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Indian Pediatr 2009;46: 61-63 |
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An Outbreak of Serratia marcescens
Septicemia in Neonates |
Ekrem Guler, Mehmet Davutoglu, Hasan Ucmak*, Hamza
Karabiber and Omer Faruk Kokoglu*
From the Departments of Pediatric and *Infectious
Diseases and Clinical Microbiology,
Kahramanmaras Sutcu Imam University, Faculty of Medicine,
Kahramanmaras, Turkey.
Correspondence to: Dr Ekrem Guler, Assistant Professor, Faculty of
Medicine,
Kahramanmaras Sutcui Imam University, Kahramanmaras 46050, Turkey.
E-mail: [email protected]
Manuscript received: November 7, 2007;
Initial review completed: March 7, 2008;
Revision accepted: April 1, 2008.
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Abstract
Serratia marcescens is a well recognized nosocomial
pathogen. We report an outbreak with this organism in 8 neonates in a
neonatal intensive care unit (NICU). Seven cases were treated
successfully with meropenem after the failure of imipenem treatment.
Although they have similar anti-microbial effects, meropenem can
effectively treat the S. marcescens sepsis resistant to imipenem.
Keywords: Imipenem, Meropenem, Newborn, Sepsis, Serratia
marcescens.
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S erratia
marcescens is a well-recognized pathogen of severe nosocomial
infections in neonatal intensive care units (NICUs)(1-5). Sepsis caused by
S. marcescens is difficult to treat because of the strain’s
resistance to antibiotics including beta-lactams and aminoglyco-sides(5).
In the present study, we managed an outbreak of S. marcescens with
meropenem after imipenem failure.
Methods
Our hospital is a 150-bed, tertiary referral care
hospital. The NICU contains 17 beds: 10 level 3 NICU beds and 7
intermediate-intensive beds. In December 2006, an outbreak of systemic
infections caused by Serratia marcescens occurred in the NICU.
Clinical details were recorded. After the first case of S. marcescens
septicemia was identified, subsequent surveillance cultures such as
pharyngeal swab, rectal swab, sputum and stool cultures were obtained in
all other neonates to trace reservoir/colonized neonates. Environmental
cultures were taken and processed by standard laboratory methods, and
susceptibility to antimicrobial agents was performed per guidelines of the
Clinical and Laboratory Standards Institute(6).
Results
Eight neonates developed clinical sepsis with positive
blood cultures and one of them died. Three patients (case 1,4,8) had
indwelling devices (mechanical ventilation for 11 to 23 days, central
lines and total parenteral nutrition for 8-20 days). The length of stay in
the NICU before S. marcescens varied from 4 to 72 days for infected
patients. The clinical characteristics, demography and associated
underlying disorders in these cases are shown in Table I.
TABLE I
Clinical Characteristics of Neonates Infected with S. marcescens
Case
no |
Age
(days) |
Problem |
Therapy
(drugs and days) |
1 |
31 |
CHD |
I:10 |
G:5 |
M:21 |
2 |
16 |
HIE |
I:10 |
G:6 |
|
3 |
44 |
HIE |
I:8 |
G:5 |
M:21 |
4 |
10 |
HIE |
I:7 |
G:7 |
M:21 |
5 |
6 |
TTN |
I:3 |
G:7 |
M:21 |
6 |
27 |
Pneumonia |
I:5 |
G:7 |
M:21 |
7* |
15 |
Sepsis |
I:15 |
G:7 |
M:21 |
8* |
72 |
RDS |
M:21 |
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HIE: hypoxic ischemic encephalopathy; RDS: respiratory distress syndrome;
CHD: Congenital heart disease; *Preterm low birth weight;
I:Imipenem; M: Meropenem; G:Gentamicin; TTN:Transient tachypnea of newborn.
The index case (case 1) of S. marcescens had
received imipenem for seven days due to E. coli sepsis. The next
day, three infected neonates (case 2, 3, and 4) were identified in the
NICU. Standard infection control measures were reinforced. Despite
efforts, four additional cases (case 5, 6, 7, and 8) of clinical
septicemia in neonates occurred within ten days. Cultures were obtained
weekly until sterile.
Infected neonates were treated empirically with
imipenem for 5-10 days before culture results were available. Four
neonates (cases 1, 5, 6 and 7) received intravenous imipenem (60 mg/kg per
day divided into three doses) before S. marcescens sepsis occurred.
After the culture results were available, gentamicin was added to the
treatment regimen because of culture-antibiogram susceptibility. Lumbar
puncture was not done due to severe thrombocytopenia and worstening in
these babies. C-reactive protein(CRP) and blood counts were
repeated frequently and cultures were repeated 72 hrs after the initiation
of the treatment. As none of the neonates showed recovery signs, both
clinically and with respect to the laboratory findings(CRP, thrombocyte,
immature/mature ratio white blood cell and white cell count), this
treatment was discontinued after 7-10 days. Case 2 died despite antibiotic
therapy including imipenem and gentamicin. We ascertained that this
resulted from in vivo resistance to imipenem, so we switched to
intravenous meropenem (60 mg/kg per day divided into three doses) instead
of imipenem for 3 weeks. A complete cure was obtained in seven patients
with 21 days of therapy with this antibiotic regimen.
Cultures of samples from incubators, antiseptics,
humidifiers, soap, distilled water, inhalation therapy equipment, hands of
all healthcare workers and stethoscopes were negative for S. marcescens.
Culture swabs from inanimate surfaces were all negative for S.
marcescens. The S. marcescens isolates during the outbreak were
uniformly susceptible to all of the antimicrobial agents tested, except
for ampicillin, amoxycillin-clavulonate and cefazolin.
Discussion
S. marcescens has emerged in recent years as an
opportunistic pathogen in a growing number of serious rapidly spreading
nosocomial infections in NICUs, particularly as bloodstream
infections(1-4). An important characteristic of S. marcescens is
its ability to produce a beta-lactamase that confers resistance to
broad-spectrum beta-lactam antibiotics, which often complicates
therapy(1,5,7). Troillet, et al.(8) reported imipenem resistance in
11% of the clinical isolates of Serratia species.
Ito, et al.(9) concluded that 19% of S. marcescens clinical
isolates were resistant to imipenem. Imipenem resistance is achieved by a
metallo-beta-lactamase that does not confer resistance to meropenem(10).
In another study, S. marcescens isolates were not resistant to
imipenem, but the resistance rate to meropenem was 89%(9). Thus,
susceptibility to the antimicrobials may differ in a manner that is
dependent on whether these antibiotics were previously used in the units.
Although our clinical S. marcescens isolates were susceptible to
gentamicin and imipenem on an antibiogram, these isolates exhibited
resistance during clinical use and treatment failure occurred. Four of our
neonates (cases 1,5,6 and 7) had already received imipenem before the
onset of S. marcescens sepsis. However, seven neonates with sepsis
were successfully treated with meropenem. This pattern may be explained by
in vitro or in vivo susceptibility. The possible development
of resistance to imipenem may be related to its long-term exposure in our
NICU. However, meropenem had not been used previously.
Acknowledgment
We thank Dr Mustafa Gul and Dr Pinar Ciragil who helped
with laboratory processing in this study.
Contributors: All authors contributed to data
search, concept, design, and reporting.
Funding: None.
Competing interests: None stated.
What This Study Adds?
• Meropenam was successfully used for treating
neonatal sepsis caused by Serratia marcescens.
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