Abstract
BACKGROUND
Mycobacterium fortuitum is a rapidly growing mycobacterium, ubiquitous in soil and water, but it is an uncommon cause of infections in immunocompetent hosts. Cardiac device infections and bloodstream infections due to non-tuberculous mycobacteria are rare.
CASE PRESENTATION
We present the case of an 85-year-old patient with infective endocarditis and pacemaker lead infection secondary to M. fortuitum.
Keywords: case, infections, Mycobacterium fortuitum, pacemakers, report
Abstract
HISTORIQUE
Le Mycobacterium fortuitum est une mycobactérie à la croissance rapide, omniprésente dans la terre et l’eau, mais est une cause d’infection peu courante chez les hôtes immunocompétents. Les infections des dispositifs cardiaques et du sang causées par des mycobactéries non tuberculeuses sont rares.
PRÉSENTATION DE CAS
Les auteurs présentent le cas d’un patient de 85 ans atteint d’une endocardite infectieuse et d’une infection de la dérivation de son stimulateur cardiaque secondaire à un M. fortuitum.
Mots-clés : cas, infections, Mycobacterium fortuitum, rapport, stimulateurs cardiaques
Case Report
An 85-year-old man was admitted to an academic hospital for elective infected pacemaker removal. He had a history of type 2 diabetes and third-degree heart block requiring a surgically implanted left-sided infraclavicular dual-chamber pacemaker in 2002. In 2014, he had an uncomplicated generator replacement for battery depletion. In 2016, the pacemaker was repositioned more centrally and inferiorly because of discomfort at the generator site and malposition of the leads. However, this pacemaker eroded the skin, and he underwent a pacemaker excision with capping of the leads in 2017. Simultaneously, a new pacemaker was inserted on the right side. Both surgical sites healed well. Approximately 2 years later, the capped left-sided leads eroded through the skin. He bent and pushed them back inside the skin. A few weeks later, the wound started draining purulent fluid, and the skin became erythematous and mildly tender. He did not seek medical attention but used a topical over-the-counter antibiotic ointment (polymyxin B and bacitracin) and covered it with bandages. No culture was obtained. He denied any fever, night sweats, rigours, weight loss, or appetite loss. He did not seek any medical attention for approximately 6 months.
On admission, he had a 2 cm left-sided chest wound with erythema and mild tenderness. The capped leads were visible. Microscopy of the purulent drainage revealed many neutrophils but no bacteria, and the culture later grew Mycobacterium fortuitum (light growth). No blood cultures were drawn initially. Chest radiograph, liver enzymes, liver function tests, leukocyte count, C-reactive protein, and kidney function tests were normal. Hemoglobin A1C was 9.6%. On day 6 of admission, he underwent lead excision, with some residual ventricular tips remaining as a result of technical difficulties. Cefazolin was started on admission and continued post-operatively for empiric coverage. Intra-operative transesophageal echocardiogram revealed no vegetation or thrombosis, although the quality of the views was insufficient to rule out endocarditis. On postoperative day 1, he had a fever of 39.4oC. Two sets of peripheral blood cultures (BD BACTEC Plus aerobic and Lytic anaerobic media) were collected. Cefazolin was changed to vancomycin, empirically. Both sets showed beaded gram-positive bacilli from the aerobic vials on day 5 of incubation. They grew on blood and chocolate agar. Acid-fast bacilli were observed on Zeihl-Neelsen stain. Subsequently, the growth from chocolate agar was identified as M. fortuitum by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry with a 99.9% confidence level (Vitek MS, bioMérieux, St Laurent, QC), and subsequent 16s rDNA sequencing by polymerase chain reaction at the National Reference Centre for Mycobacteriology (Winnipeg, MB) confirmed the subspecies to be M. fortuitum sensu stricto. The atrial lead tip culture also grew M. fortuitum. The ventricular lead grew M. fortuitum and also grew two colonies of Staphylococcus epidermidis only on the chocolate agar plate, which was susceptible to oxacillin and levofloxacin but resistant to sulfamethoxazole–trimethoprim. His therapy was changed to cefoxitin (2 g intravenously every 6 h), amikacin (500 mg intravenously daily), and levofloxacin (750 mg by mouth daily). He quickly defervesced and remained otherwise asymptomatic. Two sets of blood cultures were repeated at 1 and 2 weeks into therapy and revealed no growth. S. epidermidis did not grow from any of the blood culture sets and was therefore considered a contaminant.
A formal transesophageal echocardiogram showed vegetations on the right atrial and ventricular leads. An audiology test revealed severe sensorineural hearing loss at baseline. On day 10 of treatment, his M. fortuitum isolate was determined to be susceptible to imipenem, amikacin, ciprofloxacin, sulfamethoxazole–trimethoprim, and moxifloxacin; intermediate to cefoxitin; and resistant to clarithromycin at the National Reference Centre for Mycobacteriology, using the Clinical Laboratory Standards Institute’s (CLSI’s) standard method. On the same day, he was changed to an oral regimen given the quick defervescence, difficulty in arranging outpatient intravenous treatment, patient preference, and risk of further complications such as ototoxicity. The patient was sent home on an oral regimen of sulfamethoxazole–trimethoprim (800 mg/160 mg by mouth twice a day) and levofloxacin (750 mg by mouth daily). On follow-up 3 months later, the patient remained systemically well with good wound healing. Given the residual cardiac hardware in place, he was continued on lifelong levofloxacin and sulfamethoxazole–trimethoprim as suppressive therapy.
Discussion
Cardiovascular implantable electronic device infections are associated with significant morbidity and mortality (1, 2). The most common early infection mechanism is peri-operative microbial contamination of the generator or the leads with skin flora. Therefore, coagulase-negative staphylococci and Staphylococcus aureus are common causative microorganisms in this setting (2). In late-onset infection (6 mo or more after implantation), hematogenous seeding is more common in the absence of a pocket infection. These infections can be complicated by bacteremia and lead infection (3). Cardiovascular infections due to Mycobacterium spp are especially rare (4).
The rapidly growing mycobacteria are part of the non-tuberculous mycobacteria (NTM). They are known to cause various infections, including metalware-associated orthopedic infections and rarely endocarditis as a result of their ability to form biofilms (5). M. fortuitum complex includes several closely related species that can infect immunocompetent and immunocompromised patients. Skin infection from microtrauma can occur in immunocompetent patients and has been related to nail salon foot baths (6). Only a few cases of rapidly growing mycobacterial pacemaker infections have been reported, and among those M. fortuitum was the most common microorganism. Most of these infections had positive blood cultures and were presumed to be nosocomial on the basis of the time of presentation after implantation (7). M. fortuitum endocarditis is usually in the setting of prosthetic valves. The mortality rate with mycobacterial endocarditis is high, at 85% in one review (8). In our case, we observed a community-acquired M. fortuitum pacemaker infection.
Rapidly growing NTM are not susceptible to first-line anti-tuberculosis agents. The treatment options rely on unique in vitro susceptibility testing for amikacin, cefoxitin, imipenem, moxifloxacin, meropenem, sulfamethoxazole–trimethoprim, ciprofloxacin, doxycycline–minocycline, and linezolid on the basis of CLSI (M62) guidelines (9). Macrolides should be avoided because of inducible resistance via erm 39 (6).
We propose that the prolonged exposure of the leads to the external environment led to contamination and infection in this patient. Thus, we emphasize the importance of considering rare etiologies such as rapidly growing mycobacteria in such circumstances and to request culture for mycobacteria and other slow-growing pathogens. Also, the treatment options and time course of M. fortuitum are not well established, but a few case reports exist (2,3), and therapy for invasive infections usually requires two to three agents, which may include intravenous options for a prolonged duration. Given our patient’s circumstances, it was decided to give oral suppression therapy instead.
Ethics Approval:
N/A
Informed Consent:
Informed patient consent has been secured from all patients whose personal information is included in the manuscript or the parents or guardians of minors.
Registry and the Registration No. of the Study/Trial:
N/A
Funding:
No funding was received for this work.
Disclosures:
The authors have nothing to disclose.
Peer Review:
This manuscript has been peer reviewed.
Animal Studies:
N/A
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