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Plasmodium
vivax, the second most important species causing human malaria,
accounts for about 40% of malaria cases worldwide and is the
dominant malaria species outside Africa. It is prevalent in endemic
areas in the Middle East, Asia, Oceania and Central and South
America. In Africa, it is rare except in the Horn and it is almost
absent in West Africa. The other
two human malaria parasite species P. malariae and P. ovale are generally less
prevalent but are distributed worldwide, especially in the tropical areas of Africa.[1]
Go to
Treatment of Uncomplicated
P. falciparum |
Treatment of Severe Malaria
Treatment of clinical infection:
P. vivax is generally very
sensitive to chloroquine, although resistance is prevalent and increasing in some
areas, notably Oceania, (Irian
Jaya, Myanmar, Papua New Guinea and Vanuatu), Indonesia and Peru. Resistance to pyrimethamine has increased rapidly in some areas, and sulfadoxine-pyrimethamine
is consequently ineffective. P. vivax is sensitive to all the other antimalarial drugs; it is more
sensitive than P. falciparum to the artemisinin derivatives, and slightly less
sensitive to mefloquine (although mefloquine is still effective). However, artesunate + sulfadoxine-pyrimethamine may
not be effective against P. vivax in many areas owing to the resistance
to pyrimethamine.[1]
Both
P. ovale and P. malariae are regarded as very sensitive to chloroquine, although there is a single recent report of chloroquine resistance
in P. malariae. These species are also
susceptible to amodiaquine, mefloquine and the artemisinin derivatives.[1]
Prevention of relapses:
P. vivax and
P. ovale form hypnozoites, parasite stages in the liver that can result in
multiple relapses of infection, weeks to months after the primary infection. Therefore, treatment
of P. vivax and P. ovale infections should be aimed at
curing both the blood stage and the liver stage infections, and
thereby preventing both relapse and recrudescence. The only drugs
with significant activity against the hypnozoites are the 8-aminoquinolines
like primaquine. A combination of chloroquine + primaquine will
therefore provide
radical cure.
The frequency and pattern of relapses varies geographically.
Whereas 50–60% of P. vivax infections in South-
East Asia relapse, the frequency is lower in Indonesia (30%) and the Indian
subcontinent (15–20%). Some P. vivax infections in the Korean peninsula
have an incubation period of nearly one year. It appears that the total dose of 8-aminoquinoline
given is the main determinant of curative efficacy against liver-stage infection.
There is no evidence that the short courses of primaquine widely recommended
(such as 5-day regimens) have any efficacy. Primaquine should be given for 14
days. The usual adult oral dose is 15 mg base (0.25 mg/kg bw per day) but in
South-East Asia, particularly Indonesia, and in Oceania, higher doses (0.5 mg
base/kg bw per day) are required. Primaquine causes abdominal discomfort
when taken on an empty stomach; it should always be taken with food.
In low-transmission areas, the benefits of deploying primaquine are considered to exceed the risks, but in areas of sustained high
transmission (such as on the island of New Guinea), P. vivax infection is very
frequent, immunity is acquired, and the risks of widespread deployment of
primaquine are considered to outweigh the benefits.
Primaquine is an oxidant and causes
variable haemolysis in G6PD-deficient individuals. As primaquine is
is eliminated rapidly, haemolysis is self-limiting provided no further
medicine is taken. Screening for G6PD deficiency is not generally available
outside hospitals, although rapid tests are under development. If a patient is known to be severely
G6PD deficient, then primaquine should not be given. For the majority of
patients with mild variants of the deficiency, primaquine should be given in
a dose of 0.75 mg base/kg bw once a week for 8 weeks. If significant haemolysis
occurs on treatment, then primaquine should be stopped.[1]
Treatment of P. vivax and P. ovale infections:
Chloroquine 25 mg base/kg bw divided over 3 days, combined with
primaquine 0.25 mg base/kg bw, taken with food once daily for 14
days is the treatment of choice for chloroquine-sensitive infections.
In Oceania and South-East Asia the dose of primaquine should be
0.5 mg/kg bw.[1]
|
Treatment of P.
vivax, P. ovale, P.
malariae Infections[1,2] |
| Age
in years |
Dose of Chloroquine (as base)
(Each 250 mg tablet contains 150 mg base and
each 5 ml of suspension contains 50 mg base) |
Dose of Primaquine
For 14 days
(P.
vivax and P. ovale only) |
| 1st dose (Tab) |
2nd dose (Tab) |
3rd dose (Tab) |
4th dose (Tab) |
| 0-1 |
75 mg (½) |
37.5 mg (¼) |
37.5 mg (¼) |
37.5 mg (¼) |
Nil |
| 1-5 |
150 mg (1) |
75 mg (½) |
75 mg (½) |
75 mg (½) |
2.5 mg |
| 5-9 |
300 mg (2) |
150 mg (1) |
150 mg (1) |
150 mg (1) |
5 mg |
| 9-14 |
450 mg (3) |
225 mg (1½) |
225 mg (1½) |
225 mg (1½) |
10 mg |
| >14 |
600 mg (4) |
300 mg (2) |
300 mg (2) |
300 mg (2) |
15 mg |
For chloroquine-resistant vivax malaria, Amodiaquine (30 mg base/kg bw divided over 3 days as 10 mg/kg
bw single daily doses) combined with primaquine should be given. Where ACT has been adopted as the first-line treatment for
P. falciparum malaria, it may also be used for P. vivax malaria in
combination with primaquine for radical cure. Artesunate +
sulfadoxine-pyrimethamine is the exception as it will not be
effective against P. vivax in many places.
After 6
days of treatment, a repeat test for malarial parasites should be done to confirm
clearance of parasitemia. The 28-day
smear for malaria parasite should also be done to assess response to
treatment. Any P. vivax infection that recurs within 28 days, whatever its origin, must be resistant to chloroquine
(provided adequate treatment has been given) and should be treated accordingly.
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.[1]
Mixed infections: Mixed infections with P. vivax/P. ovale
and P. falciparum occur in 5-10% of cases. ACTs are effective against
all malaria species and are the treatment of choice. Radical treatment with
primaquine should be given to patients with confirmed P. vivax and P. ovale
infections except in high transmission settings where the risk of re-infection
is high.[1] In some cases, the tests for malarial parasite may reveal only
one of the parasite types causing the mixed infection. This is
particularly important if QBC method has been used for identifying the infection, wherein
species identification is rather difficult or if
RDTs have
been used. Therefore, all cases of P. vivax
malaria should be carefully observed during initial stages of treatment and if there are
any signs of not improving or deterioration, a possible co-infection with P.
falciparum should be considered.
See Treatment of Severe P.
vivax malaria
See
CDC Guidelines for Treatment of Malaria in the United States[3]
Treatment of P.
vivax malaria: Follow-up
Chloroquine + Primaquine |
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After 48 hours |
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 |
 |
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| Clinical Recovery |
Status quo / worse |
Continue the treatment
Repeat the MP test on the 6th day |
Suspect P. falciparum, repeat MP
test at 48 hrs.
(A thin smear examination is better for species identification and for assessing parasite
count) |
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NEGATIVE
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POSITIVE
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POSITIVE |
NEGATIVE
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Cured |
See below |
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Consider
other causes of fever, may be in association with malaria. |
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P. falciparum |
P. vivax |
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Treat as possibly chloroquine resistant |
If the patient has typical malarial complications, treat as P.
falciparum; otherwise, wait. |
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