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Differential Diagnosis

The pulmonary lesions are most commonly mistaken for tuberculosis (in some series in about half the patients). Indeed, tuberculosis is common in countries where paragonimiasis is endemic. Clinically, the usual healthy state of the average patient with paragonimiasis may allow differentiation from tuberculosis. Radiographically, pulmonary infiltrates in paragonimiasis are usually poorly-defined airspace consolidations (cotton wool opacities) that change rapidly with time, whereas infiltrates in tuberculosis are nodular lesions that change slowly. Cysts in paragonimiasis invariably have a smooth inner margin and a thin wall, with a typical ring shadow. Nodular opacities adjacent to the cysts are unusual. However, cavities in tuberculosis commonly show thicker and irregular walls, and small nodular opacities are common adjacent to the cavity, representing endobronchial spread of tuberculosis. The Paragonimus cysts have a tendency to occur in groups of three or more, often found in association with tortuous worm tracts or tunnels, the diameters of which are usually greater than the adjacent bronchi. After treatment, residual fibrosis and emphysematous change are minimal or absent in paragonimiasis, whereas these findings are usual in tuberculosis.

Subpleural linear opacities, representing worm migration tracts or peripheral atelectasis, are common in paragonimiasis, especially in the early stage, and are unusual in tuberculosis. The lesions of paragonimiasis are more peripherally located and much more common in the midlung and lower lung zones as opposed to the predominant apical location of tuberculous cavities. Hilar and mediastinal lymphadenopathy is virtually absent in paragonimiasis, whereas it is often seen dramatically in primary tuberculosis. In patients with pleurisy the amount of pleural fluid is usually less in paragonimiasis than in tuberculosis, although pneumothorax is more common in the former. Residual pleural fibrosis is absent or minimal in paragonimiasis, whereas it is a very common sequel in tuberculosis.

The lesions of paragonimiasis may be differentiated from bronchiectasis by virtue of their more peripheral location, absence of fluid levels, and the fact that the surrounding reaction is usually less transient and less marked than the pneumonitis that may develop in association with bronchiectasis. Paragonimiasis chiefly affects bronchioles. The cyst may communicate with a small or medium bronchus (Figs. 22.31 & 22.34) and the patient will expectorate eggs in the sputum. However, it is unlikely that bronchiectasis will develop in the absence of secondary infection. The wall of a Paragonimus cyst does not become as thick or irregular as occurs in a lung abscess. Lung abscesses are usually larger and there is greater surrounding parenchymal reaction, at least initially. If a nodular pattern predominates in the second stage of paragonimiasis, the disease may be mistaken for other causes of granulomatous disease.

CT or MRI findings of multiple conglomerate ring-enhancing lesions (grape-cluster appearance) strongly suggests early active cerebral paragonimiasis, particularly when observed in an endemic area. If there are no intervening normal brain tissues among the conglomerate granulomas, the lesion may be mistaken for a single lobulated neoplasm with multifocal necrotic centers. If it has the appearance of a small enhancing ring, differentiation from other granulomas such as tuberculoma, or from cysticercosis in a degenerating stage, or from abscess is impossible. The anti-Paragonimus antibody (IgG) test by ELISA is helpful in differential diagnosis (Chang et al, 1991; Cha et al, 1994).

In the chronic inactive stage of cerebral paragonimiasis, the calcified lesions may be mistaken for cysticercosis, tuberculosis, or other chronic inflammations, unless the characteristic conglomerate and soap-bubble appearances are identified on plain film radiography, CT or MR imaging (Kadota et al, 1989; Chang et al, 1991, 1993).

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