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776 19 • Diseases of the Immune System vessels. As a result of tissue destruction, symptoms of serum sickness include chills, fever, rash, vasculitis, and arthritis. Development of glomerulonephritis or hepatitis is also possible. Autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis can also involve damaging type III hypersensitivity reactions when auto-antibodies form immune complexes with self antigens. These conditions are discussed in Autoimmune Disorders. Figure 19.7 Type III hypersensitivities and the systems they affect. (a) Immune complexes form and deposit in tissue. Complement activation, stimulation of an inflammatory response, and recruitment and activation of neutrophils result in damage to blood vessels, heart tissue, joints, skin, and/or kidneys. (b) If the kidneys are damaged by a type III hypersensitivity reaction, dialysis may be required. (Credit b: Tech. Sgt. Bennie J. Davis III / US Air Force; Public Domain) CHECK YOUR UNDERSTANDING • Why is antibody excess important in type III hypersensitivity? • Describe the differences between the Arthus reaction and serum sickness. MICRO CONNECTIONS Diphtheria Antitoxin Antibacterial sera are much less commonly used now than in the past, having been replaced by toxoid vaccines. However, a diphtheria antitoxin produced in horses is one example of such a treatment that is still used in some parts of the world. Although it is not licensed by the FDA for use in the United States, diphtheria antitoxin can be used to treat cases of diphtheria, which are caused by the bacterium Corynebacterium diphtheriae. 8 The treatment is not without risks, however. Serum sickness can occur when the patient develops an immune response to non-self horse proteins. Immune complexes are formed between the horse proteins and circulating antibodies when the two exist in certain proportions. These immune complexes can deposit in organs, causing damage such as arthritis, nephritis, rash, and fever. Serum sickness is usually transient with no permanent damage unless the patient is chronically exposed to the antigen, which can then result in irreversible damage to body sites such as joints and kidneys. Over time, phagocytic cells such as macrophages are able to clear the horse serum antigens, which results in improvement of the patient’s condition and a decrease in symptoms as the immune response dissipates. 8 Centers for Disease Control and Prevention. “Diphtheria Antitoxin.” http://www.cdc.gov/diphtheria/dat.html. Accessed March 25, 2016. Access for free at openstax.org.
19.1 • Hypersensitivities 777 Clinical Focus Part 3 Kerry does not make it to the rheumatologist. She has a seizure as she is leaving her primary care physician’s office. She is quickly rushed to the emergency department, where her primary care physician relates her medical history and recent test results. The emergency department physician calls in the rheumatologist on staff at the hospital for consultation. Based on the symptoms and test results, the rheumatologist suspects that Kerry has lupus and orders a pair of blood tests: an antinuclear antibody test (ANA) to look for antibodies that bind to DNA and another test that looks for antibodies that bind to a selfantigen called the Smith antigen (Sm). • Based on the blood tests ordered, what type of reaction does the rheumatologist suspect is causing Kerry’s seizure? Jump to the next Clinical Focus box. Go back to the previous Clinical Focus box. Type IV Hypersensitivities Type IV hypersensitivities are not mediated by antibodies like the other three types of hypersensitivities. Rather, type IV hypersensitivities are regulated by T cells and involve the action of effector cells. These types of hypersensitivities can be organized into three subcategories based on T-cell subtype, type of antigen, and the resulting effector mechanism (Table 19.5). In the first type IV subcategory, CD4 T H 1-mediated reactions are described as delayed-type hypersensitivities (DTH). The sensitization step involves the introduction of antigen into the skin and phagocytosis by local antigen presenting cells (APCs). The APCs activate helper T cells, stimulating clonal proliferation and differentiation into memory T H 1 cells. Upon subsequent exposure to the antigen, these sensitized memory T H 1 cells release cytokines that activate macrophages, and activated macrophages are responsible for much of the tissue damage. Examples of this T H 1-mediated hypersensitivity are observed in tuberculin the Mantoux skin test and contact dermatitis, such as occurs in latex allergy reactions. In the second type IV subcategory, CD4 T H 2-mediated reactions result in chronic asthma or chronic allergic rhinitis. In these cases, the soluble antigen is first inhaled, resulting in eosinophil recruitment and activation with the release of cytokines and inflammatory mediators. In the third type IV subcategory, CD8 cytotoxic T lymphocyte (CTL)-mediated reactions are associated with tissue transplant rejection and contact dermatitis (Figure 19.8). For this form of cell-mediated hypersensitivity, APCs process and present the antigen with MHC I to naïve CD8 T cells. When these naïve CD8 T cells are activated, they proliferate and differentiate into CTLs. Activated T H 1 cells can also enhance the activation of the CTLs. The activated CTLs then target and induce granzyme-mediated apoptosis in cells presenting the same antigen with MHC I. These target cells could be “self” cells that have absorbed the foreign antigen (such as with contact dermatitis due to poison ivy), or they could be transplanted tissue cells displaying foreign antigen from the donor.
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Microbiology SENIOR CONTRIBUTING AU
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OPENSTAX OpenStax provides free, pe
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Contents Preface 1 CHAPTER 1 An Inv
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9.2 Oxygen Requirements for Microbi
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18.1 Overview of Specific Adaptive
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Appendix C Metabolic Pathways 1155
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Preface 1 PREFACE Welcome to Microb
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Preface 3 that often confer critica
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Preface 5 further. Our features inc
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Preface 7 and science, and pursues
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CHAPTER 1 An Invisible World Figure
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1.1 • What Our Ancestors Knew 11
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1.2 • A Systematic Approach 17 Th
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1.2 • A Systematic Approach 19 Fi
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1.2 • A Systematic Approach 21 Ta
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1.3 • Types of Microorganisms 23
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1 • Summary 31 SUMMARY 1.1 What O
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1 • Review Questions 33 17. The p
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CHAPTER 2 How We See the Invisible
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2.1 • The Properties of Light 37
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2.1 • The Properties of Light 39
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2.2 • Peering Into the Invisible
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2.3 • Instruments of Microscopy 4
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2.4 • Staining Microscopic Specim
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2 • Review Questions 71 REVIEW QU
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CHAPTER 3 The Cell Figure 3.1 Micro
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3.1 • Spontaneous Generation 75 F
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3.2 • Foundations of Modern Cell
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3.3 • Unique Characteristics of P
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3.4 • Unique Characteristics of E
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3 • Summary 125 SUMMARY 3.1 Spont
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3 • Review Questions 127 3. Which
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3 • Review Questions 129 Critical
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CHAPTER 4 Prokaryotic Diversity Fig
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4.1 • Prokaryote Habitats, Relati
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4.2 • Proteobacteria 139 for or s
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4.2 • Proteobacteria 141 Class Al
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4.2 • Proteobacteria 143 Class Be
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4.2 • Proteobacteria 145 Figure 4
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4.2 • Proteobacteria 147 Class Ga
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4.3 • Nonproteobacteria Gram-Nega
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4.4 • Gram-Positive Bacteria 157
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4.6 • Archaea 167 The class Therm
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4.6 • Archaea 169 thus is a livin
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4 • Summary 171 SUMMARY 4.1 Proka
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4 • Review Questions 173 REVIEW Q
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4 • Review Questions 175 39. Expl
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CHAPTER 5 The Eukaryotes of Microbi
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5.1 • Unicellular Eukaryotic Para
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Figure 5.7 5.1 • Unicellular Euka
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5.2 • Parasitic Helminths 193 hel
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5.2 • Parasitic Helminths 195 Fig
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5.2 • Parasitic Helminths 197 Fig
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5.2 • Parasitic Helminths 199 MIC
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5.3 • Fungi 201 Figure 5.25 Multi
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5.3 • Fungi 203 Figure 5.27 zygos
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5.3 • Fungi 205 diploid stages (F
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5.3 • Fungi 207 Figure 5.32 prese
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5.3 • Fungi 209 MICRO CONNECTIONS
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5.4 • Algae 211 and other photosy
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5.5 • Lichens 213 Figure 5.37 Chl
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5.5 • Lichens 215 marina. (b) Thi
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5 • Review Questions 217 REVIEW Q
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CHAPTER 6 Acellular Pathogens Figur
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6.1 • Viruses 221 assembly of vir
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6.1 • Viruses 223 Viral Structure
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6.1 • Viruses 225 Figure 6.5 (a)
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6.1 • Viruses 227 LINK TO LEARNIN
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6.2 • The Viral Life Cycle 229 on
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6.2 • The Viral Life Cycle 231 Fi
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6.2 • The Viral Life Cycle 237 by
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6.2 • The Viral Life Cycle 239 Ca
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6.3 • Isolation, Culture, and Ide
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6.4 • Viroids, Virusoids, and Pri
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6.4 • Viroids, Virusoids, and Pri
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6 • Summary 253 SUMMARY 6.1 Virus
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6 • Review Questions 255 18. A/an
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CHAPTER 7 Microbial Biochemistry Fi
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7.1 • Organic Molecules 259 Figur
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7.1 • Organic Molecules 261 Figur
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7.2 • Carbohydrates 263 and the m
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7.2 • Carbohydrates 265 Figure 7.
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7.3 • Lipids 267 Figure 7.11 Star
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7.3 • Lipids 269 Figure 7.13 This
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7.3 • Lipids 271 Figure 7.15 Five
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7.4 • Proteins 273 Figure 7.17 Am
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7.4 • Proteins 275 Figure 7.19 Re
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7.4 • Proteins 277 Figure 7.23 Pr
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7.5 • Using Biochemistry to Ident
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7.5 • Using Biochemistry to Ident
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7 • Review Questions 283 as hormo
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7 • Review Questions 285 19. A tr
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CHAPTER 8 Microbial Metabolism Figu
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8.1 • Energy, Matter, and Enzymes
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8.2 • Catabolism of Carbohydrates
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8.3 • Cellular Respiration 301 8.
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8.3 • Cellular Respiration 303 Fi
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8.4 • Fermentation 305 If respira
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8.4 • Fermentation 307 Common Fer
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8.5 • Catabolism of Lipids and Pr
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8.6 • Photosynthesis 311 independ
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8.6 • Photosynthesis 313 Oxygenic
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8.7 • Biogeochemical Cycles 315 L
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8.7 • Biogeochemical Cycles 317 N
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8.7 • Biogeochemical Cycles 319 F
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8.7 • Biogeochemical Cycles 321 F
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8 • Summary 323 oxygen as the fin
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8 • Review Questions 325 4. To wh
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8 • Review Questions 327 Matching
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CHAPTER 9 Microbial Growth Figure 9
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9.1 • How Microbes Grow 331 and a
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9.1 • How Microbes Grow 333 The G
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9.1 • How Microbes Grow 335 Susta
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9.1 • How Microbes Grow 337 chang
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9.1 • How Microbes Grow 339 Figur
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9.1 • How Microbes Grow 341 trans
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9.1 • How Microbes Grow 343 micro
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9.2 • Oxygen Requirements for Mic
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9.3 • The Effects of pH on Microb
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9.4 • Temperature and Microbial G
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9.4 • Temperature and Microbial G
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9.5 • Other Environmental Conditi
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9.6 • Media Used for Bacterial Gr
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9 • Summary 361 SUMMARY 9.1 How M
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9 • Review Questions 363 7. Filam
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9 • Review Questions 365 Matching
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9 • Review Questions 367 Critical
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CHAPTER 10 Biochemistry of the Geno
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10.1 • Using Microbiology to Disc
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10.2 • Structure and Function of
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10 • Summary 401 SUMMARY 10.1 Usi
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10 • Review Questions 403 3. Whic
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10 • Review Questions 405 Short A
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CHAPTER 11 Mechanisms of Microbial
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11.1 • The Functions of Genetic M
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11.2 • DNA Replication 411 Figure
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11.2 • DNA Replication 413 Figure
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11.2 • DNA Replication 415 strand
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11.2 • DNA Replication 417 telome
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11.3 • RNA Transcription 419 Figu
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11.3 • RNA Transcription 421 the
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11.4 • Protein Synthesis (Transla
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11.5 • Mutations 429 Effects of M
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11.5 • Mutations 431 In recent ye
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11.5 • Mutations 433 Figure 11.20
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11.5 • Mutations 435 formation of
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11.6 • How Asexual Prokaryotes Ac
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11.7 • Gene Regulation: Operon Th
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11 • Summary 457 SUMMARY 11.1 The
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11 • Summary 459 undamaged DNA st
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11 • Review Questions 461 11. Whi
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11 • Review Questions 463 46. ___
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71. The following figure is from Mo
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CHAPTER 12 Modern Applications of M
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12.1 • Microbes and the Tools of
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12.2 • Visualizing and Characteri
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12.3 • Whole Genome Methods and P
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12.3 • Whole Genome Methods and P
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12.4 • Gene Therapy 499 Figure 12
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12.4 • Gene Therapy 501 overall w
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12 • Summary 503 SUMMARY 12.1 Mic
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12 • Review Questions 505 11. The
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CHAPTER 13 Control of Microbial Gro
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13.1 • Controlling Microbial Grow
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13.2 • Using Physical Methods to
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13.3 • Using Chemicals to Control
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13.4 • Testing the Effectiveness
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13 • Summary 553 commonly used to
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13 • Review Questions 555 12. Ble
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CHAPTER 14 Antimicrobial Drugs Figu
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14.1 • History of Chemotherapy an
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14.1 • History of Chemotherapy an
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14.2 • Fundamentals of Antimicrob
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14.2 • Fundamentals of Antimicrob
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14.3 • Mechanisms of Antibacteria
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14.4 • Mechanisms of Other Antimi
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14.5 • Drug Resistance 591 Common
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14.5 • Drug Resistance 593 negati
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14.5 • Drug Resistance 595 Clavul
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14.7 • Current Strategies for Ant
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14.7 • Current Strategies for Ant
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14 • Summary 605 cells. • Becau
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14 • Review Questions 609 50. Why
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CHAPTER 15 Microbial Mechanisms of
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15.1 • Characteristics of Infecti
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15.2 • How Pathogens Cause Diseas
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15.4 • Virulence Factors of Eukar
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15 • Review Questions 647 protect
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15 • Review Questions 649 Critica
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CHAPTER 16 Disease and Epidemiology
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16.1 • The Language of Epidemiolo
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16.1 • The Language of Epidemiolo
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16.2 • Tracking Infectious Diseas
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16.3 • Modes of Disease Transmiss
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16.4 • Global Public Health 673 C
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16.4 • Global Public Health 675 S
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16 • Summary 677 SUMMARY 16.1 The
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16 • Review Questions 679 Matchin
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16 • Review Questions 681 20. Wha
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CHAPTER 17 Innate Nonspecific Host
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17.1 • Physical Defenses 687 know
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17.1 • Physical Defenses 689 Figu
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17.2 • Chemical Defenses 691 Phys
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17.2 • Chemical Defenses 697 Figu
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17.2 • Chemical Defenses 699 Clin
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17.3 • Cellular Defenses 701 Hema
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17.3 • Cellular Defenses 705 Clin
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17.3 • Cellular Defenses 707 Figu
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17.4 • Pathogen Recognition and P
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17.5 • Inflammation and Fever 713
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17 • Summary 719 SUMMARY 17.1 Phy
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17 • Review Questions 721 8. Hist
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17 • Review Questions 723 Short A
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20.3 • Agglutination Assays 829 s
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20.4 • EIAs and ELISAs 831 Mechan
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20.4 • EIAs and ELISAs 837 • Wh
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20 • Review Questions 849 20.4 EI
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20 • Review Questions 851 15. Sup
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CHAPTER 21 Skin and Eye Infections
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21.5 • Protozoan and Helminthic I
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21 • Summary 891 SUMMARY 21.1 Ana
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CHAPTER 22 Respiratory System Infec
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Figure 22.29 22.4 • Respiratory M
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22 • Review Questions 939 200 vir
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CHAPTER 23 Urogenital System Infect
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23 • Summary 975 SUMMARY 23.1 Ana
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CHAPTER 24 Digestive System Infecti
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24.2 • Microbial Diseases of the
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24.4 • Viral Infections of the Ga
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24.6 • Helminthic Infections of t
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24 • Summary 1033 SUMMARY 24.1 An
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CHAPTER 25 Circulatory and Lymphati
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25.1 • Anatomy of the Circulatory
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25.1 • Anatomy of the Circulatory
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25.3 • Viral Infections of the Ci
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Figure 25.26 25.3 • Viral Infecti
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25.4 • Parasitic Infections of th
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25 • Review Questions 1089 • To
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25 • Review Questions 1091 Critic
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CHAPTER 26 Nervous System Infection
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26.1 • Anatomy of the Nervous Sys
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26.1 • Anatomy of the Nervous Sys
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26.2 • Bacterial Diseases of the
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26.3 • Acellular Diseases of the
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Figure 26.19 26.3 • Acellular Dis
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26.4 • Fungal and Parasitic Disea
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26 • Review Questions 1133 are fa
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26 • Review Questions 1135 Matchi
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26 • Review Questions 1137 59. Th
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A • Fundamentals of Physics and C
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B • Mathematical Basics 1149 APPE
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B • Mathematical Basics 1151 Mult
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B • Mathematical Basics 1153 The
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C • Metabolic Pathways 1155 APPEN
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C • Metabolic Pathways 1157 Entne
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C • Metabolic Pathways 1159 Figur
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C • Metabolic Pathways 1161 Elect
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APPENDIX D Taxonomy of Clinically R
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D • Taxonomy of Clinically Releva
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E • Glossary 1177 APPENDIX E Glos
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E • Glossary 1179 destruction by
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E • Glossary 1181 pollutants from
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E • Glossary 1183 chromosome disc
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E • Glossary 1185 cysts are forme
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E • Glossary 1187 occurring ectop
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E • Glossary 1189 molecules of DN
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E • Glossary 1191 glycoprotein co
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E • Glossary 1195 discontinuously
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E • Glossary 1197 infection cause
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E • Glossary 1199 target cells by
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E • Glossary 1201 intact ribosome
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E • Glossary 1203 point source sp
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E • Glossary 1205 complexes forme
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E • Glossary 1207 antibody is fir
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E • Glossary 1209 the number of c
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E • Glossary 1211 the reciprocal
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E • Glossary 1213 vector animal (
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1215 ANSWER KEY Chapter 1 1. D 2. D
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1217 B 18. A, C, B 19. peristalsis
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Index 1219 INDEX Symbols +ssRNA 237
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Index 1221 antigen-presenting cells
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Index 1223 Bordetella 142 Bordetell
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Index 1225 chromosomes 372, 394 chr
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Index 1227 de Duve 113 dead zone 35
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Index 1229 Enteroinvasive E. coli (
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Index 1231 Gardnerella vaginalis 47
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Index 1233 shunt 298 Hfr cell 443 H
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Index 1235 iron lungs 1118 iron-sul
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Index 1237 maturation 230 mature na
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Index 1239 Health 501 National Noti
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Index 1241 patterns (PAMPs) 710 pat
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Index 1243 primary lymphoid tissue
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Index 1245 596, 1048, 1051, 1051 ri
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Index 1247 sterilant 511, 541 steri
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Index 1249 toxigenicity 633 toxin 6
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Index 1251 water activity 522 water
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Microbiology, 2021

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