Solitary SupratentorialListeria MonocytogenesBrain Abscess in an Immunocompromised Patient

Abstract

We describe an 81-year-old man receiving azacitidine monotherapy for myelodysplastic syndrome who was improving from Listeria monocytogenes bacteremia after receiving antibiotic therapy during an earlier hospital admission. Shortly after discharge he developed new-onset seizure activity, with brain imaging on subsequent admissions demonstrating a posterior right frontal lobe mass. Specimen cultures after resection of the mass revealed this to be a cerebral abscess related to L. monocytogenes. Brain abscesses related to this organism are rare.L isteria monocytogenes is a ubiquitous, opportunistic pathogen that rarely causes illness in healthy individuals. Th e immunocompromised and those with underlying illness are at greater risk for serious and potentially fatal infection. Approximately 20% of all listeriosis patients succumb to infection despite early aggressive treatment, with particularly elevated case fatality rates in those with comorbid illnesses and in immunocompromised states (1-4). While L. monocytogenes is a well-known cause of meningitis and encephalitis, brain abscesses related to this organism are rare and reported to occur in only 10% of all Listeria central nervous system (CNS) infections (4). Here we present the case of an immunocompromised man who developed L. monocytogenes bacteremia and a subsequent single supratentorial brain abscess. CASE DESCRIPTIONAn 81-year-old man with myelodysplastic syndrome was being treated with azacitidine monotherapy. He also had a remote history of acute myelogenous leukemia in remission, medically controlled atrial fi brillation, basal cell skin carcinoma resection, and treated prostate cancer. For 1 week, the patient complained only of intermittent fevers, reaching a maximum temperature of 102.4°F, and mild fatigue. Four days after the onset of fevers, blood cultures were drawn and he was started on levofl oxacin and later on amoxicillin clavulanate once Gram-positive rods were isolated. Blood cultures grew L. monocytogenes, and the patient was hospitalized.He received intravenous piperacillin-tazobactam for 2 days. When sensitivity tests revealed susceptibility to ampicillin, penicillin G, and trimethoprim sulfamethoxazole, the treatment was changed to intravenous ampicillin, which continued for his remaining 2 days in the hospital. Repeat blood cultures were negative at the time of discharge and he was afebrile. Th e patient was discharged home on continuous intravenous penicillin infusion. During the hospital admission there were no specifi c neurologic complaints, headaches, or altered sensorium.Th e morning after discharge, the patient had generalized jerking movements and left facial droop that lasted approximately 10 minutes while he remained lucid. Two additional seizure-like episodes occurred during transport to the emergency department. Noncontrast head computed tomography (CT) demonstrated a mass in the right frontoparietal region. Treatment with lorazepam and dexamethasone was initiated. Subsequent contrast-enhanced magnetic resonance imaging (MRI) ...

Serial magnetic resonance imaging findings of intracerebral spread of listeria utilising subcortical U-fibres and the extreme capsule

“…Invasive listeriosis occurs more commonly in immunocompromised individuals, and known risk factors include: diabetes mellitus, chronic illness, pregnancy, extremes of age (neonates and the elderly), immunosuppressive medications and solid-organ or haematologic malignancies. 1–3,5–7 L. monocytogenes has a striking predilection for CNS invasion, and this is particularly prevalent in neonates and the elderly, in whom it is the second leading cause of bacterial meningitis. 1–3 CNS manifestations of listerosis depend on the intracranial compartment affected and include meningitis, encephalitis, rhombencephalitis, meningoencephalitis and less commonly cerebral abscess.…”

“…1–3 CNS manifestations of listerosis depend on the intracranial compartment affected and include meningitis, encephalitis, rhombencephalitis, meningoencephalitis and less commonly cerebral abscess. 1–3,5,6,8 The distribution of brain abscesses in listerosis follows a unique pattern, and is usually observed in the reticular formation of the midbrain, pons and medulla and to lesser extent the supratentorial brain. 3,6,8,9 The predilection for brainstem involvement is likely attributed to retrograde neuronal spread of infection spread via the trigeminal nerve whereas supratentorial brain involvement is likely from hematogenous seeding.…”

“…1–3,5,6,8 The distribution of brain abscesses in listerosis follows a unique pattern, and is usually observed in the reticular formation of the midbrain, pons and medulla and to lesser extent the supratentorial brain. 3,6,8,9 The predilection for brainstem involvement is likely attributed to retrograde neuronal spread of infection spread via the trigeminal nerve whereas supratentorial brain involvement is likely from hematogenous seeding. 3,6,8,9 Our case exquisitely depicts a less well-recognised feature of listerosis brain abscesses, namely the propensity for the bacteria to spread to distant sites within the CNS utilising white-matter fibre tracts as conduits.…”

“…3,6,8,9 The predilection for brainstem involvement is likely attributed to retrograde neuronal spread of infection spread via the trigeminal nerve whereas supratentorial brain involvement is likely from hematogenous seeding. 3,6,8,9 Our case exquisitely depicts a less well-recognised feature of listerosis brain abscesses, namely the propensity for the bacteria to spread to distant sites within the CNS utilising white-matter fibre tracts as conduits. 4 A recent literature review by Bojanowski et al.…”

Cerebral Abscess Caused by Listeria monocytogenes: Case Report and Literature Review

“…Seven of 15 immunocompetent patients (46.6%) died, which was possibly due to inadequate treatment since these patients were reported before 1985 without information of the specific treatment regimen, whereas the remaining 8 patients reported after 1985 survived, which indicates that mortality in the immunocompetent population is lower. 18,21 Compared with a mortality rate of 66.6% before 1985 in the immunocompromised group, the calculated mortality rate after 1985 is 19.4%.…”