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Case Reports

Indian Pediatrics 2007;44:433-434 

Plasmodium vivax Cerebral Malaria

 

Rajoo Thapa
Vikram Patra
Ritabrata Kundu

From the Department of Pediatrics, The Institute of Child Health, 11, Dr. Biresh Guha Street,
Kolkata 700 017, India.

Correspondence to: Dr. Rajoo Thapa, The Institute of Child Health, 11, Dr. Biresh Guha Street,
Kolkata 700 017. E-mail: [email protected]

Manuscript received: August 18, 2006; Initial review completed: October 10, 2006;
Revision accepted: January 24, 2007.

Abstract:

We report two cases of Plasmodium vivax malaria (both aged 12 years) complicated by seizures and symptoms of diffuse meningoencephalitis. One had predominantly meningeal signs while in the other, purely encephalitis features were present. Both cases were treated with artesunate. Rarely, cerebral malaria is a presenting complication or occurs during the course of P. vivax infection.

Key words: Cerebral malaria, Meningoencephalitis, Plasmodium vivax, Seizures.

Cerebral malaria is usually secondary to P. falciparum infection. However, there are infrequent reports of cerebral malaria associated with P. vivax infection. To our knowledge, only 45 cases of central nervous system P. vivax malaria are reported in the English literature since 1920; about half of these cases have occurred in children(1,2).

Case Report

Two boys, each aged 12 years presented with high grade intermittent fever of more than 4 days duration. Both of them were in altered conscious-ness at the time of admission. There was history of generalized tonic clonic convulsion prior to admission in each case. Both were severely dehydrated. Their capillary blood sugar level was normal at presentation. Beside these, the differentiating features between the two are depicted in Table 1.

TABLE I

Differentiating Features Between the Two Cases
  Case 1 Case 2
Presenting features: 1.Deteriorating 1.  Unconsciousness at the time of admission
  2. consciousness for 24 hr Generalized convulsion-1 2. Generalized convulsion-3 episodes
  episode  
  3. Retention of urine 3. Recovery  – 15 hrs
  4. Recovery  – 10 hr
Examination at presentation: EMV score – 11 EMV score – 5
  Meningeal signs present Meningeal signs absent
  Plantars – extensor bilaterally Plantars – extensor bilaterally
  Pupils – normal Pupils – mid dilated
  Liver – 1 cm palpable No hepatosplenomegaly
  Spleen – 6 cm palpable
Investigations: Hemoglobin – 6 g% Hemoglobin – 13.7 g%
  Renal parameters: normal Urea and creatinine: increased

 

In both the cases, routine count, liver function tests and serum electrolytes were within normal limits. Peripheral blood smear revealed trophozoites of P. vivax. Antigen test (OptiMAL) for P. vivax was positive while that for P. falciparum was negative in both the cases. Their cerebrospinal fluid and electroencephalogram (EEG) findings were normal. They were put on supportive therapy and intravenous artesunate in the recommended dose. Repeat blood smear after 2 days showed clearance of the parasite. Both were discharged in a clinically stable condition and advised primaquine for 14 days. Follow up after one month showed no residual neurological deficit.

Discussion

Organ dysfunction characteristic of P. falci-parum malaria is unusual in P. vivax infections. Any patient infected with P. vivax who exhibits severe malaria is presumed to be suffering from mixed infection(2). However, that may not be always true. As evident from the present report, P. vivax infection can also present as cerebral malaria.

Clinical data provided by Kochar, et al. indicates that P. vivax can cause both sequestration-related and non-sequestration related complications of severe malaria, all of which are commonly associated with P. falciparum infections(3). The exact pathogenetic mechanism however remains elusive. Sachdev and Mohan(4) studied the clinico-laboratory profile of six patients with vivax cerebral malaria. The presenting features were of an acute febrile encephalopathy, convulsions and coma. Focal neurological signs were observed in one patient. Ozen, et al.(1) have recently described a case of cerebral vivax malaria that presented with status epilepticus.

Some experts also suggest that cerebral malaria subjects might have an underlying seizure disorder and those seizures are precipitated by the high fever associated with the disease.

Contributors: RT–diagnosis, manuscript design and writing; VP–data compilation and manuscript drafting and RK–guarantor, overall co-ordinator and guide.

Funding: None.

Competing interest: None stated.

 

 References

 

1. Ozen M, Gungor S, Atambay M, Daldal N. Cerebral malaria owing to Plasmodium vivax: case report. Ann J Pediatr 2006; 26: 141-144.

2. White NJ. Malaria. In: Cook GC, Zumla AI, eds. Manson’s Tropical Diseases. 21st edn. London: Elsevier Saunders; 2002; 1205-1278.

3. Kochar DK, Saxena V, Singh N, Kochar SK, Kumar SV, Das A. Plasmodium vivax malaria. Emerg Infect Dis 2005; 11: 132-134.

4. Sachdev HPS, Mohan M. Vivax cerebral malaria. J Trop Pediatr, 1985; 31: 213-215.

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