Most non-immune individuals present with falciparum malaria within 2 months of departure from a malaria-endemic area, but in semiimmune individuals and those taking malaria prophylaxis, symptomatic malaria may not develop for many months. The minimum time to developing symptoms after entering a malaria-endemic area is 7-8 days. Patients usually present with fever and headache but may have a variety of other symptoms, including cough, myalgia, arthralgia, abdominal pain, nausea, vomiting, diarrhoea, photophobia and altered conscious state. The fever may occur every 48 hours or continuously with intermittent peaks. The clinical presentation can vary substantially, depending on the level of parasitaemia and the immune status of the patient. Atypical presentations, leading to misdiagnosis as gastroenteritis, hepatitis or urinary infection are common. Asymptomatic parasitaemia is a frequent finding in semi-immune adults, hence the detection of parasites in peripheral blood should not abort the search for alternative causes of fever in such an individual.
P. falciparum infection may produce severe malaria with serious complications that may be ultimately fatal (Table 3.4). Severe malaria often develops very rapidly with specific complications,
Table 3.4 Severe malaria
Severe malaria is defined as P. falciparum infection with one or more of the following features:
• Repeated generalised convulsions
• Unrousable coma
• Acute respiratory distress syndrome or pulmonary oedema
• Renal impairment: creatinine >0.265 ^m/l
• Spontaneous bleeding
The following features may be indicative of severe malaria in selected patients:
• Parasitaemia > 5% and/or trophozoites/schizonts present in the peripheral blood
From World Health Organization (1990).
including cerebral malaria, severe anaemia, pulmonary oedema, blackwater fever or acute renal failure. Cerebral malaria is usually preceded by a history of fever for several days but the prodromal features may be much shorter. Manifestations include convulsions, hypertoni-city, opisthotonos, gaze palsies, delerium, psychosis and coma that sometimes develops rapidly after a fit. These features may also be caused by hypoglycaemia. Patients developing renal failure tend to be oliguric or anuric and often have other organ dysfunction, including coma, jaundice and lactic acidosis (Day et al., 1997). Blackwater fever (massive intravascular haemolysis and haemoglobinuria) is also a cause of acute renal failure. Any parasitaemia over 2% carries an increased risk of death, and para-sitaemias over 10% indicate a potentially dangerous infection irrespective of other features (White, 1996a; Stanley, 1997).
The clinical features of severe malaria depend on age and the immune status of the host (White, 1996a). In hyperendemic areas, major manifestations occur in young children (severe anaemia and cerebral malaria) and during pregnancy. Acute renal failure, jaundice and pulmonary oedema are more common in non-immune adults and hypoglycaemia, convulsions, shock and acidosis may occur at any age.
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