Exam 3 Flashcards
(166 cards)
1
Q
invasion of colonization of the body by a pathogen
A
Infection
2
Q
any change from a state of health
*can have infection without _________. Ex: HIV+ but not have aids
A
Disease
3
Q
develops rapidly but lasts a short time
>Common cold
A
Acute Disease
4
Q
develops slowly and is continual
>Heart disease
A
Chronic Disease
5
Q
pathogen that remains inactive (not replicating) for extended period of time
A
Latent Disease
6
Q
any disease that spreads from host to host
>Flu
A
Communicable Disease
7
Q
a type of communicable disease that spreads from host to host
A
Contagious Disease
8
Q
disease does not spread from host to host
>Heart disease, diabetes
A
Non-communicable disease
9
Q
study of the cause of an infectious disease (microbe)
A
Etiology
10
Q
objective manifestation of disease
>observed or measured by others
>fever, vomiting, rash, swelling….
A
Signs
11
Q
subjective manifestation of disease
>felt by the patient
>pain, fatigue, nausea, dizzy, headache….
A
Symptoms
12
Q
ability to cause disease
A
Pathogenicity
13
Q
disease causing microbe
A
Pathogen
14
Q
degree of pathogenicity (how bad?)
A
Virulence
15
Q
the study of where and when infectious disease occur
A
Epidemiology
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
17
Q
total number of cases of a disease in a given population or area
>HIV+ people in the US
A
Prevalence
18
Q
occurs at a relatively stable frequency in any given population or area
>Sexually transmitted pathogens
A
Endemic Disease (never ENDemic diseases)
19
Q
disease that occurs at a greater frequency in a given population or area
A
Epidemic Disease
20
Q
epidemic that occurs simultaneously on more than one continent
A
Pandemic Disease
21
Q
only a few cases occur (quite rare)
A
Sporadic Disease
22
Q
What are some virulence factors?
A
Extracellular enzymes
Toxins
Anti-phagocytic factors
23
Q
produced by bacteria. Secrete them into their environment
A
Extracellular Enzymes
24
Q
Examples of extracellular enzymes
A
Hyaluronidase
Hemolysins
Coagulase
Kinase
Leukocidins
Collagenases
25
invades deeper into tissue
>breaks down extracellular matrix
ex: lawyer scraped knee playing basketball, Staphyloccocus aureus got deep into the bone within 12 hours
Hyaluronidase
26
let bacteria lyse RBC to get iron as a trace element
Hemolysins
27
forms a blood clot, hide from immune system
Coagulase
28
digest clots to remove itself (Streptokinase injected to break clot)
Kinase
29
decrease phagocytosis because they kill WBC
Leukocidins
30
break down collagen
Collagenase
31
Do antibiotics stop extracellular enzymes?
No, they have no effect on extracellular enzymes
32
Koch's Postulates
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
33
used to determine etiological agent(BACTERIA) of an infectious disease
Koch's Postulates
34
Chemicals that harm tissues tissues or trigger host immune response that can cause damage in the host.
>Toxoid vaccines that are *disabled toxins*
Toxins
35
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
Exotoxin
36
Types of Exotoxins:
Cytotoxin
Neurotoxin
Enterotoxin
37
Kill cell or affect function of the cell
>Diphtherias cytotoxin stops protein synthesis
Cytotoxin
38
Interfere with nerve function (synapse)
>Botulism toxin, tetanus toxins
Neurotoxin
39
Kill cells that line gastrointestinal tract,
>Chloera toxin
Enterotoxin
40
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
Endotoxin
41
decreases phagocytosis (WBC engulfing material)
>Capsules decrease phagocytosis. WBC can’t eat bacteria with capsule
Anti-phagocytic factors
42
2 Organisms living together
Symbiosis
43
3 Types of Symbiosis
Mutualism
Commensalism
Parasitism
44
Type of symbiosis that involves both organisms benefit from the symbiotic relationship
ex: GI bacteria + us ; normal flora
Vaginal flora +
Mutualism
45
Type of symbiosis which involves one organism is not affected (neutral)
>Staphylococcus aureus + us
Commensalism
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Type of symbiosis that involves one organism benefits (microbe) other organism is harmed (host)
Parasitism
47
4 Types of Portals of Entry
Broken skin
Mucous membrane
Placenta
Parental Route
48
Portal of entry that deposits the pathogen directly into tissue
>Needle stick, bit
Parenteral route
49
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
Portals of Exit
50
Ways microbes hang on
-Giardia lamblia: suction cup
-Taeneia: suckers + hooks
-Having a glycocalyx
-Fimbrae
-Virus binds to its receptor on host cell
51
Reservoirs of Infectious Disease
1. Animal reservoirs (zoonotic dis.)
2. Human carriers
3. Non-living Reservoirs (water, soil, food)
52
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
Biofilm
53
send chemical signals to each other to actually coordinate biofilm formation
Quorum sensing
54
________ in biofilm can increase antibiotic resistance
Conjugation
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Part of bacterium that aid in biofilm formation, glycocalyx
Difficult for immune system to fight
Fimbrae
56
5 Stages of Infectious Disease
1. Incubation
2. Prodronal
3. Illness
4. Decline
5. Convalesence
57
3 Modes of Transmission
Contact transmission
Vehicle transmission
Vector transmission
58
Contact Transmissions sub modes
Direct
Indirect
Droplet
59
Vehicle Transmission sub modes
Airborne
Waterborne
Food borne
Body fluid
60
Vector transmission sub modes
Biological
Mechanical
61
Pathogen in acquired in a healthcare setting
40,000 die ppl/year
205 die pp/day
Healthcare Acquired Infections
62
Common sites of infection
1. Catheter
2. Central line infection
3. Ventilator/trach
63
Blood borne pathogens in occupations
Hep. B, C, HIV
64
**Hepatitis**: Transmission rate 6-30% from a single needle stick of an infected patient
>Vaccine
>Hep B immunoglobulin (antibodies) 90% effective in preventing transmission
Hep B Virus
65
**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
Hep C Virus
66
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
HIV
67
Cell wall of fungi
made of chitin and they have sterols in their cell membrane.
68
Part of the outer membrane of Gram negative bacteria. It is released when the bacteria die. May cause fever, diarrhea, hemorrhage, shock, death
Endotoxin
69
decreases phagocytosis (WBC engulfing material)
>Capsules decrease phagocytosis. WBC can’t eat bacteria with capsule
Anti-phagocytic factors
70
3 types of symbiosis:
Mutalism: both org. benefit
Commensalism: one org. is neutral
Parasitism: one org. benefits
71
4 Portals of Entry:
1. Broken skin
2. Mucous membranes
3. Placenta
4. Parenteral route (direct)
72
Bacteria send signals to each other to coordinate biofilm formation
Quorum sensing
73
can increase antibioitic resistance
Conjugation in biofilm
74
What aids in biofilm formation
Fimbrae
75
Stages of infectious disease
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
anti-viral protein that blocks synthesis step of viral replication
Interferons
77
prevent the spread of pathogen. Neutralizes bacterial toxins + aid in repair of damaged tissue
Inflammation
78
Damaged cells in the area produce 3 chemicals:
Prostaglandins
Leukotrienes
Histamine
79
Increase vessel permeability which in turn increases fluid in area and increases clotting factors
Prostaglandins + Leukotrienes
80
Increases diameter of blood vessels in area
Histamine
81
Controls body temperature
Hypothalamus
82
Bodies ability to resist infectious diseases through non-specific mechanisms
Non-specific immunity
83
First line of defenses:
Skin + mucous membranes
84
Second line of defense
Phagocytosis
Extracellular killing
Complement
Interferons
Inflammations
Fever
85
Steps in phagocytosis
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
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
Extracellular killing
87
secrete extracellular toxins that kills virus infected cells and tumor cells
are found in:
Tonsils, Lymph, Spleen, Blood, Lymph nodes
Natural killer cells
88
30 proteins in blood (inactive) that work together to destroy bacteria + some viruses
Complement
89
2 Ways to activate compliment
1.Classical: antibody bound to antigen
2.Alternative: pathogen/product
90
What happens when complement is activated?
Cell lysis or chemotaxis (phagocytes)
91
Causes hypothalamus to increase body temp
>=toxins, pathogens, products
Pyrogenes
92
All about B and T cells (lymphocytes)
Specific immunity
93
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
Interferons
94
increases vessel permeability which in turn increases fluid in area and increases clotting factors
Prostaglandins and Leukotrines
95
What is the 3rd line of defense?
Specific Immunity aka: Acquired Immunity
96
Type of IMMUNITY that is all about Lymphocytes (B+T cells)
Humoral and Cell-mediated
Specific Immunity
97
Includes B cells and antibodies present in body fluids (humors)
Humoral Immunity
98
ex: blood, lymph, mucous, breast milk
Humoral Immunity
99
What produces antibodies?
B cells
100
Antibodies circulate in fluid to do what?
Bind to pathogens + pathogen products. Tags them for destruction for phagocytes + complement
101
Uses T-cells to defend. Targets infected cells, cancerous, abnormal cells, abnormal grafts.
Cell-mediated Immunity
102
T + B cells hang in (blank) to screen (blank) for pathogen/pathogen products
Lymph nodes, lymph
103
Molecules that trigger a specific immune response
Antigens
104
Small part of antigen that stimulates a specific immune response
Epitope
105
2 Types of Antigens
Exogenous: outside cells (Humoral)
Endogenous: inside cells (Cell-mediated)
106
Where do B cells mature? In what state do they come out?
Bone marrow, inactive
107
Where do most B cells circulate?
Lymph nodes, organs, tissues
Small % in blood
108
What is the function of B cells?
To produce antibodies
109
Each B cells has (blank) and can respond to (#) of specific antigen (epitopes)
Antigen binding sites, 1
110
Is it the antigen or the B cell that binds to the other?
Antigen (strangely)
111
B cells with identical BCR
B cell clones
112
How do B cells divide?
Antigen binds to BCR + stimulates the B cell to divide by **mitosis** to produce clones
113
Result of SELECTION, ACTIVATION, and DIVISION of B cell
Swollen lymph nodes
114
Swollen lymph nodes are a sign of
**S**election
**A**ctivation
**D**ivision
of B cells
115
Gist of Clonal Selection + Activation of B cells
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
Proteins that bind to a specific antigen and tag the antigen for destruction by the immune system
Antibodies (immunoglobulins)
117
What happens when antibodies bind to antigen
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
What happens when antibodies bind to antigen
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
* Functions about 4-5 days
* Secrete antibodies
* Secrete 2,000 anitbodies per second
B cell **PLASMA** cells
119
* Don't secrete antibodies
* Long-lived
* Stays behind incase same antigen is encountered again
Memory cells
120
Classes of Antibodies:
**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
* 1st produced in responce to antigen
* 5-10% of antibodies
* short lived. few days
* pentamer increases phagocytosis
* presence of this indicates infection
IgM Class
122
* 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
IgG Class
123
* pathogens enter mucous membranes
* blocks attachment to mucousal surfafes
* found in mucous, saliva, colostrum, milk
* good against intestinal pathogens
IgA Class
124
* Acts as receptor on b cell (BCR
* 0.2% antibodies
* do not activate complement or cross placental barrier
IgD Class
125
* Triggers allergic responses + lysis of parasitic worms
* Makes ups 0.1% of antibodies
* Hypersensitivity to antigen, you will have lots of this antibody
IgE Class
126
T-cells help us fight antigens that are inside our body cells
Cell-mediated immunity
127
Where do T-cells arise?
Bone marrow
128
Where do T-cells go to mature?
Thymus
129
Where do inactive T-cells circulate?
Lymph, blood, lymph nodes, lymphoid organs, and tissues
130
T-Cell receptor (TCR) can only bind an epitope when it's associated with a (blank)
Major Histocompatability Protein/Complex
**Co-receptor**
131
T-cell has to recognize **non-self epitope** and **self Major Compatability Complex** simultaneously. What is this process called?
Double Recognition
132
T-cells recognize (blank) (blank) and (blank)(blank) simultaneously
Non-self epitope, Self Major Compatability Complex
133
What are the 2 types of T-cells?
**Helper T-cells:** help in humoral + cell-mediated immunity
**Cytotoxic T-cells:** recognize + kill abnormal cells
134
External surface of all human cells are dotted with PROTEIN MOLECULES, what is an example of one of these molecules?
MHC I + II
135
MHC molecule found on the surface of **all nucleated body cells**
ex: all cells except RBC
-recognized by **cytotoxic T-cells**
MHC 1
136
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**
MHC 2
137
Type of response **ANTIBODY RESPONSE**:
1st time encountering antigen
* IgM first rises then decreases
* IgG after about 7 days, then decreases
**Primary** Antibody Response
138
Type of response **ANTIBODY RESPONSE**:
1st time encountering antigen
* IgM first rises then decreases
* IgG after about 7 days, then decreases
**Primary** Antibody Response
139
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)
**Secondary** Antibody Response
140
What MHC and CD# pairs with Helper T-cells?
MHC 2 (epitope holder) (APC's)
CD4 (self)
4 x 2 = 8
141
What MHC and CD# pairs with Cytotoxic T-cells?
MHC 1 (nucleated cells)
CD8 (self)
142
Antibodies help fight infection by: **NAPA**
**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
Are Memory B-cells inactive or active?
Inactive
144
Are plasma cells from B cells inactive or active?
Active, looking to bing specific antigen
145
The types of T-helper cells
What are they a results of?
T-helper 1
T-helper 2
These cells are a results of Helpter T-cell Activation
146
* Produces **cytokines**: lymphokines, chemical signals
* Activates **MACROPHAGES** to increase phagocytosis
* Activates **CYTOTOXIC T-CELLS**
* Activates **NATURAL KILLER CELLS** to kill infected or abnormal cells
**T-Helper 1 cells**
147
* Produces **CYTOKINES** to help activate B cells
* Increases **B-CELL CLONAL SELECTION + ACTIVATION**
* Will results in **INCREASE IN ANTIBODIES** that can **BIND THIS ANTIGEN**
**T-Helper 2 Cells **
148
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.
Neutrophils
149
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
Eosinophils
150
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.
Basophils
151
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.
Lymphocytes
152
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
Monocytes
153
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.
Herd Immunity
154
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**
Vaccination
155
**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
Attenuated
156
**kill** the pathogen **using heat, radiation, chemicals**
>**Epitopes are altered slightly**
>Produce weaker immune response
>Multiple doses/boosters are gonna be needed
Inactivated Vaccine
157
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
Toxoid Vaccine
158
Includes only the **EPITOPES of a pathogen**
>multiple shots
Subunit Vaccine
159
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
Conjugate Vaccine
160
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
MRNA Vaccine
161
Some Vaccine Ingredients
* Suspending fluid
* Stabilizers
* Albumin
* Preservatives
* Adjuvants
* Aluminum salts
162
To increase the effectiveness of the vaccine, boost the specific immune response
Adjuvants
163
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,
ACTIVE Immunity
164
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;
PASSIVE Immunity
165
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;
PASSIVE Immunity
