An unexpected cause of fever and seizures

Abstract

In June, 2007, a 27-year-old man was brought to our emergency department by ambulance, having regained consciousness after a generalised tonic-clonic seizure. He had been having fever, chills, and rigors, on alternate days, for the previous 8 days. He had no past history of convulsions, head injury, febrile convulsions during infancy, birth trauma, meningitis, encephalitis, or psychiatric illness. There was no other past medical history of note. Until he fell ill, he had been working in a jewellery shop in Surat, Gujarat—a city where both falciparum and vivax malaria are endemic. On examination, nothing abnormal was found. The patient’s full blood count was normal; biochemistry tests, including a blood glucose measurement, also gave unremarkable results. Electrocardiography, ophthalmoscopy, examination of the cerebrospinal fl uid, and CT of the head all showed nothing of note. However, examination of the blood fi lm showed trophozoites of Plasmodium vivax, at a density of 16 200 per μL (fi gure). A rapid diagnostic test (FalciVax, Zephyr Biomedical Systems, Goa, India) indicated the presence of parasite lactate dehydrogenase, specifi c to P vivax, and the absence of histidine-rich protein 2, specifi c to P falciparum. 6 h after he arrived, the patient had another generalised seizure. He was immediately given intravenous quinine, as per the WHO guidelines for severe vivax malaria; in addition, anticonvulsant drugs were given. Over the next 12 h, the patient had a total of eight generalised seizures, with intervals of 30–120 min, without regaining full consciousness. 48 h after treatment began, the fever subsided, and the patient became fully conscious. Further blood tests—for dengue fever, leptospirosis, and HIV—gave negative results; repeat CT of the head, and electroencephalography, showed nothing remarkable. PCR, which was done as described by Kochar and colleagues, confi rmed that the patient had been infected by P vivax, but not P falciparum. The patient was discharged 8 days after his arrival. When last seen, in August, 2007, he was entirely well. P falciparum is known to cause cerebral malaria, which can manifest with seizures. The parasite multiplies in red blood cells, which adhere to the walls of small blood vessels, causing reduced cerebral blood fl ow. P vivax is less likely than P falciparum to cause severe illness— indeed, the typical 48 h interval between fevers, and benign course, have led to vivax malaria being termed “benign tertian malaria”. Classically, P vivax has not been thought to cause cerebral malaria. However, it is now known that severe P vivax infection can cause cerebral malaria—although, to our knowledge, this is the fi rst case in which the cause of seizures has been confi rmed as P vivax alone. How P vivax causes cerebral malaria is unclear, but recent studies indicate that the mechanism may be similar to that triggered by P falciparum. Other causes of seizures in malaria include hypoglycaemia, hyponatraemia, lactic acidosis—and other illnesses, such as epilepsy.