蜱叮咬相关神经系统感染性疾病(6)

fluid with normal glucose, minimally
elevated protein, no white cells, and a negative
Gram’s stain (Table 1). The erythrocyte sedimentation
rate was 4, blood cultures were sterile, and
antibody titers were negative for Borrelia burgdorferi
and Anaplasma phagocytophilum. The neurologic
symptoms progressed, and after 2 days he was
transferred to another hospital. At the time of
transfer, the peripheral-blood white-cell count was
174,800 per cubic millimeter (with 4% neutrophils
and 94% lymphocytes) (Table 1).
Findings on flow cytometry were characteristic
of CLL–SLL. Bacterial and fungal blood cultures
were sterile. Sputum cultures for tuberculosis and
legionella species were negative. No serum antibodies
to Bartonella henselae or leptospira or brucella
species were detected. One day after admission,
a repeat spinal tap showed an elevated
protein level of 192 mg per deciliter, lymphocytic
pleocytosis with 891 cells per cubic millimeter
(with 1% neutrophils and 93% lymphocytes), and
a normal glucose level (Table 1). Flow cytometry
of the cerebrospinal fluid demonstrated a predominantly
reactive T-cell population (98% of
CD45+ cells were CD3+/CD5+ small T cells), with
no evidence of CLL–SLL. Bacterial culture and
Gram’s staining of the cerebrospinal fluid were
negative. India-ink staining, cryptococcus antigen
test, and PCR analyses for herpes simplex virus
types 1 and 2 and JC–BK virus were negative in
cerebrospinal fluid.
Magnetic resonance imaging (MRI) performed
after transfer (hospital day 1) revealed abnormal
T2-weighted and fluid-attenuated inversion recovery
(FLAIR) images, with hyperintensities most
prominent in the superior cerebellum, left pons,
and bilateral basal ganglia (Fig. 1A, 1B, and 1C).
An axial diffusion-weighted image and apparentdiffusion-
coefficient sequences revealed restricted
diffusion in the superior cerebellum, suggesting
an ischemic process (Fig. 1D). The patient
remained febrile (maximum temperature, 104.5°F
[40.3°C]), and antimicrobial coverage was broadened
to include an antifungal agent. His neurologic
function deteriorated, which necessitated intubation,
and his function did not improve despite
maximal medical therapy.
On hospital day 4, his fever abated, and computed
tomographic imaging revealed a mild obstructive
hydrocephalus, leading to placement of
an external ventricular drain. On hospital day 5,
repeat MRI revealed worsening of signal abnormalities
and markedly increased hydrocephalus.
He was taken urgently to the operating room for
decompression with a suboccipital craniotomy, at
which time cerebellar biopsy was performed.
Analysis of the biopsy specimen revealed severe
meningoencephalitis with a dense meningeal lymphoid
infiltrate containing mainly reactive CD4+
T cells, lymphocytic venous invasion and destruc-

Lyme borreliosis