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Campylobacter jejuni: Enterocolitis and myopericarditis
International Journal of Cardiology 144 (2010) e14 – e16 www.elsevier.com/locate/ijcard
Letter to the Editor
Campylobacter jejuni: Enterocolitis and myopericarditis B.S.N. Alzand a,⁎, M. Ilhan a , W.F. Heesen b , J.G. Meeder b a
b
Department of Cardiology, University Hospital Maastricht, The Netherlands Department of Cardiology, VieCuri Medical Centre for Northern Limburg, The Netherlands Received 15 August 2008; accepted 12 December 2008 Available online 25 January 2009
Abstract Campylobacter jejuni enteritis is the commonest enteric infection in the developed world. There are only few reported cases in the medical literature of cardiac complications associated with C. jejuni enterocolitis, most of the patients in the reported literature were males and most of the cases followed a benign course. Severe left ventricular dysfunction complicated only two cases of C. jejuni myocarditis. We report here a young male with Campylobacter myopericarditis. We believe that this is the first reported case of Campylobacter associated myopericarditis in The Netherlands. The mechanism by which Campylobacter causes myo(peri)carditis remains uncertain, it may be caused by direct bacterial invasion of cardiac tissue, bacterial toxins, circulating immune complexes, or cytotoxic T-cells. Since the number of C. jejuni infection is increasing worldwide, cardiac complications, although rare, are a remarkable manifestation of this pathogen and should be always kept in mind. © 2008 Elsevier Ireland Ltd. All rights reserved. Keywords: Campylobacter; Myocarditis; Pericarditis; Myopericarditis
1. Case report A 21-year-old previously healthy male was admitted to our hospital because of abdominal pain with watery diarrhoea. He had no known medical history except for incidental cocaine abuse and the use of anabolic steroids, which he had not used in the last 4 weeks. During his admission he developed retrosternal pain, aggravated by movement and deep inspiration; severe enough to require transport to the coronary care unit. On physical examination, he had a pulse rate of 70 bpm and a blood pressure of 150/70 mm Hg. There was no fever. Examination of the chest revealed normal heart sounds, without any murmur or an audible pericardial rub. Pulmonary examination was normal with no signs of respiratory distress. Abdomen was diffusely tender without clinical signs of peritonitis. Laboratory testing showed an elevated CRP level of 185 mg/l with a leukocyte count of 7.4 × 109/l, as well as elevated cardiac enzymes with maximal ASAT 79 U/l, maximal LDH 644 U/l, maximal CK 2416 U/l and a troponine I of 2.5 μg/l. Chest X-ray revealed no pulmonary infiltrates with no signs of pleural effusion or pneumothorax. His electrocardiogram revealed sinus rhythm with a normal PR interval. There was slight ST-segment elevation ⁎ Corresponding author. Department of Cardiology, University Hospital Maastricht, P. Debyelaan 25, 6229 HX Maastricht, The Netherlands. Tel.: +31 43 3875102; fax: +31 43 3875104. E-mail address: [email protected] (B.S.N. Alzand). 0167-5273/$ - see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2008.12.101
with terminal negative T-waves mainly in the inferior and the precordial leads, PTa segment depressions in leads I and II were also found (see Fig. 1). Repetitive transthoracic echocardiography showed a preserved LV function without regional wall-motion abnormalities or valvular disease. The pericardium was not thickened. Pericardial effusion was absent. The patient was treated with antimicrobial therapy when Campylobacter jejuni was cultured from the stool; the chest pain was managed initially with morphine, then with Aspirin. Based on the clinical and laboratory results the diagnosis of Campylobacter enterocloitis, accompanied by myopericarditis was made. Shortly after initiating antimicrobial and antiinflammatory therapy, both diarrhoea and chest pain resolved and patient was discharged from the hospital free of complaints. A normal electrocardiogram was registered after 10 weeks in the outpatient's clinic.
2. Discussion The genus Campylobacter; which contains 16 species and 6 subspecies, is one of the most frequent bacterial causes of infectious enterocolitis. C. jejuni enteritis is the most common enteric infection in the developed world, with an annual incidence as high as 1 in 1000. The pathogenic mechanism relies on the production of enterotoxins and cytotoxins as well as direct invasion of the intestinal mucosa.
B.S.N. Alzand et al. / International Journal of Cardiology 144 (2010) e14–e16
e15
Fig. 1. ECG in the acute phase of the disease with St segment elevation, Pta segment depression en negative t waves.
Pericarditis is a very uncommon complication of Campylobacter enterocolitis. The most common cause of pericarditis is viral, with coxsackie A and B viruses, HIV, echovirus and adenovirus as the most predominant viral causes [1]. Bacterial pathogens of pericarditis are streptococci [2], staphylococci [3], Haemophilus sp. and mycobacterium tuberculosis. Other causes include mycoplasma, rickettsia, Chlamydia, fungal infection, mediastinal radiation, myocardial infarction, cardiac surgery, chest trauma, uremia, malignancy or idiopathic. Immune-complex mediated pericarditis is seen in meningococcal infections, autoimmune rheumatic diseases (SLE, systemic sclerosis, mixed connective tissue disease and rheumatoid arthritis), inflammatory bowel disease, some drugs (procaineamide, phenytoin, and hydralazine) and Dressler's syndrome. Cardiac manifestation of Campylobacter infection is highly unusual. However, several case reports now suggest that Campylobacter spp. have wider pathological manifestations than originally thought. Campylobacter fetus, type species, has been identified to cause pericarditis in more than ten documented cases. C. jejuni pericarditis is extremely rare with only two documented cases in the literature [4,5]; there are also seven reported cases of C. jejuni associated myocarditis, and another nine documented cases of myopericarditis. Almost all reported patients were males, and most cases followed a benign course. Severe left ventricular dysfunction complicated only two cases of C. jejuni myocarditis. In one of these cases it remained for several months after the infection, while it resolved within 24 h in the other case. The mechanism by which Campylobacter causes myo (peri)carditis remains uncertain. It may be caused by direct bacterial invasion of cardiac tissue, bacterial toxins, circulating immune complexes, or cytotoxic T-cells. While
C. fetus were isolated from blood in almost all cases of myo(peri)carditis, the same cannot be said for C. jejuni, where the organism was isolated from blood in only one case [4]. C. fetus may have the ability to elude the host immune system by means of complement resistant surface layer proteins which enable it to use the blood stream as a transport system, making direct microbial invasion via the blood more likely the pathogenesis of myopericarditis in C. fetus but not jejuni due to lacking of this S-layer protein. However; the short interval of about 2 to 4 days between the infection and the onset of the cardiac complication in most of the reported cases, makes an immunological aetiology also unlikely and may indicate an immediate influence of C. jejuni on myocytes through either direct damage or through circulating toxins. C. jejuni is known to produce a variety of exotoxines with cytotoxic, haemolytic and hepatotoxic effects, but none is known to cause cardiotoxicity [6]. The few reported patients that had a longer interval between the infection and the cardiac complications also had had arthritis, which may suggest immunological aetiology. The exact mechanism of myopericardial involvement is still unknown. Other reported cardiovascular complications of C. jejuni include endocarditis, atrial fibrillation and aortitis with aortic dissection. To our knowledge this is the first reported case of Campylobacter myopericarditis in The Netherlands. Since the number of C. jejuni infection is increasing worldwide, cardiac complications, although rare, are a remarkable manifestation of this pathogen and should be always kept in mind. Acknowledgement The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [7].
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B.S.N. Alzand et al. / International Journal of Cardiology 144 (2010) e14–e16
References [1] Imazio M, Trinchero R. Myopericarditis: etiology, management, and prognosis. Int J Cardiol Jun 23 2008;127(1):17–26. [2] Tatli E, Buyuklu M, Altun A. An unusual complication of pneumococcal pneumonia: acute tamponade due to purulent pericarditis. Int J Cardiol Jun 25 2007;119(1):e1–3. [3] Cakir O, Goz M. Purulent pericarditis and pleural empyema due to Staphylococcus aureus septicemia. Int J Cardiol Feb 20 2008;124(1):108.
[4] Rafi A, Matz J. An unusual case of Campylobacter jejuni pericarditis in a patient with X-linked agammaglobulinemia. Ann Allergy Asthma Immunol Oct 2002;89(4):362–7. [5] Nowakowski MLD, Freeman SR. Pericarditis associated with Campylobacter jejuni enterocolitis. Hosp Physician Jan. 2002:39–42. [6] Wassenaar TM. Toxin production by Campylobacter spp. Clin Microbiol Rev Jul 1997;10(3):466–76. [7] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131: 149–50.
Letter to the Editor
Campylobacter jejuni: Enterocolitis and myopericarditis B.S.N. Alzand a,⁎, M. Ilhan a , W.F. Heesen b , J.G. Meeder b a
b
Department of Cardiology, University Hospital Maastricht, The Netherlands Department of Cardiology, VieCuri Medical Centre for Northern Limburg, The Netherlands Received 15 August 2008; accepted 12 December 2008 Available online 25 January 2009
Abstract Campylobacter jejuni enteritis is the commonest enteric infection in the developed world. There are only few reported cases in the medical literature of cardiac complications associated with C. jejuni enterocolitis, most of the patients in the reported literature were males and most of the cases followed a benign course. Severe left ventricular dysfunction complicated only two cases of C. jejuni myocarditis. We report here a young male with Campylobacter myopericarditis. We believe that this is the first reported case of Campylobacter associated myopericarditis in The Netherlands. The mechanism by which Campylobacter causes myo(peri)carditis remains uncertain, it may be caused by direct bacterial invasion of cardiac tissue, bacterial toxins, circulating immune complexes, or cytotoxic T-cells. Since the number of C. jejuni infection is increasing worldwide, cardiac complications, although rare, are a remarkable manifestation of this pathogen and should be always kept in mind. © 2008 Elsevier Ireland Ltd. All rights reserved. Keywords: Campylobacter; Myocarditis; Pericarditis; Myopericarditis
1. Case report A 21-year-old previously healthy male was admitted to our hospital because of abdominal pain with watery diarrhoea. He had no known medical history except for incidental cocaine abuse and the use of anabolic steroids, which he had not used in the last 4 weeks. During his admission he developed retrosternal pain, aggravated by movement and deep inspiration; severe enough to require transport to the coronary care unit. On physical examination, he had a pulse rate of 70 bpm and a blood pressure of 150/70 mm Hg. There was no fever. Examination of the chest revealed normal heart sounds, without any murmur or an audible pericardial rub. Pulmonary examination was normal with no signs of respiratory distress. Abdomen was diffusely tender without clinical signs of peritonitis. Laboratory testing showed an elevated CRP level of 185 mg/l with a leukocyte count of 7.4 × 109/l, as well as elevated cardiac enzymes with maximal ASAT 79 U/l, maximal LDH 644 U/l, maximal CK 2416 U/l and a troponine I of 2.5 μg/l. Chest X-ray revealed no pulmonary infiltrates with no signs of pleural effusion or pneumothorax. His electrocardiogram revealed sinus rhythm with a normal PR interval. There was slight ST-segment elevation ⁎ Corresponding author. Department of Cardiology, University Hospital Maastricht, P. Debyelaan 25, 6229 HX Maastricht, The Netherlands. Tel.: +31 43 3875102; fax: +31 43 3875104. E-mail address: [email protected] (B.S.N. Alzand). 0167-5273/$ - see front matter © 2008 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.ijcard.2008.12.101
with terminal negative T-waves mainly in the inferior and the precordial leads, PTa segment depressions in leads I and II were also found (see Fig. 1). Repetitive transthoracic echocardiography showed a preserved LV function without regional wall-motion abnormalities or valvular disease. The pericardium was not thickened. Pericardial effusion was absent. The patient was treated with antimicrobial therapy when Campylobacter jejuni was cultured from the stool; the chest pain was managed initially with morphine, then with Aspirin. Based on the clinical and laboratory results the diagnosis of Campylobacter enterocloitis, accompanied by myopericarditis was made. Shortly after initiating antimicrobial and antiinflammatory therapy, both diarrhoea and chest pain resolved and patient was discharged from the hospital free of complaints. A normal electrocardiogram was registered after 10 weeks in the outpatient's clinic.
2. Discussion The genus Campylobacter; which contains 16 species and 6 subspecies, is one of the most frequent bacterial causes of infectious enterocolitis. C. jejuni enteritis is the most common enteric infection in the developed world, with an annual incidence as high as 1 in 1000. The pathogenic mechanism relies on the production of enterotoxins and cytotoxins as well as direct invasion of the intestinal mucosa.
B.S.N. Alzand et al. / International Journal of Cardiology 144 (2010) e14–e16
e15
Fig. 1. ECG in the acute phase of the disease with St segment elevation, Pta segment depression en negative t waves.
Pericarditis is a very uncommon complication of Campylobacter enterocolitis. The most common cause of pericarditis is viral, with coxsackie A and B viruses, HIV, echovirus and adenovirus as the most predominant viral causes [1]. Bacterial pathogens of pericarditis are streptococci [2], staphylococci [3], Haemophilus sp. and mycobacterium tuberculosis. Other causes include mycoplasma, rickettsia, Chlamydia, fungal infection, mediastinal radiation, myocardial infarction, cardiac surgery, chest trauma, uremia, malignancy or idiopathic. Immune-complex mediated pericarditis is seen in meningococcal infections, autoimmune rheumatic diseases (SLE, systemic sclerosis, mixed connective tissue disease and rheumatoid arthritis), inflammatory bowel disease, some drugs (procaineamide, phenytoin, and hydralazine) and Dressler's syndrome. Cardiac manifestation of Campylobacter infection is highly unusual. However, several case reports now suggest that Campylobacter spp. have wider pathological manifestations than originally thought. Campylobacter fetus, type species, has been identified to cause pericarditis in more than ten documented cases. C. jejuni pericarditis is extremely rare with only two documented cases in the literature [4,5]; there are also seven reported cases of C. jejuni associated myocarditis, and another nine documented cases of myopericarditis. Almost all reported patients were males, and most cases followed a benign course. Severe left ventricular dysfunction complicated only two cases of C. jejuni myocarditis. In one of these cases it remained for several months after the infection, while it resolved within 24 h in the other case. The mechanism by which Campylobacter causes myo (peri)carditis remains uncertain. It may be caused by direct bacterial invasion of cardiac tissue, bacterial toxins, circulating immune complexes, or cytotoxic T-cells. While
C. fetus were isolated from blood in almost all cases of myo(peri)carditis, the same cannot be said for C. jejuni, where the organism was isolated from blood in only one case [4]. C. fetus may have the ability to elude the host immune system by means of complement resistant surface layer proteins which enable it to use the blood stream as a transport system, making direct microbial invasion via the blood more likely the pathogenesis of myopericarditis in C. fetus but not jejuni due to lacking of this S-layer protein. However; the short interval of about 2 to 4 days between the infection and the onset of the cardiac complication in most of the reported cases, makes an immunological aetiology also unlikely and may indicate an immediate influence of C. jejuni on myocytes through either direct damage or through circulating toxins. C. jejuni is known to produce a variety of exotoxines with cytotoxic, haemolytic and hepatotoxic effects, but none is known to cause cardiotoxicity [6]. The few reported patients that had a longer interval between the infection and the cardiac complications also had had arthritis, which may suggest immunological aetiology. The exact mechanism of myopericardial involvement is still unknown. Other reported cardiovascular complications of C. jejuni include endocarditis, atrial fibrillation and aortitis with aortic dissection. To our knowledge this is the first reported case of Campylobacter myopericarditis in The Netherlands. Since the number of C. jejuni infection is increasing worldwide, cardiac complications, although rare, are a remarkable manifestation of this pathogen and should be always kept in mind. Acknowledgement The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology [7].
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B.S.N. Alzand et al. / International Journal of Cardiology 144 (2010) e14–e16
References [1] Imazio M, Trinchero R. Myopericarditis: etiology, management, and prognosis. Int J Cardiol Jun 23 2008;127(1):17–26. [2] Tatli E, Buyuklu M, Altun A. An unusual complication of pneumococcal pneumonia: acute tamponade due to purulent pericarditis. Int J Cardiol Jun 25 2007;119(1):e1–3. [3] Cakir O, Goz M. Purulent pericarditis and pleural empyema due to Staphylococcus aureus septicemia. Int J Cardiol Feb 20 2008;124(1):108.
[4] Rafi A, Matz J. An unusual case of Campylobacter jejuni pericarditis in a patient with X-linked agammaglobulinemia. Ann Allergy Asthma Immunol Oct 2002;89(4):362–7. [5] Nowakowski MLD, Freeman SR. Pericarditis associated with Campylobacter jejuni enterocolitis. Hosp Physician Jan. 2002:39–42. [6] Wassenaar TM. Toxin production by Campylobacter spp. Clin Microbiol Rev Jul 1997;10(3):466–76. [7] Coats AJ. Ethical authorship and publishing. Int J Cardiol 2009;131: 149–50.