Abstract

According to Strong (10), the genus Torula consists of an “ill-defined group of yeast-like fungi with pathogenic properties … in which the organisms reproduce only by budding, do not produce mycelium or endospores, and do not ferment carbohydrates. They rarely if ever cause lesions of the skin, but appear to have definite affinities for the tissues of the central nervous system and the lungs, though they may produce destructive granulomatous lesions in other organs of the body. The respiratory tract is regarded as the probable portal of entry. “Freeman (1931) collected a number of cases of central nervous system involvement, which suggested neoplasm or encephalitis, but were associated with the presence of yeast-like organisms, Torula histolytica. “Dodge has called this organism Cryptococcus histolyticus.” Review of Literature Levin (6), in 1937, reviewed 60 cases of Torula histolytica infection of the central nervous system. In 9 of these cases, lung involvement was also reported; 8 of the 60 cases were of generalized torulosis; in one of these the lung was apparently not involved. Thirty-seven of the 60 cases were diagnosed antemortem, but in no instance was the diagnosis made from the lung lesion. Binford (1), in 1940, supplemented Levin's collected series with a summary of 14 additional cases reported in the literature, in 5 of which either the organism or a Torula granuloma was found within the thoracic cage. Reeves, Butt, and Hammack (8), in 1941, added 6 more cases, bringing the total number collected to 80. In one of their patients, seen because of symptoms referable to the central nervous system, a large Torula granuloma was found in the lung and the diagnosis was made from purulent fluid aspirated from the chest. Treatment was with potassium iodide, sulfapyridine, and undenatured Torula antigen No. 1 (Krueger); in April 1940, two and one-half years after the onset of symptoms, the patient was still living, though organisms were obtainable from the spinal fluid. During this time there had been noteworthy regression of the pulmonary lesion. In 1943 Burger and Morton (2) again reviewed the literature, collecting about 100 cases, to which they added 4 cases of their own. They did not report the incidence of lung involvement in the isolated cases published (and reviewed by them) since Reeves, Butt, andHammack's article (8). One of their own patients was found to have “chronic bronchitis and bronchiectasis; confluent lobular pneumonia with bronchogenic abscesses, right lower lobe.” Otherwise, no evidence of lung involvement was demonstrated in their 4 cases. Lung involvement alone is rare, having been reported in one case by Sheppe (9) (though the central nervous system was not examined postmortem) and in one case by Hardaway and Crawford (4), in which during fifteen months' observation no central nervous system symptoms developed, though a roentgenogram of the chest showed persistent parenchymal involvement.

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