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The amount of medication given during a certain time interval is the **dosage**, and it must be determined carefully to ensure that optimum therapeutic drug levels are achieved at the site of infection without causing significant toxicity (side effects) to the patient. Each drug class is associated with a variety of po... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**Dosage and Route of Administration**",
"token_count": 2038,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objective**
• Describe the mechanisms of action associated with drugs that inhibit cell wall biosynthesis, protein synthesis, membrane function, nucleic acid synthesis, and metabolic pathways
An important quality for an antimicrobial drug is **selective toxicity**, meaning that it selectively kills ... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.3 Mechanisms of Antibacterial Drugs**",
"token_count": 664,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Several different classes of antibacterials block steps in the biosynthesis of peptidoglycan, making cells more susceptible to osmotic lysis (**[Table 14.2](#page-625-0)**). Therefore, antibacterials that target cell wall biosynthesis are bactericidal in their action. Because human cells do not make peptidoglycan, this... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.3 Mechanisms of Antibacterial Drugs**",
"Header 3": "**Inhibitors of Cell Wall Biosynthesis**",
"token_count": 1828,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Drugs that Inhibit Bacterial Cell Wall Synthesis**
| Mechanism of Action | Drug Class | Specific<br>Drugs | Natural or<br>Semisynthetic | Spectrum of Activity |
|----------------------------... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.3 Mechanisms of Antibacterial Drugs**",
"Header 3": "**Inhibitors of Cell Wall Biosynthesis**",
"token_count": 2037,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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This mechanism highlights the similarity between 70S ribosomes of bacteria and the 70S ribosomes within our mitochondria. The second mechanism of anemia is idiosyncratic (i.e., the mechanism is not understood), and involves an irreversible lethal loss of blood cell production known as aplastic anemia. This mechanism of... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.3 Mechanisms of Antibacterial Drugs**",
"Header 3": "**Inhibitors of Cell Wall Biosynthesis**",
"token_count": 2038,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
However, despite their selective toxicity against DNA gyrase, side effects associated with different fluoroquinolones include phototoxicity, neurotoxicity, cardiotoxicity, glucose metabolism dysfunction, and increased risk for tendon rupture.
| Mechanisms of<br>Action ... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.3 Mechanisms of Antibacterial Drugs**",
"Header 3": "**Inhibitors of Cell Wall Biosynthesis**",
"token_count": 324,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Some synthetic drugs control bacterial infections by functioning as **antimetabolites**, competitive inhibitors for bacterial metabolic enzymes (**[Table 14.6](#page-633-0)**). The **sulfonamides** (**sulfa drugs**) are the oldest synthetic antibacterial agents and are structural analogues of *para*-aminobenzoic acid (... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.3 Mechanisms of Antibacterial Drugs**",
"Header 3": "**Inhibitors of Metabolic Pathways**",
"token_count": 1158,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |

To learn more about the general principles of antimicrobial therapy and bacterial modes of action, visit **[Michigan State University's Antimicrobial Resistance](https://openstax.org/l/22MSUantireslea) [Learning Site \(https://openstax.org/l/22MSUantireslea\)](https://openstax.org/l/22M... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.3 Mechanisms of Antibacterial Drugs**",
"Header 3": "**Link to Learning**",
"token_count": 370,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objective**
• Explain the differences between modes of action of drugs that target fungi, protozoa, helminths, and viruses
Because fungi, protozoa, and helminths are eukaryotic, their cells are very similar to human cells, making it more difficult to develop drugs with selective toxicity. Additional... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.4 Mechanisms of Other Antimicrobial Drugs**",
"token_count": 219,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
The most common mode of action for antifungal drugs is the disruption of the cell membrane. Antifungals take advantage of small differences between fungi and humans in the biochemical pathways that synthesize sterols. The sterols are important in maintaining proper membrane fluidity and, hence, proper function of the c... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.4 Mechanisms of Other Antimicrobial Drugs**",
"Header 3": "**Antifungal Drugs**",
"token_count": 2044,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Jack's physician admitted him to the hospital and prescribed Bactrim, a combination of sulfamethoxazole and trimethoprim, to be administered intravenously.
*P. jirovecii* is a yeast-like fungus with a life cycle similar to that of protozoans. As such, it was classified as a protozoan until the 1980s. It lives only in... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.4 Mechanisms of Other Antimicrobial Drugs**",
"Header 3": "**Antifungal Drugs**",
"token_count": 445,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
There are a few mechanisms by which antiprotozoan drugs target infectious protozoans (**[Table 14.9](#page-641-0)**). Some are antimetabolites, such as atovaquone, proguanil, and artemisinins. Atovaquone, in addition to being antifungal, blocks electron transport in protozoans and is used for the treatment of protozoan... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.4 Mechanisms of Other Antimicrobial Drugs**",
"Header 3": "**Antiprotozoan Drugs**",
"token_count": 1390,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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Because helminths are multicellular eukaryotes like humans, developing drugs with selective toxicity against them is extremely challenging. Despite this, several effective classes have been developed (**[Table 14.9](#page-641-0)**). Synthetic **benzimidazoles**, like **mebendazole** and **albendazole**, bind to helmint... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**Antihelminthic Drugs**",
"token_count": 1355,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Unlike the complex structure of fungi, protozoa, and helminths, viral structure is simple, consisting of nucleic acid, a protein coat, viral enzymes, and, sometimes, a lipid envelope. Furthermore, viruses are obligate intracellular pathogens that use the host's cellular machinery to replicate. These characteristics mak... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**Antihelminthic Drugs**",
"Header 3": "**Antiviral Drugs**",
"token_count": 1723,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
(credit: modification of work by Thomas Splettstoesser)
#### **Common Antiviral Drugs**
| Mechanism of Action | Drug | Clinical Uses |
|---------------------------------------------|----------------------------... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**Antihelminthic Drugs**",
"Header 3": "**Antiviral Drugs**",
"token_count": 544,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Explain the concept of drug resistance
- Describe how microorganisms develop or acquire drug resistance
- Describe the different mechanisms of antimicrobial drug resistance
Antimicrobial resistance is not a new phenomenon. In nature, microbes are constantly evolving in order to overco... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.5 Drug Resistance**",
"token_count": 271,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
There are several common mechanisms for drug resistance, which are summarized in **[Figure 14.18](#page-647-0)**. These mechanisms include enzymatic modification of the drug, modification of the antimicrobial target, and prevention of drug penetration or accumulation.

**Figure 14.18** T... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.5 Drug Resistance**",
"Header 3": "**Mechanisms for Drug Resistance**",
"token_count": 1590,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Methicillin, a semisynthetic penicillin, was designed to resist inactivation by β-lactamases. Unfortunately, soon after the introduction of methicillin to clinical practice, methicillin-resistant strains of *S. aureus* appeared and started to spread. The mechanism of resistance, acquisition of a new low-affinity PBP, p... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.5 Drug Resistance**",
"Header 3": "**Methicillin-Resistant** *Staphylococcus aureus* **(MRSA)**",
"token_count": 881,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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Vancomycin is only effective against gram-positive organisms, and it is used to treat wound infections, septic infections, endocarditis, and meningitis that are caused by pathogens resistant to other antibiotics. It is considered one of the last lines of defense against such resistant infections, including MRSA. With t... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.5 Drug Resistance**",
"Header 3": "**Vancomycin-Resistant Enterococci and** *Staphylococcus aureus*",
"token_count": 438,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Gram-negative pathogens that produce **extended-spectrum β-lactamases (ESBLs)** show resistance well beyond just penicillins. The spectrum of β-lactams inactivated by ESBLs provides for resistance to all penicillins, cephalosporins, monobactams, and the β-lactamase-inhibitor combinations, but not the carbapenems. An ev... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**Extended-Spectrum β-Lactamase–Producing Gram-Negative Pathogens**",
"token_count": 790,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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To learn more about the **[top 18 drug-resistant threats \(https://openstax.org/l/](https://openstax.org/l/22CDC18drugres) [22CDC18drugres\)](https://openstax.org/l/22CDC18drugres)** to the US, visit the CDC's website.
#### **Micro Connections**
#### **Factory Farming and Drug Resis... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**Extended-Spectrum β-Lactamase–Producing Gram-Negative Pathogens**",
"Header 3": "**Link to Learning**",
"token_count": 851,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Describe how the Kirby-Bauer disk diffusion test determines the susceptibility of a microbe to an antibacterial drug.
- Explain the significance of the minimal inhibitory concentration and the minimal bactericidal concentration relative to the effectiveness of an antimicrobial drug.
T... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.6 Testing the Effectiveness of Antimicrobials**",
"token_count": 1008,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
As discussed, the limitations of the Kirby-Bauer disk diffusion test do not allow for a direct comparison of antibacterial potencies to guide selection of the best therapeutic choice. However, antibacterial dilution tests can be used to determine a particular drug's **minimal inhibitory concentration (MIC)**, the lowes... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.6 Testing the Effectiveness of Antimicrobials**",
"Header 3": "**Dilution Tests**",
"token_count": 1511,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
• Describe the methods and strategies used for discovery of new antimicrobial agents.
With the continued evolution and spread of antimicrobial resistance, and now the identification of pan-resistant bacterial pathogens, the search for new antimicrobials is essential for preventing the p... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.7 Current Strategies for Antimicrobial Discovery**",
"token_count": 2039,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
<sup>28.</sup> The White House. *National Action Plan for Combating Antibiotic-Resistant Bacteria.* Washington, DC: The White House, 2015.
<sup>29.</sup> White House Office of the Press Secretary. "Fact Sheet: Obama Administration Releases National Action Plan to Combat Antibiotic-Resistant Bacteria." March 27, 201... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.7 Current Strategies for Antimicrobial Discovery**",
"token_count": 1115,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Multiple Choice**
- **1.** A scientist discovers that a soil bacterium he has been studying produces an antimicrobial that kills gramnegative bacteria. She isolates and purifies the antimicrobial compound, then chemically converts a chemical side chain to a hydroxyl group. When she tests the antimicrobial prop... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.7 Current Strategies for Antimicrobial Discovery**",
"Header 3": "**Review Questions**",
"token_count": 1861,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
How does the insolubility of niclosamide aid its effectiveness as a treatment for tapeworm infection?
- **41.** Why does the length of time of antimicrobial treatment for tuberculosis contribute to the rise of resistant strains?
- **42.** What is the difference between multidrug resistance and cross-resistance?
- **43.... | {
"Header 1": "**Antimicrobial Drugs**",
"Header 2": "**14.7 Current Strategies for Antimicrobial Discovery**",
"Header 3": "**Review Questions**",
"token_count": 369,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Jane woke up one spring morning feeling not quite herself. Her throat felt a bit dry and she was sniffling. She wondered why she felt so lousy. Was it because of a change in the weather? The pollen count? Was she coming down with something? Did she catch a bug from her coworker who sneezed on her in the elevator yester... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**Introduction**",
"token_count": 252,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
An **infection** is the successful colonization of a host by a microorganism. Infections can lead to disease, which causes signs and symptoms resulting in a deviation from the normal structure or functioning of the host. Microorganisms that can cause disease are known as pathogens.
The **signs** of disease are object... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.1 Characteristics of Infectious Disease**",
"Header 3": "**Signs and Symptoms of Disease**",
"token_count": 776,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Nomenclature of Symptoms**
**Table 15.1**
Clinicians must rely on signs and on asking questions about symptoms, medical history, and the patient's recent activities to identify a particular disease and the potential causative agent. Diagnosis is complicated by the fact that different microorganisms can cause... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**Affix Meaning Example** cyto- cell cytopenia: reduction in the number of blood cells hepat- of the liver hepatitis: inflammation of the liver -pathy disease neuropathy: a disease affecting nerves -emia of the blood bacteremia: presence of bac... |
The World Health Organization's (WHO) International Classification of Diseases (ICD) is used in clinical fields to classify diseases and monitor morbidity (the number of cases of a disease) and mortality (the number of deaths due to a disease). In this section, we will introduce terminology used by the ICD (and in heal... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**Affix Meaning Example** cyto- cell cytopenia: reduction in the number of blood cells hepat- of the liver hepatitis: inflammation of the liver -pathy disease neuropathy: a disease affecting nerves -emia of the blood bacteremia: presence of bac... |
The five periods of disease (sometimes referred to as stages or phases) include the incubation, prodromal, illness, decline, and convalescence periods (**[Figure 15.3](#page-672-0)**). The **incubation period** occurs in an acute disease after the initial entry of the pathogen into the host (patient). It is during this... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**Affix Meaning Example** cyto- cell cytopenia: reduction in the number of blood cells hepat- of the liver hepatitis: inflammation of the liver -pathy disease neuropathy: a disease affecting nerves -emia of the blood bacteremia: presence of bac... |
In 1884, Koch published four postulates (**[Table 15.3](#page-674-1)**) that summarized his method for determining whether a particular microorganism was the cause of a particular disease. Each of Koch's postulates represents a criterion that must be met before a disease can be positively linked with a pathogen. In ord... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.2 How Pathogens Cause Disease**",
"Header 3": "**Koch's Postulates**",
"token_count": 1549,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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The ability of a microbial agent to cause disease is called **pathogenicity**, and the degree to which an organism is pathogenic is called **virulence**. Virulence is a continuum. On one end of the spectrum are organisms that are avirulent (not harmful) and on the other are organisms that are highly virulent. Highly vi... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.2 How Pathogens Cause Disease**",
"Header 3": "**Pathogenicity and Virulence**",
"token_count": 2040,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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This often occurs when microbes that reside harmlessly in one body location end up in a different body system, where they cause disease. For example, *E. coli* normally found in the large intestine can cause a urinary tract infection if it enters the bladder. This is the leading cause of urinary tract infections among ... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.2 How Pathogens Cause Disease**",
"Header 3": "**Pathogenicity and Virulence**",
"token_count": 426,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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To cause disease, a pathogen must successfully achieve four steps or stages of pathogenesis: exposure (contact), adhesion (colonization), invasion, and infection. The pathogen must be able to gain entry to the host, travel to the location where it can establish an infection, evade or overcome the host's immune response... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.2 How Pathogens Cause Disease**",
"Header 3": "**Stages of Pathogenesis**",
"token_count": 2025,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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By entering the host cells, intracellular pathogens are able to evade some mechanisms of the immune system while also exploiting the nutrients in the host cell.
Entry to a cell can occur by endocytosis. For most kinds of host cells, pathogens use one of two different mechanisms for endocytosis and entry. One mechanis... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.2 How Pathogens Cause Disease**",
"Header 3": "**Stages of Pathogenesis**",
"token_count": 1500,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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For a pathogen to persist, it must put itself in a position to be transmitted to a new host, leaving the infected host through a **portal of exit** (**[Figure 15.9](#page-685-0)**). As with portals of entry, many pathogens are adapted to use a particular portal of exit. Similar to portals of entry, the most common port... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.2 How Pathogens Cause Disease**",
"Header 3": "**Transmission of Disease**",
"token_count": 256,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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As discussed in the previous section, the first two steps in pathogenesis are exposure and adhesion. Recall that an adhesin is a protein or glycoprotein found on the surface of a pathogen that attaches to receptors on the host cell. Adhesins are found on bacterial, viral, fungal, and protozoan pathogens. One example of... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.3 Virulence Factors of Bacterial and Viral Pathogens**",
"Header 3": "**Virulence Factors for Adhesion**",
"token_count": 954,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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After exposure and adhesion, the next step in pathogenesis is invasion, which can involve enzymes and toxins. Many pathogens achieve invasion by entering the bloodstream, an effective means of dissemination because blood vessels pass close to every cell in the body. The downside of this mechanism of dispersal is that t... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.3 Virulence Factors of Bacterial and Viral Pathogens**",
"Header 3": "**Bacterial Exoenzymes and Toxins as Virulence Factors**",
"token_count": 2029,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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#### **Toxins**
In addition to exoenzymes, certain pathogens are able to produce **toxins**, biological poisons that assist in their ability to invade and cause damage to tissues. The ability of a pathogen to produce toxins to cause damage to host cells is called **toxigenicity**.
Toxins can be categorized as end... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.3 Virulence Factors of Bacterial and Viral Pathogens**",
"Header 3": "**Bacterial Exoenzymes and Toxins as Virulence Factors**",
"token_count": 2043,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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After the A subunit of the diphtheria toxin separates and gains access to the cytoplasm, it facilitates the transfer of adenosine diphosphate (ADP)-ribose onto an elongation-factor protein (EF-2) that is needed for protein synthesis. Hence, diphtheria toxin inhibits protein synthesis in the host cell, ultimately killin... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.3 Virulence Factors of Bacterial and Viral Pathogens**",
"Header 3": "**Bacterial Exoenzymes and Toxins as Virulence Factors**",
"token_count": 1820,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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Evading the immune system is also important to invasiveness. Bacteria use a variety of virulence factors to evade phagocytosis by cells of the immune system. For example, many bacteria produce capsules, which are used in adhesion but also aid in immune evasion by preventing ingestion by phagocytes. The composition of t... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.3 Virulence Factors of Bacterial and Viral Pathogens**",
"Header 3": "**Virulence Factors for Survival in the Host and Immune Evasion**",
"token_count": 2033,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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However, before viral entry into the cell can occur, a second interaction between gp120 and one of two chemokine receptors (CCR5 and CXCR4) must occur. **[Table](#page-699-0) [15.11](#page-699-0)** lists the adhesins for some common viral pathogens and the specific sites to which these adhesins allow viruses to attach.... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.3 Virulence Factors of Bacterial and Viral Pathogens**",
"Header 3": "**Virulence Factors for Survival in the Host and Immune Evasion**",
"token_count": 796,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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Pathogenic fungi can produce virulence factors that are similar to the bacterial virulence factors that have been discussed earlier in this chapter. In this section, we will look at the virulence factors associated with species of *Candida*, *Cryptococcus, Claviceps,* and *Aspergillus*.
*Candida albicans* is an oppor... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.4 Virulence Factors of Eukaryotic Pathogens**",
"Header 3": "**Fungal Virulence**",
"token_count": 957,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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Protozoan pathogens are unicellular eukaryotic parasites that have virulence factors and pathogenic mechanisms analogous to prokaryotic and viral pathogens, including adhesins, toxins, antigenic variation, and the ability to survive inside phagocytic vesicles.
Protozoans often have unique features for attaching to ho... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.4 Virulence Factors of Eukaryotic Pathogens**",
"Header 3": "**Protozoan Virulence**",
"token_count": 912,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **[15.1 Characteristics of Infectious Disease](#page-667-0)**
- In an **infection**, a microorganism enters a host and begins to multiply. Some infections cause **disease**, which is any deviation from the normal function or structure of the host.
- **Signs** of a disease are objective and are measured. **Sympto... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.4 Virulence Factors of Eukaryotic Pathogens**",
"Header 3": "**Summary**",
"token_count": 1132,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Multiple Choice**
- **1.** Which of the following would be a sign of an infection?
- a. muscle aches
- b. headache
- c. fever
- d. nausea
- **2.** Which of the following is an example of a noncommunicable infectious disease?
- a. infection with a respiratory virus
- b. food poisoning due to a preformed bacteri... | {
"Header 1": "**Microbial Mechanisms of Pathogenicity**",
"Header 2": "**15.4 Virulence Factors of Eukaryotic Pathogens**",
"Header 3": "**Review Questions**",
"token_count": 2022,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
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In the United States and other developed nations, public health is a key function of government. A healthy citizenry is more productive, content, and prosperous; high rates of death and disease, on the other hand, can severely hamper economic productivity and foster social and political instability. The burden of disea... | {
"Header 1": "**Disease and Epidemiology**",
"Header 2": "**Introduction**",
"token_count": 233,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Epidemiological analyses are always carried out with reference to a population, which is the group of individuals that are at risk for the disease or condition. The population can be defined geographically, but if only a portion of the individuals in that area are susceptible, additional criteria may be required. Susce... | {
"Header 1": "**Disease and Epidemiology**",
"Header 2": "**16.1 The Language of Epidemiologists**",
"Header 3": "**Analyzing Disease in a Population**",
"token_count": 2003,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
In each of the fatal cases, the patients had not sought medical care until their symptoms were severe; also, all of the deceased had preexisting medical conditions such as congestive heart failure, diabetes, or high blood pressure.
After reviewing the medical records, epidemiologists with the public health office dec... | {
"Header 1": "**Disease and Epidemiology**",
"Header 2": "**16.1 The Language of Epidemiologists**",
"Header 3": "**Analyzing Disease in a Population**",
"token_count": 560,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
The main national public health agency in the United States is the **Centers for Disease Control and Prevention (CDC)**, an agency of the Department of Health and Human Services. The CDC is charged with protecting the public from disease and injury. One way that the CDC carries out this mission is by overseeing the Nat... | {
"Header 1": "**Disease and Epidemiology**",
"Header 2": "**16.1 The Language of Epidemiologists**",
"Header 3": "**The Role of Public Health Organizations**",
"token_count": 657,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Explain the research approaches used by the pioneers of epidemiology
- Explain how descriptive, analytical, and experimental epidemiological studies go about determining the cause of morbidity and mortality
Epidemiology has its roots in the work of physicians who looked for patterns i... | {
"Header 1": "**Disease and Epidemiology**",
"Header 2": "**16.2 Tracking Infectious Diseases**",
"token_count": 287,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
John Snow (**[Figure 16.5](#page-716-0)**) was a British physician known as the father of epidemiology for determining the source of the 1854 Broad Street cholera epidemic in London. Based on observations he had made during an earlier cholera outbreak (1848–1849), Snow proposed that cholera was spread through a fecal-o... | {
"Header 1": "**Disease and Epidemiology**",
"Header 2": "**16.2 Tracking Infectious Diseases**",
"Header 3": "**Pioneers of Epidemiology**",
"token_count": 2014,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Today, epidemiologists make use of study designs, the manner in which data are gathered to test a hypothesis, similar to those of researchers studying other phenomena that occur in populations. These approaches can be divided into observational studies (in which subjects are not manipulated) and experimental studies (i... | {
"Header 1": "**Disease and Epidemiology**",
"Header 2": "**Types of Epidemiological Studies**",
"token_count": 1805,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Describe the different types of disease reservoirs
- Compare contact, vector, and vehicle modes of transmission
- Identify important disease vectors
- Explain the prevalence of nosocomial infections
Understanding how infectious pathogens spread is critical to preventing infectious dis... | {
"Header 1": "**Disease and Epidemiology**",
"Header 2": "**16.3 Modes of Disease Transmission**",
"token_count": 2015,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Many pathogens require contact with a mucous membrane to enter the body, but the host may transfer the pathogen from another point of contact (e.g., hand) to a mucous membrane (e.g., mouth or eye). (credit left: modification of work by Lisa Doehnert)



**Figure 17.1** Varicella, or chickenpox, is caused by the highly contagious varicella-zoster virus. The characteristic rash seen here is partly a result of inflammation associated with the body's immune response to the virus. Inflammation is a response mechanism of innate immunity that ... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"token_count": 213,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Despite relatively constant exposure to pathogenic microbes in the environment, humans do not generally suffer from constant infection or disease. Under most circumstances, the body is able to defend itself from the threat of infection thanks to a complex immune system designed to repel, kill, and expel disease-causing... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**Introduction**",
"token_count": 293,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
**Overview of Nonspecific Innate Immune Defenses**
**Table 17.1**
Physical defenses provide the body's most basic form of nonspecific defense. They include physical barriers to
#### **Clinical Focus**
#### **Part 1**
Angela, a 25-year-old female patient in the emergency department, is having some trouble comm... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "Physical barriers Physical defenses Mechanical defenses Microbiome Chemicals and enzymes in body fluids Antimicrobial peptides Plasma protein mediators Cytokines Chemical defenses Inflammation-eliciting mediators Granulocytes Cellular defenses Agran... |
The intestinal tract is lined with epithelial cells, interspersed with mucus-secreting goblet cells (**[Figure 17.6](#page-746-0)**). This mucus mixes with material received from the stomach, trapping foodborne microbes and debris. The mechanical action of **peristalsis**, a series of muscular contractions in the diges... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "Physical barriers Physical defenses Mechanical defenses Microbiome Chemicals and enzymes in body fluids Antimicrobial peptides Plasma protein mediators Cytokines Chemical defenses Inflammation-eliciting mediators Granulocytes Cellular defenses Agran... |
#### **Learning Objectives**
- Describe how enzymes in body fluids provide protection against infection or disease
- List and describe the function of antimicrobial peptides, complement components, cytokines, and acute-phase proteins
- Describe similarities and differences among classic, alternate, and lectin complem... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.2 Chemical Defenses**",
"token_count": 206,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Fluids produced by the skin include examples of both endogenous and exogenous mediators. Sebaceous glands in the dermis secrete an oil called sebum that is released onto the skin surface through hair follicles. This sebum is an endogenous mediator, providing an additional layer of defense by helping seal off the pore o... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**Chemical and Enzymatic Mediators Found in Body Fluids**",
"token_count": 983,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
The **antimicrobial peptides (AMPs)** are a special class of nonspecific cell-derived mediators with broad-spectrum antimicrobial properties. Some AMPs are produced routinely by the body, whereas others are primarily produced (or produced in greater quantities) in response to the presence of an invading pathogen. Resea... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**Chemical and Enzymatic Mediators Found in Body Fluids**",
"Header 3": "**Antimicrobial Peptides**",
"token_count": 2016,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
The term **opsonization** refers to the coating of a pathogen by a chemical substance (called an **opsonin**) that allows phagocytic cells to recognize, engulf, and destroy it more easily. Opsonins from the complement cascade include C1q, C3b, and C4b. Additional important opsonins include mannose-binding proteins and ... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**Chemical and Enzymatic Mediators Found in Body Fluids**",
"Header 3": "**Antimicrobial Peptides**",
"token_count": 1191,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Many of the chemical mediators discussed in this section contribute in some way to inflammation and fever, which are nonspecific immune responses discussed in more detail in **[Inflammation and Fever](#page-772-0)**. Cytokines stimulate the production of acute-phase proteins such as C-reactive protein and mannose-bindi... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**Chemical and Enzymatic Mediators Found in Body Fluids**",
"Header 3": "**Inflammation-Eliciting Mediators**",
"token_count": 1425,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Identify and describe the components of blood
- Explain the process by which the formed elements of blood are formed (hematopoiesis)
- Describe the characteristics of formed elements found in peripheral blood, as well as their respective functions within the innate immune system
In th... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.3 Cellular Defenses**",
"token_count": 237,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
All of the formed elements of blood are derived from pluripotent hematopoietic stem cells (HSCs) in the bone marrow. As the HSCs make copies of themselves in the bone marrow, individual cells receive different cues from the body that control how they develop and mature. As a result, the HSCs differentiate into differen... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.3 Cellular Defenses**",
"Header 3": "**Hematopoiesis**",
"token_count": 1531,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
The various types of granulocytes can be distinguished from one another in a blood smear by the appearance of their nuclei and the contents of their granules, which confer different traits, functions, and staining properties. The **neutrophils**, also called **polymorphonuclear neutrophils (PMNs)**, have a nucleus with... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.3 Cellular Defenses**",
"Header 3": "**Granulocytes**",
"token_count": 1699,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
As their name suggests, **agranulocytes** lack visible granules in the cytoplasm. Agranulocytes can be categorized as lymphocytes or monocytes (**[Figure 17.13](#page-759-0)**). Among the lymphocytes are natural killer cells, which play an important role in nonspecific innate immune defenses. Lymphocytes also include t... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**Agranulocytes**",
"token_count": 1494,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Explain how leukocytes migrate from peripheral blood into infected tissues
- Explain the mechanisms by which leukocytes recognize pathogens
- Explain the process of phagocytosis and the mechanisms by which phagocytes destroy and degrade pathogens
Several of the cell types discussed in... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.4 Pathogen Recognition and Phagocytosis**",
"token_count": 244,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Some phagocytes are leukocytes (WBCs) that normally circulate in the bloodstream. To reach pathogens located in infected tissue, leukocytes must pass through the walls of small capillary blood vessels within tissues. This process, called **extravasation**, or **diapedesis**, is initiated by complement factor C5a, as we... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.4 Pathogen Recognition and Phagocytosis**",
"Header 3": "**Extravasation (Diapedesis) of Leukocytes**",
"token_count": 1422,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Once pathogen recognition and attachment occurs, the pathogen is engulfed in a vesicle and brought into the internal compartment of the phagocyte in a process called **phagocytosis** (**[Figure 17.21](#page-770-0)**). PRRs can aid in phagocytosis by first binding to the pathogen's surface, but phagocytes are also capab... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.4 Pathogen Recognition and Phagocytosis**",
"Header 3": "**Pathogen Degradation**",
"token_count": 1526,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
An early, if not immediate, response to tissue injury is acute inflammation. Immediately following an injury, vasoconstriction of blood vessels will occur to minimize blood loss. The amount of vasoconstriction is related to the amount of vascular injury, but it is usually brief. Vasoconstriction is followed by vasodila... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.5 Inflammation and Fever**",
"Header 3": "**Acute Inflammation**",
"token_count": 572,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
When acute inflammation is unable to clear an infectious pathogen, chronic inflammation may occur. This often results in an ongoing (and sometimes futile) lower-level battle between the host organism and the pathogen. The wounded area may heal at a superficial level, but pathogens may still be present in deeper tissues... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.5 Inflammation and Fever**",
"Header 3": "**Chronic Inflammation**",
"token_count": 2041,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Although she may experience additional episodes in the future, her prognosis is good and she can expect to live a relatively normal life provided she seeks treatment at the onset of symptoms.
*Go back to the [previous](#page-762-0) Clinical Focus box.*
#### **Summary**
#### **[17.1 Physical Defenses](#page-741-0)... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.5 Inflammation and Fever**",
"Header 3": "**Chronic Inflammation**",
"token_count": 1333,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Multiple Choice**
- **1.** Which of the following best describes the innate nonspecific immune system?
- a. a targeted and highly specific response to a single pathogen or molecule
- b. a generalized and nonspecific set of defenses against a class or group of pathogens
- c. a set of barrier mechanisms that ada... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.5 Inflammation and Fever**",
"Header 3": "**Review Questions**",
"token_count": 2013,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
The overwhelming immune and inflammatory responses that occur with septic shock can cause a perilous drop in blood pressure; intravascular blood clotting; development of thrombi and emboli that block blood vessels, leading to tissue death; failure of multiple organs; and death of the patient. Identify and characterize ... | {
"Header 1": "**Innate Nonspecific Host Defenses**",
"Header 2": "**17.5 Inflammation and Fever**",
"Header 3": "**Review Questions**",
"token_count": 215,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |

**Figure 18.1** Polio was once a common disease with potentially serious consequences, including paralysis. Vaccination has all but eliminated the disease from most countries around the world. An iron-lung ward, such as the one shown in this 1953 photograph, housed patients paralyzed fro... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"token_count": 211,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
People living in developed nations and born in the 1960s or later may have difficulty understanding the once heavy burden of devastating infectious diseases. For example, smallpox, a deadly viral disease, once destroyed entire civilizations but has since been eradicated. Thanks to the vaccination efforts by multiple gr... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**Introduction**",
"token_count": 302,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Define memory, primary response, secondary response, and specificity
- Distinguish between humoral and cellular immunity
- Differentiate between antigens, epitopes, and haptens
- Describe the structure and function of antibodies and distinguish between the different classes of antibodie... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.1 Overview of Specific Adaptive Immunity**",
"token_count": 765,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Activation of the adaptive immune defenses is triggered by pathogen-specific molecular structures called **antigens**. Antigens are similar to the pathogen-associated molecular patterns (PAMPs) discussed in **[Pathogen Recognition](#page-765-0) [and Phagocytosis](#page-765-0)**; however, whereas PAMPs are molecular str... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "• List the two defining characteristics of adaptive immunity.",
"Header 3": "**Antigens**",
"token_count": 2038,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Similar to IgM, **IgD** is a membrane-bound monomer found on the surface of B cells, where it serves as an antigenbinding receptor. However, IgD is not secreted by B cells, and only trace amounts are detected in serum. These trace amounts most likely come from the degradation of old B cells and the release of IgD mol... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "• List the two defining characteristics of adaptive immunity.",
"Header 3": "**Antigens**",
"token_count": 1913,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
The **major histocompatibility complex** (**MHC**) is a collection of genes coding for MHC molecules found on the surface of all nucleated cells of the body. In humans, the MHC genes are also referred to as human leukocyte antigen (HLA) genes. Mature red blood cells, which lack a nucleus, are the only cells that do not... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**Major Histocompatibility Complex Molecules**",
"token_count": 666,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
All nucleated cells in the body have mechanisms for processing and presenting antigens in association with MHC molecules. This signals the immune system, indicating whether the cell is normal and healthy or infected with an intracellular pathogen. However, only macrophages, dendritic cells, and B cells have the ability... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**Antigen-Presenting Cells (APCs)**",
"token_count": 1233,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Describe the process of T-cell maturation and thymic selection
- Explain the genetic events that lead to diversity of T-cell receptors
- Compare and contrast the various classes and subtypes of T cells in terms of activation and function
- Explain the mechanism by which superantigens ef... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.3 T Lymphocytes and Cellular Immunity**",
"token_count": 1835,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Classes of T Cells**
| Class | Surface<br>CD<br>Molecules | Activation | Functions |
|-----------------------|----------------------------|-------------------... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.3 T Lymphocytes and Cellular Immunity**",
"token_count": 225,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
For both helper T cells and cytotoxic T cells, activation is a complex process that requires the interactions of multiple molecules and exposure to cytokines. The **T-cell receptor (TCR)** is involved in the first step of pathogen epitope recognition during the activation process.
The TCR comes from the same receptor... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.3 T Lymphocytes and Cellular Immunity**",
"Header 3": "**T-Cell Receptors**",
"token_count": 736,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Helper T cells can only be activated by APCs presenting processed foreign epitopes in association with MHC II. The first step in the activation process is TCR recognition of the specific foreign epitope presented within the MHC II antigen-binding cleft. The second step involves the interaction of CD4 on the helper T ce... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.3 T Lymphocytes and Cellular Immunity**",
"Header 3": "**Activation and Differentiation of Helper T Cells**",
"token_count": 989,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Cytotoxic T cells (also referred to as cytotoxic T lymphocytes, or CTLs) are activated by APCs in a three-step process similar to that of helper T cells. The key difference is that the activation of cytotoxic T cells involves recognition of an antigen presented with MHC I (as opposed to MHC II) and interaction of CD8 (... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.3 T Lymphocytes and Cellular Immunity**",
"Header 3": "**Activation and Differentiation of Cytotoxic T Cells**",
"token_count": 605,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
When T cell activation is controlled and regulated, the result is a protective response that is effective in combating infections. However, if T cell activation is unregulated and excessive, the result can be a life-threatening. Certain bacterial and viral pathogens produce toxins known as superantigens (see **[Virulen... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.3 T Lymphocytes and Cellular Immunity**",
"Header 3": "**Superantigens and Unregulated Activation of T Cells**",
"token_count": 1255,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
#### **Learning Objectives**
- Describe the production and maturation of B cells
- Compare the structure of B-cell receptors and T-cell receptors
- Compare T-dependent and T-independent activation of B cells
- Compare the primary and secondary antibody responses
Humoral immunity refers to mechanisms of the adaptive... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.4 B Lymphocytes and Humoral Immunity**",
"token_count": 397,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
Like T cells, B cells possess antigen-specific receptors with diverse specificities. Although they rely on T cells for optimum function, B cells can be activated without help from T cells. **B-cell receptors (BCRs)** for naïve mature B cells are membrane-bound monomeric forms of IgD and IgM. They have two identical hea... | {
"Header 1": "**Adaptive Specific Host Defenses**",
"Header 2": "**18.4 B Lymphocytes and Humoral Immunity**",
"Header 3": "**B-Cell Receptors**",
"token_count": 1731,
"source_pdf": "datasets/websources/biochem/Microbiology-LR.pdf"
} |
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