Pulmonary Paragonimiasis as a Cause of Loeffler's Syndrome

Abstract

Loeffler (1), in 1932, described a new syndrome characterized by fleeting pulmonary infiltrations and eosinophilia of the peripheral blood in association with mild clinical symptoms. The syndrome represents a hypersensitivity reaction of the lungs to various antigens, the most common of which are pollens, drugs, horse serum, and certain helminths (2–10). Some of the pollens which have been implicated as etiologic factors are privet and lily-of-the-valley. The drugs which have been reported as causative agents include penicillin, para-aminosalicylic acid, sulfadiazine, and sulfonamide. There have been reports of cases in patients with trichinosis, influenza, ascariasis, clonorchiasis, strongyloidosis, and brucellosis. A review of the literature failed to reveal any example of Loeffler's syndrome in patients with pulmonary paragonimiasis. The purpose of this report is to describe 3 cases in which pulmonary paragonimiasis is believed to have been the underlying cause of the syndrome. Report of Cases Case I: C. Y. S., a male student, aged 20 years, entered the hospital Feb. 11, 1959, because of dry cough, abdominal distress, and mild diarrhea of one month duration. Physical examination was negative except for slightly diminished breath sounds and a few râles at the left base. The temperature was 38° C., pulse 90, respirations 24. The white cell count was 10,500 to 12,300, with 16 to 39 per cent eosinophils. The sputum showed operculated ova of Paragonimus westermanii; there were no other pathogens. Serum protein was 7.3 gm. per 100 ml.: albumin 38 per cent; alpha globulin 6, alpha-2, 19, beta 14.9, and gamma 24 per cent; A/G ratio 0.61. There were Charcot-Leyden crystals in the sputum. Roentgen examination, Feb. 11, 1959 (Fig. 1), showed a small area of mottled density at the base of the left lung with obscuration of the cardiac apex and costophrenic sulcus. The right diaphragm was elevated and the right costophrenic sulcus obliterated, indicative of an infrapulmonary effusion. On Feb.18 (Fig. 2), the left basal lesion had disappeared; the right diaphragm was still elevated. One month later, there was patchy density in the left upper and mid-lung field and the right hilus shadow was enlarged. On March 31, ill-defined, fluffy densities had appeared in the left mid-lung field and there was fluid at the right base. On April 24 (Fig. 3), extensive mottling was seen at the left base and about the left hilus with fluid rising to the level of the third rib anteriorly on the right. On July 23, multiple ring-like shadows were present in the left lung field, considered typical of pulmonary paragonimiasis. By Aug. 17, 1959 (Fig. 4), the areas of density had decreased bilaterally, with pleural thickening at the right base. The patient was treated with corticosteroids and chloroquine diphosphate and appeared well when discharged from the hospital Aug. 19, 1959.