Fulminant Myocardial Failure in a Previously Healthy Young Man
1997; Lippincott Williams & Wilkins; Volume: 95; Issue: 6 Linguagem: Inglês
10.1161/01.cir.95.6.1654
ISSN1524-4539
AutoresPhilippe Chevalier, François Vandenesch, Philippe Brouqui, Gilbert Kirkorian, Alain Tabib, Jérôme Etienne, Didier Raoult, R Loire, P Touboul,
Tópico(s)Cardiomyopathy and Myosin Studies
ResumoHomeCirculationVol. 95, No. 6Fulminant Myocardial Failure in a Previously Healthy Young Man Free AccessResearch ArticleDownload EPUBAboutView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticleDownload EPUBFulminant Myocardial Failure in a Previously Healthy Young Man Philippe Chevalier, François Vandenesch, Philippe Brouqui, Gilbert Kirkorian, Alain Tabib, Jerome Etienne, Didier Raoult, Robert Loire and Paul Touboul Philippe ChevalierPhilippe Chevalier From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. , François VandeneschFrançois Vandenesch From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. , Philippe BrouquiPhilippe Brouqui From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. , Gilbert KirkorianGilbert Kirkorian From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. , Alain TabibAlain Tabib From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. , Jerome EtienneJerome Etienne From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. , Didier RaoultDidier Raoult From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. , Robert LoireRobert Loire From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. and Paul TouboulPaul Touboul From the Service de Cardiologie (P.C., G.K.), the Service de Bactériologie (F.V., J.E.), and the Department of Pathology (A.T., R.L.), Hôpital Cardiologique Louis Pradel, Lyon, and the Unité des Rickettsies, Faculté de Médecine, Marseille (P.B., D.R.), France. Originally published18 Mar 1997https://doi.org/10.1161/01.CIR.95.6.1654Circulation. 1997;95:1654–1657Case Presentation (Philippe Chevalier, MD)HistoryA 15-year-old boy was admitted to the intensive care unit of our institution in early November 1992 because of rapidly progressive heart failure with fever. The patient was a secondary school pupil, living with his parents and his brother, all of whom were well and resided in a city suburb, spending occasional weekends in the country. There was no family history of heart disease. The boy had no cardiovascular risk factors, history of intravenous drug abuse, or risk factors for human immunodeficiency virus. The patient had undergone an appendectomy 8 years earlier. He had been exposed to a parturient cat in July 1992, and his brother had been hospitalized for 2 days in October 1992 for unexplained fever and abdominal pain. The patient had been well until 7 days earlier, when headaches and fever occurred. Three days later, he developed a cough, followed by upper abdominal discomfort and vomiting. The general practitioner diagnosed an acute bronchitis and prescribed oral amoxicillin. At that time, physical examination and cardiac auscultation were noted as normal. Over the course of the following days, the patient became dyspneic and was admitted to the hospital.Initial Clinical FindingsOn admission the boy was pale and anxious. He had pyrexia of 38°C, a heart rate of 120 beats per minute, a respiratory rate of 30 breaths per minute, and a blood pressure of 110/82 mm Hg. Physical examination revealed an S3 sound with a 2/6 precordial murmur. Bibasilar inspiratory crackles were also present; the liver extended 3 cm below the right costal margin, and the jugular veins were distended to 10 cm above the sternal angle. No peripheral edema, cyanosis, rash, or lymphadenopathy was found. The abdominal and neurological examinations were normal.Most of the laboratory findings, including white blood cell count, hemoglobin, platelets, erythrocyte sedimentation rate, C-reactive protein, and serum creatinine, were within the normal ranges. The prothrombin time was markedly prolonged (international normalized ratio, 2.9); arterial blood gas analysis showed a slight hypoxemia with alkalosis (Po2, 67 mm Hg; pH, 7.5).The ECG showed sinus rhythm of 120 beats per minute, with nonspecific ST-segment and T-wave abnormalities. A radiograph of the chest showed slight cardiomegaly, with blood vessels in the upper lobes that were more engorged than those at the bases. Pulmonary interstitial edema in both bases and a left pleural effusion were also seen. On echocardiography, the left ventricle was markedly enlarged, with diffuse hypokinesis and no definite pericardial effusion.A diagnosis of viral myocarditis was initially considered, and cardiac catheterization was performed. Mean capillary wedge pressure was 22 mm Hg, mean pulmonary arterial pressure was 30 mm Hg (40/20), and cardiac index was 2 L·min−1·m−2. Coronary angiography revealed normal vessels. Right ventricular endomyocardial biopsies were made, and the specimen was used for histology and culture.Subsequent Hospital CourseOn November 11, positive serology for Q fever was obtained, and treatment with doxycycline (200 mg BID) and ofloxacin (400 mg BID) was commenced. The patient's serum antibodies reacted only against phase II of the nine mile strain of Coxiella burnetii. A first serum reacted with titers of 400 for IgG and 25 for IgM (Table). Culture of the first myocardial biopsy yielded C burnetii.On December 6, despite antibiotic treatment and inotropic support, the hemodynamic status continued to deteriorate. Because right ventricular systolic function was judged to be only moderately impaired, a left ventricular assist device (BVS 5000; Abiomed Inc) was implanted. On day 5 after implantation, attempts at weaning the patient off left ventricular assist remained unsuccessful, and a cardiac transplantation was performed.There were no signs of allograft rejection, but the posttransplantation course was complicated by pneumonia. The patient underwent a left lower lobe resection because of empyema and pyothorax. Although Enterococcus faecalis and Candida albicans were identified as the culprit microorganisms, this definitive procedure was chosen because of the posttransplantation immunosuppression. Subsequently, the patient developed edematous pancreatitis, followed by a consumptive coagulopathy refractory to transfusion of platelets and coagulation factors. Acute serum testing demonstrated a fourfold rise in titers for cytomegalovirus and respiratory syncytial virus.The patient died of multiple organ failure 2 months after initial admission.Clinical Discussion (Paul Touboul, MD, and Gilbert Kirkorian, MD)This 15-year-old boy without any medical history presented with acute myocardial dysfunction and fever. The most striking aspect of this case is the rapid progression to intractable heart failure over a 1-month period. We organize our discussion around the clinical findings. There are many causes of acute heart failure with a dilated heart.1 An acute process, myocardial or pericardial, can by itself lead to cardiac failure, but more commonly, preexisting cardiac disease is aggravated by a precipitating factor. A process of elimination determines the cause of acute heart failure. General physical examination did not reveal any evidence for an extracardiac disorder. Autoimmune disorders, such as systemic lupus erythematosus, can cause acute heart failure but are usually associated with other clinical findings and an abnormal erythrocyte sedimentation rate, which were not present in this patient.It would be unusual for a 15-year-old boy to have unrecognized ischemic heart disease in the absence of coronary risk factors. Moreover, the ECG showed no evidence of myocardial infarction. Although the heart can be directly involved in metastatic cancer, diffuse myocardial involvement is uncommon in this setting.2Pericardial disease frequently occurs in young patients, and cardiac tamponade can also present with jugular venous distension, dyspnea, and low cardiac output. Signs of pulsus paradoxus, ie, inspiratory systolic blood pressure decreased by >10 to 12 mm Hg, is usually found in pericardial tamponade but was not mentioned here. The heart sounds were not muffled, and echocardiography did not reveal pericardial fluid or a localized diastolic compression of the right atrium and the right ventricle. Preexisting cardiac disease decompensated by a benign viral infection is also unlikely, given the fatal outcome.Finally, because a preceding respiratory febrile illness was evident clinically, the history suggests that cardiac involvement may have been part of an ongoing infectious process. The absence of specific auscultatory and echocardiographic findings made a diagnosis of valvular endocarditis unlikely. Giant cell myocarditis may account for a rapid decline in left ventricular function, but the diagnosis can be made only by histological study.3 Fulminant myocarditis is capable of producing acute dilated cardiomyopathy,45 but in most cases the heart is only slightly dilated at echocardiography.6 In the present case, the echocardiographic findings could have been explained by preexisting myocardial disease, but there are no features in the clinical history suggestive of dilated cardiomyopathy. Clinically significant acute myocarditis is most commonly caused by viruses, but in our patient, initial serological findings were not suggestive of any viral infections. The exact pathogenesis of myocarditis has yet to be elucidated, although strong evidence suggests that there is an autoimmune component to myocardial destruction. In the present case, the time lag between heart failure and the initial symptoms favors this hypothesis.In our opinion, the initial symptoms of our patient were typical of acute Q fever. Pneumonia with headaches and fever, cough, upper abdominal discomfort, vomiting, and dyspnea are classic manifestations of acute Q fever.7 Thus, considering the clinical history together with culture and serological findings, we believe Q fever myocarditis associated with profound systolic dysfunction is the most likely diagnosis in this case.Pathological Findings (Robert Loire, MD, and Alain Tabib, MD)Endomyocardial biopsy, after staining with hematoxylin-eosin, did not reveal an inflammatory process despite serum studies that suggested Q fever. A sampling error may have accounted for this result.8 Examination of the heart obtained after transplantation revealed a flabby organ (weight, 450 g), with predominantly left ventricular dilatation. In both the right and left endocardium, there was a diffuse proliferation of interstitial connective tissue without cellular infiltration. The walls of some small endocardial vessels were thickened with interstitial fibrosis. There was irregular hypertrophy of myocytes and dense interstitial fibrosis without evidence of an inflammatory-cell infiltrate. The pericardium demonstrated inflammatory changes with a fibrinous pattern. There were few areas of mononuclear cell infiltrates (Fig 1).Indirect immunofluorescent antibody examination of the biopsy specimen showed C burnetii in large clusters of organisms. Culture of the myocardium after cardiac transplantation did not yield C burnetii, although indirect immunofluorescent antibody and immunoalkaline phosphatase labeling of C burnetii in the paraffin-embedded myocardium still showed small clusters of infected cells (Fig 2). Gram and silver staining of myocardial specimens did not demonstrate any microorganisms. Culture of the lung demonstrated cytomegaloviruses but did not yield C burnetii. Although isolation of C burnetii from an affected organ usually proves its pathogenetic role, one may also consider the possibility that the histological lesion corresponded exclusively to a cardiomyopathy and that the C burnetii infection was coincidental. To the best of our knowledge, C burnetii has not previously been isolated directly from human myocardium.Bacteriological Findings (Didier Raoult, MD, Jerome Etienne, MD, Philippe Brouqui, MD, and François Vandenesch, MD)C burnetii is an extremely infectious gram-negative intracellular pathogen.9 The reservoir of C burnetii is wide; cattle, goats, and sheep are frequently involved, but cats, dogs, and rabbits have been reported as a source of infection.10 In theory, any parturient mammal could be considered a source of infection. In our patient, the only risk factor found was his contact in July 1992 with a parturient cat, a well-established epidemiological exposure.11When grown in ova or in cells, C burnetii exhibits a phase-variation phenomenon caused by a lipopolysaccharide alteration that is equivalent to the smooth-rough variation observed in Enterobacteriaceae. Phase I is infectious and is recovered from infected animals, and phase II is obtained after subcultures.12 Paradoxically, the humoral response of an acutely infected human being is directed mainly against phase II. As a diagnostic test, serology with indirect immunofluorescence is the most convenient tool. The presence of an IgG anti–phase II titer of ≥200 and an IgM anti–phase II titer of ≥50 suggests recent infection.In mammals, C burnetii results in a nonsterile immunity, because the organism persists in the infected host. It is believed that factors in the host (immunosuppression or cardiovascular abnormality) allow C burnetii to cause clinical infection. The fact that few pathological changes, especially the lack of inflammation, were observed in the myocardium of this patient may, paradoxically, explain the fatal progression of disease. In acute Q fever, the most typical pathological change is the presence of granulomas in the liver or bone marrow, revealing an effective T-cell response.13 This is an unusual finding in cases of chronic Q fever,14 leading some authors to suggest that chronic Q fever occurs with the help of T-cell immunosuppression.1315 Thus, one can hypothesize that the fatal outcome in this case may be due to an unadapted T-cell response toward C burnetii. The coagulation profile, with an isolated increased prothrombin time, was supportive of the presence of a lupus-like anticoagulant in the serum frequently reported in patients with acute Q fever.16Therapy with 200 mg/d doxycycline for 3 weeks is the treatment of choice in acute Q fever. In some cases, however, short-term steroid therapy has been prescribed simultaneously, especially when acute Q fever coexists with an autoimmune response.17 The treatment failure in the present case may be explained by the severity of the disease. However, it is remarkable that C burnetii–infected cells, shown by immunohistochemistry, were still present after doxycycline therapy. In our opinion, the cause of death in this patient was due to infectious complication of heart transplantation rather than to Q fever itself.Clinical SummaryIn summary, the case of a young patient who rapidly developed intractable heart failure necessitating mechanical circulatory support followed by cardiac transplantation is presented. The initial seroimmunological profile suggested an acute form of Q fever. Culture of one specimen of an endomyocardial biopsy yielded C burnetii and thus firmly established the link between the microorganism and myocardial failure. In addition, the diagnosis of myopericarditis was suggested by histological examination. Documented cases of isolation of pathogens in human myocardium are rare. Endomyocardial biopsy is a useful diagnostic procedure and should be performed more frequently.Final DiagnosisFulminant Q fever perimyocarditis.The editor of Clinicopathological Conferences is Herbert L. Fred, MD, St Luke's Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, Room B524 (MC1-267), Houston, TX 77030-2697.Download figureDownload PowerPoint Figure 1. Photomicrograph of the pericardium. Note fibrinous pericarditis with few mononuclear cell infiltrates. Hematoxylin-eosin; magnification ×100.Download figureDownload PowerPoint Figure 2. Immunohistological demonstration of Cburnetii in the myocardium (magnification ×1000). Intracytoplasmic aggregates (red-stained pleiomorphic particles) of Cburnetii are present in mononuclear cell only. Note paucity of inflammatory response and lack of granulomas. Table 1. Patient's Antibody Titers Against Coxiella Burnetii, Nine Mile Strain, by Indirect Immunofluorescent Antibody Phase IPhase IIDateIgGIgMIgAIgGIgMIgANovember 19, 1992000400250December 17, 1992000100250December 24, 19920005000January 4, 199300050250January 21, 19930005000Presented January 8, 1996, at the Hôpital Cardiologique, Louis Pradel, Lyon, France.FootnotesCorrespondence to Paul Touboul, MD, Hôpital Cardiologique Louis Pradel, BP Lyon Montchat, 69394 Lyon Cedex 03, France. References 1 Braunwald E, Grossman W. Clinical aspects of heart failure. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. Vol 2. Philadelphia, Pa: WB Saunders; 1992:444-462. Google Scholar2 Braunwald E, Rosenthal DS. Hematological-oncological disorders and heart disease. In: Braunwald E, ed. Heart Disease: A Textbook of Cardiovascular Medicine. Vol 2. Philadelphia, Pa: WB Saunders; 1992:1752-1766. Google Scholar3 Davidoff R, Palacio I, Southern J. Giant cell versus lymphocytic myocarditis: a comparison of their clinical features and long-term outcomes. Circulation.1991; 83:953-961. CrossrefMedlineGoogle Scholar4 Dec GW, Palacios I, Fallon JT. Active myocarditis in the spectrum of acute dilated cardiomyopathies: clinical features, histologic correlates, and clinical outcomes. N Engl J Med.1985; 312:885-890. CrossrefMedlineGoogle Scholar5 Rockman HA, Adamson RM, Dembitsky WP. Acute fulminant myocarditis: long-term follow-up after circulatory support with left ventricular assist device. Am Heart J.1991; 121:922-926. CrossrefMedlineGoogle Scholar6 Pinamonti B, Alberti E, Cigalotto A. Echocardiographic findings in myocarditis. Am J Cardiol.1988; 62:285-291. CrossrefMedlineGoogle Scholar7 Tissot-Dupont H, Raoult D, Brouqui P, Janbon F, Peyramond D, Weiller PJ, Chicheportiche C, Nezri M, Poirier R. Epidemiologic features and clinical presentation of acute Q fever in hospitalized patients: 323 French cases. Am J Med.1992; 93:427-434. CrossrefMedlineGoogle Scholar8 Chow LH, Radio SJ, Sears TD. Insensitivity of right ventricular endomyocardial biopsy in the diagnosis of myocarditis. J Am Coll Cardiol.1989; 14:915-920. CrossrefMedlineGoogle Scholar9 Brouqui P, Tissot-Dupont H, Drancourt M, Berland Y, Etienne J, Leport C, Goldstein F, Massip P, Micoud M, Bertrand A, Raoult D. Chronic Q fever: ninety-two cases from France, including 27 without endocarditis. Arch Intern Med.1993; 153:642-648. CrossrefMedlineGoogle Scholar10 Marrie TF. Epidemiology of Q fever. In: Marrie TJ, ed. Q Fever: The Disease. Vol 1. Boca Raton, Fla: CRC Press; 1990:49-70. Google Scholar11 Marrie TJ, Durant H, Williams CJ, Mintz E, Waag DM. Exposure to parturient cats: a risk factor for acquisition of Q fever in maritime Canada. J Infect Dis.1988; 158:101-108. CrossrefMedlineGoogle Scholar12 Strocker MG, Fiset P. Phase variation of the nine miles and other strains of Coxiella burnetii. Can J Microbiol.1956; 2:310-321. CrossrefMedlineGoogle Scholar13 Raoult D. Host factors in the severity of Q fever. Ann N Y Acad Sci.1990; 590:33-38. CrossrefMedlineGoogle Scholar14 Brouqui P, Dumler JS, Raoult D. Immunohistologic demonstration of Coxiella burnetii in the valves of patients with Q fever endocarditis. Am J Med.1994; 97:451-458. CrossrefMedlineGoogle Scholar15 Raoult D, Brouqui P, Marchou M, Gastaut JA. Acute and chronic Q fever in patients with cancer. Clin Infect Dis.1992; 14:127-130. CrossrefMedlineGoogle Scholar16 Ordi-Ros J, O'Callaghan AS, Monegal-Ferran F, Monasterio-Aspiri Y, Juste-Sanchez C, Vilardell-Tarres M. Prevalence, significance, and specificity of antibodies to phospholipids in Q fever. Clin Infect Dis.1994; 18:213-218. CrossrefMedlineGoogle Scholar17 Levy PY, Raoult D, Razongles JJ. Q fever and autoimmunity. 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March 18, 1997Vol 95, Issue 6 Advertisement Article InformationMetrics Copyright © 1997 by American Heart Associationhttps://doi.org/10.1161/01.CIR.95.6.1654 Originally publishedMarch 18, 1997 Advertisement
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