Hypersensitivity and Hemolytic Disease of Newborn
Maternal IgG antibodies for fetal blood-group antigens cross the placenta and destroy fetal red blood cells
Hemolytic Disease of the Newborn (HDN)
Antibody class for Type I hypersensitivity
IgE
Antibody class for type III hypersensitivity
IgG
Antibody class for type II hypersensitivity
IgM or IgG
Presence of D allele for Rh antigen
Rh+
No D allele for Rh antigen
Rh-
Antibody class for type IV hypersensitivity
T-lymphocytes
Ag induces cross-linking of IgE bound to mast cells and basophils with release of vasoactive mediators. Common allergies to respiratory allergens
Type I hypersensitivity
Ag plus IgE leading to mast cell degranulation. Induced by pollens and certain foods. Systemic (anaphylactic shock)
Type I hypersensitivity
Caused by T-cell deficiency, abnormal mediator feedback, environmental factors and Ag
Type I hypersensitivity
Foreign serum, vaccines, ragweed, hayfever, trees, sulfonamides, salicylates, nuts, seafood, milk, eggs, bee wasp ant venom, dust mites, latex, mold spores, animal hair and dander, asthma, rhinitis, atopic eczema, bee sting reaction
Type I hypersensitivity
Immediate-hours response
Type I hypersensitivity
Swelling, labored respiration, tearing, runny nose, sneezing and coughing, mucous secretion, bronchoconstriction, itch, rash, vasodilation, urticaria (hives), anaphylaxia
Type I hypersensitivity
Treatment : avoid the causative agents if possible, hyposensitization, antihistamines, leukotriene antagonists, inhalation therapy, epinephrine injection
Type I hypersensitivity
Hemolytic Disease of the Newborn (HDN) is what type of hypersensitivity reaction?
Type II
Caused by exposure to Ag or foreign tissue, cells, or graft
Type II hypersensitivity
HDN, autoimmune hemolytic anemia, Graves' disease, idiopathic thrombocytopenic purpura, myasthenia gravis, blood transfusion reactions, Rhesus (Rh)/AB) blood reactions (erythroblastosis fetalis), and many DRUG allergies (notably penicillin)
Type II hypersensitivity
Minutes-hours response
Type II hypersensitivity
Redness and swelling due to cell or tissue death, hemoglobinuria, fever, increased bilirubin, mild jaundice, and anemia
Type II hypersensitivity
Result from the binding of IgG or IgM to the surface of host cells, which are then destroyed by complement or cell mediated mechanisms
Type II hypersensitivity
Surface Ag and Ab, leading to killer cells cytotoxic action or complement-mediated lysis, involve cell destruction by antibody-dependent cell-mediated cytotoxicity.
Type II hypersensitivity
Treatment: one form of clinical symptoms may be treated with Rhogam, termination of transfusion, corticosteroid, UV light
Type II hypersensitivity
Ag-Ab complex in tissue; complement activated and PMNs attracted. Can be induced with penicillin
Type III hypersensitivity
Ag-Ab complexes deposited on host cells (various tissues) induce complement activation and an ensuing inflammatory response mediated by massive infiltration of neutrophils
Type III hypersensitivity
Caused by persistent infection- microbe Ag, extrinsic environmental Ag, autoimmunity - self Ag
Type III hypersensitivity
Hours-Days response
Type III hypersensitivity
Redness and swelling (erythema and edema) pain, fever, rashes, joint pain, lymph node enlargement
Type III hypersensitivity
SLE, RA, multiple sclerosis, Arthus reaction, serum sickness, Farmer's lung disease, lupus, polyarthritis Glomerulonephritis, vasculitis, meningitis, hepatitis, mononucleosis, malaria, trypanosomiasis, penicillin and sulfonamides, hepatitis
Type III hypersensitivity
Treatment: corticosteroid, disease-modifying anti-rheumatic drugs (DMARDS), immunosuppressive agents, monoclonal antibodies (MABS), nonsteroidal anti-inflammatory drugs (NSAIDS)
Type III hypersensitivity
Severe HDN
erythroblastosis fetalis
mother and baby have different alleles of the Rhesus (Rh) antigen.
erythroblastosis fetalis
Severe reaction treatment for Rh incompatibility
fetus given intrauterine blood-exchange transfusion to replace fetal Rh+ cells with Rh- cells
Mother can be treated for Rh incompatibility with
plasmapheresis
Less severe reaction treatment for Rh incompatibility
transfusion to replace fetal Rh+ cells with Rh- cells after birth and exposure to UV light to break down bilirubin
Type of Hypersensitivity termed Allergic
type 1
Type of hypersensitivity termed cytotoxic
type 11
Type of hypersensitivity termed immune complex
type 111
Type of hypersensitivity termed delayed
type IV
Is complement activation involved in Type I hypersensitivity?
No
Is complement activation involved in Type IV hypersensitivity?
No
1-2 weeks response
Type IV hypersensitivity
Ag-sensitized T cells release lymphocytes leading to inflammatory reactions, and attract macrophages, which release mediator. An important defense agains intracellular pathogens
Type IV hypersensitivity
Caused by intradermal Ag, epidermal Ag, dermal Ag
Type IV hypersensitivity
Contact dermatitis, liver damage due to drug allergy, tuberculosis test, granuloma, graft rejections, Guillain-Barre disease, tuberculin test, poison ivy/oak, mycobacterium tuberculosis, candida albicans, herpes simplex, measles, Leishmania sp., Crohn's
Type IV hypersensitivity
Redness and hardness (erythema and induration) pain
Type IV hypersensitivity
Sensitized T cells release cytokines that activate macrophages or T cells which mediate direct cellular damage. Inappropriate T-cell activation
Type IV hypersensitivity
Treatment: immunosuppressive agents, monoclonal antibodies (MABS), corticosteroid
Type IV hypersensitivity
Is complement activation involved in Type II hypersensitivity?
Yes
Is complement activation involved in Type III hypersensitivity?
Yes
