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Imaging Diagnosis

The chest radiograph may initially suggest interstitial edema. However, close inspection can reveal multiple, diffuse, tiny nodules 2-3 mm in size. Other patients may demonstrate miliary nodulation with patchy opacification which is ill-defined and nonsegmental (Fig.26.36). Over days to weeks the radiographic findings may be quite variable, with transient shifting opacities which are ill-defined. This is similar to Loffler's pneumonia. A few septal (Kerley B) lines may be seen, and in patients with severe coughing, there may be rib fractures. Pleural effusions and mediastinal lymphadenopathy do not occur.


Fig. 26.36A-C. Tropical pulmonary eosinophilia. Chest radiographs in three patients showing different patterns. A Bilateral diffuse bronchopneumonia that is asymmetrical and greater in the left lung. The patient had a cough and minimal sputum. The eosinophil count was over 6,000 cells/mm≥. The lungs cleared with antifilarial drugs. B A patient from southern India with bilateral diffuse miliary nodules. Her absolute eosinophil count was greater than 5,000 cells/mm≥. C Another southern Indian patient showing more of a reticulonodular pattern. (Courtesy of Dr. G. Gajaraj, Madras) The end result of pulmonary eosinophilia may be quite marked interstitial fibrosis.

Differential Diagnosis

Even when there is a hypereosinophilia and high IgE, several helminth infections must be considered, including schistosomiasis, ascariasis, strongyloidiasis, and paragonimiasis. Viral, tuberculous, and mycotic infection or allergy can all present with a miliary pattern, although these entities may be associated with mediastinal lymphadenopathy, which is absent in TPE. Filarial serology (together with a persistent high eosinophilia) is most helpful in narrowing the diagnostic possibilities. A good clinical response to diethylcarbamazine would confirm filarial etiology, but this would be contraindicated in regions of endemic onchocerciasis because of the risk of a severe Mazzotti reaction.


Many other animals (apart from humans) are also infected with a variety of filarial parasites. Rarely, man becomes an accidental host of these infections. The most important example is the dog heartworm infection caused by the filarial parasite Dirofilaria immitis. This filaria was first found in 1887, when deMagalhaes noted male and female worms in the left ventricle of a Brazilian boy. Pulmonary infection was not reported until 1961, but since then there have been over 80 reported cases. This parasite of dogs is found throughout the world in tropical and temperate climates. It is uncommon in England and northern Europe, more common in southern Europe. The majority of human infections are found in the United States, Japan, and Australia. Rarely, other dirofilariae have been reported in man.

Dog to dog transmission occurs following the bite of a mosquito vector containing infective third-stage larvae. The tiny larvae burrow through subcutaneous tissue, pass into venous blood, and molt twice before finally reaching the adult stage in the dog's heart. The development in dogs takes 3-6 months, often with large numbers of worms found within the right ventricle (Fig.26.37). Following mating, the larger female worms (25-30 cm long and 1-2 mm in diameter) release large numbers of microfilariae in the dog's blood. Once these microfilariae are ingested by a suitable mosquito, further molting and development is necessary to again produce infective third-stage larvae in the mosquito vector. The parasites are then transmitted to the next dog host, completing the life cycle. In the coastal areas of the southern United States dogs used to hunt without chemoprophylaxis may not survive a second season of work due to a high worm burden and subsequent congestive heart failure.

Fig. 26.37A,B. Dirofilariasis. A Adult worms within right ventricle of a canine heart. B Dirofilaria immitis removed: there are at least four adult worms.

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