418 0 1992 Elsevier
Science
International Journal of Cardiology, 37 (1992) 418-420 Publishers B.V. All rights reserved 0167-5273/92/$05.00
CARD10 15782
Myocarditis: a rare complication during Legionella infection S.Armengol
‘, Ch. Domingo b and E. Mesalles a
’ Servei de Cures Intensives, b Servei de Pneumologia. Hospital LJniLlersitariGermans Trlas i Pujol, Badalona, Barcelona, Spain (Received 18 April 1992; revision accepted 7 August 1992)
Legionella often causes systemic manifestations. The clinical spectrum now includes cardiac legionellosis. The first case of myocarditis was reported by Gross in 1981. To date few additional cases have been described. Myocardial involvement might be more frequent than supposed in legionnaires’ disease. Key words:
Legionnaires’
disease;
Myocarditis
Introduction Since the characterization of the organism causing the 1976 Philadelphia epidemic of legionnaires’ disease and the isolation of L. pneumophila, there has been considerable progress in the understanding and identification of infections due to Legionella species [I]. There is an expanding clinical spectrum of the disease caused by the genus Legionella which now includes cardiac legionellosis [2]. Cardiac involvement can present as tachycardia, relative bradycardia, endocarditis on a prosthetic valve, pericarditis and myocarditis [2]. We report a new case of myocarditis associated with Legionella pneumonia. Case Report A 43-yr-old Caucasian male was admitted to our hospital in February 1987, with a one-week history of productive cough, fever and progressively worsening shortness of breath. He had been initially treated with an amoxicillin-clavulanic acid combination. He admitted a 20-yr 1 pack/day smoking history, and his past
medical history was unremarkable. Physical examination revealed a cyanotic man with a temperature of 39.2”C, respiratory rate of 44 breaths/min, pulse of 124 beats/min, and a blood pressure of 75/40 mmHg
CK
CKMB
(u/ml)
(u/ml)
800
600
400
200
010 0 Correspondence to: Salvador Armengol, M.D., Servei de Cures Intensives, 2’ planta, Hospital Universitari Germans Trias i Pujol, Cra de1 Canyet s/n (Can Ruti), 08916-Badalona, Barcelona, Spain. Tel. 3953161. Fax 3954206.
I
2
3
4
5
6
DAYS Fig. 1. Evolution
of CPK and CPK-MB ctuve during days after admission.
the first 6
419
without paradoxical pulse. Jugular venous distension was absent. Auscultation revealed bibasilar rales and a cardiac gallop, but murmurs or pericardial friction rubs were not detected. Significant laboratory data were: erythrocyte sedimentation rate 67 mm/h and a white blood cell count of 15,60O/mm” with a differential count of 90 polymorphonuclear leukocytes, one band form and nine lymphocytes. Serum sodium level was 136 mEq/l; potassium, 3.6 mEq/l; BUN, 18 mg/dl; creatinine, 0.9 mg/dl; bilirubin, 1.76 mg/dl; SGOT, 96 U/l; lactic acid dehydrogenase 320 U/ml (cardiac isoenzymes were notably increased); serum creatine phosphokinase 402 U/ml with an MB-fraction of 78 U/ml (Fig. 1). Arterial blood gases on room air were pH 7.46: PaO, 46 mmHg; PaCO, 33 mmHg. The chest X-ray revealed a dense alveolar infiltrate in both lower lobes; Type B Kerley lines were also observed. The ECG showed a sinus tachycardia with a left bundle branch block (Fig. 2). A positive direct fluorescent antibody test for L. pneumophila in sputum was obtained and the patient received 4 g/day of intravenous erythromycin. A posi-
Fig. 2. Electrocardiogram
tive culture for L. pneumophila was obtained several days later and also a four-fold rise in antibody titre (indirect fluorescent antibody test) confirmed the diagnosis of legionnaires’ disease, but titres to a variety of other potential pathogens (Mycoplasma pneumonia, cytomegalovirus, echo, coxsackie, influenza virus, adenovirus and toxoplasma) remained unchanged. An echocardiogram revealed a decreased left ventricular function, with moderate hypokinesia. Five days after admission in the Intensive Care Unit, the patient improved and was discharged to the pulmonary ward. Ten days later, the chest X-ray and the arterial blood gases improved, and the left bundle branch block disappeared. Three weeks after admission the patient was discharged with a normal echocardiogram and has remained well for 5 yr. Discussion The clinical spectrum of the disease caused by the genus Legionella now includes myocarditis which usually presents with pneumonia. The diagnosis of Le-
showing left bundle branch block.
420
gionella pneumophila
myocarditis was accepted on the basis of the ECG and echocardiogram changes as well as the analytical data. Attempts to demonstrate any other cause of acute myocarditis were negative. Endocarditis and dilated cardiomyopathy were ruled out by the echocardiogram as well as by the evolution. L. pneumophila pneumonia was diagnosed according to the universal criteria [l]. L. pneumophila and pneumococci were initially investigated since these are the most common bacteria isolated in those patients with community-acquired pneumonia that required admission to our Intensive Care Unit. From 1987 to 1990, 71 patients were admitted to our Intensive Care Unit because of community-acquired pneumonia. In 14 cases pneumococci were isolated and in 12 Legionella was the infective isolated agent; in another 29 cases the germ could not be identified. In the rest of the patients other germs were isolated. To date only a few cases of Legionella myocarditis have been reported. Two of them had evidence of widespread involvement [2]. In other cases, especially in childhood [3], the myocardium seems to be the only affected organ. Myocarditis seems to be evident several days after the onset of respiratory symptoms [2] and could be influenced by the prompt treatment with intravenous erythromycin (our case recovered earlier than Gross’s patient [2]). Arrhythmia or conduction blocks have been described, especially when pneumonia is absent. QT- and ST-interval abnormalities as well as T-wave inversions have also been observed with prominent respiratory symptoms [2]. In our patient, left bundle branch block
initially detected. Finally, we would like to underline that, although L. pneumophila pneumonia is a common complication of cardiac transplantations, to date myocarditis due to L. pneumophila has not been reported in cardiac transplant recipients [4]. Cardiac involvement in legionnaires’ disease is infrequent. From 1983 to 1991, 157 cases of Legionella pneumonia have been diagnosed in our hospital. Only the present case and one other case with pericardial effusion showed cardiac involvement [5]. We consider that myocarditis, if looked for, could be more frequent than supposed in legionnaires’ disease. Because of this, the indirect fluorescent antibody test for Legionella should be included as a differential diagnostic test for idiopathic myocarditis of unknown etiology, with or without pulmonary involvement.
was
References Roig J, Aguilar X, Ruiz J et al. Comparative study of Legionella pneumophila and other nosocomial-acquired pneumonias. Chest 1991;99:344-350. Nelson DP, Rensimer ER, Burke CM, Raffin TA. Cardiac legionellosis. Chest 1984;6:807-808. Pastoris MC, Nigro G, Midulla M. Arrhythmia or myocarditis: a novel infection in children without pneumonia. Eur J Pediatr 1985;144:157-159. Redd SC, Schuster DM, Quan J et al. Legionellosis in cardiac transplant recipients: results of a nationwide survey. J Infect Dis 1988;158:651-653. Domingo Ch, Roig J, Seres J. Pericardial effusion as a clinical sign of legionnaires’ disease. Int J Cardiol 1989;23:407-409.
Science
International Journal of Cardiology, 37 (1992) 418-420 Publishers B.V. All rights reserved 0167-5273/92/$05.00
CARD10 15782
Myocarditis: a rare complication during Legionella infection S.Armengol
‘, Ch. Domingo b and E. Mesalles a
’ Servei de Cures Intensives, b Servei de Pneumologia. Hospital LJniLlersitariGermans Trlas i Pujol, Badalona, Barcelona, Spain (Received 18 April 1992; revision accepted 7 August 1992)
Legionella often causes systemic manifestations. The clinical spectrum now includes cardiac legionellosis. The first case of myocarditis was reported by Gross in 1981. To date few additional cases have been described. Myocardial involvement might be more frequent than supposed in legionnaires’ disease. Key words:
Legionnaires’
disease;
Myocarditis
Introduction Since the characterization of the organism causing the 1976 Philadelphia epidemic of legionnaires’ disease and the isolation of L. pneumophila, there has been considerable progress in the understanding and identification of infections due to Legionella species [I]. There is an expanding clinical spectrum of the disease caused by the genus Legionella which now includes cardiac legionellosis [2]. Cardiac involvement can present as tachycardia, relative bradycardia, endocarditis on a prosthetic valve, pericarditis and myocarditis [2]. We report a new case of myocarditis associated with Legionella pneumonia. Case Report A 43-yr-old Caucasian male was admitted to our hospital in February 1987, with a one-week history of productive cough, fever and progressively worsening shortness of breath. He had been initially treated with an amoxicillin-clavulanic acid combination. He admitted a 20-yr 1 pack/day smoking history, and his past
medical history was unremarkable. Physical examination revealed a cyanotic man with a temperature of 39.2”C, respiratory rate of 44 breaths/min, pulse of 124 beats/min, and a blood pressure of 75/40 mmHg
CK
CKMB
(u/ml)
(u/ml)
800
600
400
200
010 0 Correspondence to: Salvador Armengol, M.D., Servei de Cures Intensives, 2’ planta, Hospital Universitari Germans Trias i Pujol, Cra de1 Canyet s/n (Can Ruti), 08916-Badalona, Barcelona, Spain. Tel. 3953161. Fax 3954206.
I
2
3
4
5
6
DAYS Fig. 1. Evolution
of CPK and CPK-MB ctuve during days after admission.
the first 6
419
without paradoxical pulse. Jugular venous distension was absent. Auscultation revealed bibasilar rales and a cardiac gallop, but murmurs or pericardial friction rubs were not detected. Significant laboratory data were: erythrocyte sedimentation rate 67 mm/h and a white blood cell count of 15,60O/mm” with a differential count of 90 polymorphonuclear leukocytes, one band form and nine lymphocytes. Serum sodium level was 136 mEq/l; potassium, 3.6 mEq/l; BUN, 18 mg/dl; creatinine, 0.9 mg/dl; bilirubin, 1.76 mg/dl; SGOT, 96 U/l; lactic acid dehydrogenase 320 U/ml (cardiac isoenzymes were notably increased); serum creatine phosphokinase 402 U/ml with an MB-fraction of 78 U/ml (Fig. 1). Arterial blood gases on room air were pH 7.46: PaO, 46 mmHg; PaCO, 33 mmHg. The chest X-ray revealed a dense alveolar infiltrate in both lower lobes; Type B Kerley lines were also observed. The ECG showed a sinus tachycardia with a left bundle branch block (Fig. 2). A positive direct fluorescent antibody test for L. pneumophila in sputum was obtained and the patient received 4 g/day of intravenous erythromycin. A posi-
Fig. 2. Electrocardiogram
tive culture for L. pneumophila was obtained several days later and also a four-fold rise in antibody titre (indirect fluorescent antibody test) confirmed the diagnosis of legionnaires’ disease, but titres to a variety of other potential pathogens (Mycoplasma pneumonia, cytomegalovirus, echo, coxsackie, influenza virus, adenovirus and toxoplasma) remained unchanged. An echocardiogram revealed a decreased left ventricular function, with moderate hypokinesia. Five days after admission in the Intensive Care Unit, the patient improved and was discharged to the pulmonary ward. Ten days later, the chest X-ray and the arterial blood gases improved, and the left bundle branch block disappeared. Three weeks after admission the patient was discharged with a normal echocardiogram and has remained well for 5 yr. Discussion The clinical spectrum of the disease caused by the genus Legionella now includes myocarditis which usually presents with pneumonia. The diagnosis of Le-
showing left bundle branch block.
420
gionella pneumophila
myocarditis was accepted on the basis of the ECG and echocardiogram changes as well as the analytical data. Attempts to demonstrate any other cause of acute myocarditis were negative. Endocarditis and dilated cardiomyopathy were ruled out by the echocardiogram as well as by the evolution. L. pneumophila pneumonia was diagnosed according to the universal criteria [l]. L. pneumophila and pneumococci were initially investigated since these are the most common bacteria isolated in those patients with community-acquired pneumonia that required admission to our Intensive Care Unit. From 1987 to 1990, 71 patients were admitted to our Intensive Care Unit because of community-acquired pneumonia. In 14 cases pneumococci were isolated and in 12 Legionella was the infective isolated agent; in another 29 cases the germ could not be identified. In the rest of the patients other germs were isolated. To date only a few cases of Legionella myocarditis have been reported. Two of them had evidence of widespread involvement [2]. In other cases, especially in childhood [3], the myocardium seems to be the only affected organ. Myocarditis seems to be evident several days after the onset of respiratory symptoms [2] and could be influenced by the prompt treatment with intravenous erythromycin (our case recovered earlier than Gross’s patient [2]). Arrhythmia or conduction blocks have been described, especially when pneumonia is absent. QT- and ST-interval abnormalities as well as T-wave inversions have also been observed with prominent respiratory symptoms [2]. In our patient, left bundle branch block
initially detected. Finally, we would like to underline that, although L. pneumophila pneumonia is a common complication of cardiac transplantations, to date myocarditis due to L. pneumophila has not been reported in cardiac transplant recipients [4]. Cardiac involvement in legionnaires’ disease is infrequent. From 1983 to 1991, 157 cases of Legionella pneumonia have been diagnosed in our hospital. Only the present case and one other case with pericardial effusion showed cardiac involvement [5]. We consider that myocarditis, if looked for, could be more frequent than supposed in legionnaires’ disease. Because of this, the indirect fluorescent antibody test for Legionella should be included as a differential diagnostic test for idiopathic myocarditis of unknown etiology, with or without pulmonary involvement.
was
References Roig J, Aguilar X, Ruiz J et al. Comparative study of Legionella pneumophila and other nosocomial-acquired pneumonias. Chest 1991;99:344-350. Nelson DP, Rensimer ER, Burke CM, Raffin TA. Cardiac legionellosis. Chest 1984;6:807-808. Pastoris MC, Nigro G, Midulla M. Arrhythmia or myocarditis: a novel infection in children without pneumonia. Eur J Pediatr 1985;144:157-159. Redd SC, Schuster DM, Quan J et al. Legionellosis in cardiac transplant recipients: results of a nationwide survey. J Infect Dis 1988;158:651-653. Domingo Ch, Roig J, Seres J. Pericardial effusion as a clinical sign of legionnaires’ disease. Int J Cardiol 1989;23:407-409.
