Microbiology Final Exam New Material

• The ability of an organism to recognize and defend itself against infectious agents
• types: specific immunity, innate immunity, acquired immunity, active immunity, passive immunity

host can defend against a particular agent

due to genetically determined characteristics

• obtained from some method beyond heredity
• can be naturally acquired or artificially acquired

from prior exposure to the agent or from antibodies through placenta or in colostrum

acquired through vaccination or antibody therapy

• hosts own immune system defends against infectious agent
• natural: happens due to environmental exposure to antigen (ie getting the flu)
• artificial: antigen given in a vaccination (triggers immune response, but doesn't make u sick)

• antibodies are given to the host to fight an infection
• natural: provided by the mother through placenta or breast milk
• Artificial: antibodies (not antigens) given through injection- ie if exposed to hep B at work youll get this

• any part of the infectious agent or host cell that is recognized as foreign by the host immune system
• proteins, polysaccharides, glycoproteins, nucleoproteins

• area on the antigen where antibodies can bind
• each antigen may have many epitopes and many different antibodies that can bind to it

small molecules that can act as an antigen IF bound to a larger molecule such as a protein

• proteins made by B cells in response to antigens
• antibodies are specific for particular epitopes on antigens

the amount of antibody necessary to bind and neutralize a certain amount of antigen

• originate as stem cells, first in yolk sac and then in fetal liver
• eventually develop in the bone marrow
• T: mature in the Thymus
• B: matuer in the Bone marrow
• they later meet up in circulation through lymph nodes and other immune organs

named for the Bursa of Fabricius in chickens

• humoral immunity
• cell-mediated immunity

• antibody mediated immunity
• antibodies in the blood made by b cells
• humors- body fluids
• secreted by b lymphocytes that neutralize antigens outside the cell
• extracellular toxins, bacteria, viruses can be combatted by this

• t cells bind with a particular antigen
• cell-bound or intracellular pathogens, viruses, bacteria, cancer cells, fungi, eukaryotic parasites, foreign tissues can be combatted by this system

• host antigens= "self"
• foreign antigens= "non-self"
• during gestation, any antigen recognized by the newly made B or T cells is regarded as self and those cells are "deleted" or inactivated.
• this produces immune tolerance to self
• if a B or T cell survives getstation and recognizes an antigen AFTER development is complete, it will respond to it
• tolerance CAN be induced by radiation (which kills off lymphocytes) and immunosuppressive drugs

body makes many lymphocytes with receptors, most will not bind self, but if any bind self antigens, meaning they react ot our cells, they experience clonal deletion or are destroyed so that they dont attack our own cells

• by Polly Matzinger
• addresses the question- why dont we attack ourselves during puberty or lactation
• if we contain many antibodies to our own DNA and proteins, why are autoimmune diseases so rare?
• this says that perhaps instead of responding to non self, maybe the immune system only responds to danger signals
• says T cells must "see" TWO danger signals in order to make a response- one from the antigen itself, the other a stress or trauma signal from the host
• one signal alone induces deletion of the T cell

• 1. (original theory) lymphocytes are activated by recognition of foreign things
• 2. (first modification) b cells die when they see antigen (signal one) unless rescued by help (signal 2)
• 3. t helper cells die when they first see antigen unless rescued by co-stimulation (signal 2) from antigen presenting cells
• 4. APCs do not costimulate unless activated by PRRS (receptors for evolutionarilly distant infectious non self)
• 5. (danger model, major change) APCS are activated by endogenous cellular alarm signals from distressed or injured cells and they can costimulate T cells as the second signal

its not enough for the Y and antigen to match up, there must also be a danger signal (stress or trauma in the body)

• immune reactions are directed towards a specific epitope on an antigen
• binding of an anitobdy to an antigen is highly specific- that antibody does not normally bind to any other antigens

• rarely, antibodies have cross reactions with similar foreign or host antigens such as
• haptens (smaller, but not recognized until bound to something larger)
• bacterial strains
• viral mimicry- sometimes viruses can mimic mhc we have in our cells (ie type one diabetes- a virus shares same epitope as beta cells resulting in cross reactive immunity, this is how you can get diabetes from a virus, even once its wiped out immune system keeps attacking this antigen in your cells)

• antibodies are specific yet flexible
• heterogeneity: immune cells make MANY different kinds of antibodies specific for a wide range of epitopes (we want to make as many antibodies as possible)
• can even recognize antigens never before seen by any immune system

• depends which genes are turned on
• pieces of DNA code for different proteins
• variable region can differ (this region makes it unique)- each antibody has a constant region and a variable region

• mix and match to give different receptors (like choosing an outfit) to get many combinations
• some people never make a good long term responsee bc they dont make enough antiboides or the right response to fight disease

• occurs randomly
• happens so we can make antibodies for antigens weve never seen before- its possible bc we make so many receptor combinations because of this (result of different variable regions)

by having primary and secondary responses

• you can get this from antigen presented in a disease or in a vaccine
• b cells respond to antigen and make antibodies
• antibodies circulate the body and recognize antigens that they have seen before
• at this time some memory B cells are produced
• the primary response happens when B cells meet their antigen match

• memory or anamnestic (not forgetting) response
• happens if you get the illness again or after vaccine
• larger and faster response than primary
• extremely rapid compared to first exposure
• binding and danger
• b cell is turned on and make clones and some antibodies
• upon second exposure cell binds to virus and acts much faster so you dont get sick

• make antibodies
• activate t cells

• b cells have antibody proteins stuck in their cell membranes
• these proteins act as receptors for specific epitopes of an antigen
• binding of an antigen activates the B cells to divide rapidly and make clones of itself
• when a b cell meets an antigen match they can differentiate into a plasma cell aka effector cell, one that secretes high levels of soluble antibody (2000 per second)

• once an antibody on the surface of a B cell interacts with an antigen, both are taken into the cell
• the antigen is broken down and presented on the surface of the B cell on a molecule called MHCII (major histocompatability complex II)
• t cells recognize antigen attached to MHC II and become activated to do their own defensive work

• Ig
• another name for antibodies
• y shaped protein
• composed of 4 chains
• Constant regions determine class (IgG, A, E, M, or D)
• variable regions determine which antigen can bind

• 2 light chains and 2 heavy chains
• held together by disulfide bonds

• an enzyme that can cleave antibodies causing them to form 2 pieces
• the two pieces are
• --> fab: binds to epidope on antigen
• --> fc: activates complement, which helps with inflammation, acts as opsonin, plays a role in allergy
• Y, fab is the branch part, fc is the base

• IgG
• IgA
• IgE
• IgM
• IgD

• Main IG found in the blood
• recruits phagocytes
• activates complement
• can cross the placenta
• found in breastmilk

• small amounds in blood
• larger amounts in secretions such as tears, milk, saliva, mucuous
• found in abundance in digestive, respiratory and urogenital tracts
• usually the first type on the scene- encountered first when something enters the system but this is before lymphocyte recognition
• surrounds pathogen and tries to prevent it from entering tissue
• secreted IgA is made up of two IgAs held together by a J (joining) chain and secretory component
• binds to microbes to keep them from invading tissues
• activates compliment

• rarely found in blood, more abundant in body fluids and skin
• has to do with allergiEs
• fab fragment binds to allergens and tissue binding site binds to basophils and mast cells causing the release of histamines

• mother of all antibodies (larger)
• first Ig to be made by fetus and first to be secreted into blood during the primary response
• made up of 5 IgM units linked by J chain
• can activate complement and cause microbes to clump together

• rarely secreted
• unknown function
• not seen in the healthy, maybe if someone is fighting an illness

• first time antigen is recognized by B cell
• b cell goes into berzerk mode and differentiates into cells that rapid fire antibodies
• effects: b cell divides to form plasma cells and memory cells, antibodies appear in blood plasma over next 1-10 weeks
• first IgM on scene then IgG

• antigen is recognized by a memory cell
• effects: memory cells divide to form plasma cells and more memory cells, Igm and IgG are rapidly produced much more than primary

• IgA attacks extraclleular toxins, bacteria, and viruses before they invade cell tissues
• -->surrounds pathogens and keeps them from adhering to the surface of cells, decreasing rate of infection
• if microbes do get into tissues, they will next encounter IgE in lymph nodes and mucus membranes which trigger histamine release
• this initiates inflammation, bringing other cells into the area and recruiting IgG and complement as well

• antigens will be engulfed by macrophages and presented to b cells there
• b cells then can divide and form plasma cells in the lymph node and form memory cells as well

• agglutination
• opsonization
• complement
• neutralization
• lysis

• clumping 
• as antibodies bind to bacterial cells, they form large complexes that clump together
• involves IgM
• viruses coated with antibodies form a clump that phagocyte will recognize and eat

• coat bacteria to aid in phagocytosis
• tag bacteria so phag can recognize and eat

• 20 proteins
• IgM and IgG (and IgA to some extent) bind to complement to activate this system

• IgG antibodies coat toxins and viruses (IgM, IgG, and IgA coat viruses) to block their action
• blocks adsorption

IgM can directly lyse some cell membranes

• while a B cell recognizes an antigen directly, T cells must be presented antigens
• also have receptors specific antigens
• essential for immunitly against Intracellular infection
• produce chemical mediators called cytokines
• only recognize antigen that has been processed by other cells and are notw located on surface MHC molecules

• Macrophages
• b cell

• t helper cells (TH1): raise the alarm to tell other cells theres a problem
• t- suppressor cells (TS): checks and balances system
• delayed type hypersensitivity cells (TD): activates macrophages and important to some allergy reactions
• Cytotoxic (killer) T cells (TC)- roam blood an lymph looking for hyjacked dying cells to kill
• Natural Killer T cells (NKT): different from NK cells, release cytokines IL4 and interferon gamma

• activated by macrophages that process antigen and produce the cytokine IL-1
• contain a receptor (CD4) that is only activated by MHCII (our cells have MHCI)
• activates TH IL-2 and gamma interferon which activate other T cells and NK cells

can shut off the immune system so to proevent a hyperactive immune system

• kill infected hosts through apoptosis
• contain a receptor (cd8) that is only activated by MHCI (like our cells have)

• DIFFERENT from NK cells
• have some surface markers of NK cells
• release IL4 and gamma interferon cytokines

• helper T cells release cytokines that help with training of b cells
• inspects b cell presentation
• if it binds, the antibodies are made and attack
• if it doesnt bind, b cell wont attack that cell (ie our cells)

• 1. toxins and bacterial or viral antigens taken up by macrophage
• 2. antigens presented on mac's MHCII receptors
• 3. tcell binds and forms activated t helper cell
• 4. TH cell divides and makes memory T cells (act if we see it again), more helper t cells (Thelper 1 cells to bind macs), and T helper 2 cells that will bind and activate b cells to make humoral immunity against the antigen

• 1. Toxins and bacterial of viral antigens taken up by cell
• 2. our own cells present the antigens on MHCI and cytotoxic t cell binds and becomes activated
• 3. cyto t cells undergoes cell division and forms another cytotoxic t cell which will recognize bad wonky cells like cancer using its CD8 receptor and will cause it to undergo apoptosis
• or if infected our cells will put viral proteins on MHCI and t cell will kill it

• only effective on virus infected cells and cancer cells
• binds to antigen-MHC on macrophages and can kill an infected macrophage
• uses 2 mechanisms

• 1. release perforin and granzyme: perforin- enzyme that makes holes in membrane; granzyme- induces apoptosis
• 2. Have Fas Ligand (FasL): on their surface. binding to Fas protein on infected cells induces apoptosis.

• After a person is infected by a pathogen (even after recovery) the person will have natural immunity from the B and T memory cells that remain.
• Can be induced artificially by vaccines
• Pathogens or products that are no longer able to cause disease as a result

Primary response: The immune response after a harmful antigen has been encountered for the first time; B lymphocytes prepare to become active to divide and produce antibodies; Antibodies improve and become better at fighting

Secondary response: Much quicker and more effective immune response if the antigen is encountered again; Memory cells recognize antigens and start producing antibodies

• Vaccines
• Toxoids

contains either dead or live attenuated organism that provokes an immune response in the host

weakened toxins that are not harmful to the host but act as antigens to sensitize the host

• often depends on the agent used
• live vaccines last longer, even the entire lifespan of the host- create a biger danger signal for a bigger reaction- also bc its the full thing to better prepare you to fight

• attenuated, toxoid and partial microbe vaccines require booster shots
• they dont give as strong of a response and dont last as long as live vaccines
• intramuscular polio, typhoid fever, tetanus, diptheria

• it does matter
• intramuscular doesnt last as long as oral or nasal for some such as the flu bc you would normally encounter the flu orally or nasally

• must take risks and apparent threat into account
• fever, pain at injection site and general malaise are common side effects but are good bc immune system is doing its job
• sever allergic rxns can occur to egg protiens and abx present in some vaccines
• live virus vaccines can cause threat to pregnant women and immunocompromised hosts

• antibodies are injected into a host after exposure to a disease to lessen the symptoms
• hyperimmune sera
• antitoxins

• gamma globulin (immune system globulin)- andibodies from many individuals are pooled
• mumps, measles help a can be fought with this
• rh- mothers with second pregnancies need this to protect baby

• immune sera that have been selected for high titers of particular antibodies
• often collected from people recovering from a certain disease (and given to the xposed pop)
• people were saved from ebola by this

• antibodies bind to specific toxins and have a countereffect
• used for botulism, tetanus, diptheria
• snake and spider bites
• antivenom

• allergic reaction
• decreased antibody production in the host

• protect against the disease
• safe (without side effects), we want minimal if any
• provide long term protection
• generate neutralizing antibodies or protective t cells to vaccine antigen- gives strong enough immune reaction
• stable and cost effective

• whole cell killed
• live attenuated
• subunit
• recombinant

• less effective than live vaccines
• all parts present to illicit response, but its dead

microbe is genetically altered in some way to make it harmless to the host, but immune system still reacts

contain only the immunogenic portion of the microbe

insert genes for antigens into nonvirulent organisms

• when a large portion of the population has become immune to an infection providing a measure of protection for individuals who are not immune
• helps control contageous disease and minimizes outbreaks

• hypersensitivity: immune system goes awry and doesnt have proper reaction
• immunodeficiency

• allergy
• autoimmune
• drug disorders

• when immune system makes an exaggerated or inappropriate response
• different parts of immune system triggered depending on the allergyhow the immune response happens

• aka- immediate response
• can cause anaphylaxis (serious, can cause death)
• a typical allergy
• mulitple exposures (prior exposure- normally most dont react' injested, inhaled, injected)
• sensitization, triggering
• localized and generalized

• initial exposure
• doesn't cause a big reaction
• b cells are activated and produce IgE (activates mast cells and basophils)

• 2nd or latter exposure which causes reactions
• mast cells and basophils release massive histamine
• ie if allergic to bee stings, first sting wont cause anaphalactic shock, could be second or seventieth

• less histamine
• red skin, watery eyes
• wheal-and-flare

• when it gets serious
• airwai contstriction, loss of blood pressure
• life threatening
• treat with epinepherine (counteracts)
• massive release of histamine

raised bump- red area with a white center = allergy

• cytotoxic response
• caused by antigen on the cells (rh factor, blood types)
• antibodies specific for an antigen activates the immune system
• increase phagocytes and turns on T killer cells and complement to kill cells
• the cells containing these cells and surrounding tissue are destroyed
• happens with blood transfusions or pregnant RH- mothers with RH+ babies

• aka erythoblastosis fetalis
• mother is RH- child is RH+
• breaks in placental membrane at delivery allow RH+ antigens to enter maternal cerculation
• mother then makes anti rh antibodies bc she is neg and hasnt seen this antigen before
• in the next pregnancy her anti rh antibodies can get into fetal circulation and attack and destroy fetal RBCs

• immune complex- things gather and congregate
• caused by antigens in vaccines, microbes or host cells
• large antigen-antibody complexes that form

• after sensitization, IgG binds to antigen to form complexes
• complement is activated --> inflammation and histamine is released
• normal: break down complexes in liver in spleen
• reactive (abnormal): dont break down properly- problem with immune system. they start to then build up and cause tissue damage. can also cause autoimmune and hypersensitivity

• Serum sickness
• arthus reaction
• rheumatoid arthritis
• lupis

• immune system reacts to proteins used to treat immune conditions
• falsley identifies a protein in an anti-serum meant to help them as harmful

• after injection with antigen, igG causes complexes at injection site
• can lead to tissue destruction due to blocked blood vessels

hard to diagnose bc it can present itself differently

• delayed (can take longer than 12 hours)
• cell mediated (Thelper) takes longer than 12 hours (normally 48-72 hours) to develop (ie rash)
• caused by exposure to foreign substances in environment (antigens, microbes, transplants)
• ie contact dermatitis

• tb test: antigen from mycobacterium tuberculosis is placed under skin, can cause induration (skin hardening)
• Poison ivy: oild turns on t cells
• dyes
• soaps and makeups: contain molecules that bind to proteins

antigen presented and t helper cell binds and brings in cytokines which activate the APC (macrophage) which causes inflammatory action and mediator release causing gczema, swelling, lesions

• hypersensitivity to host cells or tissues
• make it through colonal selection and turn against our own cells
• may be from many factors working together - epigenetics or cleanliness obsession (makes our immune system lazy)

• genetic factors (heredity, certain MHC) 
• Molecular mimcry
• Defects in Clonal Selection
• Mutations
• Viruses
• Sympathetic Nervous System Damage

• Host immune system attacks cells bc they resemle a bacterial or viral antigen
• t helper cells attack host cells with similar antigens to viral/bacterial antigens
• infection triggers response

abnormal proteins produced that are seen as foreign

can put proteins on host cells that trigger immune response

• helps regulate immune system
• if not funcitoning- can cause harm

• multiple sclerosis
• myasthenia gravis
• rheumatoid arthritis
• chrohn's disease
• celiac disease
• psoriasis
• graves disese
• hashimotos disease
• sjorgren's syndrome
• lupus

• insulating covers of nerve cells in the brain and spinal cord are damaged (myelin sheath)
• proposed cause not clear could be genetic or viral
• disease begins at 20-50yrs and more common in women and colder climates

• skeletal muscle break down
• can affect eyes speech, swallowing
• igG antibodies block message to muscle (acytlcholine receptors) and eventually die
• severity depends on number of antibodies produced

• joints
• inflammation and destruction of cartilage leave scar tissue
• patients are tested for rheumatoid factors which are IgM antibodies that specifically bind their igG antibodies

• chronic inflammation of GI tract
• not exactly autoimmune, not triggered by body itself but exposure to microbes

• reaction to gluten
• immune response that causes inflammation to small intestine

immune system causes inflammation and skin grows and causes plaques

• causes thyroid gland to produce too much thyroid hormone
• hyperthyroidism

• thyroid gland slowly destroyed by immune system
• causes hypothyroidism

• autoimmune
• immune system targets moisture producing glands (joints, ear ducts, salivary glands) 
• from genetics or infection
• dry eyes, skin

• igG, M and A antibodies are made to host DNA, blood cells, neurons, etc
• as normal cells break down these antibodies are exposed to dna causing immune complexes to form and be deposited in skin, blood vessels, joints, kidneys, CNS
• Inflammatory disease where immune system attacks different tissues
• difficult to diagnose (symptoms mimic other disorders)

• autograft: transplant from one part of the body to another
• isograft: transplant between identical twins
• allograft: transplant between non identical people
• xenograft: from one animal species to another

• caused by host t cells that recognize foreign antigen in the graft and destroy it
• cyclosporin a suppresses T cells but allows B cells to work normally

• t cells present in the graft recognize host cells as foreign and starts a site of inflammation
• host cells that are recruited to the cite actually do most of the tissue damage
• more common in immunodeficient host recipient
• recipients must take immunosuppressive drugs after transplantation

• hyperacute rejection: occurs within a few minutes
• acute rejection: first week to three months
• chronic rejection: occurs after years (ie kidney transplant)

• fools the body into thinking that tissue should be there
• rjection is caused by antigens on MHC molecules present in all cells (except RBCs)
• possible donors are tested for compatibility of their MHC antigens with those of a recipient (need to be similar to fool)
• human mHC is called HLA (Human leukocyte antigens), they have four major genes (A, B, C, D) each gene has possible alleles it would be impossilbe to test for every allele, so testing is done on HLA-DR, the gene most responsible for causing rejection

• cells in the outer portion of the fetal part of the placenta do not express MHC
• alpha fetoprotein produced by the fetus causes immunosupression (afp can be measured also to see if down syndrome or triplets)
• foreign sperm induce mother to make blocking antibodies (an antibody that doesnt have a reaction to an antigen but blocks other antibodies from combining with that antigen)

• most chemicals are too small to act as an antigen
• can bind to proteins to induce hypersensitivity
• any type  (1-1V)

• immune system makes inadequate response
• dont have functional b and t cells

• genetic disorder
• ie- severe combined immunodeficiency (SCID)
• lack of b and t cells
• bubble boy disease
• treated with bone marrow transplants or gene therapy

• acquired from malignancies and infections
• body is busy fighting other diseases
• immunosuppressant drugs
• ie- AIDS

• caused by HIV
• binds to cells that contain CD4 on their surface (thelper cells, macs, dendritic cells, langerhans cells)
• T cell count below 200 (800-1200 is normal)

• No
• die of opportunistic infection
• such as- herpes, cytomegalovirus, tb, toxoplasmosis, pneumonia, malignancies (kaposis sarcoma)

• sexual contact
• needle sharing
• contaminated blood products
• from mother to child

• gloves, mask, eye protection
• try to avoid sharps
• mouthpieces for CPR
• cover open wounds

• not promising due to high HIV mutation rate
• unsafe to use attenuated virus- can mutate back to virulent form
• whole inactivated virus leaves a person open to immunodeficiency
• recombinant virus can lead to complications