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alveolar epithelial cells (page 312).-Transmission is not well understood (Epocrates)-Slow and progressive onset-dyspnea with a gradual onset, gettingworse over the course of several weeks.-fatigue, weight loss, poor appetite-Chest x-ray will show a butterfly pattern of infiltrates that extend from the center of the chest Infection in the lung starts with the multiplication of the organism in the alveoli. As infection progresses, alveoli fill withexudates, there is type 2 pneumocyte hyperplasia, and mononuclear cells infiltrate the lung.In patients with AIDS, there are larger numbers of Pneumocystis organisms in the lungs and fewer inflammatory
(lecture notes).cells than in patients with Pneumocystis pneumonia(PCP) who are HIV-negative.mycobacterium avium complex (MAC)-Acid fast bacteria, often found in the environment-soil, water,and animals -The cell wall contains long-chained glycolipids(that make the wall thick) protect these facultative intracellular bacteria from lysosomalattack-90% to 95% of diseases in AIDS patientsFevers, night sweats,weight loss, anorexia,and lymphadenopathy (lecture notes).After entry into the body, MAI organisms colonize the respiratory and GI tracts and invade and multiply within macrophages. This phagocytosis and processing of antigens by macrophages triggersa complex immune response that includes further activation of macrophages as well as the release of cytokines such as interleukin (IL)-12, interferon gamma andtumor necrosis factor alpha.-In immune deficiency patients this can lead to unimpaired multiplication of the organisms within macrophages and subsequent dissemination.cytomegalovirus (CMV)CMV is a member of the herpes virus family. It contains a genome of double-stranded linear DNA, an icosahedral viral capsid, and a viral envelope protein that includes the highly immunogenic glycoprotein B. The most important characteristic of In a person with HIV and a low CD4 count the virus typically infects the retina and causes CMV retinitis-potentially causing blindness. (lecture notes)-CMV infected cells are protected from both T-cells, and NK cell killing because it has down-regulated MHC expressionOnce the virus is in the cell-it can inhibit cellular DNA, RNA, or protein synthesis, disruption of lysosomal membranes,
herpesviruses, includingCMV, is the ability to have latency following primary infection. Making it easier for reinfection (epocrates)resulting in release of digestive lysosomal enzymes-Promotion of apoptosis-fuses infected cells to produce multinucleated giant cells-transformation of infectedcells into cancerous cells causing unregulated growth.-alteration of the antigenicproperties, causing the immune system to attack the cell as if it were foreign (page 320).