Facial Diplegia in<i>Plasmodium vivax</i>Malaria

Fever and diarrhea developed in a 34-year-old Swiss man two weeks after his return from Madagascar. Before his visit he had not taken any prophylactic antimalarial drugs. Despite self-treatment with ciprofloxacin and metronidazole, he remained febrile. He also reported hematuria and dark urine. On admission, his temperature was 39.2°C and his vital signs and mental status were normal. The abdomen was tender, and the spleen was palpable 15 cm below the costal margin. The hemoglobin level was 12.4 g per deciliter, the hematocrit was 35 percent, the white-cell count was 8500 per cubic millimeter, and the platelet count was 15,000 per cubic millimeter. The creatinine level was 2.6 mg per deciliter (234 µmol per liter), the lactate dehydrogenase level was 1920 U per liter (normal, 187 to 443), and the bilirubin level was 11.5 mg per deciliter (197 µmol per liter); the results of other liver-function tests were in the normal range. Examination of blood smears showed severe infestation with Plasmodium falciparum, with 70 to 80 percent of red cells containing up to five parasites (small ring forms) per cell (long arrow in Panel A). Other features of P. falciparum that were present included chromatin dots (arrowheads in Panel A) and appliqué forms (short arrow in Panels A and B; Wright's stain, ¬1000). About 70 percent of the neutrophils contained hemozoin (shown in a band form [long arrows] in Panel B). The patient was treated with intravenous quinine sulfate and exchange transfusions, with dramatic improvement. The degree of parasitemia fell to 65 percent after the first exchange transfusion and to 8 percent after the second. The patient's course was complicated by acute renal failure, the acute respiratory distress syndrome, and spontaneous rupture of the spleen, necessitating continuous hemofiltration, mechanical ventilation, and laparotomy with splenectomy. Despite these complications , the patient was able to return home within three months and was well at the last follow-up visit.

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“…; Sim et al . ), acute inflammatory polyneuropathy (Chakravarty et al . ), acute disseminated encephalomyelitis (Koibuchi et al .…”

Section: Section 13: Severe Vivax Malariamentioning

confidence: 99%

Severe Malaria

2014

Tropical Med Int Health

465

354

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“…It has been postulated that malaria parasite may damage the peripheral nerves by vascular occlusion, thus causing anoxic stagnation in the vasa nervosum, which may lead to temporary demyelination and recovery after disappearance of the parasitemia and establishment of normal blood flow in the vasa nervosum [8]. In malaria, asexual-stage infections are accompanied by the release of cytokines and other immunological mediators that may mimic Guillain-Barre syndrome [9,13].…”

Section: Discussionmentioning

confidence: 99%

“…Recovery of facial paralysis due to Bell's palsy begins within three weeks of onset of the illness with complete recovery occurring within three to six months [7]. Sim et al, [8] reported facial diplegia in a 20 year old boy infected with Plasmodium vivax in Korea while Duque et al, [9] reported bilateral 6 th cranial nerve palsy caused by P. falciparum in a 14 year old Caucasian living in Democratic Republic of Congo. Haematological response to malaria infection has been documented.…”

Section: Introductionmentioning

confidence: 99%

Facial nerve palsy: an unusual feature of Plasmodium falciparum

Okike¹,

Ezeonu²,

Onyire³

et al. 2013

Paediatr Health

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A ten-year old boy who presented with headache, intermittent high grade fever for four days and left sided deviation of the mouth two days later. Examination revealed a fully conscious patient with an axillary temperature of 39.5 0 C and right facial nerve palsy, lower motor neuron lesion. No other obvious abnormality was detected in any of the systems. Laboratory examination showed positive Plasmodium falciparum (P. falciparum) with a density of 28,000 parasites/mm 3 . Cranial computerized tomographic scan and abdominal ultra-sonograghy revealed no abnormality. Cerebrospinal fluid (CSF) analysis showed normal cell count and chemistry. Culture yielded no growth. Retroviral screening test was negative. Complete blood count showed high monocytosis of 18%, other indexes were normal. Electrolytes, urea, creatinine and calcium levels were within normal limits. Urine, stool and blood cultures yielded no growth. Random blood sugar (RBS) and liver function test were normal. Symptoms subsided within 36 hours following administration of intravenous artesunate and oral paracetamol. Complete facial nerve recovery took seven days following clearance of parasitemia. The objective of this report is to draw the attention of clinicians to this uncommon presentation of malaria, though the patho-physiological mechanism remains unclear.

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“…Malaria can give rise to GBS like presentation or mononeuritic syndromes. Reports of such complications following Plasmodium falciparum (P. falciparum) infection have been previously reported [3][4][5][6][7] but are limited in children [4].…”

Section: Introductionmentioning

confidence: 99%

Guillain Barre Syndrome complicating Plasmodium falciparum malaria

Misra

Chakrabartty

2015

J Pediatr Infect Dis

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Neurological complications of falciparum malaria are quite common. Guillain Barre Syndrome (GBS) as a complication of malaria is rare especially in children but has been reported from other developing countries. We report a case of an 8 year old girl who had developed an ascending paralysis following an attack of Plasmodium falciparum malaria. She was diagnosed with GBS. The clinical presentation and nerve conduction velocity studies were helpful in taking a definitive approach. She was treated with immunoglobulin and improved remarkably.

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Facial Diplegia inPlasmodium vivaxMalaria

Cited by 10 publications

References 7 publications

Severe Malaria

Severe Malaria

Facial nerve palsy: an unusual feature of Plasmodium falciparum

Guillain Barre Syndrome complicating Plasmodium falciparum malaria

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