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Chapter 230 Histoplasmosis (Histoplasma capsulatum)
Jane M. Gould, Stephen C. Aronoff
Histoplasmosis is caused by Histoplasma capsulatum, a dimorphic fungus found in the environment as a saprophyte in the mycelial (mold) form and in tissues in the parasitic form as yeast.
The saprophytic form is found in soil throughout the midwestern USA, primarily along the Ohio and Mississippi rivers. Sporadic cases of human and animal histoplasmosis have been reported from 31 of the 48 contiguous states. In parts of Kentucky and Tennessee, almost 90% of the population >20 yr of age have positive skin test results for histoplasmin. Histoplasma is endemic to parts of the Caribbean islands, Central and South America, certain areas of Southeast Asia, and the Mediterranean. H. capsulatum thrives in soil rich in nitrates such as areas that are heavily contaminated with bird or bat droppings or decayed wood. Fungal spores are often carried on the wings of birds. Focal outbreaks of histoplasmosis have been reported after aerosolization of microconidia resulting from construction in areas previously occupied by starling roosts or chicken coops or by chopping decayed wood. Unlike birds, bats are actively infected with Histoplasma. Focal outbreaks of histoplasmosis have also been reported after intense exposure to bat guano in caves and along bridges frequented by bats. Person-to-person transmission does not occur.
Inhalation of microconidia (fungal spores) is the initial stage of human infection. The conidia reach the alveoli, germinate, and proliferate as yeast. Alternatively, spores can remain as mold with the potential for activation. Most infections are asymptomatic or self-limited. When disseminated disease occurs, any organ system can be involved. The initial infection is a bronchopneumonia. As the initial pulmonary lesion ages, giant cells form, followed by formation of caseating or noncaseating granulomas and central necrosis. Granulomas contain viable yeast, and disease can relapse. At the time of spore germination, yeast cells are phagocytosed by alveolar macrophages, where they replicate and gain access to the reticuloendothelial system via the pulmonary lymphatic system and hilar lymph nodes. Dissemination with splenic involvement typically follows the primary pulmonary infection. In normal hosts, specific cell-mediated immunity follows in approximately 2 weeks, enabling sensitized T-cells to activate macrophages and kill the organism. The initial pulmonary lesion resolves within 2-4 mo but may undergo calcification resembling the Ghon complex of tuberculosis. Alternatively, “buckshot” calcifications involving the lung and spleen may be seen. Unlike tuberculosis, reinfection with H. capsulatum occurs and can lead to exaggerated host responses in some cases.
There are 3 forms of human histoplasmosis: acute pulmonary infection, chronic pulmonary histoplasmosis, and progressive disseminated histoplasmosis.
Acute pulmonary histoplasmosis follows initial or recurrent respiratory exposure to microconidia. The majority of patients are asymptomatic. Symptomatic disease occurs more often in young children; in older patients, symptoms follow exposure to large inocula in closed spaces (e.g., chicken coops or caves) or prolonged exposure (e.g., camping on contaminated soil, chopping decayed wood). The median incubation time is 14 days. The prodrome is not specific and usually consists of flulike symptoms including headache, fever, chest pain, cough, and myalgias. Hepatosplenomegaly occurs more often in infants and young children. Symptomatic infections may be associated with significant respiratory distress and hypoxia and can require intubation, ventilation, and steroid therapy. Acute pulmonary disease can also manifest with a prolonged illness (10 days to 3 wk) consisting of weight loss, dyspnea, high fever, asthenia, and fatigue. In 10% of patients, infection is a sarcoid-like disease with arthritis or arthralgia, erythema nodosum, keratoconjunctivitis, iridocyclitis, and pericarditis. Pericarditis, with effusions both pericardial and pleural, is a self-limited benign condition that develops as a result of an inflammatory reaction to adjacent mediastinal disease. The effusions are exudative, and the organism is rarely culturable from fluid. Most children with acute pulmonary disease have normal chest radiographs. Patients with symptomatic disease typically have a patchy bronchopneumonia; hilar lymphadenopathy is variably present. In young children, the pneumonia can coalesce. Focal or buckshot calcifications are convalescent findings in patients with acute pulmonary infection.
Exaggerated host responses to fungal antigens within the lung parenchyma or hilar lymph nodes produce thoracic complications of acute pulmonary histoplasmosis. Histoplasmomas are of parenchymal origin and are usually asymptomatic. These fibroma-like lesions are often concentrically calcified and single. Rarely, these lesions produce broncholithiasis associated with “stone spitting,” wheezing, and hemoptysis. In endemic regions, these lesions can mimic parenchymal tumors and are occasionally diagnosed at lung biopsy. Mediastinal granulomas form when reactive hilar lymph nodes coalesce and mat together. Although these lesions are usually asymptomatic, huge granulomas can compress the mediastinal structures, producing symptoms of esophageal, bronchial, or vena caval obstruction. Local extension and necrosis can produce pericarditis or pleural effusions. Mediastinal fibrosis is a rare complication of mediastinal granulomas and represents an uncontrolled fibrotic reaction arising from the hilar nodes. Structures within the mediastinum become encased within a fibrotic mass, producing obstructive symptomatology. Superior vena cava syndrome, pulmonary venous obstruction with a mitral stenosis–like syndrome, and pulmonary artery obstruction with congestive heart failure have been described. Dysphagia accompanies esophageal entrapment, and a syndrome of cough, wheeze, hemoptysis, and dyspnea accompanies bronchial obstruction.
Chronic pulmonary histoplasmosis is an opportunistic infection in adult patients with centrilobular emphysema. This entity is rare in children.
Progressive disseminated histoplasmosis
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