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Letter
West Nile Virus Meningitis
in Patient with Common Variable Immunodeficiency
Augusto M. Alonto,* David M. Aronoff,* and Preeti N. Malani*
*University of Michigan Health System, Ann Arbor, Michigan, USA
Suggested citation
for this article:
Alonto AM, Aronoff DM, Malani PN. West Nile virus meningitis in patient
with common variable immunodeficiency. Emerg Infect Dis [serial online]
2003 Oct [date cited]. Available from: URL: http://www.cdc.gov/ncidod/EID/vol9no10/03-0195.htm
To the Editor: Infection by West Nile virus (WNV) was first recognized
in the Western Hemisphere in 1999 in New York (1). Subsequently,
this mosquito-borne flavivirus has spread westward and has emerged as
an important cause of infectious meningoencephalitis in the United States
(2). In September 2002, during a WNV epidemic in Michigan
(2), a 38-year-old woman with common variable immunodeficiency
(CVID) sought treatment at the University of Michigan Hospital with acute
WNV-associated meningitis. Although persons with CVID are at increased
risk for enteroviral meningoencephalitis, a greater susceptibility to
arthropod-borne flavivirus infections has not been reported.
The patient had a history of recurrent sino-pulmonary infections and
gastrointestinal giardiasis and salmonellosis; at 33 years of age, she
was diagnosed with CVID that has been subsequently treated with intravenous
immunoglobulin (IVIG) every 3 weeks. She was in her usual state of health
until 5 days before admission, when she noted the abrupt onset of severe
headache, followed by temperatures up to 39.4°C, progressive photophobia,
nausea, vomiting, and a transient papular rash on her trunk and extremities.
On arrival, the patient reported marked photophobia. Physical examination
showed a temperature of 40.6°C, heart rate 80 beats per minute, and blood
pressure 122/70 mmHg. She had cervical tenderness to palpation and active
range of motion with minimal rigidity. Small, diffuse, nontender lymphadenopathy
was noted in the cervical region. No focal or global deficits were found
on neurologic exam. Results of the remainder of the physical examination
was unremarkable. Initial laboratory values included a peripheral leukocyte
count of 3.5 K/mm3 (normal: 4.0–10.0 K/ mm3; 42%
neutrophils, 52% lymphocytes, and 7% monocytes), which was unchanged from
the patient’s baseline leukopenia. Her serum IgG level was 1,081 mg/dL
(620–1,520 mg/dL).
Cerebrospinal fluid (CSF) sampling indicated the following: erythrocytes
3/mm3, leukocytes 77/mm3 (41% neutrophils, 51% lymphocytes,
7% histiocytes), glucose 50 mg/dL (50–70 mg/dL), and protein 75 mg/dL
(15–45 mg/dL). Results of routine Gram stain, bacterial and fungal cultures,
polymerase chain reaction testing for herpes simplex virus and Cryptococcus
neoformans antigen were negative. Assay results of the patient’s CSF
for WNV by IgM-capture enzyme-linked immunosorbent assay, performed by
the Michigan Department of Community Health, were positive.
The patient was initially treated with parenteral ampicillin, ceftazidime,
and acyclovir, which were discontinued within 48 hours. Her symptoms improved
with routine medical support, and she was discharged on hospital day 5.
We were notified of the positive CSF IgM for WNV approximately 2 weeks
after the patient was discharged, at which time her symptoms had completely
resolved. At a follow-up visit 3 weeks after her hospitalization, the
patient had no residual symptoms of meningitis.
Patients with agammaglobulinemia, either common variable or X-linked,
are known to be susceptible to recurrent infections (3).
Bacterial infections are the best described; however, chronic enteroviral
meningoencephalitis is also associated with deficiencies in B-cell immunity
(4–6). Although the role of immunoglobulins in host defense
against WNV infection is not completely understood, evidence suggests
that humoral immunity protects against WNV infection and severe disease
(7–9).
WNV is a single-stranded RNA virus of the family Flaviviridae.
Its genome is processed to eight proteins, including the envelope (E)
glycoprotein, the matrix protein, the nucleocapsid protein, and five nonstructural
proteins (7). E-glycoprotein antibodies develop during
human WNV infection (8), and passive immunization of
mice with E-glycoprotein antiserum protects against WNV infection and
death (7,8). In addition, IVIG therapy was associated
with recovery from WNV meningoencephalitis of an immunosuppressed 70-year-old
woman (9). Although our patient had normal levels of
serum IgG at the time of illness, viral meningitis may occur in agammaglobulinemic
patients despite regular IVIG therapy (10).
This case demonstrates the need to consider WNV in patients with CVID.
Our patient recovered promptly, without evidence of neurologic sequelae,
despite her underlying immunodeficiency. More experience is needed to
provide a better understanding of the relationship between CVID and WNV.
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