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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 may still cause a severe and debilitating febrile
illness.
The clinical symptoms of
fever, headache, nausea and vomiting may be incapacitating, particularly for those who are
non-immune and suffering the infection for the first time.
It can also very occasionally result in severe disease as in
falciparum malaria. Severe vivax malaria manifestations that have
been reported are cerebral malaria, severe anaemia, severe
thrombocytopenia and pancytopenia, jaundice, spleen rupture, acute
renal failure and acute respiratory distress syndrome. Severe
anaemia and acute pulmonary oedema are not uncommon. 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.
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 and level of sensorium can occur in P. vivax malaria. Frank cerebral
malaria does not occur and if present, it should prompt a search for other causes, most
commonly an associated P. falciparum infection. Some of the C.N.S. manifestations
could be caused by chloroquine also.
Quartan malarial
nephropathy: In areas where P. malariae is prevalent, there is
epidemiological evidence to link P. malariae infection to immune-complex mediated
glomerulonephritis, leading to nephrotic syndrome. Because only a few of the infected
develop nephrosis, it is possible that other factors are also involved in the pathogenesis
of this entity. Histologically there is progressive focal and segmental glomerulosclerosis
with fibrillary splitting or flaking of the capillary basement membrane, producing
characteristic lacunae. Dense subendothelial deposits are seen on electron microscopy and
immunofluorescence reveals deposits of compliments and immunoglobulins. In about 25% of
patients P. malariae antigen may also be seen.
Patients usually present by the age of 15
years with typical features of nephrotic syndrome.
Treatment with antimalarial drugs,
corticosteroids or cytotoxic agents may not be useful.
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