Cardiac implantable electronic device infection due to Mycobacterium species: a case report and review of the literature
© The Author(s) 2016
Received: 22 May 2016
Accepted: 15 August 2016
Published: 24 August 2016
Infection of cardiac implantable electronic devices is a serious cardiovascular disease and it is associated with a high mortality. Mycobacterium species may rarely cause cardiac implantable electronic devices infection.
We are reporting a case of miliary tuberculosis in an Arab patient with dilated cardiomyopathy and a cardiac resynchronization therapy-defibrillator device that was complicated with infection of his cardiac resynchronization therapy-defibrillator device. To our knowledge, this is the third case in the literature with such a presentation and all patients died during the course of treatment. This underscores the importance of early diagnosis and management. We also performed a literature review of reported cases of cardiac implantable electronic devices infection related to Mycobacterium species.
Cardiac implantable electronic devices infection due to Mycobacterium species is an uncommon but a well-known entity. Early diagnosis and prompt management may result in a better outcome.
KeywordsMycobacterium Pacemaker Defibrillator Infection Endocarditis
Infection of cardiac implantable electronic devices (CIEDs) is a serious cardiovascular disease and it is associated with a high mortality. CIEDs infection may occur as a pocket infection or as infection on the leads with infective endocarditis. Cardiac device-related infective endocarditis (CDR-IE) may occur as a primary infection of the CIED system or as a secondary infection as a result of hematogenous seeding during a bacteremia secondary to a distant infected focus .
Mycobacterium tuberculosis (TB) is an infection that primarily affects the lungs, but it can involve any other organs and structures such as the kidney, spine, brain, and rarely the heart. TB disease can be fatal if not treated properly (http://www.cdc.gov).
Tuberculosis endocarditis (TBE) has been reported for many years with involvement of native or prosthetic valves mostly in cases of miliary TB . Mycobacterium species are another uncommon but well-described pathogen in CIED infections .
We are reporting a case of miliary TB in an Arab patient with dilated cardiomyopathy and a cardiac resynchronization therapy-defibrillator (CRT-D) device. His condition was complicated with TB meningitis and a CDR-IE with vegetations on the leads. He underwent surgical removal of the CRT-D device and leads and a gram stain of the vegetations was positive for acid-fast bacilli (AFB). We also performed a literature review of reported cases with Mycobacterium species related CIEDs infection.
A 50-year-old male Arab patient with non-ischemic dilated cardiomyopathy, biventricular failure with left ventricular ejection fraction (LVEF) of 20 %, moderate to severe mitral regurgitation and tricuspid regurgitation, left bundle branch block, and non-sustained ventricular tachycardia. Cardiac catheterization did not show any significant coronary artery disease. He underwent a CRT-D device implantation, as he was symptomatic with shortness of breath, New York Heart Association Functional Classification-II. He had no history of diabetes mellitus, hypertension, or dyslipidemia. He was on anti-heart failure medications and was on the heart transplantation list.
He presented to the Emergency Department 8 months after CRT-D device implantation with 2 months’ history of high-grade fever, chills, rigors, and weight loss. There was no history of concomitant respiratory, gastroenterology, cardiovascular, or neurologic localizing symptoms. There was no history of contact with febrile or TB patients. He was seen at another medical center and started on intravenous (IV) vancomycin and gentamicin for possible infective endocarditis involving his CRT-D device leads but with no improvement.
On presentation, he was looking chronically ill but not in acute distress. He was febrile with a temperature of 38.8 °C, but he was hemodynamically stable with a blood pressure of 107/57 mm Hg, and heart rate of 98 beats per minute. Oxygen saturation was 92–94 % on room air. Cardiovascular exam showed a jugular venous pressure (JVP) at 4 cm above the sternal angle; normal first and second heart sounds with a soft systolic murmur at left lower sternal border which was reported in his previous physical exam. The device site in the left upper chest was normal. There was no lower limb edema and no stigmata of infective endocarditis. Chest exam showed bilateral basal crepitations. Neurological exam was unremarkable.
Laboratory test results on admission
>60 mL/min/1.73 m2
Liver function test
Based on the clinical presentation, the chest X-ray and CT chest findings, he was started on first-line anti-TB therapy in the form of rifampin 600 mg orally once daily, ethambutol 1200 mg orally once daily, pyrazinamide 2000 mg orally once daily, and isoniazid (isonicotinylhydrazide or INH) 300 mg orally once daily, with the addition of vitamin B6 25 mg orally once daily, and prednisone 60 mg orally once daily.
The trans-thoracic echocardiogram showed moderately dilated LV with severe global hypokinesis and severely reduced function (LVEF <25 %).The CRT-D device leads were seen in the right atrium and right ventricle. There were no obvious masses on the leads or on any of the cardiac valves to suggest vegetations. There was mild to moderate mitral regurgitation. The right ventricular systolic pressure was elevated at 30–40 mmHg. There was no pericardial effusion.
The blood cultures and urine culture were all negative. The work up was negative for HACEK group (Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae), and other bacterial and viral infection including human immunodeficiency virus (HIV) and respiratory viruses.
Bronchoscopy and bronchoalveolar lavage were performed, and pathology examination showed a necrotizing granulomatous inflammation and special stains for AFB were positive. The culture showed Mycobacterium tuberculosis and sensitivity came back as sensitive to all first line anti-TB therapy.
His clinical course was complicated by acute renal failure with an increase in serum creatinine to 351 μmol/L and urea to 37 mmol/L. It was felt that the cause of his renal impairment was due to cardio-renal syndrome. It improved gradually and he did not require hemodialysis. He also had confusion and was noted to have a tonic–clonic seizure disorder. He was intubated, put on mechanical ventilation and started on anti-seizure treatment with IV levetiracetam (keppra) and phenytoin. Electroencephalogram showed a severe diffuse encephalopathy with periodic epileptiform discharges and continuous slow activity, generalized (delta coma). CT brain showed a preserved gray-white matter differentiation with no evidence of acute established territorial infarction, intra-axial or extra-axial hemorrhage, hydrocephalus, mass effect, or midline shifting.
Lumbar puncture was performed and cerebrospinal fluid (CSF) analysis showed a pale yellow, slightly turbid fluid with labs of: RBC 110 (normally 0), WBC 300 × 109/L (0–5 × 106/L) with neutrophils 72, band 1, lymphocytes 22, and monocytes 5. Glucose was 0.12 mmol/L (2.2–3.90 mmol/L), and protein 3580 mg/L (150–450 mg/L). Mycobacterium tuberculosis complex DNA was positive and Mycobacterium tuberculosis complex was isolated from the CSF. These findings were consistent with TB meningitis. Furthermore, he had melena with a drop in his hemoglobin to 69 g/L. He required transfusion of two units of packed red blood cells (PRBC). Upper gastroenterology endoscopy was performed, and it revealed a duodenal ulcer, which was cauterized. His thrombocytopenia continued and platelets dropped further to 14 × 109/L. Hematology service was involved and it was felt that his thrombocytopenia was secondary to his TB infection. Coombs test was positive and peripheral blood smear showed no significant schistocytes making thrombotic thrombocytopenic purpura (TTP) unlikely.
The vegetation was removed and sent for culture and sensitivity. The three leads were removed completely. Cardiopulmonary bypass was weaned off gradually with no difficulty. The patient tolerated the procedure and was transferred to the Cardiac Surgery Intensive Care Unit (CSICU) on inotropic support. The microbiology test of the vegetation revealed 10 colonies of Mycobacterium tuberculosis complex. In the CSICU, he was noted to have a high-grade fever and hemodynamic instability despite maximum inotropic support. He ultimately went into a multi-organ failure and died a few days later.
We are presenting a case of miliary tuberculosis (TB) with infective endocarditis involving cardiac resynchronization therapy device leads. We believe that this patient had a miliary TB that was complicated by infection of the CRT-D devices leads due hematogenous spread. There was no evidence of device pocket infection and miliary TB preceded the CDR-IE.
Infection of CIEDs is a serious cardiovascular disease which is associated with a high mortality. The incidence of CIEDs infection in a population-based study is 1.9 per 1000 device-years with a higher probability of infection after implantable cardioverter defibrillator (ICD) compared with permanent pacemaker (PPM) implantation . The diagnosis and management of CIEDs infections are difficult .
Local device infection is defined as an infection limited to the pocket of the cardiac device and is clinically suspected in the presence of local signs of inflammation at the generator pocket, including warm site, erythema, fluctuance, wound dehiscence, erosion, tenderness or purulent drainage . CDR-IE is defined as infection extending to the electrode leads, cardiac valve leaflets or endocardial surface . As stated above our patient clearly had a CDR-IE secondary to hematogenous spread of the miliary TB.
Several factors have been associated with CIED infections, which may be divided firstly into patient factors such as renal failure, corticosteroid use, congestive heart failure, hematoma formation, diabetes mellitus, anticoagulation use, and fever within the 24 h before implantation [6–11]. Secondly, procedural factors such as the type of intervention [12, 13], device revisions, the site of intervention, the number of indwelling leads, the use of pre-procedural temporary pacing, failure to administer perioperative antimicrobial prophylaxis , and operator experience  all play a role.
Our patient had a CRT-D device with three leads which put him at higher risk for CIED infection.
In terms of microbiological causes of CDR-IE, Staphylococci especially Coagulase-Negative species (CoNS), accounts for 60–80 % of cases in most of the reported series [15, 16]. A variety of CoNS species have been described [6, 15]. Corynebacterium spp., Propionibacterium acnes, Gram-negative bacilli and Candida spp. are rarely identified as pathogens in CIED infection [6, 15].
CIED infection due to Mycobacterium species is an uncommon but a well-recognized entity.
Mycobacterial infections of implanted pacemakers as reported in literature
Procedure/Type of device
Type of infection
Time from procedure
Amin et al. 
PM generator change at the age of 20 years (PM at the age of 7 years)
Pocket and proximal leads
M. avium complex
Fever, pain, and swelling over the implant site
Device extracted by thoracotomy plus antimicrobial therapy (INH, RIF, ETH for 2 weeks)
Doherty et al. 
M. tuberculosis (Miliary TB)
Purulent discharge from the pocket and pyrexial illness
Died on her 31st hospital day due to renal and respiratory failure and recurrent VF
Cutay et al. 
CABG surgery and epicardial pacing leads
Pocket and epicardial leads
Erythema and discharge from the pocket site
Device extracted, and antimicrobial therapy (CLR, FOX, AMK for 5 weeks). Patient died about 1 month later due to ESRD
Verghese et al. 
M. chelonae, and M.fortuitum
Fever, pain, purulent discharge from PM site
Device extracted, successful eradication with antimicrobial therapy (GEN, OFX for 1 month)
Sharma et al. 
Pocket and lead endocarditis Bacteremia
Fever, chills, and pain at PM site
Device extracted, successful eradication with antimicrobial therapy (DOX, CIP for 6 months)
Hemmersbach-Miller et al. 
PM in 2005
1 year later
CoNS and M. fortuitum
Subcutaneous nodules and chronic drainage
Device extracted, successful eradication with antimicrobial therapy (CIP then CIP, SXT and CLR then AMK and CIP) for 6 months
Hellwig et al. 
Epicardial PM was implanted during CP-A anastomosis surgery
New epicardial PM 5 weeks later
Pocket and epicardial leads
subcutaneous abscess at PM site
Fever, and inflammatory syndrome
Device extraction, successful eradication with antimicrobial therapy (RIF, INH, ETH, and PYR 2 months then isoniazid and rifampicin for another 7 months
Pastor et al. (Spanish) 
Pocket infection Bacteremia
18 days (started 1 week before)
Fever, malaise, drowsiness, and purulent discharge
Device left in situ, successful eradication with antimicrobial therapy (CIP, CLR for 6 weeks)
Toda et al. (Japanese) 
Generator change at 82 years
Device extraction, successful eradication with antimicrobial therapy (INH, RIP and LVX)
Giannella et al. 
Heart failure, fever, pain and erythema at PM site
Device extraction, successful eradication with antimicrobial therapy (LVX for 3 months)
Siu et al. 
DDD PM then
New DDD PM on right side
Fever and erosion purulent discharge
Old and new devices extraction, successful eradication (LVX and CLR for 6 months)
Kestler et al. 
CABG surgery and epicardial pacing wires
Pocket and leads
Painful anterior epigastric mass
Drainage of abscess cavity and the wires were cut in the abdominal cavity (INH, RIF and ETH for 16 weeks, then INH and RFP total of 25 weeks)
Marchandin et al. 
A mechanical double valve replacement with epicardial PM
Fever then purulent discharge and wound dehiscence
Antimicrobial treatment (OFX and AMK then DOX) with recovery. PM was not removed
Al Soub et al. 
PM generator change
Pocket, leads and myocardium
Discharge from surgical wound site and localized erythema and fever
Device extraction, successful eradication with antimicrobial therapy (DOX, and CIP for 6 months)
Kumar et al. 
CRT-P(pulmonary tuberculosis 15 years back)
Subcutaneous abscess of the PM site
Subcutaneous abscess at the PM site
Large lump over the pacemaker site
Device left in situ antimicrobial therapy (INH,RIF,ETH for 3 months then INH and RIF for another 9 months)
PM pocket debridement and antimicrobial
Therapy (INH, RIF, ETH and PYR for 3 months then INH and RIF for another 9 months)
PM device was explanted, antimicrobial
Therapy (RIF, INH, ETH and PYR)
Mycobacterial Infections of implanted cardioverter defibrillators as reported in literature
Procedure/Type of device
Type of infection
Time from procedure
Katona et al. 
ICD, with two epicardial patches and epicardial screw-in leads
Pain and swelling at the abdominal insertion site of ICD
INH, RIF, and ETH and defibrillator leads were relocated to the other side of the abdomen 28 days later
Kessler et al. 
Tenderness and brownish odorless discharge
Extraction of the device and CLR for 6 months
Short et al. 
Persistent erythema and a pustule
Extraction of the AICD and the leads. CIP and CLR for 6 weeks
Chrissoheris et al. 
ICD (removal of PM and ICD implantation)
Erythema, tenderness and fluctuance at the pocket site
extraction of the AICD and the leads and SXT for 8 weeks
Luckie et al. 
Revision of CRT-D
Fatigue, weight loss and anemia then pain around the ICD site, fluctuant swelling 6 months later
The ICD was explanted, and the patient discharged with a LifeVest and standard anti-tuberculous therapy
Died at home
Karnam et al. 
The device and leads were explanted and prolonged antibiotic therapy SXT, DOX for 12 months)
Yuhning et al. 
Upgrade to a CRT-D from PM then RA lead reposition
Pocket and leads
worsening pain and wound dehiscence and discharge
Antibacterial treatment (IPM, CLR and MOX; then MEM, LD and DOX) with device and lead extraction. Right MCA stroke, seizures, CoNS bacteremia, acute respiratory failure, and death
Shah et al. 
Pocket and lead
Chest wall tenderness, fevers, chills, decreased appetite, weakness and weight loss
Antibacterial treatment with device and lead extraction. (SXT for 2 months)
The device and leads were explanted and antibiotic therapy. Died due to multi-organ failure
The widespread use of AFB staining and mycobacterial cultures has undoubtedly increased diagnostic accuracy . Ziehl–Neelsen staining has a sensitivity of 50–80 % while that of blood culture is approximately 98 % [41, 42].
Early identification of the Mycobacterium species can provide predictable antimicrobial susceptibility patterns. The best chance of cure is obtained with a combination of at least two active antimicrobials given for a minimum of 4 weeks, plus removal of the CIEDs .
CIEDs infection due to Mycobacterium species is an uncommon but a well-known entity. Early diagnosis and prompt management may result in a good outcome. In case of suspected military TB early initiation of anti-TB therapy is recommended while awaiting culture results.
cardiac device-related infective endocarditis
cardiac implantable electronic devices
- CO2 :
cardiac resynchronization therapy-defibrillator
Cardiac Surgery Intensive Care Unit
- HACEK group:
Haemophilus species, Aggregatibacter species, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae
human immunodeficiency virus
implantable cardioverter defibrillator
jugular venous pressure
left ventricular ejection fraction
packed red blood cells
superior vena cava
thrombotic thrombocytopenic purpura
BAG concept/design, drafting article, critical revision of article, approval of article, statistics. HEW, MAS, JA, AAS and MH data analysis/interpretation, acquisition of data. All authors read and approved the final manuscript.
The authors want to express their appreciation to Ms. Sandra Keating and Ms. Suzanne Tobias for editing the manuscript of this research.
The authors declare that they have no competing interests.
Availability of data and materials
The dataset(s) supporting the conclusions of this article is (are) included within the article [and its additional files(s)].
Consent for publication
Written informed consent was obtained from the patient’s son for publication of this Case Report and any accompanying images..
Ethics approval and consent to participate
The study is approved by the Hospital Research Ethics Committee.
Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
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