260 Final Flashcards
i. Are well established microbes that don’t cause an overt disease but provide a protective shield against pathogens
normal body flora
- Receive nutrients from the host
2. Locate themselves depending upon their food source
Resident flora
Locate themselves depending upon their food source
a. Fatty acids
b. Mucus – proteins & carbs
c. Secretions and digested food of the digestive tract
Resident flora
i. Produced by skin’s sebaceous glands
ii. Even sweat includes nutrient molecules
fatty acids
i. Linings of
1. Respiratory
2. Digestive
3. Reproductive tract
Mucus - proteins and carbs
i. Saliva contains mucin (active ingredient in mucus) and food particles
c. Secretions and digested food of the digestive tract
ii. Few organisms survive the acids in the stomach and enzymes of the small intestines
c. Secretions and digested food of the digestive tract
iii. Large intestine supports 10 trillion microbes including Archaea
c. Secretions and digested food of the digestive tract
- Normal flora receive nutrients from host and are essential to the health of humans
iii. Maintenance of the Normal Resident Flora
- Flora create an environment that may prevent infections and can enhance host defenses
iii. Maintenance of the Normal Resident Flora
- Antibiotics, dietary changes, and disease may alter flora
iii. Maintenance of the Normal Resident Flora
- Associated with areas in direct contact with the environment
- Inhabit the body sporadically and do not acquire nutrients
iv. Transient flora
- Positive and obligatory relationship for both organisms
Mutualism
- Ex: eukaryotic cells and their mitochondria, infants, and vitamin A producing bacteria
Mutualism
- Is a positive relationship for both organisms but non-obligatory (normal body flora)
Synergism
- Humans and the bacteria in our digestive tracts
Synergism
a. Bacteria synthesize growth factors
i. Vitamins B12
ii. K
iii. Niacin
iv. Thiamin
v. Riboflavin
vi. Folic acid
Synergism
b. Assists with the breakdown of fibrous wastes
c. Stimulate development of the immune system
Synergism
- When a relationships is positive for one organism, and neutral for the other organism (normal body flora)
Commensalism
- Microbes on our skin that consume skin secretions
Commensalism
- Lactic acid bacteria that lower pH of female reproductive tract
Commensalism
- When one organism benefits and the other is harmed (disease)
Parsitism
- When both organisms are harmed
2. Disease
Competition
- When microbes are present
Contamination
- When microbes exist superficially as reproducing surface populations
Colonization
- When microbes enter the tissue
Infection
- When there is noticeable impairment of body function
Disease
i. Involves a microbe vs. noninfectious
Infectious
i. When an infectious disease can spread from one person to another person
Communicable
i. When a communicable disease is easily spread from host to host
Contagious
i. Caused by microbes from outside of the body
Exogenous
i. Caused by microbes already present in or on the body
Endogenous
i. When a microbe can cause a disease only in hosts with impaired immune systems or when relationships become unbalanced.
Opportunistic
i. Characteristics of a disease that can only be felt or observed by the patient
Symptoms
- Headache
- Cramps
- Nausea
- Pain
- Irritatio
- Malaise
- Fatigue
- Chest tightness
- Itching
- Headache
- Weakness
- Anorexia
- Sore throat
Symptoms
i. Characteristics of a disease that can be observed by examining the patients
Signs
- Changes in leukocyte count
- Inflammation and fever
- Elevated antibody titer in the blood
- Septicemia
- Microbes in tissue fluids
- Abnormal chest sounds
- Skin eruptions
- Swollen lymph nodes
- Absecesses
- Tachycardia (increased heart rate)
- Changes in urinr constituents
Signs
i. Over 10,000 white blood cells/uL
Leukocytosis
i. Under 10,000 WBC’s/uL
Leukopenia
i. Combination of signs and symptoms
Syndrome
d. Headache
i. Neutral microbe
ii. Negative to host
e. Fever
i. Negative microbe
ii. Positive to host
f. Inflammation
i. Negative microbe
ii. Positive to host
g. Cramps -> diarrhea
i. Positive microbe
ii. Positive host
h. Nausea –> vomiting
i. Positive microbe
ii. Positive host
i. Coughing
i. Positive microbe
ii. Positive host
j. Sneezing
i. Positive microbe
ii. Positive host
k. Runny nose
i. Positive microbe
ii. Positive host
nonspecific barriers to microbial entry with which a person is born; present at birth; no memory
a. Innate Immunity
- Prevents infection
- Competitive Exclusion
- Physical Barriers
- Chemical barriers
First line of defense
a. When normal flora compete with invading microbes
- Competitive Exclusion
a. Skin
b. Mucous membranes
c. Flushing mechanisms
i. Coughing
ii. Sneezing
iii. Urination
iv. Tears
v. Cilia
vi. Peristalsis
Physical barriers 1st line
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
- Prevents disease
- Chemicals
- Biological barriers
2nd line of defense
a. Complement
b. Interferon
Chemical barriers
2nd line of defense
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
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
- In response to
a. Virsues
b. RNA
c. Immune products
d. Various antigens
Interferon
- Alpha
a. Lymphocytes and macrophages - Beta
a. Fibroblasts & epithelial cells - Gamma
a. T cells
Interferon
- Induce expression of
a. Antiviral proteins
Interferon
- Inhibit expression of
a. Cancer genes
Interferon
iv. Activates an enzyme which blocks the translation of viral m-RNA and an enzyme that degrades viral m-RNA
Interferon
a. Phagocytosis
The absence of receptor sites on cell membranes
b. Inflammation
Biological barriers
2nd line of defense
- Via nonspecific leukocytes (=general WBC)
phagocytosis
- The most common WBC
- Effectively kill bacteria and other microbes
- General purpose
- React early to bacteria and other foreign materials, and to damaged tissues
- Lysozyme and defensins
Neutrophils
- The largest blood borne phagocytes
- Circulate for about 3 days in the blood;
- Then migrate into the tissues and become macrophages and dendritic cells
Monocytes
- Digest antigens into smaller antigenic determinants and present them to cells of the immune system
- APC
Macrophages
anything foreign to the body that initiates an immune response
antigens
distinctive amino acid sequences that mobilizes the immune response
ii. AKA “exogenous” antigens
iii. AKA “epitopes”
antigenic determinants
- Bind to naïve TCD4 cells and secrete the lymphokine interleukin-1
macrophages
chemicals produced by WBCs that target other WBCs and influence their behavior
=lymphokine
i. Helps activate naïve TCD4 clls
Interleukin-1
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
iii. Inflammatory agent
iv. Also induces sleeps, aches, and pains
Interleukin-1
- Will phagocytize antigen and present (epitope) to immune cells
Macrophages
- APC
- Digests antigens into epitopes (antigenic determinants)
- Present epitopes to and activate both naïve TCD4 and naïve TCD8 cells
Dendritic cells
i. When tissues are injured, WBC’s (basophils and mast cells) release chemicals such as histamines, kinins, and prostaglandins
Inflammation
ii. Includes dilation, increased permeability of blood vessels
Inflammation
- “leaky capillaries”
- Redness, swelling, pain (edema), increased temperature, delivers immune component
- Localizes microbes and chemicals used for tissue repair.
Inflammation
- Adaptive
- The recognition and elimination of foreign and/or dangerous antigens
- Takes time to respond
- Has memory
- Prevents death
Acquired Immunity
Third Line of Defense
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
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
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
vii. Help to identify self (all nucleated cells)
viii. Intracellular surveillance (cell infected or cancerous)
ix. Monitored by T cytotoxic cells
MHC-1
i. Associated with the cell membrane of macrophages, B Lymphocytes and dendritic cells
MHC-II
ii. Part of the extracellular surveillance system
MHC-II
iii. When enzymes break down phagocytized antigens into epitopes, the peptides are transported to the cell surfaced attached to these receptors
MHC-II
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
v. Only on macrophages, dendritic cells, and B lymphocytes (APC’s)
vi. Used for extracellular surveillance (cell phagocytized something)
MHC-II
vii. Used for TCD4 cells
MHC-II
a. In the bone marrow, lymphocytic stem cells differentiate into either
T or B cells
B cells stay in
T cells migrate
the bone marrow
to the thymus
- Get a T cell receptor
2. Allow T cell to recognize 1 specific antigen held in an MHC receptor
T cells in thymus
- 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
- Get a CD28 costimulatory receptor
T cells in thymus
b. Both then migrate to
secondary lymphoid tissue
a. Derived from bone marrow lymphoid stem cells that differentiate into immature lymphocytes with T cell receptors
T cells
recognition receptor that is complementary to and allows a T cell to identify an epitope from a specific microbe
T cell receptors
i. T cells whose T cell receptor an recognize “self” epitopes without binding too tightly survive their stay in the thymus
= positive selection
ii. T cells that bind inappropriately to self-epitopes are eliminated
negative selection
- Immature T cell acquires a CD8 receptor if thymic cells present self epitopes to the T cell via an
MHC 1 receptor
- Immature T cell acquires a CD4 receptor if thymic cells present self epitopes to the T cell via
MHC II
receptors are attachment receptors that help T cells bind to MHC-epitope complexes
CD4 and CD8
iii. Immature cells also acquire
CD28 recptor
i. Naïve TCD8 cells emerge from the thymus, each distinguished from the others by its unique
T cell receptor
iii. Dendritic cells have phagocytized and processed antigens into epitopes travel to lymph tissue and present those epitopes to naïve TCD8 cells in
MHC1
- If complementary, the T cell receptor binds to the
epitope
while
2. The CD8 receptor binds to
MCH 1 receptor
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
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
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
b. Synapse with MHC-I receptors presenting the foreign epitope
Effector T cytotoxic cells
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
also produce lymphokines that attract other lymphocytes and macrophages
Effector T cytotoxic cells
a. Involved in delayed hypersensitivity (allergic) reaction that may take several days to develop
- Delayed hypersensitivity cells
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
b. Are long lived cells that remain in circulation after an adaptive immune response is over
Memory T Cytotoxic Cells
c. Ready to quickly become effector T cytotoxic cells
Memory T Cytotoxic Cells
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
are most common of cells associated with adaptive immunity
TCD4
cells also emerge from the thymus, each distinguished from the other by its unique T cell receptor
TCD4
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
- If complementary, T cell receptor binds to the epitope while
- The CD4 receptor binds to the
MHCII
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
- If the synapse is complete, the naïve TCD4 cell will be
activated
will increase in size, divide and differentiate into clones of effector T-helper I & and T-helper II
TCD4
becomes effector t helper 1 in presence of
interleukin XII
becomes effector t helper 2 in presence
interleukin IV
i. Are the “commander in chief” of the immune system
Efffector T helper cells
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
facilitate the activation of naïve B lymphocytes and the production of antibodies
T Helper II
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
encourages activated B cells to stop multiplying, differentiate into plasma cells and start producing antibodies (produced by Helper II)
B cell growth factor
BCGF
= instructs B cells to stop multiplying, differentiate into plasma cells and start producing antibodies (produced by helper II)
B cell differentiation factor
BCDF
= 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
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)
i. Long lived cells that are the result of affinity maturation
Memory T Helper cell
develop from lymphoid stem cells that differentiate into naïve cells in the bone marrow
B cells
acquire Ig (immunoglobulin) or class IgD antibody receptors and ii. Undergo positive and negative selection to become
B cells
from the bone marrow, each distinguished from the others by its unique
Ig receptor
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
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
- 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
- T helper cells use their T cell receptors to examine the MHC II epitope complexes and if its receptor recognizes a ___
complementary epitope
- The T helper begins to produce the co stimulatory molecule ___ II which binds to the B cell ___
Interleukin II
B cell CD24 receptors
Recognition of the epitope plus co stimulation by ___ starts the activation of the B cell
Interleukin II
- 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
=effector B cells
plasma cells
cells secrete antibodies (humoral immunity), protein recognition molecules
plasma cells
=used as B cell receptors
IgD
are the first to be produced, but can’t pass through the placenta
IgM
appear later in primary immune response as result of class switching; most common antibodies and can pass through the placenta
IgG
= produced when plasma cells located in mucous membranes and mammary glands class switch; found in mother’s milk
IgA
normally attacks parasitic worms; allergies if attach to mast cells and basophils
IgE
b. Bind to “Free’ antigens, marking them for destruction by WBC’s
Antibodies
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
reactions where antibodies link soluble antigen molecules (toxins enzymes) making them insoluble and precipitate out of solution
Precipitation
when bacteria, coated with antibodies are more easily consumed by WBC’s
iii. Opsonization
reactions where antibodies link foreign cells to one another
iv. Agglutination
when complement reacts with antibody bound microbes; leads to microbe lysis, phagocytosis of cellular antigens and/or inflammation
v. Complement fixation
i. Can rapidly become plasma cells during a subsequent immune challenge
c. Memory B cells
- Are associated with the cell membrane of all nucleated cells of the body
- Intracellular surveillance (cell infected or cancerous)
MHC 1
- Associated with the cell membrane of macrophages, B Lymphocytes and dendritic cells
- When enzymes break down phagocytized antigens into epitopes, the peptides are transported to the cell surfaced attached to these receptors
MHC II
- T cells
2. Recognizes ONE specific antigen
T cell receptor
- B cells
2. Bind to “Free’ antigens, marking them for destruction by WBC’s
B cell receptor = IG
- T cells
2. attachment receptors that help T cells bind to MHC II-epitope complexes
CD4
- Other T cells have this receptor
2. receptors are attachment receptors that help T cells bind to MHC I-epitope complexes
CD8
- Dendritic cells
2. Co-stimulatory molecule that binds to CD28 on T cells, confirms that antigen presented is not normal.
B7
- Dendritic cells
- 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
- The T helper begins to produce the co stimulatory molecule Interleukin II which binds to the B cell ___ receptors
- Recognition of the epitope plus co stimulation by Interleukin II starts the activation of the B cell
CD24
- T cells
2. Get a costimulatory receptor
CD28
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
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”)
i. Consists of the protective mechanical barriers, phagocytes, and chemical with which you are born
Innate immunity
- Occurs when a “wild type” antigen (microbe) you encounter stimulates an adaptive immune response where
Active
Naturally Acquired Immunity
- You generate your own antibodies, effector cells and memory cells (and probably get sick)
Active
Naturally Acquired Immunity
- 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
- There’s no actual exposure to an antigen, no immune response, and no development of memory cells
Passive
Naturally Acquired Immunity
- 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
- 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
- A primary injection results in an adaptive immune response that ultimately generates memory cells
Active
Artificially Acquired Immunity
- 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
- A preventative technique that protects the individual against future encounters with a dangerous microbe
Active
Artificially Acquired Immunity
- Antibodies are provided by another person/animal
Passive
Artificially Acquired Immunity
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
- Microbes gain a stable foothold at the portal of entry;
2. Dependent on binding between specific molecules on host and pathogen
Adhesion
Attachment
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
a. Produced by some fungi (see ringworms) and digests the keratin in skin
Keratinase
a. Digests hyallyronic acid, an intracellular cementing substance between surface cells
Hyaluronidase
a. Enzyme that digests collagen, the most common protein in the body (CT)
Collagenase
a. Convert plasminogen into plasmin
b. Enzymes that breaks down blood clots
Streptokinase/Staphylokinase
causes a web-like clot that impedes WBC movement
Coagulase
a. Kills WBC’s
Leukocidin
a. Mechanically inferfere with phagocytosis
Fimbriae and Capsules
a. May inhibit digestion by phagocytes
Resistance cell walls
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
- Hemolysins
Viruses enter host cells and take over the resources and machinery of their hosts
Acquisition of host resources
i. Are the lipid A part of the outer membrane of Gram Negative bacteria
ii. Are released when gram negative bacteria die
Endotoxin
iii. Are weak, non specific and cause a fever
iv. Stimulate weak immunity
Endotoxin
v. Are stable
1. Cannot be denature and converted into a toxoid
2. Can’t be used for immunization
Endotoxin
i. Are associated with a few gram positive and a few gram negative bacteria
ii. Are secreted
exotoxin
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
v. Highly specific
1. Neurotoxins
Enterotoxins
exotoxin
a. Attack nervous system
i. Botulin
ii. Tetanospasmin
Neurotoxin
a. Attack organs of the digestive tract
i. Shiga toxin
ii. Cholera toxin
Enterotoxins
i. Clostridium botulinum
Botulism
- Normally and intoxication (toxin is consumed via contaminated food)
Botulism
- Endospores consumed by an infant (infant botulism)
Botulism
- Endospores introduced into a wound
Botulism
- Exotoxin/neurotoxin
Botulism
a. Toxin carried to neuromuscular junctions and blocks Ach release
b. Causes Flaccid paralysis
Botulism
c. Blocks release of neurotransmitter Acetylcholine, which stimulates skeletal and smooth muscle to contract
Botulism
- Paralysis of muscles, including muscles of inspiration
Botulism
iv. Treatment
1. Support
2. Antitoxins
3. Antibiotics (wound)
Botulism
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
- Hemorrhagic colitis = hemolytic uremic syndrome
=shiga toxin
i. Both caused by Escherichia coli O157:H7
=shiga toxin
- Emerged in 1975
2. First detected in 1982 and is now leading cause of acute kidney failure in children
=shiga toxin
- Outbreaks include 2 outbreaks in 1992 (including Jack-in-the-Box outbreaks in Washington)
=shiga toxin
- Transmission
a. Primarily through ground beef, leafy green and unpasteurized beverages
=shiga toxin
b. Can be person to person in households, daycare centers and other institutions
=shiga toxin
iii. Lysogenizes via a viral prophage –> shiga toxin (exotoxin)
=shiga toxin
- Binds to receptors
a. On cells lining small blood vessels
b. That are more common in children than adults
=shiga toxin
- Enters cells and
a. Inactivates ribosomes
b. Stops protein production
=shiga toxin
- Cells die
a. Break down of vessel lining –> blood clots and/or hemorrhage
b. Digestive tract –> hemorrhagic colitis (bloody diarrhea)
=shiga toxin
- Cells die
a. Kidney glomeruli
i. Kidney failure
ii. Hemolytic Uremic Syndrome - ~3000 cases/year
=shiga toxin
iv. Treatment
1. Support
2. No antibiotics
a. dead cells release lipid A
b. antibiotics activate prophage leading to more toxin production
=shiga toxin
v. Prevention
1. Cook your food
2. Avoid ground beef, leafy greens and unpasteurized beverages
=shiga toxin
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
iv. Spread via salt water
v. Exotoxin
cholera toxin
a. Binds to cell receptors lining the intestines
b. Chloride and bicarbonate ion channels open
cholera toxin
- Sodium follows the chloride out of the cell, water follows salt
cholera toxin
a. Creates salt water environment for the bacteria
b. Resultant diarrhea (rice water stools) assists transmission of the bacteria
cholera toxin
vi. Treatment
1. Re-hydration therapy
cholera toxin
vii. Prevention
1. Clean water (4 layers of sari cloth removes 99% of microbes from water in India)
cholera toxin
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
viii. Stimulation of extreme host responses
1. Extreme inflammation
2. Abscess formation
3. Inappropriate blood clotting
cholera toxin
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
i. Tetanus = Clostridium Tetani
Tetanospasmin
ii. Transmission
1. Inoculation
2. Cutting umbilical cord with dirty knife (70,000 infant African deaths/year)
Tetanospasmin
iii. Virulence factor
1. Tetanospasmin
Tetanospasmin
a. Exotoxin
b. Neurotoxin
c. 1 of 3 most powerful toxins known
Tetanospasmin
d. Follows nerve to spinal cord and brainstem
e. Inhibits release of inhibitory neurotransmitters glycine (spinal cord) and GABA (brain stem)
Tetanospasmin
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
iv. Treatment
1. Support
2. Antitoxin
3. Antibiotic
4. Muscle relaxants while anon terminal re-grows
Tetanospasmin
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
i. Agent must be isolated from host displaying the disease, grown in pure culture and characterized by testing
Koch’s postulates
ii. When the agent from the pure culture is inoculated into susceptible hosts, it must cause the disease
Koch’s postulates
iii. The agent must be re-isolated from the diseased host and identified as the original specific causative agent
Koch’s postulates
iv. A specific causative agent must be observed in every case of a disease.
Koch’s postulates
- Disease has a rapid development and course
Acute
- Diseases which are slow and persistent
Chronic
- Diseases have periods of inactivity between attacks
2. Herpes
Latent
- Diseases are confined to a specific area
2. Giardia in intestines
Localized
- When infectious agent breaks loose from a local infection and carried to other tissues
- Tetanus
Focal
- Microbes or their products are In the blood
Sepsis
a. Bacteria and viruses are present in the blood, but don’t multiply
- Bacteremia and viremia
a. Toxins are in the blood
Toxemia
- Microbes are present and multiply in the blood
2. Malaria
Septicemia
- Diseases affect the entire body
systemic
- Diseases represent an initial infection
Primary
- Diseases represent an infection that follows a primary infection, usually as the result of the patient having been weakened by the primary disease
Secondary
- The time between infection and the appearance of signs and/or symptoms
Incubation period
- The short period of time when non-specific symptoms appear (the effects of interleukin-I)
prodromal
- The period when the disease develops signs and symptoms characteristic of the disease
Invasive
- Critical stage
2. The period of the most intense symptoms
Acme
- Host immune response begins killing the pathogen
2. Symptoms characteristic of the disease begin to decrease
Decline
- The recovery phase when tissues repair and healing takes place
- No symptoms of the disease, but microbes may still be present
Convalescence
i. Selective agents
ii. Artificial passive immunization
iii. Boosting host defense mechanisms
iv. Reduce symptoms
v. Vaccine
Treatment for infectious diseases include
- Antibiotics
- Antivirals
- Sulfa drugs
Selective agents
- Homologous pooled human antibody- gamma globuins
- Homologous human yperimmune globulins
a. Convalescent serum
b. Diptheria – 1st disease cured 1891 - Heterologous hyperimmune serum
a. Antitoxin
b. Neutralizing antibodies
Artificial passive immunization
- Administering gamma interferon
- Use of interleukin II
- Good nutrition
Boosting host defense mechanisms
- Aspirin
- Fluids
- Etc.
Reduce symptoms
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
- Provides herd immunity
- Long term
- Stimulates B and T cell formation and differentiation
Artificial active immunization
a. Developed first natural vaccine for smallpox
i. Variola major and minor
Jenner
i. Small pox killed 1 in 3 (500 million victims during 20th century)
ii. Variolation
Small pox
- 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) - Live virus grown on skin of calves
- Arm to arm
small pox
a. Hybrid mix of cowpox and smallpox viruses
b. 1 dose of dried calf lymph
Dryvax
a. Smallpox eradicated – herd immunity
b. DNA virus, no mutations
c. NO question who was infected
1979
a. Discovered principle behind vaccinations
b. 1st laboratory developed a vaccines for rabies and anthrax
Pasteur
- Italian for 40 days
2. First attempted in 14th century Venice to stop Bubonic plague; ships remained at anchor for 40 days
Quarantine
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
- 1849
2. Traced a cholera outbreak to a water pump
John Snow
- Is the number of new cases of a disease seen in a specific time period
Incidence
- Corresponds to the number of people infected with a specific microbe at any one tme.
ii. Prevalence
- Number of deaths per population at risk
Mortality rate
- Disease must be communicable from person to person
2. Each host must spread the disease to at least two other people
Propagated epidemic
- Usually begins with an index case
a. =the first person to bring a disease into a community
Propagated epidemic
- When multiple hosts come in contact with the same microbe source
- The disease may not be communicable
a. Everyone eats same potato salad or water
Common source epidemic
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
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
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
a. When few new cases appear
Decline phase
Phases of epidemic disease transmission
a. If a population is small and the host is not motile, the epidemic will disappear
Epidemic aftermath
the disease spreads to at least two continents
Pandemic disease
a disease persists in a population
Endemic disease
ii. The population must be threshold for a disease
Endemic disease
iv. An endemic disease usually becomes a childhood disease
v. Controlled by vaccines (reduces the number of susceptible people)
Endemic disease
iii. Be large enough that it can continuously generate susceptible people
1. Enough children are born to keep the disease spreading
Endemic disease
- A population’s cultures
- What percent of apopulation is disadvantaged, e.g. have poor sanitation and few medical services available
- Is the population disrupted (war etc.) such that there are reduced medical services
- Is there crowding
- The present herd immunity of the population
Population factors
- Is the climate hot vs. cold
- Is there pollution
- Is there proximity to emerging microbes
Environmental factors
- How virulent is the strain of microbe e.g. does it generate symptoms that encourage the microbes spread: severe diarrhea
- What is the incubation period of the microbe
- How contagious is the microbe
Microbial factors that influence an epidemic
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)
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
a. Are spread person to person or by fomites
b. Enter the body via skin and mucous membranes
direct contact disease
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
a non living object which transmit the microbe, but on which the microbe cannot multiply
=fomites
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
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
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
i. Beef
ii. Poultry
iii. Etc.
Prevent - avoid these things
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
a. May be influenced by a dilution factor
b. The route of transmission most closely associated with epidemics
Airborne disease
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
a. May involve a vector or fomite
b. Usually stimulate good immunity
c. Not typically associated with epidemics
Inoculation diseases
- Are the sum of all constant sources of the microbe – include places where microbes replicate in nature (water, soil, animals, humans)
Reservoirs
a. Are diseases acquired in a hospital or other medical facility
nosocomial infections
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
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
d. Often involve resistant microbes
nosocomial
i. Hand washing and/or hand sanitizers
ii. Sterilizing equipment etc
iii. Controlling the generation of antibiotic resistant microbes
nosocomial
something alive that transmit a disease
vectors
i. An animal that transmits the disease microbe from one host to another
animal vector
ii. Usually involves inoculation
1. E.g. mosquitos and ticks
animal vector
- Diseases that can be transmitted to humans from animals
zoonoses
animal vector
i. A human that transmits disease
ii. May never have signs or symptoms of the disease
carriers=human vectors
- The individual is colonized
- Most transmissions occurs during the incubation period of the disease or during convalescence
- Can transmit disease via all routes of transmission
human carriers
- Increase the population’s resistance to diseases
- Reduce the number of reservoirs and vectors
- Be sure hospitals are using aseptic techniques and provide dust control and ventilation
- Encourage people to WASH THEIR HANDS/sanitize
- Increase the number of health networks to provide better suveillance
Prevention of Epidemics
