LAUSR

Neurolisteriosis, an infection caused by Listeria (L.) monocytogenes, is a rare but serious infectious disease that mainly affects immunocompromised patients [1]. Clinically, it typically manifests as a syndrome that can be difficult to distinguish from classical bacterial meningitis and rarely manifests as rhombencephalitis or abscess. Diagnosis is challenging, as it can be difficult to interpret the analysis of cerebrospinal fluid (CSF), and it is often hard to isolate the L. monocytogenes. We describe one patient with neurolisteriosis who presented with the signs and symptoms of acute coma on admission a few days after a near-drowning incident in stream water to raise awareness of the more uncommon features of this disease. A 73-year-old man slumped into stream water while cleaning at his private hydro-electric power station. He nearly drowned, aspirating a considerable amount of stream water that was contaminated with floodwater. He did not lose consciousness and managed to get out of the water on his own. After a few days, he developed diarrhea. At this time, stool probe for pathogen germs (Campylobacter, Shigella, Salmonella, Rotavirus, and Adenovirus) was negative. Days later, he developed headache, fever, drowsiness, and rapid coma. On admission in the hospital, he was comatose, with marked neck stiffness. He showed flexor responses to noxious stimuli, and his pupils were equal and reactive; all brainstem reflexes were intact. His body temperature was 39.0 °C. Routine laboratory results showed elevated levels of C-reactive protein (16.7 mg/dl; normal < 0.5), creatine (1.8 mg/dl; normal 0.6–1.3), and leucocytes (13.150/μl; normal 4300–10,000). A CCT of the brain and two CT controls on days 2 and 4 were normal without signs of rhombencephalitis, a brain abscess, or hydrocephalus. The patient had a pacemaker as a result of previous bradycardic atrial flutter, so an MRI was not performed. The analysis of CSF revealed slight mixed pleocytosis (26 cells pro μl; normal < 4/μl; 36% neutrophils, 61% lymphocytic, 3% monocytic), strongly elevated levels of protein (1959 mg/l; normal < 450 mg/l), and lactate (11.6 mmol/l; normal 1.2–2 mmol/l), as well as a strongly diminished glucose level (3 mg/dl, normal 40–80 mg/dl). Both, the blood and the CSF culture identified L. monocytogenes, and the antibiotic susceptibility profile, according to the European Committee on Antimicrobial Susceptibility Testing, showed high sensitivity to ampicillin and erythromycin and resistance to benzylpenicillin, meropenem, and trimethoprim/sulfamethoxazole (Table 1). The initially empirical antibiotic treatment regimen was switched to ampicillin (12 g/day) and gentamycin (320 mg/day) for 3 weeks after the infection was identified. After 1 week of mechanical ventilation and critical care, the patient recovered stepwise; after 3 weeks, he was transferred to a rehabilitation center. At this time, he was mentally well and mobile in the wardroom. Further history revealed nothing remarkable, except the implantation of the pacemaker. In particular, there was no evidence of an immunocompromised status. Neurolisteriosis is a severe CNS infection that continues to have a poor prognosis. In the recent MONALISA trial, only 39% of patients with neurolisteriosis survived and fully recovered after 3 months [2]. Our neurolisteriosis case vignette is notable for several reasons. First, the clinical presentation of neurolisteriosis with a coma as a severe infectious complication on hospital admission is quite rare and requires a broad work-up to confirm neurolisteriosis and to exclude other causes of the coma. Another rare presentation includes mimicking an acute stroke (own observation, unpublished), which is considered to be related to a vasculitic process triggered by the L. infection [3]. Typically, neurolisteriosis presents with an acute meningoencephalitic syndrome, fever, and a headache, * Josef G. Heckmann [email protected]