chapters 18 & 19: practical applications of immunology immune system disorders

1. chapters 18 & 19: practical applications of immunologyimmune system disorders

2. immunological memory

3. immunological memory movement via circulation memory B  bone marrow secrete Ab continuously effector memory T  tissue space central memory T  lymphatic circulation

4. Ab & TCR affinity • memory cell abundance • 100–1000x 1°response • memory affinity • 1° 1/100000 bind tightly • 2° 1/1000 bind tightly • B cells don’t require TH cells • 1° response 12–14 d • 2° response 1–2 d

5. immunity acquired immunity acquired immunity natural natural artificial active (infection) active (infection) passive (mom  baby) passive (mom  baby) active (Ag shot) passive (Ab shot)

7. childhood immunization recommendations

8. case study: Varicellavirus • March 12, 2009 15yo female ER admission • 3d Hx rash, 1d Hx shortness of breath, fever (101.1OF) • Dx: septic shock • hospital stay • Tx: acyclovir, Abx (ciprofloxacin, meropenem, STX, ticarcillin w/clavulanate, tigecycline) &mechanical ventilation • pneumonia & acute respiratory distress • multi-organ dysfunction • pancytopenia • nosocomial infections • LRI: Enterobacter cloacae • UTI: Pseudomonas aeruginosa • sepsis: Stenotrophomonas maltophilia • prognosis: dead on day 21 • Click here to read and here to listen, if you have concerns about a link between autism & vaccinations.

9. immunological identification methods immunological assays • Ag-Ab interaction • direct detect Ag • indirect detect Ab • Sensitivity: probability of false negativeSN-N-OUTSeNsitive when Negative rules OUT • Specificity: probability of false positiveSP-P-INSPecific when Positive rules IN

10. monoclonal antibodies (mAbs) hybridoma: cancerous B cell fused to Ab producing spleen cell  mAb

11. agglutination reactions 1896: Gruber-Durham reaction: cellular (particulate) Ag & Ab 1896: Widal’s serum diagnosis of Typhoid Carriage 1900: ABO & Rh blood typing Figure 18.4

12. fluorescent Ab techniques

13. enzyme-linked immunosorbent assay (ELISA) direct ELISA indirect ELISA

14. the rapid strep test • 70–85% pharyngitis cases are viral- no Abx, bacterial cases are self-limiting • S. pyogenes causes pharyngitis and long-term sequelae (rheumatic fever, kidney disease) • No symptoms are specific to streptococcal pharyngitis • rapid strep test • 95–98% specificity; 70-95% sensitivity

15. chapter 18 learning objectives • How and when is immunological memory generated? • Where do memory B cells, effector memory T cells and central memory T cells “live?” • Compare and contrast the affinity and speed of the primary vs. the secondary immune response. • Distinguish the four ways that immunity can be acquired. Be able to recognize and give an example of each. • Describe the serological tests discussed in lecture; include direct and indirect versions of each. Understand how to interpret positive and negative results for each. As technology has advanced, how has that made these serological tests more specific? • Define specificity and sensitivity. How do these terms relate to the serological tests you described above. • Describe the GENERAL mechanism for producing monoclonal Abs. Why are they necessary?

16. chapter 19: immune system disorders

17. immune deficiencies

18. Acquired Immune Deficiency Syndrome ~1930 SIVcpz crosses species barrier 1959 death in Congo 1968 HIV in U.S. (Africa  Haiti) 1981 MMWR P. carinii homosexuals, PCP, CMV, Kaposi’s sarcoma 200000 people infected 1983 discovery of HIV AIDS in 28 nations 2011 7000 new infections/day 11% under 15, 50% 15–24 yrs ~650 million infections (~37 million current) 240 deaths/hour 6th leading overall cause of death

19. infected body fluid transmission via: sexual contact (artificial insemination) blood-contaminated needles organ transplants & blood transfusion breast milk transplacental infection of fetus HIV transmission

20. HIV target cells

21. HIV infection in CD4+ T cells active infection latent infection

22. ELISA proviral PCR: 1 infected/150,000 cells, RT-PCR: 50 RNA/ml blood western blot HIV diagnostic methods

23. the stages of HIV Infection

24. where’s the Helper (CD4) T cell???

25. Ab Fluorescence and Fluorescence Activated Cell Sorting (FACS)

26. AIDS worldwide

27. HIV/AIDS in the US

28. chapter 19 learning objectives • Contrast congenital and acquired immune deficiencies. How can microbiology aid in the treatment of congenital immune deficiencies? • Describe the origin, modes of transmission, and host cells for HIV. What do each of these host cells have in common? Does HIV behave the same way in all host cells? • How is HIV transmission different in developing vs. developed countries? • How is HIV diagnosed initially? How does this differ from the monitoring that is done to track HIV conversion to AIDS? Why is it necessary that viral RNA and viral DNA is looked for? What does each tell you about HIV? • Generally speaking, AIDS is defined by a drop in a certain body cell and a serum rise in something else. What are these? • Describe why FACS is necessary to track the population of the body cell mentioned above? • Where are the majority of people living with AIDS?