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Acta Neurochir (2017) 159:2239–2241
DOI 10.1007/s00701-017-3335-5
Deep brain stimulator infection by a novel rapid
growing mycobacterium
Donna C. Moritz 1 & Amanda T. Harrington 2 & Konstantin Slavin 3 & Christy Gomez 3 &
Olamide D. Jarrett 1
Received: 5 September 2017 / Accepted: 11 September 2017 / Published online: 20 September 2017
# Springer-Verlag GmbH Austria 2017
Abstract Devise-related infections after deep brain stimulator implantation are not uncommon. However, infections due
to mycobacteria have not been reported in the medical literature. We describe the first reported case of DBS infection due
to a novel rapidly growing mycobacteria, most closely resembling Mycobacterium goodii, by rpoB gene sequencing.
Keywords Deep brain stimulator infection . Rapid growing
mycobacterial infection . Mycobacterium goodii
Deep brain stimulator
Deoxyribonucleic acid
Rapid-growing mycobacteria
Ribonucleic acid
Ribosomal ribonucleic acid
TMP-SMX Trimethoprim/sulfamethoxazole
* Donna C. Moritz
[email protected]
Division of Infectious Diseases, Department of Medicine, University
of Illinois at Chicago School of Medicine, 808 South Wood Street,
MC 735, Suite 888, Chicago, IL 60612, USA
Clinical Microbiology Laboratory, Department of Pathology, Loyola
University Medical Center, Maywood, IL, USA
Department of Neurosurgery, University of Illinois at Chicago
School of Medicine, Chicago, IL, USA
Deep brain stimulators (DBS) are a common therapeutic approach for movement disorders. Hardware infections are a
known and common complication after implantation of these
devices with reported infection rates between 0.4 to 12.7% [2,
3, 7, 11, 13]. Infections are typically due to skin commensals,
with >50% of reported infections due to Staphylococcus
aureus followed by Staphylococcal epidermidis and
Proprionibacterium acnes [2, 13]. DBS infection due to a
mycobacterium species has not been previously reported in
the medical literature. We present the first reported case of
DBS infection due to a rapid-growing mycobacterium
(RGM) not previously identified species, most closely resembling Mycobacterium goodii.
Case report
A 62-year-old male with essential tremors underwent twostage implantation of left thalamic DBS. Three weeks later
he developed generator pocket swelling with purulent drainage from the incision and mild right retro-auricular discomfort
along the extension cables. The patient was taken to the operative room for removal of the generator and washout of the
generator pocket. The retro-auricular cable track was also explored during the operation. Though there were no visible
signs of infection in this portion of the track, the cables were
cut at this level and removed inferiorly toward the generator
site. There were no immediate complications post-operation,
and the patient was started on trimethoprim/sulfamethoxazole
(TMP-SMX) to cover the most common pathogens for DBS
infections. Cultures from the generator pocket were taken
intraoperatively, and the initial gram stain showed many white
blood cells but no organisms. After 48 h, the culture grew
Bgram-positive rods,^ which were ultimately identified using
gene sequencing of bacterium-specific rpoB and 16S ribosomal RNA, as a rapidly growing Mycobacterium spp., most
closely resembling M. goodii. The mycobacterium was susceptible to TMP-SMX, doxycycline, linezolid, ciprofloxacin,
moxifloxacin, amikacin and minocycline. Thus, the decision
made was to continue TMP-SMX for at least 6 months.
Despite appropriate antibiotic therapy, 2 months later the
patient developed dehiscence of his retro-auricular incision
with drainage from the site. Doxycycline was added to his
antibiotic regimen, and he was taken back to the operating
room for removal of the extension cables and wound debridement with primary skin closure. The intra-thalamic electrodes
were left in place. Intraoperative cultures were sent, which
grew the same Mycobacterium spp. The patient completed
the course of antibiotics, and the infection resolved. The
DBS system was replaced a few months later. The patient
has had no further complications or relapse of infections since
To our knowledge, this is the first reported case of DBS infection due to any mycobacterium species. DBS hardware infections are usually due to skin flora with S. aureus comprising
the majority of infections [2, 13]. The pathogen isolated in this
case was an RGM, which are widely distributed in the soil,
water and other environments and during the past 2 decades
have been increasingly recognized as significant human pathogens [9].
Conventional laboratory identification of RGM was previously based on growth rate, pigmentation and biochemical
tests, but has largely been replaced by DNA gene sequencing
and mass spectrometry-based methods. Because antibiotic
susceptibilities can differ greatly between RGM species, correct identification of RGM is important to guide therapy. Use
of molecular techniques has allowed for more accurate identification and discrimination of Mycobacterium spp. by sequencing the 16S ribosomal RNA gene and alternative gene
targets such as the rpoB gene, which encodes the β-subunit of
bacterial RNA polymerase, and allows for more specific differentiation and speciation of mycobacterial organisms when
compared to the 16s rRNA gene [1, 10].
The RGM identified in our patient’s DBS infection
most closely resembled Mycobacterium goodii, a member
of the Mycobacterium smegmatis group, which has rarely
been reported as a pathogen in surgical site infections. At
a Colorado hospital, there was an outbreak of M. goodii
wound infections from an undetermined source after surgical implantations (two prosthetic joints and one
Acta Neurochir (2017) 159:2239–2241
inguinal hernia patch) [8]. There are also three reported
cases of pacemaker hardware infections due to M. goodii
[6, 12, 14]. M. goodii has been reported to be consistently
susceptible to sulfonamides, doxycycline, amikacin and
ethambutol, but has variable resistance to clarithromycin,
cefoxitin and doxycycline [4, 5]. While standardized
guidelines for the duration of M. goodii treatment are
not available, effective treatment with antibiotics for
4 months has been described for mild skin, soft tissue
and bone infections [4]. In more severe disease, surgical
debridement in combination with intravenous antibiotics
for 2–6 weeks followed by oral antibiotic therapy for a
total of 6 months of therapy has shown favorable results
[4, 8].
There is no standard treatment approach for the management of DBS hardware infections. Antibiotics alone are only
successful in a low percentage of superficial infections [3],
and combination therapy with partial or complete hardware
removal is usually necessary. Bhatia et al. estimated that only
20.8% of reported DBS infections were successfully treated
with complete salvage of the device and the remainder required partial or complete device removal [3]. In our case,
we eradicated the infection with near complete device removal, retaining only the intrathalamic electrodes, and 6 months of
oral antibiotic treatment.
Providers need to be aware of atypical causes of DBS infection and to consider mycobacterium infection if initial cultures
are negative for the usual skin pathogens. Close communication with the microbiology laboratory is important for the
appropriate antibiotic management of these infections. There
is no standard treatment for DBS infections due to M. goodii
or similar pathogens; however, a combination of antibiotic
therapy and surgical exploration is recommended.
Compliance with ethical standards
Conflict of interest None.
Ethical standards The manuscript does not contain clinical studies or
patient data.
The patient has consented to submission of this case report to the
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