Chapter 15

Question 1

pathogenicity

Answer 1

ability of microbes to cause disease

Question 2

virulence

Answer 2

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

Question 3

virulence factor

Answer 3

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

Question 4

portals of entry

Answer 4

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

Question 5

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

Answer 5

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

Question 6

portals of entry: skin

Answer 6

larvae of hookworm enter the host by penetrating intact skin

Question 7

portals of entry: parenteral route

Answer 7

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

Question 8

Numbers of invading microbes

Answer 8

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

Question 9

ID50

Answer 9

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

Question 10

LD50

Answer 10

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

Question 11

Adherence

Answer 11

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

Question 12

Means by which microbes attach to their host cells

Answer 12

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

Question 13

biofilms

Answer 13

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

Question 14

importance of biofilms

Answer 14

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.

Question 15

factors contributing to the ability of bacteria to penetrate host defenses

Answer 15

Capsules, cell wall components, Enzymes

Question 16

how do capsules contribute to pathogenicity

Answer 16

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

Question 17

how do cell wall components contribute to pathogenicity

Answer 17

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

Question 18

How do the bacterial exoenzymes contribute to virulence

Answer 18

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

Question 19

bacterial enzyme: coagulase

Answer 19

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

Question 20

bacterial enzyme: kinase

Answer 20

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

Question 21

bacterial enzyme: hyaluronidase

Answer 21

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

Question 22

bacterial enzyme: collagenase

Answer 22

Breaks down collagen and facilitiates spread (gas gangrene)

Question 23

bacterial enzyme: IgA protease

Answer 23

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

Question 24

bacterial enzyme: Antigenic variation

Answer 24

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)

Question 25

bacterial enzyme: penetration into host cell cytoskeleton

Answer 25

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

Question 26

Describe the function of siderophores

Answer 26

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.

Question 27

Nature of exotoxins

bacterial source
where in cell
chemistry
effect on body
heat
toxicity
fever producing
antibodies
lethal dose
diseases

Answer 27

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

Question 28

Effects of exotoxins

Answer 28

Destroying particular parts of the host’s cells

Inhibiting certain metabolic functions

Question 29

Nature of endotoxins

bacterial source
where in cell
chemistry
effect on body
heat
toxicity
fever producing
antibodies
lethal dose
diseases

Answer 29

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

Question 30

Effects of endotoxins

Answer 30

stimulate macrophages to release high concentration of cytokines

Question 31

Types of endotoxins

Answer 31

A-B toxins, membrane-disrupting toxins, superantigens

Question 32

endotoxins: a-b toxins

Answer 32

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.

Question 33

endotoxins: membrane-disrupting toxins

Answer 33

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

Question 34

endotoxins: superantigens

Answer 34

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

Question 35

mechanisms of diphtheria toxin

Answer 35

inhibits protein synthesis in eukariotic cell using A-B mechanism

Question 36

mechanisms of erythrogenic toxin

Answer 36

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

Question 37

mechanisms of botulinum toxin

Answer 37

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.

Question 38

mechanisms of tetanus toxin

Answer 38

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

Question 39

mechanisms of vibrio enterotoxin

Answer 39

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.

Question 40

mechanisms of staphylococcal enterotoxin

Answer 40

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.

Question 41

role of plasmids in bacterial pathogenicity; examples

Answer 41

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.

Question 42

role of phage DNA in bacterial pathogenicity; examples

Answer 42

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

Question 43

CPE (cytopathic events)

Answer 43

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