pathogenicity
the ability to cause disease
virulence
the extent of pathogenicity
to cause disease, pathogens must
gain access to the host, adhere to host tissue, penetrate and evade defenses and damage host tissue
some pathogens
produce waste that acculmulates or dont penetrate the body to cuase disease
mucous membrane
portal of entry, lines respiratory, gi tract, gu tract, eye; inhaled or ingested
skin
portal of entry, unbroken- most pathogens cant enter, hair follicles and sweat glands
parenteral route
route other than GI tract, punctures, injections, bites, cracked skin/ mucous membrane
preferred portal of entry
some organisms only cause disease if they enter via the preferred porta of entry
swallowed
preferred portal of entry for salmonella typhi, when rubbed on skin nothing
inhaled
preferred portal of entry for streptococci, when swallowed nothing
increase number of microbes
increase likelyhood of disease
ID50
infectious dose for 50% of the test population; way of expressing the virulence of a pathogen
LD50
lethal dose for 50% of the population; way of expressing the potency of a toxin
pathogenic adhesins/ligands
bind to complimentary surface receptors on host cells, glycoprotiens and lipoprotiens; glycocalyx; pili, fimbriae;
alterations in adhesin or receptors
will interfere with adherence, thus potentially preventing infection
biofilms
mass of microbes, clinging to a surface, taking in and sharing nutrients; resist disinfection and antibiotics; colonize teeth, medical instruments
bacteria penetrate host defenses
capsule, cell wall components, enzymes, antigenic variation, penetration into host cell cytoskeleton
capsule
glycocalyx material; prevents phagocytosis due to chemical composition; antibodies can be produced against capsule; many nonpathogenic organisms produce capsule
pathogenic capsules
Streptococcus pneumoniae; Haemophilus influenzae, Bacillus anthracis
M protiens
cell wall components that resist phagocytosis, mediate attachment to host epithelium; Streptococcus pyogenes
Opa protien
cell wall component- outer membrane protien, assists fimbriae to attach to host cells; Neisseria gonorrhoeae
mycolic acid
waxy lipid cell wall component that resist phagocytosis; Mycobacterium tuberculosis- may multiply inside phagocyte
bacterial coagulase
enzyme that converts fibrinogen to fibrin threads to form blood clot; clot protects bacteriuum from phagocytosis; some Staphylococcus
bacterial kinases
enzymes that breaks down fibrin and digest clot
fibrinolysin
streptokinase produced by streptococci used for heart attacks due to obstructed coronary arteries
hyaluronidase
hydrolyzes hyaluronic acid that holds together connective tissue; promotes spread of pathogen; produced by streptococci
collagenase
hydrolyzes collagen; produced by Clostridium spp. facilitates gas gangrene spread
IgA proteases
destroy IgA antibodies that prevent pathogen adherence to mucosal surfaces; N. gonorrhoeae
antigenic variation
allows pathogen to alter surface antigens so that they are not destroyed by host antibodies that were produced in response to prior antigens; N. gornorrhoeae has several copies of opa-encoding gene
actin
major eurkaryotic cytoskeleton component may be used by microbes to move from one cell to the next
invasins
microbe surface protiens induced by contact with host cell, enable Salmonella to alter host actin to enter a host cell
pathogens cause host cell damage
by using host nutrients, direct damage in the immediate vicinity, toxin production, inducing hypersensitivity reactions
siderophores
some pathogens secrete this to take iron from iron transport protiens and hemoglobin, and make iron available to bacterium
direct damage to cell
disrupt host function, use host for nutrients, produce waste products, rupture cell to release viruses, toxins
toxins
poisonous substances that contribute to pathogenicity, produced by some microorgansims, transported by blood or lymph
toxin range of effects
death, fever, cardiovascular disturbance, diarrhea, shock, inhibit protien syntheisis, destroy blood cells, disrupt nervous system, almost half damage eukaryote cell membrane
toxigenicity
ability to produce a toxin
toxemia
presences of tosin in the hosts blood
toxoid
inactivated toxin used in a vaccine, can stimulate antitoxin production, diphtheria, tetanus
antitoxin
antibodies against a specific toxin, provide immunity to exotoxin
exotoxins
protiens produced inside pathogenic bacteria, mostly gram +ve, released following lysis
intoxications
signs and symptoms is causes by ingestin a toxin
exotoxin names
by the type of host cell that is attacked, neurotoxins, cardiotoxins cytotoxins or associated disease, and bacterium that produced them
A-B toxins
exotoxins with a non-toxic portion (B) that binds to a host cell and a toxic portion (A) that acts on the host cell to produce an effect
Membrane disrupting toxin
lyse host cell, kill phagocytes and phagosomes, disrupt phospholipids of membrane (Clostridium perfringens), make protien channels in plasma membrane (staphylococci and streptococci)
superantigen
exotoxins that cause an intense immune response due to release of cytokines from host Tcells
cytokines
chemical mediators secreted at site of inflammation, get into blood stream and attract other cells
endotoxins
are the lipid portion of LPS that are part of the outer membrane of the cell wall of gram -ve bacteria, endotoxins are liberated when the bacteria die and the cell wall breaks apart
DIC
disseminated intravascular coagulation, activation of blood clotting protiens, formation of small blood clots
pyrogenic response
release endotoxin within macrophage, release cytokines, hypothalmus is stimulated, protaglandin is released, thermostat is reset
prostaglandin
hormonelike substance that is released by damaged cells, intensifies inflammation
rabies virus
attachment site mimics acetylcholine
viral mechanisms
have attachment sites for receptors on host cells, mimic substances useful to host cells
CPE
cytopathic effect of viruses, visible effect on a host cell, caused by a virus, that may result in cell death or damage
cytocidal effect
CPE that results in cell dealth
noncytocidal effect
CPE that results in cell damage
pathogenic effects of fungi
metabolic products may cuase symptoms, allergic response, toxins inhibit protien synthesis, attach and cause skin disease, capsule prevents phagocytosis
aflatoxin
excessive mold toxin growing on peanuts
pathogenic properties of protozoa
presense and waste products may cause symptoms
protozoan avoid host defense
by invading host cells, multiplying and rupturing cells, growing in phagocyte vacuoles, antigenic variation (Tripansoma)
pathogenic properties of helminths
cellular damage evokes symptoms, produce large parasitic masses, presence of parasites interferes with host function, waste can cause symptoms
pathogenic properties of algae
produce neurotoxins saxitoxin
portals of exit
respiratory tract, GI tract, GU tract, skin, blood