蜱叮咬相关神经系统感染性疾病(5)

chain-reaction (PCR) assay, followed by sequence confirmation. Immunohistochemical
analysis with antisera specific for deer tick virus identified numerous
immunoreactive neurons, with prominent involvement of large neurons in the
brain stem, cerebellum, basal ganglia, thalamus, and spinal cord. This case demonstrates
that deer tick virus can be a cause of fatal encephalitis.
Deer tick virus is a member of the tickborne encephalitis group
of flaviviruses and is closely related to Powassan virus. Deer tick virus was
first isolated from Ixodes scapularis ticks in 1997 in North America.1 The complete
sequence of the deer tick virus has been determined.2 The viral genome is 10.8 kb
in length and shares 84% nucleotide sequence identity and 94% amino acid sequence
identity with the Powassan virus genome. The two viruses are antigenically related,3
and it has been suggested that they share a common origin and represent two viral
lineages related to Powassan virus in North America.2 Ebel et al.4 refer to deer tick
virus as Powassan virus lineage II, and in this report we use the same terminology.
Several members of the tickborne encephalitis group of flaviviruses, including
tickborne encephalitis virus and Powassan virus, cause encephalitis in humans and
animals, with tickborne encephalitis virus causing the most serious outbreaks. These
viruses are closely related antigenically and are found predominantly in the northern
hemisphere. In Europe, tickborne encephalitis occurs mainly in eastern and central
regions and affects approximately 50 to 199 persons per 100,000 inhabitants annually.
5 The seroprevalence of antibodies to Powassan virus is estimated to be 0.5 to
4.0% in areas in which the disease is endemic.6
Infection with tickborne encephalitis virus can be mild or asymptomatic, or it can
result in meningitis and encephalitis. Powassan virus can be pathogenic in human
beings and can cause severe encephalitis with a fatality rate of up to 60% and longterm
neurologic sequelae in survivors.7 In contrast, Central European encephalitis
that is caused by tick bites typically produces mild or silent infection. Other diseasecausing
flaviviruses include West Nile virus, St. Louis encephalitis virus, dengue
virus, and yellow fever virus.8 These viruses are transmitted by mosquitoes and cause
a spectrum of diseases including meningitis, encephalitis, dengue fever, and yellow
fever.
Copyright ** 2009 Massachusetts Medical Society. All rights reserved.
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In certain locations of the northeastern and
north central United States, the prevalence of deer
tick virus in adult deer ticks is high,9,10 but human
infection has not been reported previously. This
could indicate that the virus does not easily infect
humans or that it is not particularly pathogenic.
Diagnostic testing for Powassan virus is not routinely
performed for patients with symptoms of
encephalitis. Human incidence may thus be currently
underestimated.
Case Report
In late spring, a 62-year-old man was admitted to
a local New York State hospital with a 4-day history
of fatigue, fever, bilateral maculopapular palmar
rash, and an onset of diplopia, dysarthria, and
weakness in the right arm and leg. He was a native
of New York State and had no history of recent
travel. He owned horses and spent time outdoors
in a wooded area. Reports of Lyme disease
were common in his county of residence, indicating
tick activity in the area. His medical history
included chronic lymphocytic leukemia–small lymphocytic
lymphoma (CLL–SLL), which had been
diagnosed 4 years earlier and had initially been
treated with fludarabine. He was not taking corticosteroids.
On admission, he was given nonsteroidal
antiinflammatory medication and an oral antibiotic
(amoxicillin–clavulanate), which had been
prescribed by his primary care physician for a
recent exacerbation of chronic sinusitis that had
been recurrent for more than a year. His baseline
white-cell count was 15,000 cells per cubic millimeter
and had increased to 70,000 cells per cubic
millimeter during the past 6 to 8 months. He
was started on broad-spectrum antibiotics and acyclovir
(700 mg administered intravenously every
8 hours) for presumed infection of the central nervous
system. The differential diagnosis included
cerebral ischemia, possibly related to leukostasis,
infection (viral, bacterial, or fungal), and lymphoma.
Initial laboratory results were notable for a
markedly elevated peripheral-blood white-cell
count (144,200 cells per cubic millimeter) and cerebrospinal