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الكلية كلية طب الاسنان
القسم العلوم الاساسية
المرحلة 3
أستاذ المادة علي زكي ناجي الاسدي
5/31/2011 7:35:56 AM
Mechanisms of viral injury Viruses damage host cells by entering the cell and replicating at the host s expense.
Viral tropism--the tendency to infect some cells but not others--is in part caused by the binding of specific viral surface proteins to particular host cell surface receptor proteins. For example, EBV binds to the complement receptor on macrophages , rabies virus binds to the acetylcholine receptor on neurons, and rhinoviruses bind to the adhesion protein intercellular adhesion molecule 1 (ICAM-1) on mucosal cells.
Viruses enter the cell cytoplasm by one of three ways:
(1) translocation of the entire virus across the plasma membrane.
(2) fusion of the viral envelope with the cell membrane.
(3) receptor-mediated endocytosis of the virus and fusion with endosomal membranes. Within the cell, the virus uncoats, (separating its genome from its structural components) and losing its infectivity. Viruses use host enzymes for viral synthesis, which may be present in some differentiated tissues and not in others. Newly synthesized viral genomes and capsid proteins are then assembled into progeny virions in the nucleus or cytoplasm and are released directly or bud through the plasma membrane. Viruses kill host cells in a number of ways:
1-Viruses inhibit host cell DNA, RNA, or protein synthesis. For example, poliovirus inactivates cap-binding protein, which is essential for protein synthesis directed by capped host cell mRNAs, while allowing protein synthesis from uncapped poliovirus mRNAs.
2-Viral proteins insert into the host cell s plasma membrane and directly damage its integrity.( measles virus, and herpesviruses 3-Viruses replicate efficiently and lyses host cells (e.g, neurons by poliovirus).
4-Viral proteins on the surface of the host cells are recognized by the immune system, and the host lymphocytes attack the virus-infected cells. For example, acute liver failure during hepatitis B infection may be killed by cytotoxic T lymphocytes.
5-Virus may damage defense mechanism of the body leading to different types of secondary infections, like bacterial chest infection that complicate primary viral infection to respiratory epithelium, or opportunistic infection (pneumocystic carinii) that associated with HIV viral infection.
Pathogencity (mechanisms of bacterial injury to the host):
1- Bacterial Fimbriae and Pili: these are slender processes lie on the surface of some types of bacteria, these structures coated by recognition molecules called adhesions, these are the means by which bacteria stick to the cell surface and infect that cell, the pili is a feature of Gram negative bacteria, e.g. (enterobacteria that cause gastrointestinal infection and Neisseriae that cause meningitis or genital infections).
2- Bacterial toxins:
a- Exotoxins: a group of enzymes secreted by some types of bacteria and they have local or remote effects, their effects tend to be more specific than those of endotoxins., (e.g. pseudomonas colitis caused by clostridium difficle, tetanus caused by clostridium tetani, and scalded skin syndrome caused by staphylococcus aureus).
b-Endotoxins: these are lipopolysaccarides as component of Gram negative bacterial cell wall, (e.g. E. Coli ), they released on death of the bacteria, it responsible for endotoxic shock that characterized by fever, hypotension, cardiac and renal failure.
3- Bacterial Enzymes: these are bacterial enzymes with local effects altering the tissue environment in a way that favour the growth and spread of organism (bacteria) that secreted these enzymes. Most common types of bacterial enzymes are:
a- Coagulase enzyme produced by staphylococcus aureus bacteria lead to formation of barrier between bacteria and the inflammatory reaction.
b- Streptokinase produced by streptococcus bacteria and it digest fibrin and allow bacterial spread.
c- Collagenase and hyaluronidase enzymes that digest connective tissue and facilitate bacterial invasion.
4- Undesirable consequences of immune response: bacteria can indirectly cause tissue injury by inducing an immune response that harms the host, the following three possible mechanism can occur:
a- Immune complex formation (e.g. Post-streptococcal glomerulonephritis ).
b- Immune cross reaction ( e.g. rheumatic fever).
c- Cell mediated immunity cause tissue destruction (e.g. T.B infection).
Special Techniques for Diagnosing Infectious Agents Some infectious agents or their products can be directly observed in Hematoxylin and Eosin-stained sections (e.g ,the inclusion bodies formed by CMV and herpesvirus; bacterial clumps, which usually stain blue; Candida, among the fungi; most protozoans; and all helminths).
Many infectious agents, however, are best visualized by Special stains on the basis of particular characteristics of their cell walls or coat (Gram stain, acid-fast, and Giemsa stains), or after labeling with specific antibody probes. Regardless of the staining technique, organisms are usually best visualized at the advancing edge of a lesion rather than at its center, particularly if there is necrosis. Because these morphologic techniques cannot define species of organisms, determine drug sensitivity, or identify virulence characteristics,
Cultures of lesional tissue are performed. Biochemical techniques also used to give the diagnosis of infectious agents. Serological test to detect the long list of microbial agents, (toxoplamosis, chamydia and rubella).
PCR (Polymerase Chain Reaction), which depend on DNA sequence analysis to identify microbes that grow slowly in culture (mycobacteria or CMV) or do not culture at all (hepatitis B and C viruses).
Organisms induce five major patterns of tissue reaction:
1- suppurative (polymorphonuclear) inflammation: Suppurative inflammation is characterized by increased vascular permeability and leukocytic infiltration, predominantly of neutrophils. The neutrophils are attracted to the site of infection by release of chemoattractants from the rapidly dividing, "pyogenic" bacteria that evoke this response. The bacterial chemoattractants include secreted bacterial peptides, that recognized by specific receptors on neutrophils. Alternatively, bacteria attract neutrophils indirectly by releasing endotoxin that stimulates macrophages to secrete IL-1 or TNF. Massing of neutrophils results in the formation of pus. The sizes of exudative lesions vary from tiny microabscesses formed in multiple organs in bacterial septicemia to diffuse involvement of entire lobes of the lung in pneumococcal infections.
2- mononuclear and granulomatous inflammation: Diffuse, predominantly mononuclear interstitial infiltrates occur in response to viruses, intracellular bacteria, intracellular parasites, or helminthes. Which mononuclear cell predominates within the inflammatory lesion depends on the host immune response to the organism. For example, mostly plasma cells are seen in the chancres of primary syphilis, mostly lymphocytes with active HBV infection or in viral infections of the brain) . These lymphocytes reflect cell-mediated immunity against the pathogen or the pathogen-infected cells. Granulomatous inflammation occurs when aggregates of altered macrophages form, sometimes around a central necrotic focus, or fuse together to form giant cells. These distinctive lesions are usually evoked by relatively slowly dividing infectious agents (M. tuberculosis) or by those of relatively large size (schistosome eggs).
3- cytopathic-cytoproliferative inflammation These reactions are characteristic of virus-mediated damage to individual host cells in the absence of host inflammatory response. Some viruses replicate within cells and make viral aggregates that are visible as inclusion bodies (CMV or adenovirus) or induce cells to fuse and form polykaryons (measles virus or herpesviruses). Focal cell damage may cause epithelial cells to become discohesive and form blisters (herpes Viruses can also cause epithelial cells to proliferate and form unusual individual and aggregate morphologic lesions (venereal warts caused by human papillomavirus and molluscum contagiosum caused by poxviruses). Finally, viruses can cause dysplastic changes and cancers in epithelial cells and lymphocytes.
4- necrotizing inflammation Clostridium perfringens and other organisms that secrete strong toxins cause such rapid and severe tissue damage that cell death is the dominant feature. these lesions resemble ischemic necrosis with disruption or loss of basophilic nuclear staining and preservation of cellular outlines. Similarly, the parasite Entamoeba histolytica causes colonic ulcers and liver abscesses characterized by extensive tissue destruction with liquefactive necrosis, in the absence of a prominent inflammatory infiltrate.
5- chronic inflammation and scarring The final common pathway of many infections is chronic inflammation, which may lead either to complete healing or to extensive scarring. For some organisms that are relatively inert, the exuberant scarring response is a major cause of dysfunction (the "pipe-stem" fibrosis of the liver caused by schistosome eggs or the constrictive fibrous pericarditis in tuberculosis) ..
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
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