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
endotoxins.

- 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.

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8. Describe the function of siderophores.

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

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Define and give an example of antigenic
variation.

- 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
pathogenicity.

- 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
mannose);
- 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.

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