Complications in P. vivax Malaria

Plasmodium vivax and P. ovale infections are generally benign and complications leading to significant morbidity and mortality are uncommon.

Although P. vivax malaria is considered to be a benign malaria, it has been increasingly reported to cause various manifestations of severe disease, including thrombocytopaenia, cerebral malaria, and acute renal, hepatic and pulmonary dysfunctions, with some reports of deaths. With increasing reports of drug resistance, this indeed is a cause for concern. The underlying mechanisms of severe manifestations are not well understood. Prompt and effective treatment and case management should be the same as for severe and complicated falciparum malaria.

The clinical symptoms of fever, headache, nausea and vomiting in P. vivax may be incapacitating, particularly for those who are non-immune and suffering the infection for the first time.

Rupture of spleen: Malaria is an important cause for spontaneous rupture of spleen. It is more common in vivax malaria than falciparum malaria and tends to occur in up to 0.7% of the patients.

Rupture occurs in acute, rapid, hyperplastic enlargement of spleen. It is rare in chronic malaria, despite massive enlargement. Rapid enlargement results in increased capsular tension and increased parenchymal friability.  Marked splenomegaly can occur even in low-grade parasitemia (50/ml) and it may persist for weeks or months after effective and complete treatment.

Patients present with abdominal pain, fever, tachycardia, prostration and rapidly developing anemia and hypotension. Some of these manifestations are seen in malaria itself and therefore splenic rupture can be easily missed. A degree of suspicion is required to differentiate the two conditions. Leukocytosis, severe anemia and hypotension are more in favour of splenic rupture. Ultra sound evaluation of abdomen and paracentesis of the abdomen can confirm the diagnosis.

Treatment includes replacement of fluid and blood, laparotomy and splenectomy.

Splenic rupture carries a high mortality of about 80% and this is partly attributed to lack of awareness and missed diagnosis.

Hepatic dysfunction: Hepatomegaly and non-specific hepatitis, with or without jaundice can occur in vivax malaria. Fever, jaundice, tender hepatomegaly, mild elevation in the levels of hepatic enzymes and bilirubin are observed. Liver biopsy in such cases has demonstrated brown malarial pigments in Kupffer’s cells, small to moderate sized granulomatous lesions with mononuclear infiltration and hepatocyte necrosis.

Liver function returns to normal shortly after antimalarial treatment.

Thrombocytopenia: Decrease in platelet counts can occur in vivax malaria, however, it is usually mild and bleeding does not occur.

Severe anemia: P. vivax can cause severe anemia, particularly when it is chronic and recurrent. Very rarely this can be life threatening or even fatal.

CNS manifestations: Changes in behaviour, altered sensorium, seizures, cerebral malaria, cerebellar manifestations and ataxia, hemiparesis,  aphasia, psychosis, acute inflammatory demyelinating polyneuropathy and post-malaria neurologic syndrome causing bilateral facial paralysis have all been reported in P. vivax malaria and some of these cases have had multiorgan involvement.

New paper

  1. Kochar DK, Das A, Kochar SK. Severe Plasmodium vivax malaria: A report on serial cases from Bikaner in Northwestern India. Am. J. Trop. Med. Hyg. 2009;80(2):194-198.
  2. Andrade BB, Reis-Filho A, M Souza-Neto S. Severe Plasmodium vivax malaria exhibits marked inflammatory imbalance. Malaria J 2010;9:13. doi:10.1186/1475-2875-9-13 At
  3. Tilluckdharry CC, Chadee DD, Doon R, Nehall J. A case of vivax malaria presenting with psychosis. West Indian Med J. Mar 1996;45(1):39-40.
  4. Taksande B, Jajoo U, Jajoo M. Cerebellar Malaria: A Rare Manifestation of Plasmodium vivax. The Internet Journal of Neurology. 2007;7(1)
  5. AM Taksande, KY Vilhekar Cerebellar Malaria Due to Plasmodium vivax in a Child. Iranian J Parasitol 2008;3(2):57-59. Full Text at
  6. Thapa R, Ranjan R, Patra VS, Chakrabartty S. Childhood Cerebral Vivax Malaria With Pancytopenia. Journal of Pediatric Hematology/Oncology. February 2009;31(2):116-117. doi: 10.1097/MPH.0b013e318186855a
  7.  Beg MA, Khan R, Baig SM, Gulzar Z, Hussain R, Smego RA Jr,. Cerebral involvement in benign tertian malaria. Am J Trop Med Hyg 2002;67:230–232.
  8. Sachdev HS, Mohan M. Vivax cerebral malaria. J Trop Pediatr 1985;31:213–215.
  9. Rajoo Thapa, Vikram Patra, Ritabrata Kundu. Plasmodium vivax Cerebral Malaria. Indian Pediatrics 2007;44:433-434. Full Text at
  10. Ozen M, Gungor S, Atambay M, Daldal N. Cerebral malaria owing to Plasmodium vivax: case report. Ann J Pediatr 2006;26:141-144
  11. Suman Sarkar, Prithwis Bhattacharya. Cerebral malaria caused by Plasmodium vivax in adult subjects. Indian J Crit Care Med. Oct–Dec 2008;12(4):204–205. doi: 10.4103/0972-5229.45084. Full Text at
  12. Anupkumar R. Anvikar, Dinesh K. Singh, Ruchi Singh, Aditya P. Dash, Neena Valecha. Vivax malaria presenting with cerebral malaria and convulsions. Acta Parasitologica March, 2010;55(1):96-98. DOI 10.2478/s11686-010-0013-7
  13. Mishra VN, Singh D. Cerebral malaria by Plasmodium vivax. J Assoc Physicians India. 1989 Jun;37(6):411.
  14. Parakh, A, Agarwal N, Aggarwal A, Aneja A. Plasmodium vivax malaria in children: uncommon manifestations. Annals of Tropical Paediatrics: International Child Health. December 2009;29(4):253-256.
  15. RK Patial, D Kapoor, JK Mokta. Cerebral dysfunction in vivax malaria: a case report. Ind J Med Scs. 1998;52(4):159-60.
  16. Khurshid Ahmad Abbasi, Shabir Ahmed Shaikh. Comparative study of Cerebral Malaria due to Plasmodium vivax and Falciparum. Pak Paed J Dec 1997;21(4):155-158.
  17. Jeanne R. Poespoprodjo et al. Vivax Malaria: A Major Cause of Morbidity in Early Infancy. Clinical Infectious Diseases 2009;48:1704–1712 Available at

 © ©BS Kakkilaya | Last Updated: Mar 11, 2015

One Comment:

  1. Interesting study. If it weren’t for the association with malraia endemicity apparently attested in Africa and Europe, the pure gene evolution would point to a migration out of America (ancestral state) through East Asia to Europe and Africa (derived state). India is a bridge between the east and the West and a “swing” continent. Africa still preserves the original state in some pockets such as Madagascar, Horn of Africa and northwest Africa but overall it has shifted away from the original condition. But even with the malraia association in Africa and Europe this scenario would work.The map of Hbs distribution reminds me of Y-DNA YAP+ distribution, with Africa being heavy on YAP+ but with pockets of YAP-, Europe intermediary and Asia showing a strange small pocket of YAP+. India has Hbs, Tibetans and Andaman islanders have high frequencies of YAP+. America is devoid of YAP+ completely. There’s a parallelism here, I think.

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