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9. Treatment of malaria caused by P. vivax, P. ovale or P. malariae

that have been reported are cerebral malaria, severe anaemia, severe thrombocytopenia
and pancytopenia, jaundice, splenic 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 fully understood. Prompt
and effective treatment and case management should be the same as for severe and
complicated falciparum malaria (see Section 8).

9.5 treatment of malaria caused by P. ovale and P. malariae

Resistance of P. ovale and P. malariae to antimalarials is not well characterized
and infections caused by these two species are considered to be generally sensitive
to chloroquine. Only one study, conducted in Indonesia, has reported resistance to
chloroquine in P. malariae. The recommended treatment for the relapsing malaria caused
by P. ovale is the same as that given to achieve radical cure in vivax malaria, i.e. with
chloroquine and primaquine. P. malariae should be treated with the standard regimen
of chloroquine as for vivax malaria, but it does not require radical cure with primaquine,
as no hypnozoites are formed in infection with this species.

9.6 monitoring therapeutic efficacy for vivax malaria

The antimalarial sensitivity of vivax malaria needs monitoring to track and respond
to emerging resistance to chloroquine. The 28-day in vivo test for P. vivax is similar to
that for P. falciparum, although the interpretation is slightly different. Genotyping can
distinguish a relapse or recrudescence from acquisition of a new infection, but it is not
possible to distinguish reliably between a relapse and a recrudescence as they derive
from the same infection. Relapse is unlikely if parasitaemia recurs within 16 days of
administering treatment but, after that time, relapse cannot be distinguished from a
recrudescence. Any P. vivax infection that recurs within 28 days, whatever its origin,
must be resistant to chloroquine (or any other slowly eliminated antimalarial) provided
adequate treatment has been given. In the case of chloroquine, adequate absorption can
be confirmed by measurement of the whole blood concentration at the time of recurrence.
Any P. vivax infection that has grown in vivo through a chloroquine blood concentration
of > 100 ng/ml must be chloroquine resistant. Short-term in vitro culture allows assessment
of in vitro susceptibility. There are no molecular markers yet identified for chloroquine
resistance. Antifolate resistance can be monitored by molecular genotyping of the gene
that encodes dihydrofolate reductase (Pvdhfr). Since ACTs are increasingly being used
for the treatment of vivax infections in situations where it is resistance to chloroquine,
the sensitivity of P. vivax to ACTs must also be routinely monitored.

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