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Microbiology > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

invasion of colonization of the body by a pathogen

A

Infection

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2
Q

any change from a state of health
*can have infection without _________. Ex: HIV+ but not have aids

A

Disease

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3
Q

develops rapidly but lasts a short time
>Common cold

A

Acute Disease

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4
Q

develops slowly and is continual
>Heart disease

A

Chronic Disease

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5
Q

pathogen that remains inactive (not replicating) for extended period of time

A

Latent Disease

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6
Q

any disease that spreads from host to host
>Flu

A

Communicable Disease

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7
Q

a type of communicable disease that spreads from host to host

A

Contagious Disease

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8
Q

disease does not spread from host to host
>Heart disease, diabetes

A

Non-communicable disease

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9
Q

study of the cause of an infectious disease (microbe)

A

Etiology

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10
Q

objective manifestation of disease
>observed or measured by others
>fever, vomiting, rash, swelling….

A

Signs

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11
Q

subjective manifestation of disease
>felt by the patient
>pain, fatigue, nausea, dizzy, headache….

A

Symptoms

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12
Q

ability to cause disease

A

Pathogenicity

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13
Q

disease causing microbe

A

Pathogen

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14
Q

degree of pathogenicity (how bad?)

A

Virulence

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15
Q

the study of where and when infectious disease occur

A

Epidemiology

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16
Q

the number of new cases of a disease in a given population or area
>New cases of chlamydia in AZ in October 2022

A

Incidence

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17
Q

total number of cases of a disease in a given population or area
>HIV+ people in the US

A

Prevalence

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18
Q

occurs at a relatively stable frequency in any given population or area
>Sexually transmitted pathogens

A

Endemic Disease (never ENDemic diseases)

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19
Q

disease that occurs at a greater frequency in a given population or area

A

Epidemic Disease

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20
Q

epidemic that occurs simultaneously on more than one continent

A

Pandemic Disease

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21
Q

only a few cases occur (quite rare)

A

Sporadic Disease

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22
Q

What are some virulence factors?

A

Extracellular enzymes
Toxins
Anti-phagocytic factors

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23
Q

produced by bacteria. Secrete them into their environment

A

Extracellular Enzymes

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24
Q

Examples of extracellular enzymes

A

Hyaluronidase
Hemolysins
Coagulase
Kinase
Leukocidins
Collagenases

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25
Q

invades deeper into tissue
>breaks down extracellular matrix
ex: lawyer scraped knee playing basketball, Staphyloccocus aureus got deep into the bone within 12 hours

A

Hyaluronidase

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26
Q

let bacteria lyse RBC to get iron as a trace element

A

Hemolysins

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27
Q

forms a blood clot, hide from immune system

A

Coagulase

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28
Q

digest clots to remove itself (Streptokinase injected to break clot)

A

Kinase

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29
Q

decrease phagocytosis because they kill WBC

A

Leukocidins

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30
Q

break down collagen

A

Collagenase

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31
Q

Do antibiotics stop extracellular enzymes?

A

No, they have no effect on extracellular enzymes

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32
Q

Koch’s Postulates

A
  1. Suspected pathogen must be found in every case of the disease
  2. Isolate pathogen and grow it in pure culture in the lab
  3. Inject the pure culture into a healthy host and must get the exact same disease
  4. Re-isolate the pathogen from the experimental host + verify that it’s identical to what was put in
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33
Q

used to determine etiological agent(BACTERIA) of an infectious disease

A

Koch’s Postulates

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34
Q

Chemicals that harm tissues tissues or trigger host immune response that can cause damage in the host.
>Toxoid vaccines that are disabled toxins

A

Toxins

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35
Q

Type of toxin produced by some gram + and gram - bacteria
>Exported outside of bacterium that produce them.
>Transported throughout the body via circulatory system
>Gene for exotoxin production would be on a plasmid
>Exotoxins are made of protein, heat sensitive

A

Exotoxin

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36
Q

Types of Exotoxins:

A

Cytotoxin
Neurotoxin
Enterotoxin

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37
Q

Kill cell or affect function of the cell
>Diphtherias cytotoxin stops protein synthesis

A

Cytotoxin

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38
Q

Interfere with nerve function (synapse)
>Botulism toxin, tetanus toxins

A

Neurotoxin

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39
Q

Kill cells that line gastrointestinal tract,
>Chloera toxin

A

Enterotoxin

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40
Q

Type of toxin that gram negative bacteria lyse and release lipid A in outer membrane.
>Lipid A causes fever, inflammation, clots, hemorrhage, diarrhea, shock, death
>Typhoid fever, meningococcal meningitis

A

Endotoxin

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41
Q

decreases phagocytosis (WBC engulfing material)
>Capsules decrease phagocytosis. WBC can’t eat bacteria with capsule

A

Anti-phagocytic factors

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42
Q

2 Organisms living together

A

Symbiosis

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43
Q

3 Types of Symbiosis

A

Mutualism
Commensalism
Parasitism

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44
Q

Type of symbiosis that involves both organisms benefit from the symbiotic relationship
ex: GI bacteria + us ; normal flora
Vaginal flora +

A

Mutualism

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45
Q

Type of symbiosis which involves one organism is not affected (neutral)
>Staphylococcus aureus + us

A

Commensalism

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46
Q

Type of symbiosis that involves one organism benefits (microbe) other organism is harmed (host)

A

Parasitism

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47
Q

4 Types of Portals of Entry

A

Broken skin
Mucous membrane
Placenta
Parental Route

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48
Q

Portal of entry that deposits the pathogen directly into tissue
>Needle stick, bit

A

Parenteral route

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49
Q

Usually a pathogen exits the same way they entered via secretions
Ex: GI tract exit via feces, Urinary tract exit via urine, reproductive tract exit via semen/vaginal secretions, respiratory exit via droplets

A

Portals of Exit

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50
Q

Ways microbes hang on

A

-Giardia lamblia: suction cup
-Taeneia: suckers + hooks
-Having a glycocalyx
-Fimbrae
-Virus binds to its receptor on host cell

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51
Q

Reservoirs of Infectious Disease

A
  1. Animal reservoirs (zoonotic dis.)
  2. Human carriers
  3. Non-living Reservoirs (water, soil, food)
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52
Q

forms when bacteria adhere to a surface in an aqueous environment
>Bacteria begin to secrete a slimy, glue-like substance
>65% of human infections are biofilms

A

Biofilm

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53
Q

send chemical signals to each other to actually coordinate biofilm formation

A

Quorum sensing

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54
Q

________ in biofilm can increase antibiotic resistance

A

Conjugation

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55
Q

Part of bacterium that aid in biofilm formation, glycocalyx
Difficult for immune system to fight

A

Fimbrae

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56
Q

5 Stages of Infectious Disease

A
  1. Incubation
  2. Prodronal
  3. Illness
  4. Decline
  5. Convalesence
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57
Q

3 Modes of Transmission

A

Contact transmission
Vehicle transmission
Vector transmission

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58
Q

Contact Transmissions sub modes

A

Direct
Indirect
Droplet

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59
Q

Vehicle Transmission sub modes

A

Airborne
Waterborne
Food borne
Body fluid

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60
Q

Vector transmission sub modes

A

Biological
Mechanical

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61
Q

Pathogen in acquired in a healthcare setting
40,000 die ppl/year
205 die pp/day

A

Healthcare Acquired Infections

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62
Q

Common sites of infection

A
  1. Catheter
  2. Central line infection
  3. Ventilator/trach
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63
Q

Blood borne pathogens in occupations

A

Hep. B, C, HIV

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64
Q

Hepatitis: Transmission rate 6-30% from a single needle stick of an infected patient
>Vaccine
>Hep B immunoglobulin (antibodies) 90% effective in preventing transmission

A

Hep B Virus

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65
Q

Hepatitis: Transmission rate of 1.8% from a single needle-stick from an infected patient
>No vaccine
>No immunoglobulin to prevent transmission
>test, anti-viral drug

A

Hep C Virus

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66
Q

VIRUS: transmission rate 0.3% from a single needle stick of an infected patient
>No vaccines
>No immunoglobulin to prevent transmission
>anti-HIV meds right away

A

HIV

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67
Q

Cell wall of fungi

A

made of chitin and they have sterols in their cell membrane.

68
Q

Part of the outer membrane of Gram negative bacteria. It is released when the bacteria die. May cause fever, diarrhea, hemorrhage, shock, death

69
Q

decreases phagocytosis (WBC engulfing material)
>Capsules decrease phagocytosis. WBC can’t eat bacteria with capsule

A

Anti-phagocytic factors

70
Q

3 types of symbiosis:

A

Mutalism: both org. benefit
Commensalism: one org. is neutral
Parasitism: one org. benefits

71
Q

4 Portals of Entry:

A
  1. Broken skin
  2. Mucous membranes
  3. Placenta
  4. Parenteral route (direct)
72
Q

Bacteria send signals to each other to coordinate biofilm formation

A

Quorum sensing

73
Q

can increase antibioitic resistance

A

Conjugation in biofilm

74
Q

What aids in biofilm formation

75
Q

Stages of infectious disease

A
  1. Incubation period (infection to b 4symp. begins)
  2. Prodronal period (short generalized symptoms)
  3. Illness (severe)
  4. Decline (gradually get bettter)
  5. Convalescence (recovery)
76
Q

anti-viral protein that blocks synthesis step of viral replication

A

Interferons

77
Q

prevent the spread of pathogen. Neutralizes bacterial toxins + aid in repair of damaged tissue

A

Inflammation

78
Q

Damaged cells in the area produce 3 chemicals:

A

Prostaglandins
Leukotrienes
Histamine

79
Q

Increase vessel permeability which in turn increases fluid in area and increases clotting factors

A

Prostaglandins + Leukotrienes

80
Q

Increases diameter of blood vessels in area

81
Q

Controls body temperature

A

Hypothalamus

82
Q

Bodies ability to resist infectious diseases through non-specific mechanisms

A

Non-specific immunity

83
Q

First line of defenses:

A

Skin + mucous membranes

84
Q

Second line of defense

A

Phagocytosis
Extracellular killing
Complement
Interferons
Inflammations
Fever

85
Q

Steps in phagocytosis

A

C hemotaxis: travel to where needed
A dherence: phagocyte attaches to pathogen/product
I ngestion: pseudopodia to ingest
K illing: sent to lysosome in phagocyte
E limination: exits via exocytosis

86
Q

secretes toxins (chemicals) to kill helminthes, virus infected cells or tumor cells.
>Eosinophils attach to the surface of a helminth->secrete extracellular toxins-
>inhibits and kills worm

A

Extracellular killing

87
Q

secrete extracellular toxins that kills virus infected cells and tumor cells
are found in:
Tonsils, Lymph, Spleen, Blood, Lymph nodes

A

Natural killer cells

88
Q

30 proteins in blood (inactive) that work together to destroy bacteria + some viruses

A

Complement

89
Q

2 Ways to activate compliment

A

1.Classical: antibody bound to antigen
2.Alternative: pathogen/product

90
Q

What happens when complement is activated?

A

Cell lysis or chemotaxis (phagocytes)

91
Q

Causes hypothalamus to increase body temp
>=toxins, pathogens, products

92
Q

All about B and T cells (lymphocytes)

A

Specific immunity

93
Q

Anti-viral proteins produced by some animal cells after viral infection that inhibit Viral replication and neighboring cells
-They help neighboring cells
>Interferons proteins help maintain neighboring cells
>Block synthesis step of viral replication

A

Interferons

94
Q

increases vessel permeability which in turn increases fluid in area and increases clotting factors

A

Prostaglandins and Leukotrines

95
Q

What is the 3rd line of defense?

A

Specific Immunity aka: Acquired Immunity

96
Q

Type of IMMUNITY that is all about Lymphocytes (B+T cells)
Humoral and Cell-mediated

A

Specific Immunity

97
Q

Includes B cells and antibodies present in body fluids (humors)

A

Humoral Immunity

98
Q

ex: blood, lymph, mucous, breast milk

A

Humoral Immunity

99
Q

What produces antibodies?

100
Q

Antibodies circulate in fluid to do what?

A

Bind to pathogens + pathogen products. Tags them for destruction for phagocytes + complement

101
Q

Uses T-cells to defend. Targets infected cells, cancerous, abnormal cells, abnormal grafts.

A

Cell-mediated Immunity

102
Q

T + B cells hang in (blank) to screen (blank) for pathogen/pathogen products

A

Lymph nodes, lymph

103
Q

Molecules that trigger a specific immune response

104
Q

Small part of antigen that stimulates a specific immune response

105
Q

2 Types of Antigens

A

Exogenous: outside cells (Humoral)
Endogenous: inside cells (Cell-mediated)

106
Q

Where do B cells mature? In what state do they come out?

A

Bone marrow, inactive

107
Q

Where do most B cells circulate?

A

Lymph nodes, organs, tissues
Small % in blood

108
Q

What is the function of B cells?

A

To produce antibodies

109
Q

Each B cells has (blank) and can respond to (#) of specific antigen (epitopes)

A

Antigen binding sites, 1

110
Q

Is it the antigen or the B cell that binds to the other?

A

Antigen (strangely)

111
Q

B cells with identical BCR

A

B cell clones

112
Q

How do B cells divide?

A

Antigen binds to BCR + stimulates the B cell to divide by mitosis to produce clones

113
Q

Result of SELECTION, ACTIVATION, and DIVISION of B cell

A

Swollen lymph nodes

114
Q

Swollen lymph nodes are a sign of

A

Selection
Activation
Division
of B cells

115
Q

Gist of Clonal Selection + Activation of B cells

A
  1. Antigen selects B cell by binding BCR
  2. Activated B cells divide
  3. Some made into plasma cells that secrete antibodies
  4. Some cones become memory B cells incase same antigen is encoutnered
116
Q

Proteins that bind to a specific antigen and tag the antigen for destruction by the immune system

A

Antibodies (immunoglobulins)

117
Q

What happens when antibodies bind to antigen

A
  1. Compliment activated
  2. Inflammation
  3. Bact. tocins neutralized
  4. Block receptors on host cells prevent viral replcation
  5. Bacteria can’t divide
  6. Phagocytosis increases
  7. Binds pathogens together (agglutination)
117
Q

What happens when antibodies bind to antigen

A
  1. Compliment activated
  2. Inflammation
  3. Bact. tocins neutralized
  4. Block receptors on host cells prevent viral replcation
  5. Bacteria can’t divide
  6. Phagocytosis increases
  7. Binds pathogens together (agglutination)
118
Q
  • Functions about 4-5 days
  • Secrete antibodies
  • Secrete 2,000 anitbodies per second
A

B cell PLASMA cells

119
Q
  • Don’t secrete antibodies
  • Long-lived
  • Stays behind incase same antigen is encountered again
A

Memory cells

120
Q

Classes of Antibodies:

A

IgM: 1st on scene
IgA: blocks attachment to mucousal surface, saliva, sweat, tears
IgG: most abundant, permeable, activates complement
IgD: not permeable, found on surfaces of B cells
IgE: cause ellergic reaction

121
Q
  • 1st produced in responce to antigen
  • 5-10% of antibodies
  • short lived. few days
  • pentamer increases phagocytosis
  • presence of this indicates infection
122
Q
  • principle anitbody of primary+2ndary responses
  • 80% of antibodies
  • decreases then produces more in later encounters
  • Permeable, cross placenta to protect fetus
  • can leave humor and enter tissue
  • boosters increase this antibody
123
Q
  • pathogens enter mucous membranes
  • blocks attachment to mucousal surfafes
  • found in mucous, saliva, colostrum, milk
  • good against intestinal pathogens
124
Q
  • Acts as receptor on b cell (BCR
  • 0.2% antibodies
  • do not activate complement or cross placental barrier
125
Q
  • Triggers allergic responses + lysis of parasitic worms
  • Makes ups 0.1% of antibodies
  • Hypersensitivity to antigen, you will have lots of this antibody
126
Q

T-cells help us fight antigens that are inside our body cells

A

Cell-mediated immunity

127
Q

Where do T-cells arise?

A

Bone marrow

128
Q

Where do T-cells go to mature?

129
Q

Where do inactive T-cells circulate?

A

Lymph, blood, lymph nodes, lymphoid organs, and tissues

130
Q

T-Cell receptor (TCR) can only bind an epitope when it’s associated with a (blank)

A

Major Histocompatability Protein/Complex
Co-receptor

131
Q

T-cell has to recognize non-self epitope and self Major Compatability Complex simultaneously. What is this process called?

A

Double Recognition

132
Q

T-cells recognize (blank) (blank) and (blank)(blank) simultaneously

A

Non-self epitope, Self Major Compatability Complex

133
Q

What are the 2 types of T-cells?

A

Helper T-cells: help in humoral + cell-mediated immunity
Cytotoxic T-cells: recognize + kill abnormal cells

134
Q

External surface of all human cells are dotted with PROTEIN MOLECULES, what is an example of one of these molecules?

A

MHC I + II

135
Q

MHC molecule found on the surface of all nucleated body cells
ex: all cells except RBC
-recognized by cytotoxic T-cells

136
Q

MHC molecule found on the surface of antigen presenting cells APC’s
ex: APC’s: macrophages, dendritic cells, B-cells
APC presents antigen (epitope) to helper T-cells

137
Q

Type of response ANTIBODY RESPONSE:
1st time encountering antigen
* IgM first rises then decreases
* IgG after about 7 days, then decreases

A

Primary Antibody Response

138
Q

Type of response ANTIBODY RESPONSE:
1st time encountering antigen
* IgM first rises then decreases
* IgG after about 7 days, then decreases

A

Primary Antibody Response

139
Q

Type of response ANTIBODY RESPONSE:
2 or more times encountering antigen
* Strong response due to memory B cells
* IgM increases first then decreases
* IgG produces more and faster! (thanks. tomemory B-cells)

A

Secondary Antibody Response

140
Q

What MHC and CD# pairs with Helper T-cells?

A

MHC 2 (epitope holder) (APC’s)
CD4 (self)
4 x 2 = 8

141
Q

What MHC and CD# pairs with Cytotoxic T-cells?

A

MHC 1 (nucleated cells)
CD8 (self)

142
Q

Antibodies help fight infection by: NAPA

A

N: neutralization: surrounds pathogen so it can’t spread
A: agglutination: clump big things
P: precipitation: clump small things
A: activate compliment: put holes in bacteria, call phagocytes, stimulate inflammation

143
Q

Are Memory B-cells inactive or active?

144
Q

Are plasma cells from B cells inactive or active?

A

Active, looking to bing specific antigen

145
Q

The types of T-helper cells
What are they a results of?

A

T-helper 1
T-helper 2
These cells are a results of Helpter T-cell Activation

146
Q
  • Produces cytokines: lymphokines, chemical signals
  • Activates MACROPHAGES to increase phagocytosis
  • Activates CYTOTOXIC T-CELLS
  • Activates NATURAL KILLER CELLS to kill infected or abnormal cells
A

T-Helper 1 cells

147
Q
  • Produces CYTOKINES to help activate B cells
  • Increases B-CELL CLONAL SELECTION + ACTIVATION
  • Will results in INCREASE IN ANTIBODIES that can BIND THIS ANTIGEN
A

**T-Helper 2 Cells **

148
Q

make up roughly half of the white blood cell population. They are usually the first cells of the immune system to respond to invaders such as bacteria or viruses. They** phagocytize **

As first responders, they also send out signals alerting other cells in the immune system to come to the scene.

Neutrophils are the main cells found in pus. Once released from the bone marrow, these cells live for only around eight hours. Your body produces roughly 100 billion of these cells every day.

A

Neutrophils

149
Q

also play a role in fighting off bacteria. They are very important in responding to parasitic infections (such as worms) as well.

They are perhaps best known for their role in triggering allergy symptoms. Eosinophils can go overboard in mounting an immune response against something harmless. For example, eosinophils mistake pollen for a foreign invader.

Eosinophils account for no more than 5% of the white blood cells in your bloodstream. However, there are high concentrations of eosinophils in the digestive tract.2

A

Eosinophils

150
Q

account for only around 1% of white blood cells. These cells are perhaps best known for their role in asthma. However, they are important in mounting a non-specific immune response to pathogens, organisms that can cause disease.

151
Q

are also essential in the immune system. They come in two forms: B cells and T cells. Unlike other white blood cells that provide non-specific immunity, B and T cells have specific purposes.

A

Lymphocytes

152
Q

are the garbage trucks of the immune system. Around 5% to 12% of white blood cells in your bloodstream are monocytes. Their most important function is to clean up dead cells in the body.5

153
Q

is a form of immunity that occurs when vaccination of a significant portion of a population (or herd) provides a measure of protection for individuals who have not developed immunity.

A

Herd Immunity

154
Q

inoculation with a weakened or dead microbe or microbe product in order to generate immunity
>Generate an immune response (specific immune response) by giving you the epitopes of the pathogen/pathogen product
>Produce IgG, memory B + T-cells

A

Vaccination

155
Q

weaken a virus in the lab so the virus **can’t cause disease **
>virus will replicate at a very slow rate.
>No signs or symptoms
>Produce strong **humoral + cell-mediated response **
>Lifelong immunity in 1-2 doses
>Refrigeration is required - no good in developing world
>Don’t use these on immunocompromised people

A

Attenuated

156
Q

kill the pathogen using heat, radiation, chemicals
>Epitopes are altered slightly
>Produce weaker immune response
>Multiple doses/boosters are gonna be needed

A

Inactivated Vaccine

157
Q

bacterial exotoxin is the main cause of the illness
>Innactivate the exotoxin
>Use formalin= result of inactivated toxin= toxoid
>Toxoid: will produce memory B + T-cell and antibodies that recognize the exotoxin
>Epitopes altered slightly, need multiple doses/boosters

A

Toxoid Vaccine

158
Q

Includes only the EPITOPES of a pathogen
>multiple shots

A

Subunit Vaccine

159
Q

pathogen is a bacteria that produces a capsule
>Capsules are non-antigenic
>Immune system does not see a capsule as foreign or non-self
>We conjugate (or attach) the capsule or a toxoid the the immune system sees the capsule

A

Conjugate Vaccine

160
Q

generate a mRNA sequence for the epitope. Put the
mRNA in a lipid for delivery. The mRNA inside the body will be transcribed + translated. You’ll produce the protein (eptiope)
>Presence of the epitope then stimulated a specific immune response. Memory B cells + Memory T-cell + IgG can bind
>Low cost, easy to make

A

MRNA Vaccine

161
Q

Some Vaccine Ingredients

A
  • Suspending fluid
  • Stabilizers
  • Albumin
  • Preservatives
  • Adjuvants
  • Aluminum salts
162
Q

To increase the effectiveness of the vaccine, boost the specific immune response

163
Q

develops when the immune system recognizes an antigen and responds to an antigen + produces antibodies that can bind that specific antigen as well as memory B cells and memory T cells (HUMORAL AND CELL-MEDIATED IMMUNITY)
* Can take hours or days to develop
* Can be acquired naturally by getting an infection
* Acquire it artificially with epitopes in a vaccination,

A

ACTIVE Immunity

164
Q

develops when antibodies are given to you from an outside source
* Gives immediate protection because antibodies will find and bind to that specific antigen
* Antibodies will last days to weeks
◦ They are foreign/non-self (you did not make them)
* Can be acquired naturally via IgG from mothers placenta
* Can be acquired naturally via IgA via (mucous) colostrum + breast milk
* Can be acquired artificially via an injection of antibodies;

A

PASSIVE Immunity

165
Q

develops when antibodies are given to you from an outside source
* Gives immediate protection because antibodies will find and bind to that specific antigen
* Antibodies will last days to weeks
◦ They are foreign/non-self (you did not make them)
* Can be acquired naturally via IgG from mothers placenta
* Can be acquired naturally via IgA via (mucous) colostrum + breast milk
* Can be acquired artificially via an injection of antibodies;

A

PASSIVE Immunity

Microbiology (8 decks)

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