INTRODUCTION

Malaria is a disease of global importance.

According to the World Health Organization (WHO), there are 247 million cases of malaria ann
ually, and one million people die from the disease . Plasmodium falciparum and Plasmodium
vivax malaria are endemic infections in India and are commonly associated with mild
hematological abnormalities

Plasmodium vivax is the most geographically widespread species of human malaria parasites,
affecting almost 40% of the world’s population .The invisibility of the dormant liver stages of P.
vivax to any diagnostic method may lead to an underestimation of the true prevalence of P.
vivax far more than P. falciparum.

Although severe cases of Plasmodium vivax (P. vivax) malaria in patients have been documente
d in the past ten years, Plasmodium falciparum (P. falciparum) infection is known to produce th
rombocytopenia and severe malaria.
With the use of molecular diagnostics, it became clear that P. vivax monoinfection may also be
responsible for severe disease that was life-threatening and involved multiple organ dysfunctio
n, as seen in P. falciparum infection .

Immunopathological studies have shown that platelets are an important component of the host
innate immune responses against malaria infection .Thrombocytopaenia (platelet count < 150
000/mm3) appears to be a very frequent haematological alteration in acute malaria infections.
Severe malaria is defined by a demonstration of asexual forms of the malaria parasites in the
blood of a patient with a potentially fatal manifestation or complication of malaria in whom
other diagnoses have been exclude.

Numerous reasons have also been put out for the severe signs of vivax malaria, such as platel
et adhesion to endothelium driven by tumor necrosis factor (TNF) and platelet bridges between
RBCsand endothelial cells, similar to in falciparum malaria ; activation of platelets by parasitized
RBCs causing apoptosis in endothelial cells pretreated with TNF in a mechanism mediated by tu
mor growth factor (TGF) 1; and endothelial cells, similar to in falciparum malaria .
Recent data demonstrating P. vivax infected RBCs sticking to lung endothelial cells and placenta
l tissue ex vivo suggests that mechanisms similar to those linked to the severity of falciparum m
alaria may be involved in vivax malaria.

All the complications seen in falciparum malaria are now reported with vivax also.
LITERATURE REVIEW
Thirty-three case reports of severe thrombocytopaenia (median platelet count: 21,000/μL,
range: 2000–45,000/μL) in patients with vivax malaria have been published in the medical
literature from 1993 to 2014 (the majority after 2006) . Ten individuals presented with
haemorrhagic manifestations and nine received platelet transfusions: all patients recovered
with the exception of one who died because of shock and pancreatitis .
Information regarding the relationship between vivax malaria and thrombocytopaenia adopted
as a criterion for assessing malaria severity may be also extracted from 17 clinical studies (13
from India , two from Pakistan and one each from Colombia and Sudan . In fifteen of these
studies, a cut-off value of less than 50,000 platelets per μL was used to define severe
thrombocytopaenia . Overall, platelet counts below 50,000/μL were present in 335 out of the
906 cases of severe malaria examined (36.9 %), although the prevalence varied significantly
among the studies, from 12.5 % to 93 %, because of the different selection criteria employed.
It is noteworthy that mixed P. vivax and P. falciparum infections were not ruled out in 14 out of
17 studies. In addition, coexisting infections that may contribute to thrombocytopaenia (such as
dengue fever, leptospirosis or bacterial sepsis) were not excluded in the majority of the studies.
Regarding the latter issue, a recent study conducted in the Brazilian Amazon showed that
17.6 % of patients with P. vivax malaria had concomitant dengue infection andp. these had a
higher probability to present with haemorrhagic manifestations and jaundice .
Other studies have focused on the prognostic role of thrombocytopaenia in vivax malaria.

Thrombocytopaenia (i.e., a platelet count below 150,000/μL) is a frequent haematological

finding in all types of malaria and it is observed in 29–93.3 % of patients with P. vivax malaria.
The exact mechanisms underlying the decrease in platelet counts is still unknown, but various
hypothesis have been advanced including immune-mediated phenomena, oxidative stress,
alterations in splenic function and a direct interaction between the parasite and platelets.
Recently, Coelho and coworkers demonstrated that macrophage-driven phagocytosis of
platelets may be an important contributory mechanism and that the mean platelet volume was
greater in thrombocytopaenic patients with vivax malaria than in controls . The latter finding is
particularly interesting because the presence of large circulating platelets and may be viewed as
compensatory mechanism in order to preserve primary haemostasis.

CONCLUSION
The trend of disease with P. vivax malaria is changing. Similar incidence of thrombocytopenia is
now seen in vivax and falciparum malaria patients. All complications seen in falciparum positive
cases are being seen in vivax positive cases also. Thrombocytopenia may not be a cause of
mortality by itself, but it can be a marker of increased severity and need of aggressive
management .Our findings also suggest that both the magnitude of severeity and clinical
conditions correlates with thrombocytopenia in P. Vivax malaria