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What is virulence?
- Pathogenicity = to cause disease by overcoming the defences of the host.
- Virulence = the degree or extent of pathogenicity
3 portals of entry
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
How do microbes enter the host?
- 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
What factors contribute to pathogenicity?
- 1. # of microbes - the more microbes that gain entry increases the likelihood of a disease
- ID 50 = indicator of virulence - dose needed to infect 50% of test population
= 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
How do bacteria penetrate host defenses?
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.
How do bacteria damage host cells?
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
- can carry R (resistance) factors or a toxin that determines the bacteria pathogenicity
- 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
What is a cytokine?
Cytokins are proteins that regulate immune response and mediate cell-to-cell communication. They are produced by macrophages.
What is lysogeny?
Lysogeny - insertion of phage into bacteria chromosome = bacteria can make toxin
What is a siderophore?
- 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
Difference between exotoxin & endotoxin
- 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
3 types of exotoxins?
- 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
How are viruses pathogenic?
1. They hide inside a cell (obligate intercellular parasites) to reporduce - immune system can detect them
2. Attack immune cells directly
What are the cytopathic effects of a virus? (how does it cause damage)
- 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)
What are the 5 portals of exit for a microbe?
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
What is interferon?
What is an oncogene?
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.