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Case report |
1Lysholm Department of Radiology, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG, 2Hospital for Tropical Diseases, Mortimer Market, London WC1E 6AU and 3Department of Radiology, University College London Hospital, Grafton Way, London WC1E 3BG, UK
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Introduction |
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Case history |
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The only abnormality on clinical examination was a non-specific erythematous truncal rash. Urine analysis at this time showed no red blood cells, and no parasites were identified on urine or stool microscopy. Full blood count showed an eosinophilia (1.6 x 109 l-1). There was no evidence of malaria on a blood film and biochemical indices of hepatic and renal function were normal. An ELISA for schistosomal antibody was not available at the time of initial consultation but was subsequently found to be positive at level 2. Contact with the patient was temporarily lost and she was reviewed after 2 months.
During the intervening period she experienced malaise and a persistent dry cough. On repeat testing her eosinophil count had increased to 2.1 x 109 1-1 and the ELISA was more strongly positive at level 4. A chest radiograph showed widespread, poorly-defined nodules, approximately 1 cm in diameter, with focal areas of ground-glass shadowing (Figure 1
). HRCT demonstrated widespread, ill defined nodules in a predominantly peribronchovascular and subpleural distribution, many with extensive "halos" of ground-glass opacification (Figure 2). There were no pleural effusions or hilar lymphadenopathy. Limited images of the liver and spleen acquired during imaging of the thorax were normal.
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Discussion |
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The history of exposure to infected water, the unequivocally positive serology using an IgG ELISA test, which has a specificity in excess of 97% for current infection in a non-endemic population [3], and the brisk response to treatment support the diagnosis of acute schistosomiasis, in this case almost certainly with S. haematobium. The patient's initial febrile illness with a rash and eosinophilia is typical of early schistosomal infection (Katayama syndrome), although the onset of cough in this case was late and unusually prolonged. The chest radiograph appearances were relatively non-specific but did not demonstrate the peripheral pulmonary opacification usually seen with eosinophilic lung disease. Appearances on HRCT were consistent with widespread haemorrhagic nodules. The radiological differential diagnosis for haemorrhagic nodules includes fungal infection, cytomegalovirus, herpes, intrapulmonary lymphoma, Kaposi's sarcoma, septic emboli and Wegener's granulomatosis [4–8]. No risk factors for immunosuppression could be identified and there was no cavitation of lesions to suggest septic emboli as a cause. The most common CT finding in an eosinophilic vasculitis such as Churg–Strauss syndrome is random or peripheral parenchymal opacification, although pulmonary nodules have been reported in this condition, which cannot be excluded on radiological grounds alone [9]. The clinical features and serology in this case suggested that the CT appearances were owing to pulmonary schistosomiasis. They would be in accord with the known pathophysiology of granulomatous pulmonary schistosomiasis, a granulomatous pulmonary arteritis, although this is normally considered to be a feature of long-standing disease.
As schistosomiasis is common in travellers returning from East Africa, is known to cause pulmonary arteriolar disease and is readily treatable, the patient was treated with praziquantel before embarking on further investigations, which would have included lung biopsy.
Although histological confirmation of pulmonary involvement was not obtained in this case of serologically-proven schistosomiasis, the radiological features, together with the rapid resolution of pulmonary symptoms and normalization of eosinophilia and parasite serology following treatment, strongly support this diagnosis.
Pulmonary manifestations of schistosomiasis
The type and severity of pulmonary involvement in schistosomiasis depends on the species, the parasite load, the host immune response and the stage of infection. Schistosoma haematobium, S. mansoni and S. japonicum have different patterns of organ involvement and are endemic to different geographical areas. The clinical, radiological and pathological features of acute infection and of chronic stable disease are well described. The intervening phases are less well understood. Due to the complexity of the life cycle of the parasite within the human host, the patterns of lung involvement are potentially confusing.
Acute lung disease
Invasion of migrating schistosomules (larvae) may cause a transient pneumonitis (Loeffler's syndrome). The development of adult worms in the next 2–4 weeks results in an acute sensitization process, which may cause acute damage to the lung and manifest clinically as the "Katayama syndrome" of fever, cough/wheeze and erythematous rash accompanied by eosinophilia. Rigors, headache, lymphadenopathy and hepatosplenomegaly may also occur. This manifestation of acute infection with S. haematobium is recognized in visitors to endemic areas, but is rarely seen in the indigenous population [10] and is self-limiting. The inflammatory reaction in the lungs is thought to be a form of allergic alveolitis, with high levels of circulating immune complexes and eosinophilia [11, 12]. Radiological appearances are typically transient micronodular infiltrates and, less frequently, alveolar consolidation. A recent series of cases of S. mansoni in Brazil found bronchial wall thickening to be the most frequent finding on plain chest radiographs [13].
Subacute lung disease
Worms migrate from the portal vessels to the favoured site of egg laying, depending on the species. Eggs migrate against the venous flow into the tissues drained by the vein, where they excite a vasculitic reaction and granuloma formation. In S. haematobium infection it is thought that eggs and/or worms may also embolise to the pulmonary arterioles as well as into the lung parenchyma. A granulomatous reaction results, which may be diffuse or localized; the foci of inflammation may be large enough to simulate lung neoplasm radiologically [14]. This process may be asymptomatic or, if large scale embolisation occurs, may result in cough, hypoxaemia and pulmonary oedema, which is occasionally severe and fatal. Chest radiographs may show dense patchy infiltrates, sometimes with pleural effusions [15].
Treatment may generate a reactionary pneumonitis. Dying eggs and worms in the lungs provoke inflammation, characterized by fever, dry cough and wheeze, sometimes accompanied by a blood eosinophilia [16]. Radiologically, new pulmonary infiltrates may be seen. Sometimes, approximately 2 weeks after treatment, acute pneumonia can occur. This is thought to be caused by paralysed adult worms that have lost their hold in the pelvic veins and embolised to the lungs.
Chronic lung disease
Interstitial or granulomatous pulmonary schistosomal disease ("pulmonary granulomatous schistosomiasis" and "miliary pulmonary schistosomiasis") corresponds to a granulomatous vasculitis excited by widespread deposition of ova within the pulmonary vasculature. In S. haematobium infection, this results from sustained and heavy embolisation of ova from the vesical plexus to the lungs [17].
In S. mansoni and S. japonicum, ova from the adult worms living in the mesenteric veins are deposited in intrahepatic portal venules and cause granulomata, portal occlusion and ultimately, over many years, fibrosis leading to portal hypertension. Portosystemic shunting then allows ova to pass directly to the lungs and 26% of patients with advanced hepatosplenic disease go on to develop interstitial pulmonary schistosomiasis [18].
Radiographic appearances are of interstitial infiltrates, typically nodular or micronodular, and there may be frank fibrosis. Radiographic patterns that mimic acute tuberculosis and lung neoplasms have also been reported [19]. CT appearances have been correlated with histopathological appearances in chronic stable lung involvement with S. mansoni [20]. Pulmonary hypertension develops in 7–23% of patients with chronic pulmonary schistosomal disease, owing to granulomatous endarteritis that causes progressive obliteration of pulmonary arterioles and capillaries, and leads to secondary fibrotic changes in the lung parenchyma, often over decades. The most common clinical manifestation of chronic lung disease is dyspnoea and reduced exercise tolerance, but severe hypoxaemia, chest pain and digital clubbing may also be found. Cor pulmonale develops in 5% of patients [20].
This case shows some unusual features that do not fit into the established categories of either acute or chronic pulmonary schistosomiasis. Although the patient initially presented in Africa with typical Katayama syndrome, persistence of the cough, positive serology and the radiographic appearances at the time of her subsequent presentation in the UK represent a subacute stage of infection. The radiological appearances could be due to widespread granulomatous pulmonary schistosomiasis that, in this case, are likely to have resulted from substantial embolisation of S. haematobium eggs from the venous plexus of the bladder. This particular pattern of lung infiltration, however, is more usually described in long-standing interstitial pulmonary disease. It is unclear whether persistent pulmonary disease in early schistosomiasis is unusual or underdiagnosed. To our knowledge the HRCT appearances associated with early infection have not been described previously.
Schistosomiasis should be considered in the differential diagnosis of pulmonary nodules on chest imaging in patents with a history of exposure. A chest radiograph should be performed in patients with respiratory symptoms and/or signs, especially persistent cough. Early treatment of pulmonary schistosomiasis is important to prevent the development of severe and irreversible parenchymal damage.
Received for publication October 25, 2000. Revision received July 10, 2001. Accepted for publication July 13, 2001.
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