1. Immune System
Chp. 9

2. Prokaryotic cells vs Eukaryotic cells
Organelles present
DNA stored as chromosomes
Sexual reproduction (different types)
Eg. Human cells
All Bacteria
No membrane bound organelles
single circular DNA molecule
No true sexual reproduction - adapt fast

3. Eukaryotic Cells, Bacteria, and Viruses
e.g. human cells
Inject their DNA into
host cells in order to
reproduce
Figure 9.2

4. Pathogens: Bacteria Characteristics: Types of Bacterial Infections:
Prokaryotic
Single celled
Use of variety of resources for growth & reproduction
Reproduce & adapt quickly!!
Types of Bacterial Infections:
E.g. Pneumonia, tonsillitis, tuberculosis, botulism, toxic shock syndrome, syphilis, Lyme disease.

5. Determination of Health Risk
Transmissibility: how easily is it passed from person to person
Mode of transmission: respiratory, fecal-oral, body fluids
Virulence: how much damage caused by infection & how rapid is the onset

6. Lymphatic System: Functions:
RECALL that lymph is defined as fluid derived from interstitial
fluid transported by lymphatic vessels.
Functions:
Maintenance of blood volume in cardiovascular system
Transport fats & fat soluble material from digestive system
Filtration of foreign material to defend against infection

7. Lymphatic System: Components
Lymph: protein-containing fluid transported by lymphatic vessels
Lymph nodes: cleanses lymph by filtering out materials
Spleen: cleanses blood, removes dying red blood cells, helps fight infection
Thymus: secretes chemicals to cause T lymphocytes to mature
Tonsils: protects throat

8. Physical and Chemical Barriers Include:
Skin
Tears
Saliva
Earwax
Digestive acids
Mucous
Vomiting
Urination
Defecation
Resident bacteria
Table 9.1

9. First Line of Defense: Skin
Physical & chemical barriers:
1. Skin: characteristics of barrier
Structure: dead layer, inhospitable to microorganisms
Constant replacement: many adhering microorganisms removed
pH = 5-6. pH too acidic for many microorganisms
to survive in or penetrate.

10. First Line of Defense cont.
tears, saliva, earwax, digestive acids, mucus,
vomiting, urination, defecation, resident
bacteria (normal flora)

11. Nonspecific Defenses: Second Line
Phagocytes - neutrophils & macrophages
digest “foreign” cells
Natural killer cells - chemically dissolve tumor cells &
virus-infected cells
Inflamatory response - attracts phagocytes & promotes
healing by increasing circulation to area
Interferons - stimulates producing proteins that
interefere w/ viral reproduction
Fever - helps to fight infections

12. The Inflammatory Response
Figure 9.7

13. Nonspecific Defenses: Second Line
Inflammatory response
Signs: redness, warmth, swelling, pain
Process:
1. tissue damage causes release of histamine
2. blood vessels dilate
3. proteins mark bacteria
4. phagocytic cells arrive & remove invading
microorganisms

14. Cells and Proteins Involved in Specific Defenses
Table 9.3

15. Specific Defense Mechanism: Third Line
Immune response:
Antigens: major histocompatibility complex (MHC) proteins that are part of the cell membrane or cell wall of viruses & bacteria. Once identified as an “invader” they trigger immune response.
B cells: produce circulating antibodies against an antigen.

16. Antibody Structure & Function:
Attachment of an antibody
Now marks the “invader” for
ingestion by phagocytotic cells
(eg. WBC)
The antigen binding site is
specific to the protein coat of
a given bacteria or virus
(species specific).
Figure 9.11

17. Line of Defense: Third Line
T cells: type of lymphocytes, recognize pathogen antigens, then attach to and kill pathogen.
Helper T cells: stimulate other immune cells
Cytotoxic T cells: kill abnormal & foreign cells
Memory T cells: reactivate on re-exposure
Suppressor T cells: suppresses other immune
cells

18. The Basis of Immunity Re-exposure to the same antigen
Results in a more
Rapid, stronger,
longer lasting
immune response.
Following 1st exposure ,
antibody response
declines after
approximately
1 month.
Figure 9.15

19. Immune Memory Creates Immunity: Primary Immune Response
Process: recognition of antigen, production and proliferation of B and T cells
Characteristics: lag time of 3-6 days for antibody production, peak at days

20. Immune Memory Creates Immunity: Secondary Immune Response
Process: recognition of antigen, production and proliferation of T cells and plasma cells
Characteristics: lag time in hours, peak in days

21. Medical assistance in the War Against Pathogens
Active immunization: effective against viruses
Passive immunization: effective against existing infections
Monoclonal antibodies: clones of hybrid cells
Antibiotics: effective only against bacteria, resistance is a problem. They act by disrupting the mitotic reproduction of bacteria. Not effective against viruses due to means by which viruses reproduce [see earlier ppt]

22. Tissue Rejection Transplants: 75% match essential
Recent advances: improvements in immunosuppressive drugs, better techniques for tissue typing, national organ bank systems
Immunosuppressive drugs: prevent patient’s immune system from attacking transplanted tissue

23. Inappropriate Immune Responses
Allergies: hypersensitivity reaction, excessive inflammatory response mediated by IgE
Localized: affect only the area exposed
Systemic: affect several organ systems
Anaphylactic shock: severe systemic allergic reaction
Symptoms: difficulty breathing, severe stomach cramps, swelling throughout the body, circulatory collapse, fall in blood pressure

24. Inappropriate Immune Responses: Autoimmune Disorders
Defective recognition of “self”
Lupus Erythymatosis (LE or Lupus): inflamed connective tissue
Rheumatoid Arthritis: inflamed synovial membrane

25. The Structure of HIV
Figure 9.19

26. Immune Deficiency: AIDS
HIV targets cells of your immune system-disabling it
HIV Retrovirus attaches to the immune system’s T helper cells [recall these cells stimulate production of other immune cells].
HIV Transmission: Body fluids
E.g., blood, semen, breast milk, vaginal secretions

27. Time Course of the Progression of AIDS after HIV Infection
Figure 9.21

28. Immune Deficiency: AIDS
AIDS progression:
Phase I: few weeks to a few years; flu like symptoms, swollen lymph nodes, chills, fever, fatigue, body aches. Virus is multiplying, antibodies are made but ineffective for complete virus removal
Phase II: within six months to 10 years; opportunistic infections present, Helper T cells affected, 5% may not progress to next phase
Phase III: helper T cells below 200 cells/mm., opportunistic infections and /or cancers present, clinical AIDS, death [victim actually dies from the secondary infections occurring after their immune system is destroyed by HIV]

29. AIDS Pandemic More than 36 million infected with HIV worldwide
Most infections in sub-Sahara of Africa
Increasing spread in Asia and India
Most often spread by heterosexual contact outside U.S.

30. Safer Sex Abstinence Reduce number of sexual partners
Choose sexual partners with low risk behavior
Avoid high risk sexual partners
Use latex or polyurethane condoms or barriers
GET TESTED

31. New AIDS Treatments Enzyme inhibitors: Protease inhibitors:
Early treatment may delay/prevent clinical AIDS
Vaccine: virus mutates rapidly preventing effective vaccine production at this time