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.
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