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Microbiology Hypersensitivity and Allergy Presenter: Jaycris C. Agnes 3SED-SC

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Microbiology (Introduction to Immunology)

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Page 1: Hypersensitivity with AIDS

Microbiology

Hypersensitivity and Allergy

Presenter: Jaycris C. Agnes 3SED-SC

Page 2: Hypersensitivity with AIDS

Hypersensitivity and Allergy

Hypersensitivity-An exaggerated immune response that may cause damage to the host. The trigger is often an innocuous antigen

Allergy-A hypersensitive response to an environmental antigen. Often presents as “hay fever”, asthma, dermatitis or anaphylaxis.

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Four types of Hypersensitivity

Immediate-Type Hypersensitivity:Type I (Anaphylactic/ Allergic Reactions)

IgE-mediated e.g.most common allergies

Type II (Cytotoxic Reactions) IgG-mediated e.g.ABO transfusion reaction

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Four types of Hypersensitivity

Type III (Immune Complex Reactions) Immune-complex mediated e.g.serum sickness

Delayed-Type Hypersensitivity: Type IV (Cell Mediated Reaction)

T cell-mediated; delayed type e.g.tuberculin reaction

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Type I Hypersensitivity

Allergens Proteins Examples: drugs, foods, house dust,

insect venom, latex, mold spores, & pollens.

Atopy-Predisposition to type I hypersensitivity (atopic people) Higher levels of circulating IgE Greater numbers of eosinophils

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Type I Hypersensitivity

Factors in the Development of Type I Hypersensitivity: Nature of Antigen Route of entry Amount of antigen Ability to produce IgE antibodies Frequency of exposure Length of exposure time

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Table 1. Pharmacologic Mediators of Immediate Hypersensitivity

MEDIATOR

Preformed mediators in granules

histamine bronchoconstriction, mucus secretion, vasodilatation, vascular permeability

tryptase proteolysis

kininogenase kinins and vasodilatation, vascular permeability, edema

ECF-A(tetrapeptides)

attract eosinophil and neutrophils 

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Newly formed mediators

leukotriene B4

basophil attractant

leukotriene C4, D4

same as histamine but 1000x more potent

prostaglandins D2

edema and pain

PAF platelet aggregation and heparin release: microthrombi

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Type I Hypersensitivity

Localized Anaphylaxis Allergic reaction takes place in

specific part of the body.

Systemic Anaphylaxis Allergic Reaction takes place in

different parts of the body.

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Type I Hypersensitivity

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Type I Hypersensitivity

Clinical manifestations Allergic rhinitis Asthma Food allergies Systemic anaphylaxis

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Type II Hypersensitivity

Cell associated antigens Transfusion reactions Hemagglutinins Complement mediated Clinical symptoms include fever, chills,

nausea

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Type II Hypersensitivity

A typical Type Hypersensitivity reaction might follow these sequence:1. A particular drug binds to the surface of the

cell.2. Anti-drug antibodies then bind to the drug.3. This initiates complement activation on the

cell surface.4. The complement cascade leads to the lysis

of the cell.

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Type II Hypersensitivity

Erythroblastosis fetalis Rh+ fetus born to Rh- mother First pregnancy sensitizes Subsequent pregnancies result in anti Rh

Ab Mild to severe anemia in fetus Rhogam

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Type II Hypersensitivity

Drug induced hemolytic anemia Some antibiotics can be antigenic Bind nonspecifically to RBC surface

proteins Ab fixes C and lyses RBCs

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Type III Hypersensitivity

Immune complexes consist of antigen and antibodies bound together.

Diseases involved are Systemic Lupus

Erythematosus and rheumatoid arthritis.

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Type IV Hypersensitivity

T cell mediated T helper 1 cells Effector response is through macrophages

not T cytotoxic cells Cytokine mediated

IL3 Hematopoiesis Interferon, TNF, IL 1 Extravasation MCAF Attracts macrophages MIF Retains macrophages

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Delayed hypersensitivity reactions

TypeReaction

timeClinical appearance Histology Antigen and site

contact 48-72 hr eczemalymphocytes, followed by macrophages; edema of epidermis

epidermal ( organic chemicals, poison ivy, heavy metals, etc.)

tuberculin 48-72 hr local induration

lymphocytes, monocytes, macrophages

intradermal (tuberculin, lepromin,etc.)

granuloma 21-28 days hardening macrophages, epitheloid

and giant cells, fibrosis

persistent antigen or foreign body presence (tuberculosis, leprosy, etc.)

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Type IV HypersensitivityPositive Result for TB skin test

1. Within 2-3 hours after injection of the PPD (Purified Protein Derivative), there is an influx of polymorphonuclear cells into the site.

2. This is followed by an influx of lymphocytes and macrophages while PMN’s dispersed.

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Type IV Hypersensitivity

3. Within 12-18 hours, the area become red (erythematous) and swollen (edematous).4. The erythema (redness) and edema (swell) reach maximum intensity bet. 24-48 hours.5. With time, as the swelling and redness disappear, the lymphocytes and macrophages disperse.

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Five possibilities why TB skin test may be positive:

A person has tuberculosis. A person has tuberculosis in the past. A person has been infected by M.

tuberculosis, but the organism has been killed by that person’s host defence mechanism.

A person harvors live M. tuberculosis but does not have TB.

A person had received BCG (Bacille de Calmette et Guérin) vaccine.

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Table 5 - Comparison of Different Types of hypersensitivity

Characteristicstype-I(anaphylactic)

type-II(cytotoxic)

type-III(immune complex)

type-IV(delayed type)

antibody IgE IgG, IgM IgG, IgM None

antigen exogenous cell surface soluble tissues & organs

response time 15-30 minutes minutes-hours 3-8 hours 48-72 hours

appearance weal & flare lysis and necrosiserythema and edema, necrosis

erythema and induration

histology basophils and eosinophil

antibody and complement

complement and neutrophils

monocytes and lymphocytes

transferred with antibody antibody antibody T-cells

examples allergic asthma, hay fever

erythroblastosisfetalis, Goodpasture's nephritis

SLE, farmer's lung disease 

tuberculin test, poison ivy, granuloma

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Autoimmune Diseases

Autoimmune Diseases result when a person’s immune system can no longer recognizes certain body tissues as “self” and attempt to destroy those tissues.

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Immunosuppression

Acquired Immunodeficiency maybe caused by drugs, irradiation, or certain infectious diseases.

Inherited Immunodeficiency diseases are inherited immune diseases.

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H.I.V.

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WHAT IS HIV??

“Human Immunodeficiency Virus” A unique type of virus (a retrovirus) Invades the helper T cells (CD4 cells) in

the body of the host (defense mechanism of a person)

Threatening a global epidemic. Preventable, managable but not curable.

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OTHER NAMES FOR HIV

Former names of the virus include:

Human T cell lymphotrophic virus (HTLV-III)

Lymphadenopathy associated virus (LAV)

AIDS associated retrovirus (ARV)

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WHAT IS AIDS ??? “Acquired Immunodeficiency Syndrome” HIV is the virus that causes AIDS Disease limits the body’s ability to fight

infection due to markedly reduced helper T cells.

Patients have a very weak immune system (defense mechanism)

Patients predisposed to multiple opportunistic infections leading to death.

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AIDS (definition) Opportunistic infections and

malignancies that rarely occur in the absence of severe immunodeficiency (eg, Pneumocystis pneumonia, central nervous system lymphoma).

Persons with positive HIV serology who have ever had a CD4 lymphocyte count below 200 cells/mcL or a CD4 lymphocyte percentage below 14% are considered to have AIDS.

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Modes of HIV/AIDS Transmission

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Through Bodily Fluids

Blood products

Semen

Vaginal fluids

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IntraVenous Drug Abuse

Sharing Needles Without sterilization Increases the

chances of contracting HIV

Unsterilized blades

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Through Sex

Unprotected Intercourse

Oral Anal

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Mother-to-Baby

Before Birth During Birth

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NATURAL COURSE OF HIV/AIDS

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Stage 1 - Primary

Short, flu-like illness - occurs one to six weeks after infection

Mild symptoms Infected person

can infect other people

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Stage 2 - Asymptomatic

Lasts for an average of ten years This stage is free from symptoms There may be swollen glands The level of HIV in the blood drops

to low levels HIV antibodies are detectable in

the blood

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Stage 3 - Symptomatic

The immune system deteriorates Opportunistic infections and cancers

start to appear.

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Stage 4 - HIV AIDS

The immune system weakens too much as CD4 cells decrease in number.

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Opportunistic Infections associated with AIDS

CD4<500 Bacterial infections Tuberculosis (TB) Herpes Simplex Herpes Zoster Vaginal candidiasis Hairy leukoplakia Kaposi’s sarcoma

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Opportunistic Infections associated with AIDS

CD4<200 Pneumocystic carinii Toxoplasmosis Cryptococcosis Coccidiodomycosis Cryptosporiosis Non hodgkin’s

lymphoma

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CD4 <50 Disseminated mycobacterium avium

complex (MAC) infection Histoplasmosis CMV retinitis CNS lymphoma Progressive multifocal

leukoencephalopathy HIV dementia

Opportunistic Infections associated with AIDS

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