Document oDQ9reEr63mBExdqyb5dmQG93

380 0. A. SANDER size on successive films. Ultimately central rarefaction, interpreted as,c may develop with subsequent evidence of infection in other parts'fjl, Gardner44 presents the following working hypotheses with regard,t'dJcql" lesions: .A 1. In silicotuberculosis the infection may heal so completely that its tub&r is no longer recognizable. Such an outcome has been observed in experimentai'ant to ferruginous chert and infected with attenuated tubercle bacilli. 2. Conglomerate lesions in the upper lung fields, particularly when theS^t are in the great majority of cases due to an underlying tuberculosis in healed'pifllljg In persons not exposed to dust, bilateral disease in this location proves to be tuof_ to 98 cases out of every hundred, and even unilateral disease can safely be const culous in 90 per cent of cases. i# 3. Large isolated or bilaterally symmetrical conglomerations in the lower lun|s considered tuberculous unless this origin can be excluded. In that case the pci* organizing pneumonia due to Friedlander's bacillus or other organisms should reef eration, 4. The character of the fibrosis resulting from the combined activity of 'aj organism and silica dust with or without other minerals may suggest a relatibi the time of exposure to dust and the development of the infection. . ;JJ8 (a) When the silicosis is already established before tuberculosis supervenes!!- localizes in and about the nodules which retain their form but increase in sizeiliSfl struction caused by the injection may produce widespread atelectasis with aho: proximation of the nodules in the involved area. In such cases the outlines of --= nodules in the resultant conglomeration are distinct and clearly defined. ''fit (b) When silicosis and chronic tuberculosis have developed simultaneously character of the conglomerate fibrosis is less obvious. Nodules are present but|tl rounded by a matrix of more diffuse fibrosis produced by the action of th|^p5! organizing pneumonic process. .' ,'^af (c) When the scars of a healed infection are already present before empfo' dusty industry, the inhaled particles accumulate in particularly large quantities'll mediate vicinity. Continued accumulation in the localized area produces manylno are small because they are closely packed together but typically Bpherical ii'ifutk there is no activity in the underlying infectious process to produce diffuse fibroticVe Many patients with conglomerate silicotic fibrosis are dyspneic,.bif symptoms of the associated infection may be absent. This is re'asbnai healed tuberculosis does not cause symptoms and even active infection so well encapsulated by dense fibrous tissue that no tissue reaction is jMslifi1 ,r. SiUcotiibercidosis^ '}:- ;k'M - The relationship between silica exposure and the development ofJpi has been well demonstrated in the United States as well as in .other countsi; there.has-been such exposure-Qne of -the most -remark-gbtgf&moffStfat^' relation of tuberculosis to silica dust exposure is found in the work.ofj''ifI^ dato,45 illustrated graphically in Figure 11. '+ "L. U. Gardner, "Pathological Anatomy," in B. E. Kuechle, ed,, FourthSa lory Symposium on Silicosis. Employers Mutual Liability Insurance, Wausau,-*It is /f11* 18 A. Mavrogordato, Pub. S. African Inst. Med. Research, Report No. 19u liUt))*, PULMONARY DUST DISEASES 381 fc:. Figure 11. Dust control and silicosis in South Africa. Sfe^iptomatology and clinical findings in silicosis and in silicosis compliIS^SulVeilulosis (Figure 12) have been summarized in the National Silicosis nf the C.nmmittee on Medical Control and these have been as follows: SYMPTOM'S: Dyspnea. The complaint most frequently mentioned is Depending upon the extent of the involvement, this varies from slight mpmsfip <Jt. ffipfvjS-i-V i^ressive silicotuberculosis and emphysema, with tubercle bacilli never found a*,and gastric cultures. Marked dyspnea and impaired lung function. Patient it heart failure.