chapter 15

Differentiate portal of entry and portal of exit.

- Portal of entry - how microbes enter the body
- Portal of exit - microbes leaves in secretions, excretions,
discharges, or shed tissue; commonly through respiratory and
gastrointestinal tracts

Discuss the causes of symptoms in fungal, protozoan,
helminthic, and algal disease

- Fungal - ingestion of trichothecenes inhibits protein synthesis
causing headaches, chills, severe nausea, vomiting and
visual disturbances; other fungi cause skin infections; ergot is an
alkaloid that can cause hallucinations; alfaltoxin is
carcinogenic; mycotoxins cause death
- Protozoan - reproduce within cells, digest cells and tissue
fluids, antigenic variation
- Helminthic - use host tissues for their growth, parasite blocks
lymphatic circulation, waste products
- Algal - neurotoxins (saxitoxin

13. Using examples, describe the roles of plasmids and
lysogeny in pathogenicity

- Plasmids - resistance to antibiotics, carry info. that determines pathogenicity
- Lysogeny - bacteriophages incorporate their DNA into the bacterial
chromosome; some bacterial pathogenesis is
caused by prophages

12. Identify the importance of the LAL assay.

- Laboratory test that can detect endotoxin; created from blood of
Atlantic coast horseshoe crab (large amount of lysate
that causes clotting)

11. Outlines the mechanisms of action of A-B toxins,
membrane-disrupting toxins, and super antigens.

- A-B: Released, B attached to host cell, membrane of host
invaginates and exotoxin enters by receptor-mediated
endocytosis, A-B exotoxin and receptor are enclosed by a pinched-off
portion of membrane, A-B components separate,
A alters function, B is released for reuse
- Membrane-disrupting: Cause lysis of host cells by disrupting their
membranes (form protein channels)
- Super antigens: antigens that provoke an intense immune response;
stimulate the proliferation of T cells

10. Contrast the nature and effects of exotoxins and

- Exotoxins - produced inside bacteria and are secreted into the
surrounding medium; can act over and over again; easily
diffuse into the blood; destroy particular parts of host cells cell
by inhibiting function
- Endotoxins - part of the outer cell wall of gram-negative
bacteria; lipopolysaccharides; released when bacteria die;
stimulate cytokine production

9. Provide an example of direct damage, and compare this to
toxin production.


8. Describe the function of siderophores.


7. Describe how bacteria use the host cell's cytoskeleton to
enter the cell.


Define and give an example of antigenic

- Pathogens alter their surface antigens; Influenza Virus, Neisseria
gonorrhoeae, Trypanosoma

5. Compare the effects of coagulases, kinases, hyaluronidase,
and collagenase.

- Coagulases - bacterial enzymes that clot the fibrinogen in blood
(fibrinogen is converted to fibrin)
- Kinases - enzymes that break down fibrin and digest clots
- Hyaluronidase - hydrolyzes hyaluronic acid (polysaccharide that
holds together cells in connective tissue; destroyed by
IgA proteases)
- Collagenase - Facilitates the spread of gas gangrene (breaks down
collagen, which forms the connective tissues of
muscles and other organs

4. Explain how capsules and cell wall components contribute to

- Capsules - formed by glycocalyx material, resists hosts defenses
and prevents phagocytosis
- Cell wall components - chemical substances contribute to virulence
(M protein is heat and acid-resistant/mediates
attachment; waxy lipid resists phagocytosis)

3. Using examples, explain how microbes adhere to host cells.

- Pili, fimbriae, flagella; majority of adhesins are glycoproteins or
lipoproteins (receptors are typically sugars, such as
- biofilms - masses of microbes and extracellular products (65% of
human bacterial infections)

Define ID50 and LD50

- ID50 - infectious dose for 50% of sample population
- LD50 - lethal does for 50% of sample population

1.Identify the principal portals of entry.