Vol. 299 No. 22
CORRESPONDENCE
LEGIONNAIRES' DISEASE AND OTHER CAUSES OF INTRA-ALVEOLAR PULMONARY FIBROSIS To the Editor: The case report in the August 17 issue of the Jo0umal (Case 32-1978) gives the impression that the very striking pattern of fibrosis involving alveolar ducts was caused by Legionnaires' disease. The evidence that the patient had that disease is excellent, but we believe it is doubtful whether it caused the lesions found in the biopsy. Fibrosis in this peculiar pattern was described several years ago and was identified as being associated with progressive respiratory distress.' We have recently completed a review of pulmonary morphology at autopsy in some 59 cases of adult respiratory-distress syndrome collected during a multihospital co-operative project.2 A preliminary report on the morphology3 contains several illustrations of fibrotic alveolar ducts, all from patients with processes other than Legionnaires' disease. In the complete series every one of the 25 patients who survived two or more weeks from the onset of respiratory distress had this pattern of fibrosis. Underlying original diseases in these patients ran the usual gamut of processes that commonly precede the onset of the syndrome.4 Thus, the lesion is surely not specific for a late phase of an infection. In the present case, it should be recalled that the original consolidated area was the left lower lobe rather than the lingula that was biopsied. The biopsy was done on the 16th day after the onset of respiratory distress - well within the time span noted above. The inability to demonstrate organisms in the biopsy, despite application of all the available technics, supports the concept that the lesion was not caused directly by the infection. The mechanism by which this fibrotic lesion is produced in the course of adult respiratory distress remains to be established, although one of us has presented reasons to suspect that it is largely a result of oxygen toxicity.3 Survival after reaching the severity of involvement shown in this case is unusual, but has been reported.5
Durham, NC 27710
PHILIP C. PRATT, M.D. JAMES D. CRAPO, M.D. Duke Medical Center
1. Orell SR: Lung pathology in respiratory distress following shock in the adult. Acta Pathol Microbiol Scand [A] 79:65-76, 1971 2. Blake LH: Goals and progress of the National Heart and Lung Institute Collaborative Extracorporeal Membrane Oxygenation Study, Artificial Lungs for Acute Respiratory Failure. Edited by WM Zapol, J Qvist. New York, Academic Press, 1976, pp 513-524 3. Pratt PC: Pathology of the adult respiratory distress syndrome, The Lung: Structure, function and disease. Vol. 19. Edited by WM Thurlbeck. Baltimore, Williams & Wilkins, 1978, pp 43-47 4. Petty TL, Ashbaugh DG: The adult respiratory distress syndrome: clinical features, factors influencing prognosis and principles of management. Chest 60:233-239, 1971 5. Lamy M, Fallat RJ, Koeniger E, et al: Pathologic features and mechanisms of hypoxemia in adult respiratory distress syndrome. Am Rev Respir Dis 114:267-284, 1976
The above letter was referred to one of the discussers of the case in question, who offers the following reply: To the Editor: Within the past few years two Case Records of the Massachusetts General Hospital have shown a pattern of pulmonary fibrosis similar to that observed in the case of Legionnaires' disease referred to by Drs. Pratt and Crapo. The first1 was in a woman who was placed on extracorporeal membrane oxygenation for adult respiratory-distress syndrome that was probably secondary to viral pneumonia. She was one of 15 patients dying at this hospital after extracorporeal membrane oxygenation whose lungs we have examined, and the histology illustrated in the Case Record was typical of the group as a whole. The second Case Record2 was a woman in whom adult respiratory-distress syndrome developed after massive trauma. These two previously published cases serve to illustrate that a pathological diagnosis of pulmonary fibrosis within alveolar ducts is no more specific than a clinical diagnosis of adult respiratory-distress syndrome in defining the cause. My statement that most examples of massive intra-alveolar fibrosis at this institution have been secondary to a previous infectious episode was not
1255
meant to include or exclude any of the various pathogenetic mechanisms that may be responsible for the fibrosis; I made no statement on causality. The data on the complete series of 25 patients with respiratory distress, referred to by Pratt and Crapo, are unfortunately unavailable in the literature for review. The article that they refer to as displaying the gamut of processes that commonly precede the onset of the adult respiratory-distress syndrome3 details three cases, one of smoke inhalation, one of drug intoxication and one of bronchopneumonia. In a more recent report of 15 original cases,4 eight were associated with sepsis, and an additional two patients had burns covering half the body surface. The remaining five had obvious massive trauma. The relative frequency of the various events that are known to trigger the adult respiratory-distress syndrome will obviously depend on the type of medical center in which one works, but infection is certainly a factor in many cases. I agree with Drs. Pratt and Crapo that the mechanism by which pulmonary fibrosis is produced in the course of adult respiratorydistress syndrome remains to be established. I suggest, in addition, that Legionnaires' disease could be added to the list of processes that may precede the adult respiratory-distress syndrome.
EUGENE J. MARK, M.D. Massachusetts General Hospital Boston, MA 02114 1. Case Records of the Massachusetts General Hospital (Case 21-1975). N Engl J Med 292:1174-1181, 1975 2. Case Records of the Massachusetts General Hospital (Case 22-1977). N Engl J Med 296:1279-1287, 1977 3. Petty TL, Ashbaugh DG: The adult respiratory distress syndrome: clinical features, factors influencing prognosis and principles of management. Chest 60:233-239, 1971 4. Yahav J, Lieberman P, Molho M: Pulmonary function following the adult respiratory distress syndrome. Chest 74:247-250, 1978
DEMONSTRATION OF GIARDIA IN DUODENAL FLUID BY SCANNING ELECTRON MICROSCOPY To the Editor: Giardia lamblia (Lamblia intestinalis) is a minute intestinal parasite of worldwide distribution with a relatively high incidence rate, especially in children."'2 The parasite may occur without apparent clinical symptoms; however, its presence is often associated with various gastrointestinal disorders.',2 A 34-monthold boy with a history of recurrent infections, chronic diarrhea and failure to thrive was found to have hypogammaglobulinemia. Gastrointestinal evaluation revealed a normal d-xylose test, normal small-bowel histologic findings and normal disaccharide and pancreatic enzymes. Giardia organisms were not observed in numerous stool specimens, duodenal aspirate or duodenal aspirate after secretin stimulation. Scanning electron microscopy of filter concentrated, unstimulated duodenal aspirates demonstrated the presence of giardia. For scanning electron microscopy, duodenal-aspirate fluid and phosphate-buffered 4 per cent gluteraldehyde fixative were mixed 1:1. Two milliliters was filtered with gentle pressure through a 13-mm-diameter microporous silver filter (0.45 um approximate pore diameter, Selas, Flotronics, Spring House, Pennsylvania). The filter was washed once by the passage of 2 ml of 0.1 M phosphate buffer through it. Filters were prepared for scanning electron microscopy via alcohol dehydration and critical point drying.3 Filters could be rapidly scanned at low (200 to 500 times) magnification, and small particulates examined at higher magnification to confirm their identity as giardia (Fig. 1 and 2). Less than 50 giardia organisms could be seen per filter, corresponding to a total population of approximately 50 per milliliter in the aspirate sample. Preparation and identification can be completed in a span of several hours; special staining or filter-clearing procedures are unnecessary. In addition, scanning electron microscopy permits rapid examination of large areas of filter surface, a procedure that may be tedious and inconclusive by light microscopy (especially when the density of cells on the filter surface is extremely low). Scanning electron microscopy is also helpful in the identification of abnormal, dead or dying forms of the parasite that may stain inconclusively.
The New England Journal of Medicine Downloaded from nejm.org at WEILL CORNELL MEDICAL COLLEGE LIBRARY on June 27, 2016. For personal use only. No other uses without permission. From the NEJM Archive. Copyright © 2010 Massachusetts Medical Society. All rights reserved.
1256
THE NEW ENGLAND JOURNAL OF MEDICINE
Figure 1. Dorsal View (x 5000) Showing Back, Dorsal FlagelIa (D) and Two Tail Flagella (T). ..The background is a silver °* membrane filter.
;: 2i 5
SUDDEN DEATH IN BUNDLE-BRANCH BLOCK To the Editor: The report by McAnulty et al. of their prospective study of bundle-branch-block in the August 3 issue of the Journal demonstrates an epidemiologic flaw that could modify the study results and its implications. For the 1211 abnormal electrocardiograms meeting the authors' criteria the authors got in touch with 638 patients as part of the study protocol. Only half the population at risk was studied. The demographic characteristics of the patients lost to follow-up observation are not available to determine the potential effect of selection bias. The problems of a large, prospective study are formidable, but size and a prospective design cannot guarantee a data set free of bias and epidemiologic flaws. Although 573 people were initially lost to follow-up observation, this group's demographic characteristics should be compared to those of the 638 studied patients. Negligible differences between these sets of characteristics would give proxy assurance that the groups are comparable and therefore the results in the study group indeed reflect the natural history of the disease. Perhaps more intensive follow-up study of a random sample of the 573 would help determine how representative of the target population are the 638 original patients. Birmingham, AL 35233
L
Figure 2. Ventral View (X 5000) Showing the Large, Concave Suction Disk (5) by Which the Flagellate Attaches to the Epi-
thelial Cells. In addition, the paired tail flagella (T), central flagella (C) and lateral flagella (L) are shown. The central flagellar grooves (f) are.also present.
- ~~~~~~~~~~~~~~~-
Scanning electron microscopy has been shown to be useful in the investigation of experimental giardiasis.4~ It may also be a sensitive and rapid assay to diagnose the presence of the parasite in clinical situations especially when giardiasis is suspected but the organism is not detected or its presence is questionable when samples are observed by ordinary light microscopy. R. M. ALBRECHT, PH.D. M. BORZY, M.D. G. B. ODELL, M.D. P. WHITTINGTON, M.D. S. D. HOROWITZ, M.D.
University of Wisconsin
Madison, WI 53706
Nov. 30, 1978
MAX MICHAEL, M.D. Cooper Green Hospital
To the Editor: We read with interest the recent excellent paper by McAnulty and his co-workers.' They reported a relatively high incidence of sudden death in a large (257 patients) prospectively followed population of patients with chronic bifascicular block. On the basis of their observations, they suggested that sudden death in this group of patients was infrequently due to bradyarrhythmia (trifascicular block). We were surprised that the authors did not refer to our recently published study demonstrating very similar findings.2 In our study, we reported 30 sudden cardiac deaths in a prospectively followed series of 277 patients with chronic bifascicular block. We did note some statistically significant risk factors for sudden cardiac death that were not noted by McAnulty and his co-workers: angina, previous myocardial infarction, heart failure, cardiomegaly, leftbundle-branch block (as opposed to other patterns of bifascicular block), premature ventricular beats on resting electrocardiograms and episodes of ventricular tachycardia on resting electrocardiograms. Ventricular fibrillation was the cause of death in the four cases of sudden cardiac death in which we had terminal electrocardiographic documentation available. Our conclusion was somewhat similar to that of McAnulty and his colleagues. We concluded that in patients with chronic bifascicular block, the association of sudden cardiac death with evidence of coronary disease and ventricular dysrhythmia suggested that ventricular fibrillation was the most frequent mechanism of sudden death.
Health Sciences Center
1. Peterson H Giardiasis (lambliasis). Scand J Gastroenterol 7:Suppl 14:444 1972 2. Klima M Gyorkey P, Me KW, et al: Electron microscopy in the diagnosis of giardiasis. Arch Pathol Lab Med 101:133-135, 1977 3. Albrecht RM, MacKenzie AP: Cultured and free living cells, Principles and Techniques of Scanning Electron Microscopy. Vol. 3. Edited by MA Hayat. New York, Van Nostrand Reinhold, 1975, pp 101-153 4. Erlandsen SL Scanning electron microscopy of intestinal giardiasis: lesions of the microvillous border of villous epithelial cells produced by trophozoites of giardia, Scanning Electron Microscopy/1974. Edited by o JohariR I Corvin. Chicago, IITRI, 1974, pp 775-782 5. Solov EV Chentsov I: Study of trophozoites of Lamblia intesuinalis from culture by scanning electron microscopy. Med Parazitol (Mosk) 45:650654G 1976 6. McKee AE Watson LP, Austin FA: Scanning electron microscopic study of murine giardiasis, Scanning Electron Microscopy/1978. Vol. 2. Edited by 0 Johari, RP Becker. O'Hare, Illinois, Scanning Electron Microscopy 1978, pp 321-326
Chicago, IL 60680
KENNETH M. ROSEN, M.D. PABLO DENES, M.D. RAMESH DHINGRA, M.D. CHRISTOPHER WYNDHAM, M.D. Abraham Lincoln School of Medicine
1. McAnulty JH, Rahimtoola SH, Murphy ES, et al: A prospective study of sudden death in "high-risk" bundle-branch block. N Engl J Med 299:209, 1978 2. Denes P, Dhingra RC, Wu D, et al: Sudden death in patients with chronic bifascicular block. Arch Intern Med 137:1005, 1977
The above letters were referred to the authors of the article in question, who offer the following reply:
The New England Journal of Medicine Downloaded from nejm.org at WEILL CORNELL MEDICAL COLLEGE LIBRARY on June 27, 2016. For personal use only. No other uses without permission. From the NEJM Archive. Copyright © 2010 Massachusetts Medical Society. All rights reserved.
CORRESPONDENCE
LEGIONNAIRES' DISEASE AND OTHER CAUSES OF INTRA-ALVEOLAR PULMONARY FIBROSIS To the Editor: The case report in the August 17 issue of the Jo0umal (Case 32-1978) gives the impression that the very striking pattern of fibrosis involving alveolar ducts was caused by Legionnaires' disease. The evidence that the patient had that disease is excellent, but we believe it is doubtful whether it caused the lesions found in the biopsy. Fibrosis in this peculiar pattern was described several years ago and was identified as being associated with progressive respiratory distress.' We have recently completed a review of pulmonary morphology at autopsy in some 59 cases of adult respiratory-distress syndrome collected during a multihospital co-operative project.2 A preliminary report on the morphology3 contains several illustrations of fibrotic alveolar ducts, all from patients with processes other than Legionnaires' disease. In the complete series every one of the 25 patients who survived two or more weeks from the onset of respiratory distress had this pattern of fibrosis. Underlying original diseases in these patients ran the usual gamut of processes that commonly precede the onset of the syndrome.4 Thus, the lesion is surely not specific for a late phase of an infection. In the present case, it should be recalled that the original consolidated area was the left lower lobe rather than the lingula that was biopsied. The biopsy was done on the 16th day after the onset of respiratory distress - well within the time span noted above. The inability to demonstrate organisms in the biopsy, despite application of all the available technics, supports the concept that the lesion was not caused directly by the infection. The mechanism by which this fibrotic lesion is produced in the course of adult respiratory distress remains to be established, although one of us has presented reasons to suspect that it is largely a result of oxygen toxicity.3 Survival after reaching the severity of involvement shown in this case is unusual, but has been reported.5
Durham, NC 27710
PHILIP C. PRATT, M.D. JAMES D. CRAPO, M.D. Duke Medical Center
1. Orell SR: Lung pathology in respiratory distress following shock in the adult. Acta Pathol Microbiol Scand [A] 79:65-76, 1971 2. Blake LH: Goals and progress of the National Heart and Lung Institute Collaborative Extracorporeal Membrane Oxygenation Study, Artificial Lungs for Acute Respiratory Failure. Edited by WM Zapol, J Qvist. New York, Academic Press, 1976, pp 513-524 3. Pratt PC: Pathology of the adult respiratory distress syndrome, The Lung: Structure, function and disease. Vol. 19. Edited by WM Thurlbeck. Baltimore, Williams & Wilkins, 1978, pp 43-47 4. Petty TL, Ashbaugh DG: The adult respiratory distress syndrome: clinical features, factors influencing prognosis and principles of management. Chest 60:233-239, 1971 5. Lamy M, Fallat RJ, Koeniger E, et al: Pathologic features and mechanisms of hypoxemia in adult respiratory distress syndrome. Am Rev Respir Dis 114:267-284, 1976
The above letter was referred to one of the discussers of the case in question, who offers the following reply: To the Editor: Within the past few years two Case Records of the Massachusetts General Hospital have shown a pattern of pulmonary fibrosis similar to that observed in the case of Legionnaires' disease referred to by Drs. Pratt and Crapo. The first1 was in a woman who was placed on extracorporeal membrane oxygenation for adult respiratory-distress syndrome that was probably secondary to viral pneumonia. She was one of 15 patients dying at this hospital after extracorporeal membrane oxygenation whose lungs we have examined, and the histology illustrated in the Case Record was typical of the group as a whole. The second Case Record2 was a woman in whom adult respiratory-distress syndrome developed after massive trauma. These two previously published cases serve to illustrate that a pathological diagnosis of pulmonary fibrosis within alveolar ducts is no more specific than a clinical diagnosis of adult respiratory-distress syndrome in defining the cause. My statement that most examples of massive intra-alveolar fibrosis at this institution have been secondary to a previous infectious episode was not
1255
meant to include or exclude any of the various pathogenetic mechanisms that may be responsible for the fibrosis; I made no statement on causality. The data on the complete series of 25 patients with respiratory distress, referred to by Pratt and Crapo, are unfortunately unavailable in the literature for review. The article that they refer to as displaying the gamut of processes that commonly precede the onset of the adult respiratory-distress syndrome3 details three cases, one of smoke inhalation, one of drug intoxication and one of bronchopneumonia. In a more recent report of 15 original cases,4 eight were associated with sepsis, and an additional two patients had burns covering half the body surface. The remaining five had obvious massive trauma. The relative frequency of the various events that are known to trigger the adult respiratory-distress syndrome will obviously depend on the type of medical center in which one works, but infection is certainly a factor in many cases. I agree with Drs. Pratt and Crapo that the mechanism by which pulmonary fibrosis is produced in the course of adult respiratorydistress syndrome remains to be established. I suggest, in addition, that Legionnaires' disease could be added to the list of processes that may precede the adult respiratory-distress syndrome.
EUGENE J. MARK, M.D. Massachusetts General Hospital Boston, MA 02114 1. Case Records of the Massachusetts General Hospital (Case 21-1975). N Engl J Med 292:1174-1181, 1975 2. Case Records of the Massachusetts General Hospital (Case 22-1977). N Engl J Med 296:1279-1287, 1977 3. Petty TL, Ashbaugh DG: The adult respiratory distress syndrome: clinical features, factors influencing prognosis and principles of management. Chest 60:233-239, 1971 4. Yahav J, Lieberman P, Molho M: Pulmonary function following the adult respiratory distress syndrome. Chest 74:247-250, 1978
DEMONSTRATION OF GIARDIA IN DUODENAL FLUID BY SCANNING ELECTRON MICROSCOPY To the Editor: Giardia lamblia (Lamblia intestinalis) is a minute intestinal parasite of worldwide distribution with a relatively high incidence rate, especially in children."'2 The parasite may occur without apparent clinical symptoms; however, its presence is often associated with various gastrointestinal disorders.',2 A 34-monthold boy with a history of recurrent infections, chronic diarrhea and failure to thrive was found to have hypogammaglobulinemia. Gastrointestinal evaluation revealed a normal d-xylose test, normal small-bowel histologic findings and normal disaccharide and pancreatic enzymes. Giardia organisms were not observed in numerous stool specimens, duodenal aspirate or duodenal aspirate after secretin stimulation. Scanning electron microscopy of filter concentrated, unstimulated duodenal aspirates demonstrated the presence of giardia. For scanning electron microscopy, duodenal-aspirate fluid and phosphate-buffered 4 per cent gluteraldehyde fixative were mixed 1:1. Two milliliters was filtered with gentle pressure through a 13-mm-diameter microporous silver filter (0.45 um approximate pore diameter, Selas, Flotronics, Spring House, Pennsylvania). The filter was washed once by the passage of 2 ml of 0.1 M phosphate buffer through it. Filters were prepared for scanning electron microscopy via alcohol dehydration and critical point drying.3 Filters could be rapidly scanned at low (200 to 500 times) magnification, and small particulates examined at higher magnification to confirm their identity as giardia (Fig. 1 and 2). Less than 50 giardia organisms could be seen per filter, corresponding to a total population of approximately 50 per milliliter in the aspirate sample. Preparation and identification can be completed in a span of several hours; special staining or filter-clearing procedures are unnecessary. In addition, scanning electron microscopy permits rapid examination of large areas of filter surface, a procedure that may be tedious and inconclusive by light microscopy (especially when the density of cells on the filter surface is extremely low). Scanning electron microscopy is also helpful in the identification of abnormal, dead or dying forms of the parasite that may stain inconclusively.
The New England Journal of Medicine Downloaded from nejm.org at WEILL CORNELL MEDICAL COLLEGE LIBRARY on June 27, 2016. For personal use only. No other uses without permission. From the NEJM Archive. Copyright © 2010 Massachusetts Medical Society. All rights reserved.
1256
THE NEW ENGLAND JOURNAL OF MEDICINE
Figure 1. Dorsal View (x 5000) Showing Back, Dorsal FlagelIa (D) and Two Tail Flagella (T). ..The background is a silver °* membrane filter.
;: 2i 5
SUDDEN DEATH IN BUNDLE-BRANCH BLOCK To the Editor: The report by McAnulty et al. of their prospective study of bundle-branch-block in the August 3 issue of the Journal demonstrates an epidemiologic flaw that could modify the study results and its implications. For the 1211 abnormal electrocardiograms meeting the authors' criteria the authors got in touch with 638 patients as part of the study protocol. Only half the population at risk was studied. The demographic characteristics of the patients lost to follow-up observation are not available to determine the potential effect of selection bias. The problems of a large, prospective study are formidable, but size and a prospective design cannot guarantee a data set free of bias and epidemiologic flaws. Although 573 people were initially lost to follow-up observation, this group's demographic characteristics should be compared to those of the 638 studied patients. Negligible differences between these sets of characteristics would give proxy assurance that the groups are comparable and therefore the results in the study group indeed reflect the natural history of the disease. Perhaps more intensive follow-up study of a random sample of the 573 would help determine how representative of the target population are the 638 original patients. Birmingham, AL 35233
L
Figure 2. Ventral View (X 5000) Showing the Large, Concave Suction Disk (5) by Which the Flagellate Attaches to the Epi-
thelial Cells. In addition, the paired tail flagella (T), central flagella (C) and lateral flagella (L) are shown. The central flagellar grooves (f) are.also present.
- ~~~~~~~~~~~~~~~-
Scanning electron microscopy has been shown to be useful in the investigation of experimental giardiasis.4~ It may also be a sensitive and rapid assay to diagnose the presence of the parasite in clinical situations especially when giardiasis is suspected but the organism is not detected or its presence is questionable when samples are observed by ordinary light microscopy. R. M. ALBRECHT, PH.D. M. BORZY, M.D. G. B. ODELL, M.D. P. WHITTINGTON, M.D. S. D. HOROWITZ, M.D.
University of Wisconsin
Madison, WI 53706
Nov. 30, 1978
MAX MICHAEL, M.D. Cooper Green Hospital
To the Editor: We read with interest the recent excellent paper by McAnulty and his co-workers.' They reported a relatively high incidence of sudden death in a large (257 patients) prospectively followed population of patients with chronic bifascicular block. On the basis of their observations, they suggested that sudden death in this group of patients was infrequently due to bradyarrhythmia (trifascicular block). We were surprised that the authors did not refer to our recently published study demonstrating very similar findings.2 In our study, we reported 30 sudden cardiac deaths in a prospectively followed series of 277 patients with chronic bifascicular block. We did note some statistically significant risk factors for sudden cardiac death that were not noted by McAnulty and his co-workers: angina, previous myocardial infarction, heart failure, cardiomegaly, leftbundle-branch block (as opposed to other patterns of bifascicular block), premature ventricular beats on resting electrocardiograms and episodes of ventricular tachycardia on resting electrocardiograms. Ventricular fibrillation was the cause of death in the four cases of sudden cardiac death in which we had terminal electrocardiographic documentation available. Our conclusion was somewhat similar to that of McAnulty and his colleagues. We concluded that in patients with chronic bifascicular block, the association of sudden cardiac death with evidence of coronary disease and ventricular dysrhythmia suggested that ventricular fibrillation was the most frequent mechanism of sudden death.
Health Sciences Center
1. Peterson H Giardiasis (lambliasis). Scand J Gastroenterol 7:Suppl 14:444 1972 2. Klima M Gyorkey P, Me KW, et al: Electron microscopy in the diagnosis of giardiasis. Arch Pathol Lab Med 101:133-135, 1977 3. Albrecht RM, MacKenzie AP: Cultured and free living cells, Principles and Techniques of Scanning Electron Microscopy. Vol. 3. Edited by MA Hayat. New York, Van Nostrand Reinhold, 1975, pp 101-153 4. Erlandsen SL Scanning electron microscopy of intestinal giardiasis: lesions of the microvillous border of villous epithelial cells produced by trophozoites of giardia, Scanning Electron Microscopy/1974. Edited by o JohariR I Corvin. Chicago, IITRI, 1974, pp 775-782 5. Solov EV Chentsov I: Study of trophozoites of Lamblia intesuinalis from culture by scanning electron microscopy. Med Parazitol (Mosk) 45:650654G 1976 6. McKee AE Watson LP, Austin FA: Scanning electron microscopic study of murine giardiasis, Scanning Electron Microscopy/1978. Vol. 2. Edited by 0 Johari, RP Becker. O'Hare, Illinois, Scanning Electron Microscopy 1978, pp 321-326
Chicago, IL 60680
KENNETH M. ROSEN, M.D. PABLO DENES, M.D. RAMESH DHINGRA, M.D. CHRISTOPHER WYNDHAM, M.D. Abraham Lincoln School of Medicine
1. McAnulty JH, Rahimtoola SH, Murphy ES, et al: A prospective study of sudden death in "high-risk" bundle-branch block. N Engl J Med 299:209, 1978 2. Denes P, Dhingra RC, Wu D, et al: Sudden death in patients with chronic bifascicular block. Arch Intern Med 137:1005, 1977
The above letters were referred to the authors of the article in question, who offer the following reply:
The New England Journal of Medicine Downloaded from nejm.org at WEILL CORNELL MEDICAL COLLEGE LIBRARY on June 27, 2016. For personal use only. No other uses without permission. From the NEJM Archive. Copyright © 2010 Massachusetts Medical Society. All rights reserved.
