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Journal of Clinical Microbiology, September 2001, p. 3420-3421, Vol. 39, No. 9
0095-1137/01/$04.00+0 DOI: 10.1128/JCM.39.9.3420-3421.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Peritoneal Dialysis-Associated Peritonitis Caused
by Dermabacter hominis
Andreas
Radtke,1,*
Kåre
Bergh,1,2
Cecilia M.
Øien,3 and
Lars S.
Bevanger1,2
Department of
Microbiology1 and Department of
Nephrology,3 Regional Hospital, and
Department of Laboratory Medicine, Norwegian University of
Science and Technology,2 Trondheim, Norway
Received 19 March 2001/Returned for modification 16 May
2001/Accepted 10 July 2001
 |
ABSTRACT |
Dermabacter hominis was the cause of a peritoneal
dialysis-associated peritonitis. D. hominis was identified
by phenotypic criteria and by sequencing the 16S rRNA gene. Clinical
cure was achieved with cefuroxime treatment despite the isolate's
reduced susceptibility to this drug (MIC, 12 mg/liter) on in vitro
testing. The successful treatment was probably due to the high
concentrations attained by intraperitoneal administration of the drug.
 |
CASE REPORT |
Our patient was a 67-year-old
woman with end-stage renal disease due to hypertensive kidney disease.
Since 1994 she had been receiving renal replacement therapy with
peritoneal dialysis (PD), which was exclusively performed as continuous
ambulatory peritoneal dialysis (CAPD). She was admitted to the
hospital at the end of March 2000 with symptoms of peritonitis.
Cultures of the dialysate yielded coagulase-negative staphylococci. The
infection was successfully treated with cloxacillin given
intraperitoneally. In the middle of April, the cuff of the dialysis
catheter (single-cuff Quinton-Tenckhoff catheter, 41 cm long) slid out.
The catheter was therefore exchanged. Resumption of dialysis after this
was uncomplicated. Almost 3 weeks later, while still in the hospital
awaiting transfer to a nursing home, she again became ill with
abdominal pain and a hazy dialysate. The PD effluent contained
0.54 × 109 leukocytes per liter. We routinely culture
peritoneal fluid from PD patients with signs of peritonitis in
Vital aerobic and anaerobic blood culture bottles (bioMerieux SA,
La Balmes-des-Grottes, France). Two sets of samples were obtained on
day 1, and one set of samples was obtained on each of the following 2 days. A gram-positive coryneform bacterium grew in all bottles from
days 1 and 2 and in the aerobic bottle from day 3. Growth occurred
after 18 to 24 h in the aerobic bottles and after approximately 4 days in the anaerobic bottles. A swab from the catheter exit site
yielded no growth.
From day 1 the patient was empirically treated with a combination of
intraperitoneal cloxacillin (125 mg/liter of dialysis fluid) and
netilmicin (6.25 mg/liter) in 2-liter bags in each of the four daily
instillations. New samples taken on day 6 yielded growth of the same
coryneform bacterium, although the dialysate had cleared and the
patient was improving. Because of the results of disk diffusion
susceptibility testing, treatment was changed to cefuroxime (125 mg/liter of dialysis fluid) and continued for a further 14 days,
achieving clinical cure. Cultures from days 8 and 13 were sterile.
Microbiology.
The peritoneal fluid inoculated into blood
culture bottles yielded bacteria that grew on blood agar and chocolate
agar (but best on blood agar) as 0.5- to 1-mm-diameter white
colonies after 18 h. The colonies were white, convex, slightly
viscid, and catalase positive and had a sweet, pungent odor. As judged
from the blood culture bottles, the organism was nonmotile and gram
positive and had coryneform morphology without branching. The isolate
hydrolyzed esculin and was nitrate and xylose negative. The bacterium
was identified by the API Coryne system (bioMerieux SA) as
Dermabacter hominis (code 4570365). Antibiotic
susceptibility testing was initially performed with Neo-Sensitabs
tablets (A/S Rosco, Taastrup, Denmark) on Mueller-Hinton agar with 5%
defibrinated horse blood. The isolate was resistant to chloramphenicol,
clindamycin, erythromycin, netilmicin, and penicillin and was
intermediately resistant to ampicillin. The isolate was
susceptible to cefalothin, cefuroxime, doxycycline,
trimethoprim-sulfamethoxazole, and vancomycin by disk
diffusion testing. The strain did not produce
-lactamase (nitrocefin
test). MICs were determined with E-test strips (AB Biodisk, Solna,
Sweden) on Mueller-Hinton agar with 5% defibrinated horse blood (Table
1). A discrepant result was noted for
cefuroxime by E-test (MIC, 12 mg/liter; intermediately susceptibile),
compared to the result obtained by the disk diffusion method (fully
susceptible). The 16S rRNA gene was amplified by PCR, and the amplicon
(approximately 1,500 bp) was purified from agarose gel by using a
QIAquick Gel Extraction Kit (Qiagen, Hilden, Germany). Analysis of the
nucleotide sequence was performed using a MicroSeq Full Gene 16S rDNA
Bacterial Sequencing Kit (Applied Biosystems, Foster City, Calif.) and
an automated DNA sequencer (ABI PRISM 310 Sequencer; Applied
Biosystems). The resulting 1,468-bp sequence was compared to sequences
available in databases using BLAST (1). More than 99%
similarity was found to two D. hominis and two
Dermabacter spp. published sequences.
PD has become the dialysis modality of choice for an increasing number
of patients. However, peritonitis is the major source
of morbidity and
treatment dropout in this form of renal replacement
therapy, resulting
in only a small number of long-term PD patients.
A vast number of
different species of microorganisms have been
identified as causes of
PD-associated peritonitis, and most of
the isolates are originally part
of the normal skin
flora.
D. hominis was first described in 1988 as a cutaneous
coryneform bacterium (
9). It was later found to be similar
to strains
that have been present in the special reference laboratory
collection
of the Centers for Disease Control and Protection since the
1970s
and provisionally grouped as fermentative coryneform group 3 and
5 organisms. These two groups of isolates are identical apart
from the
fact that members of group 3 are fermenters of xylose
while members of
group 5 are not (
3,
6,
8).
Chemotaxonomically,
D. hominis resembles
Brevibacterium spp. in its lack of mycolic acid and in the
fact that it has a cell
wall based on
meso-diaminopimelic
acid, but the phylogenetic distance
is large (
4,
6).
D. hominis is a recently established species,
and its
recognition as an opportunistic human pathogen is even
newer. Very few
case reports of documented infections caused by
D. hominis
have been published (
2,
7). A search in the database
of
16S rRNA gene sequences of the National Center for Biotechnology
Information for
Dermabacter sp. and
D. hominis
revealed six entries.
In our CAPD patient,
D. hominis caused
peritonitis as a nosocomial
infection. PD-associated peritonitis is
defined by three criteria:
abdominal pain, leukocyte counts above
0.1 × 10
9/liter (with 50% or more of the leukocytes
being neutrophils),
and demonstration of bacteria in the peritonal
effluent by Gram
staining or culture. Two of these three criteria are
sufficient
for the diagnosis (
10). In the present case of
peritonitis,
clinical cure with cefuroxime was achieved despite the
relatively
high MIC of this antibiotic. This was probably due to the
very
high local antibiotic concentrations employed by intraperitoneal
instillation. The present
D. hominis isolate was resistant
or
showed reduced susceptibility to several antimicrobial agents,
including penicillin, ampicillin, and cephalosporins. Apart from
cloxacillin and netilmicin, the patient had received no other
antibiotic treatment prior to the episode of peritonitis in question.
The MICs of

-lactam antibiotics tested are higher for this isolate
than has been reported previously by others (
5).
Chloramphenicol,
ciprofloxacin, clindamycin, erythromycin, and
aminoglycosides
other than amikacin have shown reduced activity against
most
D. hominis isolates (
2,
5,
6).
Susceptibility testing of
clinically important
D. hominis
isolates is therefore highly
warranted.
Nucleotide sequence accession number.
The 16S rRNA gene
nucleotide sequence of the current isolate has been given GenBank
accession number AF343728.
 |
ACKNOWLEDGMENTS |
The expert technical work on sequencing by Inger Johanne Haugen is
gratefully acknowledged.
 |
FOOTNOTES |
*
Corresponding author. Mailing address: Department of
Microbiology, Regional Hospital, N-7006 Trondheim, Norway. Phone: 47 73867470. Fax: 47 73867765. E-mail: anrad{at}gmx.net.
 |
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Journal of Clinical Microbiology, September 2001, p. 3420-3421, Vol. 39, No. 9
0095-1137/01/$04.00+0 DOI: 10.1128/JCM.39.9.3420-3421.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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