A 52-year-old diabetic female was in her usual state of health until 6 weeks prior to admission, when she had a 3-week episode of apparent “flu” characterized by fatigue, aching joints, nausea, vomiting, and headache. She recovered briefly, but then had recurrence of headaches. Two weeks prior to admission the patient became confused and was hospitalized. On admission she was found to be febrile to 104.6°F and significantly dehydrated. Hematocrit was normal. White blood count was 15,000, with 94% polymorphonuclear leukocytes. Blood sugar was 230 mg/dl, but ketones were absent. CT scan without contrast was normal. Lumbar puncture was unsuccessful, and the patient was empirically treated with cefotaxime and ofloxacin. Lumbar puncture 3 days later showed 75 white blood cells, with 48% neutrophils, protein of 111 mg/dl, and glucose of 105 with serum glucose over 330 mg/dl. Subsequent lumbar puncture was reported to show a decrease in numbers of white blood cells. The patient improved clinically and was discharged on oral ampicillin. The patient did well initially at home but then developed episodes of disorientation. On the morning of admission, she was found vomiting, incontinent of stool, and unresponsive to voice. Hospital evaluation revealed the patient to be afebrile, with white blood count of 7500. Head CT scan showed a possible brain abscess, with several patchy areas of edema. The patient was transferred for further care.
On examination, the patient was normotensive and afebrile. General physical examination was normal except for early bilateral papilledema. On neurologic examination, the patient was obtunded. She was able to move all 4 extremities spontaneously and in response to pain but was unresponsive to voice. Reflexes were hypoactive throughout and absent at the ankles. Babinski sign was absent on the left but present on the right. Head MRI showed in excess of 10 ring-enhancing and solid lesions scattered throughout both cerebral hemispheres, with surrounding edema. The patient was placed on intravenous ceftriaxone, 2 grams every 12 hours, metronidazole given as a 1 gram loading dose followed by 500 mg every 6 hours, and intravenous oxacillin at 2 grams every 4 hours. The patient stabilized and then regained consciousness, with slowed but otherwise intact mental status, mild right arm drift, and right Babinski sign; neurologic examination was otherwise intact except for distal decrease in light touch and pinprick sensation, consistent with a diabetic peripheral neuropathy. CT-guided stereotactic biopsy failed to yield organisms. The patient was maintained on all 3 antibiotics and followed with serial MRI scans to rule out enlargement of any of the lesions despite antibiotic therapy; scans were obtained at 48-hour intervals during the first week of therapy and then at progressively longer intervals as the patient improved.
After discharge from hospital, 1 month after admission, the patient was maintained on intravenous ceftriaxone and placed on oral metronidazole and oral dicloxacillin plus probenecid to increase serum concentrations and reduce active transport of the drug from cerebrospinal fluid. With antibiotic treatment, the patient’s lesions steadily diminished in size, with complete disappearance of most of the lesions. Metronidazole was discontinued after 8 weeks of therapy; ceftriaxone was discontinued after 12 weeks of therapy, and dicloxacillin was discontinued one week later. An MRI scan was obtained 1 week following discontinuation of each antibiotic to rule out recurrence of an abscess in any of the areas of residual abnormality, with a follow-up MRI 1 month after the last medication had been discontinued. The patient continued to improve mentally and was discharged to her private physician. On follow-up 4 years later, the patient was neurologically normal except for her diabetic peripheral neuropathy. An MRI scan revealed areas of gliosis at the sites of some of the previous abscesses, but no other abnormality.