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Indian Pediatr 2011;48: 397-399 |
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Stenotrophomonas maltophilia Causing Early
Onset Neonatal Sepsis |
R Viswanathan, AK Singh, C Ghosh* and S Basu†
From the Department of Neonatology, Institute of Post
Graduate Medical Education and Research, Kolkata, *SNCU,
Suri Sadar Hospital, Birbhum, and †National Institute of Cholera and
Enteric Diseases, Kolkata, West Bengal, India.
Correspondence to: Dr Rajlakshmi Viswanathan, Department
of Neonatology, IPGMER &SSKM Hospital, 244, AJC Bose Road, Kolkata 700020,
West Bengal, India.
Email: [email protected]
Received: October 6, 2009;
Initial review: October 27, 2009;
Accepted: January 13, 2010.
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Stenotrophomonas maltophilia, a multi drug resistant non fermenting
Gram negative bacillus is an increasingly common nosocomial pathogen,
especially in intensive care units. Comparatively few cases of infection
have been reported in neonatal population. We present two cases of early
onset neonatal sepsis due to S.maltophilia and a brief review of
documented isolation in neonates.
Key words: Neonate, Sepsis, Stenotrophomonas maltophilia.
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Stenotrophomonas
maltophilia (formerly Pseudomonas maltophilia/Xanthomonas
maltophilia), a multi drug resistant Gram negative bacillus, is being
increasingly implicated as a nosocomial pathogen, associated with
significant case fatality [1]. Though a well recognized opportunistic
pathogen in severely debilitated patients, comparatively few cases have
been reported in neonates. We herein present two cases of early onset
neonatal sepsis due to S.maltophilia. To the best of our knowledge,
this may be the first report of neonatal bloodstream infection from Asian
subcontinent and the first documented case of early onset neonatal sepsis.
Case Report
Case 1. A single, preterm (32 weeks) female
baby, weighing 1810 grams was delivered vaginally to a 19 year old
primipara following spontaneous onset of labour at a district hospital.
There was no history of maternal fever or any other antenatal
complication. Rupture of membranes occurred about 6 hours before delivery.
At delivery, the baby had a delayed cry and poor muscle tone, with an
Apgar score of 6 at 1 minute. He was provided with warmth and airway was
cleared. After giving stimulation and supplemental oxygen, the baby was
admitted for observational care. At 5 minutes, Apgar score was 7. The baby
did not feed well and was lethargic. Test for C Reactive protein by latex
agglutination was positive, band cells were seen on peripheral smear,
total leucocyte count was 4800/cu mm and platelet count was 230,000/cu mm.
Blood was drawn for culture. IV fluids and antibiotics (cefotaxime and
amikacin) were started. However, the baby deteriorated rapidly and died on
Day 2.
Case 2. A single, term (38 weeks) female baby
weighing 3180 grams was delivered to a 22 year old primipara by cesarean
section at a tertiary care teaching hospital, indication being foetal
distress. There was no history of maternal fever or any other illness.
Liquor was meconium stained and the baby presented with severe perinatal
asphyxia. She was immediately transferred to the NICU and ventilated. IV
fluids were started and blood for culture was drawn. Sepsis screen showed
positive CRP, leucopenia (2600/cu mm) and band cells >2% on peripheral
smear. Perfusion was poor; baby was lethargic and went into shock. Besides
management for shock, IV antibiotics (piperacillin-tazobactam and amikacin)
were started. The baby died within 48 hours.
Blood culture was done by Bactec 9050 (BD Diagnostic
Systems, Sparks, MD USA). Both cultures turned positive within 8 hours.
Gram stain showed presence of Gram negative bacilli. Subculture on Mac
Conkey Agar and 5% Sheep Blood agar (Biomerieux, Marcy l’Etoile, France)
showed growth of non lactose fermenting colonies that were catalase
positive and oxidase negative. Identification was confirmed by mini API
(analytical profile index-Biomerieux, La balme les Grottes, France) using
ID 32 GN strip. The ID percentage was 99.9% in both cases and typicity
index was 0.77 and 0.89, respectively. In both cases, maternal serology
was negative for human immunodeficiency virus, hepatitis B and syphilis.
Antibiotic sensitivity test was performed by Kirby Bauer disc diffusion
method. Isolate 1 was sensitive to cotrimoxazole alone and isolate 2 to
ciprofloxacin and cotri-moxazole. Both isolates were resistant to
amino-glycosides, extended spectrum penicillins, third generation
cephalosporins, carbapenems and monobactams.
Discussion
The first documented case of neonatal infection due to
S.maltophilia was in neonatal meningitis and conjunctivitis in 1984
[2]. Subsequently, it has been reported in superficial and deep infections
both as a colonizer and pathogen. A surveillance in our own unit during
2006-07 showed presence of S.maltophilia in gastric aspirate of
newborns, collected within 4 hours of birth [3]. Though, as yet, not so
common in Neonatal Intensive care Units (NICU), the particular danger is
because of high degree of resistance to most commonly used antibiotics
including aminoglycosides and cephalosporins, as well as intrinsic
resistance to carbapenems. It is usually susceptible to cotrimoxazole, but
emerging resistance to this drug is being documented [3]. Fluoroquinolones
have been considered a possible therapeutic option. Two cases of neonatal
meningitis were treated successfully with cipro-floxacin alone or in combination
with cotrimoxazole [4,5].
SENTRY surveillance [6], however, reports
that ciprofloxacin resistant mutants can be easily selected in vitro.
In the present report, both cases were early in onset,
presenting with features of sepsis on the first day of life. There was no
history of maternal antibiotic administration. Maternal swab, blood
culture, and environmental sampling could not be done. All documented deep
seated infections in neonates till now were late in onset and usually
involved preterm neonates [4,7-9]. The cases reported have been both from
developed and developing countries with the environmental source usually
not traced [7-9]. S.maltophilia infection is usually associated
with prolonged hospital stay, long duration of broad spectrum antibiotic
therapy, or ventilation and presence of central vascular catheter. None of
these risk factors were present in the two cases. In the first case,
delivery occurred in an overcrowded district hospital, and there may have
been lapses in asepsis. The mother also had a history of PROM for about 6
hours. It is possible that she may have been colonized and passed on the
infection to the premature baby. The second baby however was of term
gestation and a good weight. The primary cause of mortality was considered
to be perinatal asphyxia, with sepsis being a contributory factor.
However, knowing the propensity of S.maltophilia infection for
having high case fatality, it cannot be ruled out as the primary cause of
death. Asphyxia per se, is known to predispose to infection, both
due to compromised immunity and because of the interventions required.
This communication highlights that S. maltophilia,
a recognized nosocomial pathogen, is emerging as a cause of early onset
neonatal sepsis. This may be due to colonization of antenatal women in the
hospital. S.maltophilia is known to adhere to plastic surfaces and
be involved in formation of biofilms [10], which could be one of the
reasons for persistence in the hospital environment.Both clinicians and
microbiologists need to be aware of this non fermenter in neonatal
infections.
Contributors: RV, SB& AS conceptualized the paper.
RV did the microbiological work up and prepared the preliminary draft of
the manuscript. She will act as guarantor of the work. CG was involved in
collection and analysis of data and critical revision of the paper was
done by CG, SB and AS. The final manuscript was approved by all the
authors.
Funding: The authors acknowledge ‘‘Women Scientist
Scholarship Scheme for Societal programmes (WOS-B), Department of Science
and Technology, Government of India" for providing financial assistance
for this project.
Competing interests: None stated.
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