Inflammatory Responses to Infection PDF

INFLAMMATORY RESPONSES TO INFECTION In contrast with the vast molecular diversity of microbes, the morphologic patterns of tissue responses to microbes are limited. Therefore, many pathogens produce similar reaction patterns, and few features are unique to or pathognomonic for a particular microorga...

INFLAMMATORY RESPONSES TO INFECTION In contrast with the vast molecular diversity of microbes, the morphologic patterns of tissue responses to microbes are limited. Therefore, many pathogens produce similar reaction patterns, and few features are unique to or pathognomonic for a particular microorganism, adding to the challenge in histopathologic diagnosis. There are five major histologic patterns of tissue reaction in infections: 1-suppurative inflammation 2-mononuclear/ granulomatous. 3-cytopathic-cytoproliferative. 4-necrosis. 5-chronic inflammation/scarring. 1-suppurative inflammation Neutrophil-rich acute suppurative inflammation is typical of infections with many bacteria (“pyogenic” bacteria) and some fungi.  2-Mononuclear Inflammation Diffuse, predominantly mononuclear, interstitial infiltrates are a common feature of all chronic inflammatory processes, but sometimes they appear acutely in response to viruses, intracellular bacteria, or intracellular parasites. In addition, spirochetes and some helminths also provoke. Eosinophilia can be prominent with some helminthic infections. (A) Acute viral hepatitis (B) Secondary syphilis in the dermis with characterizead by a predominantly perivascular lymphoplasmacytic infiltrate lymphocytic infiltrate and endothelial proliferation. Granulomatous inflammation : is a distinctive form of mononuclear inflammation usually evoked by infectious agents that resist eradication, are capable of stimulating strong T-cell–mediated immunity (e.g., M. tuberculosis, Histoplasma capsulatum, schistosome eggs). is characterized by accumulation of activated macrophages called epithelioid cells, which may fuse to form giant cells. In some cases, there is a central area of caseous necrosis (C) Granulomatous inflammation in response to tuberculosis. Note the zone of caseation (asterisk), which normally forms the center of the granuloma, with a surrounding rim of activated epithelioid macrophages, some of which have fused to form giant cells (arrows); this in turn is surrounded by a zone of activated T lymphocytes. 3-Cytopathic-Cytoproliferative Reaction Cytopathic-cytoproliferative reactions usually are produced by viruses. The lesions are characterized by cell necrosis or cellular proliferation, usually with sparse inflammatory cells. Some viruses replicate within cells and make viral aggregates that are visible as inclusion bodies (e.g., herpesviruses or adenovirus) or induce cells to fuse and form multinucleated cells called polykaryons (e.g., measles virus or herpesviruses). Focal cell damage in the skin may cause epithelial cells to become detached, forming blisters. Finally, viruses can contribute to the development of malignant neoplasms.  (A) CMV infection in the lung. Infected cells show distinct nuclear (long arrow) and ill-defined cytoplasmic (short arrows) inclusions. (B) HSV and VZV both cause characteristic cytopathologic changes, including fusion of epithelial cells, which produces multinucleate cells with molding of nuclei to one another (long arrow), and eosinophilic haloed nuclear inclusions (short arrow). (C) HBV infection in liver. In chronic infections, infected hepatocytes show diffuse granular (“ground-glass”) cytoplasm, reflecting accumulated hepatitis B surface antigen (HBsAg). 4- Tissue Necrosis -Clostridium perfringens and other organisms that secrete powerful toxins can cause rapid and severe necrosis that tissue damage is the dominant feature. -The parasite E. histolytica causes colonic ulcers and liver abscesses characterized by extensive tissue destruction and liquefactive necrosis without a prominent inflammatory infiltrate.fibrinous exudate. This can cause The asphyxia. powerful exotoxins of C. diphtheriae cause necrosis of laryngeal epithelium giving rise to a pseudomembrane comprised of necrotic cells -viruses can cause widespread necrosis of host cells associated with inflammation, as exemplified by destruction of the temporal lobes of the brain by HSV or the liver by HBV. 5-Chronic Inflammation and Scarring Sometimes an exuberant scarring response is the major cause of dysfunction. For example, schistosome eggs cause “pipestem” fibrosis of the liver or of the bladder wall. M. tuberculosis causes constrictive fibrous pericarditis. Chronic HBV infection may cause cirrhosis of the liver, in which dense fibrous septa surround nodules of regenerating hepatocytes. Schistosoma haematobium infection of the bladder with numerous calcified eggs and extensive scarring.  PATTERNS OF HOST RESPONSES TO MICROBES Neutrophil-rich acute suppurative inflammation is typical of infections with many bacteria (“pyogenic” bacteria) and some fungi. Mononuclear cell infiltrates are common in many chronic infections and some acute viral infections. Granulomatous inflammation is the hallmark of infection with M. tuberculosis and certain fungi.  Cytopathic and proliferative lesions are caused by some viruses. Necrosis results from tissue-damaging toxins produced by microbes such as C. perfringens. Chronic inflammation and scarring represent the final common pathway of many infections.