1 / 17

Chapter 17: IR to Infectious Disease

Chapter 17: IR to Infectious Disease. In BIOL 304, we examined how pathogens can establish an infection in a susceptible host Re: the 7 components of pathogenicity !! On the other hand, humans are defended by: Physical barriers of epithelia and skin Surface chemicals, enzymes, acids

naoko
Download Presentation

Chapter 17: IR to Infectious Disease

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Chapter 17: IR to Infectious Disease • In BIOL 304, we examined how pathogens can establish an infection in a susceptible host • Re: the 7 components of pathogenicity!! • On the other hand, humans are defended by: • Physical barriers of epithelia and skin • Surface chemicals, enzymes, acids • Competitive flora • Complement and sIg • Phagocytic cells • Specific/Adaptive IR

  2. Still, infectious disease kills millions each year *Mostly, from bacterial and viral diseases

  3. Anti-viral protection: Innate • Type I IFN’s (α & β) are triggered from infected cells • IFN’s bind to nearby cells and activate JAK-STAT pathway • Induces several gene products which function to: • Degrade viral RNA • Shuts down PS in infected cells

  4. Anti-viral protection: Adaptive Neutralization by Ab’s • If Ig can bind to viral surface, prevents binding to target cell • Or Ig can trigger Complement cascade • Or bound Ig can agglutinate viruses to be phagocytized • sIgA blocks binding to mucosal surfaces

  5. Anti-viral protection: Adaptive • Cell-mediated response • Starts with TH1 cells • Release of cytokines: • IL-2, IFN-γ, TNF • IL-2/IFN- γ act. NK cells • IL-2 recruits TC cells • Within 7-10 days, most virions are elim; parallels the development of Tc’s vs the virus

  6. Evasion of Host defenses • Block intracellular effects of IFN’s (Hep C) • Block TAP function for Ag delivery to MHC I (HSV1 and 2)  prevents lysis by Tc’s • Block formation of MHC I (Adenovirus, CMV) • Block formation of MHC II (CMV, measles, HIV) • Block complement fixation (Vaccinia binds to C4b*; HSV binds to C3b**) • Antigenic variation (influenza, rhinovirus, HIV) • Imunosuppression thru immune cell infection

  7. Case study in viral mutation: Influenza • HA binds to host cells • NA aids in viral escape from host cells • 8 RNA’s code for 10 proteins • 3 types (A,B, and C) • Type A resp. for pandemics • 13 dif’t HA’s; 9 dif’t NA’s • WHO nomenclature of Type A: Ex: A/Sw/Iowa/15/30 (H1N1)

  8. Case study in viral mutation: Influenza • Antigenic change is so complete no herd immunity can build • Ag variation occurs in HA and NA from: Antigenic Drift Antigenic Shift 1934 – H0N1 1947 – H1N1 1957 – H2N2 1968 – H3N2 1977 – H1N1 1989 – H3N2 *Each Ag shift results in new pandemic outbreaks **current vaccine has both H3N2 & H1N1 strains

  9. Anti-bacterial protection • Bacterial infections are controlled by different IR’s (just as in viral infections) • The type of IR centers on: • Amount of inoculum • Degree of virulence • Extra- vs intra-cellular infection • MO’s enter mostly through mucosal surfaces (resp/g.i tract/g.u. tract) • Cuts/breaks in skin

  10. IR’s to Extra-cellular infections • Stim production of humoral Ab’s from local lymph nodes. Ab’s function to: • Opsonize bacteria  phagocytosis • Opsonize toxins  inactivation • Bind/activate complement  cell lysis • Stimulate/amplify inflammation  mast cell degran • Chemotaxis

  11. Antibody mediated responses to extra-cellular bacteria

  12. IR’s to Intra-cellular infections • Induce a Delayed-type hypersensitivity rxn • Cytokines, notably IFN-γ from CD-4 T cells activate MØ Cell-Mediated response

  13. Evasion of Host Defenses • Major steps to bacterial infection: • Attachment • Proliferation/growth • Invasion • Toxin-induced damage • Host defenses operate during each one of these steps

  14. Examples of pathogen control Diptheria • Classic example of imm bestowed by toxoid • 1923-Ramon inactivated exotoxin w/ formaledhyde • Significant drop in # of cases since then • Toxoid administered in DTP immuniz @6-8 wks w/ boosters every 10 yrs

  15. Examples of pathogen control Tuberculosis • Inhaled bacilli ingested by alveolar MØ • Bacilli grow in and lyse MØ • Cytokines (esp IFN-y) produced by TH1 cells activates MØ to kill/ inhibit bacteria • MØ wall off bacilli at focal points in the lungs – in tubercles (granulomas) • MØ secrete IL-12 -> continue TH1 response • 10% progress to chronic pulmonary or extra-pulmonary TB

  16. Emerging Infectious Diseases • Newly described pathogens • Those (which were once under control) showing rapid increases = “re-emerging infectious disease” Ex: TB Diptheria • Causes of emerging/re-emerging diseases: • Overcrowding in cities among lower socioeconomic populations • International travel • Mass distribution of food commodity

More Related