Neurologic Infections in Travelers

Malveeka Sharma, MD, MPH; Joseph R. Zunt, MD, MPH

Disclosures

Semin Neurol. 2019;39(3):399-414. 

In This Article

Malaria (Cerebral)

Epidemiology

Malaria is a mosquito-borne parasitic disease caused by the genus Plasmodium. Cerebral malaria is typically caused by Plasmodium falciparum and is one of the most severe and potentially fatal manifestations of malaria, with a mortality rate of 10 to 15%.[7] Cerebral malaria is defined as a comatose state lasting greater than 1 hour after resolution or control of fever, seizure, and hypoglycemia with evidence of asexual forms of P. falciparum on peripheral blood smear.[15] Sub-Saharan Africa carries the greatest burden of disease and mortality.

Life Cycle, Ecology, and Species

The Plasmodium parasite infects the human host via the bite of an infected female Anopheles mosquito. In mice models and postmortem analysis of Malawian children, a red blood cell infected by P. falciparum adheres and sequesters to brain vascular endothelium, leading to disruption of the blood–brain barrier, increased vasoconstriction, reduced cerebral blood flow, and vascular obstruction.[16]

Clinical Manifestations and Neurologic Symptoms

In endemic regions of sub-Saharan Africa, young children present with prodromal symptoms, followed by coma, cerebral edema, and status epilepticus.[7] In adults, the onset is more insidious over days and accompanied by multisystem complications. Seizures are not common in adults with cerebral malaria.[15] Survivors of the acute illness are prone to developing neurological deficits. At time of discharge, 6 to 29% children have neurological deficits, including cognitive difficulties, and language and behavioral problems being the most common. In adults, the prevalence of neurological sequelae is 3 to 10%, and includes psychosis, cerebellar ataxia, and extrapyramidal deficits.[17]

Diagnosis

The diagnostic gold standard is identification of the parasite on thick and thin blood film microscopy; however, immunochromatographic testing is also commonly used.[17] Positive findings of these rapid tests may not be diagnostic, as many patients in endemic areas may have incidental parasitemia. Evidence of malarial retinopathy has over 90% sensitivity and specificity for cerebral malaria.[7] Neuroimaging can demonstrate cerebral swelling, cortical infarcts, and hyperintensities in white matter, all of which are nonspecific.[17] Lumbar puncture is recommended to rule out other causes of disease.

Treatment

Cerebral malaria is a neurologic emergency. Treatment with an antimalarial medication is the mainstay, but a supportive treatment of complications is also very important. Parenteral antimalarial medications, artesunate or cinchoids (quinine or quinidine), should be started within 48 hours.[17] Seizures and status epilepticus should be treated emergently with intravenous (IV) or intramuscular (IM) benzodiazepines. Of note, IM phenobarbital was associated with higher mortality in African children, and fosphenytoin/phenytoin was ineffective in reducing seizure frequency in pediatric cerebral malaria.[7] Cerebral malaria is often associated with dysfunction of other organs and systems, and can produce severe anemia, hypoglycemia, acute renal failure, hepatic impairment, and coagulation disorders.[17] Malaria prevention has been at the forefront of many major nongovernmental organizations, with efforts focused on reducing vector burden, new drug regimens and reducing resistance, and national surveillance systems.[18]

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