Seminars in respiratory infections
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Semin Respir Infect · Sep 1990
ReviewHost responses in mediating sepsis and adult respiratory distress syndrome.
Despite significant advances in intensive care unit technology and mechanical ventilatory support, mortality due to adult respiratory distress syndrome (ARDS) or multiorgan failure (MOF) has not changed significantly within the past two decades. The key to improving survival requires understanding and modifying (or eliminating) factors that may initiate (or modulate) these syndromes. Infection, and the host responses to infection, are major etiological factors responsible for the induction and perpetuation of the injury to the lung and microvasculature in ARDS and MOF, and contribute to late mortality. ⋯ Interactions between these humoral and cellular mediators appear to set in motion an amplified cascade of events culminating in cellular and tissue injury. In this article, several of these putative inflammatory mediators are discussed in detail, and the importance of cytokine networking and the possible role of nonimmune cells in the orchestration of the inflammatory response associated with ARDS and MOF are explained. Finally, future therapeutic strategies aimed at blocking or suppressing the release or effects of endogenous mediators may be the key to improving the outcome of these disorders.
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Nosocomial infections with respiratory tract viruses, particularly influenza and respiratory syncytial viruses, account for the majority of serious nosocomial viral disease. Chronically ill, immunocompromised, elderly, and very young hosts are especially vulnerable to potentially life-threatening involvement of the lower respiratory tract. ⋯ Transmission of respiratory syncytial virus, in contrast, seems to require closer contact, with virus passed on hands, fomites, or in large droplets inoculated into the eyes and nose at close range. Strategies for control of nosocomial respiratory syncytial virus are designed to interrupt hand carriage and inoculation of virus onto mucous membranes.
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Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis, and Cryptococcus neoformans can cause acute community-acquired pneumonia. All are soil-dwelling fungi and disturbance of contaminated soil is necessary for infection in man. Each has particular epidemiologic considerations that may offer a clue to diagnosis, but the clinical presentation is not sufficiently characteristic to be of diagnostic help. ⋯ Serodiagnosis also takes several weeks and is usually not helpful while the patient is symptomatic. Treatment may not be necessary unless the patient is immunosuppressed, seriously ill, or has life threatening complications. The primary pulmonary infection may disseminate to extrapulmonary sites, which always requires treatment.
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A wide variety of noncytotoxic drugs, including antibiotics, analgesics, narcotics, and psychotrophic and cardiovascular agents, may cause lung injury accompanied by roentgenographic infiltrates. The clinical manifestations of drug-induced lung disease are protean. ⋯ Finally, some drugs may cause insidiously progressive pulmonary infiltrates that share features with granulomatous infections. The more common drug reactions are discussed in this review, and, although the features of drug-induced lung disease are often relatively nonspecific, those features that either mimic infectious causes or may be helpful in differentiating these processes from infections are given particular emphasis.
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Pulmonary vasculitis is usually caused by one of three disorders: (1) Wegener's granulomatosis (WG); (2) Churg-Strauss syndrome (CSS), or allergic angiitis and granulomatosis; or (3) a nonspecific small vessel systemic necrotizing vasculitis (SNV), or microscopic polyarteritis. WG, the most common cause of lung vasculitis, has features of a granulomatous vasculitis of the upper airway and lung and widespread small vessel vasculitis involving the kidneys and other organs. The features of pulmonary WG overlap with those of malignancy and infectious granulomatous lung disease; accurate diagnosis generally requires open lung biopsy. ⋯ Nonspecific SNV causes diffuse alveolar hemorrhage due to pulmonary capillaritis. Concomitant segmental necrotizing glomerulonephritis is almost always present. Diagnosis is made by renal biopsy, compatible extrarenal features, exclusion of nonimmune causes of lung hemorrhage, and exclusion of WG to the extent possible.