EVOLVE Module 6

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A nurse is asked about desensitization therapy for allergies. What is the nurse's best response? A) Minute amounts of allergens are given in increasing amounts. B) Decreasing amounts of IgE are injected into the body. C) Individuals with Type III hypersensitivities will benefit from this treatment. D) Antihistamines are a part of this process and will be given monthly.

A nurse is discussing the pathophysiology of bare lymphocyte deficiency. Which of the following information should the nurse include? A) Inability to produce major histocompatibility complex molecule B) Deficiencies of terminal components of the complement cascade C) Infection and destruction of the Th cell, which is necessary for development of T and B cells D) Disturbance in the immunologic tolerance of self-antigens leading to autoimmunity

A nurse is providing care to an atopic patient. Which principle should the nurse use to guide nursing care? Repeated exposure to an allergen in an atopic individual will cause the: A) allergic response to become worse. B) antibody production to become suppressed. C) autoimmune formation to increase. D) Tc cell activity to increase significantly.

A nurse is teaching about hypersensitivity reactions. Which information should the nurse include? _____________ are stimulated to release histamine by the presence of antibodies in a type I hypersensitivity reaction. A) Mast cells B) Macrophages C) B lymphocytes D) T lymphocytes

A nurse recalls Graves disease is an autoimmune disease caused by autoantibodies that: A) stimulate the production of thyroid hormone. B) block the effects of thyroid hormone. C) destroy the thyroid gland. D) destroy cells that normally respond to thyroid hormone.

A patient has DiGeorge syndrome. Which organ should the nurse discuss when describing the pathophysiology of this disease? A) Thymus B) Thyroid C) Liver D) Lung

A patient has Wiskott-Aldrich syndrome. Which typical assessment findings should the nurse monitor for in this patient? A) Decreased IgM and bleeding B) Increased IgE and clotting C) Decreased IgG and wheezing D) Increased IgA and coughing

A patient has glomerulonephritis. Which organ assessment is priority? A) Kidneys B) Eyes C) Liver D) Stomach

If blood cell counts from an individual with AIDS were analyzed, the nurse would expect to see very low quantities of: A) T helper cells and be sure to change on selected answer B) mast cells. C) red blood cells. D) neutrophils.

When a person has an allergic reaction to a bee sting, which type of hypersensitivity response is occurring? A) Type I B) Type II C) Type III D) Type IV

Which statement indicates a nurse needs more teaching regarding autoimmunity? Autoimmunity can result from: A) type I hypersensitivity. B) type II hypersensitivity. C) type III hypersensitivity. D) type IV hypersensitivity.

Active Immunization

Active immunization provides long-term protection against specific infections. Several types of vaccines are available: Attenuated (weakened) viruses - illicit a vigorous immune response but can cause disease in some individuals (e.g., measles, mumps, varicella) Killed virus - gives somewhat less protection than attenuated viruses but cannot cause disease (e.g., hepatitis A) Purified viral or bacterial antigens - work well for selected organisms and can vaccinate against several strains of the organism simultaneously (e.g., influenza, hepatitis B, Streptococcus pneumoniae, Haemophilus influenzae) Toxoids - purified toxins to protect from bacterial diseases that are produced by exotoxins, such as diphtheria, tetanus, and pertussis

Progressive Disease (Immunocompromise)

After years of combating the HIV infection, the ability of the host to replace infected and killed T helper cells begins to decline. Cells that were inactive become more active, thus providing more HIV replication. Lymph node structure begins to break down, and the numbers of active viruses in the bloodstream begin to rise. As the number of functional T helper cells declines, the immune response becomes increasingly compromised and the clinical manifestations of HIV infection such as opportunistic infections and malignancies begin to appear. This signals the progression of HIV infection to AIDS.

Allergic Rhinitis

Allergic rhinitis is commonly known as hay fever. It is the most common allergic problem, with a prevalence estimated at 20% of the U.S. population. Peak symptoms occur in decades 2, 3, and 4, but children (average age 10 years) are also affected, most commonly during times of the year when pollen counts are high. Symptoms include nasal congestion, rhinorrhea (runny nose), postnasal drainage, sneezing, itchy nose, watery eyes, headache, and loss of smell and taste. Findings on examination include swollen, pale nasal mucous membranes, nasal and pharyngeal erythema, nasal polyps, and clear fluid behind the eardrums (serous otitis media).

Allergy Testing Treatment of Type 1

Allergy testing is a broad and complex field of clinical practice. There are many ways to test for allergies. Controlled exposure to allergens can be conducted using food challenge or intradermal injection, both of which carry a small risk for anaphylaxis but which are very good at determining exactly which allergens are causing an individual's symptoms. Alternatively, measurement of IgE levels in the blood are easier to perform, but IgE levels are less correlated with clinical symptoms.

Complement Deficiencies

Antibody activation of the complement cascade is an important part of protection against infections. (See Module 04: Innate Defenses: Inflammation.) Deficiencies in complement most commonly result in infections by encapsulated organisms (e.g., Streptococcus pneumoniae and Haemophilus influenzae) because of a lack of adequate opsonization of these organisms and therefore inadequate phagocytosis and removal of the organisms from the body. Any part of the complement cascade can be defective, although deficiencies in C2 are most common, and deficiencies in C3 are most severe. C3 deficiencies are associated not only with recurrent infections by encapsulated bacteria, but also by a systemic lupus erythematosus (SLE)-like syndrome. Deficiencies in C5 through C9 are particularly associated with severe infections by Neisseria meningitidis and Neisseria gonorrhoeae.

Antimicrobials

Antimicrobials are substances that kill or inhibit the growth of bacteria, viruses, fungi, or parasites. They act through a variety of mechanisms, many of which are listed in Table 7-10 in your textbook. The most commonly used antimicrobials are the antibiotics used in the management of bacterial infections. Antibiotics are categorized according to their chemical formulas and have differing effects on various types of bacteria. For example, penicillins work best against certain kinds of gram-positive bacteria but do not work well against some gram-negative bacteria. Management of bacterial infections requires that the organism being treated is sensitive to the effects of the antibiotic that is chosen. Because viruses reproduce inside the host cell, it has been more difficult to develop safe and effective antivirals, although the tremendous research into the treatment of HIV disease has helped create new antivirals that can treat other types of viruses as well. Antifungals are frequently highly toxic and have many side effects.

HIV/AIDS epidemiology

As an overview, sub-Saharan Africa retains the highest prevalence of HIV infection in the world, where the infection is primarily spread through heterosexual sex and perinatal transmission (at delivery or through breastfeeding). In the United States, the highest prevalence rates are found among intravenous drug users and in men who have sex with men. With the advent of new treatments over the past 15 years, HIV infection has become a chronic disease. Healthcare workers, especially nurses and laboratory technicians, have a high rate of exposure to HIV-infected individuals as a part of their profession, but transmission from patient to healthcare provider is quite rare. Of the tens of thousands of infected healthcare workers, it is estimated that only a tiny fraction became infected as a result of exposure to a patient. Infection control precautions and needle-free injection systems for obtaining blood and intravenous access have further reduced the risk for developing an HIV infection as a result of patient care.

Mechanism of HIV Entry Into Host Cells

As described in the previous screen and the animation, HIV binds to the surface of target cells (e.g., dendritic cells, macrophages, and T helper lymphocytes) prior to entry into the host cell cytoplasm. The process of HIV binding occurs in several steps, including: Binding of gp120 to the CD4 molecule A conformational change in the gp120 molecule Binding to host cell co-receptors CXCR4 on T helper cells or CCR5 on macrophages and dendritic cells. gp41 membrane penetration Membrane fusion An understanding of these steps has led to the development of a two new types of therapy for HIV infection called entrance inhibitors. One called enfuvirtide prevents the conformational change of gp120, and the other called maraviroc prevents binding with the CCR5 coreceptor, thus preventing HIV entry into macrophages and dendritic cells.

Asthma

Asthma is an allergic disease that affects the lower respiratory tract with inflammation, bronchoconstriction, and mucus formation. Asthma can be extremely serious and can even result in respiratory failure and death (asthma is discussed in detail in Module 12: Alterations of Pulmonary Function).

A child has bare lymphocyte syndrome. What is the prognosis for this patient? A) Most patients have a complete recovery with treatment. B) Most patients do not live past the age of 5. C) Some patients will have remissions and exacerbations. D) Some patients will require surgery to cure this syndrome.

A nurse is asked what happens when H1 receptors are stimulated by histamine. How should the nurse respond? A) Bronchodilation B) Increased permeability C) Prolonged vasoconstriction D) Increased gastric secretions

A nurse is asked what is graft-versus-host disease (GVHD). How should the nurse respond? This occurs when: A) the recipients immune cells attack the donor. B) the donors immune cells attack the recipient. C) atypical infections overwhelm the body. D) typical infections overwhelm the body.

A nurse is describing histamine receptors. Which information should the nurse include? __________ receptors, when bound to histamine, stimulate gastric acid secretion in the stomach. A) H1 B) H2 C) H3 D) H4

A nurse recalls hyperacute allograft rejection is caused by: A) cytokines and growth factors produced by trauma to vascular endothelial cells. B) preformed antibodies that react immediately with the graft. C) Tc and NK cell destruction of the graft. D) production of antibodies to the new graft by B lymphocytes.

A patient had a hypersensitivity reaction involving the formation of antibodies against tissue-specific antigen. Which type of hypersensitivity reaction did the patient experience? A) Type I B) Type II C) Type III D) Type IV

A patient has Graves disease. Which type of hypersensitivity reaction occurred? A) Type I B) Type II C) Type III D) Type IV

A patient has a combined immune deficiency. Which important principle should the nurse remember? A patient with a combined immune deficiency lacks: A) IgA and IgG. B) T and B lymphocytes. C) Tc and Th cells. D) phagocytes and macrophages.

A patient has a complement deficiency of C5 and C7. Which type of infection should the nurse monitor for in this patient? A) Staphylococcus caused infections B) Neisseria caused infections C) Streptococcus caused infections D) Escherichia coli caused infections

A patient has an immunodeficiency disorder from an X-linked recessive disease characterized by decreased IgM production. Which diagnosis will the nurse observe documented on the chart? A) Severe combined immunodeficiency disease (SCID) B) Wiskott-Aldrich syndrome C) DiGeorge syndrome D) Bare lymphocyte syndrome

A patient is undergoing a skin test and food challenge. The nurse realizes the patient is being tested for: A) compatibility of donor tissue. B) type I hypersensitivities. C) potential surgery for obesity. D) autoimmune diseases.

A patient presents with recurrent respiratory tract infections and chronic yeast infections of the gastrointestinal tract. Which immune disease does the nurse suspect the patient is experiencing? A) Severe combined immunodeficiency B) IgA deficiency C) Bruton agammaglobulinemia D) Autoimmunity

Which characteristic does the nurse know is related to a type IV hypersensitivity reaction? A) Antibody-dependent cell-mediated toxicity B) Delayed response C) Life-threatening symptoms D) Complement system mediation

Which of the following groups should the nurse screen first for systemic lupus erythematosus (SLE)? A) Women, 50-70 years old B) Women, 20-40 years old C) Men, 50-70 years old D) Men, 20-40 years old

Which principle should the nurse use to guide nursing care for a patient with HIV? After initial infection with the HIV, some individuals may: A) receive the vaccine to destroy the virus. B) appear to have no symptoms of infection (latency). C) experience neurogenic shock. D) have primary deficiency of IgG.

Which statement indicates a nurse has a good understanding of the pathophysiology of systemic lupus erythematosus (SLE)? Disease characteristics of SLE include: A) Tc cell destruction of lung tissue and the gastrointestinal lining. B) deposition of immune complexes in the kidneys, brain, and heart. C) selective autoantibody destruction of the thyroid gland. D) absence of the antinuclear antibodies and antiDNA antibodies.

While checking lab results, the nurse notices a patient has low levels of antibodies. What term should the nurse use to describe this condition? A) Agammaglobulinemia B) Hypogammaglobulinemia C) Anemia D) Septicemia

f a transfusion of A-negative blood to an O-positive individual occurred, which result would the nurse expect? A) Improved red blood cell count B) Clumping and lysis of red blood cells C) Production of anti-B antibodies D) A type I hypersensitivity reaction

Septicemia and Septic Shock

Bacteremia is the presence of bacteria in the blood, and septicemia is the growth of bacteria in the bloodstream. Septicemia can result in bacteria seeding distant tissues, such as the brain and heart valves. It can also result in overwhelming inflammation (systemic inflammatory response syndrome [SIRS]) and dysfunction and necrosis of vital tissues (multiple organ dysfunction syndrome [MODS]). Shock that results from septicemia is called septic shock and is characterized by hypotension and myocardial suppression. Diagnosis relies on finding the organisms in the blood (blood cultures). Rapid administration of antibiotics is essential for survival.

Bacterial Disease

Bacteria are a major cause of morbidity and mortality. Infection can be acquired outside (community acquired) or inside (nosocomial or hospital acquired) healthcare facilities. Clinical manifestations of bacterial infection can range from mild to life threatening depending on the virulence of the microorganism and the immunocompetence of the host. Bacteria have developed many sophisticated mechanisms to avoid host defenses. Two of the most important are capsules and toxins.

Bacteria

Bacteria are prokaryocytes (lack a nucleus) and can be aerobic (require oxygen) or anaerobic (do not require oxygen), motile or immotile. They can take many forms; the most common bacterial forms are spherical (cocci), rodlike (bacilli), or spiral (spirochetes). Bacteria also take up common stains differently, depending on the structure of their cell walls—for example, when exposed to Gram stain, some bacteria stain light pink (gram-negative), whereas others stain dark purple (gram-positive). Subclasses of bacteria that have specialized structures and mechanisms of disease include Chlamydia, Rickettsiae, Mycoplasma, and Mycobacteria. Special stains are used for some of these subclasses of bacteria, such as the Ziehl-Neelsen (acid-fast) stain for mycobacteria.

Combined Deficiencies—Bare Lymphocyte Syndrome

Bare lymphocyte syndrome is characterized by a lack of ability by macrophages and lymphocytes to express HLA (MHC) class I or II antigens (see Module 05: Adaptive Immunity). This particularly severe form of SCID results in disrupted intercellular communication and the inability of the immune system to effectively present foreign antigens to lymphocytes. This defect causes failure of the entire immune system and results in fatal infections for most children before 5 years of age.

Flu Vaccine

Because the adaptive immune system is so antigen-specific, a vaccination must be given with an antigen that is as similar to the actual organism or toxin as possible, but it must be altered so that it does not cause disease. For example, attenuated viruses make highly effective vaccines, but can cause life-threatening infections in immunocompromised individuals. One of the most common vaccines used in the United States is the influenza vaccine. Because different strains of the virus predominate each year, the vaccine must be given annually. Some individuals have a symptomatic reaction to the vaccine characterized by low-grade fever and myalgias.

Inducible Sensitization to allergies

Being inducible means that the adaptive immune response (as compared to the innate immune or inflammatory response) is relatively slow to react to the first (primary) antigen exposure because it takes several days for B- or T-cell clones to proliferate and begin effective humoral or cell-mediated immunity.

Transformation

Both DNA viruses and RNA viruses (retroviruses) may integrate themselves into the host DNA. This can result in: A latency phase during which the virus does not replicate, but does enter a productive cycle (and cause disease) in response to stimuli such as stress, hormonal changes, or immunodeficiency. Alteration of the host cell DNA so that the cell becomes cancerous. Uncontrolled growth of the cell may be caused by disruption of its normal regulatory gene sequencing or because the virus itself contains a cancer-causing gene (viral oncogenesis).

B-Lymphocyte Deficiencies—Bruton Agammaglobulinemia

Bruton agammaglobulinemia results from defects in the bursal-equivalent tissue necessary for B-cell development. Children with this disorder have absent or very low levels of all of the immunoglobulin types and are highly prone to all types of infection, especially those by encapsulated microorganisms. Frequent infections experienced by these children include otitis media, pharyngitis, pneumonia, and septicemia.

A nurse is caring for a patient with type AB blood. Which principle does the nurse understand about this patient? This patient is likely to have: A) high titers (levels) of anti-A antibodies. B) high titers (levels) of anti-B antibodies. C) no antibodies against A or B antigen. D) high titers (levels) of anti-A antibodies and anti-B antibodies.

A nurse is describing primary immune deficiency. Which primary deficiencies should the nurse include? A) T lymphocytes and mast cells B) Phagocytes and histamine C) B lymphocytes and complement D) Combined and allergen

A nurse is describing the pathophysiology of Type IV hypersensitivities. Which information should the nurse include? Type IV hypersensitivities tissue effects are initiated by: A) B cells that release IgD 24 to 48 hours after exposure. B) the release of neutrophil chemotactic factor. C) the stimulation of cytotoxic T cells. D) the release of large quantities of IgE.

A nurse is describing the pathophysiology of the HIV infection. Which information should the nurse include? HIV inserts its genetic material by binding to the _____ on the helper T cell. A) gp 120 receptor B) CD8 receptor C) CD4 receptor D) phospholipids

A nurse is discussing the formation of antigen-antibody (immune) complexes that get deposited on vessel walls or in extravascular tissue. Which hypersensitivity reaction is the nurse describing? A) Type I B) Type II C) Type III D) Type IV

A nurse recalls Raynaud phenomenon is an example of a: A) type I hypersensitivity. B) type II hypersensitivity. C) type III hypersensitivity. D) type IV hypersensitivity.

A patient has Bruton agammaglobulinemia. Which condition would cause the nurse most concern? A) Otitis media B) Sore throat C) Septicemia D) Afebrile

A patient has DiGeorge syndrome. Which assessment findings should the nurse monitor for in this patient? A) Elevated T cells and hypocalcemia B) Enlarged parathyroid gland and erythema C) Low calcium levels and tetany D) Decreased B cells and allergies

A patient has a complement deficiency. Which patient will the nurse assess for the most severe type of deficiency? A patient with a deficiency in: A) C1 B) C2 C) C3 D) C4

A patient has human immunodeficiency virus (HIV). A nurse realizes the HIV will attack: A) neutrophils. B) gram-negative bacterium. C) helper T cells. D) IgM.

A patient needs a transplant. Which relative should the nurse assess first to have the highest chance of sharing both HLA haplotypes, making him or her a good match for an organ transplant? A) Mother B) Father C) Sibling D) Aunt/uncle

A patients body mounts an aggressive response against an organ transplanted from another person. What term will the nurse use to describe this process? A) Type I hypersensitivity B) Autoimmune C) Alloimmune D) Immunosuppressive

Original Alphabetical A patient had a hypersensitivity reaction involving the formation of antibodies against tissue-specific antigen. Which type of hypersensitivity reaction did the patient experience? A) Type I B) Type II C) Type III D) Type IV B) Type II A patient has a hypersensitivity reaction mediated by Tc cells. A nurse recalls this type of hypersensitivity reaction is called: A) Type I B) Type II C) Type III D) Type IV D) Type IV When a person has an allergic reaction to a bee sting, which type of hypersensitivity response is occurring? A) Type I B) Type II C) Type III D) Type IV A) Type I A nurse is discussing the formation of antigen-antibody (immune) complexes that get deposited on vessel walls or in extravascular tissue. Which hypersensitivity reaction is the nurse describing? A) Type I B) Type II C) Type III D) Type IV C) Type III A patient has a positive tuberculin skin test for detecting the presence of tuberculosis. A nurse realizes the patient experienced which type of hypersensitivity reaction? A) Type I B) Type II C) Type III D) Type IV D) Type IV A nurse is teaching about hypersensitivity reactions. Which information should the nurse include? _____________ are stimulated to release histamine by the presence of antibodies in a type I hypersensitivity reaction. A) Mast cells B) Macrophages C) B lymphocytes D) T lymphocytes A) Mast cells A patient has a Type I hypersensitivity reaction. Which elevated lab result should the nurse check? A) IgG B) IgD C) IgM D) IgE D) IgE A nurse is providing care to an atopic patient. Which principle should the nurse use to guide nursing care? Repeated exposure to an allergen in an atopic individual will cause the: A) allergic response to become worse. B) antibody production to become suppressed. C) autoimmune formation to increase. D) Tc cell activity to increase significantly. A) allergic response to become worse. A nurse is conducting a physical assessment on a patient. Which cluster of symptoms would indicate to the nurse that the patient experienced a Type I hypersensitivity reaction? A) Chest pain, shortness of breath, and abdominal cramping B) Weight loss, anxiety, and tremors C) Rhinorrhea, watery eyes, and pruritis D) Jaundice, fatigue, and decreased urine output C) Rhinorrhea, watery eyes, and pruritis A nurse is describing histamine receptors. Which information should the nurse include? __________ receptors, when bound to histamine, stimulate gastric acid secretion in the stomach. A) H1 B) H2 C) H3 D) H4 B) H2 A nurse is asked what happens when H1 receptors are stimulated by histamine. How should the nurse respond? A) Bronchodilation B) Increased permeability C) Prolonged vasoconstriction D) Increased gastric secretions B) Increased permeability Which finding will cause the nurse the most concern for a patient with a Type I hypersensitivity response? A) Eczema. B) Allergic rhinitis. C) Serous otitis. D) Anaphylaxis. D) Anaphylaxis. A nurse is asked about desensitization therapy for allergies. What is the nurse's best response? A) Minute amounts of allergens are given in increasing amounts. B) Decreasing amounts of IgE are injected into the body. C) Individuals with Type III hypersensitivities will benefit from this treatment. D) Antihistamines are a part of this process and will be given monthly. A) Minute amounts of allergens are given in increasing amounts. Which statement indicates the nurse needs more teaching regarding Type II hypersensitivity? Tissue injury is caused by: A) autoantibody activation of complement and subsequent destruction of target cells. B) autoantibody stimulation of NK cells that destroy target cells. C) autoantibody opsonization of target cells and subsequent phagocytosis. D) autoantibody mediation of neutrophils with detoxification of their toxic substances. D) autoantibody mediation of neutrophils with detoxification of their toxic substances. Which characteristic does the nurse know is related to a type IV hypersensitivity reaction? A) Antibody-dependent cell-mediated toxicity B) Delayed response C) Life-threatening symptoms D) Complement system mediation B) Delayed response A nurse is describing the pathophysiology of Type IV hypersensitivities. Which information should the nurse include? Type IV hypersensitivities tissue effects are initiated by: A) B cells that release IgD 24 to 48 hours after exposure. B) the release of neutrophil chemotactic factor. C) the stimulation of cytotoxic T cells. D) the release of large quantities of IgE. C) the stimulation of cytotoxic T cells. A nurse recalls Raynaud phenomenon is an example of a: A) type I hypersensitivity. B) type II hypersensitivity. C) type III hypersensitivity. D) type IV hypersensitivity. C) type III hypersensitivity. When the maternal immune system becomes sensitized against antigens expressed by the fetus, what type of immune reaction does the nurse expect to occur? A) Autoimmune B) Anaphylaxis C) Alloimmune D) Allergic C) Alloimmune A nurse recalls Graves disease is an autoimmune disease caused by autoantibodies that: A) stimulate the production of thyroid hormone. B) block the effects of thyroid hormone. C) destroy the thyroid gland. D) destroy cells that normally respond to thyroid hormone. A) stimulate the production of thyroid hormone. A patients body mounts an aggressive response against an organ transplanted from another person. What term will the nurse use to describe this process? A) Type I hypersensitivity B) Autoimmune C) Alloimmune D) Immunosuppressive C) Alloimmune Which statement indicates a nurse needs more teaching regarding autoimmunity? Autoimmunity can result from: A) type I hypersensitivity. B) type II hypersensitivity. C) type III hypersensitivity. D) type IV hypersensitivity. A) type I hypersensitivity. Which statement indicates the staff member understood the teaching from the nurse? The following is a known mechanism for the development of an autoimmune disease: A) the development of anti IgG antibodies. B) alterations in ABO blood groups. C) the breakdown of tolerance. D) the production of memory cells. C) the breakdown of tolerance. Which of the following groups should the nurse screen first for systemic lupus erythematosus (SLE)? A) Women, 50-70 years old B) Women, 20-40 years old C) Men, 50-70 years old D) Men, 20-40 years old B) Women, 20-40 years old Which statement indicates a nurse has a good understanding of the pathophysiology of systemic lupus erythematosus (SLE)? Disease characteristics of SLE include: A) Tc cell destruction of lung tissue and the gastrointestinal lining. B) deposition of immune complexes in the kidneys, brain, and heart. C) selective autoantibody destruction of the thyroid gland. D) absence of the antinuclear antibodies and antiDNA antibodies. B) deposition of immune complexes in the kidneys, brain, and heart. Which of the following assessment findings are typical of a patient with SLE? A) Wheezing, eczema, and itching B) Pulmonary edema, leg swelling, and vein distention C) Arthralgia, anemia, and rash D) Nasal polyps, headache, and rhinorrhea

When a nurse checks the patient's PPD tuberculosis skin test, the area is hard and red. Which term should the nurse use to describe the hard area? A) Helminth B) Erythema C) Induration D) Swelling

When caring for a patient with immunodeficiencies, which principle should the nurse use to guide nursing care? Patients with immunodeficiencies are most at risk for: A) hypersensitivity reactions. B) fungal infections only. C) opportunistic infections. D) transient ischemic attacks.

When the maternal immune system becomes sensitized against antigens expressed by the fetus, what type of immune reaction does the nurse expect to occur? A) Autoimmune B) Anaphylaxis C) Alloimmune D) Allergic

Which statement indicates the staff member understood the teaching from the nurse? The following is a known mechanism for the development of an autoimmune disease: A) the development of anti IgG antibodies. B) alterations in ABO blood groups. C) the breakdown of tolerance. D) the production of memory cells.

Treatment with antimicrobials

Culture of a pathogen and sensitivity testing to antimicrobials are essential if treatment is likely to be successful. Most infections are diagnosed by the use of stains (as described previously in this module) and by culturing the organisms in the laboratory. Cultures provide specific identification of the pathogen. Once the organism is growing in culture, it can be tested for its sensitivity to various antimicrobials so that the drug with the greatest effectiveness can be chosen. This process of culture and sensitivity testing commonly takes approximately 48 hours to complete. The culture plate image depicts bacteria (pale orange) that are growing on a culture medium (darker reddish orange) in the laboratory. The white circles depict paper discs impregnated with antibiotics that were placed on the culture. The two discs with a clear area of medium and no bacterial growth around them are impregnated with an antimicrobial to which the bacteria are sensitive. The other antimicrobial discs did not inhibit nearby bacterial growth and represent antimicrobials to which this particular strain of bacteria is resistant.

A nurse wants to teach about the most common primary immune deficiency condition. Which of the following should the nurse describe? A) Phagocyte deficiency B) IgG subclass deficiency C) Selective immunoglobulin A deficiency D) Common variable immune deficiency

A patient has Hashimoto disease. Which organ assessment is priority? A) Gallbladder B) Pancreas C) Lungs D) Thyroid

A patient has Raynauds phenomenon. Which situation does the nurse advise the patient to avoid? A) Meditation B) Bathing C) Gloved hands D) Cold temperatures

A patient has a B-lymphocyte deficiency. Which treatment will the nurse prepare to give? A) Physical therapy B) Heat therapy C) Live attenuated vaccine D) Gamma globulin injection

A patient has a Type I hypersensitivity reaction. Which elevated lab result should the nurse check? A) IgG B) IgD C) IgM D) IgE

A patient has a congenital disorder that affects IgA cells. A nurse recalls this type of immune deficiency is called: A) passive. B) active. C) secondary. D) primary.

A patient has a hypersensitivity reaction mediated by Tc cells. A nurse recalls this type of hypersensitivity reaction is called: A) Type I B) Type II C) Type III D) Type IV

A patient has a positive tuberculin skin test for detecting the presence of tuberculosis. A nurse realizes the patient experienced which type of hypersensitivity reaction? A) Type I B) Type II C) Type III D) Type IV

A patient has phagocytic deficiency. What component of the phagocytic process does the nurse suspect the patient is missing? A) Dendrite cells B) Halide C) Myeloperosidase D) Hydrogen peroxide

A person with type O blood has which of the following antigens present on their red blood cells? A) A and B B) Rh C) O D) No antigens

The nurse should monitor the patient for infections caused by: A) capsulated viruses. B) fermented yeast. C) wet fungi. D) encapsulated bacteria.

To prevent hemolytic disease of the newborn, which situation will cause the nurse to intervene? A) Rh negative fetus and Rh positive mom B) Rh positive fetus and Rh positive mom C) Rh negative fetus and Rh negative mom D) Rh positive fetus and Rh negative mom

Which finding will cause the nurse the most concern for a patient with a Type I hypersensitivity response? A) Eczema. B) Allergic rhinitis. C) Serous otitis. D) Anaphylaxis.

Which statement indicates the nurse needs more teaching regarding Type II hypersensitivity? Tissue injury is caused by: A) autoantibody activation of complement and subsequent destruction of target cells. B) autoantibody stimulation of NK cells that destroy target cells. C) autoantibody opsonization of target cells and subsequent phagocytosis. D) autoantibody mediation of neutrophils with detoxification of their toxic substances.

Which statement indicates the patient understood teaching provided by the nurse? When a person with HIV develops an opportunistic infection the disease is called: A) Antibody-dependent cell-mediated cytotoxicity (ADCC) B) Chronic granulomatous disease (CGD) C) Systemic lupus erythematosus (SLE) D) Acquired immunodeficiency syndrome (AIDS)

Which term can the nurse use to describe a person with type AB blood? A) Universal bone marrow transplant donor B) Universal bone marrow transplant recipient C) Universal blood donor D) Universal blood recipient

Infections

Despite great progress in the diagnosis and treatment of many infections, infectious diseases remain the number one cause of death worldwide. In developing nations, the transmittable diseases tuberculosis and human immunodeficiency virus (HIV) infection kill millions of people each year. In the United States, mortality as a result of infections is less common than it is in less-developed countries because of the widespread use of vaccinations and antibiotics. However, increasing numbers of vulnerable individuals are at great risk for serious infection: older adults, hospitalized individuals, and those on immunosuppressive medications (e.g., transplant patients). Adding to the threat of infectious diseases is the development of significant microorganismal resistance to standard therapies and the appearance of mutant organisms (such as the virus that causes severe acute respiratory syndrome [SARS]) that are highly infectious, pathogenic, and difficult to treat.

Treatment with antimicrobials cont

Empiric use of antimicrobials refers to the process of choosing a drug (or drugs) that is most likely to treat an infection effectively, even though the specific organism and its sensitivity to antimicrobials have not yet been determined. In serious infectious disease, it is unwise to wait the 48 hours necessary for culture and sensitivity testing, and treatment must begin immediately. Empiric antimicrobial selection is usually one of "broad-spectrum coverage." This means that the drug chosen is effective in treating a large range of potential organisms. If culture and sensitivity of the pathogen are subsequently completed, the choice of antimicrobial treatment can be "narrowed" to use only the most effective and least toxic drugs.

Capsules

Encapsulated bacteria such as Streptococcus pneumoniae and Neisseria meningitidis can avoid phagocytosis by neutrophils and macrophages because their capsules make it difficult for the phagocytes to adhere to and engulf the organisms. Effective phagocytosis must await opsonization of the organism by complement and antibodies. (See Module 05: Adaptive Immunity.) This allows the organisms time to replicate and invade tissues before adequate defense mechanisms are activated.

Fungal Disease

Fungi are capable of causing serious systemic infection, especially in immunocompromised individuals who have decreased phagocytic and T lymphocyte function (opportunistic infection). For example, Candida albicans can involve the mouth (see image), throat, esophagus, intestines, and bloodstream (fungemia). Another fungus that causes serious opportunistic infection of the lung and central nervous system is Cryptococcus neoformans. Fungi are usually diagnosed by staining with india ink or potassium hydroxide and by culture. Treatment for mild skin infections is usually with a topical fungicide. Serious infection requires highly toxic antifungal medications, such as amphotericin.

Fungi

Fungi have thick polysaccharide walls that make them relatively impervious to most antibiotics. These organisms can live anywhere in the body, although they are found most commonly on the skin (dermatophytes). Common examples of fungal infections (mycoses) of the skin include tinea pedis (athlete's foot as seen in this picture), onychomycosis (fungal infection of the nail), and Candida albicans, which thrives in warm moist skin folds (intertrigo) and in the vagina (yeast vaginitis). Fungi can adapt to the host environment and frequently colonize the skin. They can survive in a wide variety of conditions and will spread rapidly whenever host defenses are compromised, such as when commensal bacterial colonization is lost (use of widespread antibiotics) or when phagocytic activity or cellular immunity is reduced.

Fungi

Fungi take the form of yeasts (single-celled spheres) or molds (multicelled filaments or hyphae), or both (dimorphic). They are not motile and have thick polysaccharide cell walls that render them resistant to most antibacterial drugs.

HIV life cycle

Fusion: Infection begins with attachment of the virus to the surface of the target cell via the binding of the viral envelope glycoproteins gp120/gp41 to CD4 receptors on the host macrophages, dendritic cells, and T helper cells. (See Module 05: Adaptive Immunity.) Coreceptor binding: Effective viral attachment requires the subsequent interaction of host cell co-receptors CXCR4 on T helper cells and CCR5 on macrophages and dendritic cells. There are small numbers of individuals who have genetic mutations in these co-receptors and are therefore immune to HIV infection. Reverse transcription: The virus moves into the host cell cytoplasm and uncoats and makes a DNA copy of its RNA, using the viral enzyme reverse transcriptase. Integration: This new viral DNA is then incorporated into the host cell chromosomes, using another viral enzyme called integrase. Protease activity: As the host cell divides, it makes numerous copies of this integrated viral genetic material and produces the viral components needed to make new virions. These components are separated into their active forms by another viral enzyme called protease. Budding: Finally, the virus is reassembled and buds from the surface of the host cell are ready to infect other host macrophages and T helper cells. The virus takes a part of the host cell membrane with it when it buds, making the virus harder to detect by the immune system.

Gene Therapy for Primary Immune Deficiences

Gene therapy has been used increasingly for primary immune disorders, although the greatest success has been with SCID caused by adenosine deaminase (ADA) deficiency. Gene therapy for immunodeficiencies uses a virus as a vector for inserting normal genes into stem cells which are then infused into affected individuals. Gene therapy remains one of the areas of most active research for the treatment of immune deficiencies.

HIV structure

HIV is a retrovirus, meaning that it contains only single stranded viral RNA (not DNA). The virus is surrounded by a lipid envelope from which protrude important glycoproteins called gp120 and gp41. Within the envelope is a capsid (p24), and within the capsid are two copies of viral RNA and three enzymes: reverse transcriptase, integrase, and protease.

High Proliferation Rates

High proliferation rates: Many microorganisms have proliferation rates that allow the pathogen to surpass the development of a protective inflammatory and immune response. For example, cholera and some forms of streptococci can cause severe illness and even death within a few days of infection.

Action of IGE

IgE binds to mast cells and causes the mast cell to degranulate with release of histamine, prostaglandins, leukotrienes, and chemotactic agents. (See Module 04: Innate Defenses: Inflammation.) In addition, eosinophils are stimulated by the immune cytokine interleukin-5 (IL-5) to release eosinophil cationic protein, major basic protein, and platelet-activating factor. These cytokines result in activation of cellular receptors in tissues throughout the body, and the inflammatory response is initiated. Refer to Module 04: Innate Defenses: Inflammation to review these inflammatory cytokines and their effects. Even though IgE has a relatively short half-life in the blood, IgE molecules that have yet to bind to allergen can remain attached to mast cell receptors for a prolonged period of time. Reexposure to antigen not only will induce additional IgE production as described on the last screen, but will also result in cross-linking of IgE molecules already bound to mast cells. This will cause rapid degranulation of the mast cells and acute onset of allergic symptoms.

Types of Infections

Immunocompromised individuals are at risk for many potential problems, the most important of which is infection by both usual and opportunistic organisms. Careful monitoring for symptoms and signs of infection is crucial, and it is important to note that a lack of significant innate and adaptive immunity can make these signs and symptoms more subtle (for example, the individual may not develop fever or exude pus). Individuals with long-term immunocompromise are also at risk for other complications, such as chronic infections with organ failure, poor wound healing, malnutrition, growth failure, diarrhea, and cancers. These individuals require comprehensive interprofessional coordinated care in order to prevent these serious sequelae.

Diagnosis of AIDS

In addition to measuring antibodies and/or virus in the blood, important diagnostic tests used in HIV infection include measurement of CD4 (T helper) cells and detection of opportunistic infections and malignancies. The criteria for diagnosis of AIDS, as defined by the Centers for Disease Control and Prevention, are: Documented HIV infection with an associated indicator disease, including: Certain opportunistic infections Certain cancers such as Kaposi sarcoma, lymphomas, and invasive cervical or anal carcinomas Wasting syndrome Associated neurologic diseases Recurrent pneumonias HIV infection and a CD4 (T helper) count of <200 cells/mL

Pediatric AIDS

Infants infected with HIV during pregnancy, delivery, or breastfeeding have a much more rapidly progressive clinical course than adults. Most untreated children will die before age 2. Neurologic involvement is especially severe in the infected developing central and peripheral nervous system. Children with untreated HIV infections may present clinically with failure to thrive, intellectual deficits, motor deficits, and impaired brain growth (diminished head circumference). Rapid diagnosis and treatment is essential

Intracellular Survival

Intracellular survival: Many microorganims have the ability to move inside cells and thus evade the host immune response. Examples include Listeria and Mycobacterium tuberculosis. These bacteria avoid being killed by phagocytes by producing substances that neutralize these lysosomal enzymes.

Primary (Congenital) Immune Deficiencies

Lymphocyte dysfunction is the most common form of primary immunodeficiency, although failure of phagocytes or inflammatory systems, such as complement, are also important causes. (See Table 7-11 in your textbook.) Primary immunodeficiencies can be classified into 5 major categories of defects, including deficiencies of: B lymphocytes T lymphocytes Combined T and B lymphocytes Complement Phagocytes Any of these defects leads to a reduction in the ability of the host to respond to invasion by microorganisms, as well as other types of organ dysfunction. The following examples of congenital immunodeficiencies will help to illustrate some of the pathophysiologic disorders that characterize immune dysfunction and the challenges that individuals with these disorders face.

AIDS

Macrophages, dendritic cells, and T helper cells are the main targets for HIV infection because they have CD4 molecules on their surfaces that allow attachment of the virus to their cell membranes. When active lymphocytes become infected with HIV (and the viral genetic code is integrated into the host cell chromosomes), these target cells become "factories" for HIV replication until they are found and destroyed by the T cytotoxic cells of the immune system. (See Module 05: Adaptive Immunity.)

Secondary Immunodeficiency Disorders

Many conditions are associated with secondary immunodeficiency states including stress, trauma, malnutrition, malignancy, and infection. Also, many medications can suppress immune function, especially those drugs used for the treatment of cancer, inflammation, or transplant rejection. Table 2 in your text lists many of these conditions.

Leukocytosis

Many individuals with infection will develop an increased white blood count. Bacterial infection is commonly associated with an increase in polymorphonucleocytes, while viral infections may cause an increase in the number of circulating lymphocytes.

Parasitic Infection

Many of parasitic infections are associated with only limited disease in immunocompetent hosts. Others are the cause of serious morbidity and mortality, especially in the developing world. Malaria is one of the most serious global infectious diseases. It is transmitted through the bite of an infected mosquito and invades the liver and red blood cells. Treatment frequently requires the use of toxic antibiotics with many side effects. Individuals who are immunocompromised (e.g., HIV/AIDS or post-transplant) are at greater risk for significant parasitic disease. One example of a parasite that commonly causes illness in AIDS patients is Toxoplasma gondii. This protozoan is transmitted via undercooked meat, dairy foods, or cat feces. Toxoplasmosis is associated with central nervous system infection (abscesses), retinal infection, lymphadenopathy, myocarditis, and pneumonitis, especially in immunocompromised patients. Treatment requires a combination of pyrimethamine, folic acid, and sulfadiazine.

Antigenic Variation

Many pathogens can evade the host immune system (at least temporarily) by altering their immunologic appearance (antigenic variation). There are three primary mechanisms of antigenic variation: Antigenic drift - emergence of new strains of organisms Antigenic shift - recombination of genes from one strain of pathogen to another Gene switching - the switching on and off of genes that control surface antigens Antigenic drift (variation) in viruses is most often the result of random mutations that occur during rapid viral replication. Some of these mutations confer a selective advantage such that increased infectivity, invasiveness, and resistance to both host immune defenses and antimicrobials emerge. Influenza A has two important virulence factors: hemagglutinin (HA) and neuraminidase (NA) that undergo frequent antigenic variation. Different strains of influenza viruses are described by assigning numbers to the different mutations of these molecules. For example, common influenza infections worldwide are caused by H1N2 and H3N2 strains of influenza. Influenza viruses are especially able to undergo another kind of antigenic variation called antigenic shift. When antigenic shift occurs, different strains of influenza are exposed to one another when they infect the same host (human, swine, bird). Segments of the viruses' genomes undergo recombination such that a new hybrid virus is formed.

Clinical Evaluation of Immunity and Replacement Therapies for Immune Deficiencies

Most individuals suffering from an immunodeficiency disorder will present to the healthcare provider with the symptoms and signs of infection. Discovering the cause of the immunodeficiency may be as simple as learning that the patient has recently been placed on immunosuppressive medications, or it may be as difficult as identifying a specific genetic metabolic defect that affects certain immune cells. The management of immune deficiencies includes not only the prevention and treatment of infection, but increasingly involves the use of replacement therapies. When a specific immunodeficiency disorder is diagnosed, it may be possible to correct the deficiency by replacing the missing elements (e.g., replacement of missing immunoglobulins). In other cases, it may be necessary to restore the immune system through bone marrow transplantation, although graft-versus-host disease (GVHD) remains a significant complication of this procedure. GVHD results from transplanted T cells that attack the recipient of the transplant and cause severe rash, liver dysfunction, and damage to the gastrointestinal tract. New treatments for GVHD include the administration of mesenchymal stem cells which suppress the immune reaction of the graft to the host. For many acquired immunodeficiencies, treating the underlying disorder and supporting the immune system through good nutrition, exercise, avoidance of alcohol, and counseling are essential.

Progressive and Late Disease

Once immune dysfunction develops (average of 10 to 11 years in otherwise healthy adults, but occurs much sooner in infants, the elderly, and those with comorbid conditions such as hepatitis), individuals experience nonspecific conditions such as fungal infections (e.g., thrush), eczema, or sexually transmitted diseases such as venereal warts and vaginitis. Progressive deterioration in immune function results in more serious opportunistic infections with organisms such as Pneumocystis jerovici (previously called Pneumocystis carinii), Mycobacterium tuberculosis, Toxoplasmosis gondii, and cytomegalovirus. In addition, malignancies such as Kaposi sarcoma (caused by coinfection with a herpesvirus) and lymphomas may develop. Other complications of HIV infection include wasting syndrome and AIDS-related dementia. Your textbook contains many illustrations of these conditions.

Urticaria

One common manifestation of allergy is urticaria (hives). Histamine-induced increased vascular permeability in the skin results in fluid exudation that presents as pruritic fluid-filled blisters surrounded by redness

Recent Pathogenic Adaptations

One of the most serious challenges that confront the effective management of infectious disease is the concept of drug resistance. Many microorganisms undergo a mutation of genes that renders them resistant to available antimicrobials. Many infections that had been historically managed with drug therapy have reemerged as drug- and antibiotics-resistant. At least 25% of the Streptococcus pneumoniae isolates are penicillin resistant. There are multiple antibiotic-resistant forms of Staphylococcus aureus present in the endemic portions in some hospitals. Some forms of this microorganism that were once sensitive to only vancomycin are vancomycin resistant. Antimicrobial resistance is now routinely seen in such disease processes as tuberculosis (TB) and sexually transmitted infections (STIs). The overuse of antimicrobials to treat minor infections and the use of broad-spectrum antibiotics to treat simple infections have led to a dramatic increase in multidrug-resistant strains of many pathogens, including bacteria, viruses, and fungi. Although new antimicrobials are being developed to overcome drug-resistant infections, mutations occur frequently and new resistant strains are discovered regularly. Mutations leading to resistance also occur in response to vaccines, and this has been a major barrier to the development of an effective vaccine against HIV.

Parasites

Parasites are organisms that are dependent on the human body during at least a part of their life cycle and can be classified into three major groups: protozoa (single-celled), arthropods, helminths. Protozoa are frequently motile single-celled intracellular parasites that are larger than bacteria and have an organized nucleus. These organisms frequently infect the gastrointestinal tract, although infection of the liver, lungs, and central nervous system is possible. Protozoal infections usually occur in the presence of infected water (e.g., amebiasis), venereal transmission (e.g., Trichomonas vaginalis), ingestion (e.g., Toxoplasmosis gondii), or insect vectors (e.g., malaria). Arthropods are invertebrate animals with jointed appendages that frequently cause skin disease (e.g., scabies). Helminths are large parasites that can infect the gut, skin, eyes, and lymphatics; they are acquired through ingestion (e.g., pinworms or tapeworms) or through skin penetration (e.g., hookworms, flukes).

Parasitic Disease

Parasites can take many forms and are classified into three major groups: protozoa (single-celled), arthropods, and helminths. Parasites are organisms that are dependent on the human body during at least a part of their life cycle. Some reach the human body via transmission by a vector (e.g., fly bites), and others by ingestion of contaminated food or water into the gastrointestinal tract. Still others penetrate through the skin or are inhaled into the respiratory tract. One of the primary immune responses to parasitic infection is the activation of eosinophils. Parasites exhibit many virulence factors that decrease the effectiveness of the host immune response including intracellular survival, coating with host self proteins, antigenic variation, and release of immunosuppressive factors. Parasites can "hide" from the immune system by remaining dormant in tissues (such as the liver) for years and then reemerge when conditions are favorable.

Passive Immunization

Passive immunization refers the procedure by which preformed antibodies are given to an individual when a more rapid immunologic response is needed. This can occur after exposure to an infection when active immunization was not obtained previously (as in hepatitis B exposure), when potential exposure to a pathogen is imminent (travel), or when an active vaccine is not available (rabies).

Fever

Pathogenesis of feverFever is defined as an elevated core body temperature and is commonly part of the host defense against infection. It is caused by the production of inflammatory cytokines (endogenous pyrogens) or by microorganism components (exogenous pyrogens) that alter the temperature-regulating function of the hypothalamus. Exogenous pyrogens include some exotoxins and endotoxin. These toxins may interact directly with the hypothalamus, or they may induce fever by interacting with toll-like receptors on macrophages, which causes the release of endogenous pyrogens such as tumor necrosis factor-alpha (TNF-alpha), interleukin 1 (IL-1), interleukin 6 (IL-6), and prostaglandin E2. These inflammatory cytokines act on the thermoregulatory center of the hypothalamus to induce an increase in core body temperature.

Phagocytic Deficiences

Phagocytic deficiencies are often associated with inadequate opsonization of encapsulated bacteria as described on the previous screen. Phagocytosis can also be impaired by inadequate numbers of phagocytes, especially neutrophils. Most neutrophil deficiencies are acquired, but there is a primary form of neutropenia called severe congenital neutropenia. While most primary neutropenias are chronic disorders, some are considered cyclic. There are also disorders of defective phagocytic activity that include defects in adhesion molecules and complement receptors. Phagocyte activity can also be defective because of an inability to kill organisms intracellularly. Defects in intracellular killing most commonly result from abnormal cytoplasmic granule formation (e.g., Chediak-Higashi syndrome) or deficiencies in lysosomal enzymes such as myeloperoxidase (e.g., chronic granulomatous disease).

Prevention

Prevention of HIV has been successful in many populations in the United States through education about how to reduce transmission of the virus. Unfortunately, many of those at highest risk for HIV infection are adolescents and intravenous drug users who are less likely to adhere to safe practices. In pregnant women infected with HIV, perinatal transmission can be greatly reduced through the proper use of antiviral medications. An effective HIV vaccine remains elusive because of the dangers inherent in using a live virus, the rapid rate of viral mutation, the intracellular spread of the virus throughout the body on exposure, and the relative ineffectiveness of HIV antibodies in combating infection. In 2009, it was reported that a vaccine in Thailand resulted in a 31% reduction in HIV infection, a modest response at best. Research to find an effective HIV vaccine continues.

Purulent exudate (pus)

Pus is the result of the inflammatory and immune processes. (See Module 04: Innate Defenses: Inflammation and Module 05: Adaptive Immunity.) Fluid and cells move out of the blood vessels and into the area of infection in an effort to dilute toxins and bring phagocytes such as neutrophils and macrophages to the area. The organ system involved frequently determines symptoms associated with the production of purulent exudates. For example, infections of the lung are characterized by sputum production, and infections of the middle ear result in purulent fluid pressing on the eardrum, causing pain. When pus collects within a tissue and cannot be extruded from the body, it may form an abscess that must be drained therapeutically to relieve symptoms and allow for clearance of the infectious organism. The image shown represents acute otitis media.

Screening and Diagnosis of HIV

Screening recommendations for HIV have changed over the years. The CDC now recommends that everyone be screened when they are seen in a healthcare facility, and counseling is no longer essential prior to screening. Home-use rapid testing for HIV is now available. Measuring antibodies to HIV remains the most commonly used screening (e.g., enzyme immunoassay, EIA or ELISA) and diagnostic test for HIV. There are two main problems with this test: "False positives"-meaning that the test falsely detects antibodies in the blood even when infection is not present "False negatives"-meaning that antibodies are not detected even though HIV infection is present The number of false positives is decreased by doing an additional test called a Western blot, which can help confirm the actual presence of infection. False negatives are more difficult to prevent. False negatives may occur because individuals may not become seropositive for the antibodies for several weeks or months after primary infection, leaving a "window period" during which the person may be infectious to others but still be HIV antibody negative. The point at which antibodies can be detected in an HIV-infected individual is called seroconversion. The presence of HIV in the blood can be detected very early in the course of infection by measuring viral proteins using a technique called a polymerase chain reaction (PCR). Unfortunately, this test is expensive and complicated and is not yet appropriate for general screening of the population. Instead, it is used to monitor the progression of infection and the response to treatment in those already known to be infected with HIV.

B-Lymphocyte Deficiencies—Selective IgA Deficiency

Selective IgA deficiency is characterized by a lack of IgA production and results from an inability of plasma cells to class-switch to IgA (although they can continue to produce the other antibody types). Because the secretory immune system is compromised, infections of the gastrointestinal (GI) tract are most common, along with lung and sinus infections. Many individuals with this disorder develop chronic intestinal candidiasis and are also prone to autoimmune diseases and allergy. A major concern is the possibility of transfusion reactions because most individuals with IgA deficiency develop anti-IgA antibodies through exposure to intrauterine leakage of maternal IgA or though milk. Transfused blood contains significant IgA and will cause a severe transfusion reaction; therefore blood washed of IgA must be used and the patient pretreated for a possible anaphylactic reaction.

Combined Deficiencies—Severe Combined Immunodeficiency Disease (SCID)

Severe combined immunodeficiency disease (SCID) is caused by a failure of stem cell development into mature lymphocytes. Most children with SCID have few or no T and B lymphocytes, but they do have normal numbers of neutrophils and macrophages. SCID can also arise from inherited enzymatic defects that result in the accumulation of toxic purines within rapidly dividing cells such as lymphocytes. Children with this disorder lack both cellular and humoral immunity and are highly susceptible to infections from viruses, bacteria, fungi, and parasites. A famous case of SCID was described in Ian Strachan's book, The Boy in the Bubble, and in the movie The Boy in the Plastic Bubble (1976) starring John Travolta.

Lysis

Some viral replication results in lysis of the cell as the progeny virions are released. Host cells also may be lysed as a result of viral disruption of lysosomes with autodigestion of the cell by lysosomal enzymes.

T-Lymphocyte Deficiencies—DiGeorge Syndrome

T-lymphocyte deficiencies can affect both humoral and cellular immunity because they frequently result in a decrease in the important interleukins necessary for full adaptive immune responses. DiGeorge syndrome results from congenital thymic aplasia (absence of thymus gland) or hypoplasia and diminished parathyroid gland development. T-cell number and function are severely compromised, resulting in numerous fungal infections (especially of the GI tract) and bacterial and viral pneumonias. Parathyroid dysfunction leads to hypocalcemia and tetany. Abnormal facial development is also common.

Histamine 3

The H3 receptor is still not fully understood but appears to modulate the release of neurotransmitters in the central nervous system.

Histamine 4

The H4 receptor is on mast cells, histamine results in chemotaxis of more mast cells to the area of allergen exposure.

Clinical Progression of Infection

The human body passes through four distinctly different stages as the infectious process progresses. These stages include incubation (pathogens present but numbers are still insufficient to cause symptoms), prodrome (highly contagious period), invasion (immune and inflammatory responses are triggered), and convalescence (identifying symptoms begin to decline). Fever is the hallmark of most infectious disease processes and is believed to be an adaptive host-defense response.

Early Disease (Clinical Latency)

The immune response to the infection destroys T helper cells (and the viruses they carry), thus reducing the "viral load" (as measured by the number of copies of HIV RNA per milliliter in the blood). Billions of T helper cells are infected, destroyed, and replaced by the bone marrow each day throughout the years of clinical "latency" (no symptoms of infection). Other less active immune cells, such as dendritic cells in the lymph nodes, memory cells, and cells in the central nervous system, also become infected shortly after primary exposure to the virus. Because they are inactive, the virus does not replicate and the infected cells may remain undetected by immune defenses for many years, therefore serving as "reservoirs" for HIV.

Memory Sensitization

The memory characteristic means that the adaptive immune system becomes "primed" for another (secondary) exposure to that same antigen because of the presence of long-lived B and T memory cells that were created in response to the primary antigen exposure. The secondary immune response is faster with higher antibody titers and more vigorous cell-mediated immunity. In the upper figure on this screen, the immune responses depicted are those of IgM and IgG. This is the classic humoral response seen with most exogenous antigens such as infectious organisms. However, in allergy, the primary and secondary responses are characterized by the production of IgM and IgE. The increasing amounts of IgE with each exposure means that the affected individual is more likely to have serious consequences from reexposure to the allergen. The lower figure demonstrates that repeated exposure to allergens results in increasing production of IgE which results in sensitization of the individual to that allergen.

Antigenicity

The presence of an intracellular pathogen such as a virus can cause the host cell to present foreign antigen on its surface (endogenous antigen), resulting in a cellular immune response that causes death of the host cell. (See Module 05: Adaptive Immunity.)

Histamine 2 Receptor

The primary action of histamine at this receptor is to increase gastric acid secretion in the stomach. H2 receptors are also found in cardiac muscle, where histamine can act as a stimulant.

Clinical Manifestations of primary infection

The progression of HIV-1 infection to AIDS may vary greatly from patient to patient. Primary infection with HIV is characterized by a flu-like illness with fever, myalgia, and adenopathy that often goes unrecognized as HIV infection. In subsequent weeks, months, and years, the immune system is able to combat the HIV infection so that the individual is most often asymptomatic. During this time, the individual may be unaware that the virus is being shed in body secretions and therefore may unwittingly infect others.

Microorganisms and Humans: Normal Flora and Opportunistic Organisms

The relationship between humans and microrganisms can be considered in three different categories: normal flora, opportunistic organisms, and true pathogens. Humans and certain microorganisms (called "normal flora" or commensal bacteria) maintain a mutually beneficial relationship. Normal bacterial flora helps digest dietary molecules and produce metabolites such as vitamins B and K. Another important activity of these resident organisms is that they produce factors that keep pathogenic organisms in check. Serious infection by normal flora is prevented through skin and mucosal barriers and the innate and adaptive immune systems. An opportunistic organism is usually harmless to its host body unless it is presented with exactly the right set of circumstances. The primary risk factor for the human is a compromised immune system. When the body's defenses are weakened or suppressed, the usually benign organism seizes the opportunity to become pathogenic to the host. A true pathogen, on the other hand, has the ability to cause illness in the host regardless of the status of its immune system because it has developed the means to circumvent the body's defenses.

Food Allergies

The symptoms and signs of allergy depend on the tissues most affected by allergen exposure in an individual. The most common forms of atopic disease are allergic rhinitis, bronchial asthma, atopic dermatitis (eczema), and anaphylaxis. Gastrointestinal allergy is usually caused by foods and medicines and results in nausea, vomiting, and abdominal cramping. However, in highly sensitized individuals, ingestion of allergens can lead to a life-threatening form of allergic reaction called anaphylaxis, which also affects the respiratory and cardiovascular systems. Common food allergens are contained in milk, peanuts, tree nuts, eggs, wheat, and fish. Food preservatives (for example MSG, monosodium glutamate) may also cause allergy. Another important source of gastrointestinal allergy is medications.

Toxins

The two major categories of bacterial toxins are exotoxins and endotoxins. Exotoxins are proteins from gram-positive bacteria that are released during cell growth and are directly cytotoxic. They include cyotoxins, neurotoxins, pneumotoxins, and hemolysins. Endotoxins are lipopolysaccharides (lipid A and lipid O) that are released from the cell walls of gram-negative bacteria when the cell wall is injured during lysis or exposure to antibiotics. Endotoxins set off a severe inflammatory response that can result in shock and dysfunction in many organs.

Histamine 1 Receptor

This receptor is important in causing smooth muscle effects in blood vessels and in bronchi, resulting in vasodilation and bronchoconstriction. It also causes increased capillary permeability by stimulating endothelial cells to retract, opening the spaces between cells, which allows cells and proteins to move out of the vessel and into the tissues (edema). Histamine receptors located on white blood cells help to activate polymorphonucleocytes and macrophages that provide the cellular inflammatory response. Tissues commonly affected by histamine via its H1 receptor during allergic symptoms include the nasal mucosa, conjunctiva, skin, bronchi, and the gastrointestinal tract.

Treatment of AIDS

Treatment of HIV infection centers around 5 classes of drugs: 1) block the viral enzyme reverse transcriptase (e.g., azidothymidine [AZT; zidovudine]), 2) block protease (e.g., indinavir) 3) block integrase, 4) block fusion of the virus to the CD4 cell membrane (fusion inhibitors), and 5) block the coreceptor CCR5 (maraviroc) which is found on macrophages and dendritic cells. Unfortunately, HIV has the capacity to mutate at an astonishing rate, such that resistance to these medications occurs very rapidly when they are used singly. In an effort to diminish the likelihood of drug resistance, several of these medications are used in combinations of two or three drugs at the same time. This use of a drug "cocktail" to prevent drug resistance is called highly active anti-retroviral therapy (HAART). The use of HAART has dramatically reduced the progression of HIV infection to AIDS and mortality but is characterized by difficulties in adherence, toxicities (e.g., lipodystrophies associated with protease inhibitors), and expense. Experts no longer believe that HIV can be eradicated from the body; rather, these drugs serve to keep the infection under control so that the immune system can remain functional. Management of the complications of HIV infection and AIDS requires a multidisciplinary team of expert clinicians who can detect the presence of infections, malignancies, and other disorders (e.g., wasting and dementia) early and respond quickly. Many antimicrobials are needed during the course of AIDS to prevent and treat potentially fatal opportunistic infections.

Treatment of Type I

Treatment of allergies is tailored to the specific allergic disorder (e.g., allergic rhinitis, asthma, anaphylaxis), the severity of the disorder, and the age of the affected individual. Management begins with allergen avoidance. Pharmacologic therapies that can be used in allergic disorders include: Antihistamines Anti-inflammatories (e.g., inhaled corticosteroids, nasal steroids, prednisone) Bronchodilators (e.g. inhaled beta 2 agonists, anticholinergics) Anti-leukotrienes Anti-IgE antibody (omalizumab) Desensitization (allergy shots; immunotherapy) Epinephrine (use is restricted to acute allergic reactions such as anaphylaxis)

Vaccines

Vaccines induce a primary immune response, thus priming the immune system so that exposure to the actual organism in the future is met with a vigorous and effective defense. (See Module 05: Adaptive Immunity.) Vaccines have been developed against bacteria and viruses and some of the toxins that they produce (e.g., diphtheria and tetanus toxins). Vaccines must be given at the right time in the life span of an individual to provide an appropriate immune response, and "boosters" may be required at intervals to maintain immunity. Some individuals fail to mount an adequate immune response to certain vaccines. In rare instances, stimulation of the immune system by a vaccine may inadvertently elicit autoimmune responses that can result in damage to healthy organs.

Viral Disease

Viral infections are emerging as some of the world's most widespread and dangerous forms of infectious disease. Some common viral infections include adenovirus, influenza, herpes, measles, hepatitis, and human immunodeficiency virus to name just a few. Viruses can often hide from the host defenses because they reproduce intracellularly. Viral replication depends on their ability to penetrate a permissive host cell. The first step requires binding of the virus to the surface of the host cell. This is followed by penetration into the cytoplasm, which can occur by endocytosis (the host cell envelops the virus), viral envelope fusion with the host cell wall, or direct penetration of the cell membranes. The virus then sheds its protective coating (uncoating). Most RNA viruses and a few DNA viruses can replicate in the cytoplasm. Conversely, a few RNA viruses (influenza and retroviruses) and most DNA viruses move into the nucleus and use the cells' normal replicative mechanisms to produce the necessary genetic and structural components for viral replication. New viruses are assembled in the cytoplasm and then are released from the cell so that they can infect other cells. Release of viruses may result from lysis of the host cell or may occur through budding of the virus from the host cell surface. This may spare the cell from death but also renders it a persistent "factory" for viral replication. (See HIV Life Cycle Animation later in this module.) Other viruses are able to set up a latent phase and remain integrated into the cell for many years, but may cause active disease in the future should the host become immunocompromised (e.g. herpes zoster virus and shingles).

Fusion

Virally infected cells also may fuse together with healthy cells into structures called multinucleated giant cells, or syncytia.

Dysfunction

Virally infected cells may not be able to perform normal functions such as DNA, RNA, or protein synthesis.

Viruses

Viruses are intracellular microorganisms that take over the metabolic machinery of host cells and use it for their own survival and replication, frequently resulting in destruction of the infected cell. Arthropods are invertebrate animals with jointed appendages that frequently cause skin disease (e.g., scabies). Helminths are large parasites that can infect the gut, skin, eyes, and lymphatics; they are acquired through ingestion (e.g., pinworms or tapeworms) or through skin penetration (e.g., hookworms, flukes)

Pathogenic Defense Mechanisms

When the host loses the ability to generate adequate defense (immunocompromise), that individual becomes vulnerable to many organisms, even those that are not normally pathogenic. In healthy individuals, infections can still occur because pathogens devise means to circumvent host defenses. Pathogens have their own set of defense mechanisms. Infectious processes can be better understood when viewed as an interaction among host, pathogen, and environment. Click on the illustration to see how a parasite interacts with the host and environment. Note the normal defense mechanisms of both the host and the parasite. Microorganisms become pathogens when they breach the normal host defense mechanisms and develop pathogenic defense mechanisms that allow them to replicate within the host.

Wiskott-Aldrich Syndrome

Wiskott-Aldrich syndrome is an X-linked recessive disorder characterized by decreased IgM antibody production. (See Module 01: Genes and Genetic Diseases.) This markedly inhibits the ability of an affected individual to defend against encapsulated bacteria such as Streptococcus pneumoniae and Haemophilus influenzae, as well as many viruses. Platelet dysfunction also occurs, leading to bleeding problems.

Desensitization Treatment of Type 1

also known as immunotherapy or allergy shots) is the process by which allergic individuals are exposed to minute quantities of allergens at increasing doses over a prolonged period. This process results in the production of IgG blocking antibodies that bind to the allergen and prevent it from being bound to IgE. Desensitization may also result in the activation of T regulatory lymphocytes. (See Module 05: Adaptive Immunity.)

Nutritional Deficiencies

including zinc, B vitamins, and vitamins A and E, can result in significant depression of T- and B-cell function. These deficiencies most commonly result from malabsorption, renal, or GI diseases but can also occur in malnutrition. Maintaining adequate nutritional intake of these nutrients is essential to normal immune function and is especially important in individuals with other underlying immune disorders.

Malignancy

is also associated with decreased immune function. Cancers that directly involve the bone marrow or the lymphatics deplete lymphocytes and phagocytes. Some cancers secrete immune suppressants (e.g., transforming growth factor beta [TGF- β]). Cancer contributes to malnutrition, which can depress immunity. And finally, cancer treatment commonly damages the bone marrow and protective barriers (skin, mucous membranes), thus making infections more likely.

Trauma and Stress

lso depress host defenses by affecting all parts of the immune and inflammatory responses. The complicated relationship between the hypothalamus, endocrine system, autonomic nervous system, and white blood cell function is an area of intense study. A relatively new field of investigation, called psychoneuroimmunology (PNI), explores these relationships and their impact on health and disease. PNI is the study of how the consciousness, brain, and central nervous system interact with the body's defenses against infection and abnormal cell division.

AIDS

nfection with the human immunodeficiency virus (HIV) and the subsequent development of AIDS remains a major source of morbidity and mortality in the United States and throughout the world. Two kinds of HIV virus have been identified to cause human disease: HIV-1, which is responsible for the vast majority of morbidity and mortality, and HIV-2, which is less common and less lethal. There are also many subtypes of HIV called clades. As an example of an acquired immunodeficiency disorder, an in-depth exploration of HIV infection and AIDS will serve to illustrate many important principles of lymphocyte dysfunction and its associated complications.

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