SUPORTED By :

7 Mei 2009

Pneumocystis Pneumonia

English Version

Pneumocystis pneumonia remains the most prevalent opportunistic infection in patients infected with the human immunodeficiency virus (HIV). First identified as a protozoan nearly 100 years ago and reclassified as a fungus in 1988, pneumocystis cannot be propagated in culture. Few treatment options exist for patients with pneumocystis pneumonia. The number of patients who are receiving chronic immunosuppressive medication or who have an altered immune system and are thus at risk for pneumocystis pneumonia is rapidly growing. Although the prevalence of the acquired immunodeficiency syndrome (AIDS) has decreased in the Western hemisphere owing to the routine use of highly active antiretroviral therapy (HAART), many patients worldwide do not have the resources for HAART. The increased reservoir for infection among such patients leads to concern that resistance to trimethoprimsulfamethoxazole, the most common treatment for pneumocystis pneumonia, will emerge, although this has yet to happen. The application of molecular techniques to the study of pneumocystis has provided new insights into the complex cell biology of this fungus. In this article we summarize advances that have resulted from studies of the cell biology, biochemistry, and genetics of pneumocystis in the past several years and include recommendations for the diagnosis of pneumocystis pneumonia, as well as for prophylaxis and treatment.

Clinical Features of Pneumocystis Pneumonia

Pneumocystis pneumonia is often the AIDS-defining illness in patients infected with HIV, occurring most frequently when the T-helper cell count (CD4+) is less than 200 cells per cubic millimeter. Common symptoms of pneumocystis pneumonia include the subtle onset of progressive dyspnea, nonproductive cough, and low-grade fever. Acute dyspnea with pleuritic chest pain may indicate the development of a pneumothorax. Physical examination typically reveals tachypnea, tachycardia, and normal findingson lung auscultation. Patients with AIDS and pneumocystis pneumonia have a significantly increased number of pneumocystis organisms in their lungs, with fewer neutrophils, than do patients with pneumocystis pneumonia in the absence of AIDS. This greater organism burden results in a higher diagnostic yield of induced sputum and bronchoalveolar lavage fluid to confirm pneumocystis pneumonia in patients with AIDS as compared with other conditions associated with immunosuppression. The smaller number of inflammatory cells in patients with AIDS-related pneumocystis pneumonia also correlates with better oxygenation and survival as compared with pneumocystis pneumonia in patients without AIDS.

Patients with mild symptoms of pneumocystis pneumonia can often be treated as outpatients with the use of oral therapy and close follow up. However, patients with significant hypoxemia should be hospitalized for the administration of intravenous therapy. The development of worsening pneumonia with respiratory failure in these patients is the most common reason for admission to an intensive care unit. Among most patients with AIDS and pneumocystis pneumonia, the mortality rate is 10 to 20 percent during the initial infection, but the rate increases substantially with the need for mechanical ventilation.

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