PC3071: Enterobacter Ludwigii in Neonatal Sepsis and Complicated Meningitis- an Emerging Threat!

Introduction: There are case reports of neonatal meningitis caused by Enterobacter ludwigii in neonates with central lines, urinary catheters, post neurosurgical interventions, and in the immunocompromised but none in healthy infants. We present an 11-day old previously healthy neonate with rapidly progressive Enterobacter ludwigii meningitis who eventually succumbed to the infection.

Case Description: An 11-day old previously healthy female, born at term, presented to the emergency room with decreased appetite and activity and persistent grunting hours prior to arrival. The infant was being fed expressed breast milk supplemented by powdered infant formula. She was febrile but other vitals and exam were normal. Labs revealed bandemia and elevated CRP. Chest and abdomen imaging were normal. CT head concerning for mass in the right frontal lobe with a midline shift. MRI brain showed large area of diffusion restriction in right frontal lobe extending to the left frontal white matter with midline shift. Patient started on ampicillin and gentamicin after collecting blood and urine cultures, lumbar puncture deferred due to midline shift. Pediatric Neurosurgery and Neurology consulted, MRA+MRV ordered due to concerns for ischemia, resulted negative for arterial or venous abnormality. Blood culture grew Enterobacter ludwigii. Cefepime and gentamicin started based on susceptibility pattern. On day 3 of admission, anisocoria noted, and stat Head CT showed evidence of obstructive hydrocephalus with cerebellar herniation. MRI brain+MRV repeated the same day, showed cortical venous thrombosis. Patient was intubated and antibiotic coverage broadened to include metronidazole and acyclovir. Her condition rapidly deteriorated, and she developed central diabetes insipidus, refractory thrombocytopenia in the following days. Subsequently, there were minimal signs of clinical cerebral activity and EEG showed electrocerebral silence. All supportive care was withdrawn on day 7 per family’s wishes and autopsy ordered. Brain autopsy showed liquefactive necrosis of brain, abscesses, and widespread vessel thrombosis. Postmortem CSF analysis identified E. cloacae species and partial ribosomal DNA sequencing confirmed same species in blood.

Discussion: Enterobacter ludwigii is a species within Enterobacter cloacae complex, closely related to Cronobacter sakazakii which is known to thrive in dried infant formulas and even in contaminated breast pump parts. Both the species are known to cause meningitis, brain abscesses and venous thrombosis in infants with high case fatality rate of 40-80% , but ECC is not yet reported as a contaminant in infant formulas or breast pump parts. Most species in this complex are intrinsically resistant to most first-line antibiotics including Ampicillin, Amoxicillin and first generation cephalosporins.

Conclusion: Enterobacter ludwigii and other enterobacteria from Enterobacter cloacae complex are rapidly emerging as a potential cause of neonatal sepsis and rapidly progressive meningitis with high morbidity and mortality as seen in recent outbreaks associated with Cronobacter sakazakii.