Leclercia adecarboxylata Causing Spontaneous Bacterial Peritonitis in a Child with Nephrotic Syndrome: A Case Report and Review of Literature

Introduction

Nephrotic syndrome (NS) is a common childhood glomerular disease, with infections as an important cause of morbidity and mortality. Of all infections, spontaneous bacterial peritonitis (SBP) and pneumonia is common. Studies have shown that gram-negative microorganisms like Escherichia coli can cause SBP.¹ As far as we know, there is no report of Leclercia adecarboxylata (LAD) causing SBP in NS children. We report a case of NS presenting with LAD peritonitis and a review of other LAD infections in pediatric cases reported in literature.

Discussion

Infective complications in NS children occur because of various reasons like altered serum levels of immunoglobulins, abnormality of the complement system, and altered T-cell subpopulation and function.²

LAD was first identified by Leclerc in 1962. It is a motile, facultative, anaerobic, gram-negative bacilliform bacteria which has been isolated from food, water, and other environmental sources and is regarded as part of normal flora of animals and humans. However, now it is recognized as a pathogenic organism. This is partly because of enhanced detection by new bacterial assays like Micronaut-E (Merlin-Diagnostika, Bornheim, Germany), API 20E (bioMérieux, Marcy l’Etoile, France), and MALDI-TOF MS, which can distinguish LAD from other Escherichia species.^3,4 Our isolate was also identified using MALDI-TOF MS.

As far as pathogenicity of LAD, exact mechanism is still not known, although cytotoxic effect has been demonstrated in vitro on human epithelial cells type 2.⁵ Since majority of infections caused by LAD are soft tissue infections post trauma, the route of entry of LAD is considered to be skin disruption or catheter-related. Massive edema causing devitalization of skin may be the explanation of LAD causing SBP in NS.

Anuradha had reported two cases of infection with LAD from India, one from vaginal discharge in a 31-year-old female and another from a gluteal abscess in a healthy 50-year-old man. These isolates were pan-sensitive to tested antibiotics (cephalosporins, amikacin, fluoroquinolones, and carbapenems). The first patient was treated with moxifloxacin and second one with doxycycline for 10 days, respectively.⁶

Case reports of children infected with LAD worldwide have been enumerated in ►Table 1. Hurley et al reported a pediatric case in a healthy 2-year-old child who presented with post traumatic right thumb abscess. The isolate was pan sensitive, except for intermediate sensitivity for piperacillin/tazobactam and child improved with parenteral ampicillin—sulbactam.⁷ In another report, a 9-year-old immunocompetent child who had post-traumatic LAD foot abscess, improved after surgical drainage and levofloxacin usage for 14 days.⁸ However, case reports of fatalities have also been reported in pediatric population. One child with colonic neuropathy and pseudo-obstruction acquired LAD infection, culminating into LAD sepsis.⁹ Another case who expired was a preterm, very low birth weight baby who had LAD sepsis and succumbed on day 54 of life in spite of receiving sensitive antibiotics for 21 days.¹⁰

No case of LAD causing SBP in NS has been reported so far, although one case of peritonitis has been reported from the West in a 5-year-old boy, who was on chronic peritoneal dialysis for end-stage renal disease. This child improved after receiving ceftazidime and intravenous plus intraperitoneal amikacin for a total of 10 days.¹⁴

Conclusion

We present a case report of peritonitis in a nephrotic child where the organism isolated was facultative anaerobic gram-negative bacilliform bacteria LAD using MALDI-TOF MS. Our isolate was sensitive to all the first line antibiotics and ceftriaxone was efficient in clearing the infection.