Legionnaires’ Disease A Cause of Severe Abscess-Forming
SIIARON LEWIN, M.D. LEE R. BRETTMAN, M.D. iZ’r,n,\‘or!i. Ar,~c York EI,LlE J, C. GOLDSTEIN,
M.D.
I~rookl!~n,New York ROBERT S. HOLZMAN, Non.
M.D.
York, New York
l1ERNANDO DEVILA, M.D. FELIX TAUBMAN. M.D. MARCELINO F. SIERRA, Ph.D. I~rooklyn.
New
York
PAUL H. EDELSTEIN. M.D.
Pneumonia
In two previously well nonsmokers fatal pneumonia developed with extensive abscess formation. Legionnaires’ bacillus was the only pathogen isolated. These cases indicate that Legionnaires’ bacillus is capable of causing extensive necrosis of the lung. Over 1,000 cases of sporadic and epidemic Legionnaires’ disease have been reported. The spectrum of disease has ranged from a mild selflimited illness in which no pneumonia and few respiratory symptoms were observed [l] to a severe and rapidly fatal pneumonia 12-41. Smokers, the elderly and those receiving immunosuppressive therapy have a predilection for the severe form of Legionnaires’ disease [5]. In fatal cases, the underlying lung structure has remained relatively intact histologically. Although abscess formation has been reported [6], microbiologic data were not adequate to determine if the Legionnaires’ bacillus was the sole pathogen. We report two cases of Legionnaires’ disease in young nonsmokers with no underlying illness. Both patients died from an extensive abscess-forming pneumonia. Pus from the abscesses in both cases was cultured using optinial aerobic and anaerobic techniques. Legionnaires’ bacillus was the only organism which could be demonstrated either by culture or histology. CASE REPORTS
From the Infectious Disease and Immunology Division, Department of Medicine, New York llnivcrsity Medical Center. New York, New York: the Infectious Disease Division, Departmonts of Medicine and Pathology, State Univarsity of New York Downstate Medical Center, Brooklyn, New York; Departments of Medicine and Pathology, St. Johns Episcopal Hospital, Brooklyn, New York: and the Research Service, Wadsworth Veterans Administration Hospital. Los Angeles, California. Requests for reprints should be addressed to Dr. Robert S. Holzman, Department of Medicine, New York University Medical Center, 550 First Avenue, New York, Now York 10016. Manuscript accepted January 4. 1979.
Case 1. A 44 year old black man employed in the garment district of Manhattan was admitted to Bellevue Hospital in August 1978 with complaints of dyspnea, chest pain and fever for three days. He had been in excellent health until four days before admission when he sustained trauma to the right side of his chest. A day later he noted shortness of breath. a nonproductive cough, high fevers and malaise. The patient’s mother added a history of headache, anorexia, abdominal discomfort and severe diarrhea. Physical examination revealed an acutely ill, lethargic man in cxtremc respiratory distress. The temperature was 40°C, blood pressure 150/86 mm Hg, pulse rate 136/min and respirations 36/min. There was dullness to percussion at the bases of both lungs. Diffuse bilateral rhonchi were heard without ralcs or wheezes. The remainder of the examination was within normal limits except for tachycardia and intermittent episodes of confusion. The urinalysis showed 3+ proteinuria and a 1-t test for blood. The urinary sodiment contained 1 white blood cell, z red blood cells and 2 to 3 granular casts per high power field (hpf). The hemoglobin level was 14.7 g/100 ml and the hcmatocrit value 42 per cent. The white blood cell count was 9.900/mm3 with
August 1979
The American Journal of Medicine
Volume 67
339
LEGIONNAIRES’
DISEASE-LEWIN
ET AL.
Case 1. Gram-negative intracellular bacilli are seen. Original magnification X 1200, reduced by 29 per cent.
27 per cent neutrophils, 71 per cent band forms, 1 per cent lymphocytes and 1 per cent monocytes with toxic granulations noted in the neutrophils. The erythrocyte sedimentation rate was 73 mm/hour. The sodium was 125 meq/liter, chloride 83 meq/liter, potassium 3.1 meq/liter and bicarbonate 17 meq/ liter. The-blood urea nitrogen was 22 mg/lOO ml, creatinine 3.3 mg/lOO ml, glucose 164 mg/lOO ml, creatinine phosphokinase 450 IU, lactic dehydrogenase 790 IU, serum glutamic oxnloacetic transaminase (SGOT) 440 IU and serum pyruvic oxaloacetic transaminase (SGPT) 360 IU. Arterial blood gases with the patient breathing room air were oxygen tension (~0s) 24 mm Hg, carbon dioxide tension (pCOZ) 30 mm Hg and pH 7.37. An x-ray film of the chest showed alveolar infiltrates involving the apex, lower lobe, middle lobe of the right lung and lingula. There was a right pleural effusion. Culture of oxpcctorated sputum grew Neisseria catarrhalis and viridans streptococci. Cu4ture of blood, urine and spinal fluid revealed no growth. The pleural effusion was not tapped. An orotracheal tube was placed and the patient artifically ventilated. Gram stain of sputum from the tube showed 5 to 6 ncutrophils hpf with approximately one field of 10 showing intracellular faintly staining gram-negative rods (Figure 1). Dieterle stain revealed both intracellular and extracellular blunt coccobacillary bacteria. A stain for acid-fast organisms was negative. Several aerobic and anaerobic cultures of the sputum obtained through the orotracheal tube were sterile. The patient was at first treated with penicillin and gentamicin. On the second hospital day, he was stuporous. The pleural effusion was no longer present on a chest film. The antibiotics he was receiving were changed to erythromycin. 500 mg intravenously every 6 hours, ampicillin and amikacin. Episodes of hypotension developed, the abdomen became progressively distended, and the patient continued to have profuse diarrhea. On the third hospital day, ampicillin and amikacin therapy was discontinued, and the administration of rifampin and chloramphenicol was begun. The patient’s renal function continued to deteriorate. On the fourth hospital day, the chest film revealed extensive bilateral alveolar infiltrates. During the hospital course, the patient’s orotracheal tube was changed six times because of obstruction by tenacious
340
August 1979 The American Journal of Medicine
Figure 2. Photograph of cut lung at postmortem examination in Case 1. Extensive abscess formation is seen. In this view the lung has been cut from periphery to hilum and opened like a book. The hilar structures are seen in the center.
secretions. This occured despite good hydration and frequent orotracheal suctioning. Hemodialysis was begun on the fifth hospital day. On the eighth hospital day, a chest film suggested cavitation in the upper lobe of the right lung. The patient died on the ninth hospital day. At autopsy, the lung’s cut surface showed diffuse areas of pneumonic consolidation and large abscess cavities ranging in size from 1 to 10 cm with relative sparing of the upper lobe of the right lung (Figures 2 and 3). There were larger cavities which appeared to represent the confluence of numerous smaller abscess cavities. A gram stain of the pus showed sheets of gram-negative rods which stiined with direct fluorescent antibody to the Knoxville strain (serotype I) of the Legionnaires’ bacillus in the laboratories of the Center for Disease Control (CDC] [7]. Material from the abscesses yielded no growth when cultured aerobically on blood, Columbia CNA. phcnylethanol agars and anaerobically in Gas-PakTM jars on brucella agar and phenylethanol agar both enriched with vitamin K, hemin and yeast. Legionnaires’ bacillus, however, was cultured using Mueller-Hinton agar supplemented with I per cent hemoglobin and I per cent IsoVitaleX. When tested at CDC. the patient’s indirect fluorescent antibody titer to the Knoxville strain of Legionnaires’ bacillus was 1:1024 on the fourth hospital day [8]. Case 2. A 31 year old black man employed in the garment district of Manhattan was admitted to St. John’s Episcopal Hospital in August 1978 with dyspnea, chest pain, fever and chills of several days’ duration. He was well until one week prior to admission when he noted a persistent headache. Several days prior to admission he experienced right pleuritic pain, fever, chills and a nonproductive cough. The patient was a nondrinker and nonsmoker. Physical examination revealed a coherent man in mild respiratory distress. The temperature was JO%, blood pressure 130/90 mm Hg, pulse rate llO/min and respirations 26/min. Examination of the chest revealed rales in the right mid-axil-
Volume 67
Figure 3. F’hotomicrographsof lung in Case 1. A, low power view showing consolidated lung bordering a large abscess cavity. Original magnification X 50. B, higher power view of abscess wall showing cellular infiltrate of polymorphonuclear and mononuclear leukocytes. Original magnification X 50 (A) and X 310 (B), reduced by 10 per cent.
lary line and at the base of the right lung. The remainder of the examination was within normal limits. The hemoglobin level was 15.5 g/100 ml and the hematocrit value 42 per cent. The white blood cell count was 13,900/mm3 with 81 per cent neutrophils, 11 per cent band forms and 8 per cent lymphocytes. The serum electrolytes and blood urea nitrogen were within normal limits. An x-ray film of the chest showed an infiltrate in the hilum and middle lobe of the right lung. Gram stain of the sputum showed a few neutrophils and scanty gram-positive cocci. Acid-fast stain of the sputum was negative. Urine, blood and stool cultures were negative for pathogens. Cold agglntinins were absent. The patient was treated with penicillin. After 36 hours he was still febrile, and a repeat x-ray film showed progression of the infiltrates to involve the entire right lung. He experienced diarrhea and abdominal bloating. Therapy with penicillin was stopped, and cephalothin and gentamicin therapy was started. On the fifth hospital day, the patient became hypothermic, hypotensivc and required intubation. Erythromycin, 500 mg every 6 hours, and clindamycin were added to his therapeutic regimen. On the eighth hospital day, an x-ray film showed a new infiltrate at the base of the left lung and bilateral pleural effusions. The pleural effusions were not tapped. The patient died on the eighth hospital day. At autopsy, there was 1.000 ml clear amber transudate in the pleural cavities. The lungs were grossly edematous with consolidation involving the entire right lung and less severely the lower lobe of the left lung. There was extensive necrosis with 1 to 3 cm abscesses bilaterally, most marked in the lower lobe of the right lung. Microscopic examination showed alveoli distended with polymorphonuclear leukocytes, lymphocytes and pigmented macrophages. Areas of the intcralveolar septums showed necrosis. Perivascular edema was also noted. Culture of the hmg yielded no growth when incubated aerobically on brucella blood agar, blood agar with phenylethyl alcohol, and chocolate agar in a
candle jar, and anaerobically in a Gas-Pak’rM jar on brucella blood agar supplemented with hemin and vitamin K, and on kanamycin-vancomycin laked-blood agar. Cultures for acidfast organisms and fungi were also negative. Legionnaires’ bacillus was demonstrated in the lung by direct immunofluorescent antibody against the Knoxville strain and was cultured by inoculating embryonated chicken eggs and subculturing the yolk sac after five days on charcoal yeast agar [prcpared using 10g DIFCO yeast extract, 1.5g &ivated charcoal, 0.4 g l-cysteine HCI. 0.25 g ferric pyrophosphatc. 17 g agar diluted with water to 1 liter and adjusted to pieI 6,!1). COMMENTS
Past reports of the pulmonary pathology in Legionnaires’ disease have emphasized the presence of consolidation with an alveolar exudate consisting of polymorphonuclear leukocytes, macrophages, cellular debris and fibrin [6,9]. Winn et al. [6] reported the pathologic findings in 14 cases of Legionnaires’ disease confirmed by direct fluorescent antibody staining of lung tissue. An extensive necrotizing pneumonia was not described although in some cases there was histologic evidence of focal destruction of alveolar septums. Areas of coagulation necrosis were also seen. Abscesses of undisclosed size and extent were present in two of the 14 cases. It could not be determined if these abscesses were due to Legionnaires’ bacillus or to concomitant secondary infection. In fact, other bacteria and fungi were grown in autopsy specimens of the lungs from four patients. In two reports [lO,ll] the roentgenologic findings in a total of 45 cases of Legionnaires’ disease were reviewed. In both reports, the absence of cavitation, cmpyema or necrotizing pneumonia was specifically noted. In the cases we report, severe Legionnaires’ disease
August 1979
The American
Journal of Medicine
Vohrme 67
341
LEGIONNAIRES’ DISEASE-LEWIN
ET AL.
peated efforts to isolate other aerobic and anaerobic pathogens failed. The cases reported here represent two of the three fatalities of the Manhattan garment center outbreak. No autopsy was performed in the third case. Our cases are unusual because they occurred in two young, previously healthy nonsmokers in whom postmortem examination failed to reveal any serious underlying disease. They also differ from other reported cases because of the presence of an extensive necrotizing and abscessforming pneumonia. The failure to isolate other pathogens-in these cases suggests that the Legionnaires’ bacillus is capable of causing gross as well as microscopic necrosis of lung.
developed in two previously healthy men. Despite specific therapy with intravenous erythromycin and extensive supportive care, both patients died. A chest film obtained on the eighth hospital day in Case 1 suggested the presence of abscess formation. Extremely tenacious pulmonary secretions which necessitated six orotracheal tube changes further complicated the management of this patient. Postmortem examination in both cases revealed an extensive necrotizing pneumonia. In Case 1, visible abscesses ranged from 1 to 10 cm in diameter. The upper lobe of the left lung was almost entirely replaced by a large abscess. In Case 2, the abscesses were smaller, ranging from 1 to 3 cm in diameter. Despite eight days of intravenous erythromycin therapy in Case 1 and three days in Case 2, Legionnaires’ bacillus was grown from postmortem material. In both cases intensive and re-
ACKNOWLEDGMENT
We wish to thank the Center for Disease Control in Atlanta, Georgia and the house staff at Bellevue Hospital.
REFERENCES I.
Glick TH. Gregg MB, Berman B. et al.: Pontiac fever: an epidemic of unknown etiology in a health department: 1. Clinical and epidemiologic aspects. Am ] Epidemiol 107: 149.1978. 2. Fraser DW, Tsai TR, Orenstein W, et al.: The Field Investigation Team: Legionnaires’ disease; description of an epidcmic of pneumonia. N Engl J Med 297: 1189,1977. 3. Kirby BD, Snyder KM, Meyer RD, et al.: Legionnaires’ discase: clinical features of 24 cases. Ann Intern Med 89; 297, 1978. 4. Beaty HN, Miller AA, Broome CV, et al.: Legionnaires’ disease in Vermont, May to October 1977. JAMA 240: 127, 1978. 5. Bock BV, Kirby BD, Edelstein PH. et al.: Legionnaires’ disease in renal transplant recipients. Lancet 1: 410, 1978. (i. Winn WC, Glavin FL, Per1 DP, et al.: The pathology of Legionnaires’ disease. Arch Path01 Lab Med 102: 344, 1978.
342
August 1979
The American
Journal of Medicine
7.
Cherry WB: Detection in clinical specimens by direct immunofiuorescence, “Legionnaires’ “: The Disease, the Bacterium, and Methodology (Jones CL, Hebert GA, eds). Atlanta, U.S. Public Health Service, 3978,99. 8. Wilkinson HW: Indirect fluorescent antibody test. “Legionnaires’ “: The.Disease, the Bacterium, and Methodology (Jones GL. Hebert GA, eds], Atlanta, U.S. Public Health Service, 1978, p 117. 9. Chandler FW, ‘Hicklin MD, Blackman JA: Demonstration of the agent of Legionnaires’ disease in tissue. N Engl J Med 297: 1218,1977. IO. Dictrich PA, Johnson RD. Fairbank JT. et al.: The chest radiograph in Legionnaires’ disease. Radiology 127: 577, 1978. ‘Il. Kirby BD, Peck H, Meyer RD: Radiologic features of 21 cases of Legionnaires’ disease. Program and Abstracts, 18th Intcrscience Conference on Antimicrobial Agents and Chemotherapy, October l-4, Atlanta, Ga., 1978, p 374.
Volume 67
SIIARON LEWIN, M.D. LEE R. BRETTMAN, M.D. iZ’r,n,\‘or!i. Ar,~c York EI,LlE J, C. GOLDSTEIN,
M.D.
I~rookl!~n,New York ROBERT S. HOLZMAN, Non.
M.D.
York, New York
l1ERNANDO DEVILA, M.D. FELIX TAUBMAN. M.D. MARCELINO F. SIERRA, Ph.D. I~rooklyn.
New
York
PAUL H. EDELSTEIN. M.D.
Pneumonia
In two previously well nonsmokers fatal pneumonia developed with extensive abscess formation. Legionnaires’ bacillus was the only pathogen isolated. These cases indicate that Legionnaires’ bacillus is capable of causing extensive necrosis of the lung. Over 1,000 cases of sporadic and epidemic Legionnaires’ disease have been reported. The spectrum of disease has ranged from a mild selflimited illness in which no pneumonia and few respiratory symptoms were observed [l] to a severe and rapidly fatal pneumonia 12-41. Smokers, the elderly and those receiving immunosuppressive therapy have a predilection for the severe form of Legionnaires’ disease [5]. In fatal cases, the underlying lung structure has remained relatively intact histologically. Although abscess formation has been reported [6], microbiologic data were not adequate to determine if the Legionnaires’ bacillus was the sole pathogen. We report two cases of Legionnaires’ disease in young nonsmokers with no underlying illness. Both patients died from an extensive abscess-forming pneumonia. Pus from the abscesses in both cases was cultured using optinial aerobic and anaerobic techniques. Legionnaires’ bacillus was the only organism which could be demonstrated either by culture or histology. CASE REPORTS
From the Infectious Disease and Immunology Division, Department of Medicine, New York llnivcrsity Medical Center. New York, New York: the Infectious Disease Division, Departmonts of Medicine and Pathology, State Univarsity of New York Downstate Medical Center, Brooklyn, New York; Departments of Medicine and Pathology, St. Johns Episcopal Hospital, Brooklyn, New York: and the Research Service, Wadsworth Veterans Administration Hospital. Los Angeles, California. Requests for reprints should be addressed to Dr. Robert S. Holzman, Department of Medicine, New York University Medical Center, 550 First Avenue, New York, Now York 10016. Manuscript accepted January 4. 1979.
Case 1. A 44 year old black man employed in the garment district of Manhattan was admitted to Bellevue Hospital in August 1978 with complaints of dyspnea, chest pain and fever for three days. He had been in excellent health until four days before admission when he sustained trauma to the right side of his chest. A day later he noted shortness of breath. a nonproductive cough, high fevers and malaise. The patient’s mother added a history of headache, anorexia, abdominal discomfort and severe diarrhea. Physical examination revealed an acutely ill, lethargic man in cxtremc respiratory distress. The temperature was 40°C, blood pressure 150/86 mm Hg, pulse rate 136/min and respirations 36/min. There was dullness to percussion at the bases of both lungs. Diffuse bilateral rhonchi were heard without ralcs or wheezes. The remainder of the examination was within normal limits except for tachycardia and intermittent episodes of confusion. The urinalysis showed 3+ proteinuria and a 1-t test for blood. The urinary sodiment contained 1 white blood cell, z red blood cells and 2 to 3 granular casts per high power field (hpf). The hemoglobin level was 14.7 g/100 ml and the hcmatocrit value 42 per cent. The white blood cell count was 9.900/mm3 with
August 1979
The American Journal of Medicine
Volume 67
339
LEGIONNAIRES’
DISEASE-LEWIN
ET AL.
Case 1. Gram-negative intracellular bacilli are seen. Original magnification X 1200, reduced by 29 per cent.
27 per cent neutrophils, 71 per cent band forms, 1 per cent lymphocytes and 1 per cent monocytes with toxic granulations noted in the neutrophils. The erythrocyte sedimentation rate was 73 mm/hour. The sodium was 125 meq/liter, chloride 83 meq/liter, potassium 3.1 meq/liter and bicarbonate 17 meq/ liter. The-blood urea nitrogen was 22 mg/lOO ml, creatinine 3.3 mg/lOO ml, glucose 164 mg/lOO ml, creatinine phosphokinase 450 IU, lactic dehydrogenase 790 IU, serum glutamic oxnloacetic transaminase (SGOT) 440 IU and serum pyruvic oxaloacetic transaminase (SGPT) 360 IU. Arterial blood gases with the patient breathing room air were oxygen tension (~0s) 24 mm Hg, carbon dioxide tension (pCOZ) 30 mm Hg and pH 7.37. An x-ray film of the chest showed alveolar infiltrates involving the apex, lower lobe, middle lobe of the right lung and lingula. There was a right pleural effusion. Culture of oxpcctorated sputum grew Neisseria catarrhalis and viridans streptococci. Cu4ture of blood, urine and spinal fluid revealed no growth. The pleural effusion was not tapped. An orotracheal tube was placed and the patient artifically ventilated. Gram stain of sputum from the tube showed 5 to 6 ncutrophils hpf with approximately one field of 10 showing intracellular faintly staining gram-negative rods (Figure 1). Dieterle stain revealed both intracellular and extracellular blunt coccobacillary bacteria. A stain for acid-fast organisms was negative. Several aerobic and anaerobic cultures of the sputum obtained through the orotracheal tube were sterile. The patient was at first treated with penicillin and gentamicin. On the second hospital day, he was stuporous. The pleural effusion was no longer present on a chest film. The antibiotics he was receiving were changed to erythromycin. 500 mg intravenously every 6 hours, ampicillin and amikacin. Episodes of hypotension developed, the abdomen became progressively distended, and the patient continued to have profuse diarrhea. On the third hospital day, ampicillin and amikacin therapy was discontinued, and the administration of rifampin and chloramphenicol was begun. The patient’s renal function continued to deteriorate. On the fourth hospital day, the chest film revealed extensive bilateral alveolar infiltrates. During the hospital course, the patient’s orotracheal tube was changed six times because of obstruction by tenacious
340
August 1979 The American Journal of Medicine
Figure 2. Photograph of cut lung at postmortem examination in Case 1. Extensive abscess formation is seen. In this view the lung has been cut from periphery to hilum and opened like a book. The hilar structures are seen in the center.
secretions. This occured despite good hydration and frequent orotracheal suctioning. Hemodialysis was begun on the fifth hospital day. On the eighth hospital day, a chest film suggested cavitation in the upper lobe of the right lung. The patient died on the ninth hospital day. At autopsy, the lung’s cut surface showed diffuse areas of pneumonic consolidation and large abscess cavities ranging in size from 1 to 10 cm with relative sparing of the upper lobe of the right lung (Figures 2 and 3). There were larger cavities which appeared to represent the confluence of numerous smaller abscess cavities. A gram stain of the pus showed sheets of gram-negative rods which stiined with direct fluorescent antibody to the Knoxville strain (serotype I) of the Legionnaires’ bacillus in the laboratories of the Center for Disease Control (CDC] [7]. Material from the abscesses yielded no growth when cultured aerobically on blood, Columbia CNA. phcnylethanol agars and anaerobically in Gas-PakTM jars on brucella agar and phenylethanol agar both enriched with vitamin K, hemin and yeast. Legionnaires’ bacillus, however, was cultured using Mueller-Hinton agar supplemented with I per cent hemoglobin and I per cent IsoVitaleX. When tested at CDC. the patient’s indirect fluorescent antibody titer to the Knoxville strain of Legionnaires’ bacillus was 1:1024 on the fourth hospital day [8]. Case 2. A 31 year old black man employed in the garment district of Manhattan was admitted to St. John’s Episcopal Hospital in August 1978 with dyspnea, chest pain, fever and chills of several days’ duration. He was well until one week prior to admission when he noted a persistent headache. Several days prior to admission he experienced right pleuritic pain, fever, chills and a nonproductive cough. The patient was a nondrinker and nonsmoker. Physical examination revealed a coherent man in mild respiratory distress. The temperature was JO%, blood pressure 130/90 mm Hg, pulse rate llO/min and respirations 26/min. Examination of the chest revealed rales in the right mid-axil-
Volume 67
Figure 3. F’hotomicrographsof lung in Case 1. A, low power view showing consolidated lung bordering a large abscess cavity. Original magnification X 50. B, higher power view of abscess wall showing cellular infiltrate of polymorphonuclear and mononuclear leukocytes. Original magnification X 50 (A) and X 310 (B), reduced by 10 per cent.
lary line and at the base of the right lung. The remainder of the examination was within normal limits. The hemoglobin level was 15.5 g/100 ml and the hematocrit value 42 per cent. The white blood cell count was 13,900/mm3 with 81 per cent neutrophils, 11 per cent band forms and 8 per cent lymphocytes. The serum electrolytes and blood urea nitrogen were within normal limits. An x-ray film of the chest showed an infiltrate in the hilum and middle lobe of the right lung. Gram stain of the sputum showed a few neutrophils and scanty gram-positive cocci. Acid-fast stain of the sputum was negative. Urine, blood and stool cultures were negative for pathogens. Cold agglntinins were absent. The patient was treated with penicillin. After 36 hours he was still febrile, and a repeat x-ray film showed progression of the infiltrates to involve the entire right lung. He experienced diarrhea and abdominal bloating. Therapy with penicillin was stopped, and cephalothin and gentamicin therapy was started. On the fifth hospital day, the patient became hypothermic, hypotensivc and required intubation. Erythromycin, 500 mg every 6 hours, and clindamycin were added to his therapeutic regimen. On the eighth hospital day, an x-ray film showed a new infiltrate at the base of the left lung and bilateral pleural effusions. The pleural effusions were not tapped. The patient died on the eighth hospital day. At autopsy, there was 1.000 ml clear amber transudate in the pleural cavities. The lungs were grossly edematous with consolidation involving the entire right lung and less severely the lower lobe of the left lung. There was extensive necrosis with 1 to 3 cm abscesses bilaterally, most marked in the lower lobe of the right lung. Microscopic examination showed alveoli distended with polymorphonuclear leukocytes, lymphocytes and pigmented macrophages. Areas of the intcralveolar septums showed necrosis. Perivascular edema was also noted. Culture of the hmg yielded no growth when incubated aerobically on brucella blood agar, blood agar with phenylethyl alcohol, and chocolate agar in a
candle jar, and anaerobically in a Gas-Pak’rM jar on brucella blood agar supplemented with hemin and vitamin K, and on kanamycin-vancomycin laked-blood agar. Cultures for acidfast organisms and fungi were also negative. Legionnaires’ bacillus was demonstrated in the lung by direct immunofluorescent antibody against the Knoxville strain and was cultured by inoculating embryonated chicken eggs and subculturing the yolk sac after five days on charcoal yeast agar [prcpared using 10g DIFCO yeast extract, 1.5g &ivated charcoal, 0.4 g l-cysteine HCI. 0.25 g ferric pyrophosphatc. 17 g agar diluted with water to 1 liter and adjusted to pieI 6,!1). COMMENTS
Past reports of the pulmonary pathology in Legionnaires’ disease have emphasized the presence of consolidation with an alveolar exudate consisting of polymorphonuclear leukocytes, macrophages, cellular debris and fibrin [6,9]. Winn et al. [6] reported the pathologic findings in 14 cases of Legionnaires’ disease confirmed by direct fluorescent antibody staining of lung tissue. An extensive necrotizing pneumonia was not described although in some cases there was histologic evidence of focal destruction of alveolar septums. Areas of coagulation necrosis were also seen. Abscesses of undisclosed size and extent were present in two of the 14 cases. It could not be determined if these abscesses were due to Legionnaires’ bacillus or to concomitant secondary infection. In fact, other bacteria and fungi were grown in autopsy specimens of the lungs from four patients. In two reports [lO,ll] the roentgenologic findings in a total of 45 cases of Legionnaires’ disease were reviewed. In both reports, the absence of cavitation, cmpyema or necrotizing pneumonia was specifically noted. In the cases we report, severe Legionnaires’ disease
August 1979
The American
Journal of Medicine
Vohrme 67
341
LEGIONNAIRES’ DISEASE-LEWIN
ET AL.
peated efforts to isolate other aerobic and anaerobic pathogens failed. The cases reported here represent two of the three fatalities of the Manhattan garment center outbreak. No autopsy was performed in the third case. Our cases are unusual because they occurred in two young, previously healthy nonsmokers in whom postmortem examination failed to reveal any serious underlying disease. They also differ from other reported cases because of the presence of an extensive necrotizing and abscessforming pneumonia. The failure to isolate other pathogens-in these cases suggests that the Legionnaires’ bacillus is capable of causing gross as well as microscopic necrosis of lung.
developed in two previously healthy men. Despite specific therapy with intravenous erythromycin and extensive supportive care, both patients died. A chest film obtained on the eighth hospital day in Case 1 suggested the presence of abscess formation. Extremely tenacious pulmonary secretions which necessitated six orotracheal tube changes further complicated the management of this patient. Postmortem examination in both cases revealed an extensive necrotizing pneumonia. In Case 1, visible abscesses ranged from 1 to 10 cm in diameter. The upper lobe of the left lung was almost entirely replaced by a large abscess. In Case 2, the abscesses were smaller, ranging from 1 to 3 cm in diameter. Despite eight days of intravenous erythromycin therapy in Case 1 and three days in Case 2, Legionnaires’ bacillus was grown from postmortem material. In both cases intensive and re-
ACKNOWLEDGMENT
We wish to thank the Center for Disease Control in Atlanta, Georgia and the house staff at Bellevue Hospital.
REFERENCES I.
Glick TH. Gregg MB, Berman B. et al.: Pontiac fever: an epidemic of unknown etiology in a health department: 1. Clinical and epidemiologic aspects. Am ] Epidemiol 107: 149.1978. 2. Fraser DW, Tsai TR, Orenstein W, et al.: The Field Investigation Team: Legionnaires’ disease; description of an epidcmic of pneumonia. N Engl J Med 297: 1189,1977. 3. Kirby BD, Snyder KM, Meyer RD, et al.: Legionnaires’ discase: clinical features of 24 cases. Ann Intern Med 89; 297, 1978. 4. Beaty HN, Miller AA, Broome CV, et al.: Legionnaires’ disease in Vermont, May to October 1977. JAMA 240: 127, 1978. 5. Bock BV, Kirby BD, Edelstein PH. et al.: Legionnaires’ disease in renal transplant recipients. Lancet 1: 410, 1978. (i. Winn WC, Glavin FL, Per1 DP, et al.: The pathology of Legionnaires’ disease. Arch Path01 Lab Med 102: 344, 1978.
342
August 1979
The American
Journal of Medicine
7.
Cherry WB: Detection in clinical specimens by direct immunofiuorescence, “Legionnaires’ “: The Disease, the Bacterium, and Methodology (Jones CL, Hebert GA, eds). Atlanta, U.S. Public Health Service, 3978,99. 8. Wilkinson HW: Indirect fluorescent antibody test. “Legionnaires’ “: The.Disease, the Bacterium, and Methodology (Jones GL. Hebert GA, eds], Atlanta, U.S. Public Health Service, 1978, p 117. 9. Chandler FW, ‘Hicklin MD, Blackman JA: Demonstration of the agent of Legionnaires’ disease in tissue. N Engl J Med 297: 1218,1977. IO. Dictrich PA, Johnson RD. Fairbank JT. et al.: The chest radiograph in Legionnaires’ disease. Radiology 127: 577, 1978. ‘Il. Kirby BD, Peck H, Meyer RD: Radiologic features of 21 cases of Legionnaires’ disease. Program and Abstracts, 18th Intcrscience Conference on Antimicrobial Agents and Chemotherapy, October l-4, Atlanta, Ga., 1978, p 374.
Volume 67
