Chpt 15 Microbial Mechanisms of Pathogenicity

Microbial Mechanisms of Pathogenicity
Chapter 15

Pathogenicity: the ability to cause disease in a host.
Virulence: the degree of pathogenicity. A measure of pathogenicity.

I. Portal of entry: the avenue by which a microbe gains access to the body. (There is also a portal of exit, which like portal of entry is often a characteristic of a disease.)
A. Mucous membranes: unlike skin, mucous membranes are warm, moist, thin living cells.
1. respiratory tract: the easiest, most frequently used route of entry for infectious microorganisms. (Sushma said best portal is broken skin)
a. common cold
b. pneumonia
c. TB
d. influenza
e. measles
f. small pox
2. gastrointestinal tract: microorganisms enter by contact with food, water, or fingers
a. poliomyelitis
b. hepatitis A
c. typhoid fever
d. amoebic dysentery
e. shigellosis
f. cholera
3. genitourinary tract
a. HIV/AIDS
b. Chlamydia
c. syphilis
d. gonorrhea
4. conjunctiva (eyes)
B. Skin
1. sweat glands
2. cuts (broken skin is the best portal of entry * according to Sushma)
C. Parenteral route: microorganisms entering through skin or mucous membranes that are punctured or injured (traumatized).
D. Preferred portal of entry (did not go over)
E. Numbers of invading microbes (did not go over)
F. Adherence: attachment between pathogen and host by the use of surface adhesions.
1. Suckers and hooks (helminthes)
2. Ligands: proteins on surface of bacteria and viruses found on fimbraie, flagella and glycocalyces.
a. adhesions: proteins on surface of bacteria
b. attachment proteins: proteins on surfaces of viruses.
3. Surface receptors: complementary receptors on host cells to which ligands attach.

II How bacterial pathogens penetrate host defenses.
A. Capsules: resist phagocytosis
1. Streptococcus pneumoniae
2. Haemophilus influenzae
B. Cell wall components: waxes in cell walls resist digestion by macrophages.
1. Mycobacterium tuberculosis
C. Enzymes
1. Extracellular enzymes: dissolve structural components/chemicals
a. Hyaluronidase and collagenase allow bacteria to invade deeper tissues
b. Coagulase: coagulates blood clot proteins, “hiding” the bacteria protecting it from phagocytosis. (produced by S. aureus)
c. Kinase: dissolves clots, releases bacteria from clots. A modified version can be used to dissolve blood clots.
i. Streptokinase
ii. Staphylokinase
D. Antigenic variation (did not go over)
E. Penetration into host cell cytoskeleton
1. Adhesins: microbes attach to host cells by adhesions.
III How bacterial pathogens damage host cells
A. Siderophores (did not go over)
B. Toxins: poisonous substance produced by certain microorganisms. Chemicals that harm tissue or elicit host immune response, damaging tissue.
1. Definitions:
a. Toxigenicity: the capacity to produce toxins.
b. Toxemia: the presence of toxins in the blood and lymph. Toxins enter the bloodstream and are carried to other parts of the body.
2. Types:
a. Exotoxins: proteins secreted by the bacterium, mostly gram +, into the surrounding medium or released following lysis. Destroy host cells or interfere with host cell metabolism by secreting toxin from cell.
i. highly specific
ii. among the most lethal substances known
iii. antitoxins: antibodies (produced by the body) that provide immunity to exotoxins.
iv. both gram + and gram – but mostly gram +
v. types of exotoxins
a. cytotoxins: attack any type of cell
b. neurotoxins: attack nerves. Cause paralysis, stiff muscles. (Clostridium gram +)
c. enterotoxins:attack the stomach (E coli gram -)

vi. hemolysins: toxins that target red blood cells. Streptococci
vii. representative extoxins (did not go over): named for the tissues they affect, such as neurotoxins, cardiotoxins, etc.
b. Endotoxins: not secreted by bacteria, but are part of the outer portion of the cell wall of gram – bacteria.
i. gram – cell wall
ii. have lipopolysaccharide layer on outer membrane (LPS)
iii. lipid A: the lipid part of LPS
a. released upon bacterial cell death often causing fever and inflammation. Also can be released during bacterial multiplication.
iv. at high levels can cause hemorrhaging and septic shock
v. released only after bacteria have died. (therefore to give antibiotics is wrong in this case because the dead bacteria would release all of the endotoxins. Hydrate patient.)
C. Anti-phagocytic factors: (whenever you see this term you should remember macrophages)
1. macrophages: white blood cells that engulf and remove invading pathogens.
a. capsules
i. made up of chemicals normally found in a host
ii. slippery glycocalyx blocks phagocytosis
b. antiphgocytic chemicals: chemicals that prevent the fusionof lysosomes with phagocytic vesicles.
i. M protein: protein produced on its cell wall by Streptococcus pyogenes
ii. Leudocidins: kill white blood cells
iii. Mycolic acid: lysozomes cannot enter. Mycobacterium
IV Plasmids, Lysogeny, and Pathogenicity (did not go over)
V Pathogenic properties of nonbacterial microorganisms (did not go over)
A. Viruses
1. Cytopathic effects of viruses:
B. Fungi
C. Protozoa
D. Helminths
E. Algae







Extra

This outline follows the book format which is different from Sushma’s format. All of the information that Sushma discussed is included on this outline, just in a way that is easier for me to understand. I hope it helps. :0)


Virulence: a measure of pathogenicity (the ability of an organism to cause disease)
Viurlence factors: (besides adhesions these can be classified into three categories)
I Adhesins
II Extracellular enzymes
II IToxins
IV Anti-phagocytic factors


Possible questions:
Which produces an endotoxin? Gram – (neg)

Need to know which bacteria are gram – for above question.

See table 15.3 page 464

Denatured proteins can renature when cooled causing food poisoning.
Protein in endotoxins are lipids

Damage to host cells occur in the Log phase.