A 76-year-old female patient was admitted to the emergency department of our hospital with fever, headache, mental alteration, and dysarthria, starting approximately 24 hours before admission. Her medical history included a curatively treated VIPoma of the pancreas—in this context, splenectomy had occurred two years ago. She was currently in remission and had been vaccinated according to guidelines in the context of the splenectomy. Parkinson's disease, arterial hypertension, and diabetes mellitus type 2 were also present. Her medication included levodopa with decarboxylase inhibitor, mirtazapin, rivotril, insulin, pancreatic enzymes, esomeprazol, aspirin, metoprolol, and enalapril.
The clinical examination showed an encephalopathic patient with Glasgow Coma Score (GCS) of 14, an oxygen saturation of 91%, hypertonus, abdominal tenderness on palpation and terminal meningism.
The laboratory findings demonstrated a leucocytosis (19 G/l) and an elevated C-reactive protein (CRP) with a value of 50 mg/l. The cerebrospinal fluid (CSF) revealed a high cell count with 1078 white blood cells/m3 with 72% polymorphonucleocytes, hyperproteinorrachia (2.25 g/l), and a very high lactate level (8.0 mmol/l). Brain computed tomography image did not show relevant pathological findings. With the diagnosis of meningoencephalitis an empiric antibiotic therapy with ceftriaxone, amoxicillin, and aciclovir was started. Dexamethasone was additionally administered. The patient showed a good response to the initial therapy, but some symptoms like dysarthria, ataxia, slight left leg paresis and a persistent meningism were still observed in the following days. A multiplex Polymerase Chain Reaction (PCR) of the CSF, including Varicella zoster virus and Herpes simplex virus 1 and 2, identified no pathogen and therefore aciclovir was discontinued. Admission blood cultures became positive for gram-negative rods (Figs. 3 and 4) and the microbiological laboratory later reported growth of a Flavobacterium species pending further identification. At this point, amoxicillin, dexamethasone and ceftriaxone were replaced by sulfamethoxazole/trimethoprim in combination with ciprofloxacin, as we found reports in the literature that these bacteria usually are resistant to beta-lactam antibiotics but show variable susceptibility to quinolones and sulfamethoxazole/trimethoprim. On the following day, Flavobacterium lindanitolerans was identified by MALDI-TOF mass spectromety after 24h from bacterial growth on Columbia blood agar (Fig. 1). There was no growth on McConkey agar. Flavobacterium lindanitolerans was also found in the CSF after 48h incubation on Columbia blood agar and Chocolate agar from CSF (Fig. 2). The minimal inhibitory concentration (MIC) was evaluated for amoxicillin, ceftriaxone, sulfamethoxazole/trimethoprim, ciprofloxacin, levofloxacin and minocyclin (Table 1). There are no standadized interpretation criteria available for this pathogen. Based on these results the antimicrobial therapy was again changed to intravenous levofloxacin 500mg twice daily on the seventh day of hospitalization and continued by oral levofloxacin from day 13 on until day 21.
Table 1
| Analysis | Results |
| Microbiology | |
| Blood culture, periphery | |
| Aerob flask Micr. | Gram-negative rods visible through the microscope |
| Aerob flask culture + | Flavobacterium species |
| | exact identity: Flavobacterium lindanitolerans |
| | Ceftriaxone MIC 32.0 mg/l |
| | Sulfamethoxazole/trimethoprim MIC 32.0 mg/l |
| | Ciprofloxacin MIC 3.0 mg/l |
| | Levofloxacin MIC 1.0 mg/l |
| | Minocycline MIC 0.19 mg/l |
| | Susceptibility examination to be interpreted with caution. |
| | No interpretation standards exist |
| Anaerob flask culture | no growth |
A brain magnetic resonance imaging (MRI) was additionally performed and showed purulent sediments in the lateral ventricles and leptomeningeal inflammation without signs of encephalitis (Figs. 5 and 6). Therapeutic response to treatment was good. Apart from splenectomy and type 2 diabetes mellitus, no other cause of immunosuppression was found. The patient was discharged from the hospital into a geriatric rehabilitation after 14 days. During the first 20 days of rehabilitation, the patient showed improvement of mental status, dysarthria and gait with slightly remaining disbalance and disorientation.
Given the absence of data in the literature, we chose a treatment duration of 21 days analogous to other gram-negative meningitis pathogens [1]. Before discontinuation of the antibiotic therapy, a follow up MRI showed the absence of abscess and a reduction of the ventricular sediments. In the performed laboratory parameters, no signs of systemic inflammation were evident.
Taking into account that the entry point of the bacteria remains unknown, a colonoscopy is planned.