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143 terms

Microbiology Immunity and Disease

What is the Germ Theory of disease? What did Robert Koch discover?
Theory that proposes that microorganisms are the cause of many diseases. Robert Koch discovered anthrax was caused by the bacterium Bacillus anthracis > This validated the Germ Theory.
Koch's Postulates?
To follow these: (1) microbe must me associated with infected organism at all stages of disease (2) microbe must be isolated into pure culture and characterized (3) when a healthy organism is inoculated with the suspect microbe, the original signs and symptoms must be reproduced (4) microbe must be reisolated from the newly infected organism and the identification confirmed.
Procedures of Koch's Postulates
(1) Suspected pathogen is isolated into pure culture from a diseased organism. (2) The characteristics of the pathogen are noted and an initial identification is made.(3) Pathogen is introduced into a healthy host. (4) Test subjects are examined for signs and symptoms to see if they match the initial disease. (5) Pathogen is reisolated into pure culture. (6)
Identification is confirmed.
What is symbiosis?
Relationship between you and your normal microbiota; literally means living together.
Describe the types of symbiotic relationships.
(1) Mutualism: both partners provide a benefit to each other; example: E. Coli in your large intestine synthesizes Vit. K, which you need and can absorb into the blood. In return, you provide E. coli with a perfect environment with lots of food. (2) Commensalism = if only one partner derives a benefit, but the other is not harmed (3) Parasitism = if one partner derives a benefit at the expense of the other; example: anytime a microbe has made you sick, multiplying itself at the expense of your cells.
*Remember - if conditions change, relationships change; "opportunistic pathogens"
Both partners provide a benefit to each other; Exl - E. Coli in your large intestine synthesizes Vit. K, which you need and can absorb into the blood. In return, you provide E. coli with a perfect environment with lots of food.
The relation between two different kinds of organisms when one receives benefits from the other without damaging it. Exl - The bacteria on our skin is commensalism. Bacteria on our hands are getting food/good environment, but do not typically harm us.
If one partner derives a benefit at the expense of the other; Exl - anytime a microbe has made you sick, multiplying itself at the expense of your cells.
Normal Flora
Good Bacteria. Part of Body's Natural Defense. Began colonizing you at birth, rapidly establishing unique microbial communities in the different environments of your body. Protect you from colonization by transient microbiota, bacteria that might live temporarily on your body. Metabolic activites of your normal flora may change the pH of body environments, preventing colonization by certain organisms. Some might even fight against certain bacteria by producing
bacteriocins, chemicals that prevent bacterial growth.
What is an opportunist?
Organisms that are harmless in one circumstance but that can cause disease under certain conditions. Members of your normal microbiota can be opportunistic pathogens. (ex. E. coli)
How is an opportunist different than a true pathogen?
Primary Pathogens are the microorganisms that cause diseases in healthy individual. Opportunistic Pathogens are the microorganisms that are ordinarily in contact with the host and cause disease when the host's resistance is low.
What is disease?
Occurs when there is an abnormal change in the physiology of the body.
What is an infection?
Any colonization of the body by a pathogenic microbe; not all infections result in disease
How are signs, symptoms, and syndromes different?
Symptoms - subjective and may not be observable by a health care worker. Signs - physiological changes that can be observed. Syndrome - combo of signs and symptoms associated with particular disease.
Subclinical infection
an infectious disease not detectable by the usual clinical signs
Primary infection
an original infection from which a second infection can occur. directly leads to disease.
Secondary Infection
If body's defenses are weakened by a primary infection, then disease may result from a secondary
infection by an opportunistic pathogen. (ex. When HIV weakens immune system and makes it
susceptible to second infections; death from AIDS typical results from one of these secondary
Seven Steps to Cause Disease
1st: Maintaining a Reservior 2nd: Enter Host 3rd: Attach to Host Cell 4th- Invade Deeper 5th- Evade Defenses 6th- Multiple and Cause Disease
Three types of Reservoirs?
humans, non-human animals (called
zoonoses), and nonliving surfaces.
What is a reservoir?
anything (a person or animal or plant or substance) in which an infectious agent normally lives and multiplies
Give examples of the three types of reservoirs - an example of a virus at each one.
Humans- staphylococcus aureus, carried in their noses.
Animals- West Nile Virus, rabies - zoonotic diseases that can spread from animal to human
Nonliving surfaces- Vibrio cholera and Salmonella typhi, both can multiply in water, cause diarrhea
What is the difference between someone who is sick and someone who is a carrier?
Someone who is sick shows signs of the pathogen being present and has the symptoms of
disease. Someone who is a carrier has the opportunistic pathogen colonized in them, but does not
have signs of the disease. These people can spread the pathogen to other and make them sick.
What happens after a reservoir is maintained?
Transmission, pathogen enters the host through portal of entry.
What is transmission?
Transmission is the way of the pathogen traveling from the reservoir to the host.
Direct contact transmission
Occurs when the host actually touches the reservoir. Such as
when kissing, touching, etc.
Indirect contact transmission
Occurs when the pathogen is transferred from the reservoir
to a nonliving object where it colonizes. These objects are called fomites which are these nonliving objects. Examples are toothbrushes, and drinking glasses.
Droplet Transmission
Occurs when pathogens are transmitted in mucus as it travels short distances owing to sneezing and coughing. Considered indirect transmission.
Vehicle transmission
A vehicle such as water, food, or air may bring the pathogen from the reservoir to the person.
Fecal-oral transmission
When the diarrheal pathogen is transmitted from the feces of one person and then consumed by another.
Airborne transmission
Common for transmission respiratory illnesses such as the flu, tuberculosis, and the common cold.
Vector transmission
Pathogens are brought from the reservoir to people by the action of animal vectors. Most common vectors are insects and arthropods such as ticks and fleas.
Two different types of vector transmission?
Mechanical & Biological
Mechanical Vector Transmission
The pathogen is carried on the surface of the vector, basically hitch- hiking a ride. Great example is when flies bring the pathogen from feces to food.
Biological Vector Transmission
Biological- when the pathogen enters the body of the vector and is transmitted to the host by biting, defecation, or vomiting of the vector. Example- biting by ticks.
What is a virulence factor?
Any molecules that a microorganism makes and that help them to cause disease. Basically they are a tool kit of a pathogen.
How do microbes attach to cells?
Microbes have adhesins on the surface of them, which are molecules that the bacteria use to attach to receptors on the host cell. These adhesins are often found on structures used for attachment like fimbriae and glycocalyx.
Why are biofilms good if you are a bacterium?
Biofilms are dense communities of microbes consisting of one or more species of microbes embedded in a matrix of sticky molecules. An example is the slick coating on our teeth in the morning or the smooth rock coated with slippery substances at the beach. The matrix helps the
members of the biofilm attach and protects them from drying out and from being killed off by antimicrobial substances.
What virulence factors help adhesion?
Name enzymes that help microbes invade. How do these work?
(1) Enzyme Collagenase (2) Hyaluronidase (3) Enzyme Fibrinolysin. (4) Some bacteria produce hemolysins that enable them to lyse red blood cells (5) Enzyme Invasins allow pathogens to rearrange the cytoskeleton of the host cell.
Enzyme Collagenase and Hyaluronidase
Help break down molecules like collagen and
hyaluronic acid that support cells and hold them together. This allows the pathogens to penetrate into the host tissues.
Enzyme Fibrinolysin
Breaks down the fibrin that holds blood clots together and may enable a bacterium to move beyond a clot and continue its spread through the body.
Enable them to lyse red blood cells, which contain
nutrients like iron that may be essential for bacterial growth.
allow pathogens to rearrange the cytoskeleton of the host cell. This can allow the pathogens to enter the cell and even use the cytoskeleton to move through the cell and then infect neighboring cells.
Why do bacteria want to invade
deeper instead of remaining on the surface of tissues?
Bacteria want to invade deeper instead of remaining on the surface of tissues in order to grow, spread, and multiply faster. If they are on the surface of tissues, they are more likely to be killed off by TcCells. By invading deeper, they are able to hide inside of tissue/cells in order to evade the body's defense system.
What is coagulase, how does it work?
The enzyme used to convert host fibrinogen to fibrin, the material that is the basis for blood clots. Staphylococcus aureus uses this enzyme to hide under a pile of the fibrin molecules to effectively hide from phagocytes.
How does a capsule help a bacterial pathogen evade defenses?
The capsule is used by pathogens in order to evade phagocytosis. If the pathogen is inside a capsule, it is considered virulent and phagocytes cannot bind to it to kill it. If it does not have a capsule, then they are not considered virulent and generally don't survive in the body.
How can bacteria deactivate antibodies, complement?
When complement proteins cannot bind to molecules on the
surface of bacteria. This can be because of a surface protein that is present to which the complementary protein does not bind to. Other pathogens avoid complement activation by
causing it to occur at a safe distance from the surface of the cell. An example is when some gram-negative bacteria have long polysaccharides that trail off their surfaces, while others
may actually shed their polysaccharides.
How do other pathogens evade immunity?
Evasion of adaptive immunity is more challenging for pathogens to avoid. (1) Some bacteria
produce IgA Protease which destroys IgA antibodies that are common on the surfaces of mucous membranes.
(2) Bacteria/viruses that multiply in host cells can hide their antigens from being displayed on the cell surface. If they were displayed, then they would be subject to
destruction by Tc Cells. (3) Other bacteria turn their genes on and off to change their antigens. This is called
Antigenic Variation. After the B-cells are activated, antibodies are produced. By this time, the pathogen has changed and the antibodies will not bind to the new antigens on the pathogen.
Antigenic Variation
Bacteria turn their genes on and off to change their antigens. It prevents the immune system from making the correct antibodies to attack the pathogen. After the B-cells are activated, antibodies are produced. By this time, the pathogen has changed and the antibodies will not bind to the new antigens on the pathogen.
What is the goal in life of a bacterium?
Multiply and then show signs and symptoms of disease by
destructing host tissues and having the body respond to the infection.
What does a bacterium need in order to fulfill this goal?
A lot of bacteria require Fe to grow. They also need to be able to cause damage to the host cells or impair their function in order to survive and operate the way that they need to.
These negative effects on virally infected host cells are called Cytopathic Effects.
A siderspore is a protein that is produced by bacteria because they are able to take away iron from host proteins like transferrins that carry iron around in the body.
How are exotoxins and endotoxins different?
Exotoxins are toxic substances secreted by bacteria and released outside of the cell. Whereas Endotoxins are bacterial toxins composed of lipids that are within a cell.
Proteins that are made inside the cell and then released. They are made by both gram-positive and gram-negative bacteria. Since they are proteins, each exotoxin has
a specific function and they may be denatured by heat or chemicals. They are highly immunogenic. Because of this, effective vaccines against exotoxins can be produced.
Denatured Endotoxins
Three types of Endotoxins
A-B Toxins, Superantigens, Membrane-disrupting toxins
A-B Toxins
Type III toxins, all are similar in structure. Made of an Active subunit and a Binding subunit. When synthesized in a bacterial cell, they are inactive. Once it leaves the bacterial cell, the B-subunit lets it bind to and uptake into a host cell and
then the A-subunit is activated and carries out the specific function of the subunit.Some act as neurotoxins and inhibit neurotransmission.
Type I toxins, cause nonspecific activation of TH Cells. Usual
activation is about 0.01% of the total population of these cells. Presence of Superantigens may cause an activation of up to 25% of the total population which leads to an abnormally strong immune response. Causes a mass overproduction of
cytokines, resulting in fever, nausea, vomiting, diarrhea, and an excessive drop in blood pressure, and even death.
Membrane-disrupting toxins
Type II toxins, disrupt membranes by forming protein
channels in the membrane or by affecting the phospholipids. Some of these toxins disrupt plasma membranes.
The lipid-A portion of the lipopolysaccharide found on gram-negative cell walls, which are released from the wall as these bacteria die. Since they are lipid, they are
not activated by heat. Even though they trigger an immune response, it is not sufficient to protect fully against the toxin. Because of these 2 factors, effective vaccines against
endotoxins cannot be produced. They are not as specific as exotoxins. All endotoxins form a wide variety of gram-negative bacteria essentially functioning in the same way.
How are portals of exit similar to portals of entry?
For most pathogens, the portals of exit are the same as the portal of entry. This means that most
pathogens leave the body the exact same way they came in. The pathogen is not required to leave
the same way, but in most cases they do leave the same exact way.
Why should we be concerned about global health?
Infectious disease is still highly prevalent globally
Global Health
*Low-income African and Asian countries - infectious disease caused 45% of deaths
*For children, infectious disease responsible for 65% of deaths in children younger than age 5
*Respiratory illness and diarrheal diseases are the two leading killers of children.
*Infectious disease prevalent because of economics, culture, education, sanitation systems are expensive, war, etc.
How did Dr. Snow end the Cholera epidemic?
Between 1831 and 1854, four cholera outbreaks in London resulted in deaths of tens of thousands of
people. The last outbreak was the worst, killing 127 people in the first 3 days alone.
Dr. Snow who lived in the area examined the water from the well and found that it contained white
He thought this was the source of cholera and has authorities to remove the handle from the pump
so that no one could drink out of the well; as soon as this happened, incidence of cholera dropped
dramatically and epidemic ended.
What is Dr. Snow the founder of?
Science of epidemiology.
# of new cases of a particular disease is greater than what is normally expected in the
When they are spread around the globe and affect more than one continent or population.
Certain diseases are constantly present at a relatively stable; "endemic" to that region
Diseases that occur occasionally within a population
nosocomial infection
hospital-acquired infectious
What contributes to these nosocomial infections?
1. Hospitals filled with sick people, so many reservoirs of disease
2. Patients in hospital may be compromised; their immune systems may be weakened by a
primary infection, or surgery or burns may have broken their skin
3. Lots of opportunities for transmission of disease as health care workers travel from patient to patient
Give examples of chemical surface defense in the epidermal? How does each prevent microbes from gaining access to our system?
Chemicals >>> Epidermal: (1) PH - Slightly acidic Why? Due to the fatty acid component of sebum (the oily
secretion from your sebaceous glands)
Give examples of chemical surface defense in the mucous membrane? How does each prevent microbes from gaining access to our system?
(1) mucus (a thick substance that traps microbes as they are inhaled or eaten).
(2) Lysozyme in perspiration, tears, saliva, nasal, tissue fluids (breaks down peptidoglycan and
causes the lyse of bacteria)
(3) Mucous Membrane is also protected by the PH. Gastric PH is around
Body PH
Give examples of physical surface structures that defend in the mucous membrane/epidermal? How does each prevent microbes from gaining access to our system?
Epidermal: (1) Flakes off routinely taking microbial visitors with them. (2) Keratin - a hard tough
protein that reinforces the epithelial cells - microbes would need to get past this in order to
penetrate the skin. (3) Microbes would also have to penetrate the many layers of closely packed
cells which make up the epidermis/mucous membranes.
Give examples of mechanical surface defense in the mucous membrane/epidermal? How does each prevent microbes from gaining access to our system?
Mucous Membrane: (1) Ciliary Escalator: rows of cila that sweep rows of microbe laden mucous
toward the throat where it can be coughed out of the body. (2) mechanical washing: tears (eyes),
urine (urethra), saliva (mouth), secreations (vagina)
Describe the steps of phagocytosis.
1st- Finding. Phagocytes need to find the pathogens. - they are attracted to the scene of the crime
by chemoattractants (released from the damaged cell, or part of microbes themselves)
2nd-Adherence. Receptors on the phagocyte bind to molecules on the microbe.
3rd. Phagosome Engulfs! Phagocyte forms pseudopods. Pseudopods surround the microbe and fuse
together, enclosing the microbe in a membrane bound sac called phagocytic vesicle, or phagosome.
4th-Digestion. Triggered when the lysomsomes fuse with the phagosome forming a phagolysome.
Microbe in the fused vesicle is digested by lysomomal enzymes within the whole phagolysome
5th- Removal - Digestion leaves a residual body, which is filtered out of the cell along with the
indigestiable material (this is called exocytosis)
Which white blood cells are important phagocytes?
1. Neutrophils (highly phagocytic, #'s increase in early infections, most abundant WBC in blood
2. Eosinophil (Somewhat Phagocytic. Important Defense against parasitic worms)
3. Monocytes (Migrates to tissues and differentiate into Macrophages)
What are the classic signs of inflammation?
Redness (Erythema), Pain, Swelling (Edema), Heat
Summarize acute inflammation by giving its purpose: (1) Destroy/Contain invading organism, (2)
Repair/Replace Wounded Tissue
Systemic response.
Affects the entire body.
How does fever help our body fight an infection?
Fever has the benefits of: (1) Enhances several of our defenses (2) slow growth rate of some
organisms and speeds up the repair in the body (3) Releases the protein, "transferrins" (which
binds up Fe and keeps it away from microbes that need Fe for growth) (4) Increased production of
4 Parts of Complement
(1) Made out of protein (2) works as a cascade (starts off as a small response but gets larger and larger.) (3) Complement enhances inflammation and phagocytosis. This tells us, that the C3 protein has been activated and has activated other proteins leading to the lysis of microbial cells. (4) Complement results in formation of the Membrane Attack Complex.
What is the effect of the Membrane Attack Complex?
Cytoplasm leaks out through the ring of proteins causing the microbial cell to lyse.
How do Interferons protect against virus infections?
Interferons - help defend by warning neighbor cells to prepare against a viral infection.
By (1) Signaling neighboring cells to produce antiviral proteins (AVPs) such as nucleases that
degrade viral nucleic acid when it enters cell.
(2) Activate proteins that are involved in apoptosis (this makes neighbor cells more likely to
commit suicide if infected)
Circulate blood and lymph, migrate into tissues.
Purpose - Immunity
Wandering macrophages migrate through tissues, fixed macrophages remain in a tissue.
Purpose - Highly phagocytic
Granulocyte, granules stained with basic stain, circulate in blood, can migrate into tissues.
Purpose- Release histamine.
Granulocyte, grandules stained with acidic stain, released into blood migrate into tissues.
Purpose- Somewhat Phagocytic. Important in defense of worms.
Granulocyte, Leukocytes owing to the highly bobed nucleus relased into blood, migrate
to tissue.
Purpose - Highly Phagocytic. Number increase early in infections.
How is active and passive immunity different?
Active immunity is a form of immunity that develops after a primary immune response which is a response to exposure to a live pathogen and development of symtoms. The cells produce the antibodies themselves.

Passive immunity is a form of immunity in which a person's cells do not produce the antibodies, they receive them by an injection of antibodies or antitoxin.
Active immunity
any time our immune system responds to a pathogen; typically called long-lasting
Naturally acquired active immunity
if active immunity is triggered in response to an infection
Artificially acquired active immunity
if active immunity is triggered by vaccine
Passive immunity
short-term; acquired by receiving defensive proteins called antibodies from someone else
Naturally acquired passive immunity
breast-fed babies receive antibodies from their mothers
Artificially acquired passive immunity
if you are exposed to some pathogens, such as hepatitis
virus, it is possible to receive an injection of antibodies to help clear the virus from your system.
*Chemicals released by T helper cells that stimulate B cells
*Lymphocytes communicate with each other and with phagocytes by means of these special communicating
special type of cytokines that are often used to communicate between white blood cells; effectiveness of immune system depends on the communication
*Antigens = molecules that trigger the production of defensive proteins called antibodies.
*A microbe entering the body is basically a little ball of antigens; typically large molecules like proteins
and polysaccharides.
*For WBC to respond to antigen, must have a receptor on its surface that can bind to it; each receptor
is very specific and can only bind to a particular subunit of the antigen called "epitope" or "antigenic
When is the immune response activated?
Immune response is activated when the cells of the immune system recognize that something foreign
has entered the body; they are actually responding to antigens
What are antigen presenting cells? How do they work?
For antigens to trigger an immune response, they must be recognized by lymphocytes, esp. T
lymphocytes or T cells. T cells arise from stem cells in the bone marrow and are then processed in the
thymus, after which they can differentiate into several different types of T cells. Helper T cells (T H cells)
play a central role in coordination of immune response, releasing cytokines that activate phagocytes
and other lymphocytes. Cytotoxic T cells (TC cells) recognize and destroy body cells that are infected or
cancerous. All T Cells recognize and bind to antigen with a receptor called the T-cell receptor. Different
types of T cells can be distinguished by another surface protein, which has different forms. T H cells have
a surface protein called CD8.

Activation of TH cells by antigen is important to immune response; For TH cells to antigen with their T-cell
receptor, the antigen must be presented to them by antigen-presenting cell (APC), such as a phagocyte,
dendritic cell, or B Cell. When phagocytes or dendritic cells encounter microbes, they take them in
and break them down. As the microbe is being broken down into its component parts, fragments of
microbial antigen are then displayed on the surface of the antigen-presenting cell where they can be
recognized by TH cells.
IgM - Structure
pentamer (5 bivalents)
IgA - Structure
dimer (two bivalents attached by secretory component or J chain)
IgG - Structure
IgD - Structure
IgE - Structure
IgM - Location
in blood and lymph, monomer (bivalent) is surface receptor on B cells
IgA - Location
secretions such as mucous and breast milk, blood, lymph
IgG - Location
IgG = circulates in blood and lymph, present in intestine, can cross into tissues including the placenta
IgD - Location
IgD = surface of B cells, blood, lymph
IgE - Location
IgE = bound to surface of basophils and mast cells
IgM - Function
IgM = produced 1st in response to infection, very effective at "agglutination" (clumping of antigens)
IgA - Function
IgA = naturally acquired passive immunity to newborns, defends against pathogens on mucosal surfaces
IgG - Function
IgG = defends against circulating bacteria and viruses; protects fetus
IgD - Function
IgD = antigen receptor
IgE - Function
IgE = antigen receptor
What is the difference between Helper T cells and Cytotoxic T cells?
Helper T Cells play central role in coordination of immune response, releasing cytokines that activate
phagocytes and other lymphocytes.

Cytotoxic T cells recognize and destroy body cells that are infected or cancerous.
Humoral immunity
= production of antibodies by B cells; B cells arise from stem cells in bone marrow ad
then mature and migrate to lymphoid tissues, where they produce antibodies. Each B cell has surface
receptors specific to that epitope. For antibody production to occur, B cells must be activated by
Two categories of antigens that activate B cells:
T-dependent antigens and T-independent antigens
Activation by T-dependent antigens requires ...
... requires cytokines from TH cells. Activation my T-independent antigens does not require cytokines from Thelper cells.
Activation by T-dependent antigens gives ____ response, resulting in __________
... gives stronger response, resulting in development of immunologic memory. Activation by T-independent antigens is weaker and does not result in immunologic memory.
Explain what happens when a B-cell is activated
In order for a B cell to be activated, it must first encounter antigen. T-dependent antigens are processed
by the B cell and resented to TH cells within the MHCII on the surface of the B cell. A TH cell that
recognizes this antigen binds to the MHCII-antigen complex on the B cell, receives a co-stimulatory
signal, and releases cytokines that stimulate the B cell to divide and differentiate. This "clonal selection"
and "expansion" of B cell results in proliferation of B cells that can respond to this particular antigen.
Some of the B cells differentiate into antibody-producing cells called plasma cells, which are relatively
short-lived. Antibodies produced by the plasma cells are released into the blood and tissues where they
will bind to the antigen recognized by the B cell. Some of the B cells differentiate into memory B cells,
long-lived B cells that can rapidly divide and differentiate when they encounter antigens. Memory B and
T cells are the basis for the immunologic memory that protects you from repeated infections by some
cell mediated immunity
Any adaptive immune response in which antigen-specific effector T cells dominate. It is defined operationally as all adaptive immunity that cannot be transferred to a naive recipient with serum antibody. Cell-mediated immune responses include CD4+ T cell-mediated activation of macrophages that have phagocytosed microbes and CD8+ cytolytic T lymphocyte killing of infected cells.
Describe the steps in the activation of specific immunity starting with an infected cell and ending
with a Cytotoxic T cell and apoptosis. [This is cell mediated immunity.]
(1) Activated TC binds to MHCI of infected host cell with its T-cell receptor. (2) TC releases perforins (3) Perforins penetrate host cell membrane and cause cytoplasm to leak out.
*Cytotoxic T cells recognize abnormal antigen displayed in major histocompatibility complex type I and
destroy the infected or cancerous cells. (p. 386, Fig. 19.7 for diagram)
Humoral immunity
Refers to the production of antibodies by B cells. B cells arise from stem cells in bone marrow and then mature and migrate to lymphoid tissues where they produce
How are plasma and memory B cells different?
Plasma cells are short-lived; antibody-producing; antibodies produced by plasma cells are released into
blood and tissue where they will bind to the antigen recognized by the B cell.

Some of the B cells differentiate into memory B cells, long-lived B cells that can rapidly divide and
differentiate when they encounter antigen. Memory B and T cells are the basis for the immunologic
memory that protects you from repeated infections by some pathogens.
T-independent antigens
*can stimulate antibody production, but they don't usually trigger the production of memory B cells, and therefore don't establish immunologic memory.
*are long, repetitive molecules like certain polysaccharides that have many copies of one epitope. If the epitope simultaneously bind to enough B-cell antigen receptors, it can
trigger the B cell to divide and differentiate into plasma cells that produce antibodies specific to the epitope.
How is the secondary immune response different than the primary response?
**Activation of B cells by T-dependent antigens also generates beneficial long-term response = secondary
immune respond (aka immunologic memory or anamnestic response). This response is mediated by
memory B cells and memory T cells leads to very rapid clearance of the pathogen upon a second intro to
the body.

**Primary response - when the body first encounters an antigen and the immune response is triggered,
the first class of antibody to be produced is IgM. These large antibodies are good at agglutinating the
pathogen and helping to restrict its spread. After a few days, the B cells switch into production of IgG
antibodies which circulate through the body, helping to clear the pathogen. During primary response, it
can take more than a week before there is strong production of IgG antibody.

*Look at diagram on p. 392
What is one consequence of an overreaction of the immune system? How does our immune system
prevent this?
Allergies - hypersensitive responses to antigens called allergens, overactive immune responses

Allergy shots - desensitization (immunotherapy); get an injection with allergens that you are allergic to;
this causes isotype switch from IgE back to IgG. Can take years.
Who first instituted hand washing as a control of microbial growth?
Dr. Ignaz Semmelweis first demonstrated that handwashing can reduce disease transmission.
Complete killing of all organisms (including spores, viruses - typically achieved by a combination of heat and pressure)
Only vegetative cells are killed and spores and viruses remain. Removal of microbes from inanimate objects. Achieved by: chemicals (aka disinfectants)
Living tissue is disinfected (sepsis - decay). Achieved by: chemical called antiseptic
aseptic technique
steps necessary to ensure an environment free from pathogens - Used in Micro Lab. Used in surgery.
Living tissue is wiped clean.
Indicates Killing.
Indicates inhibition of growth.
What affects chemical control methods? How are they affected?
1- Number of Microorganisms present in the population: the greater the number of
microrganisms present in the population, the longer it takes to kill them.
2- Duration of Exposure - the longer the exposure the greater the reduction in the microbial
3- Composition: If resistant organisms (endospore producers, unenveloped viruses) it will be
more difficult to sterilize.
4- Concentration: Typically, the greater the concentration the greater the antimicrobial activity
(not true with rubbing alchols)
5 - Temperature of the environment - Some chemical disinfectants work better at a slightly
elevated temperature - This is why it's best to clean with hot water.
Think back to chapter 6... Describe three examples of how changing the physical properties of an
environment can control growth. Which is sterilization and which is disinfection?
Changes in physical properties which affect growth: Temperature, PH, Concentration, Osmotic
Pressure, Presence of Nutrients.
1) Heat is the most widely used method to control Microorganisms. Moist heat denatures
microbial proteins, where a dry heat oxides various microbial components. Both Sterilize.
2) Autoclave - pressure cooker, uses heat and pressure to sterilize liquids and equipment's
3) Filtration - useful way to sterilize materials that would be damaged by heat such as prescription drugs. Filtration physically screens microbes out of solution to be sterilized.
Who discovered antimicrobial drugs?
• The first synthetic drug was discovered in 1910 by German scientist Paul Ehrlich Discovered this by seeing that some dyes would stain microbes but not animal cells.That led to the concept called Selective Toxicity where the microbial cells are attacked and the host cells are left unaffected.
Who discovered antibiotics?
•The first antibiotic, Penicillin, was first used in the 1940's during the Second World War. But it was discovered in 1928 by a Scottish physician named Alexander Fleming.
Discovered this by an unusual clear area around the mold in which no bacteria grew there. Realized that the fungus was inhibiting the growth of the bacteria.
How are drugs and antibiotics
different? What is selective toxicity?
Drugs are synthetically made while antibiotics are naturally occurring.
What is selective toxicity?
Selective toxicity- when the microbial cells are attacked and host cells are not harmed.
Describe Robert Koch's Experiment
Robert Koch proved that microbes could cause disease in 1872. Koch examined samples of diseased cattle's blood and found that a large rod-shaped bacterium were associated with diseased cattle but NOT with blood of healthy cattle. Koch developed a system for culturing these bacteria in sterile interior of an ox eyeball. Koch achieved a pure culture of the suspect bacteria, then took some of the bacteria and introduced them into healthy cattle. When healthy cattle developed anthrax, Koch took fresh samples of their blood and confirmed that the same bacterium was present bygrowing it in pure culture and examining it again. The two samples of bacteria matched, and Koch has his proof that this bacterium was the causative agent of anthrax. The bacterium is Bacillus antracis, and the series of steps that Kock demonstrated to prove that a particular organism causes a particular disease is called Koch's postulates.