ARTICLE
Auteur(s) : Marie-Luise Langrock1, Hans-Jörg
Linde2, Michael Landthaler1, Sigrid
Karrer1
1Department of Dermatology,
2Institute of Medical Microbiology and Hygiene,
University of Regensburg, 93042 Regensburg, Germany
accepté le 28 Mai 2008
Serratia marcescens is a gram-negative bacillus belonging to the
family of Enterobacteriaceae [1]. It is facultatively anaerobic,
non-sporeforming and can be found in the ground, water, on plants
and in animals. S. marcescens produces hydrolytic enzymes like
DNAses, gelatinases and lipases and a variety of red pigments
(prodigiosins) with antimycotic, immunosuppressive and
antiproliferative properties. Intrinsic resistance to many
β-lactam-antibiotics is conferred by chromosomally encoded extended
spectrum β-lactamases. Therefore, antibiotic therapy should be
carried out with third generation cephalosporines, carbapenems or
fluoroquinolones.
S. marcescens may cause a variety of infections, such as
pneumonia, bacteremia, meningitis, endocarditis or septic
arthritis. However, only a few cases of skin infections caused by
this organism have been reported in the literature [1-3]. We report
a male patient with multiple leg ulcers and abscesses caused by S.
marcescens. He had a medical history of chronic venous
insufficiency and long-term low-dose oral corticosteroid therapy
for chronic obstructive pulmonary disease.
Case report
A 73-year-old man presented with multiple ulcers and painful
nodules on the lower right leg and abscesses on the right malleolus
lateralis (figure
1A). The skin lesions had appeared 4 weeks beforehand,
starting with an erythema, hyperthermia, swelling and pain on the
lower right leg. The patient was first treated under the tentative
diagnosis of thrombophlebitis of the lower right leg. However,
neither topical nor oral antibiotic therapy with penicillin
improved the skin lesions, but multiple red nodules as well as
abscess formation developed.
The patient’s medical history revealed a bursitis of the right
elbow 7 weeks beforehand. After wound incision, the ulcer did not
show any sign of healing. Furthermore, the patient suffered from
chronic venous insufficiency with multiple deep vein thromboses on
the right leg as well as two-time pulmonary embolism. Because of
severe chronic obstructive pulmonary disease, the patient had been
taking low-dose corticosteroids (prednisolone 10 mg/day) for
many years.
Upon examination, he was non-febrile with normal vital signs,
but with reduced breath sound intensity. He also showed a reduced
general state of health. Laboratory tests revealed elevated
C-reactive protein (22.58 mg/L) and a high normal leukocyte
count (10.21/mL). Doppler ultrasonography of both legs showed no
signs of an acute thrombophlebitis, but post-thrombotic lesions of
the deep veins. We could not find any signs of circulatory
disorders on either leg.
Cardiovascular and neurological examinations were unremarkable.
The lower right leg showed multiple, sharply demarcated round
ulcers with livid edges and a yellow coating. The largest ulcer was
about 2 × 1.5 cm in size, the other lesions measured about 1 ×
0.5 cm. On the right malleolus lateralis two abscesses
presented with erythema and livid surrounding skin. The whole lower
right leg was hyperthermic and swollen. The lower left leg showed
some scaring and hyperpigmentation resulting from venous
insufficiency. There was no inguinal lymphadenopathy. Both feet
displayed tinea pedis with severe interdigital maceration.
Furthermore, after surgery because of bursitis, the right elbow
showed a yellow coated wound, sized approximately 3 × 2 cm,
that extended nearly up to the joint. No microbiological samples
were available from this lesion.
Having taken samples for culture from several lesions of the
right leg, we started an intravenous antibiotic therapy with
clindamycin 3 × 600 mg. Microscopy showed leukocytes and
detritus. The culture revealed growth of S. marcescens in small
quantities. Other bacilli, such as Streptococcus or Staphylococcus
spp., could not be detected. Cultures for atypical mycobacteria,
actinomyces and nocardia remained sterile. Within a few days the
original ulcers increased in size and showed progressive yellow
coatings. The abscesses on the right malleolus lateralis showed
massive fluctuation (figure 1B). The abscess
was incised and the new sample was highly positive for S.
marcescens. According to the microbial sensitivity test and the
therapeutic efficiency in culture, antibiosis was adapted to
ertapenem 1 g/day, given intravenously for 10 days.
Echocardiography, abdominal sonography and blood cultures to
exclude systemic bacteremia were unremarkable. The immunological
investigation of complementary factors and serum IgG, IgA and IgM
showed normal values. There were no signs of hepatitis or
HIV-infection.
Under topical therapy, repeated incision and draining of the
abscesses, as well as the continuation of intravenous ertapenem,
the skin lesions continued to improve (figure 2). After 10 days
of intravenous therapy, ertapenem was changed to oral ciprofloxacin
500 mg 1-0-1 for a further 7 days. Under this therapy, the
lesions improved gradually and the infection ceased completely,
leaving hyperpigmented scars.
Discussion
Skin infections with fluctuating foci and violaceous edges
accompanied by multiple abscesses are rare manifestations of S.
marcescens [1-3]. Often, immunocompromised patients are affected,
but also alcoholism or chronic diseases may favor an infection.
More commonly, S. marcescens causes urinary tract infection,
pneumonia, endocarditis, meningitis, septic arthritis, otitis and
sepsis [4]. Even soft tissue infections can be caused by S.
marcescens. Rare cases of necrotizing fasciitis, frequently of
nosocomial origin [5, 6] have been reported. S. marcescens causing
cellulitis has been described in some cases [7-9].
In this patient, the most remarkable clinical feature was the
occurrence of multiple abscesses on the right leg. Skin infections
or abscesses are often caused by staphylococcal or streptococcal
species, most notably Staphylococcus aureus carrying
Panton-Valentine leukocidin [10]. Differential diagnoses of
multiple abscesses include atypical mycobacteria, nocardia,
pyoderma gangraenosum, rosacea fulminans, severe acne, diabetes or
fungi [11, 12]. In our patient, chronic venous insufficiency and
long-term immunosuppression by low-dose corticosteroid therapy were
predisposing factors. The portal of entry could have been the
post-thrombotic lesions on the lower right leg or the preexisting
tinea pedis. Recently, gram-negative skin infections and a few
cases of rare soft tissue infections caused by S. marcescens have
been described in the literature [13].
Although uncommon, suddenly appearing painful nodules and
abscesses in immunocompromised patients or on pre-damaged skin may
be caused by S. marcescens. This is a ubiquitous bacterium, which
needs a specific microbiological diagnosis and adapted
antibiosis.
Acknowledgements
Financial support: none. Conflict of interest: none.
References
1 Friedmann ND, Peterson NB, Summer WT,
Alexander BD. Spontaneous dermal abscesses and ulcers as a
result of Serratia marcescens. J Am Acad Dermatol 2003; 49: 193-4.
2 Joao AM, Serrano PD, Cachao MP,
Bartolo EA, Brandao FM. Recurrent Serratia marcescens
cutaneous infection manifesting as painful nodules and ulcers. J Am
Acad Dermatol 2008; 58: 55-7.
3 Nieves DS, James WD. Painful red nodules of the
legs: a manifestation of chronic infection with gram-negative
organisms. J Am Acad Dermatol 1999; 41: 319-21.
4 Garcia FR, Paz RC, Gonzalez RS, Ruiz ES,
Martin-Neda FG, Rodriguez MS, Martin MR,
Sarto MS, Arguelles HA, Bustinduy MG,
Cabrera AN. Cutaneous infection caused by Serratia marcescens
in a child. J Am Acad Dermatol 2006; 55: 357-8.
5 Huang JW, Fang CT, Hung KY, Hsueh PR,
Chang SC, Tsai TJ. Necrotizing fasciitis caused by
Serratia marcescens in two patients receiving corticosteroid
therapy. J Formos Med Assoc 1999; 98: 851-4.
6 Liangpunsakul S, Pursell K. Community-Acquired
Necrotizing Fasciitis Caused by Serratia marcescens: Case Report
and Review. Eur J Clin Microbial Infect Dis 2001; 20: 509-21.
7 Hsieh S, Babl FE. Serratia marcescens Cellulitis
Following an Iguana Bite. Clin Infect Dis 1999; 28: 1181-2.
8 Bogaert MA, Hogan DJ, Miller Jr. AE.
Serratia cellulitis and secondary infection of leg ulcers by
Serratia. J Am Acad Dermatol 1991; 25: 565.
9 Cooper CL, Wiseman M, Brunham R. Bullous
cellulitis caused by Serratia marcescens. Int J Infect Dis 1998; 3:
36-8.
10 Lina G, Piemont Y, Godail-Gamot F, Bes M,
Peter MO, Gauduchon V, Vandenesch F, Etienne J.
Involvement of Panton-Valentine Leukocidin-Producing Staphylococcus
aureus in Primary Skin Infections and Pneumonia. Clin Infect Dis
1999; 29: 1128-32.
11 Roth RR, James WD. Microbiology of the skin:
resident flora, ecology, infection. J Am Acad Dermatol 1989; 20:
367-90.
12 Bonnetblanc JM. Leg ulcerations: a clinical appraisal.
Eur J Dermatol 2005; 15: 127-32.
13 Marzano AV, Gasparini G, Caputo R. Cutaneous
infection caused by Serratia marcescens. Cutis 2000; 66: 461-3.
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