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| Factors influencing infection by a pathogen |
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Communicability Immunogenicity Infectivity Mechanism of action Pathogenicity Portal of entry Toxigenicity Virulence |
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| ability to spread from one individual to others |
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| ability of pathogens to induce an immune response |
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| ability of the pathogen to invade and multiply in the host |
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| manner in which the microorganism damages the tissue |
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| ability of an agent to produce disease |
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| - route by which a pathogenic microorganism infects the host: direct contact, inhalation, ingestion, or bites from animal or insect |
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| - ability to produce soluble toxins or endotoxins, factors that greatly influence the pathogen’s degree of virulence |
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| capacity of a pathogen to cause severe disease |
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| change of appearance by altering surface antigens (influenza virus mutates key surface antigen H and N allowing emergence of new strains of virus) |
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| major changes in antigenicity that occur from recombination of genes for H and N among different strains of viruses and can result in pandemics. |
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| a vaccine prepared from live microorganisms or viruses cultured under adverse conditions, leading to loss of their virulence but retention of their ability to induce protective immunity |
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| An inactivated vaccine (or killed vaccine) consists of virus particles which are grown in culture and then killed using a method such as heat or formaldehyde. These viruses are grown under controlled conditions and are rendered non-infectious as a means to reduce antigenicity. Large doses, adjuvants, and multiple doses are required to confer immunity. |
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| vaccine prepared from living, attenuated organisms. A weakened or killed vaccine containing a virus that will be injected into the host. This triggers an active immune response for a particular antibody which will be memorized by t-cells for future reference. |
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| how bacterial resistance to antibiotic occur. |
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| Lack of compliance concerning the necessity of completing the therapeutic regimen with antibiotics allows the selective resurgence of microorganisms that are more relatively resistant to the antibiotic. |
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| Primary (congenital) Immune Deficiency |
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most are the result of a single gene defect. Generally the mutations are sporadic and not inherited. The sporadic mutations occur before birth, but the onset of symptoms may be early or later, depending on the particular syndrome. *B lymphocyte deficiencies *T lymphocyte deficiencies *Combined T an B cell deficiencies * complement defects * phagocyte defects |
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| Secondary (Acquired) Immune Deficiency |
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| usually result in recurrent infections with the same group of microorganisms (encapsulated bacteria) associated with antibody and complement deficiencies. |
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| is a member of the retrovirus. use a viral enzyme, reverse transcriptase, to convert RNA into double-stranded DNA. Using a second viral enzyme, an integrase, the new DNA is inserted into the infected cell's genetic material, where it may remain dormant. If the cell is activated, translation of the viral information may be initiated, resulting in the formation of new virons, lysis and death of the infected cell, and shetting of infections HIV particles. During that process the viral protease is essential in processing proteins needed from the viral internal structure. |
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| HIV clinical manifestations |
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| serologically negative, serologically positive but asymptomatic. (uses a western blot analysis). Atypical or opportunistic infections present. |
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| CD4+T cells number decrease to less than 200/mm^3 |
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| HAART- highly active antiretroviral therapy. it reverses transcriptase inhibitors and are protease inhibitors. |
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| deleterious effects of hypersensitivity to environmental (exogenous) antigens. |
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| disturbance in the immunologic tolerance of self-antigens (lupus, MS) |
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| alloimmunity (isoimmunity) |
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| immune reaction to tissues of another individual (rejection of transplant) |
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against environmental antigens (allergens), IgE binds to Fc receptors on surface of mast cells (cytotropic antibody)- "sensitized", *itching/urticarial/conjunctivitis/ rhinitis/hypotension/bronchospasm/ dysrhythmias/GI cramps/malabsorption |
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| Type II: Tissue-specific reactions |
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| specific cell or tissue is the target of an immune response. 1.cell is destroyed by antibodies and complement 2.cell destruction through phagocytosis 3.soluble antigen may enter the circulations and deposit on tissues; tissues destroyed by complement and neutrophil granules 4. antibody dependent cell mediated cytotoxicity (ADCC) 5. Causes target cell malfunction. EXAMPLE-GRAVES |
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| Type III: immune complex mediated |
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