Acute pericarditis is a not uncommon, frequently idiopathic disorder that mostly follows a benign clinical course. Some myocardial involvement often accompanies acute pericarditis, with the term myopericarditis indicating the pericardium as the primary focus [3]. Viruses are often implicated when acute pericarditis or myopericarditis are linked to infection, with bacterial causes less commonly described [3]. Diagnostic criteria for acute pericarditis include chest pain, pericardial friction rub, ST segment elevations and pericardial effusion, with a clinical diagnosis made when two of these criteria are met [3]. A clinical diagnosis of myopericarditis includes the additional detection of elevated cardiac enzymes or a new onset of depressed left ventricular systolic function [3].

Campylobacter spp. have an uncommon but increasingly recognised link with myopericarditis, as supported by a growing body of case reports and reviews of literature [4–6]. Our report is notable in terms of the observed differences in both pathogen and host characteristics. Firstly, our patient was positive for C. coli, a species well recognised as a cause of enterocolitis, but not previously reported in association with myopericarditis. Secondly, the patient was a healthy, middle-aged female, in contrast to previous patients where most were younger immunocompetent males [4–6]. Although Campylobacter does show tendency to cause higher rates of disease in men compared to women, the apparent predilection towards men in myopericarditis is striking. However despite this observation, epidemiological evidence of a causal association between campylobacteriosis and myopericarditis is lacking. We identified a single study that showed a greater incidence of myocarditis in Campylobacter positive cases than controls at 16.1 cases per 100,000 person-years (95% CI 2.3–114.4) compared to 1.6 cases per 100,000 person-years (95% CI 0.2–11.4), but the result was not significant and absolute case numbers were small [7].

It is important to make distinction between myopericarditis associated with C. jejuni or C. coli and that with C. fetus. The former are recognised causes of enteric disease in humans and likely represent archetypal causes of Campylobacter myopericarditis. Conversely C. fetus is an atypical, invasive species, capable of evading the host immune system by means of complement resistant surface proteins [8]. As such it is more frequently isolated from blood and pericardial fluid, with enteric symptoms either absent or less pronounced [9]. For C. jejuni (and C. coli) associated myopericarditis, the putative mechanisms include direct infection of the pericardium or myocardium, an immune hypersensitivity reaction, or the effect of bacterial toxins [10]. Currently evidence for direct infection is limited to two reports of C. jejuni detection in pericardial fluid [11, 12]. A dominant immune-mediated response also seems less likely given the short window between the onset of enteric and cardiac symptoms, as distinct to that seen with C. jejuni and development of other immune-mediated disease (e.g., Guillain–Barré syndrome and reactive arthritis) [10]. Although there is a lack of evidence for a specific Campylobacter-associated cardiotoxin [13], the short window period surely favors a toxin-mediated mechanism [4, 6]. Furthermore, the infrequency of C. coli myopericarditis as highlighted by our case might possibly be explained by the dominance of C. jejuni at the species level, along with the lower incidence of cytotoxin and enterotoxin production by C. coli compared to C. jejuni [13].

It is unclear whether antibiotic treatment influences the outcome of Campylobacter spp. myopericarditis, however a recent examination of C. jejuni-associated myopericarditis cases showed treatment with either macrolide or fluoroquinolone antibiotics to be a common practice although without any apparent consensus on dosage and treatment duration [5]. However campylobacteriosis is generally regarded as a self-limiting illness with antimicrobial therapy recommended for immunocompromised patients, patients whose symptoms are severe or persistent, or who develop extra-intestinal infections [1]. For our case confirmation of Campylobacter spp. in stool occurred following hospital discharge, with a mechanism for myopericarditis such as direct infection or toxin-mediated response not able to be readily determined. As such antimicrobial therapy was not commenced. Treatment for the myopericarditis was conservative, using nonsteroidal anti-inflammatory drugs (NSAIDS) and colchicine. Among case reports describing Campylobacter-associated myopericarditis we identified a single episode where colchicine, as an adjunctive to aspirin, was used in treating myopericarditis, with the case reported as fully recovered at a 3-month review [14]. Anecdotally, clinical outcomes for C. jejuni (and C. coli) associated myopericarditis appear favourable [5] with low rates of morbidity, mortality, evolution to heart failure and worsening ventricular function [15].