Clin Res Cardiol (2023). https://doi.org/10.1007/s00392-023-02302-4

Erysipelas and Myocarditis

K. Wosgien1, D. O h-Ici1, K. Seidenspinner1, A. Bärisch1, S. Kische1

1Klinik für Innere Medizin - Kardiologie und konserv. Intensivmedizin, Vivantes Klinikum im Friedrichshain, Berlin;

Case: A man aged 26 years presented to the emergency department with acute chest pain. Two days previously, a blister had formed on his right foot. This had become infected with redness and swelling. There was no history of drug abuse or other medication. He denied dyspnoea, and any other infections in the past. Bilateral congestion was present in the X-ray. ECG showed an incomplete right bundle branch block, ST-elevation in leads V5 – V6 and PQ segment depression in leads II, III, avF. The troponin level I and CRP was elevated. The patient showed no signs of fever. An intravenous antibiotic was started for the clinically diagnosed Erysipelas. Transthoracic echocardiogram revealed a dilated left ventricle with a reduced ejection fraction  (EF) of 40 % and global hypokinesia,. The coronary angiography showed normal coronary arteries. Transesophageal echocardiography showed no Patent Foramen Ovale and no signs of endocarditis. Blood cultures were negative. Immunologic studies were normal but Antistreptolysin (ASL) test showed a significantly increased value. The CMR established the diagnosis of a myocarditis with a mild LV dilatation and normalised systolic EF of 58 %. It revealed an acute oedema subepicardial inferolateral basal with significantly increased T2 values in this area. T1 mapping demonstrated significantly increased native T1 values (pre-contrast), and significantly decreased post-contrast values in the area of interest. The Late Gadolinium Enhancement (LGE) showed a pronounced subepicardial scar inferolateral basal to apical. The modified Lake Louise Criteria 2018 were met. Discussion: Myocarditis is an inflammatory disease of the myocardium and the clinical presentation is highly variable. Patients with acute myocarditis often present with non-specific symptoms of chest pain, dyspnoea, or palpitations; however, acute viral myocarditis can cause cardiac damage without symptoms. The most frequent cause of this disease in developed countries is viral infection. Nevertheless, cases of bacterial myocarditis have been reported. The most common bacterial causes are Staphyloccus aureus and Streptococcus spp. Bacterial infection seems to be a poorly reported etiologic cause of myocarditis. Erysipelas is mainly caused by infection with group A ß-hemolytic Streptococcus.  There are only two cases described of patients with erysipelas and acute myocarditis. Streptococcal infection associated to cardiac disease is most commonly described with acute rheumatic fever. Our patient did not meet the revised Jones criteria for acute rheumatic fever. As in the case Dominguez et al. reported we assume that our patient suffered from a toxin-induced myocarditis. Three factors support this thesis as already demonstrated by Friedman: 1. Local wound identified as the portal of entry of the pathogen, 2. A significantly increased value of ASL as evidence for an infection with Streptococcus spp., 3. met criteria for myocarditis in the CMR. The exact pathophysiological mechanisms of acute non-rheumatic streptococcal myocarditis are still not fully understood. Possible causative mechanisms are cross-reactivity as well as streptococcal toxins. Overall, in the cases of non-rheumatic streptococcal myocarditis linked to pharyngitis the toxin theory seems to be of the most probability. Our Patient, similar to the other patients described in the literature, had an excellent clinical response following antibiotic treatment of the offending organism.

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