Sequential infections of Campylobacter jejuni and Salmonella gastroenteritis complicated by myocarditis: a case report

Abstract

Background:

Myocarditis is a rare but serious complication of bacterial gastroenteritis, occurring when intestinal infections extend to systemic inflammation involving the myocardium. Although viral etiologies are most prominent in the literature, increasing evidence implicates that certain bacterial pathogens, usually regarded as confined to the gastrointestinal tract, provoke cardiac inflammation through mechanisms that are poorly understood.

Case presentation:

We report a case of recurrent myocarditis in a 34-year-old previously healthy male, with each episode temporally associated with a distinct episode of enteric infection – initially due to Campylobacter jejuni and subsequently Salmonella enterica. The latter presentation was characterized by constitutional symptoms, biochemical evidence of myocardial injury, and confirmatory imaging findings, necessitating a high index of suspicion to establish the diagnosis. The patient responded well to a combination of targeted antimicrobial therapy and anti-inflammatory pharmacologic intervention.

Conclusion:

The presence of this pattern involving two different bacterial pathogens raises significant questions regarding host susceptibility, immune system activation, and overall immunopathogenesis of bacterial myocarditis. It highlights the need to broaden the differential diagnosis in patients with gastrointestinal illness who present with systemic or cardiac-related clinical manifestations. As this phenomenon is likely underrecognized, particularly in the absence of classic cardiac symptoms, timely identification and multidisciplinary management are crucial for optimizing outcomes and reducing the risk of long-term myocardial complications. By presenting this rare and illustrative case, we aim to contribute to the evolving recognition of bacterial myocarditis as a distinct clinical entity and to prompt further inquiry into the host-pathogen dynamics that may underlie its pathophysiology.

Background

Acute infectious gastroenteritis is one of the most prevalent illnesses globally, often perceived as self-limiting and benign[1]. However, in rare circumstances, its clinical trajectory may transcend gastrointestinal boundaries, unmasking life-threatening complications such as myocarditis[2]. Myocarditis is an inflammatory condition of the myocardium that can present with a clinical spectrum of severity, from subclinical disease to fulminant heart failure and sudden cardiac death. Although viral etiologies remain the dominant cause, a growing body of literature identifies bacterial pathogens, including Salmonella enterica and Campylobacter jejuni, as rare but significant causes^[3–5^].

HIGHLIGHTS

• Recurrent myocarditis occurred sequentially following Campylobacter jejuni and later Salmonella enterica gastroenteritis in the same previously healthy patient.

• Bacterial gastroenteritis can lead to myocardial inflammation, mimicking acute coronary syndrome with ST-segment elevation and elevated troponin.

• Cardiac magnetic resonance imaging was essential in confirming the diagnosis of acute myocarditis.

• The recurrence following two distinct enteric pathogens suggests possible host-specific susceptibility and immune-mediated mechanisms.

• Early recognition and multidisciplinary management are critical to prevent long-term myocardial complications.

This report is a unique case of recurrent bacterial gastroenteritis-associated myocarditis in the same patient. The patient developed two distinct episodes, the first episode following C. jejuni infection, and more recently, the second episode after confirmed S. enterica infection. This clinical recurrence raises intriguing questions regarding host susceptibility, the possibility of immune priming, and the broader immunopathogenesis of bacterial myocarditis. By presenting this case, we aim to contribute to the growing recognition of this phenomenon and advocate for increased diagnostic vigilance when evaluating patients with systemic symptoms in the context of foodborne illness.

Case presentation

A 34-year-old previously healthy male presented to the emergency department with a 4-day history of high-grade fever reaching 40 °C, watery diarrhea, and multiple episodes of non-bloody, non-projectile vomiting. The symptoms began shortly after consuming buffet food at his workplace. He had been hospitalized 2 days prior with similar complaints, which temporarily improved following supportive care but subsequently recurred.

The patient’s medical history was significant for two prior episodes of C. jejuni gastroenteritis in March 2023 and May 2024, both confirmed by stool culture. The latter episode was complicated by myocarditis, which had presented with chest discomfort and elevated cardiac biomarkers, managed conservatively at the time. He had a remote history of a femoral fracture in childhood and chronic neck pain managed with tramadol and co-codamol. He denied alcohol use, illicit drug use, or any known drug or food allergies. There was no known family history of cardiomyopathy, autoimmune disease, or sudden cardiac death.

On admission, the patient appeared well and was hemodynamically stable. Vital signs revealed a temperature of 36.9 °C, heart rate of 85 beats per minute, blood pressure of 97/67 mm Hg, respiratory rate of 17 breaths per minute, and oxygen saturation of 99% on room air. Physical examination revealed no signs of distress, dehydration, or focal abdominal tenderness. Cardiovascular and respiratory examinations were unremarkable. There were no cutaneous lesions, lymphadenopathy, or neurological deficits.

Initial laboratory investigations revealed leukocytosis, elevated inflammatory markers, and a rising troponin level, suggestive of myocardial involvement. A detailed summary of laboratory findings is presented in Table 1. Stool PCR testing was positive for S. enterica, which demonstrated susceptibility to trimethoprim-sulfamethoxazole and intermediate susceptibility to ciprofloxacin. Clostridium difficile PCR was negative. Serum IgA and IgG levels were normal, and serum electrolytes and renal and liver function test results were within normal limits.

Table 1.

Laboratory investigations at the time of hospital admission, highlighting evidence of systemic inflammation and myocardial injury.

Test	Result	Reference range	Interpretation
White blood cell count	13.3 × 109/l	4.0–10.0 × 109/l	Elevated
Hemoglobin	13.3 g/dl	13.5–17.5 g/dl	Slightly low-normal
Platelets	206 × 109/l	150–400 × 109/l	Normal
C-reactive protein	18.5 mg/l	<5.0 mg/l	Elevated
High-sensitivity troponin (initial)	4.1 ng/ml	<0.04 ng/ml	Elevated
High-sensitivity troponin (repeat)	13.2 ng/ml	<0.04 ng/ml	Markedly elevated
Creatine kinase	239 U/l	30–200 U/l	Mildly elevated
Serum lactate	1.1 mmol/l	0.5–2.2 mmol/l	Normal

Electrocardiography (ECG) revealed ST-segment elevations in leads V2 through V6, as demonstrated in Figure 1. Transthoracic echocardiography showed a mildly dilated left ventricle with global hypokinesia and left ventricular ejection fraction of 40–45%. Right ventricular systolic function was also mildly reduced. Cardiac magnetic resonance imaging confirmed the presence of patchy subepicardial late gadolinium enhancement in the lateral wall of the left ventricle, consistent with acute myocarditis, as demonstrated in Figure 2.

Figure 1.

ST elevation in V2 through V6.

Figure 2.

Cardiac magnetic resonance imaging showing subepicardial late gadolinium enhancement consistent with acute myocarditis (A–D). Red arrows indicate areas of myocardial inflammation.

Computed tomography of the abdomen ruled out intra-abdominal pathology. The patient was admitted to a telemetry-monitored medical unit. Management included intravenous fluid rehydration, electrolyte replacement, and antibiotic therapy with ciprofloxacin. The administration of colchicine (0.5 mg) twice everyday was initiated for myocardial inflammation. Throughout his hospitalization, the patient’s symptoms steadily improved. Cardiac enzyme levels trended downward, gastrointestinal symptoms resolved, and repeat echocardiography showed no worsening of systolic function. He was discharged home in stable condition on colchicine, with scheduled follow-ups for cardiology and gastroenterology.

Discussion and conclusions

Although viral infections are generally recognized as the major cause of myocarditis, recent reports have drawn attention to enteric bacterial pathogens as underrecognized etiologies – particularly in the context of enteric infections. Notably, S. enterica and C. jejuni, though typically associated with self-limiting gastroenteritis, have been implicated in systemic complications, including cardiac involvement^[3–5^]. This case adds to the growing evidence by illustrating a rare instance of recurrent bacterial myocarditis in the same individual, each episode triggered by a distinct gastrointestinal pathogen.

S. enterica, a facultative intracellular Gram-negative bacillus, is a prominent foodborne pathogen responsible for millions of cases of gastroenteritis each year. Although typically confined to the gastrointestinal tract, it can disseminate systemically, especially in vulnerable individuals, potentially seeding extraintestinal sites such as the myocardium. The mechanisms proposed for Salmonella-induced myocarditis include direct bacterial invasion, endotoxin-mediated myocardial damage, and systemic immune activation^[3,6^]. Documented cases have shown electrocardiographic changes mimicking acute coronary syndromes, with ST-segment elevations, elevated cardiac enzymes, and sometimes ventricular dysfunction – highlighting the diagnostic challenges and the need for non-invasive imaging such as cardiac MRI^[7,8^].

Similarly, C. jejuni, one of the leading global causes of bacterial diarrhea, is best known for its association with post-infectious neurological syndromes, particularly Guillain-Barré syndrome. However, cardiac involvement, including myocarditis and pericarditis, has also been reported. The underlying pathophysiology likely involves molecular mimicry, whereby bacterial antigens resemble cardiac self-antigens, triggering an autoimmune response. In addition, toxin-mediated myocardial damage, including the effects of cytolethal distending toxin, has been proposed^[4,9^].

The recurrence of myocarditis in the patient – first following C. jejuni and then after S. enterica – raises the possibility of host-specific vulnerability to bacterial myocarditis. This could reflect genetic predisposition, dysregulated immune responses, or altered gut barrier integrity, allowing for systemic translocation of enteric pathogens. Although speculative in this case, such susceptibility warrants further investigation and underscores the importance of considering bacterial etiologies in patients with a history of myocarditis who present with systemic symptoms.

These findings align with previously reported cases of cardiac complications associated with bacterial gastroenteritis. For instance, Mohamed et al described two cases of C. jejuni–associated myocarditis in adults aged 21 and 35 years, both of whom presented with chest pain and ST-segment changes. The diagnosis was confirmed by cardiac MRI[10]. Similarly, Jin et al documented S. Typhimurium–induced myopericarditis with ECG abnormalities mimicking myocardial infarction, successfully managed with supportive care and antibiotics[11]. Additional literature reviews have identified similar cases, reinforcing the need for clinicians to maintain a high index of suspicion for cardiac symptoms in the setting of recent bacterial gastroenteritis^[12,13^].

Diagnosis of bacterial myocarditis relies on a high index of suspicion, especially when gastrointestinal illness is followed by chest discomfort, ECG abnormalities, or elevated troponin. Cardiac MRI remains the non-invasive diagnostic modality of choice, capable of identifying myocardial edema and fibrosis with high sensitivity[2]. Treatment for bacterial myocarditis typically includes pathogen-directed antibiotics and supportive cardiac care. In our case, ciprofloxacin was initiated despite intermediate susceptibility, due to its established efficacy against systemic Salmonella infections and broad activity against Gram-negative pathogens[14]. In addition, colchicine was added to reduce myocardial inflammation. Colchicine has shown benefits against recurrent pericarditis and is increasingly investigated for myocarditis due to its anti-inflammatory and antifibrotic properties[15].

In conclusion, this case contributes to a growing awareness of bacterial myocarditis as a rare but serious complication of bacterial gastroenteritis. While S. enterica and C. jejuni are traditionally viewed as enteric pathogens, their potential for systemic involvement, particularly cardiac, should not be underestimated. The recurrence of myocarditis in the same patient following distinct bacterial infections suggests a possible host predisposition to immune-mediated myocardial injury.

Clinicians should maintain a high index of suspicion for myocarditis in patients with gastrointestinal infections who present with chest discomfort, ECG changes, or elevated cardiac biomarkers. Early diagnosis and comprehensive assessment through appropriate imaging, prompt initiation of supportive and targeted therapy, and interdisciplinary follow-up are critical to improving outcomes and preventing long-term complications.

Ethical approval

The ethical committee of Johns Hopkins Aramco Healthcare Hospital in Dhahran approved the publication of this case report.

Consent

Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review from the editorial office upon request.

Sources of funding

Not applicable.

Author contributions

R.J.A.G.: conceptualization, data collection, supervision, analysis, interpretation of data, investigation, writing – original draft preparation, and writing – review and editing; H.A.S.: data collection, analysis, interpretation of data, writing – original draft preparation, and writing – reviewing and editing; L.A.: data collection, investigation, and writing – original draft preparation; E.A.: writing – reviewing, and editing.

Conflicts of interest disclosure

The authors declare that they have no conflicts of interest.

Research registration unique identifying number (UIN)

Not applicable.

Guarantor

Rawan AlGhawi.

Provenance and peer review

This article was not commissioned and was internally peer-reviewed.

Data availability statement

The datasets generated or analyzed during the current study are included in the published article.