Chap 15 Flashcards

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1
Q

Pathogenicity

A

the ability to cause disease

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2
Q

Virulence

A

the degree of pathogenicity

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3
Q

Portals of entry for microorganisms

A

Mucous membranes
Skin
Parenteral route

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4
Q

Parenteral route

A

Portal of entry beneath the skin and mucous membranes

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5
Q

Moth pathogens have a preferred

A

portal of entry

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6
Q

ID 50

A

infectious dose for 50% of a sample population

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7
Q

ID 50 MEASURES

A

Measures virulence of a microbe

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8
Q

LD50

A

lethal dose for 50% of a sample population

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9
Q

LD50 MEASURES

A

POTENCY OF A TOXIN

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10
Q

endospores

A

What are left behind when a bacteria is in an environment that it cant survive in. last hope for survival

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11
Q

Which portal of entry is most likely to cause infection?

A

The one with the lower ID 50 because it needs less endosppores to cause disease

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12
Q

adherence

A

pathogens attach to host tissues

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13
Q

adhesins (ligands)

A

on the pathogen bind to receptors on the host cells

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14
Q

receptors can be on

A

Glycocalyx
Fimbriae

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15
Q

microbes form biofilms that are

A

communities that share nutrients

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16
Q

capsules

A

Glycocalyx around the cell wall

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17
Q

function of capsules

A

Impair phagocytosis

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18
Q

Examples of microbes with capsules

A

Streptococcus pneumoniae—pneumonia
Haemophilus influenzae—pneumonia and meningitis
Bacillus anthracis—anthrax
Yersinia pestis—plague

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19
Q

Cell wall components

A
  1. M protein
  2. Opa protein
  3. Waxy lipid
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20
Q

M protein

A

resists phagocytosis
Streptococcus pyogenes

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21
Q

Opa protein

A

allows attachment to host cells
Neisseria gonorrhoeae

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22
Q

Waxy lipid

A

(mycolic acid) resists digestion
Mycobacterium tuberculosis

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23
Q

Coagulases

A

coagulate fibrinogen

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24
Q

Kinases digest

A

digest fibrin clots

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25
Q

Hyaluronidase

A

digests polysaccharides that hold cells together

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26
Q

Collagenase

A

breaks down collagen

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27
Q

IgA proteases:

A

destroy IgA antibodies

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28
Q

Antigenic variation

A

Pathogens alter their surface antigens (and antibodies are rendered ineffective)

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29
Q

How do invasins penetrate the host?

A

Surface proteins produced by bacteria that rearrange actin filaments of the cytoskeleton
Cause membrane ruffling

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30
Q

Use actin to move from one cell to the next

A

Shigella and Listeria

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31
Q

Survival inside phagocytes

A

Requirement for low pH in phagolysosome
Escape from phagosome before lysosomal fusion
Prevention of fusion of lysosome with phagosome

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32
Q

Fimbriae

A

Very specific to bacteria, strands that go out to help bacteria communicate and attach

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33
Q

Biofilms play a role in invading phagocytes

A

Biofilm bacteria more resistant to phagocytosis, shielded by extracellular polymeric substance (EPS) of biofilm

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34
Q
A
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34
Q

_____ is required for most pathogenic bacteria

A

Iron

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35
Q

Siderophores

A

proteins secreted by pathogens that bind iron more tightly than host cells

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36
Q

Direct damage disrupts

A

host cell function

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37
Q

Direct damage uses

A

host cell nutrients

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38
Q

Direct damage produces

A

waste products

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39
Q

Direct damage multiplies in

A

host cells and causes ruptures

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40
Q

Virulence factors

A

certain traits that help pathogens attach to and penetrate the host tissues and escape host defenses

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41
Q

Type of virulence factor that helps pathogen penetrate tissues

A

enzymes

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42
Q

Why do pathogens like to penetrate host tissues?

A

To have better access to nutrients and be able to reproduce

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43
Q

Examples of microbes that release hyaluronidase

A

Clostridium perfringens
Some streptococcus species

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43
Q

Collagen fibers are found in the base of

A

superficial tissues

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44
Q

Streptococcus and clostridium also secrete

A

Collagenase

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45
Q

What causes strep throat & necrotizing facitis

A

Streptococcus pyogenes

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46
Q

Secretes streptokinase that digests blood clots by breaking down fibrin proteins

A

Streptococcus pyogenes

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47
Q

fibrinolysin

A

aka streptokinase

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48
Q

staphylokinases

A

secreted by some staphylococcus do same as streptokinase

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49
Q

Streptococcus pyogenes & staphylococcus live on the

A

skin

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50
Q

Enteric pathogens

A

intestinal pathogens

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51
Q

Examples of enteric pathogens

A

Salmonella and Shigella

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52
Q

Etiologic agent of salmonellosis, typhoid and shigella

A

Salmonella

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53
Q

causes shigellosis

A

Shigella

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54
Q

Both can live within host cells as parasites

A

Salmonella and shigella

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55
Q

Flagella

A

on salmonella, helps it move in its environment

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56
Q

Toxins

A

poisonous substances produced by microorganisms

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57
Q

Toxins produce effects such as

A

fever, cardiovascular problems, diarrhea, and shock

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58
Q

Toxigenicity

A

ability of a microorganism to produce a toxin

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59
Q

Toxemia

A

presence of toxin in the host’s blood

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60
Q

Intoxications

A

presence of toxin without microbial growth

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61
Q

Exotoxins

A

Proteins produced and secreted by bacteria
Soluble in bodily fluids; destroy host cells and inhibit metabolic functions

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62
Q

Antitoxins

A

antibodies against specific exotoxins

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63
Q

Toxoids

A

inactivated exotoxins used in vaccines

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64
Q

Proteins produced inside pathogenic bacteria, most commonly gram-positive bacteria, as part of their growth and metabolism. The exotoxins are then secreted into the surrounding medium during log phase.

A

exotoxins

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65
Q

: toxic substances
released outside the cell

A

exotoxins

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66
Q

example of a gram-positive bacterium that produces exotoxins

A

Clostridium
botulinum

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67
Q

bacterial proteins that are secreted by a living organism into its surroundings

A

Exotoxins

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68
Q

What happens to exotoxins in a host?

A

exotoxins circulate and cause damage to host cells in various ways.

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69
Q

________ can cause severe damage or death at very low concentrations

A

Exotoxins

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70
Q

How can exotoxins be classified?

A
  1. Location (neurotoxins)
  2. Structure and function
    3.
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71
Q

tetanus and botulism are caused by species of Clostridium that secrete

A

neurotoxins

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72
Q

Enterotoxins like those secreted by cholera bacterium can target

A

lining of intestinal tract

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73
Q

Cytotoxin

A

kills or seriously damages host cells in general.

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74
Q

Corynebacterium diptheriae is a bacterium that secretes a cytotoxin that

A

inhibits protein synthesis in host cells

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75
Q

Most exotoxins are proteins with two domains _ & _

A

A & B

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76
Q

A” domain of exotoxin is

A

an enzyme that has a particular function.

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77
Q

“B” domain of an exotoxin is

A

the binding component

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78
Q

B domain binds to

A

specific receptor (usually a carbohydrate ) on the host cell

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79
Q

Once the B domain attaches to the host cell,

A

the host cell uses endocytosis to bring the exotoxin inside.

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80
Q

Once the B domain opens a pore in the endosome…

A

this allows the A domain to escape into the cytosol

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81
Q

What happens when the A domain escapes into the cytosol?

A

It can inhibit protein synthesis or interfere with the host cytoskeleton. This usually results in the death of the host cell

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82
Q

Membrane disrupting toxins exert their effect without

A

entering the cytosol

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83
Q

How do membrane disrupting toxins exert their effect without entering the cytosol?

A
  1. Form protein pores in the host plasma membrane.
  2. Disrupt phospholipid portion of the membrane
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84
Q

Membrane disrupting toxins result in

A

The cell lysing

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85
Q

Superantigens

A

bacterial exotoxins that stimulate an excessive immune response.

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86
Q

Superantigens first cause a proliferation of

A

T cells

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87
Q

After causing a proliferation of T cells, then it

A

causes those T cells to release excessive amounts of cytokines

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88
Q

The cytokines can stimulate

A

fever, inflammation & shock. This intense immune response can lead to death.

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89
Q

The toxin secreted by staphylococcus aureus in food poisoning and Toxic shock syndrome is an example of a

A

Super antigen

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90
Q

contain an enzyme component (A part) and a binding component (B part)

A

AB toxins

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91
Q

Example of A-B toxin

A

Diphtheria toxin

92
Q

Genotoxins

A

damage DNA (causing mutations, disrupting cell division, and leading to cancer)

93
Q

lyse host cells by disrupting plasma membranes

A

Membrane-disrupting toxins

94
Q

Leukocidins

A

kill phagocytic leukocytes

95
Q

Hemolysins

A

kill erythrocytes by forming protein channels

96
Q

Streptolysins

A

hemolysins produced by streptococci

97
Q

cause an intense immune response due to release of cytokines from host cells (T cells)

A

Superantigens

98
Q

Cause symptoms of fever, nausea, vomiting, diarrhea, shock, and death

A

superantigens

99
Q

Lipid A

A

portion of lipopolysaccharides (LPS) of gram-negative bacteria

100
Q

Lipid A released during

A

bacterial multiplication and when gram-negative bacteria die

101
Q

Lipid A stimulates macrophages

A

macrophages to release cytokines

102
Q

Lipid A causes

A

disseminated intravascular coagulation

103
Q

LPS are part of

A

outer membrane of the cell wall of gram-negative bacteria (lipid A).

104
Q

The endotoxins are liberated when

A

the bacteria die and the cell wall lyses, or breaks apart.

105
Q

example of a gram-negative bacterium that produces endotoxins

A

Salmonella
typhimurium

106
Q

Endotoxins are composed of

A

lipids that are part of the cell wall

107
Q

First step of the pyrogenic response

A

A macrophage ingests a
gram-negative bacterium.

108
Q

Step 2 of the pyrogenic response

A

Bacterium gets degraded in a vacuole.
Releases endotoxins that induce the macrophage to produce
cytokines, interleukin-1
(IL-1), and tumor necrosis
factor alpha (TNF-α).

109
Q

Releases endotoxins that induce the macrophage to produce

A

cytokines, interleukin-1
(IL-1), and tumor necrosis
factor alpha (TNF-α).

110
Q

Step 3 of pyrogenic response

A

cytokines are
released into the blood-
stream by the macrophages,

111
Q

Through the macrophages, the cytokines travel to

A

to the
hypothalamus, the temperature
control center of the brain.

112
Q

Step 4 of the pyrogenic response

A

The cytokines induce the
hypothalamus to produce
prostaglandins

113
Q

Effect of releasing the prostaglandins

A

reset
the body’s “thermostat” to a
higher temperature, producing
fever.

114
Q

Limulus amebocyte lysate (LAL) assay

A

is used to test for endotoxins

115
Q

Blood of horseshoe crabs contains

A

amebocytes

116
Q

Amebocytes lyse in the presence of

A

endotoxin, producing a clot

117
Q

“A” portion of the LPS in the outer membrane

A

Endotoxin

118
Q

Endotoxins are only released when

A

The cell dies or during cell division

119
Q

Interleukin 1 is a

A

protein messenger that ravels to the hypothalamus

120
Q

Cause fever, an early sign of an infection

A

prostaglandins

121
Q

Help stimulate phagocytosis, complement activation and antibody production by B lymphocytes

A

Endotoxins and interleukin 1

122
Q

What happens when endotoxin is released in large amounts or within the bloodstream

A

serious and deadly effects.

123
Q

Massive amounts of cytokines and interleukin 1 and tumor necrosis factor cause

A

1.loss of fluid from capillaries
2 vasodilation,
3.which lower BP. 4.Can lead to shock

124
Q

cytokines and interleukin 1 also cause

A

coagulation, making it more severe. Most often occurs in bacterial sepsis

125
Q

Bacterial sepsis is commonly caused by

A

E. Coli or meningococci in the blood stream or spinal fluid

126
Q

metabolic product of growing the cell

A

exotoxins

127
Q

Can be made by gram positive and gram negative bacteria

A

exotoxins

128
Q

Bacterial source is gram negative bacteria

A

endotoxins

129
Q

Present in LPS of outer membrane of cell wall and released with destruction of cell or during cell division

A

Endotoxins

130
Q

Metabolic product of growing cell

A

Exotoxins

131
Q

Proteins, usually with two parts A-B

A

exotoxins

132
Q

Lipid portion (lipid A ) of LPS of outer membrane

A

Endotoxins

133
Q

Specific for a particular cell structure or fucntion in the host (Mainly affects cell functions, nerves and GI tract)

A

Exotoxins

134
Q

General such as fever, weaknesses, aches and shock, all produce same effects

A

endotoxins

135
Q

Unstable, can usually be destroyed at 60-80 C except for staphylococcal enterotoxin

A

Exotoxins

136
Q

Stable, can withstand autoclaving (121 C for one hour)

A

Endotoxins

137
Q

High toxicity

A

Exotoxins

138
Q

Low toxicity

A

Endotoxins

139
Q

Fever producing: no

A

exotoxins

140
Q

Fever producing: Yes

A

Endotoxins

141
Q

Can be converted to toxoids to immunize against toxin; neutralized by antitoxin

A

Exotoxins

142
Q

Not easily neutralized by antitoxin; therefore effective toxoids cannot be made to immunize against toxin

A

endotoxins

143
Q

Small lethal dose

A

Exotoxins

144
Q

Considerably larger lethal dose

A

Endotoxins

145
Q

Gas gangrene, tetanus, botulism, diphtheria, scarlet fever, cyanobacterial intoxication

A

Representative Diseases

146
Q

Typhoid fever, UTIs, Meningococcal meningitis

A

Endotoxins

147
Q

Plasmids may carry genes for

A

1.toxins,
2.production of antibiotics,
3.enzymes

148
Q

Lysogenic conversion

A

changes characteristics of a microbe due to incorporation of a prophage

149
Q

Cytopathic effects (CPE)

A

visible effects of viral infection on a cell

150
Q

Stopping cell synthesis

A

Cytopathic effects CPE

151
Q

Causing cell lysosomes to release enzymes

A

Cytopathic effects CPE

152
Q

Creating inclusion bodies in the cell cytoplasm

A

Cytopathic effects CPE

153
Q

Inclusion bodies

A

non-living chemical compounds and by-products of cellular metabolism

154
Q

Fusing cells to create a syncytium

A

Cytopathic effects CPE

155
Q

Changing host cell function or inducing chromosomal changes

A

Cytopathic effects (CPE)

156
Q

Inducing antigenic changes on the cell surface

A

Cytopathic effects (CPE)

157
Q

Loss of contact inhibition in the cell, leading to cancer

A

Cytopathic effects (CPE)

158
Q

Contact inhibition

A

animal cell movement and division stop as a result of contact with other cells.

159
Q

Alpha and beta interferons produced by

A

virally-infected cells

160
Q

Alpha and beta interferons protect

A

neighboring cells from viral infection

161
Q

How do Alpha and beta interferons Protect neighboring cells from viral infection

A
  1. Inhibit synthesis of viral proteins and host cell proteins
  2. Kill virus-infected host cells by apoptosis
162
Q

Some _______ have metabolic products that are toxic to human hosts

A

fungi

163
Q

Can provoke an allergic response

A

fungi

164
Q

Trichothecene toxins inhibit

A

Protein synthesis

165
Q

fungal toxins that inhibit protein synthesis in eukaryotic cells.

A

Trichothecene

166
Q

Two fungi that can cause skin infections, Candida albicans and Trichophyton (trik-ō-Fī-ton), secrete ________.

A

proteases

167
Q

proteases

A

modify host cell membranes

168
Q

Cryptococcus neoformans is a fungus that causes a type of meningitis; it produces a ________ that helps it resist phagocytosis.

A

capsule

169
Q

prevent phagocytosis

A

capsule

170
Q

Ergot

A

alkaloid toxins that cause hallucinations

171
Q

Aflatoxin

A

carcinogenic toxin produced by Aspergillus

172
Q

Ergot comes from

A

fungi

173
Q

Aflatoxin comes from

A

Aspergillus which is fungi

174
Q

Mycotoxins

A

produced by mushrooms and are neurotoxic

175
Q

Phalloidin and amanitin are examples of

A

mycotoxins

176
Q

produced by Amanita phalloides , commonly known as the deathcap. These neurotoxins are so potent that ingestion of the Amanita mushroom may result in death.

A

Phalloidin and amanitin

177
Q

Presence of protozoa and their waste products causes

A

symptoms

178
Q

Protozoa avoid host defenses by

A
  1. Digesting cells and tissue fluids
  2. Growing in phagocytes
  3. Antigenic variation
179
Q

helminths use host tissue for

A

growth

180
Q

Helminths produce large masses which cause

A

cellular damage

181
Q

Helminths produce waste products that

A

cause symptoms

182
Q

saxitoxin made by

A

Made by algae,

183
Q

People who eat the mollusks develop paralytic shellfish poisoning, with symptoms similar to botulism. Caused by which neurotoxin?

A

saxitoxin

184
Q

Portals of exit

A

Route by which a pathogen leaves the body

185
Q

pathogens leave the Respiratory tract via

A

Coughing and sneezing

186
Q

pathogens leave the GI tract via

A

Feces and saliva

187
Q

pathogens leave the Genitourinary tract via

A

Urine; secretions from the penis and vagina

188
Q

Other portals of exit

A

Skin
Blood

189
Q

How do pathogens leave the blood?

A

Arthropods that bite; needles or syringes

190
Q

15-17 Which are the most often used portals of exit?

A

respiratory and gastrointestinal tracts.

191
Q

When the balance between host and microbe tips in favor of the microbe, an infection or _______ results

A

disease

192
Q

Learning these mechanisms of microbial pathogenicity is fundamental to understanding

A

how pathogens are able to overcome the host’s defenses

193
Q

portals of entry via mucous membranes include

A
  1. Respiratory tract
  2. Gastrointestinal tract
  3. Genitourinary tract
  4. Conjunctiva
194
Q

Parenteral route

A

entry for pathogens by deposition directly into tissues beneath the skin and mucous membranes.

195
Q

How does penetration or evasion of host defenses occur?

A

Capsules
Cell wall components
Enzymes
Antigenic variation
Invasins
Intracellular growth

196
Q

Invasins

A

surface proteins that rearrange nearby actin filaments of the cytoskeleton.

197
Q

Capsules increase virulence by

A

increases the virulence of pathogenic species. The capsule resists the host’s defenses by impairing phagocytosis

198
Q

Bacteria get iron from the host using _________.

A

siderophores

199
Q

_____ is required for the growth of most pathogenic bacteria. However, the concentration

A

Iron

200
Q

the concentration of free iron in the human body is fairly low because

A

most of the iron is tightly bound to iron-transport proteins, such as lactoferrin, transferrin, and ferritin, as well as hemoglobin.

201
Q

siderophores

A

bacterial iron-binding proteins

202
Q

they take the iron away from iron-transport proteins by binding the iron even more tightly.

A

siderophores

203
Q

Once the iron-siderophore complex is formed, it is taken up by

A

siderophore receptors on the bacterial surface

204
Q

taken up by siderophore receptors on the bacterial surface. Then the iron is brought into the

A

bacterium

205
Q

In some cases, the iron is released from the complex to enter

A

The bacterium

206
Q

in other cases, the iron enters as part of

A

the complex

207
Q

Direct damage toxins

A

endotoxins and exotoxins

208
Q

After entering the host, most pathogens adhere to

A

host tissue,
penetrate or evade host defenses, and damage host tissues

209
Q

Pathogens usually leave the body via specific portals of exit, which are

A

generally the same sites where they entered initially

210
Q

M protein is found in

A

Streptococcus pyogenes

211
Q

Opa protein is found in

A

Neisseria gonorrhoeae

212
Q

Waxy lipid is found in

A

Mycobacterium tuberculosis

213
Q

Exotoxins are ________ produced and secreted by _______

A

Proteins produced and secreted by bacteria

214
Q

Exotoxins are soluble in

A

bodily fluids;

215
Q

Exotoxins destroy

A

host cells

216
Q

Exotoxins inhibit

A

metabolic functions

217
Q

poisonous substances produced by microorganisms

A

Toxins

218
Q

inactivated exotoxins used in vaccines

A

Toxoids

219
Q

Once the host cell brings the exotoxin inside via phagocytosis?

A

B domain opens a pore in the endosome.

220
Q

The ________ are then secreted into the surrounding medium during log phase.

A

exotoxins

221
Q

Exotoxins are produced in

A

pathogenic bacteria, most commonly gram-positive bacteria

222
Q

What happens after the bacterium gets degraded in a vacuole?

A

Releases endotoxins that induce the macrophage to produce
cytokines, interleukin-1
(IL-1), and tumor necrosis
factor alpha (TNF-α).

223
Q

disseminated intravascular coagulation caused by

A

LIPID A

224
Q

produced by mushrooms and are neurotoxic

A

Mycotoxins

225
Q

alkaloid toxins that cause hallucinations

A

Ergot

226
Q

carcinogenic toxin produced by Aspergillus

A

Aflatoxin

227
Q

produced by mushrooms and are neurotoxic

A

Mycotoxins

228
Q

Saxitoxin is what kind of toxin?

A

neurotoxin

229
Q
  • Paralytic shellfish poisoning is caused by
A

Saxitoxin