260 Final Flashcards
(329 cards)
1
Q
i. Are well established microbes that don’t cause an overt disease but provide a protective shield against pathogens
A
normal body flora
2
Q
- Receive nutrients from the host
2. Locate themselves depending upon their food source
A
Resident flora
3
Q
Locate themselves depending upon their food source
a. Fatty acids
b. Mucus – proteins & carbs
c. Secretions and digested food of the digestive tract
A
Resident flora
4
Q
i. Produced by skin’s sebaceous glands
ii. Even sweat includes nutrient molecules
A
fatty acids
5
Q
i. Linings of
1. Respiratory
2. Digestive
3. Reproductive tract
A
Mucus - proteins and carbs
6
Q
i. Saliva contains mucin (active ingredient in mucus) and food particles
A
c. Secretions and digested food of the digestive tract
7
Q
ii. Few organisms survive the acids in the stomach and enzymes of the small intestines
A
c. Secretions and digested food of the digestive tract
8
Q
iii. Large intestine supports 10 trillion microbes including Archaea
A
c. Secretions and digested food of the digestive tract
9
Q
- Normal flora receive nutrients from host and are essential to the health of humans
A
iii. Maintenance of the Normal Resident Flora
10
Q
- Flora create an environment that may prevent infections and can enhance host defenses
A
iii. Maintenance of the Normal Resident Flora
11
Q
- Antibiotics, dietary changes, and disease may alter flora
A
iii. Maintenance of the Normal Resident Flora
12
Q
- Associated with areas in direct contact with the environment
- Inhabit the body sporadically and do not acquire nutrients
A
iv. Transient flora
13
Q
- Positive and obligatory relationship for both organisms
A
Mutualism
14
Q
- Ex: eukaryotic cells and their mitochondria, infants, and vitamin A producing bacteria
A
Mutualism
15
Q
- Is a positive relationship for both organisms but non-obligatory (normal body flora)
A
Synergism
16
Q
- Humans and the bacteria in our digestive tracts
A
Synergism
17
Q
a. Bacteria synthesize growth factors
i. Vitamins B12
ii. K
iii. Niacin
iv. Thiamin
v. Riboflavin
vi. Folic acid
A
Synergism
18
Q
b. Assists with the breakdown of fibrous wastes
c. Stimulate development of the immune system
A
Synergism
19
Q
- When a relationships is positive for one organism, and neutral for the other organism (normal body flora)
A
Commensalism
20
Q
- Microbes on our skin that consume skin secretions
A
Commensalism
21
Q
- Lactic acid bacteria that lower pH of female reproductive tract
A
Commensalism
22
Q
- When one organism benefits and the other is harmed (disease)
A
Parsitism
23
Q
- When both organisms are harmed
2. Disease
A
Competition
24
Q
- When microbes are present
A
Contamination
25
1. When microbes exist superficially as reproducing surface populations
Colonization
26
1. When microbes enter the tissue
Infection
27
1. When there is noticeable impairment of body function
Disease
28
i. Involves a microbe vs. noninfectious
Infectious
29
i. When an infectious disease can spread from one person to another person
Communicable
30
i. When a communicable disease is *easily* spread from host to host
Contagious
31
i. Caused by microbes from outside of the body
Exogenous
32
i. Caused by microbes already present in or on the body
Endogenous
33
i. When a microbe can cause a disease only in hosts with impaired immune systems or when relationships become unbalanced.
Opportunistic
34
i. Characteristics of a disease that can only be felt or observed by the patient
Symptoms
35
1. Headache
2. Cramps
3. Nausea
4. Pain
5. Irritatio
6. Malaise
7. Fatigue
8. Chest tightness
9. Itching
10. Headache
11. Weakness
12. Anorexia
13. Sore throat
Symptoms
36
i. Characteristics of a disease that can be observed by examining the patients
Signs
37
1. Changes in leukocyte count
2. Inflammation and fever
3. Elevated antibody titer in the blood
4. Septicemia
5. Microbes in tissue fluids
6. Abnormal chest sounds
7. Skin eruptions
8. Swollen lymph nodes
9. Absecesses
10. Tachycardia (increased heart rate)
11. Changes in urinr constituents
Signs
38
i. Over 10,000 white blood cells/uL
Leukocytosis
39
i. Under 10,000 WBC’s/uL
Leukopenia
40
i. Combination of signs and symptoms
Syndrome
41
d. Headache
i. Neutral microbe
| ii. Negative to host
42
e. Fever
i. Negative microbe
| ii. Positive to host
43
f. Inflammation
i. Negative microbe
| ii. Positive to host
44
g. Cramps -> diarrhea
i. Positive microbe
| ii. Positive host
45
h. Nausea --> vomiting
i. Positive microbe
| ii. Positive host
46
i. Coughing
i. Positive microbe
| ii. Positive host
47
j. Sneezing
i. Positive microbe
| ii. Positive host
48
k. Runny nose
i. Positive microbe
| ii. Positive host
49
nonspecific barriers to microbial entry with which a person is born; present at birth; no memory
a. Innate Immunity
50
1. Prevents infection
2. Competitive Exclusion
3. Physical Barriers
4. Chemical barriers
First line of defense
51
a. When normal flora compete with invading microbes
2. Competitive Exclusion
52
a. Skin
b. Mucous membranes
c. Flushing mechanisms
i. Coughing
ii. Sneezing
iii. Urination
iv. Tears
v. Cilia
vi. Peristalsis
Physical barriers 1st line
53
a. Acids in
i. Stomach
ii. Female reproductive tract (vagina)
b. Lysozyme found in
i. Tears
ii. Saliva
iii. Digests bacterial cell walls
Chemical barriers 1st line
54
1. Prevents disease
2. Chemicals
3. Biological barriers
2nd line of defense
55
a. Complement
| b. Interferon
Chemical barriers
| 2nd line of defense
56
i. Group of 20 blood proteins
ii. Bind to microbe membranes --> chain reaction leading to the insertion of pores in membranes of microbes (microbe lysis)
Complement
57
i. Antiviral
ii. Is produced by fibroblast and WBC’s invaded by a virus
iii. Attaches to receptor sites on neighboring host cells
iv. Activates an enzyme which blocks the translation of viral m-RNA and an enzyme that degrades viral m-RNA
Interferon
58
4. In response to
a. Virsues
b. RNA
c. Immune products
d. Various antigens
Interferon
59
1. Alpha
a. Lymphocytes and macrophages
2. Beta
a. Fibroblasts & epithelial cells
3. Gamma
a. T cells
Interferon
60
1. Induce expression of
| a. Antiviral proteins
Interferon
61
2. Inhibit expression of
| a. Cancer genes
Interferon
62
iv. Activates an enzyme which blocks the translation of viral m-RNA and an enzyme that degrades viral m-RNA
Interferon
63
a. Phagocytosis
The absence of receptor sites on cell membranes
b. Inflammation
Biological barriers
| 2nd line of defense
64
1. Via nonspecific leukocytes (=general WBC)
phagocytosis
65
1. The most common WBC
2. Effectively kill bacteria and other microbes
3. General purpose
4. React early to bacteria and other foreign materials, and to damaged tissues
5. Lysozyme and defensins
Neutrophils
66
1. The largest blood borne phagocytes
2. Circulate for about 3 days in the blood;
3. Then migrate into the tissues and become macrophages and dendritic cells
Monocytes
67
2. Digest antigens into smaller antigenic determinants and present them to cells of the immune system
- APC
Macrophages
68
anything foreign to the body that initiates an immune response
antigens
69
distinctive amino acid sequences that mobilizes the immune response
ii. AKA “exogenous” antigens
iii. AKA “epitopes”
antigenic determinants
70
3. Bind to naïve TCD4 cells and secrete the lymphokine interleukin-1
macrophages
71
chemicals produced by WBCs that target other WBCs and influence their behavior
=lymphokine
72
i. Helps activate naïve TCD4 clls
Interleukin-1
73
ii. Stimulates the brain (hypothalamus) to raise the body’s temperature, FEVER, which
1) helps activate naïve TCD4 cells;
2) enhances the activity of immune cells (T cell production increases 20 fold if temperature up to 102.2) and interferon;
3) increases microbial demand for iron;
4) reduces host’s absorption of iron
Interleukin-1
74
iii. Inflammatory agent
| iv. Also induces sleeps, aches, and pains
Interleukin-1
75
4. Will phagocytize antigen and present (epitope) to immune cells
Macrophages
76
1. APC
2. Digests antigens into epitopes (antigenic determinants)
3. Present epitopes to and activate both naïve TCD4 and naïve TCD8 cells
Dendritic cells
77
i. When tissues are injured, WBC’s (basophils and mast cells) release chemicals such as histamines, kinins, and prostaglandins
Inflammation
78
ii. Includes dilation, increased permeability of blood vessels
Inflammation
79
1. “leaky capillaries”
2. Redness, swelling, pain (edema), increased temperature, delivers immune component
3. Localizes microbes and chemicals used for tissue repair.
Inflammation
80
1. Adaptive
2. The recognition and elimination of foreign and/or dangerous antigens
3. Takes time to respond
4. Has memory
1. Prevents death
Acquired Immunity
| Third Line of Defense
81
i. Are unique to each individual
ii. Identify self
iii. Are associated with the cell membrane of all nucleated cells of the body
1. NOT red blood cells
MHC-1
82
iv. Part of intracellular surveillance system, whereby enzymes regularly break down cytoplasmic proteins into peptides (epitopes) and transport the epitopes to the cell surface attached to said receptors
MHC-1
83
v. Its epitope complexes are examined by effector T killer/cytotoxic cells.
vi. Normal “self” epitopes are ignored while epitopes from an antigen that has infected the cell (or a cancer cell) will instigate an attack by the T-cellls
MHC-1
84
vii. Help to identify self (all nucleated cells)
viii. Intracellular surveillance (cell infected or cancerous)
ix. Monitored by T cytotoxic cells
MHC-1
85
i. Associated with the cell membrane of macrophages, B Lymphocytes and dendritic cells
MHC-II
86
ii. Part of the extracellular surveillance system
MHC-II
87
iii. When enzymes break down phagocytized antigens into epitopes, the peptides are transported to the cell surfaced attached to these receptors
MHC-II
88
i. Dendritic cells and macrophages present these complexes to naïve TCD4 cells while naïve B lymphocytes present its epitope complex to effector T helper cells
MHC-II
89
v. Only on macrophages, dendritic cells, and B lymphocytes (APC’s)
vi. Used for extracellular surveillance (cell phagocytized something)
MHC-II
90
vii. Used for TCD4 cells
MHC-II
91
a. In the bone marrow, lymphocytic stem cells differentiate into either
T or B cells
92
B cells stay in
| T cells migrate
the bone marrow
| to the thymus
93
1. Get a T cell receptor
| 2. Allow T cell to recognize 1 specific antigen held in an MHC receptor
T cells in thymus
94
3. Have to be able to identify “self”
| 4. Get a CD4 or CD8 receptor which allows them to attach to either MHC1 or MHC2 receptor
T cells in thymus
95
5. Get a CD28 costimulatory receptor
T cells in thymus
96
b. Both then migrate to
secondary lymphoid tissue
97
a. Derived from bone marrow lymphoid stem cells that differentiate into immature lymphocytes with T cell receptors
T cells
98
recognition receptor that is complementary to and allows a T cell to identify an epitope from a specific microbe
T cell receptors
99
i. T cells whose T cell receptor an recognize “self” epitopes without binding too tightly survive their stay in the thymus
= positive selection
100
ii. T cells that bind inappropriately to self-epitopes are eliminated
negative selection
101
1. Immature T cell acquires a CD8 receptor if thymic cells present self epitopes to the T cell via an
MHC 1 receptor
102
2. Immature T cell acquires a CD4 receptor if thymic cells present self epitopes to the T cell via
MHC II
103
receptors are attachment receptors that help T cells bind to MHC-epitope complexes
CD4 and CD8
104
iii. Immature cells also acquire
CD28 recptor
105
i. Naïve TCD8 cells emerge from the thymus, each distinguished from the others by its unique
T cell receptor
106
iii. Dendritic cells have phagocytized and processed antigens into epitopes travel to lymph tissue and present those epitopes to naïve TCD8 cells in
MHC1
107
1. If complementary, the T cell receptor binds to the
epitope
108
while
| 2. The CD8 receptor binds to
MCH 1 receptor
109
If dendritic cell’s ___ receptor have been activated (bound to antigens recognized as dangerous, e.g. flagellin), the dendritic cells will display co-stimulatory molecule ___ which bind to CD28 receptors on the TCD8 cell
toll-like
| B7
110
increase in size, multiply, and differentiate into clones of specific effector T Killer/cytotoxic cells, and delayed hypersensitivity cells (involved in allergic reactions)
Activated T cells
111
a. Leaves lymphoid tissue and search for cells presenting MHC 1 epitop complexes with foreign epitopes complementary to their T cell receptor
Effector T cytotoxic cells
112
b. Synapse with MHC-I receptors presenting the foreign epitope
Effector T cytotoxic cells
113
c. Release lymphotoxins (like perforin) which form pores in the cell membrane of the infected cell and protreases which enter the infected cell through the pores and cuase the infected cell to undergo
apoptosis=programmed cell death
Effector T cytotoxic cells
114
also produce lymphokines that attract other lymphocytes and macrophages
Effector T cytotoxic cells
115
a. Involved in delayed hypersensitivity (allergic) reaction that may take several days to develop
2. Delayed hypersensitivity cells
116
a. Result of affinity maturation where the cytotoxic cells with the best binding T cell receptors survive to reproduce and generate the “best” progeny
Memory T Cytotoxic Cells
117
b. Are long lived cells that remain in circulation after an adaptive immune response is over
Memory T Cytotoxic Cells
118
c. Ready to quickly become effector T cytotoxic cells
Memory T Cytotoxic Cells
119
d. Provide the basis for the quick anamnestic or secondary immune response, that occurs when the same antigen is encountered again (the basis of immunization programs)
Memory T Cytotoxic Cells
120
are most common of cells associated with adaptive immunity
TCD4
121
cells also emerge from the thymus, each distinguished from the other by its unique T cell receptor
TCD4
122
iii. Dendritic cells and macrophages that have phagocytized and processed antigens into epitopes present those epitopes to naïve TCD4 cells in
MHC II epitope complexes
123
1. If complementary, T cell receptor binds to the epitope while
2. The CD4 receptor binds to the
MHCII
124
If ___ have been activated on dendritic cell and/or macrophage, the presenting cells will display co-stimlatory molecules such as
___ which bind to receptors on the ___ cell
toll like receptors
b7 receptors
tcd4 cell
125
4. If the synapse is complete, the naïve TCD4 cell will be
activated
126
will increase in size, divide and differentiate into clones of effector T-helper I & and T-helper II
TCD4
127
becomes effector t helper 1 in presence of
interleukin XII
128
becomes effector t helper 2 in presence
interleukin IV
129
i. Are the “commander in chief” of the immune system
Efffector T helper cells
130
produce lyphokines that facilitate the activation of naïve TCD8 cells, the maturation of effector T cytotoxic cells and the efficiency of macrophages
T helper 1
131
facilitate the activation of naïve B lymphocytes and the production of antibodies
T Helper II
132
produced by both helper I and helper II;
stimulates T helper cells and helps activate naïve TCD8 cells;
helps activates naïve B lymphocytes by binding to CD24 receptors
Interleukin II
133
encourages activated B cells to stop multiplying, differentiate into plasma cells and start producing antibodies (produced by Helper II)
B cell growth factor
BCGF
134
= instructs B cells to stop multiplying, differentiate into plasma cells and start producing antibodies (produced by helper II)
B cell differentiation factor
BCDF
135
= helps activate T cytotoxic cells, increases the ability of plasma cells to produce antibodies, keeps macrophages at the site of an infection and helps them digest the cells they have engulfed, stimulates suppressor cells (produced by helper I and helper II)
=Gamma interferon
136
i. TCD4 cells that produce inhibitory lymphokines that help call off an adaptive immune response when the antigen (microbe) that elicited the immune response has been eliminated
Regulatory (Suppressor T cells)
137
i. Long lived cells that are the result of affinity maturation
Memory T Helper cell
138
develop from lymphoid stem cells that differentiate into naïve cells in the bone marrow
B cells
139
```
acquire Ig (immunoglobulin) or class IgD antibody receptors and
ii. Undergo positive and negative selection to become
```
B cells
140
from the bone marrow, each distinguished from the others by its unique
Ig receptor
141
c. Naïve B cells migrate to lymphoid tissue and areas frequented by microbes
i. Near the skin
| ii. Lining of the digestive tract etc where they await activation
142
i. B cells become activated when their ___ receptors interact directly with epitopes on the surface of whole, free antigens e.g. viruses or bacteria
Ig
143
1. The B cell uses its Ig receptor to bind to and ingest the microbe
a. The microbe is processed into epitopes which are
b. Presented to T helper II cells by B cell
____
MHC II receptors
144
2. T helper cells use their T cell receptors to examine the MHC II epitope complexes and if its receptor recognizes a ___
complementary epitope
145
3. The T helper begins to produce the co stimulatory molecule ___ II which binds to the B cell ___
Interleukin II
| B cell CD24 receptors
146
Recognition of the epitope plus co stimulation by ___ starts the activation of the B cell
Interleukin II
147
5. The T helper cell subsequently produces BCGF, BCDF, interleukin IV, and gamma interferon to orchestrate the development of naïve B cells into ___ and ___
memory cells and plasma cells
148
=effector B cells
plasma cells
149
cells secrete antibodies (humoral immunity), protein recognition molecules
plasma cells
150
=used as B cell receptors
IgD
151
are the first to be produced, but can’t pass through the placenta
IgM
152
appear later in primary immune response as result of class switching; most common antibodies and can pass through the placenta
IgG
153
= produced when plasma cells located in mucous membranes and mammary glands class switch; found in mother’s milk
IgA
154
normally attacks parasitic worms; allergies if attach to mast cells and basophils
IgE
155
b. Bind to “Free’ antigens, marking them for destruction by WBC’s
Antibodies
156
reactions where the antibodies bind to and block the activity of a virus, toxin, or enzyme; immobilized antigen is then eaten by WBCs or may deteriorate on its own (toxins will have a half life)
Neutralization
157
reactions where antibodies link soluble antigen molecules (toxins enzymes) making them insoluble and precipitate out of solution
Precipitation
158
when bacteria, coated with antibodies are more easily consumed by WBC’s
iii. Opsonization
159
reactions where antibodies link foreign cells to one another
iv. Agglutination
160
when complement reacts with antibody bound microbes; leads to microbe lysis, phagocytosis of cellular antigens and/or inflammation
v. Complement fixation
161
i. Can rapidly become plasma cells during a subsequent immune challenge
c. Memory B cells
162
1. Are associated with the cell membrane of all nucleated cells of the body
2. Intracellular surveillance (cell infected or cancerous)
MHC 1
163
1. Associated with the cell membrane of macrophages, B Lymphocytes and dendritic cells
2. When enzymes break down phagocytized antigens into epitopes, the peptides are transported to the cell surfaced attached to these receptors
MHC II
164
1. T cells
| 2. Recognizes ONE specific antigen
T cell receptor
165
1. B cells
| 2. Bind to “Free’ antigens, marking them for destruction by WBC’s
B cell receptor = IG
166
1. T cells
| 2. attachment receptors that help T cells bind to MHC II-epitope complexes
CD4
167
1. Other T cells have this receptor
| 2. receptors are attachment receptors that help T cells bind to MHC I-epitope complexes
CD8
168
1. Dendritic cells
| 2. Co-stimulatory molecule that binds to CD28 on T cells, confirms that antigen presented is not normal.
B7
169
1. Dendritic cells
2. If receptor have been activated (bound to antigens recognized as dangerous, e.g. flagellin), the dendritic cells will display other co-stimulatory molecules
Toll-like
170
3. The T helper begins to produce the co stimulatory molecule Interleukin II which binds to the B cell ___ receptors
4. Recognition of the epitope plus co stimulation by Interleukin II starts the activation of the B cell
CD24
171
1. T cells
| 2. Get a costimulatory receptor
CD28
172
i. Has a long latent period (about a week) during which naïve cells are activated and become effector cells
ii. Because of the delay, a person will become sick
primary immune response
173
i. Has no significant delay
ii. Is based on memory cells
iii. Is much bigger/aggressive and
iv. Should keep a person from ever expressing disease signs or symptoms
b. Secondary = anamnestic immune response (Anamnestic = “without forgetting”)
174
i. Consists of the protective mechanical barriers, phagocytes, and chemical with which you are born
Innate immunity
175
1. Occurs when a “wild type” antigen (microbe) you encounter stimulates an adaptive immune response where
Active
| Naturally Acquired Immunity
176
2. You generate your own antibodies, effector cells and memory cells (and probably get sick)
Active
| Naturally Acquired Immunity
177
3. Improves with the number of times you are exposed to the same antigen as memory cells increase in number and become more efficient
Active
| Naturally Acquired Immunity
178
1. There’s no actual exposure to an antigen, no immune response, and no development of memory cells
Passive
| Naturally Acquired Immunity
179
2. When a fetus or infant acquires antibodies from their mother via the placenta (igG) and /or her milk (igA) and is temporarily protected (antibodies have a half-life and eventually disappear
Passive
| Naturally Acquired Immunity
180
1. Occurs when a person is immunized with a dead or living (attenuated) microbe, epitopes from a microbe or microbe products such as toxins
Active
| Artificially Acquired Immunity
181
2. A primary injection results in an adaptive immune response that ultimately generates memory cells
Active
| Artificially Acquired Immunity
182
3. Later, when the person actually encountes the living, “Wild” microbe or its products, memory cells quickly differentiate into effector cells which initiate a rapid, dramatic anamnestic response and another generation of even more effective memory cells
Active
| Artificially Acquired Immunity
183
4. A preventative technique that protects the individual against future encounters with a dangerous microbe
Active
| Artificially Acquired Immunity
184
1. Antibodies are provided by another person/animal
Passive
| Artificially Acquired Immunity
185
i. Due to age (very young, elderly)
ii. Due to malnutrition
iii. Due to treatments: chemo/radiation therapy, anti-transplant rejection drugs
iv. Due to diseases that depress/destroy the immune response, e.g. AIDS
Reduced immunity
186
1. Microbes gain a stable foothold at the portal of entry;
| 2. Dependent on binding between specific molecules on host and pathogen
Adhesion
| Attachment
187
a. Fimbriae
i. G+/G- to help stick to you
b. Flagella
c. Glycocalyx
i. Sticky
ii. Slime layer
d. Cilia
e. Suckers
f. Hooks
g. Barbers
Adhesian Attachment
188
a. Produced by some fungi (see ringworms) and digests the keratin in skin
Keratinase
189
a. Digests hyallyronic acid, an intracellular cementing substance between surface cells
Hyaluronidase
190
a. Enzyme that digests collagen, the most common protein in the body (CT)
Collagenase
191
a. Convert plasminogen into plasmin
| b. Enzymes that breaks down blood clots
Streptokinase/Staphylokinase
192
causes a web-like clot that impedes WBC movement
Coagulase
193
a. Kills WBC’s
Leukocidin
194
a. Mechanically inferfere with phagocytosis
Fimbriae and Capsules
195
a. May inhibit digestion by phagocytes
Resistance cell walls
196
a. Are toxins that act as pores
b. Lyse red blood cells
c. Iron released from RBCs is appropriated for microbial use
d. Alpha’s cause partial hemolysis leaving a greenish ring around microbial colonies
e. Beta’s cause complete hemolysis leaving a clear ring around microbial colonies
Hemolysins
197
1. Hemolysins
| Viruses enter host cells and take over the resources and machinery of their hosts
Acquisition of host resources
198
i. Are the lipid A part of the outer membrane of Gram Negative bacteria
ii. Are released when gram negative bacteria die
Endotoxin
199
iii. Are weak, non specific and cause a fever
| iv. Stimulate weak immunity
Endotoxin
200
v. Are stable
1. Cannot be denature and converted into a toxoid
2. Can’t be used for immunization
Endotoxin
201
i. Are associated with a few gram positive and a few gram negative bacteria
ii. Are secreted
exotoxin
202
iii. Are polypeptides, unstable, powerful, do not tend to cause fever, and stimulate strong immunity
iv. Can be denatured and converted to a toxoid which can be used for immunization
exotoxin
203
v. Highly specific
1. Neurotoxins
Enterotoxins
exotoxin
204
a. Attack nervous system
i. Botulin
ii. Tetanospasmin
Neurotoxin
205
a. Attack organs of the digestive tract
i. Shiga toxin
ii. Cholera toxin
Enterotoxins
206
i. Clostridium botulinum
Botulism
207
1. Normally and intoxication (toxin is consumed via contaminated food)
Botulism
208
2. Endospores consumed by an infant (infant botulism)
Botulism
209
3. Endospores introduced into a wound
Botulism
210
1. Exotoxin/neurotoxin
Botulism
211
a. Toxin carried to neuromuscular junctions and blocks Ach release
b. Causes Flaccid paralysis
Botulism
212
c. Blocks release of neurotransmitter Acetylcholine, which stimulates skeletal and smooth muscle to contract
Botulism
213
2. Paralysis of muscles, including muscles of inspiration
Botulism
214
iv. Treatment
1. Support
2. Antitoxins
3. Antibiotics (wound)
Botulism
215
v. Prevention
1. Properly prepare food to destroy endospores
2. Avoid feeding honey/corn syrup to infants under age of 2 (associated w/SIDS)
Botulism
216
- Hemorrhagic colitis = hemolytic uremic syndrome
=shiga toxin
217
i. Both caused by Escherichia coli O157:H7
=shiga toxin
218
1. Emerged in 1975
| 2. First detected in 1982 and is now leading cause of acute kidney failure in children
=shiga toxin
219
3. Outbreaks include 2 outbreaks in 1992 (including Jack-in-the-Box outbreaks in Washington)
=shiga toxin
220
5. Transmission
| a. Primarily through ground beef, leafy green and unpasteurized beverages
=shiga toxin
221
b. Can be person to person in households, daycare centers and other institutions
=shiga toxin
222
iii. Lysogenizes via a viral prophage --> shiga toxin (exotoxin)
=shiga toxin
223
1. Binds to receptors
a. On cells lining small blood vessels
b. That are more common in children than adults
=shiga toxin
224
2. Enters cells and
a. Inactivates ribosomes
b. Stops protein production
=shiga toxin
225
3. Cells die
a. Break down of vessel lining --> blood clots and/or hemorrhage
b. Digestive tract --> hemorrhagic colitis (bloody diarrhea)
=shiga toxin
226
1. Cells die
a. Kidney glomeruli
i. Kidney failure
ii. Hemolytic Uremic Syndrome
1. ~3000 cases/year
=shiga toxin
227
iv. Treatment
1. Support
2. No antibiotics
a. dead cells release lipid A
b. antibiotics activate prophage leading to more toxin production
=shiga toxin
228
v. Prevention
1. Cook your food
2. Avoid ground beef, leafy greens and unpasteurized beverages
=shiga toxin
229
i. Vibrio cholerae
ii. Bengal cholera is a new, virulent strain and
iii. Threatens to become the world’s 8th cholera pandemic since 1837
cholera toxin
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iv. Spread via salt water
| v. Exotoxin
cholera toxin
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a. Binds to cell receptors lining the intestines
| b. Chloride and bicarbonate ion channels open
cholera toxin
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2. Sodium follows the chloride out of the cell, water follows salt
cholera toxin
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a. Creates salt water environment for the bacteria
| b. Resultant diarrhea (rice water stools) assists transmission of the bacteria
cholera toxin
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vi. Treatment
| 1. Re-hydration therapy
cholera toxin
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vii. Prevention
| 1. Clean water (4 layers of sari cloth removes 99% of microbes from water in India)
cholera toxin
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i. Prevention
1. Vaccine evaluated in Africa (2003) is 90% effective
a. Need for cold chain distribution
b. Short shelf life
c. High cost 7-12$
d. Multiple doses
cholera toxin
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viii. Stimulation of extreme host responses
1. Extreme inflammation
2. Abscess formation
3. Inappropriate blood clotting
cholera toxin
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ix. Evasive strategies
1. Depression of the immune response
2. High mutation rate
3. Intracellular
4. Triggering an autoimmune response
5. Mimicking host molecules
6. Formation of biofilms
cholera toxin
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i. Tetanus = Clostridium Tetani
Tetanospasmin
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ii. Transmission
1. Inoculation
2. Cutting umbilical cord with dirty knife (70,000 infant African deaths/year)
Tetanospasmin
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iii. Virulence factor
| 1. Tetanospasmin
Tetanospasmin
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a. Exotoxin
b. Neurotoxin
c. 1 of 3 most powerful toxins known
Tetanospasmin
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d. Follows nerve to spinal cord and brainstem
| e. Inhibits release of inhibitory neurotransmitters glycine (spinal cord) and GABA (brain stem)
Tetanospasmin
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f. There is an increase in number of impulses sent to the skeletal muscle
g. Muscle spasms
i. Lock jaw
ii. Muscles of inspiration becomes non-functions --> breathing stops
Tetanospasmin
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iv. Treatment
1. Support
2. Antitoxin
3. Antibiotic
4. Muscle relaxants while anon terminal re-grows
Tetanospasmin
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v. Prevention
1. Toxoid vaccine (denatured tetanospasmin)
a. DTaP (children <6)
b. Tdap (adolescent and adult 1 time booster)
c. Td booster every 8-10 years
Tetanospasmin
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i. Agent must be isolated from host displaying the disease, grown in pure culture and characterized by testing
Koch's postulates
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ii. When the agent from the pure culture is inoculated into susceptible hosts, it must cause the disease
Koch's postulates
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iii. The agent must be re-isolated from the diseased host and identified as the original specific causative agent
Koch's postulates
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iv. A specific causative agent must be observed in every case of a disease.
Koch's postulates
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1. Disease has a rapid development and course
Acute
252
1. Diseases which are slow and persistent
Chronic
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1. Diseases have periods of inactivity between attacks
| 2. Herpes
Latent
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1. Diseases are confined to a specific area
| 2. Giardia in intestines
Localized
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1. When infectious agent breaks loose from a local infection and carried to other tissues
2. Tetanus
Focal
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1. Microbes or their products are In the blood
Sepsis
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a. Bacteria and viruses are present in the blood, but don’t multiply
2. Bacteremia and viremia
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a. Toxins are in the blood
Toxemia
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1. Microbes are present and multiply in the blood
| 2. Malaria
Septicemia
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1. Diseases affect the entire body
systemic
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1. Diseases represent an initial infection
Primary
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1. Diseases represent an infection that follows a primary infection, usually as the result of the patient having been weakened by the primary disease
Secondary
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1. The time between infection and the appearance of signs and/or symptoms
Incubation period
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1. The short period of time when non-specific symptoms appear (the effects of interleukin-I)
prodromal
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1. The period when the disease develops signs and symptoms characteristic of the disease
Invasive
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1. Critical stage
| 2. The period of the most intense symptoms
Acme
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1. Host immune response begins killing the pathogen
| 2. Symptoms characteristic of the disease begin to decrease
Decline
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1. The recovery phase when tissues repair and healing takes place
2. No symptoms of the disease, but microbes may still be present
Convalescence
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i. Selective agents
ii. Artificial passive immunization
iii. Boosting host defense mechanisms
iv. Reduce symptoms
v. Vaccine
Treatment for infectious diseases include
270
1. Antibiotics
2. Antivirals
3. Sulfa drugs
Selective agents
271
1. Homologous pooled human antibody- gamma globuins
2. Homologous human yperimmune globulins
a. Convalescent serum
b. Diptheria – 1st disease cured 1891
3. Heterologous hyperimmune serum
a. Antitoxin
b. Neutralizing antibodies
Artificial passive immunization
272
1. Administering gamma interferon
2. Use of interleukin II
3. Good nutrition
Boosting host defense mechanisms
273
1. Aspirin
2. Fluids
3. Etc.
Reduce symptoms
274
i. Good nutrition
ii. Good sanitation
iii. Artificial active immunization
iv. Eliminate non human vectors
v. Treat carriers
vi. Good surveillance
vii. Quarantine
Prevention of Diseases include
275
1. Provides herd immunity
2. Long term
3. Stimulates B and T cell formation and differentiation
Artificial active immunization
276
a. Developed first natural vaccine for smallpox
| i. Variola major and minor
Jenner
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i. Small pox killed 1 in 3 (500 million victims during 20th century)
ii. Variolation
Small pox
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1. Used to prevent serious smallpox infections (person inoculated with Variola from a mild case of smallpox)
iii. Jenner, first “natural” vaccine based on Cowpox virus (vaccination)
1. Live virus grown on skin of calves
2. Arm to arm
small pox
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a. Hybrid mix of cowpox and smallpox viruses
| b. 1 dose of dried calf lymph
Dryvax
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a. Smallpox eradicated – herd immunity
b. DNA virus, no mutations
c. NO question who was infected
1979
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a. Discovered principle behind vaccinations
| b. 1st laboratory developed a vaccines for rabies and anthrax
Pasteur
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1. Italian for 40 days
| 2. First attempted in 14th century Venice to stop Bubonic plague; ships remained at anchor for 40 days
Quarantine
283
a short term increase (from months to years) in the incidence of a specific microbial disease in a limited population (confined in time and space)
=epidemic
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1. 1849
| 2. Traced a cholera outbreak to a water pump
John Snow
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1. Is the number of new cases of a disease seen in a specific time period
Incidence
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1. Corresponds to the number of people infected with a specific microbe at any one tme.
ii. Prevalence
287
1. Number of deaths per population at risk
Mortality rate
288
1. Disease must be communicable from person to person
| 2. Each host must spread the disease to at least two other people
Propagated epidemic
289
3. Usually begins with an index case
| a. =the first person to bring a disease into a community
Propagated epidemic
290
1. When multiple hosts come in contact with the same microbe source
2. The disease may not be communicable
a. Everyone eats same potato salad or water
Common source epidemic
291
a. Corresponds to the length of the incubation period
b. Is when the disease is asymptomatic
c. The microbe can be spread during this phase
Latent (lag) phase
| Phases of epidemic disease transmission
292
a. Corresponds to rapid transmission of the disease
b. Depends upon the number of contacts made by contagious individuals
c. Continues until a high percentage of the population has encountered the organism and the number of new cases begins to decline
Logarithmic phase
| Phases of epidemic disease transmission
293
a. Is when there is low incidence (few new cases are reported) and some of the population have started to recover (or have died)
b. Is when antibodies are building in the population
Stationary phase
| Phases of epidemic disease transmission
294
a. When few new cases appear
Decline phase
| Phases of epidemic disease transmission
295
a. If a population is small and the host is not motile, the epidemic will disappear
Epidemic aftermath
296
the disease spreads to at least two continents
Pandemic disease
297
a disease persists in a population
Endemic disease
298
ii. The population must be threshold for a disease
Endemic disease
299
iv. An endemic disease usually becomes a childhood disease
| v. Controlled by vaccines (reduces the number of susceptible people)
Endemic disease
300
iii. Be large enough that it can continuously generate susceptible people
1. Enough children are born to keep the disease spreading
Endemic disease
301
1. A population’s cultures
2. What percent of apopulation is disadvantaged, e.g. have poor sanitation and few medical services available
3. Is the population disrupted (war etc.) such that there are reduced medical services
4. Is there crowding
5. The present herd immunity of the population
Population factors
302
1. Is the climate hot vs. cold
2. Is there pollution
3. Is there proximity to emerging microbes
Environmental factors
303
1. How virulent is the strain of microbe e.g. does it generate symptoms that encourage the microbes spread: severe diarrhea
2. What is the incubation period of the microbe
3. How contagious is the microbe
Microbial factors that influence an epidemic
304
b. The longer the incubation period,
the greater the risk for generating an epidemic (the disease has more time to spread before it’s detected)
305
c. The shorter the incubation period,
the more rapidly a person gets sick and stays home, reducing the microbe spread and the risk of an epidemic
306
a. Are spread person to person or by fomites
| b. Enter the body via skin and mucous membranes
direct contact disease
307
c. Are caused by microbes that
i. Are sensitive to drying and temperature variation
ii. Are associated with capsules and pus formation
iii. Produce toxins, enzyme, etc. that the microbe uses to invade
iv. Stimulate an immune response only if the microbe contacts cells of the immune system
direct contact disease
308
a non living object which transmit the microbe, but on which the microbe cannot multiply
=fomites
309
a. Enter the body via the mouth
b. Are influenced by a dilution factor
c. Feces are the usual source of contamination
d. The pathogen is usually an intestinal G- negative rod
e. Prevention will increasingly depend upon controlling contamination of feed and water and animals themselves
Food and waterborne diseases
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i. The greater dilution of microbes in water generates a long incubation with few cases of the disease appearing
ii. Less dilution by food generates a shorter incubation period and more cases of the disease
311
i. Usually have animal reservoirs
ii. Contamination tends to occur early in the production process
iii. Centralized production and wide distribution of products encourages widespread epidemics
feces source of contamination
312
i. Beef
ii. Poultry
iii. Etc.
Prevent - avoid these things
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a. Enter the body via the inhalation of droplets, dust, dry skin or spores
b. Involve microbes that are the least susceptible to drying
Airborne disease
314
a. May be influenced by a dilution factor
| b. The route of transmission most closely associated with epidemics
Airborne disease
315
i. The greater dilution of microbes outdoor reduces exposure to the microbe
ii. The reduced dilution indoors explains the need for good ventilation and dust control to reduce the spread of airborne diseases
316
a. May involve a vector or fomite
b. Usually stimulate good immunity
c. Not typically associated with epidemics
Inoculation diseases
317
1. Are the sum of all constant sources of the microbe – include places where microbes replicate in nature (water, soil, animals, humans)
Reservoirs
318
a. Are diseases acquired in a hospital or other medical facility
nosocomial infections
319
i. During the 60’s and 70’s, Gram negative bacteria were the leading cause
ii. Gram + bacteria have emerged as the leading cause, eg.g. MRSA, VRE, and Clostridium difficile
nosocomial infections
320
c. Transmission of these diseases include
i. Invasive procedures involving individuals in an already weakened state (increasing numbers of imunodeficient patients)
ii. Person to person contact
iii. Contact with contaminated equipment
iv. Airborne
nosocomial
321
d. Often involve resistant microbes
nosocomial
322
i. Hand washing and/or hand sanitizers
ii. Sterilizing equipment etc
iii. Controlling the generation of antibiotic resistant microbes
nosocomial
323
something alive that transmit a disease
vectors
324
i. An animal that transmits the disease microbe from one host to another
animal vector
325
ii. Usually involves inoculation
| 1. E.g. mosquitos and ticks
animal vector
326
1. Diseases that can be transmitted to humans from animals
zoonoses
| animal vector
327
i. A human that transmits disease
| ii. May never have signs or symptoms of the disease
carriers=human vectors
328
1. The individual is colonized
2. Most transmissions occurs during the incubation period of the disease or during convalescence
3. Can transmit disease via all routes of transmission
human carriers
329
1. Increase the population’s resistance to diseases
2. Reduce the number of reservoirs and vectors
3. Be sure hospitals are using aseptic techniques and provide dust control and ventilation
4. Encourage people to WASH THEIR HANDS/sanitize
5. Increase the number of health networks to provide better suveillance
Prevention of Epidemics
