Am Fam Physician. 2000 Aug 1;62(3):507-508.
to the editor: Infection with the malaria parasite remains the most prevalent parasitic infection in the world and affects more than 400 million persons,1 with about 2.6 billion persons at risk of contracting the disease. Although malaria is primarily a disease of tropical and subtropical areas of the world, it can occur in any country because of increased global travel.2 This letter reports a case of malarial infection that illustrates the neuropsychiatric sequelae of acute and chronic malaria.
A 37-year-old man was admitted to the medicine unit of a teaching hospital after presenting with the sudden onset of fever, chills, headache, nausea, vomiting and dark urine with reduced output. In addition, he had been irritable and easily frustrated. The symptoms began seven days after he returned from a trip to West Africa.
Physical examination revealed a temperature of 38.9°C (102°F), pulse of 96 beats per minute, blood pressure of 110/71 mm Hg and respiration rate of 20 per minute. He had bilateral icterus with dry mucous membranes. Examination of the neck revealed no nuchal rigidity. The rest of the physical examination was unremarkable. The patient was cooperative but anxious, and the results of mental status examination were otherwise within normal limits.
A blood smear obtained during the emergency department examination revealed ring forms of malaria parasites consistent with Plasmodium falciparum malaria of 82,000 per μL. On admission, additional investigation revealed a white blood cell count of 8,200 per mm3 (8.2 × 109 per L), hemoglobin of 12.2 g per dL (122 g per L) and a platelet count of 18,000 per mm3 (18.0 × 109 per L). Blood urea nitrogen (BUN) was 93 mg per dL (33.0 mmol per L), and serum creatinine was 6.4 mg per dL (570 μmol per L). The lactate dehydrogenase (LDH) level was elevated at 1,624 U per L, and the aspartate aminotransferase (AST) level was 113 U per L. Total bilirubin was 13.5 mg per dL (230 μmol per L), with the direct portion being 11.2 mg per dL (192 μmol per L).
The admitting diagnosis was P. falciparum malaria complicated by acute renal failure. He was treated with intravenous doxycycline in a dosage of 100 mg twice daily and oral quinine in a dosage of 650 mg twice daily for three days. He was rehydrated with normal saline. The BUN and creatinine levels continued to fall steadily and were within normal limits two weeks after discharge from the hospital. Two weeks later, the patient noticed that he was apathetic and depressed. These feelings were accompanied by irritability, reduced appetite, insomnia, anhedonia and reduced energy. He was diagnosed as having adjustment disorder with depressed mood and was treated with brief psychotherapy.
Neurologic sequelae are well recognized with malarial infestation (especially cerebral malaria). Up to 12 percent of persons surviving cerebral malaria may have persistent neurologic abnormalities that include impaired consciousness, confusion and seizures.3 P. falciparum malaria has been associated with other self-limited neurologic deficits including cerebellar ataxia, generalized convulsions and fine postural tremors. Although the neurologic sequelae of cerebral malaria are well documented, its long-term neurocognitive effects are more controversial. The extent of central nervous system involvement may reflect the virulence of the parasite, host immune status, time of onset of symptoms to initiation of treatment or a combination of these factors.
Acute psychiatric complications that have been described in acute cerebral malaria include schizophrenic and manic syndromes, typical and atypical depression, acute anxiety attacks, acute confusional states, possession or trance-like states, delirium, amnesia, acute personality changes and twilight states.2 However, the exact causal relationship has not been fully investigated. There is no solid evidence that malaria psychosis exists.
Other psychiatric symptoms that have been described as sequelae to malaria infestation include irritability, violence, impaired memory, personality changes, anxiety and depression.1 The treatment of patients with psychiatric symptoms following malarial infestation should involve treating the acute infection aggressively. Patients with mild anxiety or depression may be treated with psychotherapy; pharmacotherapy may be required in patients with moderate and severe symptoms of depression.
1. Dugbartey AT, Dugbartey MT, Apedo MY. Delayed neuropsychiatric effects of malaria in Ghana J Nerv Ment Dis. 1998;186:183–6.
2. Osuntokun BO. Malaria and the nervous system Afr J Med Sci. 1983;12:165–72.
3. Gorbach SL, Bartlett JG, Blacklow NR, eds. Infectious disease. 2d ed. Philadelphia: Saunders,1998.
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