Microbiology Ch 18/19

Vaccine = fractions of organisms that are used to produce immunity

Herd immunity = most of the population is immune - no epidemics

• 1. Attenulated whole agent - live but weakened - gain immunity quickly but can back mutate & cause disease in the immune compromised
• 2. Inactivated whole agent - dead - treated with phenol/ formalin
• 3. Toxoids - inactivated toxins - diptheria & tetanus
• 4. Subunits - fragments of organism - Hep B
• 5. Conjugated - toxoid + T independent Ag -for immature immune systems - childrens immune system s do not respond well to T ind Ag but itself until 15 month of age
• 6. nucleic acid - DNA vaccines

• I. Bacterial
• a. DPT -diptheria, pertussis, tetanus - toxoids, fragments
• b. meningicoccal
• c. H- flu
• d. Pneumococcal

• II. Viral
• a. smallpox - live attenuated
• b. polio - dead
• c. rabies - dead
• d. hep A - dead
• e. influenza - dead
• f. MMR - measels, mumps, rubella, -live attenuated
• g. chicken pox - live attenuated
• h. Hep B - fragments

• Adults w/ chronic diseases
• people over 65
• children 2-23 months

• Dead (Salk)
• used to use live attenuated (Sabin)

Hypersensitivity reactions - host responds to an allergen (Ag) - all 4 require sensitizing dose

• Type I - Anaphylaxis - systemic vs. localized
• Type II - Cytotoxic Rh ABO reactions
• Type IIII- Serum Sickness - immune complezes
• Type IV- Delayed hypersensitivity - T cell mediated

hypersensitivity - an Ag response beyond what is considered normal - also called an allergy

Allergen - the Ag to which the body is responding

Person is sensitized by previous exposure to the Ag

Ag (allergen) + IgE (on mast cell) → degranulation=histamine (from mast cell) → edema, redness, bronchoconstriction

Ag must bind to & bridge two IgE Abs to trigger degranulation → release of granules (histamine & other mediators)

• Systemic reaction - anaphlactic shock = vasodilation -low BP, bronchoconstriction →death
• Rx = EPI, steroids, antihistamine, IV fluid, O₂

• Localized reaction - also called a anaphylactoid reaction - hives, hay fever, allergic asthma
• Rx = antihistamines (block histamine receptor sites)

Can skin test to see if allergic -" wheal" - rapid local inflammation

can desensitize person to allergen - give progressively larger doses of allergen - produced blocking Ags = IgG that binds to Ag before it binds to mast cell

Mast cells are dereived from Basophils and are only found in CT - not in the blood

Involves Ag on cell / Ab (Host cell) + complement

• I. Transfusion reaction (Does not require sensitization for ABO reaction):
• RBC Ag + Host Abs + complement = RBC hemolysis of donor blood (complment activation -MAC = RBC lysis)

• II. Erythroblastosis Fetalis (requires sensitization)
• 1. Rh (-) Mother + Rh (+) Baby
• 2. Maternal anti-Rh Abs bind to fetal RBCs → hemolysis
• 3. Rx = RhoGAM - passive immunity to mother - anti-Rh Abs bind to fetal Rh Ags - prevent mother from becoming sensitized
• (Rh named for Rhesus Monkey)

• Drug Induced thrombocytopenic purpura
• 1. drug (haptens)+ platelet → drug/platelet Ag → cytolysis of platelet
• 2. thrombocytopenia = low # of platelets
• - purpura = bruise

• reaction to drugs or allergens - floating Ags, not attached to cellsAg
• (allergen) + serum IgG = Ag/ IgG complex → lodges in basement membrane (under endothelial cells) of blood vessels & causes inflammatory response (damages basement membrane)

immune complex glomeuronephritis - damage to kidney glomeruli = renal failure

Cell Mediated - hypersensitivity caused by T cells

Delayed due to travel time of T cell to tissue (24-48 hours)

• Ag = hapten (allergen) + skin protein
• primary response = sensitization
• secondary response = memory T cells cytokins activate macrophages & initiate tissue damage

poison ivy, latex, metal, some drugs (PCN), transplant rejection

TB - tine test - reaction if memT cells exist

Autoimmne Diseases are hypersensitivity reactions agaist self Ags - lack of self tolerance caused by a failure of clonal deletion mechanism

Self Ags - trigger immune response → disease

• Type II - Ab react with cell surface Ags
• Graves Disease - anti-thyroid Abs blocks TSH→hyperthyroid (goiter, bulging eyes)
• Myasthenia Gravis - anti ACH receptor Abs → receptors coated - muscle weakness

• Type III - immune complexes - deposit in tissue
• RA - rheumatiod arthritis - complex deposited in joints (synovum)

• Type IV - cell mediated - T cells -
• MS - multiple sclerosis - T cell attack myline sheaths of nerves

• cell mediated immune response
• T cell reaction against non-self HLA Ags - by t cells, cytokins, complement, macrophages, complement fixing Abs

• Rx = cyclosporin -lowers cytokins (supresses secreation of IL-2) which disrupts cell-mediated immunity by cytotoxic T cells
• - steroids also decrease immune response

transplats to immune privleged sites do not cause immune response - no host Abs (no blood flow to area)- corneal transplants

Privleged donor tissue - no Ags for host to react to - pig heart valves

• Autograft - from self (skin graft)
• Isograft - same genetically (twin)
• Allograft- another person
• Xenograft - another species (pig heart valve)
• Graft-vs-host-reaction - graft rejects host (bone marrow transplant to an immune compromised host)

• HIV = Human Immunodeficiency Virus (RNA retrovirus)
• AIDS = Acquired Immuno Deficiency Syndrome (disease)

• 1. 2 identical strands of RNA
• 2. capsid
• 3. reverse transcriptase attached to RNA
• 4. envelope - with spikes
• 

1. Spikes on envelope bind to CD4 on host T cell + co-receptor MUST bind also- CCR5 or CXCR4

• 2. Viral RNA + reverse transcriptase = double stranded DNA → provirus (inserts in host DNA)
• -replicates when T cell replicates
• - can be transcribed into RNA =HIV viron

3. HIV can infect a macrophage after it is eaten

Category A: lymphadenopathy - assympathetic - swollen lymph notes

Cat B: persistent Candida albicans infection (thrush) -fungal infection

• Cat C: Clinical AIDS - opportunistic infections called AIDS defining infections
• Clinical AIDS defined at CD4 T cell population < 200/mm³

Median time of HIV infection to AIDS onset =9-10 years

Opportunistic infections -healthy people dont get these diseases

• Kaposi's sarcoma - skin & mouth cancer - ADI
• neumocystis carinii - ADI
• TB
• taxoplasmosis

Exopsed by not infected - 1% of population have no CCR5 co-receptors on thier T cells - cant become infected with HIV

Long-Term nonprogressors - HIV infected but does not progress from latent stage - no known reason

Can take up to 3 month before HIV Ab can be detected in patients serum - Red Cross has it down to two weeks (for testing blood donors)

ELISA test - detects patients Abs to HIV-quick

Western Blot test - detects HIV Ags- used to confirm ELISA

Plasma viral load - tells amount of virus in blood

• spread in body fluids - but NOT SALIVA
• -blood
• -semen
• -breast milk
• -transplacental

.3% 1 in 333

• Treat every patient as if they have HIV
• a. gloves, gowns, masks, goggles
• b. do not recap needles - into sharps box

• male-to-male sexual contact
• then heterosexual
• then drug users

1 million

HIV subtype

• 1. mutations - rapid
• 2. Clades - many subtypes

1. Reverse transcriptase inhibitors (nucleoside analogues)

2. Protease inhibitors - block viral assembly

3, Fusion inhibitors - block viral attachment

4. Integrase inhibitors - block provirus formation

• AZT = Zidovuedine - reverse transcriptase inhibitor
• HAART = highly active anti-retroviral therapy - combination of the above drugs used simulaneously

some cancer cells present specific Ags

immune surveillance - T cells recognize and destroy some cancer cells - this funciton deteriorates with age