Page 944 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

CHAPTER 72: Encephalomyelitis 675

abnormalities, transverse myelitis, radiculitis, and cerebellar ataxia parenchyma, spinal cord and present as tuberculous meningitis, brain
have also been reported with CSD. A small percentage of patients tuberculomas, and spinal tuberculosis. Another entity named tuber-
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with CSD may also develop neuroretinitis. Patients with neuroretinitis culous encephalopathy (TBE) was described by Dastur and Udani in a
often present with unilateral visual acuity abnormalities. Examination paper published in 1966. However, TBE as a disease entity remains
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reveals retinal hemorrhages, cotton wool exudates, and stellate macular controversial. Tuberculomas are caseous foci within the brain paren-
exudates. In patients with CNS involvement, pleocytosis is often present chyma and may present as single or multiple nodular lesions, and may
in the CSF. Diagnosis of CSD is based on history of exposure to cats, be associated with Tb meningitis or miliary Tb. Tuberculomas often
clinical findings suggestive of CSD, and laboratory testing such as serol- manifest with focal neurological signs and symptoms of an intracranial
ogy, culture or PCR of blood, CSF, and tissue. However, the yield from mass lesion. Systemic symptoms or signs of meningeal inflammation
culture and PCR is low. Treatment is with doxycycline or azithromycin. may or may not be associated with this depending on whether it is
Rifampin is sometimes added to these antibiotics. Patients with CSD associated with Tb meningitis or with miliary Tb without meningitis.
and CNS involvement recover with treatment but may have permanent Tuberculomas appear as enhancing lesions on CT scan or MRI of the
neurological defects. brain. CSF analysis may show elevated protein and low glucose con-
■ LISTERIA MONOCYTOGENES centrations with a mononuclear pleocytosis. If the meninges are not
involved, the CSF may be normal. CNS Tb presenting as tuberculoma
Listeria is one of the common causes of bacterial meningitis in neonates, is uncommon in the USA. This entity is seen more often in children in
adults over the age of 50 years, and immunosuppressed patients. Patients Asia. Patients with tuberculous encephalopathy present predominantly
may present only with meningitis or a combination of meningitis with signs of diffuse cerebral involvement, with or without clinical and
and encephalitis. In rare instances Listeria can present as encephalitis CSF changes seen in Tb meningitis. TBE is quite distinct from tuber-
without any signs of meningitis. Patients with encephalitis present culomas or tuberculous meningitis, where the brain parenchyma may
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with fever, headache, altered sensorium, or cognitive dysfunction and become involved. TBE as described by Dastur and Udani is seen less
may mimic herpes encephalitis. A complication of encephalitis is the commonly and has been reported more often in children. Presentation
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progression to brain abscess formation. Another rare form of listerial of TBE is similar to encephalitis with seizures, stupor, and coma often
brain infection is rhomboencephalitis, which typically occurs, in healthy without meningeal signs. The common neuropathological feature seen
adults. Rhomboencephalitis typically presents as a biphasic illness; the in TBE is diffuse brain edema with diffuse or patchy rarefaction of white
initial phase of headache, fever, nausea, and vomiting for a few days is matter and demyelination. The pathogenesis of TBE is not well under-
followed by the development of cranial nerve palsies, cerebellar signs, stood. It has been postulated that TBE may represent immune-mediated
altered sensorium, seizures, and hemiparesis. Development of respira- white matter damage similar to acute disseminated encephalomyelitis.
tory failure has been reported in about 40% of patients. CSF analysis Some researchers have put forth other hypotheses that lead to TBE such
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reveals pleocytosis with either polymorphonuclear cell or mononuclear as hypoxia with ischemic damage of brain parenchyma, direct toxic
cell predominance. CSF protein concentration is moderately elevated effect of some of the antituberculosis drugs such as streptomycin and
with a low glucose concentration. In rhomboencephalitis, the CSF find- isoniazid on the brain, and hypersensitivity reaction to the tuberculo-
ings may be only mildly abnormal. Culturing blood or CSF specimens protein in the brain. TBE may be a heterogeneous group of conditions
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can establish the diagnosis. MRI imaging of the brain is helpful in both immune and nonimmune, affecting the brain parenchyma.
demonstrating rhomboencephalitis. Combined intravenous ampicil- Varying manifestations of TBE have been reported from acute fulminant
lin and gentamicin is the treatment of choice. In penicillin allergy, disease resulting in death within a few days to chronic disease lasting
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trimethoprim-sulfamethoxazole as a single agent is a good alternative. over months. Clinical features of TBE without clinical evidence of Tb
■ MYCOPLASMA PNEUMONIAE ors, ophthalmoplegia, papilledema, involuntary movements, myoclonic
meningitis reported in the literature are fever, vomiting, tongue trem-
M pneumoniae, a common cause of community acquired respiratory jerks, seizures, decerebrate spasm, hypotonia, stupor, and coma.
CSF is usually normal, but in some cases an increase in protein, low
tract infections, has been associated with extrapulmonary disease glucose, and lymphocytic pleocytosis may be seen. Diagnosis of TBE
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including the CNS. It is unclear if the CNS manifestations are due to may be difficult if the CSF does not show any abnormalities, as TBE
direct infection or an immune-mediated illness. 116,117 CNS involvement, may mimic many other forms of encephalopathies and encephalitis.
most often presenting as encephalitis, is seen year round and is more The level of adenosine deaminase in the CSF may not be elevated as in
common in children. Other manifestations of CNS involvement that Tb meningitis. MRI may show diffuse hyperintense lesions in the white
have been reported are aseptic meningitis, transverse myelitis, Guillain- matter on T2-weighted images and disseminated gadolinium enhance-
Barré syndrome, cranial nerve palsies, and cerebellar ataxia. Peripheral ment on T1-weighted images. CSF culture and PCR for mycobacteria
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neuropathy has also been reported. The development of CNS manifes- are not helpful as the yield is very low in TBE. Brain biopsy may help
tations preceded by a recent upper or lower respiratory tract infection in the diagnosis with characteristic histopatholgy and reveals acid-fast
may be a clue to the diagnosis. CSF in patients with neurologic involve- bacilli with specific stains. Treatment of tuberculomas and TBE is with
ment typically shows pleocytosis with lymphocytic predominance, a four-drug regimen that includes isoniazid(INH), rifampin(RIF), pyra-
elevated protein and normal glucose concentration. Diagnosis is made zinamide, and either ethambutol or streptomycin for 2 months followed
by serology detecting serum IgM and IgG antibodies against M pneu- by INH and RIF alone, if the isolate is fully susceptible. Adjunctive
moniae. PCR to detect M pneumoniae in respiratory samples has a high glucocorticoid therapy with either dexamethasone or prednisone is
sensitivity and specificity, but CSF PCR is not a sensitive test to aide in beneficial in reducing mortality and is recommended. 123
the diagnosis. Antimicrobial therapy for M pneumoniae includes mac-
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rolides, doxycycline, or fluoroquinolones. In one case report, addition of
glucocorticoids to the antimicrobial agent in a child with M pneumoniae PROTOZOAN
CNS infection appeared to be beneficial. Patients who develop neuro-
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logic complications with mycoplasma infections appear to have a higher ■ TOXOPLASMOSIS
incidence of morbidity and mortality compared to those without CNS Toxoplasma gondii is a ubiquitous intracellular protozoan that causes
involvement. 116 asymptomatic toxoplasmosis in nearly half of the world’s population.
■ MYCOBACTERIUM TUBERCULOSIS Encephalitis is the most common manifestation of toxoplasma, which
was historically a rare disease seen sporadically in immunocompro-
The CNS involvement in tuberculosis is approximately 10% to 15% of mised patients. However, with the HIV epidemic this has risen to promi-
all cases of tuberculosis infections. This may involve meninges, brain nence and is one of the most frequent and life-threatening opportunistic

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