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Internal Medicine Journal 45 (2015)

L E T T E R S TO T H E E D I TO R

Clinical-scientific notes

Non-enhancing subcortical white
matter lesions in central nervous
system Listeriosis
Listeria monocytogenes infection is a devastating disease,
especially in high-risk groups, consisting of infants, pregnant women and immunosuppressed individuals.1
Listeria is one of the most important organisms transmitted by the foodborne route.2

A 66-year-old, previously independent Caucasian
man, was referred to the neurology service for acute
onset left-sided hemiplegia and drowsiness 2 days after
total colectomy. Four days earlier, he was admitted for a
severe exacerbation of ulcerative colitis. There was no
clinical response to the initial treatment with mesalazine,
azathioprine, prednisone and a single dose of infliximab.
On clinical examination, he was conscious and drowsy
with dense left-sided hemiplegia. Blood tests showed

Figure 1 T2 and fluid-attenuation inversion recovery axial images (A–C) images shows a diffuse white matter high signal abnormality in the right
subinsular region, posterior frontal and parietal lobes with sparing of the cortex. Restricted diffusion is identified (D). There is no enhancement in any of
the described lesions on post-contrast images (E,F). There is effacement of sulci in the right posterior parietal region (F).
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228

Letters to the Editor

leucopenia of 1.9 × 109/L (neutrophils 1.18 × 109/L) and
anaemia with haemoglobin of 72 g/L. C-reactive protein
was 129 mg/L. Computed tomography brain showed a
hypodensity in the right fronto-parietal and subinsular
region. Magnetic resonance imaging (MRI) brain revealed
a diffuse high signal abnormality in the white matter of the
right subinsular region, right parietal and posterior frontal
lobe without perilesional oedema, with restricted diffusion, which were not typical of ischaemia, and did not
demonstrate contrast enhancement (Fig. 1). Lumbar
puncture showed clear cerebrospinal fluid (CSF) with 37 ×
106/L white cells (polymorphs 4%, lymphocytes 96%),
elevated protein (1000 mg/L) and low glucose
(3.2 mmol/L; blood glucose 11 mmol/L). CSF Herpes
Simplex virus 1 and 2, Cytomegalovirus, JC virus and
Epstein Barr virus were negative. Blood and CSF culture
grew Listeria monocytogenes sensitive to ampicillin. Antibiotic therapy with ampicillin at 2 g 4 hourly was initiated
and planned for a period of 4 weeks. Two sets of blood
cultures sent after 1 week of ampicillin showed no growth.
The patient’s sensorium improved with treatment.
However, the dense left hemiplegia persisted. Unfortunately, the patient passed away 4 weeks later due to
complications from aspiration pneumonia. On autopsy,
cerebral tissue from the right fronto-parietal lobe showed
L. monocytogenes on gram staining and culture.
Our patient was immunosuppressed and prone to
developing L. monocytogenes meningoencephalitis and
Listeria septicaemia. With Listeria septicaemia, cerebral
parenchymal involvement can occur from cerebral invasion via endothelial cells of capillaries, and meningeal
involvement can occur via epithelial cells of the choroid

References
1 Dee RR, Lorber B. Brain abscess due to
Listeria monocytogenes: case report and
literature review. Rev Infect Dis 1986; 8:
968–77.
2 Wing EJ, Gregory SH. Listeria
monocytogenes: clinical and experimental
update. J Infect Dis 2002; 185(Suppl 1):
S18–24.

plexus.3 While cerebral abscesses, Listeria rhombencephalitis and Listeria encephalitis are well described in the
literature, the imaging appearance of our patient’s cerebral lesions was unique. The lesions involved the
subcortical U fibres and white matter diffusely and did
not enhance with contrast. There was minor perilesional
oedema. There was no enhancement with contrast which
is well described with Listeria abscesses and encephalitis,
and there was no cortical involvement.4,5
The MRI findings of Listeria encephalitis in our patient
were similar to progressive multifocal leucoencephalopathy with diffuse white matter lesions that do not
enhance with contrast.6 Another possibility is that our
patient’s lesion was an atypical subcortical early cerebritis
stage of Listeria abscess formation. We acknowledge that
the lack of enhancement of our patient’s lesions could
also have been due to chronic immunosuppression and
ongoing steroid use. This case adds that involvement of
only white matter with diffuse non-enhancing lesions is
possible in central nervous system Listeriosis. Central
nervous system Listeriosis should be considered in such
patients with an appropriate clinical history, investigated
and treated accordingly.
Received 18 June 2014; accepted 24 July 2014.
doi:10.1111/imj.12654
1

A. Salonga-Reyes, M. S Badve,2,3 S. Bhuta,3,4
S. Broadley2,3 and A. Jones3,5
5

Departments of 1Medicine, 2Neurology, 4Medical Imaging and
Infectious Diseases, Gold Coast University Hospital and 3School of
Medicine, Griffith University, Gold Coast, Queensland, Australia

3 Limmahakhun S, Chayakulkeeree M.
Listeria monocytogenes brain abscess: two
cases and review of the literature.
Southeast Asian J Trop Med Public Health
2013; 44: 468–78.
4 Horta-Baas G, Guerrero-Soto O,
Barile-Fabris L. Central nervous system
infection by Listeria monocytogenes in
patients with systemic lupus
erythematosus: analysis of 26 cases,

including the report of a new case.
Reumatol Clin 2013; 9: 340–7.
5 Alper G, Knepper L, Kanal E. MR
findings in listerial rhombencephalitis.
AJNR Am J Neuroradiol 1996; 17: 593–6.
6 Osborn AG. Central nervous system
infections. In: Renlund AR, ed. Osborn’s
Brain: Imaging, Pathology and Anatomy, 1st
edn. Salt Lake City, UT: Amirsys; 2013;
371–93.

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