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doi:10.1111/j.1750-3639.2009.00347.

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COM AUGUST 2009 CASE 2

35-YEAR-OLD HIV-POSITIVE WOMAN WITH BASAL


FOREBRAIN MASS bpa_347 265..268

Cristina Vincentelli, MD ; Matthew J. Schniederjan, MD2; Daniel J. Brat, MD, PhD2


1

1
Mount Sinai Medical Center Department of Pathology and Laboratory Medicine Miami Beach, FL 33140
2
Emory University School of Medicine, Department of Pathology and Laboratory Medicine, Atlanta, GA

CLINICAL HISTORY PATHOLOGY


The patient was a 35-year-old African American woman with HIV/ The brain weight in the fresh state was 1,220 g. Gross examina-
AIDS (CD4 count 95/ml) and no history of HAART therapy, who tion of the external surface was unremarkable. Serial coronal
was admitted from an outside hospital for further management of sections revealed a poorly circumscribed area of softening with
altered mental status and hypercarbic respiratory failure. Upon surrounding hemorrhage within the basal forebrain, measuring
admission, the patient was unresponsive and ventilator dependent. 2.7 ¥ 2.3 ¥ 1.2 cm (Figure 2). Similar lesions were identified
On neurologic exam she had no response to painful stimuli, as well bilaterally in the middle temporal lobes within the anterior hip-
as decreased deep tendon and pupillary reflexes. A chest X-ray pocampi measuring 1.0 cm each. The ventricles were slightly
failed to demonstrate any pulmonary lesions. A CT of the head dilated. The cortical ribbon and deep gray structures appeared
without IV contrast revealed an infiltrating hypodense mass within unremarkable, as well as the brainstem and cerebellum.
the basal forebrain extending inferiorly to the level of the basilar Microscopic examination of the areas of softening demonstrated
cisterns, involving the thalami and cerebral peduncles bilaterally necrotizing encephalitis with a predominantly lymphocytic inflam-
(Figure 1). Diffuse brain volume loss was also noted. A lumbar matory infiltrate in a perivascular pattern and marked reactive
puncture was performed for CSF analysis, which showed lympho- gliosis (Figure 3). Many of the reactive glia showed a variety of
cytic pleocytosis (56 nucleated cells/ml with 92% lymphocytes), intranuclear and intracytoplasmic inclusions, ranging from amor-
low glucose (23 mg/dl) and elevated protein (208 mg/dl). An infec- phous and basophilic to discreet and eosinophilic (Figure 4).
tious disease was suspected. PCR analysis of the CSF was negative Similar changes were identified around the fourth ventricle, at the
for Mycobacterium tuberculosis, HSV, VZV, CMV and JC virus. level of the mid-pons. Numerous microglial nodules without multi-
There was low positivity for EBV DNA. Serologic studies were nucleated giant cells were present around the lesions and in the
consistent with past infections with EBV and CMV and were nega- grossly normal brain.
tive for toxoplasmosis, histoplasmosis, Cryptococcus and West Stains for JC virus (SV40), HSV, CMV and EBV were negative.
Nile virus. VDRL was non-reactive. CSF and blood cultures for Beta amyloid and tau protein stains were also negative. Diagnostic
bacteria, fungal organisms and acid fast bacilli were negative. The immunohistochemistry showed strong nuclear and cytoplasmic
patient received empiric therapy for bacterial meningitis, including positivity within neurons and glia (Figure 5) and the diagnosis was
Mycobacterium tuberculosis, HSV/VZV encephalitis and cover- confirmed by electron microscopy (Figure 6).
age for fungi with amphotericin. Her neurologic status progres- What is the diagnosis?
sively deteriorated. She lost all deep tendon reflexes and her left
pupil became fixed and dilated. The presence of corneal reflexes
was the only sign of remaining brain stem function. The decision to
end life sustaining treatment was made and the patient expired.
Consent for limited autopsy of the brain was obtained from the
family.

Figure 1. Figure 2.

Brain Pathology 20 (2010) 265–268 265


© 2010 The Authors; Journal Compilation © 2010 International Society of Neuropathology
Correspondence

Figure 3.

Figure 4.

266 Brain Pathology 20 (2010) 265–268


© 2010 The Authors; Journal Compilation © 2010 International Society of Neuropathology
Correspondence

Figure 5.

Figure 6.

Brain Pathology 20 (2010) 265–268 267


© 2010 The Authors; Journal Compilation © 2010 International Society of Neuropathology
Correspondence

necrotic changes resembling herpes encephalitis (5). Mild brain


DIAGNOSIS atrophy has also been reported. In the adult population, some find-
Acute adenovirus encephalitis. ings described on MRI imaging include linear high-signal intensity
Immunohistochemistry for adenovirus showed strong nuclear in the hippocampi on T1, and hyperintense signaling on FLAIR
and cytoplasmic positivity within neurons and glia. Electron sequencing in both temporal lobes (1, 2). Zagardo et al reported a
microscopy of tissue from the basal forebrain lesion revealed case of adenoviral rhombencephalitis in an immunosuppressed
numerous non-enveloped virions with icosahedral symmetry that patient which was found to have T2 signal abnormalities in the
ranged in diameter from 70 to 75 nm, consistent with adenovirus brain stem and cerebellum with mild patchy enhancement and
(Figure 6). No other virions were identified. mass effect on MRI (5). To our knowledge, the CT findings of an
infiltrating mass due to adenovirus has not been previously
described. We conclude that adenovirus is a rare and sometimes
DISCUSSION unsuspected cause of encephalitis that may present as a mass
Patients with HIV/AIDS frequently present with neurological signs lesion, and should be considered in the differential diagnosis once
and symptoms and require neuroimaging studies as part of their the major etiologies have been ruled out.
diagnostic workup. The detection of intracranial pathology consist-
ing of a focal brain lesion raises the possibility of an opportunistic REFERENCES
infection versus a neoplastic process. The major diagnoses in these
1. Dubberke ER, Tu B, Rivet DJ, Storch GA, Apisarnthanarak A, Schmidt
patients include Toxoplasma gondii infection, primary CNS lym- RE, Weiss S, Polish LB (2006) Acute meningoencephalitis caused by
phoma, progressive multifocal leukoencephalopathy (PML) and adenovirus serotype 26. J Neurovirol 12:235–40.
focal HIV encephalopathy, with some variation seen in the fre- 2. Nagasawa H, Wada M, Kurita K, Iseki C, Katagiri T, Kato T (2006) A
quency of these entities with the advent of highly active antiretrovi- case of non-herpetic acute limbic encephalitis associated with a type-2
ral therapy. CD4+ T lymphocyte counts and a history of ongoing adenovirus infection. Rinsho Shinkeigaku 46:322–7.
prophylaxis for opportunistic infections are also factors that may 3. Ohtsuki N, Kimura S, Nezu A (2000) Three cases with acute
influence the differential diagnosis of a focal brain lesion in HIV/ encephalopathy with adenovirus type 7 infection. No To Hattatsu
AIDS patients. Other well known infectious etiologies of focal 32:68–72. Review.
brain lesions in HIV/AIDS patients are fungal organisms, CNS 4. Schnurr D, Bollen A, Crawford-Miksza L, Dondero ME, Yagi S (1995)
Adenovirus mixture isolated from brain of an AIDS patient with
tuberculosis and neurosyphilis. In rare cases, ring-enhancing and
encephalitis. J Med Virol 47:168–71.
space occupying lesions have been described with cytomegalovirus 5. Zagardo MT, Shanholtz CB, Zoarski GH, Rothman MI (1998)
(CMV) infection of the CNS. Rhombencephalitis caused by adenovirus: MR imaging appearance.
In the present case, the patient was a neurologically impaired AJNR Am J Neuroradiol 19:1901–3.
woman with HIV/AIDS who was found to have a brain mass in a
CT scan of the head. The extensive workup performed to rule out
the major causes of this clinical scenario failed to reveal an etiol-
ABSTRACT
ogy. With this unusual presentation, CNS adenoviral infection was A 35-year-old African American woman with HIV/AIDS presented
not suspected. with altered mental status. A CT of the head revealed an infiltrating
Adenoviruses are common pathogens which may cause a wide hypodense intra-axial mass within the basal forebrain. Lumbar
spectrum of diseases depending on the infecting serotype. Clinical puncture showed a lymphocytic pleocytosis, elevated protein and
entities include respiratory illnesses, pharyngitis, conjunctivitis, low glucose. PCR analysis of the CSF was negative for Mycobacte-
gastroenteritis and cystitis, and may produce severe disease in rium tuberculosis, HSV, VZV, CMV and JC virus. There was low
immunosuppressed hosts. Although known to be capable of positivity for EBV DNA. Serologic studies were consistent with
causing meningoencephalitis, CNS infection by adenovirus (ADV) past infections with EBV and CMV and were negative for toxo-
is infrequent in both immunocompetent and immunosuppressed plasmosis, histoplasmosis, Cryptococcus and West Nile virus.
patients. Of the 51 known adenovirus serotypes, some that have VDRL was non-reactive. CSF and blood cultures were negative.
been implicated in CNS infections are 2, 3, 7 and 26, as well as She soon expired. Post-mortem examination of the patient’s brain
serotype 31 in mixture with 49 (1–4). Adenoviral meningoen- showed a poorly delineated area of softening and hemorrhage
cephalitis has most frequently been reported in the setting of pneu- within the basal forebrain. Histologic examination revealed necro-
monia or as one component of a disseminated infection in immuno- tizing encephalitis with perivascular lymphocytes and glial cells
compromised patients. Only rarely does adenovirus infection with numerous cytoplasmic and intranuclear inclusions. Immuno-
present primarily as a CNS disease (1). histochemistry was strongly positive for adenovirus and negative
Neuroimaging patterns of CNS adenoviral infection depend on for HSV, CMV, SV40 and EBV. Electron microscopy confirmed
the patient age, location and clinical course. In children, hydro- the presence virions consistent with adenovirus. We conclude that
cephalus with periventricular radiolucency and multiple parenchy- adenovirus is a rare and sometimes unsuspected cause of encepha-
mal hypodensities have been described on CT scan, as well as litis that may present as a forebrain mass lesion.

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© 2010 The Authors; Journal Compilation © 2010 International Society of Neuropathology

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