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Case Report

Indian Pediatr 2011;48: 397-399

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.
 


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.


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.

References

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