Journal of Clinical Neonatology

: 2022  |  Volume : 11  |  Issue : 3  |  Page : 182--186

Fulminant late-onset sepsis due to elizabethkingia meningoseptica in term newborns

Sudhir Malwade, Manas Nayak, Anand Gangadharan, Sharad R Agarkhedkar 
 Department of Paediatrics, Dr. DY Patil Medical College, Dr. DY Patil Vidyapeeth, Pune, Maharashtra, India

Correspondence Address:
Anand Gangadharan
Dr. DY Patil Medical College, Dr. DY Patil Vidyapeeth, Pune, Maharashtra


Elizabethkingia meningosepticum is not usually found in the human body. Just a few cases have been reported in neonates in India to date. We provide a series of two different cases of Elizabethkingia meningoseptica encephalitis that were admitted to our newborn intensive care unit (NICU). At our NICU we observed two cases of Elizabethkingia meningoseptica, during a period of 1 month. Both the babies presented with refractory status epilepticus and decreased feeding. The organism was isolated from cerebrospinal fluid (CSF) and blood in the first baby whereas it was isolated from postmortem CSF sample in the second case. In both the cases, the organism was resistant to multiple antibiotics. The first baby was found to have ventriculitis and hydrocephalus and was discharged after complete recovery although had neurological deficits. The second baby presented at 2nd day of life and succumbed to death at 8th day of life. A difficult treatment, poor associated prognosis, and its multidrug resistance warrants a better understanding of the organism.

How to cite this article:
Malwade S, Nayak M, Gangadharan A, Agarkhedkar SR. Fulminant late-onset sepsis due to elizabethkingia meningoseptica in term newborns.J Clin Neonatol 2022;11:182-186

How to cite this URL:
Malwade S, Nayak M, Gangadharan A, Agarkhedkar SR. Fulminant late-onset sepsis due to elizabethkingia meningoseptica in term newborns. J Clin Neonatol [serial online] 2022 [cited 2023 Jan 27 ];11:182-186
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Elizabethkingia meningosepticum (or meningoseptica) formerly known as Flavobacterium meningosepticum is a member of the Flavobacteriae family that is found in natural and hospital environments.[1] They are not usually found in the human body, but several cases of meningitis, pneumonia, endocarditis, and bacteremia have been reported in newborn and adult intensive care units. Prolonged hospitalization, immunosuppression, indwelling catheters, and invasive procedures are risk factors.[2] The organism usually colonizes in the respiratory tract. The organism has been found resistant to beta-lactam antibiotics, aminoglycosides, tetracyclines, and chloramphenicol groups and sensitive to trimethoprim-sulfamethoxazole, quinolones, and vancomycin.[3],[4],[5],[6],[7],[8]

Although Elizabethkingia meningoseptica sepsis is a well-known disease, just a few cases have been reported in neonates in India to date. The multidrug resistance character of this bacterium makes treatment a difficult task. It is known to cause newborn meningitis, with high fatality rate of 57%.[1],[9] It is imperative to have a better understanding of this bacteria, to deal with rising incidence of sepsis. In this report, we provide a series of two lethal cases of Elizabethkingia meningoseptica encephalitis that were admitted to our newborn intensive care unit (NICU).

 Case Report 1

2.7 kg male child born to a 23-year-old Primigravida at 38 weeks of gestation through a difficult and prolonged vacuum-assisted delivery. Baby at birth had HR <60, no respiratory efforts, and was cyanosed and limp, with SPO2 of 70%–72%, capillary refill time of 6 s, and an APGAR score of 3 and 5 at 1 min and 5 min, respectively. The baby was resuscitated following the steps of neonatal resuscitation program and was shifted to NICU for further care poststabilization. The baby was put on mechanical ventilation and euthermia and euglycemia were maintained. Umbilical vein catheter was secured and started intravenous D10, dobutamine and antibiotics. At 8 h of life, the baby started to have tonic-clonic seizures and antiepileptic drugs were started. Three antiepileptic (phenobarbitone, levetiracetam, and midazolam) and one anesthetic agent (fentanyl) were needed to control the seizures.

Cranial Ultrasonography revealed cerebral edema and caput succedaneum. First C-reactive protein (CRP) sent at 10 h of life was 62 mg/L, reports of blood c/s were awaited. The baby's condition was deteriorating with respect to oxygen requirement, pressure support and the baby started to have multiple cyclical movements of both upper and lower limbs with desaturation and bradycardia, for which IV sodium valproate, IV phenytoin and topiramate were added. A plan to do 48 hourly CRP and repeat blood culture was made which revealed CRP on days 4, 6, and 8 to be 134 mg/L, 154 mg/L, and 150 mg/L, respectively. By this time, the first blood culture revealed Acinetobacter sepsis and plating of the second blood culture revealed E. meningosepticum sensitive to tigecycline [Figure 1] and [Figure 2]. Once the culture report was obtained infectious disease specialist's advice was taken and was started on IV tigecycline. Cerebrospinal fluid (CSF) culture done on day 8 also revealed E. meningosepticum. The CSF appeared white and turbid with total leukocyte counts >50,000 cells/microL and proteins 290 mg/dL.{Figure 1}{Figure 2}

Seizure control was achieved on multiple anti epileptic drug by day 11 of life. Magnetic resonance imaging (MRI) 3T was done on 12th day of life which revealed changes of hypoxic-ischemic insults in bilateral basal ganglia and thalamic and perirolandic cortices, acute infarcts in the vermis and left cerebral hemisphere, gliotic areas in the left cerebellar hemisphere, multiple subdural hemorrhage or empyema along the cerebral convexities in bilateral frontotemporoparietal region, debris intraventricular hemorrhage in the occipital horns of the bilateral lateral ventricles, there was increased CSF signals with multiple adhesions in the cisterns and sulcal spaces along with ventriculomegaly and effacements of the sulcal spaces, these changes were suggestive of meningoencephalitis [Figure 3].{Figure 3}

Antibiotics given were 21 days of IV ceftazidime, 10 days of IV tigecycline and IV linezolid, and were started on IV levofloxacin. The baby was extubated on 13th day [Figure 4]. The baby was discharged on day 26 of life, parents were counseled about long-term consequences, regular follow-up, and early intervention. The child was on breastfeeds at the time of discharge, able to maintain temperature without a warmer, gaining weight, and stable vitals. The baby lost follow-up after the first 2 follow-ups, that is at 48 h and 1 week postdischarge.{Figure 4}

 Case Report 2

2.1 kg female child born through vaginal delivery to 20-year-old primi at 37 weeks of gestation with uneventful antenatal and immediate postnatal period. Feeds were started at 30 min after delivery. The baby and mother were shifted to postnatal ward.

At 48 h of life, the baby had refusal to feeds and abnormal cyclical movements, for which the baby was shifted to the NICU. On admission, blood sugar was low (26 mg/dl), the baby was lethargic with decreased activity, tone, and reflexes. Intravenous D10 through umbilical line was started, child had increasing respiratory distress for which she was kept on B-continuous positive airway pressure. Critical samples and BSL were sent. Antibiotics (Amoxicillin-clavulanic acid, gentamicin) were initiated.

The baby started posturing with jerky movements. This was associated with desaturation and hence the child was ventilated, loaded with phenobarbitone and levetiracetam. Inotropes were added as the baby had a mean blood pressure of 30 mmHg and poor perfusion. Lumbar puncture was withheld in view of patient's critical condition.

Clinical presentation and lab reports were suggestive of early-onset sepsis with a CRP of 25.82. First blood culture report isolated Klebsiella Pneumoniae sensitive to colistin, tigecycline, and ofloxacin. Antibiotics were upgraded to colistin. An MRI brain done on the 5th day of life displayed gross diffusion restriction in bilateral parieto-occipital cortex evident of neonatal hypoglycemic brain injury.

The child had a rough intensive care unit course and succumbed to death on the 8th day of life due to septic shock secondary to Klebsiella positive sepsis with neonatal hypoglycemic brain injury. Postmortem LP was performed, the CSF fluid was turbid and was sent for culture. Report obtained after 3 days of inoculation isolated E. meningoseptica.


E. meningosepticum is the most pathogenic species in the Chryseobacterium genus. It has been found out to cause neonatal meningitis outbreaks in NICU classically in early weeks of life. Premature newborns are the most commonly affected, and outbreaks are common.[10] Prematurity is a major risk factor for E. meningosepticum infection, with neonates weighing <2500 g accounting for half of all infections. It has a mortality rate of up to 57% with severe postinfectious sequelae such as brain abscess, hydrocephalus, deafness, and developmental delay. E. meningosepticum has been observed to cause less pneumonia and bacterial sepsis.[1] Neonate meningitis outbreaks have been associated with contaminated saline usage for eye cleaning, sink drains, contaminated ventilator tubing, and aerosols.[9]

There is not enough data on the clinical profile in Indian newborns. [Table 1] summarizes the characteristics of a handful of the most recently reported cases. Both cases in our study manifested before the 3rd day of life, indicating early-onset sepsis. Both of them had a similar picture of respiratory distress and refractory seizure, which were seen in all of the cases cited except in Sandhya Bhat et al.'s[9] where it was an incidental finding in a baby with epidermolysis bullosa. Hypoglycemia was an additional feature in one of our cases. Despite the fact that preterms are more susceptible to E. meningosepticum sepsis, both of our cases were term, similar to other research with the exception of preterm case in Chamalla et al.[11]{Table 1}

A striking feature in our first case was that both blood and CSF showed organism growth. In all previously reported cases, the organism was isolated from either CSF or blood. This organism's sensitivity pattern varies greatly from case to case [Table 1], making the management tricky. Chryseobacteria are resistant to a wide range of antibiotics. They have class A extended-spectrum-lactamases and class B metallo–lactamases, providing resistance to carbapenems, which are used to treat multidrug-resistant Gram-negative infections.[12] The majority of the reported cases were treated with multiple antibiotics, except the one reported by Joshi et al. where they tried intraventricular vancomycin. Outcomes remained the same with both the interventions.[3]

Despite the differences in sensitivity patterns, the illness trajectory remains the same in all cases, with meningitis advancing to ventriculitis and hydrocephalus. The majority of the cases post E. meningosepticum sepsis developed neurological deficits warranting aggressive neurodevelopmental follow-up and management.


A previously unheard entity E. meningosepticum needs no introduction anymore. A difficult treatment, poor associated prognosis, and its multidrug resistance warrants a better understanding of the organism. NICU must practice strict aseptic protocols to keep a check on the hospital-acquired sepsis and thus decreasing associated comorbidities.


Department of Microbiology, Dr. DY Patil Vidyapeeth, Dr. DY Payil Medical College, Pimpri, Pune.

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Written informed consent was provided by the legally authorized representative.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form, the legal guardian has given consent for images and other clinical information to be reported in the journal. The guardian understands that name and initials will not be published and due efforts will be made to conceal identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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