A Pediatric Case of Fusobacterium necrophorum Mastoiditis and Meningitis Case Report in a Healthy Child and Review of the Literature

Abstract

In infants and children, bacterial meningitis caused by anaerobic bacteria is rare. However, a serious infection with the anaerobe Fusobacterium necrophorum can occur in previously healthy children with a peak incidence in preschool children and in adolescents. As the clinical presentation can be very similar to meningitis caused by aerobic bacteria, one should consider Fusobacterium necrophorum as the causative agent when preceded by or associated with otitis media with purulent otorrhea or mastoiditis, in combination with minimal or no improvement on empiric antibiotic treatment. As this pathogen can be difficult to culture, anaerobic cultures should be obtained. Prompt treatment with a third-generation cephalosporin and metronidazole should be initiated once suspected or confirmed. Surgical source control is often necessary, but even with adequate and prompt treatment, the morbidity and mortality in children with a Fusobacterium necrophorum meningitis remains high. In this report, we describe a case of Fusobacterium necrophorum meningitis in a previously healthy child and review the available literature.

Figure 1

MRI day 1. Vessel wall imaging (axial 3D T1 TSE SPACE Dante) after IV gadolinium administration. (a) There is diffuse supratentorial and infratentorial pathological leptomeningeal contrast enhancement compatible with meningitis. Also note the pathological contrast enhancement of the walls of the cerebral arteries, indicative of associated vasculitis. (b) The cavernous sinus appears thickened on the left side and enhances more heterogeneously, suggestive of inflammation. There is secondary narrowing of the left cavernous carotid artery.

Figure 2

MRI day 1. Axial postcontrast T1 TSE SPACE (a), b1000 diffusion-weighted image (b), and ADC map (c). There is a right-sided and an interhemispheric subdural empyema, characterized by pathological pachymeningeal and leptomeningeal contrast enhancement (short arrows), and increased diffusion restriction (long arrows). Also, note the mild hydrocephalus.

Figure 3

MRI day 1. Axial maximum intensity projection (MIP) of the 3D time of flight MR angiography (3D TOF MRA) (a) and ADC map at the level of the basal ganglia (b). The left internal carotid artery (long arrows) and proximal middle cerebral artery (short arrows) are narrowed on the 3D TOF MRA MIP reconstruction. There is a secondary ischemic infarct in the left basal ganglia, insular region, and temporal lobe, seen as low signal on the ADC map.

Figure 4

Gram stain of the cerebrospinal fluid with multiple Gram-negative bacilli clearly visible.

Figure 5

Follow-up MRI 18 months later. Vessel wall imaging (axial 3D T1 TSE SPACE Dante) after IV gadolinium administration. The diffuse leptomeningeal contrast enhancement and vessel wall contrast enhancement are no longer visible. There is limited residual contrast enhancement of the cerebellar tentorium (short arrow), and focal cystic encefalomalacia in the left mesial temporal lobe (long arrow) and basal ganglia (not shown) after ischemic infarction.

Figure 6

Distribution of age and primary infection site in children with F. necrophorum meningitis.