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676 PART 5: Infectious Disorders

infection in severe AIDS patients. It is believed that toxoplasmic enceph- of inflammation and demyelination involving cerebral subcortical and
alitis results from reactivation of chronic latent infection seen in patients deep cortical white matter, and gray matter. Spontaneous recovery
132
with CD4 counts less than 50 cells/µL. However, with the introduc- or recovery with corticosteroids is usually reported, though permanent
124
tion of antiretroviral therapy and prophylaxis with trimethoprim- sequelae can occur in few patients. Once infection is ruled out, the
sulfamethoxazole, the incidence is decreasing. Clinically, cerebral recommended treatment regime is intravenous methylprednisolone 1 g
involvement is more common and takes the form of cerebral mass daily with a cumulative dose of 3 to 5 g followed by 1 to 2 months of oral
lesions, meningoencephalitis, or diffuse encephalitis. The symptoms are prednisolone on a tapering regimen. Plasma exchange and intravenous
nonspecific, and include fever, seizures, headache, hemiparesis, altered immunoglobulin can be considered in patients who fail to respond to
mental status, and coma. CT or MRI of the brain in toxoplasmosis corticosteroids. 130
shows multiple homogenous or ring-enhancing lesions with mass effect
commonly in the region of the basal ganglia, midbrain, or brainstem.
Imaging may be normal in diffuse toxoplasmosis. MRI is reportedly KEY REFERENCES
more sensitive than CT. The diagnostic serologic studies for toxoplas-
125
mosis are seldom seen in AIDS patients. Detection of Toxoplasma DNA • Centers for Disease Control and Prevention (CDC). Update:
on PCR testing of CSF may facilitate diagnosis and follow-up care. 126,127 measles–United States, January-July 2008. MMWR Morb Mortal
In AIDS patients with suspected toxoplasmic encephalitis, it is desirable Wkly Rep. 2008;57(33):893-896.
to have a confirmed diagnosis because similar lesions may be due to • Dedicoat M, Livesley N. Management of toxoplasmic encepha-
tuberculosis, other bacteria or fungi, or even lymphoma. Brain biopsy litis in HIV-infected adults (with an emphasis on resource-poor
is reserved for patients who fail to respond to therapy or whose neuro- settings). Cochrane Database Syst Rev. 2006;3:CD005420.
logic status is rapidly deteriorating. In AIDS patients with encephalitis • Gilden DH, et al. Neurologic complications of the reactivation of
that is clinically and radiographically compatible with toxoplasmosis, a varicella-zoster virus. N Engl J Med. 2000;342(9):635-645.
therapeutic trial with pyrimethamine and sulfadiazine should be initi-
ated early. The standard treatment regimen includes pyrimethamine, • Gutierrez J, Issacson RS, Koppel BS. Subacute sclerosing panen-
folinic acid, and sulfadiazine. Trimethoprim-sulfamethoxazole can be cephalitis: an update. Dev Med Child Neurol. 2010;52(10):901-907.
used as an alternative treatment and clindamycin can be used in sulfa • Hatipoglu HG, Sakman B, Yuksel E. Magnetic resonance and
allergic patients. Primary therapy is continued for at least 6 weeks. diffusion-weighted imaging findings of herpes simplex encephali-
128
In AIDS patients, discontinuation of therapy has been associated tis. Herpes. 2008;15(1):13-17.
frequently with relapse of toxoplasmic encephalitis, so maintenance • Hayes EB, et al. Virology, pathology, and clinical manifestations of
therapy should be continued at reduced doses. The duration of main- West Nile virus disease. Emerg Infect Dis. 2005;11(8):1174-1179.
tenance therapy depends on the response to highly active antiretroviral • Hviid A, Rubin S, Muhlemann K. Mumps. Lancet. 2008;
therapy (HAART) and can be discontinued when persistent CD4 counts
are greater than 200 cells/µL and if lesions have disappeared on MRI. 129 371(9616):932-944.
• Kramer AH. Viral encephalitis in the ICU. Crit Care Clin.
2013;29:621-649.
POSTINFECTIOUS • Lindquist L, Vapalahti O. Tick-borne encephalitis. Lancet.
■ ACUTE DISSEMINATED ENCEPHALOMYELITIS 2008;371(9627):1861-1871.

Acute disseminated encephalomyelitis (ADEM) is an inflammatory • Tunkel AR, et al. The management of encephalitis: clinical prac-
demyelinating disease of the central nervous system. It is usually mono- tice guidelines by the Infectious Diseases Society of America. Clin
phasic but a multiphasic variety has also been recognized. ADEM Infect Dis. 2008;47(3):303-327.
130
includes postinfectious and postvaccination encephalomyelitis, which • Whitley RJ, et al. Vidarabine versus acyclovir therapy in herpes
together make up more than three-quarters of cases of ADEM. ADEM simplex encephalitis. N Engl J Med. 1986;314(3):144-149.
is one of the categories of the inflammatory demyelinating diseases,
others being multiple sclerosis, transverse myelitis, optic neuropathy,
and neuromyelitis optica (Devic disease). Postinfectious ADEM has
been described with both viral and bacterial infections, including mea- REFERENCES
sles, mumps, rubella, varicella-zoster, EBV, CMV, herpes simplex virus, Complete references available online at www.mhprofessional.com/hall
hepatitis A or B, coxsackievirus, influenza A or B, human immunode-
ficiency virus (HIV), human T-cell lymphotropic virus-1 (HTLV-1),
human herpes virus 6, Rocky Mountain spotted fever, human corona
virus, Mycoplasma pneumoniae, Borrelia, Campylobacter, Leptospira,
Chlamydia, Legionella, and group A beta-hemolytic streptococci. ADEM CHAPTER Life-Threatening Infections
has been described postvaccination with rabies, mumps measles rubella, of the Head, Neck, and
diphtheria pertussis, tetanus, polio, influenza, and hepatitis B vaccines. 73
ADEM has an estimated annual incidence of 0.8 per 100,000 with a Upper Respiratory Tract
median age of onset of 6.5 years. ADEM has a distinct pattern of
131
perivenous inflammation surrounding small vessels in both the CNS Anthony W. Chow
gray and white matter. Most of these lesions seem of similar age with
predominant lymphocytic infiltration. Eventual demyelination in a
“sleeve-like” fashion is pathognomic. In ADEM, the timing of a febrile KEY POINTS
131
event is associated with the onset of neurological disease. Symptoms
occur rapidly with a combination of altered consciousness and multifo- • A thorough knowledge of the deep cervical fascial spaces and their
cal neurological deficits. Multiple sclerosis (MS) is an important dif- interrelationships and anatomic routes of spread is a prerequisite to
ferential for ADEM but encephalopathy, fever, seizures, and meningeal optimal management of life-threatening head and neck infections.
signs are very rare in MS. Infection should be ruled out first with lumbar • The microbial etiology of deep infections of the head and neck is
puncture, microbiological and serological tests. MRI is the imaging complex and typically polymicrobial.
modality of choice and shows scattered, focal, or disseminated areas

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