Lec 13 Mmi

ability to cause disease by evading or overcoming the host defenses

the extent to which the microorganism is pathogenic

molecules produced by pathogens that contribute to their pathogenicity

1. cracks in mucous membranes

2. skin, abrasions and cuts

3. parenteral route

can provide routes to bypass traditional means for pathogens as surgical sites open up cavities

some microorganisms have a preferred portal of entry, only capable of causing disease via a specific route ex. stds

pathogens with a preferred type of cell to infect

1. distribution of cell receptors for microbes

2. accessibility of correct host cell types

3. requirement for appropriate cellular elements that will allow the microbe to grow

4. physical and innate defences at the site of infection, strong immune system= no infection

5. other microbes may be competing

microbes can produce exotoxins that get into cells through proteins that attaches to the host cell, spreading the disease process

1. adhere to host

2. proliferate and multiply

3. break off and infect new host

during proliferation, infected cells also:

1. invade host cells

2. avoid destruction by producing toxins to kill WBC

3. share virulence factors

first step towards establishment of infection

facilitated by structures on pathogens called adhesins or ligands and structures on the host cells that recognize and bind with these "receptors"

glycoproteins are or lipoproteins

sugars like mannose

Glycocalyx; initially prevents the phagocyte from recognizing adn ingesting bacteria

bacteria can produce capsules in the right environmental conditions, sugars, etc.

Fc receptors on microorganism binds the Fc portion of antibodies produced to the capsule of bacteria.

Phagocytes also have Fc receptors and are looking to bind the Fc portion on organisms that are opsonized.

Fc portion of the molecule is not available for binding to the phagocyte

in streptococcus pyogenes

heat an acid resistant protein in the cell wall that allows attachment of the bacteria epithelial cells and inhibits phagocytosis, it holds itself away from phagocyte wit protein M, which acts like a stick

in mycobacterium tuberculosis, waxy substances in cell walls that make the bacterium resistant to digestion inside the phagocyte

community of bacteria, often surrounded by shared glycocalyx

reduces antibiotic penetration, increasing resistance

destroys WBC cells

break down fibrin and dissolve clots formed by the body to isolate infection

breakdown red blood cells

clots: converts fibrinogen to fibrin, clot can wall the bacteria off from host defenses

ex. staphlycoccus aereus not epidermidis

break down collagen, a connective tissue

destroy plasma membrane

inactivate antibodies and other body proteins, like IgA protease

surface proteins on some bacteria which activate actin, the cytoskeleton on eukaryotic cell, rearranging and facilitating bacterial engulfment into the host cell

some bacteria use their invasins to move from one host cell to another, moving laterally and from the outside in.

also called type 1 exotoxins

protein antigens that stimulate a large immune response, activating 20% of T cells

result in excessive release of cytokines due to binding to MHC II and TCR

which results in nausea, fever, diarrhea, shock, death

L

1. often primary virulence factor

2. usually proteuns that can produce fever, cause heart failure, diarrhea, edema or shock

3. can destroy cells as well as inhibit protein synthesis leading to cell death

something that contributes to the structure of the bacteria

ex. LPS, Lipid A portion

ex. superantigens

an extra protein that is made by bacterium to affect cells other than itself

heat sensitive

L

causes chills, fevers, weakness, aches, shock adn death

activates the blood clotting system (DIC- disseminated intravascular coagulation)

life threatening loss of blood pressure

if caused by bacteria

if caused by gram - bacterium

are carried on bacteriophages or plasmids

1. cytotoxins

2. neurotoxins

3. enterotoxins

antitoxins

type III secretion apparatus allows bacteria to inject proteins into a host cell, killing or altering it

a chromosomal region in some bacteria, esp. Gram - have genes encoded for pathogenic characteristics like that of a type III secretion apparatus

pathogens have antigens on their surfaces to which B cells produce antibodies

some pathogens change the makeup of their antigens= immune system sees them now as new pathogens

can only grow inside of host cells, often in a protected vacuole

bacteria that can multiply outside of host cells, but often use intracellular growth as a means of evading host defenses

mutate or take up small pieces of DNA that can change their virulence

pieces of DNA can either be integrated into the bacterial chromosome or exist as free floating genes in the bacterial cell

advantage for pathogens

more efficient to have them packed closely together to be transferred as a unit between bacteria

transferral of plasmids containing genes for virulence or antibiotic ressitance

acquisition of genes for toxin production

acquiring gene for toxin, capsule production, etc.

small circular DN molecules separated from main bacterial chromosome

responsible for transferring the genes for antibiotic resistance

viruses which infect specific bacteria

transfer genes by transduction

most effects caused by inflammation and activation of the immune system, producing disease

cytopathic effects: alteration of cells

1. killing or damaging of host cell

2. different strains of virus cause different CPE

1. infected cells fuse to from giant cell with many nuclei

2. giant cell dies when virus use up all building material and cause necrosis of tissue

3. permits viral multiplication w/o exposing virus to antibodies