chapter 15 Microbial mechanisms of pathogenicity

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