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The diagnosis is made primarily via CT scanning or MRI demonstrating calcified, hypodense or ring-enhancing
larval cysts. Antibody assays detecting IgG to T. solium in the CSF and serum are the confirmatory diagnostic tests
available via the CDC and multiple commercial laboratories. Serum serologies are more sensitive than CSF
serologies.
Neurocysticercosis treatment has to be individualized on the basis of the number and viability of cysts present
on neuroimaging and where they are located. Calcified, or nonviable cysts, only require symptomatic treatment
and anticonvulsant therapy in children with seizures. Parenchymal cysts without enhancement typically respond to
antihelminthic treatment: albendazole (15 mg/kg/day, max 1,200 mg, in two doses for 14 days). Praziquantel (50
mg/kg/day in 3 doses × 9–13 days) should be considered for patients with >2 viable cysts. Albendazole is better
tolerated than praziquantel, is indicated for children of all ages, and does not interact with most antiepileptic
medications. One large meta-analysis found that antihelminthic treatment was associated with decreased seizure
frequency and more rapid radiographic resolution of granulomas that form around cysts. Coadministration of
corticosteroids for the initial 2 to 3 days of treatment is recommended if extensive CNS involvement is suspected,
but is not associated with improved neurologic outcomes. Clinicians should be aware that patients may have
paradoxical worsening during therapy, as most of the CNS effects of neurocysticercosis are immune mediated and
often worsen as the host inflammatory response is activated. Anticonvulsant therapy is recommended until
resolution of neurologic symptoms and patient has been seizure free for 2 years. Surgical excision is generally
recommended for intraventricular and ocular cysts. Standard precautions should be observed.
Rabies
Rabies is an almost uniformly fatal zoonotic infection caused by a rhabdovirus. While most commonly spread to
humans from dogs internationally (more than 95% of cases occur in Africa and Asia), the majority of U.S. cases
are caused by exposure to bats and wild carnivores (raccoons, skunks, foxes, coyotes). Among domesticated
animals, cats are reported as rabid three times more commonly than dogs. The incubation period is longer for bites
on the distal extremities than on the trunk or face. The two major clinical syndromes are furious and paralytic
rabies; each lasts approximately 2 to 10 days. Furious rabies consists of hyperesthesia at the bite site, agitation,
confusion, hallucinations, aerophobia, and hydrophobia; in the absence of an exposure history, early symptoms can
be difficult to differentiate from psychiatric illness. Paralytic rabies (approximately 30% of all cases) begins with
paresis of the muscles surrounding the bite site and progress to generalized paralysis. This form often is
underreported. There are a few case reports of rabies survivors (protocol available at www.mcw.edu/rabies ), but
treatment generally is supportive; contact precautions should be used. Pre-exposure prophylaxis with the rabies