lecture 21 pathogenesis Flashcards
what is an infection
when an pathogen us growing or multiplying in or an host.
when the host is not capable of controlling g microbial activity, this iscalled __
infectious disease
the numbe rof microbes needed to kill the dose
lethal dose
what is the dose that kills 50% of hosts
LD 50
LOWER ld50 =
greater virulence
number of microbes needed to see the signs of infection in 50% of the hosts
ID 50
number of microbes needed to cause an infection
Infectious DOse
what can be said about professional poathogens
alwasy cause diseases
descirbe opportunistic pathogenes
wait for an opportunity to cause disease, like break in barrier, drop in immune system, compromised host
streptococcus pyogenes
strep throat
staphylococcus aureus
skin infections
proprionibacterium acnes
acne
examples of opportunistic pathogen
strep throat, skin infections, acne
two major branches of immunity
Nonspecific mechanisms (Innate immunity)
Specific mechanisms (Acquired immunity)
example of innate community
phagocytosis, inflammation
types of acquired immunity
humoral (antibody)
cell-mediated (cytotoxic T cells)
what immunity attacks extra-cellular pathogenes
Humoral (antibody mediated), like bloood, lymph
what immunity attacks intra cellular pathogens
cytotoxic T cell.
types of pathogenes
extracellular pathogens
intracellular pathogens
what are extracellular pathogens and what do they infect
resid eoutside of the cells and infect typical bacterium
Host defenses for innate immunity
phagocytosis
process of phagocytosis
- phagocytes digest foreign particles
- degraded in lysosomes
- cause inflammation
what clears bacteria in tack punctured skin
neutrophils and macrophage
host defenses using adaptive immunity
certain phagocytes present bits of what they captured (microbe) to T cells. T cells produce pro-inflammatory molecules.
antigen presenting cells active
T cells, b cells
viral pathogenesis steps
APSAR attachement, penetration synthesis, assemble/packaging release
what is tropism
this is a specific receptor and lignad needed/ present to bind
release is done by
lysis and budding
what is the outcome of viral poathogenesis
cell death (apoptosis), chronic infection, latent infection, cancer.
how is bacteria pathogenessis different from virus
they are looking for a niche
what happens after a bacteria finds a niche
infect host
attach to a surface
invade tissue
multiply
exit host
parts of bacteria pathogenesis
genome
pathogenicity islands
virulence plasmids
attachment of microorganism to a surface is called
binding
what is the establishmant of a microorganism in a particular niche (growth there)
colonization
what are the adhesins added
pilli, other protein
what is involved in binding
the bacteria produce adhesive struictures, adhesins, recognize specific receptors
pilli is also known as
fibriae
what can be said about the afimbiral adhesins
no pilus but still bind a receptor
what does variable domain or conserved domain need
m protein , and bind to many different receptors
other adhesive structurs
teichoic acids
capsules
flagella
non specific
how does invading into a host cell happen
induce uptake, actively invade
how doe invading int he tissues occur
lytic enzymes
transcytosis (intestinal epithelium)
penetrate deeper tissues
systemic : enter blood stream
how does salmonella invasion
through induce uptake, reorganize the actin and membrane ruffles
how does toxoplasma gondii invade the cell
bumps into target cell, releases toxins into host cell. then reorganize and allow the receptors into the adhesins. forcefil entry
what molecules alter host cell function
toxin
disease that results from a toxin
intoxication
example of toxins
botulism
tetanus
endotoxin _______ to the microbes
attach
example fo endotoxin
LPS
how does LPS work
lipid A is most immunogenic part
they induyce cells to release pyrogens
septic shock
function ofn pyrogens
induce fever
secreted toxins are called
exotoxins
types of exotoxins
- AB toxins
- Cytolytic
- Superantigens
AB toxins component
A is enzymatic subunit, B is the binding subunit
examples of AB toxins
diphtheria Toxins
cholara toxin
anthrax toxin
ways to evade phagocytosis
kill the phagocyte
phase variation=change antigen
molecules that bind natibodies
Protein A & Protein G
Bio film formation
are antibiotic resistance, rsisitance to immune activity cause chronic infection
explain frustrated phagocytosis
when white blood cells cannot phagocytose biofilm bacteria. bacteria areee resistant to antibodies and antibiotics
when are biofilm suspectible for phagocytosis
when seed is used for disoersal and dissemination
