Microbiology Ch 15

• Pathogenicity = to cause disease by overcoming the defences of the host.
• Virulence = the degree or extent of pathogenicity

1. Mucous membranes - first line of defense - lungs, GI, GU (STDs) , conjunctiva (gonorrhea, chlamudia)

2. Skin -first line of defence -largest organ - breaks, ducts in glands, on top of skin

3. Parentieral - entry other than through the mouth or GI tract - directly deposited into tissue - punctures, bites, cuts

• 1. Portals of entry - mucous membranes, skin, parenteral
• 2. Preferred portals - most microbes have one preferred entry point - some diseases can only result from one specific one

• 1. # of microbes - the more microbes that gain entry increases the likelihood of a disease
• I_D 50 = indicator of virulence - dose needed to infect 50% of test population

L_D50 = indicator of lethality - dose needed to kill 50% of test population

• 2. Adherence - ability of microbes to adhere to tissue
• a. Microbe ligand binds to host receptor
• b. biofilms - communities of microbes that cling together and share nutrients - able to resist disinfection - 65% of human infections

1. Capsule - outside cell wall -well organized glycocalyx - not slime later - used for attachment & prevention of phagocytosis

2. Cell Wall components on bacteria - used to attach and prevent phagocytosis - eg, mycolic acid

3. Enzymes - produced by bacteria - used to wall themselves off, spread more easily, & destroy host IgA (which is designed to block microbes ability to adhere)

4. Antigenic vatiaiton on bacteria - some can alter their surface Ags to fool host defenses - Influenza mutates it envelope spikes (H1, N1), conjugation plasmid gives new surface Ags

5. Use of host's cytoskeleton - bacteria use proteins called "invasins" to rearrange the actin filaments of the host cell cytoskeleton - causes membrane ruffling (rearranging of microtubules) - allows bacteria to enter -move around on microtubules & can use gap junctions to move from cell to cell.

1. Using hosts nutrients - uses siderophores (proteins) to bind Fe so host can have it for Hgb production

2. Direct damage - entry→growth→host cell lysis

• 3. Production of Toxins - Toxins can enter the bloodstream and effect all areas. Two types:
• a. exotoxin - bacteria makes & releases into BS
• b. endotoxin - embedded in Gram (-) cell wall - released when the bacteria dies

4. Induce hypersensitivity immune response

5. Plasmids - can carry R (resistance) factors or a toxin that determines the bacteria pathogenicity

6. Lysogeny - insertion of phage into bacteria chromosome = bacteria can make toxin

poisonous substance (protine) that can be produced by some bacteria - adds to pathogenicity - Toxin can travel in the blood or on dead bacteria

- most toxins damage cell membrane

the ability of a bacteria to make toxin

toxin in hosts blood

pieces of heat inactivated toxin used in vaccines - host can make Ags against the toxin

Abs against a certain toxin (Ag) that inactivates the toxin - used to treat botulism & tetanus

Cytokins are proteins that regulate immune response and mediate cell-to-cell communication. They are produced by macrophages.

Lysogeny - insertion of phage into bacteria chromosome = bacteria can make toxin

• Siderophores are proteins that are released by bacteria.
• - take Fe from iron transport proteins (transferrin, Hgb) by binding it even more tightly.

- also one way that bacteria cause damage - taking nutrients from host cells

• Exotoxin = gram (+) bacteria (mostly) - toxin is made by the cell and secreted or is released at lysis
• - protein (enzyme) - soluble in blood - can travel in blood stream
• - very potent and potetially lethal
• - destroy host cell membrane components
• - sometimes host can produce antitoxin (Ab)
• - usually produced from gene on plasmid

• Endotoxin - Toxin is inserted on Gram (-) outer cell membrane
• - lipidpolysaccharides
• - released only when cell dies (why infection sometimes gets worse when you start antibiotics)
• - cause macrophages to release large amounts of cytokins (abnormal immune response) which leads to shock

• 1. AB toxins - most commom exotoxin - enters host cell & inhibits protein synthisis
• - A= acitve part - does damage- stays in host cell
• - B= binding part - binds to host cell membrane - after A delivered it releases

• 2. Membrane-disrupting toxins
• - lyse host cells by
• a. making protein channels in plasma membrane
• - - leukocidins - kill WBC's
• - - hemolysins - kills RBC's

b. disrupt host cells phospholipid bilayer

• 3. Superantigen - super toxins - cause a super out of control immune response -
• - cause macrophages to release large amounts of cytokins
• - cytokins cause all Sx = fever, nausea, vomiting, diarrhea, shock, death

1. They hide inside a cell (obligate intercellular parasites) to reporduce - immune system can detect them

2. Attack immune cells directly

• 1. stop host cell proteinsysthesis
• 2. causes lysosomal digestive enzymes to be released - cell eats itself
• 3. damages host cell DNA
• 4. turns oncogenes on - transformed cells have no contact inhibition → uncomtrolled cell growth == tumor
• 5. Make surface Ag changes on host cell - host attacks itself (RA)

Pathogenicity inclused exit from host - to infect another host

- Most microbes use same entrance & exit ports

• 1. Respiratory tract - cough, sneeze
• 2. GI - hand to mouth
• 3. GU (Genitourinary) - STDs
• 4. Skin/ open wounds
• 5. Blood

Interferon - proteins (cytokins) that interfere with viral replication inside a host cell

Oncogene - mutated from of normal cellular genes - once turned on, it transform the cell and begins rampant replicaiton.