Term
Symbiosis
Mutualism
Commensalism
parasitism |
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Definition
Microbial Interactions with the Host
types of interactions |
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Term
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Definition
| the relationship between 2 organisms in which neither organism can survive without the other. |
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Definition
the relationship that benefits both organisms.
ex. flowers and bees- flowers provide nectar for the bees. bees pollinate
the flowers. |
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Definition
| a relation that benefits one organism while the other is not affected. |
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Definition
| relationship in which one organism benefits at the expense of the other (one is harmed) |
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Term
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Definition
| bacteria in an on our body (we have a lot of them. Two types: transient and resident |
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Term
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Definition
those that colonize the body for only a short period of time (few
days/months). we pick these up by touch, ingest, inhale. |
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Term
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Definition
live in and on your body for a long period of time (sometimes
your whole life). |
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Term
| Skin: the part of our body that is exposed. It has relatively low Normal Flora. mainly because: |
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Definition
our skin is relatively dry (bacteria like a little moisture--armpit/groin have
more Normal Flora than others) produces an odor
our skin is constantly shedding dead skin (its hard for the bacteria to gain a
good "foothold")
our skin has sebaceous glands is secretes sebum and it has antibacterial
properties
our sweat greats an hypertonic environment that make it unfavorable for germs to survive. |
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Term
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Definition
have very low normal flora:
we are constantly blinking our eyes, and our eyes are bathed in tears which
have antibodies and antibacterial proteins. |
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Term
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Definition
have the same normal flora as the skin, but throw in a little more fungi
some evidence that ear wax has anti bacterial properties. |
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Term
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Definition
| has very little Normal Flora because it is very acidic (pH of 2). |
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Term
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Definition
the farther down you go...the more normal flora (gram +). As you go down it becomes increasingly
gram - and more anaerobic. |
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Term
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Definition
has the most normal flora and the most diverse normal flora
anaerobic gram + and gram - (not E. coli). |
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Term
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Definition
under normal circumstances we have no normal flora in the kidney and UTI
the urethra of both men and women are colonized by normal flora of the
skin. a healthy genital tract depends on a heathy concentration of
Lactiobacillus. it ferments glycogen and therefore creates a slightly acidic genital tract preventing anything else from growing down there.
March |
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Term
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Definition
| a living transmitter of disease (ticks, fleas, other people) |
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Term
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Definition
| where the pathogen naturally occurs (chickens, cattle, water, soil) |
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Term
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Definition
| bacteria that can cause disease |
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Term
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Definition
causes a severe or serious disease
(the fewer organisms it takes to cause and infection the more pathogenic it is)
Vibrio cholerae (100 million this one is more virulent) Shigella (10-100 more pathogenic) |
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Term
| In order to cause disease, a pathogen must |
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Definition
1) have a means of reaching the host (transmission)
2) colonize or invade host tissue
3) Multiply or complete life cycles
4) Survive or evade body defenses
5) Have a means of harming the host |
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Term
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Definition
| inhalation, ingestion, Direct contact, Indirect contact, Insect/Animal bites, injury or trauma |
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Term
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Definition
(sneezing, talking, stirred up dust...anything that produces an
aresol that is tiny enough to be inhaled)...tiny airborne particles that contain germs and can be inhaled are known as droplet nuclei |
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Term
| ingestion of contaminated food or water |
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Definition
fecal-oral transmission
(associated with good hygiene) |
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Term
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Definition
directly from one host to another either person to person
or animal to person (STDS, kissing, or touching an open sore, snuggling a
diseased pet) |
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Term
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Definition
person to person transmission by means of an inanimate
object (fomite) (bowling, iceskating, skiing, doorknob, table) Pinworms (tiny
nematode parasites that live in your large intestines....come out of your butt
(OMG) |
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Term
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Definition
| introducing the germ directly into the tissue/blood |
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Term
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Definition
| introducing the germ directly into the tissue/blood |
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Term
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Definition
| the pathogen must have receptor for that tissue |
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Term
| How does Normal Flora protect your body from infection? |
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Definition
Normal Flora have already taken up most of the binding sites therefore
competing with pathogens for tissue binding sites. It also competes with the pathogen for the nutrients leaving very little available for pathogens. |
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Term
| Obligate intracellular parasites |
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Definition
| those that can only grow inside of a host cell |
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Term
| facultative intracellular parasites |
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Definition
they can grow on a culture plate, but in the
body they grow as inside the cell |
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Term
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Definition
| phagocytosis by white blood cells |
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Term
| Ability to survive phagocytosis by white blood cells... |
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Definition
especially if the WBC is
somewhat impaired in its function |
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Term
| Intracellular growth (advantages) |
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Definition
if it can grow inside the host cell then
antibodies and white blood cells can't get to it. they are in their own little bubble. |
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Term
| Some produce enzymes that |
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Definition
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Term
| Some have Antigenic Variation |
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Definition
| by changing the surface antigen they can stay one step ahead of the bodies defenses. |
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Term
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Definition
molecule that stimulates an immune response (antibody
production)
they are found on the surface of microorganisms that cause the infection |
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Term
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Definition
| if the body is producing antibodies against surface antigens on the germ, the bacteria just simply needs to stop making antigens so that the antibodies don't have anything to attach to. |
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Term
| Extensive tissue destruction |
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Definition
when the infection has become well
established (flesh eating disease), the broken down tissue provides a great growth medium for the bacteria, but the tissue damage has destroyed the blood vessels to the tissue. that means WBC nor antibiotics can get to the area, so surgical removal is required. |
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Term
| Multiply faster than killed |
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Definition
| germ grows faster than it's being killed (ex. anthrax) |
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Term
| intracellular growth usually results in |
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Definition
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Term
| Extracellular enzymes (protease, DNase, hyalusonidase, ect) |
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Definition
degrade
connective tissue which facilitates the spread of that infection to that tissue.
almost all pathogens produce some combination of extracellular enzymes |
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Term
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Definition
| heat-sensitive proteins secreted by bacteria (inactivated by boiling) |
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Term
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Definition
heat-resistant lipopolysaccharide of gram-negative bacteria
(resistant to bacteria...only gram neg. bacteria have these) |
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Term
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Definition
cytotoxin
Enterotoxin
Neurotoxin |
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Term
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Definition
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Term
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Definition
does NOT kill cells ...it causes secretion of large amounts
of H2O and electrolytes into the intestinal tract causing watery diarrhea |
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Term
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Definition
they disrupt neurotransmission
in doing this you disrupt the ability to breathe. |
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Term
| Minute amounts of endotoxins |
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Definition
promotes fever which is actually a good thing...it helps
stop the growth of the bacteria. stimulates the production of antibodies,
stimulates complement (group of serum proteins that interact together to
kill bacteria) |
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Term
| Large amounts of endotoxins |
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Definition
inability to regulate body temperature, leakage of blood
plasma into tissues (vasodilation), disseminated intravascular coagulation
(DIC)--where the plasma forms clots that can clog blood vessels.
the combination of the leakage and the DIC can result in impaired blood
flow to vital organs which in turn can result in these organs not receiving
enough oxygen and eventually organ failure and endotoxic shock and if not
treated soon then death. |
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Term
| Why is the large amounts of endotoxins so important? |
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Definition
because that's why gram neg. bacteria are more dangerous than gram positive.
also can be more severe. Also why killing them can be dangerous because
it can release more endotoxins. you can't treat the endotoxin, you can
only treat the bacteria. |
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Term
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Definition
| nonspecific (first line of defense) |
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Term
| Types of innate immunity: |
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Definition
gag reflexes
skin
eyes
mucous membranes
Circulating factors
white blood cells (leukocytes) |
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Term
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Definition
| coughing, sneezing, swallowing |
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Term
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Definition
(shedding, dryness, sweating...) the reasons why we don't have alot of
normal flora |
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Term
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Definition
(blinking, tears) prevent bacteria from colonizing the eyes.
note our tears- contain antibacterial proteins |
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Term
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Definition
| anything we ingest come into contact with the mouth,GI tract, UT, respiratory tract. |
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Term
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Definition
| complement, a group of serum proteins that interact together to kill bacteria. (transferrin, a protein that binds iron which therefore deprives the bacteria of the iron that they need for growth.) |
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Term
| white blood cells (leukocytes)types: |
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Definition
| neutrophils (PMNs), Monocytes, Eosinophils, Basophils, and Lymphocytes |
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Term
| neutrophil (polymorphonuclear leukocyte or PMNs): |
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Definition
they are the most
common WBC in the body, they are phagocytic WBC and they are
usually the first to arrive at the site of injury or infection. |
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Term
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Definition
large WBC with a large nucleus. they are also phagocytic.
when monocytes reside in tissues and organs they are referred to as
Macrophages. |
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Term
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Definition
these are important during parasitic worm infections (hooke
worm...). |
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Term
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Definition
| are involved in allergic responses (body-wide). |
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Term
| Lymphocyte,there are 3 types: |
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Definition
the cell in almost entirely nucleus
natural killer cells
B-cells
T-cells |
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Term
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Definition
they kill cells that are infected with viruses or intracellular bacteria, they kill by apoptosis (programmed cell death signal
the cell to kill itself). |
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Term
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Definition
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Term
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Definition
| mediate cell-mediated immunity |
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Term
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Definition
| specific germ or specific antigen. Two types Humoral immunity and Cell-mediated immunity |
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Term
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Definition
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Term
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Definition
| activation of cells and proteins to kill pathogens |
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Term
| Phagocytic killing of bacteria |
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Definition
bacteria enclosed in phagosome
lysosome attache to phagosome and release digestive enzyme
it uses what it can as nutrients for the cell, and expels what it can't |
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Term
| some bacteria survive phagocytosis by: |
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Definition
Inhibit lysosome binding to phagosome or
Escape the phagosome into cytoplasm |
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Term
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Definition
a nonspecific response to injury or infection and is a very imp.
component of our innate immunity. |
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Term
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Definition
the injured tissue cells release mediators that activate lining of
nearby capillaries and attract WBC to that site of injury or infection
Inflammatory mediatory |
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Term
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Definition
| creates openings in blood vessels--> movement of plasma and WBC into tissue. bind mast cells in tissue |
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Term
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Definition
| activate mast cells to release more mediators |
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Term
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Definition
it makes the opening in the blood vessels even larger so that
more plasma can leak into tissue, and it increases mucus production. |
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Term
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Definition
| it binds free nerve endings causing pain (OUCH!) |
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Term
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Definition
| mediators that attract WBC |
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Term
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Definition
Increased blood flow to affected site
Capillary dilation- the seepage of the plasma of the capillaries into the tissue
along with serum
Fever- increased blood flow causes the affected site to feel warm
Can slow down the growth of the bacteria causing the bacteria
Can also activate other immune factors such as phagocytes
Formation of fibrin clot- purpose of clot is to try and contain the bacteria and
prevent it from spreading to other sites.
Influx of WBC thanks to the chemotaxins |
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Term
| Signs of inflammation (clinical) |
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Definition
Redness and Heat because of the influx of blood into that area
Swelling because of the seepage of the plasma into the tissue
pain because of the prostaglandins binding to the free nerve tissue
Loss of function (sometimes)
sometimes the symptoms we experience when we are sick are symptoms of
inflammation (like the common cold)-when we have a common cold we take the antihistamines but we are inhibiting
our own bodies immune system to fight off that infection. |
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Term
| Humoral Immunity--in response to a specific antigen |
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Definition
Mediated by B cells
Each B cell has a receptor to 1 specific antigen (Ag)When the body is exposed to an antigen (A) clonal selection results
clonal section- only the B cells that have receptors to that antigen will be
activated.
Activation involves several rounds of cell division, B cell differentiation into Plasma cells and Memory B cells.Plasma cells- produce antibodies
Memory B cells- Primed for next exposure to antigen (important part of
a vaccine is the production of these guys...they stick around for a
while...a booster shot makes even more of these.) |
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Term
| Antibody (Immunologlobulin) |
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Definition
made of polypeptides
long chain is referred to H chain= heavy chain (Fc)-stem like part
short chain = L chain they are referred together as the FAB-the antigen binding region |
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Term
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Definition
the most abundant class of antibody (found in serum) the only class of
antibody that can cross the placenta to protect the child during pregnancy. |
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Term
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Definition
usually presented as a dimer of two. the major antibodies that are found
in mucus secretion, tears, saliva, and milk. (why mothers are encouraged
to breast feed.) |
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Term
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Definition
| polymer of 5 Ig (wheel type appearance). first class of antibody produced in response to an antigen. |
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Term
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Definition
| antibody that is involved in response to allergic reactions. |
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Term
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Definition
| least abundant class of antibody that is found only in the surface of B cells. this is what they used in receptor to antigens. |
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Term
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Definition
| by binding an antigen, they are marking that antigen for elimination |
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Term
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Definition
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Term
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Definition
enhanced phagocytosis by WBC (WBC have receptors to
the Fc portion of antibodies). antibodies can now get a better grip on these
bacteria (capsule bacteria) |
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Term
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Definition
causes the bacteria to clump together. makes it easier for the
cell to take in, and harder for the bacteria to attach to tissue.
Inhibit bact./viral attachment to tissue by coating the bacteria/virus they cannot attach to tissue |
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Term
| Neutralization of bacterial toxins |
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Definition
by attaching to the toxin it cannot attach to the part of the body that it is suppose to have it's affect on.
antibody-dependent cell-mediated cytotoxicity (ADCC) by natural killer
cells. natural killer cells kill cells coated with antibodies |
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Term
Antibody response to antigen:
primary response |
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Definition
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Term
Antibody response to antigen:
secondary response |
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Definition
secondary lag=shorter lag period
secondary IgG=stronger antibody response
reason is for the memory B cells
booster shots boost the memory B cells |
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Term
| Cell-mediated immunity (T cells) |
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Definition
| these cells activate other defense mechanisms to clear the infections (rather than antibodies) |
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Term
| Humoral immunity is most effective with- |
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Definition
| bacterial infection and initial viral infections. |
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Term
| Cell-mediated immunity is most effective with |
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Definition
| fungal infections, established viral infections, intracellular pathogens, and tumors |
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Term
| different types of T cells |
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Definition
T-helper cells (Th cells)
T-cytotoxic cells (Tc cells)
T-regulatory cells (Treg cells |
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Term
| T-helper cells (TH Cells) |
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Definition
| stimulate immune response. They produce mediators that activate B cells, macrophages, other T-cells, ect.) |
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Term
| T-cytotoxic cells (Tc cells) |
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Definition
kill virus-infected cells, cells with intracellular pathogens.
Different from natural killer cells because they recognize cells with specific antigens on their cells. they are involved tumor immunology. |
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Term
| T-regulatory cells (Treg cells) |
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Definition
once the disease has been cleared something is needed to turn off the response. they also regulate how strong the response will
be as well as prevent autoimmune diseases. (make antibodies against your own tissue- systemic lupus erythematosis). results from over stimulation |
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Term
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Definition
nonspecifically kill virus infected cells, tumor cells, cells with
intracellular pathogens. (don't recognize a specific antigen, but they have different
surface markers on them than an uninfected cell). it's assumed that those subtle
difference are associated with that cell being unhealthy.
the also functions in ADCC- they kill cells that are coated with antibodies |
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Term
| T-Cells produce cytokines |
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Definition
| which are chemical mediators |
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Term
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Definition
chemotaxins
Interleukins
Hematopoietins
Interferons |
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Term
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Definition
| attract WBC (can even regulate what type of WBC is attracted) |
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Term
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Definition
| activate or inactivate specific WBC |
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Term
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Definition
| stimulate the production of more WBC |
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Term
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Definition
cytokines with antiviral activity. they have 2 effects (act to contain
the viral infection). inhibit viral replication inside cells
protect neighboring cells from infections |
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Term
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Definition
IFN-Alpha
IFN-Beta
IFN-Gamma |
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Term
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Definition
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Term
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Definition
| produced by fibroblasts (tissue cells) |
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Term
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Definition
produced by TH Cells
also involved in activation of macrophages which enables them
to kill more effectively (people with AIDS have this problem
too). |
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Term
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Definition
exaggerated immune response that results in tissue damage.
used to be classified by either immediate(get a reaction with in a few min. after
being exposed to an antigen) or delayed (don't feel anything until a day or two) now classified into 4 types based on the immune reaction that is involved |
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Term
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Definition
mediated by IgE- occurs immediately after the person's second
exposure to the antigen (bee sting, peanuts)
1st exposure to antigen-B cells differentiate into plasma cells that secrete
IgE. IgE binds Fc receptors on mast cells (or basophils)- they become
sensitized to antigen. during this the person is not experiencing
any symptoms.
2nd exposure- Ag binds IgF on mast cell (or basophil). causing mast cells
to release inflammatory mediators. |
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Term
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Definition
mediated by Ab to tissue Ag (results in the death of the tissue). (ex.
blood transfusion rxn, autoimmune disease (systemic lupus)). |
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Term
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Definition
mediated by immune (Ab-Ag)-compexes. normally they are cleared
in the body, but sometimes you might have an excess that can't be cleared.
sometimes they can form deposits in various parts of the body. (deposit in
capillaries --> vasculitis)
cause by:
persistent infection combined with a weak antibody response
continued production of auto antibodies continued/repeated exposure to Ag |
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Term
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Definition
mediated by T cells- Ag interacts with T cell. T cell is activated and
releases cytokines that attract lymphocytes, eosinophils, macrophages. (ex.
organ transplant rejection, TB, and TB skin test, poison ivy...contact
dermatitis.) |
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