many holes, causing cell lysis

210
Q

What do pore forming cytolysins do at low concentrations?

A

They allow influx of calcium ions, which causes membrane damage and induces apoptosis

211
Q

How does perfringolysin work?

A

It binds to membrane cholesterol and contributes to tissue destruction in gas gangrene

212
Q

What are the characteristics of gas gangrene?

A

Muscle necrosis and intense gas productions

BIO 315 (12 decks)

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