10. Pathology of infectious disease Questions By what mechanisms do microorganisms damage tissues? How does the host respond pathologically to infection? Symptoms of infection arise from direct damage to tissues, ‘poisoning of cells’, immune-mediated damage (immunopathology) or a combination of these. Subclinical infection may occur, however, without any such damage. Disease severity depends on both host factors and virulence determinants of the microorganism. Host determinants of disease severity include age, nutritional status, genetic constitution, immune status, local environment (e.g. gastric pH), presence of normal flora and presence of physical barriers (such as intact skin). Factors that affect the virulence of a pathogen include the infectious titre, the route of entry and genetic expression (e.g. of virulence factors). Both host and microbial factors can be altered by environmental changes such as ambient temperature and use of antibiotics. Even in an outbreak arising from a single pathogen, there is often a spectrum of clinical presentation. Damage to tissues Most viruses cause damage to the cells they infect. Viruses abort host replicative mechanisms and may thus cause death of the cell or, when mature, they may lyse the cell as they erupt. If a large fraction of the cells is infected, then there is extensive tissue damage. Programmed cell death (apoptosis) is also now recognized as a common mechanism that many viruses, such as HIV and influenza A, use to cause cell damage. Macroscopically, extensive tissue necrosis is, however, rare, and patchy necrosis with oedema owing to membrane damage is all that is seen. Viral infection is also characterized by changes in the cytoskeleton and organelles. There may be shrinkage of the nucleus (pyknosis) and aggregations of newly formed virus may be seen as inclusion bodies. Some viruses, such as paramyxoviruses, also cause cell-to-cell fusion to yield multinucleate cells. Viruses such as hepatitis B virus, herpesviruses (particularly Epstein–Barr virus) and papillomaviruses are known to be oncogenic. The precise mechanisms of cancer causation are not fully elucidated but genes that provide oncogenic potential have been identified; for example, the product of the X gene of hepatitis B virus has been shown to inhibit DNA repair mechanisms and, therefore, allow the accumulation of mutations. Bacteria may exist intracellularly within phagocytic cells. These cells may then be destroyed. Parenchymal cells are, however, more commonly damaged by extracellular products such as toxins, enzymes and pH change. Helicobacter pylori, for example, produces urease, which causes hydrogen ion changes, and mucinase, which degrades the protective mucous layer of the stomach cavity; both of these mechanisms are thought to contribute to the cell damage that results in gastritis and peptic ulceration.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Epidemiology of infectious diseases Infections of the immunocompromised host Principles of hospital infection control Infections of bone, joints and muscle Tuberculosis and other mycobacterial diseases Innate host defences to infectious disease Stay updated, free articles. Join our Telegram channel Join Tags: The Flesh and Bones of Medical Microbiology Jul 3, 2016 | Posted by admin in MUSCULOSKELETAL MEDICINE | Comments Off on Pathology of infectious disease Full access? Get Clinical Tree
10. Pathology of infectious disease Questions By what mechanisms do microorganisms damage tissues? How does the host respond pathologically to infection? Symptoms of infection arise from direct damage to tissues, ‘poisoning of cells’, immune-mediated damage (immunopathology) or a combination of these. Subclinical infection may occur, however, without any such damage. Disease severity depends on both host factors and virulence determinants of the microorganism. Host determinants of disease severity include age, nutritional status, genetic constitution, immune status, local environment (e.g. gastric pH), presence of normal flora and presence of physical barriers (such as intact skin). Factors that affect the virulence of a pathogen include the infectious titre, the route of entry and genetic expression (e.g. of virulence factors). Both host and microbial factors can be altered by environmental changes such as ambient temperature and use of antibiotics. Even in an outbreak arising from a single pathogen, there is often a spectrum of clinical presentation. Damage to tissues Most viruses cause damage to the cells they infect. Viruses abort host replicative mechanisms and may thus cause death of the cell or, when mature, they may lyse the cell as they erupt. If a large fraction of the cells is infected, then there is extensive tissue damage. Programmed cell death (apoptosis) is also now recognized as a common mechanism that many viruses, such as HIV and influenza A, use to cause cell damage. Macroscopically, extensive tissue necrosis is, however, rare, and patchy necrosis with oedema owing to membrane damage is all that is seen. Viral infection is also characterized by changes in the cytoskeleton and organelles. There may be shrinkage of the nucleus (pyknosis) and aggregations of newly formed virus may be seen as inclusion bodies. Some viruses, such as paramyxoviruses, also cause cell-to-cell fusion to yield multinucleate cells. Viruses such as hepatitis B virus, herpesviruses (particularly Epstein–Barr virus) and papillomaviruses are known to be oncogenic. The precise mechanisms of cancer causation are not fully elucidated but genes that provide oncogenic potential have been identified; for example, the product of the X gene of hepatitis B virus has been shown to inhibit DNA repair mechanisms and, therefore, allow the accumulation of mutations. Bacteria may exist intracellularly within phagocytic cells. These cells may then be destroyed. Parenchymal cells are, however, more commonly damaged by extracellular products such as toxins, enzymes and pH change. Helicobacter pylori, for example, produces urease, which causes hydrogen ion changes, and mucinase, which degrades the protective mucous layer of the stomach cavity; both of these mechanisms are thought to contribute to the cell damage that results in gastritis and peptic ulceration.< div class='tao-gold-member'> Only gold members can continue reading. Log In or Register to continue Share this:Click to share on Twitter (Opens in new window)Click to share on Facebook (Opens in new window) Related Related posts: Epidemiology of infectious diseases Infections of the immunocompromised host Principles of hospital infection control Infections of bone, joints and muscle Tuberculosis and other mycobacterial diseases Innate host defences to infectious disease Stay updated, free articles. Join our Telegram channel Join
