1. Chapter 16 Host- Microbe Interaction
Biology 261
Medgar Evers College
Dr. Santos

2. Establishing cause of infectious disease
1- Koch’s postulate
a- the microorganism must be present in every case of the disease
b- the organism must be grown in pure culture from dispersed hosts.
c- the same disease must be produced when a pure culture of the organism is introduced into a host.
d- the organism must be removed or isolated from experimentally infected hosts.

4. Molecular Koch’s postulates
a- the virulence factor or its product should be found in pathogenic strains of the organism.
b- mutating the virulence gene to disrupt its function should reduce the virulence of the pathogen.
c- reversion of a mutated virulence gene or replacement with a wild type version should restore virulence to the strain.

5. Pathogenicity/Virulence
Pathogenicity refers to the ability of an organism to cause disease (harm the host).
Virulence- the extend of pathogenicity

6. Mechanism of pathogenicity
1- establishment of infection
2- invasion and breach of anatomical barriers
3-avoiding host defense
4-damage to the host

7. Principles of infectious disease
Incubation period- time between infection and onset of disease.

8. Establishment of infection
Adherence- the use of adhesin proteins to bind to host.
Adhesin proteins are found at tip of pili.
Pili used for attachment are called fimbriae.
The binding of an adhesin to host surface receptor is highly specific.

9. Colonization
Colonization- this involves taking over sites that are already populated by a normal flora. The pathogen must compete for nutrients, space, and overcome the host’s immune system.

10. Invasion of Anatomical barriers
I Penetration of skin to get in or get in by means of a vector such as an arthropod or a cut.
II Penetration of the mucous membrane.

11. 2 ways to invade mucous membranes
1- Directed uptake by cells 2- Exploit antigen sampling system

12. Directed uptake by cells
Pathogen induces cells to
engulf via endocytosis
Salmonella uses type III
secretion system to inject
effector proteins; actin
molecules rearrange, yield
membrane ruffling

13. Type III secretion system
(injectisome)
Effector proteins
induce changes
(e.g., altering of cell’s
cytoskeleton structure)
Can induce uptake
of bacterial cells

14. Antigenic sampling
Special cells called M cells are located between the intestinal lumen and secondary lymphoid tissues called peyer’s patches.
These M cells sample fluids of the intestine and if a microbe is detected, it delivers the microbe to a macrophage that destroys it.

15. Some strains of shigella exploit this system to get into the mucous membranes and induce apoptosis in the phagocyte.

17. Avoiding the host defense
I Hiding inside the host
II Avoiding killing by complement system proteins
III Avoiding destruction by phagocytosis by avoiding recognition, attachment, and eventually escaping from the phagosome.

18. IV Avoiding antibodies by using proteases to destroy them and antigenic variation
Ig A antibodies circulating the host bind to adhesin proteins of pathogen preventing their attachment to host receptor.
To overcome this, a rapid turnover of the pili occurs, antigenic variation of the pili can occur and the activation of IgA protease to destroy IgA.
Ex; Neisseria gonorrhoeae varies antigenic structure of pili

19. V mimicking “self cells”.
Streptococcus pyogenes form capsule from hyaluronic acid, a polysaccharide found in tissues

20. Avoiding recognition
1- capsule proteins inactivate the C3b complement component
2- M proteins found in strains of Streptococcus pyogenes also inactivate the C3b complement component.
3- Fc receptors found on the surface of Staphylococcus and Streptococcus bind to the fc region of an antibody preventing it from binding correctly!

22. Damage to the host 3 main mechanisms; Release of exotoxins
Use of endotoxins
Damaging effect of the Immune system

23. Exotoxins
These are proteins that have very specific damaging effects. There are 4 types;
1- A-B toxins, the A subunit is the toxin while the b subunit binds to specific receptors on target cell.
2- Super-antigens interfere with T cell responses by causing non-specific activation of T cells. This leads to a massive release of cytokines that can promote tissue damage.

25. Examples of AB toxins Cholera exotoxin Enterotoxins Pertussis toxin
Anthrax toxin
Botulin toxin
Tetanus toxin
Neutrophil activating protein

26. Examples of superantigens
1- Toxic shock syndrome toxin-1- secreted by S. aureus leading to fever, rash and shock 2- Staphylococcal enterotoxin- secreted by S.aureus leading to vomiting, fever, diarrhea, and nausea.

28. 3- Membrane damaging toxins that disrupt the integrity of the cell membrane by forming pores or removing the polar head group on phospholipids
4-Hydrolytic enzymes that can break down tissues.
Example is exfoliatin toxin secreted by S. aureus to cause scalded skin syndrome.

29. Endotoxin
a toxin that is confined inside the microorganism and is released only when the microorganism is broken down or dies.

30. Endotoxins
This involves the Lipid A of the LPS of a cell wall of a bacteria. The host immune system produces massive amounts of pro- inflammatory cytokines in response to its presence.
The immune system will mount a massive attack against lipid A. This can lead to systemic shock or endotoxic shock.