IJCCR 2013, Vol.3, No.3, 17
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Discussion
Unlike severe falciparum malaria, severe vivax
malaria (SVM) in adults is a less described entity
(
Warrell, 1993; Mohapatra et al., 2002; World Health
Organization, 2000). The present one revealed that
non-parasitological risk factors are important for
development of SVM and Artesunate is an effective
antimalarial drug for its treatment with good outcome.
The present study showed that vivax malaria was
found in 25.3% (n=300) of total patients of malaria
and of them 20.0% (60 of 300) developed severe
malaria. The incidence of severe malaria due to Pv
(11.1%)
is less than Pf malaria (85.0%,
p
<0.001). The
incidence of severe Pv malaria is variable in different
studies showing a geographical variation of SVM.
From Mumbai, the hospital incidence of severe vivax
malaria was 66.8% (488 of 711, whereas from another
hospital from Mumbai the percentage of vivax malaria
was only 14. 8%) (Nadkar et al., 2012; Limaye et al.,
2012).
But in Eastern India still falciparum malaria is
predominant species causing SVM (Mohapatra et al.,
2002;
Mohaptra, 2006). In Papua New Guinea (PNG)
and Indonesia it is more found in paediatric
population whereas in India adult population is
affected (Genton et al., 2008; Tjitra et al., 2008).
Apart from geographic heterogeneity, seasonal
variation also influences the prevalence of Pv malaria.
In this study area vivax malaria in general and SVM
in particular occurred more in wet season than dry
season. This seasonal variation may be due to relative
abundance of the species in a geographical area
(
Mohapatra et al., 2012). Thus the incidence of SVM
has been influenced both by geographical heterogenei-
ty and seasonal variation.
The clinical pictures of SVM were different from
UVM. Fever was present in majority of cases with
typical paroxysm. However, in SVM nonfebrile
complaints like head ache, abdominal pain and organ
specific complaints are more common than UVM. The
organ specific complaints are more because of severe
malaria.
In the present study severe malaria was found in Pv
malaria but it is about 8 times less than Pf mono
infection (11.1% vs 85.0%,
p
<0.001). Thus severe
malaria was higher in Pf malaria than Pv malaria.
However, in a study from rural PNG, Pv is responsible
for 21% of all cases severe malaria where as Pf and
mixed infection for 71% and 5% respectively (Genton
et al., 2008).
All forms of severe malaria like cerebral malaria,
anaemia, renal failure, jaundice, multi organ failure
had been encountered in adult patients with SVM.
Affection of different systems is also encountered in
paediatric population. The study from PNG showed
that neurological manifestation, anaemia, respiratory
distress was found in 2.0%, 1.6%, and 5.1%
respectively (Anstey et al., 2009). The increased risk
of severe malaria in children has been attributed to
higher overall parasite burden.
There are some distinct differences between Pv and Pf
malaria which are responsible for the benign nature of
Pv malaria. Firstly, Pv can only invade young red
blood cells i.e. reticulocytes. Hence the density of
parasites is lower than Pf that invades all stages of
RBCs causing high density of parasites (Gilles and
Warrell, 1996). Secondly, the pyrogenic threshold of
Pv is 150~200 parasites/µL which is much lower than
that of Pf (1 500~2 000 /µL). Therefore, patients with
Pv infection develop fever earlier than Pf mono
infection resulting in early medical attention and
treatment reducing the chance of development of
severe disease (Mohapatra et al., 2012). Thirdly,
resistance to drugs particularly, chloroquine is not
commonly found in vivax malaria (Mohapatra et al.,
2002;
Tjitra et al., 2008). Fourthly, P. vivax does not
sequester within the microvasculature of different
internal organs (Gilles and Warrell, 1996). Therefore,
the mechanisms of organ development in vivax
malaria are debatable.
However, the later 3 factors seemed to alter recently.
The delay in treatment due to inappropriate and
inadequate drugs is a risk factor for development of
severe disease. Thev drug resistance is also another
important risk factor. Though chloroquine resistance
has not been a problem for vivax malaria in India, in
our earlier study we emphasized on the possibility of
chloroquine resistance as a risk factor for SVM
(
Mohapatra et al., 2002). Multi drug resistance has
been described as a factor for SVM in Indonesia
(
Tjitra et al., 2008). But recent studies showed that P.
vivax infected erythrocytes may sequester within
pulmonary microvasulature causing alveolar-capillary