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