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Human Anatomy & Physiology (11th Edition)
Human Anatomy & Physiology (11th Edition)
11th Edition
ISBN:9780134580999
Author:Elaine N. Marieb, Katja N. Hoehn
Publisher:Elaine N. Marieb, Katja N. Hoehn
Chapter1: The Human Body: An Orientation
Section: Chapter Questions
Problem 1RQ: The correct sequence of levels forming the structural hierarchy is A. (a) organ, organ system,...
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It was important for Lilly to understand how the bacteria were able to cause disease in patients. The mechanism of pathogenesis by M. tuberculosis starts in the lung alveoli. The cell wall of M. tuberculosis allows it to resist phagocytolysis by the alveolar macrophages, where they can multiply. They can then induce apoptosis in macrophages, which die, and the bacteria is free to infect other macrophages. As the cycle of infection slowly progresses, the body's response to the infection is to try to wall off the bacteria in granulomas (wall of immune cells, both dead and alive, surrounding the bacteria to restrict its spread). Eventually, the bacteria can escape the granuloma and infect other parts of the lung. Transmission of Mtb Initial infection and Granuloma cavitationy replication of Mtb in macrophages and dissemination of Mtb in the lung Infected macrophages Caseating granuloma Recruitment of Innate and adaptive immune cells Infected cells undergo necrosis resulting in the formation of the caseum Solid granuloma, containment of Mtb Figure 6. Granuloma development during TB progression. The initial stages of TB infection involve inhalation of M. tuberculosis (Mtb) bacilli into the lung and phagocytosis by resident alveolar macrophages. Mtb can survive phagocytosis and grow within macrophages for a while. Once their number reaches a certain threshold and the bacteria has spread locally to other macrophages, they can elicit a local inflammatory response resulting in the recruitment of monocytes and macrophages and other immune cells to the site of infection, resulting in the formation of a granuloma around the infectious agent. This is the balanced solid state in which many granulomas persist and restrict the bacilli at their center. However, as the disease progresses, increased necrotic breakdown of granuloma cells leads to the accumulation of caseum (cheese-like loose collection of dead and live cells), which may result in cavitation of granulomas. Ultimately, as the granuloma cavitates and collapses into the lung, Mtb bacilli are released into the airway and can spread to other parts of the lung.
Transcribed Image Text:It was important for Lilly to understand how the bacteria were able to cause disease in patients. The mechanism of pathogenesis by M. tuberculosis starts in the lung alveoli. The cell wall of M. tuberculosis allows it to resist phagocytolysis by the alveolar macrophages, where they can multiply. They can then induce apoptosis in macrophages, which die, and the bacteria is free to infect other macrophages. As the cycle of infection slowly progresses, the body's response to the infection is to try to wall off the bacteria in granulomas (wall of immune cells, both dead and alive, surrounding the bacteria to restrict its spread). Eventually, the bacteria can escape the granuloma and infect other parts of the lung. Transmission of Mtb Initial infection and Granuloma cavitationy replication of Mtb in macrophages and dissemination of Mtb in the lung Infected macrophages Caseating granuloma Recruitment of Innate and adaptive immune cells Infected cells undergo necrosis resulting in the formation of the caseum Solid granuloma, containment of Mtb Figure 6. Granuloma development during TB progression. The initial stages of TB infection involve inhalation of M. tuberculosis (Mtb) bacilli into the lung and phagocytosis by resident alveolar macrophages. Mtb can survive phagocytosis and grow within macrophages for a while. Once their number reaches a certain threshold and the bacteria has spread locally to other macrophages, they can elicit a local inflammatory response resulting in the recruitment of monocytes and macrophages and other immune cells to the site of infection, resulting in the formation of a granuloma around the infectious agent. This is the balanced solid state in which many granulomas persist and restrict the bacilli at their center. However, as the disease progresses, increased necrotic breakdown of granuloma cells leads to the accumulation of caseum (cheese-like loose collection of dead and live cells), which may result in cavitation of granulomas. Ultimately, as the granuloma cavitates and collapses into the lung, Mtb bacilli are released into the airway and can spread to other parts of the lung.
Practice question 14 p. 225 Steps to pathogenesis Multiple events, each a limiting barrier for infection, need to occur before a full-fledged bacterial infections translate into symptoms and pathology. The infection process The disease process TOXICITY Toxin effects are local or systemic EXPOSURE ADHERENCE INVASION MULTIPLICATION to pathogens TISSUE OR SYSTEMIC DAMAGE to skin or mucosa Growth and production of virulence factors and toxins through epithelium INVASIVENESS Further growth at original and distant sites Break in barrier Knowing the pathogenesis of TB, what virulence factors would you expect to see in this microorganism at each stage (main steps seen in class) of pathogenesis? Note: Don't give the specific name of molecules, the general mechanism described above does not name them, so we don't know them. I want important categories of molecules and their function in TB pathogenesis for each theoretical infection stage as seen in class (exposure, adherence, ..). Please do NOT waste your time Googling and reading papers about TB pathogenesis.
Transcribed Image Text:Practice question 14 p. 225 Steps to pathogenesis Multiple events, each a limiting barrier for infection, need to occur before a full-fledged bacterial infections translate into symptoms and pathology. The infection process The disease process TOXICITY Toxin effects are local or systemic EXPOSURE ADHERENCE INVASION MULTIPLICATION to pathogens TISSUE OR SYSTEMIC DAMAGE to skin or mucosa Growth and production of virulence factors and toxins through epithelium INVASIVENESS Further growth at original and distant sites Break in barrier Knowing the pathogenesis of TB, what virulence factors would you expect to see in this microorganism at each stage (main steps seen in class) of pathogenesis? Note: Don't give the specific name of molecules, the general mechanism described above does not name them, so we don't know them. I want important categories of molecules and their function in TB pathogenesis for each theoretical infection stage as seen in class (exposure, adherence, ..). Please do NOT waste your time Googling and reading papers about TB pathogenesis.
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