Seminars in respiratory infections
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Cystic fibrosis (CF) is an autosomal-recessive disorder and affects about 60,000 people worldwide. The CF gene, the cystic fibrosis transmembrane conductance regulator (CFTR), was found in 1989 and over 800 mutations have been sequenced. Although our understanding of the pathophysiology of CF has increased, pulmonary infections remain the major cause of morbidity and mortality. ⋯ However, prophylactic strategies to prevent initial infection or to delay chronic infection with P. aeruginosa or chronic maintenance therapy to slow deterioration of lung function may also improve clinical status. Recognition of the role of inflammation, even early in life, in the absence of clinical symptoms, has led to treatment with anti-inflammatory agents. Novel strategies to disrupt biofilm formation, stimulate chloride conductance, and replace abnormal CFTR are currently being studied.
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The epidemic of pediatric acquired immunodeficiency syndrome (AIDS) in the United States, which peaked during the mid-1980s and early 1990s, was characterized by a variety of opportunistic infections in children infected with human immunodeficiency virus (HIV), often as the presenting illness of their HIV infection. Pneumocystis carinii pneumonia (PCP) during infancy was responsible for significant morbidity and mortality, followed by many other opportunistic infections, including recurrent, serious bacterial infections; disseminated cytomegalovirus infection; and disseminated Mycobacterium avium complex (MAC) infection. ⋯ Far fewer children are at risk for clinical progression of HIV disease and for opportunistic infections. Despite these successful trends, pulmonary opportunistic infections and pulmonary disease remain common clinical manifestations of pediatric HIV disease.
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A variety of antibiotics, both parenteral and oral, are available to the clinician caring for a child with pneumonia. Although viral pathogens are the common etiologic agents causing community-acquired pneumonia, significant morbidity and mortality exists from disease caused by bacteria and atypical pneumonia agents. Treatment of nosocomial bacterial pneumonia has become particularly difficult with ever-increasing resistance documented in hospital-acquired organisms. This article discusses antibiotic therapy based on clinical presentation and based on identified pathogens, with a discussion of mechanisms of antibiotic resistance and the newer agents that have been designed to meet this continually evolving challenge.