Subramanian Senthilkumaran1, Chidambaram Ananth2, Sandeep B Gore3, Ponniah Thirumalaikolundusubramanian4. 1. Department of Emergency and Critical Care Medicine, Sri Gokulam Hospital, Salem, Tamil Nadu, India. 2. Department of Anaesthesiology, Chennai Medical College and Research Center, Irungalur, Trichy, India. 3. Department of Accident and Emergency Medicine, Fortis Hospital, Mulund, Mumbai, Maharashtra, India. 4. Department of Internal Medicine, Chennai Medical College and Research Center, Irungalur, Trichy, India.
Sir,The letter by Gosh et al.[1] once again emphasizes that Plasmodium vivaxinfection is not always a simple and self-limiting infection. In comparison with Plasmodium falciparum, P. vivax runs a benign course and is rarely fatal. However, in recent times, scenarios have changed and there are reports of severe malaria due to P. vivaxinfection.[2] In this context, we would like to suggest the probable mechanisms based on our earlier observations[3] and measures to tackle such situations.Though the exact mechanism of subdural hemorrhage in this patient is not known, there is a possibility of rupture of small vessels plugged by infected red cells in combination with severe thrombocytopenia.[4] This hypothesis has been supported by histopathological studies disclosing widespread cerebral vasculopathy due to parasite-specific factors such as adhesion and sequestration of parasitized erythrocytes in vascular endothelium with increased endothelial permeability, perivascular infiltrations, and cerebral edema; capillaries and venules are also distended and packed with erythrocytes.[5]In P. vivaxinfections, parasitemia seldom exceeds 2-5% of circulating RBCs, and high parasite indices are not attributed to the severity of the disease. However, cytokine production during P. vivaxinfections is higher than that during P. falciparum infections with similar degree of parasitemia.[6] By up-regulating endothelial adhesion molecules, TNF-α may promote cerebral sequestration of platelets and red cells thus leading to hemorrhage. The serum TNF-α level correlates well with the severity of disease. In addition, patient-specific factors such as oxidative stress, enhanced host inflammatory responses, and alterations in splenic functions might have played a pivotal role. Thus, patient susceptibility to develop vascular complications may be attributable to gene polymorphism.This is common for all clinical conditions and not specific for plasmodium vivax complications.
Authors: Ritesh G Menezes; Sadip Pant; Magdy A Kharoshah; Subramanian Senthilkumaran; M Arun; K R Nagesh; Nishanth B Bhat; D R Mahadeshwara Prasad; Raj Kumar Karki; S H Subba; Abul Fazil Journal: Leg Med (Tokyo) Date: 2012-02-26 Impact factor: 1.376
Authors: Ric N Price; Emiliana Tjitra; Carlos A Guerra; Shunmay Yeung; Nicholas J White; Nicholas M Anstey Journal: Am J Trop Med Hyg Date: 2007-12 Impact factor: 2.345