Broncholithiasis due to Histoplasma capsulatum Subsequently Infected by Actinomycetes

Broncholithiasis due to Histoplasma capsulatum Subsequently Infected by Actinomycetes

18 Goodwin JS. Immunologic effects of nonsteroidal anti-inftammatory drugs. Am J Med 1984; 77(supplement 4B):7-15 19 Bacon PA. Nonsteroidal anti-infta...

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18 Goodwin JS. Immunologic effects of nonsteroidal anti-inftammatory drugs. Am J Med 1984; 77(supplement 4B):7-15 19 Bacon PA. Nonsteroidal anti-inftammatory drugs and immunologic function: overview of the European experience. Am J Med 1984; 77(supplement 4B):26-31

Broncholithiasis due to Histoplasma capsulatum Subsequently Infected by Actlnomycetes* Larry S. Hirschfield, M.B., B.Ch .;t

L. Michael Graver; M.D., F.C .C .P.;t and Henry D. Isenberg, Ph.D.§

A case of broncholithiasis in which both Histoplasma and actinomycotic organisms were demonstrated is presented. The etiology ofbroncholithiasis is discussed, with particular emphasis on the relationship between the organisms identified. (CheBt 1989; 96:218-219)

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roncholithiasis as originally defined' is an uncommon condition in which a calcified mass is found either within or eroding into the lumen of a bronchus. The source of the calcified mass is usually a lymph node that, foUowing inflammation and necrosis, has undergone dystrophic ~alcification. Aided by constant respiratory movements, the calcified node eventually erodes through the wall of an adherent bronchus. Although theoretically any lesion that calcifies, such as a pulmonary infarction, hematoma, or abscess, could give rise to a broncholith, in practice most cases are caused by lymph nodes involved by an infectious process. The underlying cause is usually tuberculosis or histoplasmosis, although other infectious agents such as Coccidioides, Cryptococcus, Actinomyces, and Nocardia have been considered in the differential etiology. 2 We present a case of broncholithiasis in which both Histoplasma capsulatum and Actinomyces-like organisms were identified by special stains and immunofluorescent techniques on tissue sections. CASE REPORT A 63-ye~old man had a 20-month history of nonproductive cough. He had dated the start of symptoms to cessation of smoking. He related an extensive travel history that included Europe, Hong Kong, Tahiti, and South America, but did not recall any illness. A chest x-ray 61m three months prior to his hospitalization revealed an in6ltrate in the superior segment of the left lower lobe and calci6cation of the lymph nodes in the pulmonary hilum. A onemonth course of oral antibiotics failed to improve his symptoms, and a CT scan of the chest was obtained. This study revealed bronchiectatic changes in the large airways of the superior segment of the left lower lobe with segmental consolidation (Fig 1). There was a small pleural effusion and grouped calci6cations of the lymph nodes surrounding the bronchus to the superior segment and in the hilum. The spleen was also found to contain multiple small calci6c *From Long Island Jewish Medical Center, New Hyde Park, and State University of New York, Stony Brook. tStalf Pathologist, Department of Pathology. :!:Attending Surgeon, Division ofCardio Thoracic Surgery. §Chief, Division of Microbiology. Reprint requests: Dr. Hirschjaeld, lbthology Department, Long Island jewish Medical Center, New Hyde Ebrk, NY 11042

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FIGURE 1. CT of chest showing in6ltrate and bronchiectatic changes of superior segment of left lower lobe. Extensive calci6cation in lymph nodes surrounding the bronchus to the superior segment

(arrows).

densities. A bronchoscopic examination revealed widening of the secondary and tertiary carinae by lymphadenopathy, and an obstructive lesion at the takeoff of the superior segmental bronchus of the left lower lobe. Washings ofthis area revealed only atypical cellular material. A thoracotomy was performed, and the superior segment was resected. At surgery the lobe was densely consolidated and inftamed. The vascular and bronchial structures entering the segment were densely adherent to the local lymph nodes. The patient made an uneventful recovery from this procedure. PATHOLOGY Gross examination of the resected specimen revealed large, calci6ed lymph nodes eroding the main bronchus to the segment of lung. There were, also, multiple small calci6ed nodules within the lung parenchyma and bronchial wall. Extensive bronchiectatic changes and consolidation were associated with the obstructive calci6ed masses. Histologic examination of the larger calculi after decalci6cation showed predominantly necrotic structureless material with calci6cation. Within these necrotic and calci6ed areas, there were zones of suppuration in which typical sulphur granules, containing branching bacteria were identi6ed (Fig 2A). Extensive further sampling revealed rare necrotizing and partially calci6ed granulomas surrounded by palisading histiocytes and Langhans type giant cells. Within the central areas of necrosis numerous budding yeast forms were identi6ed by GMS stain (Fig 2B). The CDC

FIGURE 2 (A). Sulphur granule composed of branching bacteria (PAS x 450). (B). Budding yeast forms of Histoplasma capsulatum (GMS x 450).

Bronc:holllhias

Hlstop/uma capsulatum and Actinomycetes (Hirschfield, Grall!ll; IHflberg)

confirmed a diagnosis of H CG,.,Jatum on the basis of immunofluorescent staining of the yeast forms. The branching bacteria, although members of the order Actinomycetales. could not be identified Immunologically as AcHnomgcea UrGeU or NoctJrdlo IJiferoldu. Culture studies were not helpthl.

'Thlnslent Complete AV Block In Lyme Disease* Electrophyslologlc

Observations

Marcel R. oan dsr Unde, M.D.; Harry JG.M. Crijru, M.D.; and Kong I. lJe, M.D.

DISCUSSION

It is widely accepted that most cases of broncholithiasis result from calcification of lymph nodes following tuberculosis or Histoplasma infection. However, few studies have directly addressed the question of etiology by use of special staining techniques or culture. The inability to demonstrate organisms by these techniques in fact does not exclude infection either, as the broncholith in reality represents the burned out and inactive stage of the disease. In an attempt to define the etiology of broncholithiasis, w,ed and Anderson3 from the Mayo Clinic applied special staining and culture techniques to 12 broncholiths of nine patients with broncholithiasis. Although the culture results were thought to be unhelpful, the special stain findings were of interest. Five stones from five patients contained structures with the morphologic features of H copBUlatum, while eight stones from five patients contained acid-fast branching filaments consistent with N tJBterofdes. In two stones from two patients, structures resembling both Histoplasma and Nocardia were present in generous numbers. The branching organisms that we identified had morphologic features similar to those illustrated by w,ed and Anderson,3 but the acid-fast stain performed by our technique was negative. In addition, we were able to exclude an Actinomyces or Nocardia species on the basis of immunologic techniques applied to tissue sections. Actinomyces and related organisms have a tendency to colonize devitalized tissue, and they have been identified in association with the calcified lymph nodes of tuberculosis. 4 The presence of these Actinomyceslike organisms in both our case and the Mayo Clinic study probably represents a phenomenon of secondary invasion of tissue previously devitalized by earlier Histoplasma infection. The secondary infection may have resulted from bloodhome seeding or aspiration. Only the Actinomyces-like organisms were identified on our initial sections, resulting in the false impression that the broncholiths were caused by these bacteria. Further sections, however, revealed budding yeasts and the true etiology became unmasked. Negative cultures probably were a result of inappropriate collection of specimens. ACKNOWLEDGMENTS: The authors would Uke to thank the Center of Infectious Disases Mycolotw ~ent of the Center for Disease Control, Atlanta, for tlieir help in identifvimr the microorganisms. \1\e are most grateful to Bill Oxberry fOr photographic assistance and Francine \Werio for preparation this manuscript.

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REFERENCES 1 Schmidt HW, Clagett OT, McDonald JR. Broncholithiasis. J Thorac Cardiovasc Surg 1950; 19:226-45 2 Kelley WA. Broncholithiasis. Postgrad Med 1979; 66:81-90 3 \\Mcl LA, Andersen HA. Etiology of broncholithiasis. Chest 1960; 37:?:70. 77 4 Lee BY. Actinomycosis of the lung coexisting with pulmonary tuberculosis. Chest 1966; 50:211-13

1he 6nclings in a patient with complete AV block and intraatrial conduction disturbances due to Lyme disease ue presented. 1he electrocardiographic follow-up and serial EP &ndings suggest that complete AV block in Lyme disease may signify a more extensiw afJection of the AV conduction system (with eventually attendant intra-atrial conduction disturbances) than described in earlier reports. An almost complete resolution of the considerable damage to the conduction system oecurred within two weeks.

(Chm 1989; 96:!19-!1)

T yme disease is nowadays known as an infectious disease L caused by the bite of a tick or a flea, by which the

spirochete, Borrelia burgclorferi, can affect skin, joints, nervous system, and heart. 1.s Although the clinical expression of Lyme disease is highly variable, 1.. the most common and clinically most troublesome cardiac manifestation is AV block. 14 The electrophysiology of AV block in Lyme disease has not received much attention, and serial EP investigations have not, to our knowledge, been performed before. This report describes a patient with Lyme disease in whom complete AV block was the presenting and main clinical problem and in whom the course of the AV (and intra-atrial) conduction disturbances was pursued with surface electrocardiographic follow-up and serial EP investigations. CASE REPORT

A 4o.year-old athlete was admitted to our hospital because of complete AV block of unknown origin, with recurrent dizziness and near collapse, which had been occurring for two days. For three weeks, he had had arthritis-Uke symptoms in the toes of his right foot. No erythema migrans had been noticed. On physical eumination the temperature was normal, the pulse rate was regular at 40 beats per minute, and the blood pressure was 12«V70 mm Hg. There were cannon-wave pulsations in the jugular veins and a &rst heart sound of variable intensity. No pulmonary rales were heard. Four toes of the patients right foot were warm, red, and painful, but not swollen. There were no dermatologic abnormalities. The surface ECG showed complete AV block with an escape rhythm of 37/min; the QRS oon&guration suggested a focus in the left bundle branch. The con&guration of the P wave was abnormal, and its duration was prolonged. In spite of administration of atropine and isoproterenol (isoprenaline~ there were recurrent periods of ventricular asystole, sometimes lasting as long as 10 seconds. The erythrocyte sedimentation rate was 22 mmlh. Other routine laboratory tests yielded normal results. The chest roentgenograms and echocardiogram also proved to be normal. A gallium scan showed difFuse uptalce in the myocardium (Fig 1~ Serologic tests forB burgtlorferi were positive fOr IgM (1:128) and weakly positive for lgG (1:64). Tests for chlamydia and cytomegalo*From the Department of Cardiolotw, Thorucentre, University Hospital Groningen, Groni!lgen, the""Netherlands. Reprint ~: Dr. oan tlir Unde, DeJJartment of Cardlolotz.rJ, ~. Unicernty Ho,ual, 9713 EZ Groningm, NetherltJrlill CHEST I 88 I 1 I JULY, 1888

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