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Chapters 18 & 19: practical applications of immunology immune system disorders.

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

2 immunological memory

3 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/ bind tightly –2° 1/1000 bind tightly B cells don’t require T H cells 1° response 12–14 d 2° response 1–2 d vaccine functions vaccine types

5 immunity acquired immunity natural active (infection) passive (maternal Ab) acquired immunity natural active (infection) passive (maternal Ab) artificial active (Ag inoculation) passive (Ab inoculation)

6

7 childhood immunization recommendations DiseaseVaccine TDaP- Tetanus, Diptheria, Pertussis tetanus & diptheria toxoid, acellular fragments of B. pertussis Pneumococcal PneumoniaS. pneumoniae polysaccharide conjugates Hib H. influenzae type b meningitis polysaccharide conjugated with protein Hepatitis Ainactivated virus Human Papillomavirusantigenic fragments of virus Influenza A injection: inactivated virus; nasal: attenuated Hepatitis Bantigenic fragments of virus MMR- Measles, Mumps, Rubellaattenuated viruses Chickenpoxattenuated Varicellavirus

8 case study: Varicellavirus March 12, yo female ER admission –3d Hx rash, 1d Hx shortness of breath, fever (101.1 O F) –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.here

9 immunological identification methods immunological assays Ag-Ab interaction direct detect Ag indirect detect Ab Sensitivity: probability of false negative SN-N-OUT SeNsitive when Negative rules OUT Specificity: probability of false positive SP-P-IN SPecific when Positive rules IN

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

11 agglutination reactionsagglutination reactions: naked eye results ~1900: Gruber-Durham reaction “agglutination” Widal’s serum diagnosis of Typhoid carriers Landsteiner: ABO & Rh blood typing Crypotococcus neoformans Ab: Pneumonia/Meningitis Figure 18.4

12 enhancing visibility: fluorescent Abs & FACS direct Lyssavirus rabies test

13 enhancing visibility: complement fixation Borrelia burgdorferi Abs for Lyme Disease diagnosis

14 enzyme-linked immunosorbent assay (ELISA) indirect ELISAdirect ELISA

15 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

16 chapter 18 learning objectives 1.How and when is immunological memory generated? 2.Where do memory B cells, effector memory T cells and central memory T cells “live?” 3.Compare and contrast the affinity and speed of the primary vs. the secondary immune response. 4.Distinguish the four ways that immunity can be acquired. Be able to recognize and give an example of each. 5.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? 6.Define specificity and sensitivity. How do these terms relate to the serological tests you described above. 7.Describe the GENERAL mechanism for producing monoclonal Abs. Why are they necessary?

17 chapter 19: immune system disorders

18 immune deficiencies immune deficiencies congenital defective genes gene therapy acquired artificial immunosuppressants natural cancer infection

19 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 –200,000 people infected 1983 –discovery of HIV –AIDS in 28 nations 2012 –>35 million people with HIV/AIDS, 3.3 million <15 YO –2.3 million infected, 260,000 <15YO –6,300 new infections daily –1.6 million people died, 210,000 <15YO 75 million total infections, 36 million total deaths

20 infected body fluid transmission via: –sexual contact (MSM, MSW, WSW, artificial insemination) –blood-contaminated needles –organ transplants & blood transfusion –breast milk –transplacental infection of fetus HIV transmission

21 HIV target cells

22 HIV infection in CD4+ T cells active infection latent infection

23 proviral PCR: 1/150,000 cells RT-PCR: 50 RNA/ml blood (replaced western blot) HIV diagnostic methods ELISA P24 Ag & HIV Ab % specificity

24 Treatment: HAART Highly Active AntiRetroviral Therapy 1987: Retrovir (azidothymidine) (N)NRTIs: (N)Nucleoside analog Reverse Transcriptase Inhibitors PIs: Protease Inhibitors  IIs: Integrase Inhibitors FIs: Fusion Inhibitors  CRAs: Chemokine Receptor Antagonists (prevent CD4 binding)

25 the stages of HIV Infection

26 Ab Fluorescence and Fluorescence Activated Cell Sorting (FACS)

27 HIV/AIDS worldwide 70% of world’s HIV/AIDS (20 million) 88% of world’s HIV/AIDS children 1.6 million infected in million died (75% of deaths worldwide)

28 HIV/AIDS in the US 1.1 million have HIV/AIDS, 1/5 don’t know they’re infected 1.7 million have been infected, 650,000 have died 50,000 new infections per year –MSM: 44x MSW, 40x women –54% blacks –20% women –Southerners

29 chapter 19 learning objectives 1.Contrast congenital and acquired immune deficiencies. How can microbiology aid in the treatment of congenital immune deficiencies? 2.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? 3.How is HIV transmission different in developing vs. developed countries? 4.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? 5.Generally speaking, AIDS is defined by a drop in a certain body cell and a serum rise in something else. What are these? 6.Describe why FACS is necessary to track the population of the body cell mentioned above? 7.Where are the majority of people living with AIDS?


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