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ability of microbes to cause disease



capacity of a pathogen to invade and cause damage to the host; it's a measure of pathogenicity


virulence factor

characteristics or structures of the microbes that contribute to their capacity to attach, enter, and survive in the host/cause damage


portals of entry

mucous membranes (respiratory, GI, genitourinary, conjunctiva); skin; parenteral route


portals of entry: mucous membranes, GI, Genitourinary, conjunctiva

majority enter through:
EX of respiratory diseases
EX of GI diseases and defenses
EX of Genitourinary diseases
Explanation of conjunctiva and EX of diseases

most pathogens enter through the mucous membranes of the gastrointestinal and respiratory tracts. Respiratory: easiest & most frequent--common cold, pneumonia, tuberculosis, influenza, measles. GI tract: most microbes are destroyed by the hydrochloric acid and enzymes in the stomach or by the bile and enzymes in the small intestin; pathogens enter through this route are adapted to sruvive. --polio, hepatitis A, typhoid fever, amebic dysentery, giardiasis, shigellosis, cholera. Genitourinary: sexually transmitted diseases. Conjunctiva: lines the eyelids, covers the whites of eyeballs--conjunctivitis, trachoma, ophthalmia neonatorium


portals of entry: skin

larvae of hookworm enter the host by penetrating intact skin


portals of entry: parenteral route

microbes are deposited directly into the tissues when the skin/mucous membranes are penetrated


Numbers of invading microbes

increase the number of pathogens, increase the likelihood of disease.



infectious dose of 50% of a sample population; indicates the virulence of a microbe.



Lethal dose for 50% of a sample population; indicates the potency of a toxin



adhesion, the attachment of pathogens to their host tissue at their portal of entry


Means by which microbes attach to their host cells

adhesins: interaction/binding between the adhesins (surface molecules) on pathogens with the surface receptors on the host; biofilms (see next)



slimy community of microbes growing on a surface; formed by the masses of microbes and their extracellular products attach to living/nonliving surfaces.


importance of biofilms

resistant to disinfectants, antibiotics; involved in 65% of all human bacterial infections. Example: strep mutans attach to teeth by glycocalyx and the fimbrae of Actinomyces adhere to glycocalyx of Strep mutans. Together, they form a biofilm and contribute to dental plaque and tooth decay.


factors contributing to the ability of bacteria to penetrate host defenses

Capsules, cell wall components, Enzymes


how do capsules contribute to pathogenicity

bacteria secrete glycocalyx to its cell surface that forms capsules; resists the phagocytosis of host; increases virulence. Examples: strep pneumoniae


how do cell wall components contribute to pathogenicity

Involved in attachment of host cells and resistance to phagocytosis by the host. Example: strep pyogenes M protein, Neisseria gonorrhoeae fimbrae & Opa (outer membrane protein), and mycolic acid of cell wall of mycobacterium tuberculosis


How do the bacterial exoenzymes contribute to virulence

digests materials between cells and forms or digests blood clots, among other functions.


bacterial enzyme: coagulase

CLOTS blood: staph produces bacterial coagulase that converts fibrinogen to fibrin clot, protects bacterium from phagocytosis and other host defense


bacterial enzyme: kinase

BREAKS DOWN CLOTS: Strep pyogenes produces fibrinolysin that breaks down fibrin clots formed by host to confine infection


bacterial enzyme: hyaluronidase

hydrolyzes hyaluronic acid, an extracellular substance outside of host cells, so the connection among cells is disrupted. Involved in the tissue blackening and spreading of the infected pathogen.

EX: streptococci and clostridium perfringes


bacterial enzyme: collagenase

Breaks down collagen and facilitiates spread (gas gangrene)


bacterial enzyme: IgA protease

Destroys IgA antibodies by the host defense against adherance to pathogens to mucosal surfaces - Neisseria gonorrhea


bacterial enzyme: Antigenic variation

Alter surface antigens so not to be recognized by the antibodies from the host.

EX: Neisseria gonorrheoeae (Opa-encoding gene) and influenza (this is why you need annual flu shot)


bacterial enzyme: penetration into host cell cytoskeleton

Salmonella - invasins that rearrange the host actin filaments; leads to membrane ruffling, the bacterium sinks into ruffle and is engulfed by host cell.

Shigella & Listeria - actin to propel through host cytoplasm.

Bacteria can also move from cell to cell via the adherin of cell junctions


Describe the function of siderophores

proteins secreted by pathogens to score free iron--they are released, and take away iron from iron-transporting proteins by binding to iron even more tightly.


Nature of exotoxins

bacterial source
where in cell
effect on body
fever producing
lethal dose

gram positive and negative
inside cell
protein A & B
specific for tissue
unstable in heat
very toxic
not fever producing
converts to toxoids
low lethal dose
gas gangrene, tetanus, botulism, diptheria, scarlet fever


Effects of exotoxins

Destroying particular parts of the host's cells

Inhibiting certain metabolic functions


Nature of endotoxins

bacterial source
where in cell
effect on body
fever producing
lethal dose

gram negative only
outer membrane
lipid A
systemic, same signs & symptoms for all
stable in heat
not as toxic
fever producing
cannot convert to toxoids
high lethal dose
typhoid fever, uti, meningitis


Effects of endotoxins

stimulate macrophages to release high concentration of cytokines


Types of endotoxins

A-B toxins, membrane-disrupting toxins, superantigens


endotoxins: a-b toxins

consists of polypeptide A (active) and B (binding). B binds to cell receptors, then A-B toxins enter cell by receptor mediated endocytosis. Once inside, A disrupts cellular functions, and inhibits protein synthesis of the cell.


endotoxins: membrane-disrupting toxins

Disrupts cell membrane and causes lysis of host cells by forming protein channels (S. aureus) and disrupting the phospholipid of cell membrane (Clostridium perfringes)


endotoxins: superantigens

induce T cell proliferation and excessive release of cytokines by T cells that lead to fever, diarrhea, shock. EX: staphylococcal toxins


mechanisms of diphtheria toxin

inhibits protein synthesis in eukariotic cell using A-B mechanism


mechanisms of erythrogenic toxin

superantigens that damage plasma membranes of blood capillaries under skin and produce red skin rash. EX: Scarlet fever from Strep. pyogenes


mechanisms of botulinum toxin

acts at the neuromuscular junction (btw nerve & muscle cells), and prevents the transmission of impulses from nerve cell to the muscle. Binds to nerve cells and inhibits release of neurotransmitter Acetylcholine. Botulism toxin causes paralysis in which muscle tone is lacking.


mechanisms of tetanus toxin

produces neurotoxin (A-B toxin) that reaches CNS and binds to nerve cells that control contraction of skeletal muscles that normally send inhibiting impulses that prevent random contractions and terminate completed contractions. Result is uncontrollable muscle contractions, producing the convulsive symptoms of tetanus


mechanisms of vibrio enterotoxin

produces A-B enterotoxin. Subunit B binds to epithelial cells, subunit A causes cells to secrete large amounts of fluids & electrolytes. Normal muscular contractions are disturbed, leading to severe diarrhea that may be accompanied by vomiting.


mechanisms of staphylococcal enterotoxin

produces a superantigen that affects the intestines the same way as a vibrio enterotoxin. One strain of S. aureus also produces a superantigen that results in TSS.


role of plasmids in bacterial pathogenicity; examples

plasmids carry information that determine resistance factors and virulence factors - some plasmid genes include toxin genes (tetanus neurotoxin, heat-labile enterotoxin, staph enterotoxin), some contain info about enzymes (Strep. Mutans involved in tooth decay), adhesins & coagulase info, etc.


role of phage DNA in bacterial pathogenicity; examples

some bacteriophages can incorporate their DNA into bacterial chromosome, becoming a prophage, thus remain latent (lysogeny) EX: diptheria toxin, erythrogenic toxins, staphylococcal enterotoxins, etc.


CPE (cytopathic events)

Visible effects of viral infection. Includes cytocidal effects (CPE that result in cell death) and noncytocidal effects (CPE that results in cell damage but not cell death). Some potential effects include: stopping host synthesis machinery or mitosis, destroy intracellular contents & cause cell death, form inclusion bodies, form syncytium, reduce production of cytokine, induce production of inferons, induce antigenic changes on the surface of infected cells, induce chromosomal changes, loss of contact inhibition