A 36-year-old woman with no medical or epidemiological history of interest was admitted to the Intensive Care Unit for sepsis and meningitis due to meningococcal type B isolated from blood cultures and cerebrospinal fluid.
He received fluid therapy support, ceftriaxone and vancomycin for 10 days with disappearance of clinical and analytical parameters of the patient although daily fever persisted. Thirty-eight patients had severe abdominal sepsis and an ultrasound did not show any other infectious focus.
She was admitted to an internal medicine ward to complete the study and evolution; she remained hemodynamically stable and in good general condition, fever up to 38.5oC in poor extremities and normal subclavian central venous access pet without infection data, neurological stage.
Complete blood count, hemostasis, renal, hepatic, thyroid and lipid profiles were normal, with a ferritin value of 775 μg/dl, ESR 90 mm1h, CRP of 23.8 mg/dl and CRP of 0.2 mg/dl.
Serology for hepatitis B and C virus, HIV, EBV, CMV, HSV types 1 and 2, burnetti, normal immunoglobulins and complements were negative; autoimmunity with ANA, ANCA.
Negative Mantoux reaction; hemocultives through central catheter, peripheral blood and urocultives were repeatedly negative; the control cerebrospinal fluid was of normal characteristics except for a smear-negative protein and culture also negative.
Eye fundus, electrocardiogram, echocardiography and contrast-enhanced toco-abdominal CT were also normal.
A cranial MRI with contrast was requested, showing a slight generalized meningeal uptake and multiple lesions measuring between 7-10 mm, hypointense on T1 and hyperintense on the left periventricular capsule with marked frontal edema and Flair.
regarding the few complications associated with brain abscesses secondary to meningeal infection, an extensive literature search (clinical practice guidelines, systematic reviews, bibliographic databases, peer-reviewed metasearches) was performed.
At this point, it was decided to perform a PET-CT in order to rule out other possible findings and absence of fever, justifying the persistence of the fever, corroborating the hypermetabolic uptake of the brain lesions described.
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No other source of infection fever was ruled out in the outpatient follow-up. Treatment was continued with parenteral ceftriaxone for 8 weeks, with progressive disappearance of the recurrence, a paulatin decrease until CRP and SGV normalization.
