K Jagadish Kumar, VG Manjunath, HR Nandish, A Ratna

Abstract

Background: Enterobacter cloacae (E. cloacae) has been recognised as one of the important nosocomial pathogens in recent times and causes a broad spectrum of infections involving the lower respiratory tract, urinary tract, central nervous and musculoskeletal system. E. cloacae causing systemic bacterial infection is uncommon in children and primarily affects younger children or those with associated underlying medical problems. Case Presentation: We are reporting a 5-year-old immune-competent boy with community-acquired E. cloacae septicaemia, who presented with septic shock requiring vasopressor therapy, and mild encephalitis with a reversible splenial lesion of the corpus callosum. He recovered completely without any sequelae after treatment. Conclusions: Even though an E. cloacae bloodstream infection is typically a nosocomial pathogen that affects those with co-morbidities; it can rarely lead to severe and life-threatening community-acquired septicaemia.

Introduction

Enterobacter cloacae (E. cloacae) is a gram-negative bacterium that belongs to the genus Enterobacter.^1,2 E. cloacae is one of the commensal flora of the human intestinal tract and is also widely distributed in environmental sources such as water, soil, and food.^1,3 Nowadays, E. cloacae has been recognised as an important nosocomial pathogen and causes a broad spectrum of infections involving the lower respiratory tract, urinary tract, central nervous system, joints, bones, skin and soft tissues.^1,3 E. cloacae causing systemic bacterial infection is rare in children and usually affects younger children or those with underlying medical problems.⁴ Even though most of the cases are due to nosocomial infections, community-acquired infections can also occur and can be equally fatal.² We are reporting a 5-year-old healthy male child with community-acquired E. cloacae septicaemia who presented with septic shock, and mild encephalitis with a reversible splenial lesion of the corpus callosum (MERS). He recovered completely without any sequelae following prompt treatment.

Case Report

A 5-year-old developmentally normal boy presented with fever, loose stools, vomiting for 1 day, and convulsions over 6 hours. Loose stools were watery, and profuse with no blood in them. He had 2 episodes of tonic-clonic seizures for 20 minutes each with loss of consciousness. There was no history of trauma/ear discharge/headache/ body ache. On examination, he was dehydrated with a Glasgow coma scale (GCS) of 7/15. He had a temperature of 99.6oF, Pulse Rate (PR) of 148/minute, low volume and feeble with cold extremities, Respiratory Rate (RR) of 40/minute, only manually recordable systolic Blood Pressure (BP) of 74 mm of Hg, and Capillary Filling Time (CFT) of 6 seconds. Per abdomen examination revealed 4 cm hepatomegaly. Respiratory (RS) and Cardio Vascular System (CVS) examinations were unremarkable. Immediately oxygen, IV (Intra venous) Levetiracetam, and two fluid boluses (20 ml/kg of normal saline) were initiated along with correction of dehydration. However, despite fluids infusion, he continued to have feeble peripheral pulses, cold extremities and CFT of 3 seconds, and hence a preliminary diagnosis of shigella gastroenteritis, with encephalopathy and septic shock was made. Inj Noradrenaline at a dose of 0.1 mg/kg/minute was started along with Inj Ceftriaxone and Inj Meropenam. Investigations are depicted in Table 1 and Figure 1. MRI brain revealed hyperintense signal changes of the splenium of the corpus callosum (SCC) visible on diffusion-weighted imaging (DWI) sequences. Twelve hours after admission, the patient continued to have fever spikes. His GCS improved to 15/15 and urine output to 2 mL/kg/hour. Vital signs were as follows: PR 128/min with good volume and warm peripheries, RR 32/min, BP of 80/42 mm Hg, and a CFT of 2 seconds. At 24 hours post-admission, the child was conscious with a GCS of 15/15 with normal urine output. His vitals are as follows: Temperature 100oF, RR 30/minute, PR 120/minute, good volume with warm peripheries, BP of 98/72 mm of Hg, and CFT 2 seconds. Inj noradrenaline infusion was slowly tapered and stopped while antibiotics continued for ten days. He gradually improved and was discharged on the 10th day of hospitalisation.

Figure 1 MRI Brain: Hyperintense signal changes of the splenium of the corpus callosum (SCC) visible on diffusion-weighted imaging (DWI) sequences.

Discussion

The clinical significance of E. cloacae is that it is frequently multidrug-resistant and associated with a mortality risk of up to 40%, thus making it a huge challenge for the treating clinician.^2,5 Factors associated with mortality due to invasive E. cloacae include low haemoglobin levels, increased C-reactive protein (CRP), septic shock, and renal failure.² Our case hailing from a rural area of south India presented with acute gastroenteritis, shock and status epilepticus. There was no history of previous hospitalisation, underlying medical conditions, or immunodeficiency. The presenting symptoms at admission made us think of a provisional diagnosis of shigella diarrhoea with encephalopathy. He had leucopenia, thrombocytopenia, elevated CRP, and pneumonia on chest X-ray. Blood culture grew Enterobacter cloacae sensitive to most of the drugs. His stool culture was sterile. Even though he presented with septic shock with MERS, he responded well within 2 days of starting inj meropenem and inj ceftriaxone as E. cloacae is sensitive to both antibiotics.

The classic triad of muscle pain, weakness, and dark urine for the diagnosis of rhabdomyolysis was not present in our child. Serum CK levels in rhabdomyolysis are usually at least five times the upper limit of normal but range from approximately 1500 to 100,000 units/L.⁶ Serum CK levels were 2434 U/L at presentation and decreased to 81 U/L after recovery in this child. Falasca et al reported myositis and rhabdomyolysis in association with E. cloacae infection.⁷

MERS is characterised by a transient mild encephalopathy and a reversible lesion in the splenium of the corpus callosum on MRI.⁸ In MERS, hyper-intense signal changes in the splenium of the corpus callosum are visible on DWI in the brain MRI is associated with various other neurological symptoms like disturbed consciousness, behavioural disorders, incoherent speech, seizures, drowsiness, headaches, and hallucinations. The present case had gastroenteritis, altered consciousness, seizures and MRI features of MERS (Figure 1). There is a well-known association between MERS and hyponatremia, which was also seen in our patient, who presented with a serum sodium level of 129 mEq/L. A variety of other infectious agents have also been known for the development of MERS, including Rotavirus, Cytomegalovirus, Adenovirus, Influenza virus, Epstein-Barr virus, Mycoplasma pneumoniae, Salmonella, Escherichia coli and Shigella.⁸ For a decade, E. cloacae has emerged as one of the most common nosocomial pathogens causing outbreaks in neonatal units.⁹ Bonadio et al reported 30 children with E. cloacae bacteraemia over 12 years. Among the 30 cases, 14 were infants less than one year of age, out of which the majority were younger than two months. In 17 children, bacteraemia was nosocomial acquired in the ICU. Four children had hypotension requiring vasopressors and 3 patients died. The most common underlying condition was immune deficiency followed by gastrointestinal tract lesions.⁴ In another study, all children with E. cloacae bacteraemia had at least one underlying condition, the most common being neuromuscular (35%), end-stage renal disease (27%), and short bowel syndrome (15%). In 75% of cases, a central venous catheter was present and hypotension was noted in 38% of cases. One-third of them had severe sepsis and mortality was 8%.⁵ This child also presented with septic shock, requiring noradrenaline infusion for hemodynamic support. Öz et al reported a child who was treated with ACTH for infantile spasm developing rotavirus gastroenteritis complicated by nosocomial E. cloacae bacteraemia.¹⁰ Wutor et al reported the unsuccessful treatment of sepsis due to multidrug-resistant E. cloacae sepsis in a 25-month-old child.²

E. cloacae have the ability to secrete various cytotoxins (enterotoxins, haemolysins, pore-forming toxins) and to form biofilms, which are important in the pathogenicity of E. cloacae infections.¹

Conclusions

Although E. cloacae bloodstream infections are classically associated with nosocomial settings and primarily affect individuals with underlying comorbidities, they can rarely, cause community-acquired septicaemia, which may manifest as a severe and potentially life-threatening condition.

Conflicts of Interest

None

References

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