Mechanisms of Pathogenesis Flashcards

Chapter 14 and Chapter 15

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1
Q

Define Pathology

A

scientific study of disease

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2
Q

Define Etiology

A

Cause of a disease

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3
Q

Define Pathogenesis

A

How a disease develops (structural/functional)

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4
Q

Define Infection

A

Invasion/Colonization of the body by a pathogenic microbe

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5
Q

Define Disease

A

Infection changes the normal status of health

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6
Q

Define Host

A

Organism that harbors another organism

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7
Q

Define Normal Flora

A

Permanent, (typically) nonpathogenic microbes

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8
Q

What is resident flora?

A

Microbes that are always present on/in the human body

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9
Q

What is transient flora?

A

Microbes that come and go

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10
Q

Do babies in the womb encounter microbes?

A

No

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11
Q

When do babies begin encountering microbes?

A

At birth

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12
Q

What common microbes do babies encounter? (2)

A
  • lactobacilli (mother’s vagina)
  • feeding and breathing (URT and GIT)
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13
Q

(T/F) There are more cells than bacteria in the body

A

False, bacteria > cells

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14
Q

Define symbiosis

A

Association between 2+ species

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15
Q

Example of Symbiosis

A

Host and Normal Flora

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16
Q

Define Commensalism

A

One organisms benefits, other organism not affected

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17
Q

Example of Commensalism

A

Staphylococcus epidermis (on our skin)

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18
Q

Define Mutualism

A

Both organisms benefit

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19
Q

Example of Mutualism

A

E. coli in the intestines (produce vitamins for the body)

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20
Q

Define Antagonism

A

Competition between the microorganisms

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21
Q

Define Competitive Exclusion

A

Normal Flora vs Pathogen over resources (food)

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22
Q

Example of Antagonism

A

Bacteriocins in the large intestine (inhibit other bacteria)

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23
Q

Define Parasitism

A

One organism benefits, other is harmed

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24
Q

Example of Parasitism

A

Any successful pathogenic microorganism

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25
Q

Describe Probiotics

A

Live microbial cultures are applied/ingested to benefit the host

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26
Q

Define Opportunistic

A

Become pathogenic under certain circumstances

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27
Q

What are ways opportunistic pathogens are given opportunity? (3)

A
  • normal flora disrupted/destroyed
  • defense mechanisms compromised
  • normal protective barriers disrupted
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28
Q

Examples of Opportunistic Pathogens (3)

A
  • S. aureus (TSS)
  • Pneumocystis jirovecii (pneumonia in AIDS patients)
  • E. coli (UTI if moved to urethra)
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29
Q

Define Symptoms

A

Changes in body functions (pain and malaise)

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30
Q

Define Signs

A

VISIBLE changes (rash, fever, swelling)

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31
Q

Define Syndrome

A

Specific symptoms and signs associated with a disease

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32
Q

Define Infectious

A

Caused by bacteria, viruses, fungi, protozoa, and helminthes

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33
Q

Define Communicable Infectious Diseases

A

Contagious (directly or indirectly)

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34
Q

Define Non-Communicable Infectious Diseases

A

Caused by individual’s normal flora, ingestion or preformed toxins, organisms in the environment (not contagious)

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35
Q

Define Non-Infectious

A

Caused by any other factor than infectious organisms

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36
Q

Define Incidence

A

Number of new cases contracted within a set population during a set time period

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37
Q

Define Prevalence

A

TOTAL number of people infected within a population at ANY time

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38
Q

Define Sporadic

A

Occurs occasionally in a population

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39
Q

Define Endemic

A

Disease that is always found in the region

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40
Q

Define Epidemic

A

Disease that many people acquire in a very SHORT period of time

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41
Q

Define Pandemic

A

An epidemic that is worldwide

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42
Q

Define Acute Disease

A

Symptoms develop rapidly, lasts a SHORT time

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43
Q

Define Chronic Disease

A

Symptoms develop slowly

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44
Q

Define Subacute Disease

A

Intermediate (between acute-chronic)

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45
Q

Define Latent Disease

A

Inactive until activation, then produces symptoms

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46
Q

Define Herd Immunity

A

Immunity in MOST of a population

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47
Q

(T/F) Pathogens can live without a host

A

False

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48
Q

Define Reservoir

A

Continual source of the disease causing organisms (living or inanimate objects)

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49
Q

Describe Human Reservoirs (3)

A
  • transmit microorganisms directly/indirectly
  • carries (asymptomatic people)
  • convalescing patients (gradual recovery)
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50
Q

Describe Animal Reservoirs (3)

A
  • wild and/or domestic
  • zoonoses (primarily in animals, possible in humans)
  • transmitted: bites, contaminated hides/feathers, food, insect vectors
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51
Q

What are examples of nonliving reservoirs of infection? (2)

A
  • soil (fungal diseases)
  • water (feces)
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52
Q

What are the modes of disease transmission (3)

A
  • contact
  • vehicle
  • vector
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53
Q

Where do pathogens leave the host from?

A

The same way it came in (portal of entry)

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54
Q

What is direct transmission?

A

person-to-person

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55
Q

What is congenital transmission?

A

mother to fetus/newborn

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56
Q

What is indirect transmission?

A

fomites (nonliving objects)

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57
Q

What is droplet transmission?

A

coughing, sneezing, talking

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58
Q

What is vehicle transmission?

A

Through a medium

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59
Q

How is water a vehicle of transmission?

A

fecal contamination

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60
Q

How is food a vehicle of transmission?

A

incompletely cooked food or improperly refrigerated foods; food poisoning

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61
Q

How is air a vehicle of transmission?

A

mucus droplets by droplet nuclei

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62
Q

What are the four vehicles of transmission?

A
  • water
  • food
  • air
  • body fluids and blood
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63
Q

What is vector transmission?

A

Through an arthropod (insect)

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64
Q

What are two examples of vector transmission?

A
  • biological
  • mechanical
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65
Q

What is an example of biochemical transmission?

A
  • bitten by infected insect (lyme disease, malaria)
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66
Q

What is an example of mechanical transmission?

A
  • transfer of microbe from feet or other body parts of insects to food/skin of person
  • passive; no replication of microbe within vector (shigellosis, typhoid fever)
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67
Q

What are nosocomial infections?

A

Acquired in a hospital/medical facility

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68
Q

What are the three factors of nosocomial infections?

A
  • microbe in hospital
  • compromised patient
  • chain of transmission
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69
Q

What are common bacterial nosocomial infections? (5)

A
  • S. aureus (urinary and respiratory)
  • Pseudomonas aeruginosa (burns & surgical wounds)
  • E. coli (urinary tract, neonatal meningitis)
  • Enterococcus (urinary tract & wound)
  • Clostridium difficile (diarrhea)
70
Q

What plasmids are antibiotic resistant?

A

R Plasmids

71
Q

What causes endogenous infections?

A

Opportunistic microbes in an individual’s normal flora

72
Q

What causes exogenous infections?

A

Microbe that enter an individual through the environment

73
Q

What increases an individual’s risk to infection? (4)

A
  • broken skin/mucous membranes
  • surgery
  • burns
  • catheters
74
Q

What suppresses an immune system? (4)

A
  • drugs
  • diabetes
  • stress
  • HIV
75
Q

What are 4 ways a disease can be transmitted to a patient in a hospital?

A
  • hospital staff
  • other patients
  • fomites
  • ventilation system
76
Q

How can we control the spread of nosocomial infections? (3)

A
  • educate personnel
  • practice good aseptic techniques
  • monitor for drug resistance
77
Q

What are emerging infectious diseases?

A

New or changing diseases

78
Q

What causes emerging infectious diseases? (7)

A
  • new strain (more virulent)
  • overuse of antibiotics (resistance)
  • global warming (increases survival rates of reservoirs/vectors)
  • modern transportation
  • natural transportation
  • animal control measures
  • failure to comply with public health measures
79
Q

4 Contributing Factors to Emerging Infectious Diseases:

A
  • genetic recombination
  • evolution of new strains
  • overuse of antibiotics
  • changes in weather patterns
80
Q

What is pathogenicity?

A

Ability of organism to cause disease

81
Q

What is virulence?

A

Degree of pathogenicity

82
Q

Steps for microbes to cause infection/disease are (4)

A
  • ENTER organism
  • ADHERE to tissues
  • PENETRATE tissues
  • DAMAGE cells
83
Q

What are 3 portals of entry?

A
  • mucous membranes
  • skin
  • parenteral route
84
Q

What are examples of mucous membranes? (4)

A
  • respiratory
  • gastrointestinal
  • genitourinary tract
  • conjuncitva (eyes)
85
Q

Describe skin

A

Largest organ & outermost protective layer

86
Q

Examples of the parenteral route (4)

A
  • bites
  • punctures
  • burns
  • injections
87
Q

How many microbes are needed to cause disease?

A

Number varies from person to person

88
Q

What is ID50

A

Infectious dose for 50% of population, indication of virulence

89
Q

What is LD50

A

Lethal dose of a toxin in 50% of population

90
Q

Define Adhesins

A

Surface molecules on pathogen that bind to receptors on host cells/tissues

91
Q

Where are adhesins found? (4)

A
  • capsules
  • fimbriae
  • capsid
  • virus envelope
92
Q

What are biofilms?

A

Masses of microbes

93
Q

Pathogen exits the GI tract by (2)

A
  • diarrhea
  • vomiting
94
Q

Pathogen exits the Urogenital tract by (2)

A
  • sexual contact
  • urine
95
Q

Pathogen exits blood by (2)

A
  • insects
  • needles
96
Q

Pathogen exits the Respiratory tract by (3)

A
  • coughing
  • sneezing
  • speaking
97
Q

How do most bacteria cause disease?

A

Penetrating tissues

98
Q

What are virulence factors?

A

Characteristic that help microbes cause infection/disease

99
Q

Structural example of a virulence factor:

A

Pili (adhesion)

100
Q

Physiological examples of a virulence factor (2):

A
  • enzymes
  • toxins
101
Q

Describe adhesins

A

Proteins/glycoproteins that adhere to host

102
Q

Describe Colonization of microbes

A

Microbe growth on epithelial cell surfaces (skin, mucous membranes)

103
Q

Describe Invasiveness

A

Degree that microbe can invade and grow in host tissues

104
Q

Describe Toxins

A

Poisonous substance to other organisms

105
Q

What do capsules do

A

Resist Host Defenses
- phagocytosis
- complement

106
Q

What are Streptococcus pyogenes cell wall made of?

A

Protein M

107
Q

What are Mycobacteria cell wall made of?

A

Waxes (mycolic acid)

108
Q

What are Neisseria gonorrheae cell wall made of?

A

Fimbriae (Opa proteins)

109
Q

How do extracellular enzymes help microbes?

A

Breakdown and dissolve material found near cells

110
Q

What does Hyaluronidase do?

A

Digests hyaluronic acid (bacterial cell membranes)

111
Q

What does Coagulase do?

A

Increases clotting

112
Q

What do IgA Proteases do?

A

Destroy antibodies

113
Q

What does Streptokinase do?

A

Dissolves clots (digests fibrin)

114
Q

What does Collagenase do?

A

Breaks down collagen

115
Q

What do Hemolysins do?

A

Destroys RBCs

116
Q

Alpha Hemolysis

A

Partially digests hemoglobin (green)

117
Q

Beta Hemolysis

A

Completely digests hemoglobin (clear)

118
Q

Gamma Hemolysis

A

No digestion

119
Q

What do Leukocidins do?

A

Destroy neutrophils

120
Q

(T/F) If phagocytosis occurs after entry, no damage occurs

A

True

121
Q

What causes damage to the host cells (4)

A
  • using host nutrients (siderophores)
  • direct damage by injury (cell rupture)
  • toxins
  • causing hypersensitivity reactions
122
Q

What uses a host cell’s nutrients?

A

Siderophores

123
Q

What are toxins?

A

Poisonous substances made by some microbes

124
Q

What do toxins cause (5)

A
  • fever
  • cardiovascular disturbances
  • neurological disturbances
  • diarrhea
  • shock
125
Q

What is Toxemia?

A

Toxins in the blood

126
Q

What is Intoxication?

A

Disease caused by ingestion of toxin

127
Q

What are Exotoxins?

A

Produced INSIDE bacteria, released into SURROUNDING medium

128
Q

What are Endotoxins?

A

Lipid A portion of LPS released from cell wall of GRAM NEGATIVE bacteria

129
Q

Where are endotoxins located

A

Outer portion of the LPS (lipopolysaccharide) of gram - bacteria (Lipid A)

130
Q

When are endotoxins released

A

When the gram - cell dies (cell wall breaks)

131
Q

Symptoms of endotoxins (6):

A
  • chills
  • fever
  • weakness
  • aches
  • shock
  • death
132
Q

Explain how Disseminated Intravascular Coagulation (DIC) occurs:

A

Endotoxins activate clotting cascade causing blockage of blood supply = tissue death

133
Q

Outcomes possible because of endotoxins:

A
  • fever/pyrogenic response
  • septic shock
134
Q

How do endotoxins cause pyrogenic/fever response? (5)

A
  • Macrophage eats Gram - cell (phagocytosis)
  • cell degrades = endotoxin released
  • endotoxin stimulates macrophage to secrete IL-1
  • IL-1 causes hypothalamus to produce prostaglandins
  • PGs causes body temperature to rise
135
Q

What does IL-1 stand for?

A

Interleukin 1 (Endogenous pyrogen)

136
Q

What else could the macrophage secrete during endotoxic shock? (2)

A
  • Tumor Necrosis Factor (TNS)
  • Cachetin
137
Q

What causes the release of Mediators?

A

Tumor Necrosis Factor & IL-1

138
Q

What do Mediators cause? (3)

A
  • increased permeability of capillaries (loss of fluids)
  • rapid decrease in B.P.
  • Impaired blood flow to kidneys
139
Q

What does Endotoxic Septic Shock cause? (8)

A
  • chills
  • fever
  • vomiting
  • diarrhea
  • rapid decrease in blood pressure
  • convulsions
  • shock
  • death
140
Q

Which bacteria are major producers of Endotoxic Septic Shock? (6)

A
  • P. aeruginosa
  • E. coli
  • Klebsiella
  • Proteus
  • Enterobacteria
  • Salmonella typhi
141
Q

What are Exotoxins?

A

Proteins/Enzymes produced by Gram + bacteria (& some Gram -) that destroy/inhibit parts/functions of cells

142
Q

How can we destroy Exotoxins?

A

Heat or chemicals

143
Q

Where are Endotoxin genes carried in? (2)

A
  • plasmids
  • bacteriophages
144
Q

What are antitoxins?

A

Things the body produces that gives immunity against exotoxins

145
Q

What are toxoids used for? (2)

A
  • vaccines
  • stimulate antitoxins
146
Q

How are Exotoxins named?

A

According to the cell they attack or the disease they are associated with

147
Q

What pathogen secretes Diphtheria Toxin?

A

Corynebacterium diptheriae

148
Q

What do Diphtheria toxins do?

A

Inhibits protein synthesis (A-B toxin)

149
Q

What pathogen secretes Erythrogenic Toxin?

A

Streptococcus pyogenes

150
Q

What do Erythrogenic Toxins do?

A

Damages blood capillaries under the skin

151
Q

What pathogen secretes Botulinum Toxin?

A

Clostridium botulinum

152
Q

What do Botulinum Toxins do?

A
  • prevents nerve impulses
  • inhibits release of acetylcholine
  • flaccid paralysis
153
Q

Describe Clostridium botulinum (4)

A
  • gram +
  • spore forming
  • anaerobic rod
  • found in soil, canned foods, water, intestinal tracts of animals
154
Q

How long does it take for symptoms of Clostridium botulism to appear?

A

12-46 hours

155
Q

What are the symptoms of Clostridium botulism? (5)

A
  • poor vision
  • difficulty swallowing
  • weakness
  • faulty speech
  • death
156
Q

How would you treat a patient with the Adult Form of Botulism?

A

Trivalent antitoxin to A,B, & E

157
Q

How can we prevent Infant Botulism?

A

Do not give infants honey

158
Q

What do Tetanus Toxins do?

A

Inhibit nerve cell impulses form muscle relaxation

159
Q

What pathogen secretes Tetanus Toxins?

A

Clostridium tetani

160
Q

What do Vibrio Entertoxins (Cholera Toxin) do?

A

Release large amounts of fluid & electrolytes (“rice water stools”)

161
Q

What do Staphylococcal Enterotoxins do?

A

(Superantigen) Affects intestinal tract in releasing fluid & electrolytes

162
Q

What do Staphylococcal TSS Toxin do?

A

(Superantigen) Toxic Shock Syndrome Toxin

163
Q

What gram bacteria do endotoxins occur in?

A

Gram -

164
Q

What are exotoxins made of?

A

Protein

165
Q

What are endotoxins made of?

A

Lipid

166
Q

What gram bacteria do exotoxins occur in?

A

Gram + and Gram -

167
Q

Which toxins can be made into toxoids?

A

Exotoxins

168
Q

Which toxin is found in LPS of gram - cells?

A

Endotoxins

169
Q

Can Endotoxins be destroyed by heat?

A

No

170
Q

Can endotoxins be made into toxoids?

A

No

171
Q

How are viruses able to avoid host defenses? (2)

A
  • grow inside cells where the immune system cannot reach
  • they attack immune cells (HIV)
172
Q

What are the Cytopathic Effects (CPE) of viruses?

A
  • kills cell
  • inhibits protein, DNA, RNA synthesis
  • toxic to cells
  • syncytia formation
  • antigenic changes cause destruction by immune system
  • chromosomal damage can activate oncogenes