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From Service de Cardiologie (A.D.C., G.K., P.C., P.T.), Hôpital
cardiovasculaire et pneumologique, Lyon, France; and Laboratoire de
bactériologie (H.L., M.C., F.V., J.E.), Hôpital cardiovasculaire
et pneumologique, Lyon.
Correspondence to Prof Paul Touboul, Hôpital Cardiovasculaire et Pneumologique Louis Pradel, BP Lyon Montchat 69394 Lyon Cedex 03 France.
Methods and ResultsSpecimens were collected at the site of
implantation for culture from the skin and the pocket before and after
insertion in a consecutive series of patients who underwent elective
permanent pacemaker implantation. Microorganisms isolated both at the
time of insertion and of any potentially infective complication were
compared by using conventional speciation and ribotyping. There were
103 patients (67 men and 36 women) whose age ranged from 16 to 93 years
(mean±SD, 67±15). At the time of pacemaker implantation, a total of
267 isolates were identified. The majority (85%) were staphylococci.
During a mean follow-up of 16.5 months (range, 1 to 24), infection
occurred in four patients (3.9%). In two of them, an isolate of
Staphylococcus schleiferi was recognized by molecular
method as identical to the one previously found in the pacemaker
pocket. In one patient, Staphylococcus aureus, an
organism that was absent at the time of pacemaker insertion, was
isolated. In another patient, a Staphylococcus
epidermidis was identified both at the time of pacemaker
insertion and when erosion occurred; however, their antibiotic
resistance profiles were different.
ConclusionsThis study strongly supports the hypothesis that
pacemaker-related infections are mainly due to local contamination
during implantation. S schleiferi appears to play an
underestimated role in infectious colonization of implanted
biomaterials and should be regarded as an important opportunistic
pathogen.
Surgical Technique
Follow-up
Bacteriologic Procedures
Statistical Analysis
Bacteriologic Results at the Time of Implantation
Follow-up
Epidemiological Analysis of Bacterial Strains
In this prospective study, 4 patients out of 103 (3.9%) developed
infection. Two of them developed bacteremia shown by positive blood
cultures (patients 1 and 2), one developed a wound abscess (patient 3),
and one a local infection (patient 4). S schleiferi was
associated with two of these four cases of infection and was also
isolated at the time of pacemaker implantation (Table 2
Although a local antisepsis was applied, several organisms
(mostly staphylococci) were cultured in the pocket and over the
generator before suturing. This phenomenon plays an important role,
suggesting a local contamination with the staphylococci present
within the skin appendages (including hairs, sebaceous glands, and
sweat glands), which might contaminate the wound margins during
surgical procedure, probably during the pocket achievement. The
present study also showed that S epidermidis, although
representing the majority of strains isolated at the time
of implantation, was very rarely responsible for subsequent infection.
In a previous study, Ramsdale et al 8 took
preoperative microbiologic specimens in more than 470 patients, but the
results of preoperative culture were not found to be predictive of
subsequent infection. In their series, six patients had pathogens over
the skin before surgery (among which five were S aureus),
but none of the six patients developed
infection.8 No data are available concerning
bacteriologic findings in the pacemaker pocket and wound margins in
their study. Bacteriologic examinations were also performed by Bluhm et
al.10 Samples were obtained from tissue fluid of
the pacemaker pocket 1 day after surgery. Out of 34 patients not
receiving an antibiotic prophylaxis regimen, cultures were positive in
10 but none developed subsequent infection.10
Another study from the same authors led to the same
conclusions.9 Only one study was made to predict
the causative organism in postoperative
infection.18 Specimens for culture were taken
from the nose, the throat, and from the wound margins at the end of the
operation. A needle aspiration was performed from the pacemaker pocket
in each patient with suspected infection. Identity of a strain of
S aureus isolated from the nose before surgery to that
collected at the time of infection from a wound culture was
demonstrated by phage typing, with no molecular marker being available
in 1983.18 For the other seven patients in their
series, no definitive conclusion could be drawn by analysis of
the preoperative and postoperative microbiologic flora. In contrast,
our prospective study evidenced the pathogenic role of the preaxillary
flora, notably that of S schleiferi, in early and late
pacemaker infections.
Another important finding deals with pacemaker erosion. Our
results support the hypothesis that apparently clinical pacemaker
erosion without obvious local infection may be primarily caused by
infection (two of three patients in our series); systematic local
sampling and blood cultures should be recommended in this setting.
Indeed, specific microorganisms such as S schleiferi or
S epidermidis can be responsible for nosocomial infections,
especially in the presence of foreign
bodies.17
Conclusions
Received September 5, 1997;
revision received January 5, 1998;
accepted January 9, 1998.
2.
Frame R, Brodman RF, Furman S, Andrews C, Gross JN.
Surgical removal of infected transvenous peacemakers leads.
PACE. 1993;16:23432348.
3.
Hill PE. Complications of permanent transvenous
cardiac pacing: a 14-year review of all transvenous pacemakers inserted
at one community hospital. PACE. 1987;10:564570.
4.
Bluhm G. Pacemaker infections: a clinical study with
special reference to prophylactic use of some isoxazolyl
penicillins. Acta Med Scand. 1985;699:162.
5.
Arber N, Pras E, Capperman Y, Schapiro JM, Meiner V,
Lossos IS, Militianu A, Hassin D, Pras E, Shai A, Moshkowitz M, Sidi Y.
Pacemaker endocarditis: report of 44 cases and review of the
literature. Medicine. 1994;73:299305.[Medline]
[Order article via Infotrieve]
6.
Klug D, Lacroix D, Savoye C, Goullard L, Grandmougin
D, Hennequin JL, Kacet S, Lekieffre J. Systemic infection related to
endocarditis on pacemaker leads: clinical presentation and
management. Circulation. 1997;95:20982107.
7.
Wade JS, Cobbs CG. Infections in cardiac pacemakers.
Curr Clin Top Inf Dis. 1988;9:4461.
8.
Ramsdale DR, Charles RG, Rowlands DB, Singh SS, Gautam
PC, Faragher EB. Prophylactic antibiotics for cardiac
pacemaker implantation: a prospective randomised trial.
PACE. 1984;7:844849.
9.
Bluhm G, Jacobson B, Julander I, Lindgren ML, Olin C.
Antibiotic prophylaxis in pacemaker surgery: a prospective study.
Scand J Thorac Cardiovasc Surg. 1984;18:227234.[Medline]
[Order article via Infotrieve]
10.
Bluhm G, Norlander R, Ransjö U. Antibiotic
prophylaxis in pacemaker surgery: a prospective double blind trial with
systemic administration of antibiotic versus placebo at implantation of
cardiac pacemakers. PACE. 1986;9:720726.
11.
Bluhm G, Jacobson B, Ransjö U. Antibiotic
prophylaxis in pacemaker surgery: a prospective trial with local or
systemic administration of antibiotics at generators replacements.
PACE. 1985;8:661670.
12.
Choo MH, Holmes DR, Gersh BJ, Maloney JD, Merideth J,
Pluth JR, Trusty J. Permanent pacemaker infections: characterization
and management. Am J Cardiol. 1981;48:559564.[Medline]
[Order article via Infotrieve]
13.
Grattard F, Etienne J, Pozzetto B, Tardy F, Gaudin OG,
Fleurette J. Characterisation of unrelated strains of
Staphylococcus schleiferi by using ribosomal DNA
fingerprinting, DNA restriction patterns, and plasmid profiles.
J Clin Microbiol. 1993;31:812818.
14.
Crichton PB, Anderson LA, Phillips G, Davey PG, Rowley
DI. Subspecies discrimination of staphylococci from revision
arthroplasties by ribotyping. J Hosp Inf. 1995;30:139145.[Medline]
[Order article via Infotrieve]
15.
Izard NC, Hachler H, Grehn M, Kayser FH. Ribotyping of
coagulase-negative staphylococci with special emphasis on intraspecific
typing of Staphylococcus epidermidis. J Clin
Microbiol. 1992;30:817823.
16.
Celard M, Vandenesch F, Darbas H, Grando J, Jean-Pierre
H, Kirkorian G, Etienne J. Pacemaker infections caused by
Staphylococcus schleiferi, a member of the human
pre-axillary flora. Clin Inf Dis. 1997;24:10141015.[Medline]
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17.
Vandenesch F, Eykyn SJ, Etienne J. Infections
caused by newly described species of coagulase-negative staphylococci.
Rev Med Microbiol. 1995;6:94100.
18.
Jacobson B, Bluhm G, Julander I, Nord CE.
Coagulase-negative staphylococci and cloxacillin prophylaxis in
pacemaker surgery. Acta Path Microbiol Scand [B] Microbiol
Immunol. 1983;91:9799.
19.
Da Costa A, Kirkorian G, Cucherat M, Delahaye F,
Chevalier P, Cerisier A, Isaaz K, Touboul P. Antibiotic prophylaxis for
permanent pacemaker implantation: a meta-analysis.
Circulation. 1998;97:17961801.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Role of the Preaxillary Flora in Pacemaker Infections
A Prospective Study
![]()
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
Addendum
References
BackgroundInfection remains a
severe complication after pacemaker implantation. The purpose of our
prospective study was to evaluate the role of the local bacteriologic
flora in its occurrence.
Key Words: pacemakers follow-up studies genes
![]()
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
Addendum
References
Despite improvement
as the result of better surgical techniques, infection of the pacemaker
pocket or lead still remains a potential complication after permanent
pacemaker implantation. Rates varying between 0.5% and 5.1% have been
reported in retrospective and prospective
studies.1 2 3 4 Bacteremia and/or endocarditis have
also been reported in up to 0.5% of patients.5
When they occur, they carry a high morbidity and
mortality.5 6 Infection can involve the pacemaker
pocket itself (abscess) or can be disseminated to the blood by the lead
that lies within the venous system and impinges on the endocardium
(bacteremia/endocarditis). The precise mechanisms involved are
incompletely understood. It is currently considered that infections are
first due to local bacterial contamination acquired at the time of
surgery. Virulent organisms such as Staphylococcus aureus
cause infections early after pacemaker
implantation,4 whereas coagulase-negative
staphylococci (CNS) such as Staphylococcus epidermidis are
responsible for delayed infections. Second, infection can occur after
seeding of the microorganisms through the hematogenous
route.4 Alternatively, skin erosion may be the
primary mechanism by which local infection occurs. There are very few
data available on operative bacteriologic findings and their
implications in pacemaker infection.7 8 9 10 11 12 In a
prospective study, we evaluated the role of local bacteriologic flora
on pacemaker-related infection and skin erosion. Microorganisms
isolated at the time of insertion and of any pertinent clinical event
were compared by using phenotypic and molecular methods when
consecutive isolates were of the same species.
![]()
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
Addendum
References
Study Patients
From January 1995 through January 1996, specimens were
systematically and prospectively collected at the site of implantation
for bacteriologic culture in a consecutive series of patients who
underwent elective permanent pacemaker implantation. Patients were
systematically submitted to shaving and to an antiseptic shower with
povidone iodine 10% aqueous solution on the night before the
operation. The first specimen was taken preoperatively from the skin at
the implantation site over the relevant right or left pectoral region
before any skin preparation or desinfection. Antisepsis was performed
immediately before surgery; the skin was painted with two solutions,
successively: aqueous povidone iodine 10% solution and povidone iodine
7.5% solution. The second specimen was sampled from the pocket as soon
as it had been done and the third one from the same pocket after
generator insertion immediately before suturing. Specimens were taken
with sterile dry swabs. Infectious risk factors were systematically
searched: diabetes mellitus, long-term corticosteroid
therapy or anticoagulant agents, postoperative hematoma, malignancy,
and temporary electrodes.
Pacemaker implantation was standardized. Operations were
performed under local anesthesia. All operators were
trained in the technique of pacemaker implantation during the course of
the trial. New leads were inserted transvenously through the cephalic
vein or alternatively through the subclavian vein. Generators were
positioned subcutaneously over the pectoral major muscle. Drains and
antibiotics, local or systemic, were never used.
Patients were discharged 3 to 5 days after implantation, and the
site was inspected at 3 days, then 3, 6, and 12 months after
implantation. In patients with suspected postoperative infections,
specimens were taken with swabs or by needle aspiration from the
pacemaker pocket. In the presence of potentially infectious
complications, blood cultures were systematically sampled by
venipuncture. Patients and/or their physicians were
systematically called on January 1997. No patient was lost to
follow-up.
Bacterial isolates collected at the time of implantation were
stored and compared with the isolates cultured at the time of any
infection. Bacterial culture and identification were performed
according to standard methods by using commercially available reagents.
All staphylococcal isolates were identified at the species level by
using ID32 STAPH gallery (bioMérieux). When consecutive isolates
of the same species were identified from the same patient, their
genetic relatedness was evaluated by ribotyping. It consisted of
comparing ribosomal DNA (rDNA) restriction fingerprints of the studied
isolates. Briefly, whole-cell DNA was restricted by HindIII,
separated by agarose gel electrophoresis, and vacuum transferred to
nylon membranes as previously described.13
Plasmid pKK3535 labeled by random priming with digoxigenin-11-dUTP (DIG
DNA Labeling Kit, Boehringer Mannheim) was used as a probe
specific for genes coding for rRNA.13 14 15
Hybridization was detected by addition of antidigoxigenin antibodies
conjugated to alkaline phosphatase, revelation by addition of the
chemiluminescent substrate provided by the manufacturer
(Boehringer Mannheim), and exposition of the filter to x-ray
film.
Results are reported as mean value±SD. We used Kaplan-Meier
survival estimates to describe the long-term event-free rate. The
analysis was performed with the StatView F-4.5 software (Abacus
Concepts Inc).
![]()
Results
Top
Abstract
Introduction
Methods
Results
Discussion
Addendum
References
Population Characteristics
There were 103 patients (67 men and 36 women). Their age ranged
from 16 to 93 years (67±15, mean±SD). Implanted pacemakers were dual
chamber in 56 and single chamber in 47. Infectious risk factors were
found in 28 patients; none of them developed subsequent infection.
At the time of surgery, a total of 293 samples were collected.
Data were missing and nonavailable for 16 samples. Positive culture was
obtained in 88.3% of the preoperative skin samples, 48% of the
pacemaker pocket samples before insertion, and 37.1% of the pocket
samples at the end of surgery (Table 1
).
A total of 267 isolates were identified. The majority of the isolates
were members of the human cutaneous flora, 227 (85%) being
staphylococci. S aureus was isolated in nine instances from
seven patients, eight of nine times on the preoperative skin. S
epidermidis was the most represented species.
Staphylococcus schleiferi was isolated in five instances
from five patients.
View this table:
[in a new window]
Table 1. Results of Preoperative and Operative Cultures
During a mean follow-up of 16.5 months (range, 1 to 24), infection
occurred in four patients (3.9%): wound abscess in one, erosion and
local infection in one, erosion and bacteremia in one, and bacteremia
in one, occurring 10, 1, 16, and 4 months, respectively, after
implantation. Infection occurred 7.7±6.7 months after implantation.
The 2-year infection rate was 4.6%. S schleiferi was
responsible for bacteremia in two patients (patients 1 and 2) and was
also isolated over the generator in patient 1 (Table 2
). Interestingly, erosion was the
initial clinical diagnosis for patient 1 before systematic blood
cultures showed evidence of infection. In this patient, two strains of
S epidermidis were also cultured from the generator and the
skin, respectively. Their antibiotic resistance profiles were
significantly different to reject any clonal relatedness between the
two strains. In a third patient (patient 3), a strain of S
aureus was isolated from a wound abscess and in patient 4, a
strain of S epidermidis was identified at the site of skin
erosion. No organism could be cultured in an additional patient
(patient 5) at the site of erosion although a strain of
Staphylococcus haemolyticus had been isolated on the
preoperative skin 9 months earlier. Hence this patient was not
considered as infected.
View this table:
[in a new window]
Table 2. Complications and Results of Bacteriologic Findings
The organisms collected at the time of infection were compared
with those collected at the time of pacemaker implantation. No strain
of S aureus was recovered at the time of pacemaker
implantation for patient 3, although a strain of S
epidermidis was isolated on the preoperative skin and a strain of
S schleiferi from the pacemaker pocket. A strain of S
epidermidis was isolated at the time of pacemaker insertion in
patient 4; however, this strain was different from the one isolated at
the time of skin erosion on the basis of different antibiotic
resistance profiles. In patients 1 and 2, S schleiferi was
isolated over the generator (patient 1) or on the preoperative skin
(patient 2), together with other microorganisms that were not cultured
afterward (Table 2
). Antibiotic resistance and biochemical profiles of
the different isolates of S schleiferi were identical, and
ribotypes of the consecutive isolates of each patient were identical
(Figure
). However, the ribotypes of strains isolated
from patients 1 and 2 were unrelated (Figure
). Ribotype of the strain
of S schleiferi isolated on the preoperative skin of patient
3 was not determined.

View larger version (84K):
[in a new window]
Figure 1. HindIII restriction patterns of rDNA from
Staphylococcus schleiferi isolates. Lane 1:
S schleiferi ATCC 43808type strain;
lane 24, isolates from patient 1 cultured from the generator at
implantation (lane 2), blood culture (lane 3), and generator at the
time of complication (lane 4); lane 56, isolates from patient 2
cultured from the preoperative skin (lane 5) and blood at the time of
complication (lane 6).
![]()
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
Addendum
References
Infection is a serious, potentially life-threatening complication
after pacemaker surgery; morbidity and mortality are reported to be
high.6 Its prevention would greatly benefit from
a better knowledge of mechanisms involved. Several mechanisms have been
advocated,7 although none has been fully
validated. Local perioperative wound contamination is
usually described as the major mechanism predisposing to local or
systemic pacemaker infection.7 The presence of a
superficial foreign body can predispose to skin erosion or necrosis and
also cause infection. Besides, microorganisms can colonize foreign
bodies such as pacemaker leads by the hematogenous route. The
predictive values of preoperative and operative local bacteriologic
flora have not been fully explored; conclusions drawn from small series
are elusive.8 9 10 11 12
). The frequency
of association of S schleiferi with infections in this
series is surprising compared with its low frequency of isolation in
the prospective samples (5 out of 267 isolates). Four other cases of
pacemaker infection caused by S schleiferi have been
reported previously.16 When analyzing these six
cases (two from the present study plus four from the previous
study16 ), the interval between pacemaker
implantation and infection varied between 6 weeks and 16 months, with a
median of 10 to 12 months. In the present study we have
demonstrated by a molecular method that the strain associated with
pacemaker infection and present in blood cultures was already
present in the operative sample at the time of pacemaker insertion.
This supports a previous hypothesis that delayed infections caused by
CNS are due to local bacterial contamination acquired at the time of
surgery. This also strongly suggests that infection is likely to begin
at the pacemaker pocket and extend down the lead. Furthermore, strains
of S schleiferi isolated from our two patients displayed
different ribotypes (Figure
) assessing the lack of pathogenic link
between them and allowing exclusion of a specific operator
contamination. Besides pacemaker infections, S schleiferi
has been associated with other human conditions such as infections of
wounds, hip prostheses or vascular devices, brain empyema, and
bacteremia, but the frequency of these infections is extremely low
compared with those caused by other species of staphylococci such as
S aureus or S
epidermidis.17 However, S
schleiferi may be misidentified as S aureus because
both species express a fibrinogen affinity factor (clumping factor), a
characteristic frequently used to identify S aureus. Hence
the actual responsibility of S schleiferi in human
infections especially on biomaterials may have been underestimated as
coagulase-negative staphylococci from infected materials are not
systematically identified at the species level senso stricto by all
laboratories. Moreover, bacteriologic cultures from pacemaker skin
erosion are not currently done if signs of infection are not patent.
The peculiar association of S schleiferi with pacemaker
infection may reflect the expression by this species of specific
virulence factors such as surface receptors that are presently
unknown.
Our study shows that numerous strains of organisms are present
in the pacemaker pocket at the time of implantation despite careful
preoperative preparation of the skin, suggesting their subcutaneous
origin. They are very rarely responsible for subsequent infection.
Among these organisms, S schleiferi appears to play a
particular and so far underestimated role in infectious colonization of
implanted biomaterials and should be regarded as an important
opportunistic pathogen. This study gives new insights into the
pathogenesis of infections secondary to pacemaker infections and
strongly supports the hypothesis that pacemaker-related infections are
mainly due to local contamination during implantation. These data
equally support the hypothesis that pacemaker erosion can be caused by
primary infection. Our findings further raise the question of a likely
benefit of antibiotic prophylaxis in this setting to prevent subsequent
major infections.19
![]()
Addendum
Top
Abstract
Introduction
Methods
Results
Discussion
Addendum
References
Since submission of this paper, an additional patient was
admitted for pacemaker erosion 29 months after implantation. A strain
of S schleiferi was cultured from the pacemaker pocket, skin
sample and pacemaker itself at the time of complication, while a strain
of S schleiferi has also been isolated from the pocket at
the time of implantation. Molecular analysis confirmed the genetic
relationship between the two strains. Hence, 4 patients out of 5 in
whom a strain of S schleiferi had been isolated at the time
of implantation presented an infective complication: 3 were associated
with S schleiferi and 1 with S aureus.
![]()
References
Top
Abstract
Introduction
Methods
Results
Discussion
Addendum
References
1.
Kearney RA, Eisen HJ, Wolf JE. Nonvalvular
infections of the cardiovascular system. Ann
Intern Med. 1994;121:219230.
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