Capnocytophaga canimorsus Sepsis Complicated by Myocardial Infarction in Two Patients with Normal Coronary Arteries

Hans-Ulrich Ehrbar 0 1 Jacques Gubler 0 1 Stefan Harbarth 0 1 Bernhard Hirschel 0 1 0 Received 29 January 1996; revised 18 April 1996. This work was presented in part at the annual session of the Swiss Society of Internal Medicine held on 8-9 September 1994 in Lausanne , Switzerland . Stadtspital Triemli, CH - 8063 Zurich, Switzerland 1 From the Stadtspital Triemli, Zurich ; and the Hopital Cantonal Universitaire , Geneva, Switzerland We describe two patients who had acute myocardial infarctions during episodes of Capnocytophaga canimorsus sepsis. C. canimorsus is associated with severe infection in patients who are immunocompromised; one of these patients had undergone splenectomy for Hodgkin's disease 11 years earlier, and the other consumed significant amounts of alcohol regularly. Both patients owned dogs that had licked them or produced minor skin wounds shortly before they became ill. Coronary angiographic findings were normal for both patients. The association of acute myocardial infarction and sepsis with a specific pathogen is unique. This finding suggests that endothelial damage and coronary thrombosis due to C. canimorsus sepsis is a possible mechanism of acute myocardial necrosis. Case Reports Patient 1. A 52-year-old male had been superficially bitten on the forearm by his poodle ~ 7 days before his illness. He had smoked 20- 30 cigarettes and consumed ~ 100 g of alcohol daily for several years. The patient went into acute cardiac arrest 18 hours after experiencing an initial episode of typical retrostemal chest pain. Cardiopulmonary resuscitation and oro tracheal intubation were performed at his home. When he arrived in the emergency department, he was found to have supraventricular tachycardia, which was electrically converted; a diagnosis of acute myocardial infarction was made on the basis of electrocardiographic tracings (ST elevations of 1.5 mV in leads I and aVL) and evidence of corresponding regional hypomotility on an echocardiogram. Thrombolysis with recombinant tissue-type plasminogen activator was started, and the patient was mechanically ventilated and re ceived vasopressor therapy for 24 hours. At the time of admis sion, laboratory studies revealed thrombocytopenia (platelet count, 13,OOO/fiL); a C-reactive protein level of 302 mg/L (normal level, 0 - 5 mg/L); and a serum creatinine-kinase level of 3,729 U/L (normal level, 10-190 U/L) with an MB-fraction of 406 U/L (normal value, < 27 U/L), both of which decreased thereafter. On day 2, the patient was hemodynamically stable, and he was extubated; however, he developed a fever. Blood for cul tures was drawn, and intravenous therapy with amoxicillin/ clavulanic acid (2.2 g every 8 hours) and netilmicin (150 mg every 12 hours) was initiated. The blood cultures subsequently yielded C. canimorsus, which was identified by standard meth ods [5]. The patient made an uneventful recovery. Exercise tests performed on day 10 showed no signs of ischemia; findings on an echocardiogram were normal, and coronary angiography on day 14 showed normal vessels with no myocardial hypomo tility. Patient 2. A 53-year-old man with no history of chest pain or coronary artery disease was admitted to the hospital because of high fever, chest pain, and malaise of 1 day's duration. He had had Hodgkin's disease 11 years earlier and had apparently been cured with splenectomy, radiation therapy, and three cy cles of chemotherapy. During the weeks before admission, his dog had licked a superficial wound on his right leg. On admission, the patient had a severe headache, intermittent retrostemal chest pain, and extensive purpuric lesions on the face and both arms and legs. His temperature was 40.2C; respirations, 32/min; pulse, l40/min; and blood pressure, 90/ 50 mm Hg. The WBC count was 5,000/pL with a significant left shift. The platelet count was 15,c)00/fiL. An arterial blood gas analysis performed while the patient was breathing 40% oxygen by mask showed a pH of 7.31, a Pco, of 30 mm Hg, and a P0 2 of 109 mm Hg. The serum lactate level was 5.98 mmol/L (normal level, < 1.9 mmol/L), Further laboratory investigations revealed diffuse intravascu lar coagulation (DIC), with a partial thromboplastin time of 179 seconds (normal time, <32 seconds) and a prothrombin time of 35% of normal. The fibrinogen level was 1.2 giL (nor mal level, >2.0 giL), and fibrin split products were present. The serum creatinine level was 152 /LmoVL; the creatinine kinase level was 481 UIL (normallevel, 5-270 U/L) and subse quently rose to 1,539 UIL, with a significant MB-fraction (max imal value, 122 U/L; normal value, <30 U/L). The patient was treated empirically with intravenous ceftazi dime (2 g every 6 hours), gentamicin (120 mg every 12 hours), and metronidazole (500 mg every 8 hours). His hypotension persisted, requiring treatment with systemic epinephrine and dopamine. Fresh plasma, thrombocytes, and antithrombin III were given because of the severe DIC. Twelve hours after admission, electrocardiographic tracings revealed an evolving lateral myocardial infarction. Blood for cultures that was drawn on admission yielded long, thin, gram-negative bacteria that were subsequently identified as C. canimorsus. Treatment with intravenous clindamycin (900 mg every 8 hours) was continued for 2 weeks. He recovered fully. On day 18, exercise tests revealed no signs of ischemia, findings on an echocardiogram were normal, and coronary an giography showed normal coronary arteries with mild myocar dial hypomotility of the lateral left ventricle. The ejection frac tion was 60%. The patient was asymptomatic when he was discharged after 3 weeks of hospitalization. Discussion Both patients presented with typical clinical and laboratory signs of acute myocardial infarction. In the first patient, the cardiac event preceded the manifestations of sepsis, while in the second patient, myocardial infarction evolved during sepsis. The high levels of cardiac enzymes, together with the rapid resolution of cardiac dysfunction and the documented regional hypomotility observed in patient 1, are best explained by tem porary coronary occlusion and not by diffuse septic myocardial necrosis. Significant atherosclerotic disease was excluded on the basis of the normal coronary angiographic findings. Although chronic infections with Chlamydia pneumoniae or Helicobacter pylori have been linked epidemiologically to chronic atheromatous disease of the coronary arteries [6], our search of the literature revealed only two recent reports con cerning sepsis as a cause of acute myocardial infarction [3, 4]. Guest and co-workers [4] described 209 critically ill patients and found evidence of myocardial injury in 32, five of whom had sepsis [4]. C. canimorsus was not the offending agent in any of these patients (A. S. Jaffe, personal communication). To our surprise, the second report also concerned a case of sepsis due to C. canimorsus [3]. The patient, a 24-year-old kennel operat (...truncated)