Compare the pathogens discussed in the previous chapters with zoonotic pathogens.? Discuss what the different character
Compare the pathogens discussed in the previous chapters with zoonotic pathogens.
- Discuss what the different characteristics are
- Describe how they cause disease
- Explain the transmission processes.
Microbiology FUNDAMENTALS A Clinical Approach Third Edition
Marjorie Kelly Cowan
&
Heidi Smith
with
Jennifer Lusk
BSN RN CCRN
©McGraw-Hill Education. All rights reserved. Authorized only for instructor use in the classroom. No reproduction or further distribution permitted without the prior written consent of McGraw-Hill Education.
Chapter 14
Disorders in Immunity
©McGraw-Hill Education
Learning Outcomes Section 14.1
Define immunopathology, and describe the two major categories of immune dysfunction.
Identify the four major categories of hypersensitivities, or overreactions to antigens.
©McGraw-Hill Education
Immune Response: A Two-Sided Coin(1)
The human immune system is powerful and intricate, with the potential to cause injury and disease
Defects in the immune system can range from hay fever to dermatitis
Abnormal immune functions are involved in:
Asthma
Anaphylaxis
Diabetes
Rheumatoid arthritis
Graft rejection
©McGraw-Hill Education
Immune Response(2)
Immunopathology: the study of disease states associated with the overreactivity or underreactivity of the immune response
Hypersensitivity or overreactivity:
Allergy and autoimmunity
Tissues are attacked by immunologic functions that cannot distinguish between self and nonself
Hyposensitivity or immunodeficiency:
Immune system is incompletely developed, suppressed, or destroyed
©McGraw-Hill Education
Disorders of the Immune System
Courtesy Baylor College of Medicine, Public Affairs (primary); ©McGraw-Hill Education/Christopher Kerrigan, photographer (secondary); ©Pixtal/age fotostock (type I); ©Roc Canals Photography/Getty Images (type II); ©Dynamic Graphics/JupiterImages (type III); ©BW Folsom/Shutterstock (type IV)
©McGraw-Hill Education
Hypersensitivity: Four Types
Type I: “common” allergy and anaphylaxis
Type II: IgG- and IgM-mediated cell damage
Type III: immune complex
Type IV: T-cell response
| Type | Systems and Mechanisms Involved | Examples | |
| I | Immediate hypersensitivity | IgE-mediated; involves mast cells, basophils, and allergic mediators | Anaphylaxis, allergies such as hay fever, asthma |
| II | Antibody-mediated | IgG, IgM antibodies act upon cells with complement and cause cell lysis; includes some autoimmune diseases | Blood group incompatibility; pernicious anemia; myasthenia gravis |
| III | Immune complex-mediated | Antibody-mediated inflammation; circulating IgG complexes deposited in basement membranes of target organs; includes some autoimmune diseases | Systemic lupus erythematosus; rheumatoid arthritis; serum sickness; rheumatic fever |
| IV | T-cell-mediated | Delayed hypersensitivity and cytotoxic reactions in tissues; includes some autoimmune diseases | Infection reactions; contact dermatitis; graft rejection |
©McGraw-Hill Education
Concept Check (1)
Which of the following is not a result of an abnormal or undesirable immune function?
Asthma
Anaphylaxis
Contact dermatitis
Fever
Lupus
©McGraw-Hill Education
Learning Outcomes Section 14.2
Summarize genetic and environmental factors that influence allergy development.
Identify three conditions caused by IgE-mediated allergic reactions.
Identify the two clinical forms of anaphylaxis, explaining why one is more often fatal than the other.
List the three main ways to prevent or short-circuit type I allergic reactions.
©McGraw-Hill Education
Type I Allergic Reactions: Atopy and Anaphylaxis
Allergy: exaggerated immune response that is manifested by inflammation
Allergens: innocuous substances that induce allergy in sensitive individuals
Atopy: chronic local allergy such as hay fever or asthma
Anaphylaxis: systemic, sometimes fatal, reaction that involves airway obstruction and circulatory collapse
©McGraw-Hill Education
Who Is Affected?(1)
In the U.S., nearly half the population is affected by airborne allergens (dust, pollen, mold)
Type I allergies:
Majority are relatively mild
Asthma and some food allergies may require hospitalization and can cause death
Some allergies last for a lifetime, some are “outgrown,” and others develop later in life
©McGraw-Hill Education
Who Is Affected?(2)
Generalized susceptibility to allergens is inherited, not the allergy to a specific substance
Genetic basis for atopy:
Increased IgE production
Increased reactivity of mast cells
Increased susceptibility of target tissue to allergic mediators
The prospect of a child developing an atopic allergy is 25% if parents are afflicted and 50% if siblings or grandparents are also afflicted
©McGraw-Hill Education
Hygiene Hypothesis
The industrialized world has created a hygienic environment: antimicrobial substances, well-insulated homes, etc.
Immune systems need to be “trained” by interaction with microbes as we develop
It has been shown that children who grow up on farms have lower incidences of several types of allergies
Delivery by cesarean section and maternal history of allergy elevates childhood risk of allergy by a factor of eight
©McGraw-Hill Education
Effect of Breast Feeding
Newborns breast fed exclusively for the first 4 months have a lower risk of asthma and eczema
Cytokines and growth factors in human milk act on the baby’s gut mucosa to induce tolerance to allergens
Human Microbiome Project: 600 species of bacteria can be transferred to infants through breast milk
Important role in the development of tolerance to foreign antigens
©McGraw-Hill Education
Nature of Allergens
As with all antigens, allergens have certain immunogenic characteristics
Proteins are more allergenic than carbohydrates, fats, or nucleic acids
Some are haptens, nonprotein substances with a molecular weight of less than 1,000 that can form complexes with carrier molecules in the body
Organic and inorganic chemicals found in industrial and household products, cosmetics, food, and drugs are haptens
©McGraw-Hill Education
Allergen Portals of Entry(1)
Mucosa of the gut and respiratory tract:
Thin, moist surface that is normally quite penetrable
Skin:
Dry, tough keratin is generally less permeable
Access occurs through tiny breaks, glands, and hair follicles
©McGraw-Hill Education
Allergen Portals of Entry(2)
Inhalants: airborne environmental allergens such as pollen, house dust, dander, or fungal spores
Ingestants: allergens that enter by mouth that cause food allergies
Injectants: allergies triggered by drugs, vaccines, or hymenopteran (bee) venom
Contactants: allergies that enter through the skin; many are type IV (delayed) hypersensitivities
©RubberBall/Alamy Stock Photo
©McGraw-Hill Education
Role of Mast Cells and Basophils in Type I Allergy
Mast cells are located in all connective tissues, but in particularly high concentrations in the lungs, skin, gastrointestinal tract, and genitourinary tract
Each cell carries 30,000 to 100,000 cell receptors that bind IgE and degranulate, releasing inflammatory cytokines
Symptoms of allergy are not caused by the direct action of allergen on tissues, but the physiological effects of mast-cell-derived allergic mediators on target organs
©McGraw-Hill Education
Cytokines, Target Organs, and Allergic Symptoms(1)
Histamine:
Most profuse and fast-acting allergic mediator
Constricts smooth muscle in the small bronchi and intestine, causing labored breathing and increased intestinal motility
Relaxes vascular smooth muscle and dilates arterioles and venules, resulting in wheal-and-flare reactions in the skin and itching
Stimulates eosinophils to release inflammatory cytokines, escalating symptoms
Bradykinin:
Prolonged smooth muscle contraction of the bronchioles
Dilation of peripheral arterioles
Increased capillary permeability
Increased mucus secretion
Serotonin:
Effects complement those of histamine and bradykinin
©McGraw-Hill Education
Cytokines, Target Organs, and Allergic Symptoms(2)
Leukotriene:
“Slow-reacting substance of anaphylaxis”
Induces gradual contraction of smooth muscle
Prolonged bronchospasm, vascular permeability, and mucus secretion of the asthmatic individual
Stimulates polymorphonuclear leukocytes
Prostaglandins:
Regulate smooth muscle contraction; stimulate uterine contractions during delivery
Vasodilation
Increased vascular permeability
Increased sensitivity to pain
Bronchoconstriction
Nonsteroidal anti-inflammatory drugs (NSAIDs) prevent the actions of prostaglandins
©McGraw-Hill Education
Cellular Reactions During Type I Allergic Response(1)
©Ingram Publishing (headache); ©robeo/Getty Images (hives); ©Brand X Pictures (stomachache); ©Science Photo Library (asthma); ©Ingram Publishing (blowing nose)
©McGraw-Hill Education
Cellular Reactions During Type I Allergic Response(2)
©Ingram Publishing (headache); ©robeo/Getty Images (hives); ©Brand X Pictures (stomachache); ©Science Photo Library (asthma); ©Ingram Publishing (blowing nose)
©McGraw-Hill Education
Hay Fever
A generic term for allergic rhinitis
Seasonal reaction to inhaled plant pollen or molds, or a chronic, year-round reaction to airborne allergens or inhalants
Targets: respiratory membranes
Symptoms: nasal congestion; sneezing; coughing; profuse mucus secretion; itchy, red, and teary eyes; mild bronchoconstriction
©McGraw-Hill Education
Asthma
Respiratory disease characterized by episodes of impaired breathing due to severe bronchoconstriction
Airways of asthmatics are extremely sensitive to minute amounts of inhalants, ingestants, or other stimuli, such as infectious agents
Symptoms range from labored breathing to fatal suffocation
Rales: clicking, bubbling, or rattling sounds in the lungs
Lungs are overreactive to leukotrienes and serotonin
Natural killer cells are also recruited and activated
©McGraw-Hill Education
Atopic Dermatitis/Eczema
Intensely itchy inflammatory condition of the skin
Sensitization occurs through ingestion, inhalation, and skin contact with allergens
Usually begins in infancy and is characterized by reddened, encrusted skin lesions on the face, scalp, neck, and inner surfaces of limbs and trunk
Progresses to a dry, scaly, thickened skin condition in adults
Lesions are itchy, painful, and predisposed to secondary bacterial infections
©Dr. P. Marazzi/Science Source (a); ©Biophoto Associates/Science Source (b)
©McGraw-Hill Education
Food Allergy
Most common food allergens come from peanuts, fish, cow’s milk, eggs, shellfish, and soybeans
Mode of entry is intestinal
Symptoms include vomiting, diarrhea, and abdominal pain
Other manifestations include hives, rhinitis, asthma, and occasionally anaphylaxis
Hypersensitivity involves IgE and degranulation of mast cells, but not all reactions involve this mechanism
Care should be taken vaccinating individuals with egg allergies
©McGraw-Hill Education
Drug Allergy
Drugs are foreign compounds capable of stimulating allergic reactions
Drug allergies are one of the most common side effects of treatment, affecting 5 to 10% of hospitalized patients
Reactions range from a mild rash to fatal anaphylaxis
Compounds implicated:
Antibiotics: penicillin
Synthetic antimicrobials: sulfa drugs
Aspirin
Opiates
Contrast dye used in X rays
Allergen is not the intact drug itself, but a hapten given off when the liver processes the drug
©McGraw-Hill Education
Anaphylaxis: An Overpowering IgE-Mediated Allergic Reaction
Anaphylaxis/anaphylactic shock: swift reaction to allergens:
Cutaneous anaphylaxis: wheal-and-flare inflammatory reaction to the local injection of allergen
Systemic anaphylaxis: characterized by sudden respiratory and circulatory disruption that can be fatal within minutes due to airway blockage
Bee stings and injection of antibiotics or serum are most commonly implicated
Result of the sudden, massive release of chemicals into the tissues and blood, which act rapidly on target organs
©McGraw-Hill Education
Diagnosis of Allergy: In Vitro Methods
Blood testing:
Radioallergosorbent (RAST) test: measures levels of IgE to specific antigens
Tryptase test: measures tryptase, an enzyme released by mast cells that increases during an allergic response
Differential blood cell count can reveal high levels of basophils and eosinophils
Leukocyte histamine-release test: measures the amount of histamine released from the patient’s basophils when exposed to a specific allergen
©McGraw-Hill Education
Diagnosis of Allergy: In Vivo Methods
Skin testing: in vivo method to detect precise atopic or anaphylactic sensitivities
Skin is injected, scratched, or pricked with a small amount of pure allergen extract
A wheal-and-flare result 20 minutes after antigenic challenge is indicative of histamine release
The diameter of the wheal is measured and rated on a scale from 0 (no reaction) to 4 (greater than 15 mm)
©Southern Illinois University/Science Source (a)
©McGraw-Hill Education
Treatment and Prevention of Allergy
Take drugs that block the action of lymphocytes, mast cells, or chemical mediators
Avoid the allergen, although this may be difficult in many instances
Desensitization: controlled exposure to the antigen through ingestion, sublingual absorption, or injection to reset the allergic reaction
©McGraw-Hill Education
©McGraw-Hill Education
Concept Check (2)
Which of the following is not an IgE- and/or mast-cell-mediated allergic condition?
Asthma
Food allergy
Systemic lupus erythematosus
Allergy to penicillin
Eczema
©McGraw-Hill Education
Learning Outcomes Section 14.3
List the three immune components causing cell lysis in type II hypersensitivity reactions.
Explain the role of Rh factor in hemolytic disease development and how it is prevented in newborns.
©McGraw-Hill Education
Type II Hypersensitivities: Reactions That Lyse Foreign Cells
A complex group of syndromes that involve complement-assisted destruction (lysis) of cells by antibodies (IgG and IgM) directed against those cells’ surface antigens:
Transfusion reactions
Some types of autoimmunities
Alloantigens:
Molecules that differ in the same species that are recognized by the lymphocytes of the recipient
Not an immune dysfunction; the immune system is functioning normally by reacting to foreign cells in an organ or tissue transplant
©McGraw-Hill Education
Rh Factor and Its Clinical Importance
First discovered in experiments exploring genetic relationships among animals:
Rabbits injected with the RBCs of rhesus monkeys produced an antibody that also reacted with human RBCs
This monkey antigen (Rh for rhesus) was present in about 85% of humans and absent in about 15%
Rh+ is a dominant gene; Rh- is recessive
The only way to develop antibodies against this factor is through placental sensitization or transfusion
©McGraw-Hill Education
Hemolytic Disease of the Newborn and Rh Incompatibility
Placental sensitization occurs when the mother is Rh- and the unborn child is Rh+:
Fetal RBCs may leak into the mother’s circulation during childbirth when the placenta detaches.
Mother’s immune system detects the foreign Rh factors on fetal RBCs and is sensitized to them by producing antibodies and memory B cells
Does not usually affect the first child because the process occurs so late in pregnancy
In the next pregnancy with an Rh+ fetus:
Fetal blood cells escape into maternal circulation late in pregnancy, eliciting a memory response.
Maternal anti-Rh antibodies cross the placenta, affix to fetal RBCs, and cause complement-mediated lysis.
Outcome is potentially fatal hemolytic disease of the newborn (HDN), also called erythroblastosis fetalis, characterized by severe anemia and jaundice
©McGraw-Hill Education
Development and Control of Rh Incompatibility
©McGraw-Hill Education
Preventing Hemolytic Disease of the Newborn
Once sensitization has occurred, all other Rh+ fetuses will be at risk
A careful history of the Rh– pregnant woman is needed:
Rh types of children and Rh status of the father are needed
If the father is Rh-, there is no risk
If the father is Rh+, the fetus may be Rh+.
RhoGAM antiserum:
Passive immunization for an Rh- mother with an Rh+ fetus
Immunoglobulin fraction of human anti-Rh serum prepared from pooled human sera
Injected at 28 to 32 weeks and again immediately after delivery
Sequesters fetal RBCs that have escaped into maternal circulation and prevents sensitization
Must be given with each pregnancy with an Rh+ fetus
©McGraw-Hill Education
Concept Check (3)
When is the RhoGAM shot needed?
Rh+ mother, Rh+ fetus
Rh+ mother, Rh– fetus
Rh– mother, Rh– fetus
Rh– mother, Rh+ fetus
All of the choices are correct. The mother always responds to the fetus as foreign tissue and mounts an immune response against it.
©McGraw-Hill Education
Learning Outcomes Section 14.4
Identify commonalities and differences between type II and type III hypersensitivities.
©McGraw-Hill Education
Type III Hypersensitivities: Immune Complex Reactions
Involves the reaction of soluble antigen with antibody, and deposition of resulting complexes in various tissues in the body:
Involves the production of IgG and IgM antibodies
Also involves the activation of complement
Unlike type II hypersensitivities, antigens are not attached to the surface of a cell
Immune complex reaction: produces free-floating complexes that are deposited into tissues
©McGraw-Hill Education
Mechanisms of Immune Complex Disease
Large quantities of antibodies are produced in response to an exposure to a profuse amount of antigen
Upon second exposure, antigen-antibody complexes are formed:
These recruit complement and neutrophils that would normally eliminate these complexes
In immune complex disease, complexes are deposited in the basement membranes of epithelial tissues:
Neutrophils release lysosomal granules that digest tissues and cause a destructive inflammatory condition
©McGraw-Hill Education
Stages in the Course of Infection and Disease
Arthus reaction and serum sickness are associated with certain types of passive immunization
Similar to anaphylaxis in that all require sensitization and preformed antibodies
Differences from anaphylaxis:
Depend on IgG, IgM, or IgA rather than IgE
Require large doses of antigen
Symptoms are delayed hours to days
©Koshi Johnson/Medical Images (a); Courtesy Gary P. Wiliams, M.D. (b)
©McGraw-Hill Education
Concept Check (4)
Which of the following antibody types is not involved in serum sickness or the Arthus reaction?
IgA
IgE
IgG
IgM
All of the choices are involved.
©McGraw-Hill Education
Learning Outcomes Section 14.5
Describe one example of a type IV delayed hypersensitivity reaction.
List four classes of grafts, and explain how host versus graft and graft versus host diseases develop.
©McGraw-Hill Education
Type IV Hypersensitivities: Cell-Mediated (Delayed) Reactions
Involves primarily the T-cell branch of the immune system
Results when T cells respond to antigens displayed on self tissues or transplanted foreign cells
Traditionally known as delayed hypersensitivity:
Symptoms arise one to several days following the second contact with antigen
©McGraw-Hill Education
Infectious Allergy
Tuberculin reaction:
Acute skin inflammation at the tuberculin extract injection site
Mainstay diagnostic tool for TB infections
TH1 cells release cytokines that recruit macrophages, neutrophils, and eosinophils to the site, causing a red bump
Source: CDC/Donald Kopanoff (a)
©McGraw-Hill Education
Contact Dermatitis
Caused by exposure to resins in poison ivy and poison oak, haptens in household and personal articles, and certain drugs
Requires a sensitizing dose followed by a provocative dose
Allergen penetrates the outer skin layers:
Processed by skin dendritic cells and presented to T cells
Subsequent exposures attract lymphocytes and macrophages
Cells release enzymes and cytokines that damage the epidermis in the immediate vicinity
©carroteater/Shutterstock (b)
©McGraw-Hill Education
T Cells and Their Role in Organ Transplantation
Transplantation or grafting of organs and tissues is a common medical procedure
Although it is life-giving, it is plagued with the natural tendency of lymphocytes to seek out and destroy foreign antigens
The bulk of the damage that occurs in graft rejections are attributed to cytotoxic T-cell action
©McGraw-Hill Education
Genetic and Biochemical Basis for Graft Rejection
MHC or HLA classes I and II markers are extremely important for recognizing self and in regulating the immune response
Although a person can exhibit variability in the pattern of these markers, the pattern is identical in different cells in the same person
Similarity is seen in related siblings and parents, but the more distant the relationship, the less likely that the MHC genes and markers will be alike
When a donor tissue (graft) displays surface molecules of a different MHC class, the T cells of the recipient will react to it as a foreign substance
©McGraw-Hill Education
Host Rejection of Graft
Cytotoxic T cells of a host recognize foreign class I MHC markers on the surface of grafted cells
Release IL-2 as part of general immune mobilization
Helper and cytotoxic T cells bind to the grafted tissue and secrete lymphokines that begin the rejection process within 2 weeks of transplantation
Antibodies formed against the transplanted tissue contribute to damage
The result is destruction of the vascular supply and death of the graft
©McGraw-Hill Education
Graft Rejection of Host
Some grafted tissues (bone marrow) contain indigenous populations of passenger lymphocytes
These lymphocytes create an immune response to the host
Graft versus host disease:
Graft attacks any host tissue bearing foreign MHC markers
Effects are systemic and toxic
Papular, peeling skin rash is the most common symptom; other organs are also affected
Occurs within 100 to 300 days of the graft
©McGraw-Hill Education
Development of Incompatible Tissue Graft Reactions
©McGraw-Hill Education
53
Classes of Grafts
Autograft: tissue transplanted from one site on an individual’s body to another site
Isograft: tissue from an identical twin is used
Allograft: exchanges between genetically different individuals belonging to the same species; the most common types of grafts
Xenograft: a tissue exchange between individuals of a different species
©iStockphoto/Getty Images
©McGraw-Hill Education
54
Types of Transplants
Transplantation has been performed on every major organ, but most often involves the skin, liver, heart, kidney, coronary artery, cornea, and bone marrow
Sources of organs: live donors, the recently deceased, fetal tissues
Bone marrow transplantation:
Used in individuals with immune deficiencies, aplastic anemia, leukemia, and other cancers, and radiation damage
Patient is treated with chemotherapy and whole-body irradiation to destroy their own blood cells, preventing rejection
Closely matched donor marrow is infused
GVHD can still occur, and antirejection drugs may be necessary.
After transplantation, a recipient’s blood type may change to the blood type of the donor
©McGraw-Hill Education
Concept Check (5)
Match the class of tissue graft with its description.
Allograft
Autograft
Isograft
Xenograft
Graft between identical twins
Graft between different species
Graft within an individual
Graft between non-identical twins
©McGraw-Hill Education
Learning Outcomes Section 14.6
List at least three autoimmune diseases and the most important immunologic features in them.
©McGraw-Hill Education
Inappropriate Response to Self: Autoimmunity
Autoimmune diseases: individuals actually develop hypersensitivity to themselves
Autoantibodies, T cells, or both, mount an abnormal attack against self antigens
Systemic: involves several major organs
Organ specific: involves only one organ or tissue
| Disease | Target | Type of Hypersensitivity | Characteristics |
| Systemic lupus erythematosus (SLE) | Systemic | III | Inflammation of many organs; antibodies against red and white blood cells, platelets, clotting factors, nucleus DNA |
| Rheumatoid arthritis and ankylosing spondylitis | Systemic | II, III, and IV | Vasculitis; frequent target is joint lining; antibodies against other antibodies (rheumatoid factor), T-cell cytokine damage |
| Graves’ disease | Thyroid | III | Antibodies against thyroid-stimulating hormone receptors |
| Myasthenia gravis | Muscle | III | Antibodies against the acetylcholine receptors on the nerve-muscle junction alter function |
| Type 1 diabetes | Pancreas | IV | T cells attack insulin-producing cells |
| Multiple sclerosis | Myelin | II and IV | T cells and antibodies sensitized to myelin sheath destroy neurons |
©McGraw-Hill Education
Genetic and Gender Correlation in Autoimmune Disease
Cases cluster in families, and even unaffected members tend to develop autoantibodies for the disease
Particular genes in class I and II MHC coincide with certain autoimmune diseases:
Rheumatoid arthritis and ankylosing spondylitis are more common in persons with B-27 HLA type
Molecular mimicry:
Microbial antigens bearing molecular determinants similar to human cells induce the formation of autoantibodies
One explanation for the pathology of rheumatic fever
Psoriasis flare-ups after strep throat infections may also be due to T cells primed to react with keratin in the skin
©McGraw-Hill Education
Examples of Autoimmune Diseases: Systemic Autoimmunities
Systemic lupus erythematosus (SLE, or lupus):
Name originated from the characteristic butterfly-shaped rash that drapes across the nose and cheeks
Manifestations vary, but all patients develop autoantibodies against organs, tissues, or intracellular materials
Viral infection and loss of normal immune response suppression are suspected as causes
Rheumatoid arthritis:
Causes progressive, debilitating damage to the joints and at times to the lungs, eyes, skin, and nervous system
Autoantibodies form immune complexes that bind to the synovial membrane of joints, activating cytokine release by macrophages
Chronic inflammation develops, leading to scar tissue and joint destruction
Cytokines trigger additional type IV delayed hypersensitivity responses
©McGraw-Hill Education
Common Autoimmune Diseases
©ISM/CID/Medical Images (a); ©Aaron Roeth Photography (b)
©McGraw-Hill Education
61
Autoimmunities of the Endocrine Glands
Graves’ disease:
Attachment of
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