Published on 10/04/2015 by admin

Filed under Neurology

Last modified 10/04/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 5 (1 votes)

This article have been viewed 2373 times



In 1909 John D. Rockefeller declared, “Deprivation in the agriculturally rich Southern States is not due to stupidity or laziness, but to parasite infestation.”1 The human immunodeficiency virus pandemic and global warming have resurrected the study of parasitology. In general, parasitic diseases are treatable and should be considered when geography, patient susceptibility, and exposure make infection possible.

More than 2 million people die each year of falciparum malaria; 200 million are infected with schistosomiasis. Toxoplasma species flourish in patients with acquired immunodeficiency syndrome (AIDS). Epilepsy from neurocysticercosis affects more than 1% of the population in some regions. Most cases of neurocysticercosis in Mexico remain undiagnosed despite the people having cognitive and psychiatric problems throughout life. Sleeping sickness affects 300,000 Africans and threatens many more. Intestinal helminths dull children’s minds.2

This chapter addresses the major neuroparasites, as is customary in the neurosciences, by location and clinical presentation. The aim is to present the clinician with a catalog of possibilities so that a treatable disease is not overlooked (Table 94-1).

TABLE 94-1 Clinical Findings Associated with Neuroparasites

CSF, cerebrospinal fluid; MRI, magnetic resonance imaging.

The pathophysiology of parasites illustrates how they have adapted to evade the host’s immune system through pleomorphism and antigenic variation (malaria and sleeping sickness) or how they avoid killing their host to ensure their survival (hookworms). Parasites stimulate the secretion of prostaglandins, nitric oxide, and interleukin-10, which downregulate the immune response (Plasmodium, Trypanosoma, and Toxoplasma), ensuring their quiet multiplication and perhaps teaching us how to find and eliminate them when they cause disease.

Amebic Encephalitis

Various features of primary amebic meningoencephalitis (a fulminant encephalitis) and granulomatous amebic encephalitis (a subacute granulomatous disease) are summarized in Table 94-2.

TABLE 94-2 Central Nervous System Amebiasis

Feature PAM GAE
Risk factors Swimming Diabetes, pregnancy, alcohol/cirrhosis, corticosteroids, AIDS, chemotherapy/radiotherapy
Organism Naegleria Acanthamoeba27,28
Route to CNS Olfactory epithelium/nerves Intranasal/intracranial vasculitis leading to thrombosis and infarction
CNS disease Culture-negative, fulminant, purulent meningitis; mostly PMN, unlike TB or viral Focal or diffuse encephalitis with meningism, giant cell reaction29
Organism can harbor Yes30 Yes
Legionella, Vibrio cholerae
CSF laboratory findings Glucose variable; protein >1 g/L Glucose variable
CSF microscopic findings Motile Naegleria move 1-3 body lengths/min11 Lymphocytic pleocytosis; trophozoite seldom found in CSF31,32

AIDS, acquired immunodeficiency syndrome; CNS, central nervous system; CSF, cerebrospinal fluid; GAE, granulomatous amebic encephalitis; PAM, primary amebic meningoencephalitis; PMN, polymorphonuclear neutrophils; TB, tuberculosis.

African Trypanosomiasis

Clinical Presentation

A painful chancre is seen in approximately 50% of patients infected with T. b. rhodesiense but is seldom seen in patients infected with T. b. gambiense. The chancre is more common in non-Africans. It develops 5 to 15 days after the bite and heals in 3 to 4 weeks. It occasionally ulcerates and may be associated with regional lymphadenopathy.

The first stage of illness is associated with intermittent fever, headache, intense pruritus, facial edema, ocular symptoms, and arthralgia. Posterior cervical lymphadenopathy (Winterbottom’s sign) is prominent in T. b. gambiense infections. This is followed by an asymptomatic phase for several months or years.

The second stage, the meningoencephalitic stage, occurs after months to years (earlier with T. b. rhodesiense infections) and is associated with various neurological abnormalities. The parasite is found in the basal ganglia of laboratory animals, which is confirmed with magnetic resonance imaging in case reports. Fasciculations, tremor, rigidity, chorea, and ataxia are observed. Typically, the patient complains of severe frontal head pain, tremors, delayed hyperesthesia (Kerandel sign, which is pain elicited by a tap on a tendon and is common in Caucasians), pronounced lethargy, and day-night inversion (sleeping sickness). Cognitive decline is common, with memory loss, dementia, depression, agitation, and hallucinations. In addition, T. b. rhodesiense can cause myocarditis, pericardial effusion, and heart failure.


If CSF is positive for leukocytes and IgM concentrations are high, melarsoprol (a trivalent arsenic compound) is the drug of choice (Table 94-3). Relapse rates are high, and up to 20% of patients infected with T. b. gambiense do not respond to melarsoprol. Eflornithine is an alternative therapy for infections from T. b. gambiense but not from T. b. rhodesiense. Melarsoprol may cause post-treatment reactive encephalopathy in up to 10% of cases, with a mortality rate of 50%. Thus, the overall mortality from melarsoprol is 5% from arsenic encephalopathy.

TABLE 94-3 Treatment of Trypanosoma brucei gambiense and Trypanosoma brucei rhodesiense Sleeping Sickness*

Stage West African (T. b. gambiense) East African (T. b. rhodesiense)
Early stage
Endemic countries According to national legislation or guidelines According to national legislation or guidelines
Other countries Pentamidine isethionate, 4 mg/kg body weight daily or on alternate days for 7 to 10 days intravenously or intramuscularly Suramin, test dose of 4-5 mg/kg body weight at day 1, followed by 5 injections of 20 mg/kg body weight every 7 days (e.g., days 3, 10, 17, 24, 31); the maximum dose per injection is 1 g
Late stage
Endemic countries According to national legislation or guidelines According to national legislation or guidelines
Other countries If available: eflornithine, 100 mg/kg body weight at 6-hour intervals for 14 days (150 mg/kg body weight in children) by short infusions over a period of at least 30 minutes Eflornithine not recommended (low efficacy38)
Alternative: melarsoprol, 3 series of 3.6 mg/kg body weight at 24-hour intervals for 3 days; the series are spaced by intervals of 7 days Melarsoprol,§ 1 series of 1.8, 2.16, 2.52 mg/kg body weight at 24-hour intervals; 1 series of 2.52, 2.88, 3.25 mg/kg body weight at 24-hour intervals; and 1 series of 3.6, 3.6, 3.6 mg/kg body weight at 24-hour intervals; the series are spaced by intervals of 7 days (the maximum dose is 5 mL)

* No firm recommendations exist for the use of the trypanocidal drugs; the schedules indicated are those most commonly used. A concise treatment schedule for treatment of T. b. gambiense sleeping sickness consisting of 10 days of melarsoprol, 2.2 mg/kg body weight daily, is under final evaluation.39,40 Note: This 10-day schedule must not be used for treatment of T. b. rhodesiense sleeping sickness, because there are no data available.

Very slow intravenous injection or short infusion, only under well-controlled circumstances.

The concomitant application of 1 mg/kg body weight prednisolone has been shown to reduce the incidence of encephalopathic syndromes in one large-scale clinical trial.41

§ A single dose of Suramin is often applied before the stage determining lumbar puncture.

From Burri C, Brun R: Human African trypanosomiasis. In Cook GC, Zumla AI, eds: Manson’s Tropical Diseases, 21st ed. Edinburgh: Saunders, 2003, pp 1303-1323. Used with permission.

A lumbar puncture should be performed 1 day after a course of therapy for late-stage disease. All patients should be monitored for 2 years with lumbar punctures every 6 months. A relapse is suspected if the CSF cell count is more than 20 cells/μL. Reinfection is likely when CSF has more than 50 cells/μL, when the count has doubled since the previous count, or when there are 20 to 49 cells/μL in a symptomatic patient.25,39

Cysticercus of Taenia solium


On the basis of autopsy findings in Mexico, most cases of neurocysticercosis remain undiagnosed despite the patient having cognitive and psychiatric problems throughout life. Subcutaneous cysts are palpable. In striated muscle, they rapidly calcify and may be noted on imaging studies. Stool examination is unrewarding. Peripheral eosinophilia is inconsistent and nonspecific.

Blood and CSF serological analyses have improved. Many clinicians use the enzyme-linked immunoelectrotransfer blot (EITB) assay. It derives from coproantigens of adult T. solium and ignores nonspecific bands of antigen. EITB results may revert to negative after the cysticercus dies. The assay is not always readily available. In the blood, sensitivity is 92.5% and specificity is 100%. However, EITB sensitivity has been reported to be as low as 28% in subjects with a single parenchymal lesion, as is commonly seen in India.46 EITB sensitivity may be less in CSF.47

Enzyme-linked immunosorbent assay (ELISA) is based on crude antigen to cysticercal fluid. It is inexpensive and rapid. ELISA cross-reacts with other cestodes (other taeniae and echinococci). It seems more sensitive in CSF (sensitivity, 62% to 90%; specificity 98% to 100%) than in blood.

The diagnosis requires neuroimaging, with the goal of identifying the scolex (2 to 3 mm). Only since the frequent use of computed tomography in the 1980s has cysticercosis emerged as the most common cause of epilepsy in many areas. (Cerebral malaria is likely the most common cause of febrile seizures.) Magnetic resonance imaging may show a diagnostic invaginated scolex but not show the calcific stage, for which computed tomography is best. Magnetic resonance imaging can show ventricular cysts. In brain parenchyma, the cysts mature in 3 months to 10mm in size (occasionally up to 20mm); in the ventricles, they can exceed 5 cm. Therefore, serum EITB, CSF ELISA, and neuroimaging have become useful diagnostic tools48,49 (Figs. 94-1 through 94-7).


Figure 94-1 Inactive form (nodular stage) of cysticercosis. Axial computed tomography shows small calcification in the left occipital lobe.

(From Castillo M: Imaging of neurocysticercosis. Semin Roentgenol 2004; 39:465-473. Used with permission.)