Plasmodium vivax malaria presenting with severe thrombocytopenia

Abstract

Plasmodium falciparum and Plasmodium vivax malaria are endemic infections in India and are commonly associated with mild hematological abnormalities. Severe thrombocytopenia is common in isolated falciparum and mixed falciparum/vivax malaria, but is very rare in isolated P.vivax infection. We hereby report a case of severe thrombocytopenia (platelet count of 8x10 9 /L) in a case of vivax malaria. This is only the second case ever reported in the literature of such profound thrombocytopenia in a case of isolated P.vivax malaria. Key Words: Plasmodium vivax, malaria, severe thrombocytopenia. Malaria is common in most parts of India and is usually caused by P. falciparum and P. vivax. Though mild thrombocytopenia is common in both falciparum and vivax malaria, severe thrombocytopenia is reported especially in P. falciparum malaria and is very rare in isolated P. vivax infection. Both non-immunological as well as immunological destruction of platelets have been implicated in causing thrombocytopenia in such cases but the mechanisms involved are still not completely clear. Case ReportA 43-year-old male, resident of eastern India, arrived at the hospital emergency room with complaints of high grade, intermittent fever associated with chills and rigors during seven days. He also had a two-day history of mild spontaneous bleeding from the gums. There was no history of bleeding from any other site and no past or family history suggestive of bleeding diathesis. There was no history of any drug ingestion. On examination, the patient was febrile with a temperature of 40 o C. He had slight pallor and the liver and spleen were palpable 2 cm and 3 cm below the costal margin, respectively. There were no purpuric spots and the tourniquet test was negative.Routine blood investigations revealed 7.5 g/dL hemoglobin and a WBC count of 6.3x10 9 /L, with 54% neutrophils, 39% lymphocytes, 4% eosinophils and 3% monocytes. The platelet count was 8x10 9 /L. The peripheral blood smear showed numerous gametocytes of P. vivax in a background of marked thrombocytopenia. The 'OptiMAL® Rapid Malaria Dipstick Test' (DiaMed AG,Switzerland) for P. falciparum was negative but was positive for P. vivax. The bleeding time was prolonged to 9 minutes while the clotting time was 3 minutes, with a prothrombin time of 14 seconds (control 13 seconds) and activated partial thromboplastin time of 40 seconds (control 36 seconds). Glucose-6-phosphate dehydrogenase levels were normal and disseminated intravascular coagulation (DIC) was ruled out by normal levels of fibrinogen degradation products (FDP). Total serum bilirubin was 1.4 mg/dL with normal serum transaminase levels. Dengue serology (IgG and IgM) and Elisa for HIV were nonreactive. The patient was treated with antimalarials (quinine sulphate 10 mg/kg thrice daily) for 7 days and was given 6 units of platelet transfusions

The Unusual Presentation of a Usual Organism – the Changing Spectrum of the Clinical Manifestations of Plasmodium Vivax Malaria in Children: A Retrospective Study

“…In our study, the most common manifestation was thrombocytopaenia, which was reported in 90.2% of the cases and in about 37.0% children, severe thrombocytopaenia (<20,000/cumm) was present, with the lowest platelet count of 6000/cumm, which was probably the lowest count which was recorded among children in the literature [14][15][16][17][18]. There have been occasional reports of thrombocytopaenia with P.vivax malaria, either as an isolated or a more commonly associated complication [14][15][16][17][18].…”

Evaluation of clinical profile of febrile thrombocytopenia: an institutional based study

“…These cases are often asymptomatic and are discovered under routine haematological investigations. 8 Hence, we planned the present study to analyse the clinical profile of febrile thrombocytopenia.…”

A Study of Different Hematological Parameters in Malaria

“…Although sever thrombocytopenia is commonly reported to be associated with Plasmodium falciparum infection and has been reported to occur in patients co infected with both Plasmodium falciparum and Plasmodium Vivax, its occurrence has been rarely reported in cases of Plasmodium vivax malaria. 16 The precise mechanism behind thrombocytopenia, however, remains unclear. Both the immunological as well as the nonimmunological destruction of platelets have been implicated.…”

“…Other postulates include peripheral destruction and the consumption of platelets. 16 Immune complexes which are generated by the malarial antigen lead to the sequestration of the injured platelets by the macrophages in the spleen. This is supported by the finding that malaria patients have elevated levels of platelet-bound IgG.…”