Bacterial Meningoencephalitis in Newborns

Abstract

Bacterial meningoencephalitis in newborns is a severe and life-threatening pathology, which results from meningeal infection and the subsequent involvement of the brain parenchyma. The severity of the acute onset of symptoms and the risk of neurodevelopmental adverse sequelae in children strongly depend on the timing of the infection, the immunological protection transmitted by the mother to the fetus during pregnancy, and the neonate's inflammatory and immune system response after birth. Although the incidence of neonatal meningitis and meningoencephalitis and related mortality declined in the past twenty years with the improvement of prenatal care and with the introduction of intrapartum antibiotic prophylaxis against Streptococcus beta Hemolyticus group B (Streptococcus Agalactiae) in the 1990s, bacterial meningitis remains the most common form of cerebrospinal fluid infection in pediatric patients. To date, the rate of unfavorable neurological outcomes is still from 20% to 60%, and the possibility of containing its rate strongly depends on early diagnosis, therapy, and a multidisciplinary approach, which involves neonatologists, neurologists, neuroradiologists, and physiotherapists. Neonatal meningitis remains difficult to diagnose because the responsible bacteria vary with gestational age at birth, age at presentation, and environmental context. The clinical presentation, especially in the newborn, is very ambiguous. From a clinical point of view, the definitive test for diagnosis is lumbar puncture in patients with symptoms suggestive of neurological involvement. Therefore, neuroimaging is key for raising clinical suspicion of meningitis or corroborating the diagnosis based on clinical and laboratory data. Our pictorial review offers a practical approach to neonatal meningoencephalitis by describing the epidemiology, the pathophysiology of bacterial meningoencephalitis, defining the indications and suggesting optimized protocols for neuroimaging techniques, and showing the main neuroimaging findings to reach the diagnosis and offering proper follow-up of bacterial meningitis. Moreover, we tried identifying some peculiar MRI patterns related to some bacteria.

Keywords: CT; MRI; US; bacterial meningoencephalitis; encephalitis; meningitis; meningoencephalitis; newborns; pediatric.

Figure 1

Flowchart illustrating the pathophysiology and progression of bacterial meningoencephalitis.

Figure 2

A 10-day-old boy with Serratia Meningitis, presenting with plexitis. Axial DWI (a) and axial ADC (b) show infection of the choroid plexus characterized by diffusion restriction (arrows in (a,b)), and sagittal T2 SPACE shows engorgement and infection of the choroid plexus (arrow in (c)).

Figure 3

A 9-day-old boy affected by meningitis caused by Listeria Monocytogenes with ventriculitis. There are hypointense in T2 (arrow in (a), axial T2WI) and hyperintense detritus in T1 (arrow in (b), axial T1-weighted images); a slight contrast enhancement of ventricle wall is visible in (d), axial post- contrast T1 WI, especially if compared with (c) axial pre-contrast T1 WI. There is also a ventriculomegaly visible on both MRI ((e), coronal T2WI; (f), sagittal T1 WI) and US ((g), coronal plane and (h), parasagittal plane). In (f,h), there are also visible hyperintense ((f), arrow) and hyperechogenic detritus ((h), arrow).

Figure 4

Newborn affected by Escherichia Coli meningitis and undergoing brain and spine MRI. Axial post-contrast T1WI of the brain (a–d) and sagittal post-contrast T1WI (e) of the spine show intense and diffuse pachymeningeal and leptomeningeal enhancement.

Figure 5

Sagittal T2 SPACE WI (a,b) showing multiple membranes and adhesions that cause hydrocephalus, visible in (c) (axial T2 images), in a boy with neonatal meningoencephalitis.

Figure 6

MRI of a newborn affected by Group B Streptococcus meningoencephalitis and presenting with left frontoparietal subdural effusion appearing hypointense on T1WI (a) and hyperintense on T2WI (c) with no appreciable contrast enhancement on post-contrast T1WI (b).

Figure 7

MRI of a newborn affected by Group B Streptococcus meningoencephalitis and presenting with left frontotemporal subdural empyema presenting diffusion restriction on axial DWI/ADC (arrow in (a), (b)) and intense pachymeningeal and leptomeningeal enhancement on post-contrast coronal T1WI (arrow in (d)). T2WI (c) shows hyperintensity of the frontal lobes WM, the left temporo-insular WM, and the deep WM bilaterally, associated with cystic degeneration of the frontal WM, frontal cortical atrophy, and laminar necrosis.

Figure 8

A patient affected by Bacillus Cereus meningoencephalitis. MRIs were acquired at 30 days, 43 days, and 63 days from birth and show the brain abscess evolution during the patient’s follow-up. At 30 days from birth (a–d), the parenchymal abscess in the left temporal lobe presents a necrotic core, appearing inhomogeneously hyperintense on T2WI (a) with diffusion restriction on DWI/ADC (b,c), and a thick capsule, appearing hypointense on T2WI with intense enhancement on post-contrast T1WI (d). At 43 days from birth, the parenchymal abscess shows a dimensional decrease and similar radiological features on T2WI (e), DWI (f), ADC (g), and post-contrast T1WI (h). At 63 days we can appreciate a hemosiderin scar appearing hypointense on T2WI (i) and SWI (l) with no diffusion restriction on DWI/ADC (j,k).

Figure 9

Two cases of newborns, namely a 1-month-old girl and (e–h) a 2-month-old girl, affected by Group B Streptoccoccus meningoencephalitis (a–d). In both cases, there are multiple punctate ischemic lesions with a massive brain involvement characterized by diffusion restriction on axial DWI sequences (arrows in (a,b,e,f)) and low ADC values (arrowheads in (c,d,g,h)).

Figure 10

Three different cases of newborns with brain sequelae caused by Listeria Monocytogenes meningoencephalitis. The first case (a–e) refers to a boy of 9 days of life, who presented with meningoencephalitis characterized by ventriculitis with enlarged ventricles ((a), axial T2WI) with ependymal contrast enhancement (arrow in (b), axial post-contrast T1WI) and an encapsulated abscess in the right white matter (arrow in (c), axial post-contrast T1WI). At the 3-month FU, the brain MRI showed massive cystic encephalomalacia and periventricular cavitations (arrowheads in (d,e), axial T2WI). The second case (f,g) shows the 3-month FU MRI of a girl affected by listeria meningoencephalitis at 6 days of life, evolved in multiple periventricular cysts (arrows in (f), axial and (g), coronal T2WI). The third case (h,i) refers to a boy who presented with Listeria meningoencephalitis at 5 days of life, whose 2-month FU MRI showed encephalomalacia with multiple cysts (arrow in (h), axial and (i), coronal T2WI).

Figure 11

Two cases of neonatal Klebsiella meningoencephalitis abscess characterized by hypointense capsule on SWI due to macrophages and free radicals deposits. Case one (a–d) refers to a 5-day-old boy with multiple abscesses in bilateral white matter, whose thin capsule appears slightly visible on post-contrast axial T1WI (arrows in (a,b)) and optimally visible as a thick hypointense capsule on axial SWI (arrows in (c,d)). Case two (e,f) refers to a 1-month-old girl with a parietal abscess characterized by peripheral contrast enhancement (arrow in (e), axial post-contrast T1WI) and a thick hypointense capsule on SWI (arrow in (f), axial SWI).

Figure 12

A 15-day-old boy presenting with pneumocephalus caused by Proteus meningoencephalitis and characterized by multiple hypointense round lesions on SWI ( (a–c), axial SWI) representing air in the intra- and extra-axial spaces.