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PATHOLOGY OF BACTERIAL INFECTION {ST1}

PATHOLOGY OF BACTERIAL INFECTION {ST1}. BY RANJEET RAMAN. Host response factors that influence infection:

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PATHOLOGY OF BACTERIAL INFECTION {ST1}

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  1. PATHOLOGY OF BACTERIAL INFECTION {ST1} BY RANJEET RAMAN

  2. Host response factors that influence infection: ​intrinsic defenses (skin barriers, cilia, lysozyme in mucosal secretions) ​innate immunity (complement, PMN efflux and adhesion, toll-like receptors) ​adaptive immunity (B and T cells, resident dendritic cells and monocytes to ​present antigens, cytokine release)

  3. Bacterial factors that influence infections: ​route of entry ​size of inoculum ​bacterial products that damage host tissue and alter host physiology ​evolutionary adaptation to host

  4. Histopathology of bacteria Extracellular bacteria cause acute inflammations with lots of PMNs and edema. Depending ​on species there may be necrosis, with pus or abscess. Over time, inflammation ​becomes chronic. Extracellular bacteria are clinically much more common. ​examples include Strep pneumoniae, Staph aureus, H. pylori, Vibrio vulnificus

  5. Intracellular bacteria cause chronic inflammations, sometimes with acute or ​granulomatous inflammation as well. Lots of macrophages, lymphocytes, ​sometimes epithelioid macrophages. May be caseous necrosis or small abcesses. ​examples include Mycobacterium tuberculosis, Salmonella typhi, Rickettsia rickettsii

  6. Host tissue responses to bacterial infection 1. Exudative inflammation. Vascular permeability brings in PMNs. Lots of pus. ​Typically caused by localized extracellular pyogenic bacteria. Pathology results ​from inflammatory responses (consolidation in lungs, edema).

  7. 2. Necrotizing inflammation. The exudative response plus necrosis (“suppuration”). ​Pathology results directly from bacterial toxins. 3. Granulomatous inflammation. Characterized by accumulation of activated epithelioid ​macrophages. Caused by bacteria that resist PMN attack, usually obligate ​intracellular bacteria. Granulomas form when macrophages secrete cytokines like ​IL1 and GM-CSF.

  8. 4. Interstitial inflammation. A non-specific chronic inflammation. Even when arising ​acutely, infiltrates with lymphocytes, macrophages, plasma cells. This suggests a ​viral or spirochete bacterial infection, such as Treponema pallidum (syphilis). When ​seen with inflammation/necrosis of the vascular wall, suggests Rickettsia rickettsii.

  9. 5. Cytopathic or host proliferative changes. Typically from viral infections. 6. The Null reaction. Absence of inflam, necrotizing, or cytopathic signs. Rarely occurs in ​bacterial infections. May be seen in hosts with physiological, inflammatory, or ​immune defects.

  10. Host tissue responses to bacterial infection 1. Exudative inflammation. Vascular permeability brings in PMNs. Lots of pus. ​Typically caused by localized extracellular pyogenic bacteria. Pathology results ​from inflammatory responses (consolidation in lungs, edema).

  11. 2. Necrotizing inflammation. The exudative response plus necrosis (“suppuration”). ​Pathology results directly from bacterial toxins.

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