Microbal Mechanisms of Pathogenicity

provoke intense immune response. T cells produce too many cytokines. you hurt yourself. TSS, staph antigens.
diptheria toxin
inhibits protein synthesis. A-B toxin. diptheriae only produces toxin when infected by phage.
erythrogenic toxins
strep. pyogenes synthesizes 3 types of cytotoxins that are superantigens that damage the plasma membranes of blood caililaries. Scarlet fever caused by strep. pyogenes
botulinum toxin
Clostridium botulinum. A-B toxin
tetanus toxin
A-B toxin binds to nervous system controlling skeletal muscles causeing contractions
Vibrio Enterotoxin
vibrio cholerae A-B binds to epithelial cells, causeing them to secrete large amounts of fluids and electrolytes. causes diarrhea and vomiting. E. Coli can produce a similar toxin
Staphlococcal Enterotoxin
staph aureus produces a superantigen in the intestines.
caused by endotoxins. causes blood clots.
study chart pg. 438
lacrimal apparatus
system that protects the eyes by flushing them
prevents hair from drying, protective layer over the skin
white blood cells
type of white blood cells that have large granules. Neutrophils, basophils, eosinphils.
stain in neutral dye, active in initial stage of infection. they can leave teh blood, enter an infected tissue, and destroy microbes.
stain in basic dye. release histamine for inflammation in allergic responses.
stain with acidic dye called eosin. produces toxic proteins that fight parasites such as helminths. they can also leave the blood.
have granules, but you can’t see them. 3 types: monocytes, dendritic cells, lymphocytes
not actively phagocytic until they leave the blood and mature into macrophages
dendritic cells
found on skin, mucous membranes, thymus, lymph nodes. phagocytosis and initiating adaptive immune response (communicates with T and B cells)
include natural killer cells, T cells, and B cells.
natural killer (NK) cells
hunt and kill infected cells using toxic stuff stored in granules. example of toxic stuff: perforin creates channel in membrane causeing cytolysis, granymes cause cells to self destruct
increase of white blood cells in response to infection
differential white blood cell count
percentage of kinds of white blood cells
blood clotting
fixed macrophages/ histiocytes
resident in certain tissues and organs of the body. all have different names. the other kind of macrophages wander.
mononuclear phogocytic system
all the macrophages of the body
attraction of phagocytes to mircobes
coating process that promotes phagocytosis
fusion of phagosome (membrane formed around microbe when it is brought into the macrophage) with a lysosome
hydrolyzes peptidoglycan
redness, pain, heat, swelling, sometimes loss of function. acute (shoret but severe) or chronic (long but not as bad)
dilation of blood vessels, increasing blood flow to damaged areas and is resonsible for redness and heat associated with inflammation
accumulation of fluid
chemicals released by damaged cells in response to injury
histamine, kinins, prostaglandins, leukotrienes
Complement system
destroys microbes by 1: cytolysis 2:inflammation 3:phagocytosis
coating microbe to enhance phagocytosis. makes it easier for phagocyte to bind to a microbe.
MAC membrane attack complex
C5b- C9 in the complement system. causes cytolysis
C3 convertase
C3a:binds to mast cells with C5a and cause them to relase histamine and other chemicals that increase blood vessel permeability during inflammation. this happens because they release histine.
C3b: binds to microbe, causing opsonization
classical pathway
antibodies attach to antigens. C1 binds to antibodies, starts cascade.
alternative pathway
B,D,P factors are surface proteins that bind to C3.
Lectin pathway
lectin binds to mannoose, working as an opsonin and activating C2 and C4, which cascades to C3.
type of cytokine. interfere with viral replication. alpha and beta (causes uninfected cells to synthesize AVPs), gamma (causes macrophages to produce nitric oxide that appears to kill bacteria).
AVPs (antiviral proteins)
disrupt viral multiplication
iron-binding proteins
Lactoferrin, transferrin, ferritin, hemoglobin
AMPs (antimicrobial peptides)
attract dendritic cells, kill microbes, recruit mast cells. broad spectrum of activity.
perforin/ granzyme
pore-forming protein that lets granzyme into the cell. granzyme then apoptosizes (chops up the DNA) of the cell.
T Cytotoxic cells (CD8+ T cells)
matures into CTL (cyutotoxic T lymphocyte) that destroys cells on contact using perforin and granzymes.
T Regulatory cells
stop T cells from reacting against self. maintains tolerance.
T helper cells
activated when come into contact with APC. produce cytokines and activates all cells related to cell-mediated immunity: mactophages, T cytotoxic cells, and NKs.
Dendritic cells
primary APCs to induce immune responses by T cells.
cell eaters. activated by ingesting antigenic material or by cytokines made by helper T cells. activated macrophages are better phagocytes adn APCs. notable: eat cancer cells.
Natural Killer Cells (NKs)
don’t have to be activated by antigen. kill cells that don’t display MHC class I slef-antigens
chemical messengers. soluble proteins or glycoproteins produced by immune cells in response to a stimulus. communicate between white blood cells.
cytokines that bring leukocytes into area of infection important for inflammation
tumor necrosis factor
TNF- alpha. targets tumor cells. factor in inflammatory responses
cytokine storm
harmful overproduction of cytokines caused by a feedback loop.
Humoral immunity
B cells. targets free circulating patogens using antibodies
cellular immunity
t cells- targets infected cells, or intracellular pathogens. mostly uses specialized phagocytic or NK cells
B cells
lymphocytes that mature in bone marrow. involved in humoral immunity. produces Antibodies. mature into plasma cells that make antibodies or memory cells.
T cells
lymphocytes that mature in the thymus. involved in cellular immunity.
stem (Fc region)and V region on tips of the Y. V region binds to epitope, Fc region binds to host cell or complement.

Leave a Reply

Your email address will not be published. Required fields are marked *