A 52-year-old woman with a history of recurrent urinary tract infection and bronchial asthma was treated with corticosteroids intermittently.
The patient was admitted to hospital with fever (low antipyretics), blood pressure 90/60mmHg, pulse 94, after 2 days of low back pain, fever and headache.
He had muscle contracture and pain exacerbated by percussion.
Urine examination showed leukocytes: 5-10 p/c, pyocytes, leukocytes: 1-3 p/c, nitrites(+), bacteria+++.
Hematocrit was 36.5%, leukocytes 12,500 mm3, platelets 244,000 mm3, C-reactive protein 44.2 mg/L (VN: < 4.9).
Renal ultrasound was normal.
Acute pyelonephritis was diagnosed and ceftriaxone 2 g/ day was indicated.
On the third day, due to fever and vomiting, amikacin and waveform were added.
On the fourth day the uroculture showed a multisensitive E. coli.
Headache caused a brain scanner that showed no abnormalities.
On the sixth day, the patient was stupor, the cerebrospinal fluid showed hypoglycorrhachi (9 mg/dl), proteinorrhachi (360 mg/dl) and pleocytosis (18 mm3), adeno-philus, for pneumo-phenolate
Ceftriaxone was increased to 4 g/day and dexamethasone, vancomycin 1 g c/12 h, and intravenous therapy were added.
After a few hours the level of consciousness improved and diplopia in the lateral view, central nystagmus, bilateral dysmetria and generalized hyperreflexia was observed.
The symptoms and Gram stain of CSF with Gram (+) bacilli raised a listerial rhomboencephalitis and started ampicillin (8 g/day).
Fever ceased that day, and in the following cases there was paresis of the velum of the palate, mild right hemiparesis and a tremor of action in the upper limbs.
Magnetic resonance imaging showed hyperintensity in T2 and FLAIR sequences in the cerebellum and diffuse cerebellum cerebellum regions, in the same areas as in the ventricular system, particularly in the third.
Upon bacteriological confirmation of a rhomboencephalitis due to monocytogeneous listeria, and ruling out other etiologies, vancomycin and ceftriaxone were discontinued.
On day 13 of treatment, a new lumbar puncture and magnetic resonance showed persistent hypoglycorrhachia and pleocytosis with polyformonuclear predominance, consolidation of microabscesses on the trunk and increased antibiotic uptake.
While receiving between 600 and 1,300 mL of saline daily, on day 20 there was polyuria of 6,150 mL/day associated with hyponatremia (132.9 mEq/L), natriuresis of 529 normal fraction excreted tachycardia, tachycardia
He suffered autonomic nervous system dysfunction and EPS increased the supply of oral and intravenous sodium.
Three days later, the brain natriuretic peptide (BNP) concentration was normal.
In the following weeks, her neurological status improved but she continued with polyuria, natriuresis higher than intake, hypotension, low uricemia and a tendency to hyponatremia.
Antibiotic therapy was discontinued one month (21 days with ampicillin).
She was discharged 36 days after admission, with only diplopia persisting in the upward gaze.
Examinations prior to discharge showed mild hyponatremia (133.5/L), low uricemia (2.9 mg/dl), excreted fraction of high creatinine clearance (773 mEq/day, elevated creatinine clearance (11.2%-NV: < 10%), hyperuricemia
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In subsequent outpatient controls it was found that their renal sodium management and blood pressure normalized only five weeks later and there were no neurological sequelae.
Later, she remembered that she had taken artisanal cheese the week before the onset of her disease, which could have been the source of infection.
