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A fit and healthy 48-year-old farm mechanic from Yorkshire gradually developed unsteadiness over 24 h associated with nausea, vomiting and malaise. The next day he developed a dull occipital headache and his unsteadiness worsened. His symptoms progressed over the next 48 h with slurring of speech, diplopia, rotational vertigo and intractable hiccups. He did not seek medical attention until day 4 when he woke with right-sided weakness and pareasthesia.
On arrival at the accident and emergency department, he was afebrile, mildly dysarthric and had an ataxic gait. MRI of the brain showed abnormal high T2 signal within the brainstem (figure 1). Treatment with dexamethasone was commenced, but his symptoms worsened after 48 h to include dyspnoea, cough and stridor, the last prompting laryngoscopy, which showed vocal cord paresis, and arterial blood gas analysis showed a type 1 respiratory failure.
As he continued to deteriorate, he was transferred to the intensive care unit, where he was intubated following acute respiratory arrest. At this point, he was transferred to our hospital, where his sedation was stopped to allow for a full neurological examination. This revealed that he was able to obey motor commands, open eyes spontaneously and communicate appropriately with his head and fingers while intubated, the last allowing for assessment of light touch and pain, which was reduced in his right face and limbs. There were no other signs on full examination of each system. Blood tests (including autoimmune screen) showed no abnormalities other than C reactive protein of 41 mmol/l and random plasma glucose of 10 mmol/l. Lumbar puncture demonstrated a leucocyte count of 60/mm3 (100% mononuclear cells), normal protein, glucose and Gram stain. HIV testing was negative and CT body found no evidence of malignancy.
With working differential diagnoses of infectious or autoimmune brain stem encephalitis, the patient was treated with high-dose intravenous ampicillin and aciclovir alongside a 3-day course of intravenous methylprednisolone. At this point, his neurological decline was halted. After 3 days, the results of blood culture showed the growth of Listeria monocytogenes, allowing for more appropriate antimicrobial treatment. Aciclovir was replaced by gentamicin to be infused with ampicillin for 21 days.
Thirty-one days after the onset of symptoms, the patient was discharged with normal gait, limb and bulbar function. With the benefit of hindsight, further questioning of the patient revealed that he had consumed a buffet at a New Year's party 3 weeks prior to the onset of symptoms, where he had consumed soft cheese that he recalled tasting ‘off’. No dairy goods were produced at his farm.
L monocytogenes is a motile non-spore-forming Gram-positive rod transmitted via ingestion of raw vegetables, unpasteurised milk, fresh soft cheese and delicatessen meats, with a median incubation period of 3 weeks. It is able to grow at lower temperatures (4°C) which is important for its aetiology.1
Although central nervous system (CNS) listerial infections occur predominantly in immunocompromised patients, rhomboencephalitis has been more commonly reported in immunocompetent individuals.2 Previous studies have hypothesised that, rather than a haematogenous spread, a retrograde axonal spread occurs, originating from the oropharynx.3
We think that it is important for clinicians to be informed of the possibility of a listerial CNS infection in immunocompetent patients presenting with features of brainstem encephalitis.
Acknowledgments
This paper was refereed by Tom Solomon.
Footnotes
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Competing interests None.
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Provenance and peer review Commissioned; externally peer reviewed.
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