Unusual Campylobacter jejuni infection causing life- threatening cardiac tamponade

Abstract

The incidence of Campylobacter jejuni enterocolitis is increasing, with this bacterium being the leading cause of acute bacterial diarrhea. However, cardiac complications associated with C. jejuni remain rare. A 47-year-old man presented with sudden chest pain and shortness of breath. Echocardiography revealed pericardial tamponade and pleural effusion over time. Despite the patient having no prior gastrointestinal complaints, Campylobacter jejuni was identified in pericardial aspirates and stool samples by microbiological analysis. Exclusive pericarditis caused by C. jejuni remains an extremely rare complication. To date, the successful isolation of the pathogen from pericardial fluid has only been reported three times. Despite being immunocompetent, relevant bacteremia appears to be a likely cause of the infection. Isolated pericarditis is a rare but serious complication of Campylobacter jejuni infection. Regarding pathogenesis, direct bacterial invasion is becoming increasingly likely. The emergence of antimicrobial-resistant strains must be considered when selecting a therapeutic regimen.

Highlights

• •Campylobacter pericarditis can occur in otherwise healthy young patients.
• •Direct bacterial invasion of the pericardium is possible, even in immunocompetent hosts.
• •Early diagnosis and prompt antibiotic therapy is critical for a favorable outcome.
• •Consider rising antimicrobial resistance, as demonstrated in previous cases, when selecting empirical therapy.

Introduction

Campylobacter jejuni is the leading cause of acute diarrhea in developed countries, with peak incidence observed in infancy and early adulthood [1], [2], [3], [4]. Typical Campylobacter enteritis presents with diarrhea, fever and abdominal cramps, and stool cultures remain the mainstay of diagnosis. ⁴ In recent years, however, it has become apparent that C. jejuni may have a broader pathogenic potential beyond the gastrointestinal tract [2], [3].

We report a rare case of C. jejuni infection resulting in critical pericardial tamponade occurring in the absence of any gastrointestinal symptoms. Unusually, the bacterium was detected in both stool and pericardial fluid, while blood cultures remained negative. Previously, complications of C. jejuni infections were largely attributed to toxin-mediated immune responses rather than direct bacterial invasion. ¹ ⁰ In this case, however, direct invasion appears to be the most likely pathogenic mechanism. This clinical presentation remains extremely rare, with only four cases having been published to date. Consequently, there are no clear management guidelines. However, given the rising incidence of C. jejuni enterocolitis, such complications may become more frequent in the future, emphasizing the importance of rapid diagnosis and timely therapeutic intervention.

Case presentation

A 47-year-old man attended our emergency department complaining of shortness of breath and acute chest pain. On arrival, he exhibited tachycardia, hypotension and mild respiratory distress. His heart rate was 110 beats per minute, his systolic blood pressure was 100 mmHg and his room air oxygen saturation was 93%. Baseline blood work revealed the following: C-reactive protein: 13 mg/dL; leukocyte count: 15.4 thousand/µL; hemoglobin: 13.6 g/dL; D-dimer: 1.29 µg/ml; creatinine: 0.9 mg/dL. All laboratory parameters are presented in Table 1.

Table 1.

Laboratory parameters at time of admission, AST Aspartate Aminotransferase, CRP C-reactive protein, PCT Procalcitonin, INR international normalized ratio, MCV mean corpuscular volume, MCH mean corpuscular hemoglobin.

Laboratory value	Reference range	Patient value at admission
AST	10–50 U/L	28
CRP	10.0.50 mg/dl	13.00
PCT	0.00–0.50 ng/ml	0.50
hsTroponin T	10.14.0 pg/ml	8.0
Creatinine	0.70–1.2 mg/dl	0.9
Natrium	135–145 mmol/l	136
Kalium	3.5–5.1 mmol/l	3.9
Quick	70–120%	61
INR	-	1.4
D-Dimer	10.0.50ug/ml	1.29
Leucocytes	3.98–10.04Tsd/µl	15.4
Hemoglobin	13.7–17.5 g/dl	13.6
MCV	79.0–92.2fl	80.0
MCH	25.7–32.2 pg	27.5
Thrombocytes	163–337Tsd/µl	191

Electrocardiography and a routine physical examination were unremarkable. There were no signs of ST-segment alteration and hsTroponin T was within the normal range.

Screening with two-dimensional transthoracic echocardiography revealed a large, circular pericardial effusion with a maximum extension of 35 mm. No significant heart defects were identified, and left ventricular function was hyperdynamic. However, the right atrium and right ventricle were compromised and the inferior vena cava was congested.

The patient reported having had a mild respiratory infection approximately 14 days prior to presentation. Apart from this, the patient had no other known medical conditions. However, the patient's family history suggested mild gastroenteritis in two family members, approximately two and four weeks before presentation to the emergency department, respectively.

The patient underwent a computed tomography (CT) scan and angiography of the chest to rule out acute aortic dissection. The pericardial effusion previously identified was confirmed (Fig. 1). There were also no signs of pneumonia or pulmonary embolism.

Fig. 1.

Contrast-enhanced computed tomography (CT) of the chest demonstrating extensive pericardial effusion. (a) Axial CT image showing compression of the right atrium, (b) left ventricle, and (c) a large pericardial effusion measuring 3.5 cm. (d) Coronal contrast-enhanced CT reconstruction demonstrating a dilated inferior vena cava measuring 2.6 cm.

An ultrasound-guided pericardial puncture was subsequently performed. Due to the emergency setting and technical issues with the echocardiography equipment, echocardiographic images could not be stored prior to the puncture.

Microbiological, pathological and laboratory chemical samples were obtained, as well as PCR swabs for SARS-CoV-2, respiratory syncytial virus (RSV), influenza A and B, and Mycoplasma pneumoniae.

The patient was admitted to our intermediate care unit for further observation.

Differential diagnosis

The patient presented with laboratory evidence of systemic infection and early hemodynamic instability. The initial differential diagnosis included sepsis of pulmonary origin, but the absence of fever and cough suggested otherwise. Echocardiography revealed a large pericardial effusion. The sudden onset of chest pain and dyspnea raised concerns about pulmonary embolism or pneumothorax, but both were ruled out by CT. Imaging also ruled out acute aortic dissection, the most critical differential diagnosis. The rapid onset of symptoms over two days and the absence of aortic valve disease made dissection unlikely. Overall, the findings were consistent with acute pericardial tamponade of an initially unclear etiology being the cause of the patient's dyspnea, chest pain and hemodynamic instability. Urgent pericardiocentesis was therefore performed to evaluate and stabilize the patient further.

Treatment

An ultrasound-guided pericardial puncture was subsequently performed. This procedure drained 1000 ml of hemorrhagic effusion. Microbiological, pathological and laboratory chemical samples were obtained. Due to significantly elevated infection parameters in the patient's bloodwork (see Table 1) and a high white blood cell count (leukocyte count: 23,470/μL, with 92.7% granulocytes and 7.3% mononuclear cells, hemoglobin of 5.3 g/dL) in the pericardial puncture, antibiotic therapy with piperacillin/tazobactam (4.5 g three times a day) was initiated.

Later that day, the patient exhibited renewed tachycardia, hypotension and significant respiratory distress. A CT scan was performed to rule out post-procedural complications (Fig. 2). The patient was then transferred to the intensive care unit for two days. Intermittent CPAP therapy was necessary. In retrospect, this symptom constellation was most consistent with septic shock, despite negative blood cultures, likely due to the prior initiation of broad-spectrum antibiotic therapy.

Fig. 2.

Axial chest CT after pericardiocentesis showing a small residual pericardial effusion without haemodynamic significance (a).

Four days later, microbiological samples revealed the presence of Campylobacter jejuni in the pericardial effusion. The antibiotic therapy was subsequently deescalated to azithromycin (500 mg once a day) in accordance with the resistance profile (Table 2).

Table 2.

Antibiotic resistance profile. S= Susceptible, I= Intermediate, R= Resistant.

Antibiotic	Interpretation
Erythromycin	S
Clarithromycin	S
Azithromycin	S
Doxycycline	R
Tetracycline	R
Ciprofloxacin	R

Incidentally, a left-sided pleural effusion was detected, with a total of 400 ml of hemorrhagic fluid being evacuated. Laboratory tests ruled out empyema, with the pH level being found to be 7.48. Campylobacter jejuni could not be detected in the effusion. A small, hemodynamically insignificant pericardial effusion remained unchanged (Fig. 3, Fig. 4). By this time, the patient had undergone a total of seven days of antibiotic treatment.

Fig. 3.

Transthoracic echocardiography performed 4 days after pericardiocentesis demonstrating a persistent pericardial effusion measuring 13 mm lateral to the right ventricle, 11 mm lateral to the left ventricle, and 15 mm at the apex.

Fig. 4.

Transthoracic echocardiography performed 6 days after pericardiocentesis demonstrating a small residual pericardial effusion measuring 9 mm anterior to the right ventricle.

To rule out an immune deficiency, an HIV test and protein electrophoresis were performed. Both tests were inconclusive. Similarly, there was no clinical evidence of an underlying malignant disease. A stool sample confirmed a Campylobacter jejuni infection, despite there being no clinical signs of gastrointestinal involvement. According to the patient's medical history, the only potential source of the infection was consuming raw milk cheese approximately three weeks before admission to hospital.

Outcome and follow- up

At discharge, the patient's leukocyte count had returned to normal and their C-reactive protein levels continued to decline (leukocytes: 7.1 thousand/µL; CRP: 8.82 mg/dL). TTE revealed only a small pericardial effusion measuring less than 5 mm at end-diastole.

Outpatient follow-up echocardiography 26 days after discharge showed normal biventricular function and no evidence of pericardial effusion (Fig. 5). The patient remained asymptomatic and was able to perform everyday activities and return to work. They were advised to attend outpatient cardiology follow-up appointments for ongoing monitoring.

Fig. 5.

Transthoracic echocardiography 26 days after discharge demonstrating normal biventricular function with no pericardial effusion.

Discussion

The incidence of Campylobacter jejuni enterocolitis has been steadily increasing. It is recognized as the leading cause of acute diarrhea in developed countries, with peak incidences observed during infancy and early adulthood [1], [2], [3], [4]. A typical case of Campylobacter enteritis is characterized by symptoms such as diarrhea, fever and abdominal cramps [4]. Stool cultures remain the easiest way to diagnose the infection [4].

However, in recent years, it has become apparent that C. jejuni may have a broader pathogenic potential, extending beyond the gastrointestinal tract. Extraintestinal infections caused by Campylobacter are rare, but can result in severe complications such as cholecystitis, meningoencephalitis, brain abscesses, septic arthritis and lung abscesses. Although cardiac complications associated with C. jejuni are rare, they can result in severe sequelae [2], [3]. Nevertheless, these manifestations are more commonly associated with Campylobacter fetus, which is caused by direct bacterial invasion, than with Campylobacter jejuni [3].

Here, we present the case of a previously healthy, immunocompetent individual who did not exhibit gastrointestinal symptoms, yet developed critical pericardial tamponade due to Campylobacter jejuni pericarditis. To our knowledge, this is the fifth reported case of isolated Campylobacter jejuni pericarditis in the absence of concomitant myocarditis and the third case in an immunocompetent host with direct detection of Campylobacter jejuni in the pericardial fluid [5], [6], [7], [8]. In the remaining two reported cases, no Campylobacter jejuni was detected in the pericardial fluid [5], [6]. Unlike most previously reported cases, our patient did not exhibit gastrointestinal symptoms throughout the illness [5], [6], [7], [8]. A summary of the previously reported cases is presented in the Supplementary Table 1.

Conversely, given that Campylobacter jejuni has only been directly detected in pericardial samples on three occasions, direct hematogenous invasion of the pericardium appears to be an uncommon pathogenesis of Campylobacter jejuni pericarditis [3], [6], [8], [9]. Corroborating this hypothesis bacteremia secondary to Campylobacter jejuni infection is considered relatively uncommon and has been reported in approximately 1% of cases in the literature [10], [11]. Previous studies have shown that clinically significant bacteremia with C. jejuni is generally only observed in immunocompromised patients [4], [5]. Although immunocompetent individuals may experience only transient bacteremia, most likely due to bacterial susceptibility to serum-mediated killing, it typically resolves rapidly without the need for antibiotic therapy [5], [11]. This transient bacteremia is most frequently associated with the acute phase of Campylobacter enteritis, during which bacterial translocation from the intestinal lumen into the bloodstream may occur [11]. Furthermore a previous study suggested toxin-induced damage rather than bacterial invasion [9]. However, this toxin-mediated immunological reaction generally develops several weeks after the initial infection, as exemplified by the onset of Guillain–Barré syndrome or reactive arthritis following Campylobacter jejuni infection [3], [5], [9].

In contrast, the present case now involved an immunocompetent host with no pre-existing conditions who suffered from relevant bacteremia, ultimately leading to pericarditis, with the pathogen being isolated directly from the pericardial fluid. The patient most likely had an asymptomatic gastrointestinal Campylobacter jejuni infection, as indicated by the positive stool sample. A mild respiratory infection two weeks prior may have temporarily suppressed immunity, facilitating bacterial colonization of the pericardium. However, despite the absence of gastrointestinal symptoms, Campylobacter jejuni remained detectable in both the pericardial fluid and stool. Acute cardiac symptoms manifested 1.5 days before admission, indicating an atypical clinical course. The negative blood cultures and the microbiologically unremarkable pleural fluid may be explained by the administration of a broad-spectrum antibiotic a few days prior to the pleural puncture, as well as by the brief and intermittent nature of Campylobacter jejuni bacteremia [10], [11]. Additionally, it would be conceivable that a concomitant toxin-mediated immunological reaction, previously described as a potential pathomechanism in the literature, may have contributed to the development of the pleural effusion [9]. These findings align with previous reports in which C. jejuni could not be detected in blood cultures [3], [8].

This case highlights the serious and rare possibility of Campylobacter jejuni-associated pericarditis in an immunocompetent host. Despite its current rarity, the frequency of the disease may be increasing, partly due to growing clinical awareness. In this context, the global emergence of antimicrobial-resistant Campylobacter strains, largely driven by the widespread use of antibiotics in livestock production, must be considered when developing future therapeutic strategies. ⁴ Fortunately, complications from Campylobacter jejuni infections are uncommon, and most patients recover without antibiotic treatment [5].

CRediT authorship contribution statement

Marie Biedermann: Writing – review & editing, Writing – original draft, Visualization, Project administration, Methodology, Investigation, Formal analysis, Data curation, Conceptualization. Felix Lampe: Writing – review & editing, Data curation. Ulrich Saueressig: Writing – review & editing, Data curation. Peter Hafkemeyer: Writing – review & editing, Validation, Supervision. Sascha Kocher: Writing – review & editing, Validation, Supervision, Formal analysis, Data curation.

Ethical approval and Consent

Ethical approval was not required because this was a single, retrospective, anonymized case report. Patient’s consent was obtained both in writing and verbally.

Declaration of Generative AI and AI-assisted technologies in the writing process

During the preparation of this work the author(s) used ChatGPT for English language editing. Queries were made regarding correct grammatical phrasing, assistance was sought in identifying appropriate words and synonyms, and it was partially used as a translation aid. After using this tool/service, the author(s) reviewed and edited the content as needed and take(s) full responsibility for the content of the published article.

Declaration of Competing Interest

The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Appendix A. Supplementary material

Supplementary material