microbiology exam 4

Immunology

study of the molecular and cellular interactions between a host and introduced foreign molecules (immune system)

What are the several layers of defense?

First line: nonspecific tactics
Second line: innate cellular responses
Third line: adaptive cellular responses

Susceptibility

lack of resistance to a disease

Immunity

ability to ward off disease

Innate immunity

defenses against any pathogen

Adaptive immunity

immunity or resistance to a specific pathogen; slower to respond, has memory component

What line of defense is Innate (nonspecific) Immunity?

first and second line of defense

What line of defense is adaptive (acquired) immunity?

third line of defense

first line of defense

intact skin, mucous membranes and their secretions, normal microbiota

second line of defense

natural killer cells and phagocytic white blood cells, inflammation, fever, antimicrobial substances

third line of defense

specialized lymphocytes: T cells and B cells, antibodies

Innate (nonspecific) immunity

immediate actions of the host immune system that prevent infection without conferring immunity

barriers in nonspecific innate immunity

physical barriers (intact skin), chemical barriers (lysozyme, salt secretions), and fever

nonspecific cellular attacks

phagocytes (pathogen-ingesting cells), complement, cytokines (signaling proteins secreted by white blood cells)

highly specific (adaptive immunity)

recognizes and reacts only to a given pathogen

establishing memory (adaptive immunity)

allows a faster immune response to previously encountered pathogens

what is adaptive immunity characterized by?

B cells and T cells

physical factors blocking microbial infection:

skin, mucous membranes, ciliary escalator, lacrimal apparatus (tear ducts), saliva (washes microbes off), urine (flushing), heat (fever)

what happens when microbes are trapped in mucus? (ciliary escalator)

they are transported away from the lungs

benefits of a fever

Elevated body temperature reduces bacterial growth and survival

chemical factors blocking microbial infection

Fungistatic fatty acid in sebum.
Low pH (3-5) of skin.
Lysozyme in perspiration, tears, saliva, and tissue fluids.
Low pH (1.2-3.0) of gastric juice.
Acidity of urine
Acidity of vaginal lumen
Transferrins in blood limit iron available to microbes

biological factors blocking microbial infection

-Normal Microbiota
(Compete with pathogens for space & nutrients
Microbial antagonism/competitive exclusion)

-Misdiagnosis and over-use of antibiotics remove this natural defense

anatomy of the immune system

contains components of circulatory system, lymphatic system, and reticuloendothelial system (RES)

circulatory system

moves blood throughout the body

lymphatic system

moves lymph (fluid leaked from blood) to lymph nodes and then back into circulatory system

primary lymphoid organs

bone marrow and thymus

secondary lymphoid organs

spleen, lymph nodes, and mucosal associated lymphoid tissue (MALT)

blood cell types

red blood cells, white blood cells, platelets

the differential count

determines the proportion of each WBC type

neutrophils

A type of white blood cell that engulfs invading microbes and contributes to the nonspecific defenses of the body against disease. (phagocytic)

Phagocytis

ingestion of microbes or particles performed by phagocytes

phagocytic cells are

neutrophils, macrophages, dendritic cells

how can some cells survive phagocytosis?

by inhibiting leukocyte function

inflammation

redness, heat, swelling, and pain in response to tissue injury due to physical trauma, chemical damage, or pathogen attack

functions of inflammation:

-mobilizes phagocytic cells and directs them to site of injury
- contains and eliminates pathogens
-repairs tissue damage to facilitate resumption of normal function

steps of inflammation:

acute phase proteins released, vasodilation, margination, diapedesis, tissue repair

steps of inflammation (pt 2)

1. Injury to capillaries and tissue cells
2. Release of bradykinin from injured cells
3. Bradykinin stimulates pain receptors.
4. Pain causes release of histamine.
5. Bradykinin and histamine cause capillary dilation.
6. Break in skin allows bacteria to enter tissue
7. Neutrophils phagocytize bacteria.
8. Macrophages (mature monocytes) leave the bloodstream and phagocytose microbes.

types of inflammation

acute and chronic inflammation

acute inflammation

persists only a few days; primarily involves neutrophils and monocytes
example: healing of infected skin abrasion

chronic inflammation

-inflammation that persists and is not resolved
- typically leads to host damage
-examples: hepatitis, granulomas, and abscesses (may require surgical excision)

fever

abnormally high body temperature

hypothalamus is normally set at what temperature?

37 degrees celsius

what are some advantages to a fever?

slows microbial growth rate, intensifies the effect of anti-viral interferons, and enhances WBC/leukocyte production

what are some disadvantages to a fever?

tachycardia (increased heart rate), dehydration, may cause delirium and ultimately coma

benefits of fever

elevated body temperature reduces bacterial growth and survival

anti-microbial substances

the complement system, interferons, and transferrin, anti-microbial peptides

the complement system

group of proteins circulating in serum. the activation of one starts a cascade reaction activating others.

the activation of the complement system is started either by \______ or \________

-antibody-antigen interaction (classical pathway)
-pathogen (microbe) itself (alternative pathway)

complement activation leads to

enhanced phagocytosis, inflammation, and cytolysis

Effects of Complement Activation

Opsonization or immune adherence: Enhanced phagocytosis
Inflammation: increase of blood vessel permeability and chemotactic attraction of phagocytes
Cytolysis:
bursting of microbe due to the inflow of extracellular fluid through transmembrane channel formed by membrane attack complex

classical activation

Requires an antibody to activate it.

alternative activation

Nonspecific, binds directly to targets

Interferons (IFNs)

proteins (cytokines) secreted by T cells and other cells to aid and regulate the immune response

IFN alpha and beta

-produced by virus-infected cells
-causes neighboring uninfected cells to produce antiviral proteins that inhibit viral replication

IFN gamma (INF-y)

-produced by lymphocytes
-induces neutrophils and macrophages to phagocytize bacteria

Action of interferons

proteins produced in response to presence of viruses, bacteria, cancer, and other foreign invaders

antigen (Ag)

a substance that causes the body to produce specific antibodies or sensitized T cells

antibody (Ab)

proteins made in response to an antigen and can combine with that antigen

complement

serum proteins that bind to antibodies in an Ag-Ab reaction; cause cell lysis

humoral immunity

specific immunity produced by B cells. these cells recognize antigens through antibodies displayed on their surfaces

cell mediated immunity

involves T cells (lymphocytes). T cells recognize antigens through receptors on their surfaces

Where do B and T cells come from?

bone marrow

antigenic determinants

parts of antigen that antibodies or lymphocyte receptors bind to

antibodies recognize and react with what?

antigenic determinants or epitopes on an antigen

clonal deletion

The process of destroying B and T cells that react to self antigens

some diseases are a consequence of autoimmune (self attack) disorders:

eczema, arthritis, Crohn's disease/ulcerative colitis

activation of B cells can either be

T cell independent (humoral response)
T cell dependent ( cell-mediated response)

functions of T cells

- help in fight against infection
-are activated by antigen presenting cells (APCs) such as macrophages

T helper cells

-activate B cells to make antibodies (TH1)
-stimulate other immune cells to attack pathogen (TH2)
-Missing or defective in HIV infected/AIDS patients

Cytotoxic T cells

induced infected cells to kill themselves (apoptosis)

two main types of APCs

dendritic cells and macrophages

dendritic cells

present in lymph nodes and skin, good antigen presenters, poor phagocytosers

Macrophages

usually found in "resting" state, very phagocytic once activated, activated by ingestion of antigen or by T helper cells

APCs activate what?

T helper cells

virus infected( & cancer) cells can present antigens to what?

cytotoxic T cells

extra-cellular killing

some microbes (usually parasites) are larger than the immune cells so they cannot be digested

immunological memory

The capacity of the immune system to generate a secondary immune response against a specific antigen for a lifetime

primary response

occurs after initial contact with antigen

secondary (memory) response

after subsequent exposure (stronger and more specific)

vaccination is an attempt to push you to what?

second response before encountering the infectious agent or toxin

antibody titer

amount of antibody in serum

primary and secondary immune responses illustrate what?

specificity and memory in adaptive immunity

types of adaptive immunity

-Naturally acquired active immunity
-Naturally acquired passive immunity
-Artificially acquired active immunity
-Artificially acquired passive immunity

naturally aquired active

antigens enter the body naturally; body induces antibodies and specialized lymphocytes

naturally acquired passive

antibodies pass from mother to fetus via placenta or to infant via the mother's milk

artificially acquired active

antigens are introduced in vaccines; body produces antibodies and specialized lymphocytes

artificially acquired passive

preformed antibodies in immune serum are introduced by injection

vaccination (aka immunization)

administering a non-virulent antigen to stimulate an adaptive immune response and trigger the development of immunological memory

variolation

using scabs from smallpox patients to induce immunity in uninfected

who practiced variolation?

the chinese, 3000 years ago

who modified variolation?

Edward Jenner

what was used to prevent patients from developing smallpox?

cowpox scabs

what happened in 1980?

smallpox was declared eliminated thanks to vaccine programs

vaccine

the immunogenic material used to induce artificially acquired active immunity

what requirements do successful vaccines try to meet? (none do all)

-activate humoral and cell-mediated responses
-provide long-term memory response
-protect fully against all aspects of pathogen infection
-cause minimal side effects or discomfort
-easy to administer, require few doses, dont need boosters
-affordable
-stable suspensions that store well for extended periods

Live attenuated vaccines

contains live whole agent in a weakened or less virulent form

advantages for live attenuated vaccines

most closely mimics a natural infection

disadvantages for live attenuated vaccines

-not recommended for immunocompromised
-small possibility of reversion to pathogenicity

inactivated vaccines

pathogen has been inactivated by treatment with antibiotics, heat, radiation, or chemicals
(ex: rabies, hepatitis A, cholera, influenza

advantages of inactivated vaccines

pathogen cannot reproduce