1. Host- Microbe Interactions
Biology 261
Medgar Evers College
Dr. Santos

2. Infection process!

3. Section 16.1 Symbiosis- relationship between organisms; three types
Mutualism
Commensalism
Parasitism

4. Section 16.2
Normal Microbiota

5. Beneficial roles of Normal flora
Protection against infection
Aids in digestion
Producing substances important for human health.

6. 16.3 Terms to know
Colonization- microorganism establishes itself and multiplies itself in an environment.
Infection- the host-microbe relationship is parasitic.
Symptoms- subjective effects of the disease such as pain and nausea
Signs- objective evidence such as rash, pus formation or swelling.
Subclinical- symptoms are mild enough to go unnoticed or do not appear.

7. Contagious disease/communicable- disease that spreads from one host to another.
Infectious dose- the number of microbes needed to establish infection.
Localized infection- the microbe is limited to one small area.

8. Systemic infection- the infectious agents spreads throughout the body.

9. Bacteremia- bacteria circulating in blood
Toxemia- toxins circulating in blood
Viremia- viruses circulating in blood

10. 16.4 Establishing cause of infectious disease
1- Koch’s postulate- four criteria that were established to identify the causative agent of a particular disease.
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.

12. 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.

13. Pathogenicity
Pathogen- disease causing organism that contain certain “virulence factors” that allow them to cause disease.
Pathogenesis- the process pathogens use to cause disease
Virulence- degree of pathogenicity

14. Pathogenicity islands- where many virulence genes reside.
Plasmids- some virulence genes are found on plasmids such as certain pathogenic E.coli strains that cause diarrhea and C. diphtheriae (diphtheria toxin gene)

15. Virulence factors
Virulence factors- factors that aid the organism in the disease causing process. These factors include pili for attachment, toxins, enzymes, proteins that “reprogram’ the host by disrupting normal signaling processes.

16. Mechanism of pathogenicity
1- Establishing infection; adhesion, colonization, delivering effector molecules to the host cell
2-Invasion; penetration of skin and mucous membranes
3- avoiding host defense
4- damage to the host

17. 16.5 Establishing infection/adherence
First step towards infection is attachment or adhesion.
Adhesins on bacteria promote attachment.
Include Pili (type I and IV)

18. 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.

19. Delivering effector proteins to the host cells
Some gram – organisms deliver proteins to host by using syringe like systems known as type III secretion system. Some of the effector proteins induce host ot take up the pathogen.

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

21. 16.6 invasion- breaching the anatomical barrier
Penetration of skin
Penetration of mucous membrane
1- Directed uptake by cells
2- Exploit antigen sampling system

22. 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

23. Exploiting antigenic sampling system
Some strains of shigella exploit this system to get into the mucous membranes and induce apoptosis in the phagocyte.

24. 16.7 Avoiding the host defense
I Hiding inside the host

25. II Avoiding destruction by phagocytosis
preventing encounter with phagocytes
avoiding recognition, attachment,
surviving within the phagocyte (escape, prevent fusion, surviving).

26. 1-Preventing encounter with phagocyte
C5a peptidase- destroys C5a, which recruits phagocytes to area of infection.
Membrane damaging toxins to destroy phagocytes.

27. 2-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!

29. 3- surviving within the phagocytes

30. III Avoiding killing by complement system proteins Microorganisms bind to regulatory proteins involved in the complement system not allowing it to function properly.

31. IV Avoiding antibodies
IgA proteases
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, preventing the antibodies from binding.
Ex; Neisseria gonorrhoeae varies antigenic structure of pili
mimicking “self cells”.
Streptococcus pyogenes form capsule from hyaluronic acid, a polysaccharide found in tissues.

32. 16.8 Damage to the host 3 main mechanisms; Release of exotoxins
Use of endotoxins
Damaging effect of the Immune system

33. 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.

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

35. 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.

36. 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.

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

38. 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.

39. Progression of Disease
Incubation period-----illness  convalescence
Acute (strep throat)
Chronic (TB)
Latent (herpes)