Type II Hypersensitivity and Type IV Hypersensitivity

Type II Hypersensitivity and Type IV Hypersensitivity ORDER NOW FOR CUSTOMIZED AND ORIGINAL ESSAY PAPERS ON Type II Hypersensitivity and Type IV Hypersensitivity As a learner in Pathophysiology, it’s important to take the information you are absorbing from your coursework and connect it to real life. Throughout the semester you will be invited to make connections by locating, reviewing, and summarizing current and relevant journal articles. Type II Hypersensitivity and Type IV Hypersensitivity Use the following link to learn how to find and evaluate an online source: https://www.nia.nih.gov/health/online-health-information-it-reliable#where (Links to an external site.) Please follow the instructions below: Locate a current (medical or scientific) news or journal article based on one of the topics listed below: Type II Hypersensitivity (ch 8) Type IV Hypersensitivity (ch 8) Note: As you read through the article, think about how it connects to Pathophysiology and why is it relevant. Provide a write-up summarizing the article. Within your document, include how the information connects to Pathophysiology, and why it is relevant. Aim to include 150 – 200 words in the summary. Remember to cite your source(s) in APA Format! attachment_1 Understanding Pathophysiology FIRST CANADIAN EDITION Mohamed Toufic El-Hussein, RN, PhD Associate Professor, School of Nursing Faculty of Health, Community & Education Mount Royal University Calgary, Alberta Kelly Power-Kean, MHS, NP, RN Center for Nursing Studies Memorial University St. John’s, Newfoundland Stephanie Zettel, BN, MN Associate Professor 2 School of Nursing and Midwifery Mount Royal University Calgary, Alberta U.S. AUTHORS Sue E. Huether, MS, PhD Professor Emeritus College of Nursing University of Utah Salt Lake City, Utah Kathryn L. McCance, MS, PhD Professor Emeritus College of Nursing University of Utah Salt Lake City, Utah U.S. Section Editors Valentina L. Brashers, MD Professor of Nursing and Woodard Clinical Scholar Attending Physician in Internal Medicine University of Virginia Health System Charlottesville, Virginia Neal S. Rote, PhD Academic Vice-Chair and Director of Research Department of Obstetrics and Gynecology University Hospitals Case Medical Center William H. Weir, MD, Professor of Reproductive Biology and Pathology Case Western Reserve University School of Medicine 3 8 Infection and Defects in Mechanisms of Defence Neal S. Rote, Stephanie Zettel CHAPTER OUTLINE Infection, 177 Microorganisms and Humans: A Dynamic Relationship, 177 Countermeasures Against Infectious Microorganisms, 188 Deficiencies in Immunity, 190 Initial Clinical Presentation, 190 Primary (Congenital) Immune Deficiencies, 191 Secondary (Acquired) Immune Deficiencies, 193 Evaluation and Care of Those With Immune Deficiency, 193 Replacement Therapies for Immune Deficiencies, 193 AIDS, 195 Hypersensitivity: Allergy, Autoimmunity, and 546 Alloimmunity, 199 Mechanisms of Hypersensitivity, 202 Antigenic Targets of Hypersensitivity Reactions, 208 The defensive system protecting the body from infection is a finely tuned network, but it is not perfect. Sometimes infectious agents can inhibit or escape defence mechanisms or the system may break down, leading to inadequate protection or inappropriate activation. An inadequate response (commonly called an immune deficiency) may range from relatively mild defects to life-threatening severity. Inappropriate responses (hypersensitivity reactions) may be (1) exaggerated against noninfectious environmental substances (allergy); (2) misdirected against the body’s own cells (autoimmunity); or (3) directed against beneficial foreign tissues, such as transfusions or transplants (alloimmunity). Several of these inappropriate responses can be serious or life-threatening. This chapter provides an overview of conditions under which our protective systems have failed. Infection Modern health care has shown great progress in preventing and treating infectious diseases. In Canada, heart disease and malignancies greatly surpass infectious disease as major causes of death.1 However, since the severe acute respiratory syndrome (SARS) epidemic that took place in 2003, the challenge in treating 547 infectious diseases has become a key issue. Type II Hypersensitivity and Type IV Hypersensitivity Hospitals have implemented measures geared toward controlling health care– associated infections.2 Most deaths related to infections occur in individuals whose protective systems are compromised (children, older adults, and those with chronic disease). Infectious disease remains a significant threat to life in many parts of the world, including India, Africa, and Southeast Asia.3 Sanitary living conditions, clean water, uncontaminated food, vaccinations, and antimicrobial medications have improved the health of many; but inefficient health care systems, endemic poverty, political unrest, and other factors have slowed progress in some regions. As a result of initiatives to prevent and treat infectious diseases, smallpox has been eradicated from the globe (the last reported case was in 1975 in Somalia). Worldwide, polio has declined by more than 99% and been eradicated from the Western hemisphere. Measles was decreased by 78% and was nearly eliminated in the Western hemisphere. Although vaccines and antimicrobials have diminished the frequency of some infectious diseases, new diseases have emerged, such as West Nile virus, SARS, Middle East respiratory syndrome coronavirus (MERS-CoV), and Hantavirus. Some diseases have spread uncontrollably, such as Ebola virus disease, into new regions of Africa. As well, many multiple medication–resistant microorganisms continue to develop. All of these examples reflect the ongoing intense challenges in the struggle to prevent and control infectious diseases. In Canada, First Nations people and the Inuit have higher rates of contagious disease, resulting in shorter life expectancies. Human immunodeficiency virus (HIV)/acquired immunodeficiency syndrome (AIDS), influenza, West Nile virus, and tuberculosis (TB) are just a few of the common conditions found in the Indigenous population4 (see Health Promotion: Tuberculosis and the Indigenous Population in Canada). Health Promotion Tuberculosis and the Indigenous Population in Canada 548 Indigenous people have one of the highest rates of tuberculosis (TB) in Canada. In 2012, Indigenous people in Canada accounted for 4% of the population, but 23% of the active cases of TB. TB incidence in the Inuit population was 400 times higher than TB incidence in the Canadian-born non-Indigenous population, and the incidence rate for First Nations people was 32 times higher. The rate of TB incidence in the Indigenous population can be explained partly by the living conditions on reserves. For example, many homes on reserves are overcrowded and poorly ventilated. A lack of proper nutrition can further increase the risk for those with latent TB infection to progress to an active disease state. Many individuals in First Nations communities also have pre-existing comorbidities such as diabetes and HIV that further contribute to this risk. Moreover, many of these communities are remote and isolated, which results in decreased access to health care services. In 2014, the federal government developed a framework for action to lower the incidence of TB in Canada. The key areas of focus for this framework are as follows: 1. Optimizing and enhancing current efforts to prevent and control active TB disease 2. Facilitating the identification and treatment of latent TB infection for those at high risk for developing active TB disease 3. Championing collaborative action to address the underlying risk factors for TB The report Tuberculosis Prevention and Control in Canada: A Federal Framework for Action presents the federal government’s framework for action and associated initiatives in relation to addressing TB in Canada. © All rights reserved. Type II Hypersensitivity and Type IV Hypersensitivity Tuberculosis Prevention and Control in Canada: A Federal Framework for Action. Public Health Agency of Canada, 2014. Adapted and reproduced with permission from the Minister of Health, 2017. Retrieved from http://www.phac-aspc.gc.ca/tbpclatb/pubs/tpc-pct/assets/pdf/tpc-pcta-eng.pdf. Microorganisms and Humans: A Dynamic Relationship 549 The increase in antibiotic resistance, in particular, places more importance on maintenance of an intact inflammatory and immune system. Individuals with immune deficiencies become easily infected with opportunistic microorganisms—those that normally would not cause disease but seize the opportunity provided by the person’s decreased immune or inflammatory responses. Unlike opportunistic infections, true pathogens have devised means to circumvent the normal controls provided by the innate and adaptive immune systems. Several factors influence the capacity of a pathogen to cause disease: • Communicability: The ability to spread from one individual to others (e.g., measles and pertussis spread very easily; HIV is of lower communicability) • Infectivity: The ability of the pathogen to invade and multiply in the host (e.g., herpes simplex virus can survive for long periods in a latent stage) • Virulence: The capacity of a pathogen to cause severe disease (e.g., measles virus is of low virulence; rabies and Ebola viruses are highly virulent) • Pathogenicity: The ability of an agent to produce disease—success depends on communicability, infectivity, extent of tissue damage, and virulence (e.g., HIV can kill T lymphocytes [T cells]) • Portal of entry: The route by which a pathogenic microorganism infects the host (e.g., direct contact, inhalation, ingestion, or bites of an animal or insect) • Toxigenicity: The ability to produce soluble toxins or endotoxins, factors that greatly influence 550 the pathogen’s degree of virulence Infectivity is facilitated by the ability of pathogens to attach to cell surfaces, release enzymes that dissolve protective barriers, multiply rapidly, escape the action of phagocytes, or resist the effect of low pH. After penetrating protective barriers (invasion), pathogens then multiply and spread through the lymph and blood to tissues and organs, where they continue multiplying and cause disease. In humans the route of entrance of many pathogenic microorganisms also becomes the site of shedding of new infectious agents to other individuals, completing a cycle of infection. Infectious disease can be caused by microorganisms that range in size from 20 nm (poliovirus) to 10 m (tapeworm). Classes of pathogenic microorganisms and their characteristics are summarized in Table 8-1. Some mechanisms of tissue damage caused by microorganisms are summarized in Table 8-2. The multiple layers of defence against infection are described in Chapters 6 and 7. Table 8-3 contains examples of microorganisms that defeat our protective systems. TABLE 8-1 Classes of Microorganisms Infectious to Humans Class Size Site of Reproduction Example Virus Chlamydiae Rickettsiae Mycoplasma Bacteria 20–300 nm 200–1 000 nm 300–1 200 nm 125–350 nm 0.8–15 mcg Fungi 2–200 mcg Protozoa 1–50 mm Helminths 3 mm to 10 m Intracellular Intracellular Intracellular Extracellular Skin Mucous membranes Extracellular Intracellular Skin Mucous membranes Extracellular Intracellular Mucosal Extracellular Intracellular Extracellular Poliomyelitis Urethritis Rocky Mountain spotted fever Atypical pneumonia Staphylococcal wound infection Cholera Streptococcal pneumonia Tuberculosis Tinea pedis (athlete’s foot) Type II Hypersensitivity and Type IV Hypersensitivity Candidiasis (e.g., thrush) Sporotrichosis Histoplasmosis Giardiasis Sleeping sickness Trichinosis Filariasis TABLE 8-2 Examples of Microorganisms That Cause Tissue Damage 551 Pathogens That Directly Cause Tissue Damage Produce Exotoxin Streptococcus pyogenes Tonsillitis, scarlet fever Staphylococcus aureus Boils, toxic shock syndrome, food poisoning Corynebacterium diphtheria Diphtheria Clostridium tetani Tetanus Vibrio cholerae Cholera Produce Endotoxin Escherichia coli Gram-negative sepsis Haemophilus influenzae Meningitis, pneumonia Salmonella typhi Typhoid Shigella Bacillary dysentery Pseudomonas aeruginosa Wound infection Yersinia pestis Plague Cause Direct Damage With Invasion Variola Smallpox Varicella-zoster Chickenpox, shingles Hepatitis B virus Hepatitis Poliovirus Poliomyelitis Measles virus Measles, subacute sclerosing panencephalitis Influenza virus Influenza Herpes simplex virus Cold sores Pathogens That Indirectly Cause Tissue Damage Produce Immune Complexes Hepatitis B virus Kidney disease S. pyogenes Glomerulonephritis Treponema pallidum Kidney damage in secondary syphilis Most acute infections Transient renal deposits Cause Cell-Mediated Immunity Mycobacterium tuberculosis Tuberculosis Mycobacterium leprae Tuberculoid leprosy Lymphocytic choriomeningitis virus Aseptic meningitis Borrelia burgdorferi Lyme arthritis Herpes simplex virus Herpes stromal keratitis Data modified from Janeway, C.A., Travers, P., Walport, M., et al. (2001). Immunobiology: The system in health and disease (5th ed.). New York: Garland. TABLE 8-3 Examples of Mechanisms Used by Pathogens to Resist the Immune System Mechanisms Example of Specific Microorganisms Effect on Immunity Destroy or Block Component of Immune System Produce toxins Kills phagocyte or interferes with chemotaxis Prevents phagocytosis by inhibiting fusion between phagosome and lysosomal granules Produce Prevents killing by oxygen-dependent 552 Staphylococcus Streptococcus Mycobacterium tuberculosis Mycobacterium antioxidants (e.g., catalase, superoxide dismutase) Produce protease to digest IgA mechanisms Promotes bacterial attachment Produce surface Prevents activation of complement system molecules that Prevents antibody functioning as opsonin mimic crystallizable fragment (Fc) receptors and bind antibodies Mimic Self-Antigens Produce surface Resembles individual’s own tissue; in some antigens (e.g., M individuals, antibodies can be formed against selfprotein, red antigen, leading to hypersensitivity disease (e.g., blood cell antibody to M protein also reacts with cardiac tissue, antigens) that are causing rheumatic heart disease; antibody to red similar to selfblood cell antigens can cause anemia) antigens Change Antigenic Profile Undergo Delays immune response because of failure to mutation of recognize new antigen antigens or activate genes that change surface molecules sp. Salmonella typhi Neisseria gonorrhoeae (urinary tract infection), Haemophilus influenzae, and Streptococcus pneumoniae (pneumonia) Staphylococcus Herpes simplex virus Group A Streptococcus (M protein) Mycoplasma pneumoniae (red cell antigens) Influenza HIV Some parasites Bacterial Disease Bacteria are prokaryotes (lacking a discrete nucleus) and are relatively small. They can be aerobic or anaerobic and motile or immotile. Spherical bacteria are called cocci, rodlike forms are called bacilli, and spiral forms are termed spirochetes. Gram stain differentiates the microorganisms as Gram-positive or Gramnegative bacteria. Examples of human diseases caused by specific bacteria are listed in Table 8-4.Type II Hypersensitivity and Type IV Hypersensitivity The general structure of bacteria is reviewed in Figure 8-1. TABLE 8-4 Examples of Common Bacterial Infections Microorganism Gram Stain 553 Respiratory Pathway Intracellular or Extracellular Respiratory Tract Infections Upper Respiratory Tract Infections Corynebacterium diphtheriae (diphtheria) Gram + Haemophilus influenzae Gram ? Streptococcus pyogenes (group A) Gram + Otitis Media Haemophilus influenzae Gram ? Streptococcus pneumoniae Gram + Lower Respiratory Tract Infections Bacillus anthracis (pulmonary anthrax) Gram + Bordetella pertussis (whooping cough) Chlamydia pneumonia Escherichia coli Gram ? Not stainable Gram ? Haemophilus influenzae Gram ? Legionella pneumophila Gram ? Facultative anaerobic Facultative anaerobic Extracellular Facultative anaerobic Aerobic Aerobic Extracellular Facultative anaerobic Facultative anaerobic Aerobic Extracellular Extracellular Extracellular Extracellular Obligate intracellular Extracellular Extracellular Aerobic Aerobic Extracellular Aerobic Aerobic Facultative anaerobic Facultative anaerobic Facultative anaerobic Extracellular Extracellular Extracellular Facultative anaerobic Anaerobic Facultative anaerobic Facultative anaerobic Extracellular Gram ? Aerobic Intracellular Gram ? Gram + Microaerophilic Extracellular Aerobic Intracellular Gram ? Gram ? Anaerobic Facultative anaerobic Extracellular Extracellular Gram + Facultative Extracellular Gram + (weakly) Mycoplasma pneumoniae Not stainable Neisseria meningitidis (develops into meningitis) Gram ? Pseudomonas aeruginosa Gram ? Streptococcus agalactiae (group B; develops into Gram + meningitis) Streptococcus pneumoniae Gram + Yersinia pestis (plague) Gram ? Gastro-intestinal Infections Inflammatory Gastro-intestinal Infections Bacillus anthracis (gastro-intestinal anthrax) Gram + Clostridium difficile Escherichia coli O157:H7 Gram + Gram ? Vibrio cholerae Gram ? Food Poisoning Bacillus cereus Extracellular Facultative intracellular Extracellular Mycobacterium tuberculosis Invasive Gastro-intestinal Infections Brucella abortus (brucellosis, undulant fever, leading to sepsis, heart infection) Helicobacter pylori (gastritis and peptic ulcers) Listeria monocytogenes (leading to sepsis and meningitis) Salmonella typhi (typhoid fever) Shigella sonnei Facultative anaerobic Facultative anaerobic Facultative anaerobic 554 Extracellular Extracellular Extracellular Extracellular Extracellular anaerobic Anaerobic Anaerobic Facultative anaerobic Extracellular Extracellular Extracellular Not stainable Gram ? Aerobic Intracellular Aerobic Treponema pallidum (spirochete; syphilis) Skin and Wound Infections Bacillus anthracis (cutaneous anthrax) Gram ? Aerobic Facultative intracellular Extracellular Gram + Extracellular Borrelia burgdorferi (Lyme disease; spirochete) Clostridium tetani (tetanus) Clostridium perfringens (gas gangrene) Mycobacterium leprae (leprosy) Pseudomonas aeruginosa Rickettsia prowazekii (rickettsia; typhus) Gram ? Gram + Gram + Gram + (weakly) Gram ? Gram ? Facultative anaerobic Aerobic Anaerobic Anaerobic Aerobic Aerobic Aerobic Staphylococcus aureus Gram + Extracellular Obligate intracellular Extracellular Streptococcus pyogenes (group A) Gram + Clostridium botulinum Clostridium perfringens Staphylococcus aureus Gram + Gram + Gram + Sexually Transmitted Infections Chlamydia trachomatis (pelvic inflammatory disease) Neisseria gonorrhoeae (urethritis) Eye Infections Chlamydia trachomatis (conjunctivitis) Facultative anaerobic Facultative anaerobic Extracellular Extracellular Extracellular Extracellular Extracellular Aerobic Haemophilus aegyptius (pink eye) Type II Hypersensitivity and Type IV Hypersensitivity Not stainable Gram ? Zoonotic Infections Bacillus anthracis (anthrax) Gram + Extracellular Extracellular Intracellular Obligate intracellular Obligate intracellular Extracellular Facultative anaerobic Brucella abortus (brucellosis, also called undulant fever) Borrelia burgdorferi (spirochete; Lyme disease) Listeria monocytogenes Rickettsia rickettsii (rickettsia; Rocky Mountain spotted fever) Rickettsia prowazekii (rickettsia; typhus) Gram ? Facultative anaerobic Aerobic Gram ? Gram + Gram ? Aerobic Aerobic Aerobic Gram ? Aerobic Yersinia pestis (plague) Gram ? Facultative anaerobic Health Care–Associated Infections Enterococcus faecalis Gram + Enterococcus faecium Gram + Escherichia coli (cystitis) Gram ? Pseudomonas aeruginosa Gram ? Staphylococcus aureus Gram + Staphylococcus epidermidis Gram + Facultative anaerobic Facultative anaerobic Facultative anaerobic Obligate anaerobic Facultative anaerobic Facultative anaerobic 555 Obligate intracellular Extracellular Intracellular Extracellular Extracellular Extracellular Extracellular Extracellular Extracellular FIGURE 8-1 General Structure of Bacteria. A, The structure of the bacterial cell wall determines its staining characteristics with Gram stain. A Gram-positive bacterium has a thick layer of peptidoglycan (left). A Gram-negative bacterium has a thick peptidoglycan layer and an outer membrane (right). B, Example of a Gram-positive (darkly stained microorganisms, arrow) group A Streptococcus. This microorganism consists of cocci that frequently form chains. C, Example of a Gram-negative (pink microorganisms, arrow) Neisseria meningitides in cerebrospinal fluid. Neisseria form complexes of two cocci (diplococci). (A, from Murray, P.R., Rosenthal, K.S., & Pfaller, M.A. [2013]. Medical microbiology [7th ed.]. Philadelphia: Saunders; B, C, from Murray, P.R., Rosenthal, K.S., Kobayashi, G.S., et al. [2002]. Medical microbiology [4th ed.]. St. Louis: Mosby.) Bacterial survival and growth depend on the effectiveness of the body’s defence mechanisms and on the bacterium’s ability to resist these defences. A vast amount of information has been published 556 about bacterial pathogenesis. The main aspects of how bacteria cause disease may be illustrated in how o … Get a 10 % discount on an order above $ 100 Use the following coupon code : NURSING10