Chapter 15: Mechanisms of Pathogenicity

Question 1

Entry Points

Answer 1

1. Mucous Membranes
   a. Respiratory mechanism
   eg. pneumonia, TB, influenza
   b. G.I. tract
   eg. E Coli, hepatitis virus
   c. Genitourinary tract
   eg. STD, HIV
   d. Conjunctiva
   eg. Pink eye
2. Skin
   eg. Streptococcus aureus, fungus (athlete’s foot)
3. Parental Route
   eg. injection site, insect bite, wound, catheter insertion route, surgery

Question 2

Adherence

Answer 2

A necessary step in pathogenicity

1. Establishment
2. Invasion

Pathogen:

1. adhesin
2. glycoprotein or lipoprotein
3. could be a capsule on the cell wall
4. fimbriae, flagella

Host

1. receptor
2. Sugars, never glucose. eg. mono/fuco sugars
3. found on the plasma membrane

Question 3

Streptococcus mutans (adhesin)

Answer 3

• glycocalyx (capsule)
• uses enzyme glucosyltransferase to turn glucose into glucan/dextran.
• this increases plaque formation (300 cells thick) on teeth
• uses enzyme glucosyltransferase to change fructose into organic acids by degenerating structures
• it loosens the tooth. this allows for an increase chance of infection and tooth loss 10%)

Question 4

Escherichia coli (adhesin)

Answer 4

Gammaproteobacteria 
Enterobacteriales
- also called coliforms
- agencies: use it for purity assessments (water supplies)
- "lab pet"
- transmits in hospital by food-borne illnesses (ground beef). This causes traveler's diarrhea. 
- can also cause UTI's (~70-75%) 
- adheres to fimbriae

Question 5

Streptococcus pyogenes (adhesin)

Answer 5

• M protein
• acid/heat resistance
• escapes phagocytosis
• adheres on the fibrils on the cell wall

Question 6

Mycobacterium tuberculosis (adhesin)

Answer 6

Gram Positive Bacteria
Actinobacteria (high GC ratio)
- TB 
- rods
- has a cell wall
- has mycolic acid
 - use an acid-fast stain
 - mycolic acid = resistance against drying/desiccation, antiseptics and antibiotics
- treatment ~9 months
- nutrients enter slowly
- colonies appear slowly, 4-6 weeks

Question 7

Coagulase

Answer 7

Exoenzyme

• coagulates blood
• fibrinogen -> fibrin (clot)
  eg. S. aureus (coagulates )
  eg. Streptococcus

Question 8

Kinases

Answer 8

Exoenzyme

• digests fibrin clots
• streptokinase - commercial to break down blood clots
  eg. S. pyogenes
  eg. a few staph

Question 9

Hyaluronidase

Answer 9

Exoenzyme

• hyaluronic acid: connective and muscle tissue
• can cause blackening of skin
• the infection starts to spread with hyaluronic acid is borken
  eg. C. perfringens (gangrene)
  eg. S. pyogenes

Question 10

Collagenase

Answer 10

Exoenzyme

• hydrolyzes collagen
  eg. C. perfringens
  eg. S. pyogenes

Question 11

Toxins Definitions

Answer 11

Toxins: substances that contribute to pathogenicity
Toxigenicity: ability to produce a toxin
Toxemia: presence of toxins in the host’s blood
Toxoid: inactivated toxin used in a vaccine
Antitoxin: antibodies against a specific toxin

Question 12

Endotoxins

Answer 12

1. Lipid A from Lipopolysaccharides (LPS)
2. In gram negative cells, outer membrane of the cell wall
   - Chemistry: lipid
   - Fever: yes, accompanied by nausea, diarrhea or dysentery
   - Neutralized by antitoxin? No.
   - Shock? Yes.
   - Ig, most common

Question 13

Exotoxins

Answer 13

1. In both gram negative and gram positive cells
2. Produced during metabolism
   - Chemistry: protein
   - Fever: no.
   - Neutralized by antitoxin? Yes.
   - Soluble by body fluid
   - Produces Ig
   - Used in vaccines after they are chemically changed. Called toxoids. eg. DTP

Question 14

Classic A-B Exotoxins

Answer 14

• Polypeptide
• B is used for entry
• A damages the cells
  1. Diotheriotoxin
• forms a pseudomembrane
• binds: leads to cell death in protein synthesis
• pseudomembrane forms in respiratory tract causes death

2. Tetanospasmin
   - B -> A in the nerves at the neuromuscular junction
   - shuts down the relaxation pathyway
   - spams can case lockjaw and opsithotonos. both can lead to death
   - opisthotonos leads to spinal fracture, and eventually spasms in the cardiovascular/respiratory systems
3. Botulinum
   - release of Ach
   - falcid
   - neuromuscular junction paralysis
4. Vibriotoxin
   - B -> A in cAMP. Triggers the bind to intestinal cells
   - “little pumps”
   - Diarrhea

Question 15

Membrane Disrupting Exotoxins

Answer 15

eg. Hemolysins (blood agar)
eg. S. pyogenes (RBC)
eg. Leukocidin (WBC), S. pyogenes
eg. Erythrogenic toxins
- skin and blood
- red skin and rash (scarlet fever)
- S. pyogenes

Question 16

Superantigen Exotoxins

Answer 16

Provokes an immune response

• T cells secrete cytokines
• Travels to various parts
  eg. GI tract, resp. tract, kidneys
• Symptoms are nausea, vomiting, diarrhea and shock
  eg. Toxic Shock Syndrome
  eg. Food poisoning (violent), S. aureus
• 1-6 hours

Question 17

Endotoxins

Answer 17

Fever

- gram negative bacteria is engulfed by the macrophage/monocyte. enzymes begin to break it down into smaller fragments

Question 18

Cell Wall of Gram Negative, Lipid A

Answer 18

• Interleukin-1 is a cytokine
• messengers that travel through the blood vessels and reach the hypothalamus
• Lipid A - IL-1 - blood vessels - brain - hypothalamus secretes prostaglandins - FEVER

Question 19

Stages of Fever

Answer 19

1. Chills
   - Interleukin-1 is in abundance
   - Shivering
2. Crisis
   - Interleukin-1 has decreased
   - Sweating

Question 20

Shock

Answer 20

• any life threatening change in blood pressure
  1. release of cachetin
  TNF, tumor necrosis factor
  2. Travels through the blood vessels
  3. Vital organs
  e.g G.I. tract, kidneys
  4. Kidney failure, death