Disease relevance of Malaria, Vivax

• When combined with the newly recognized roles of iNOS in renal and pulmonary function and glucose metabolism, synergy between inflammatory cytokines and hypoxia in iNOS induction provides a framework to help explain, at a molecular level, the differences in the pathology seen in falciparum and vivax malaria [1].
• We conducted a double-blind, placebo-controlled trial to determine the prophylactic efficacy of azithromycin against multidrug-resistant P. falciparum malaria and chloroquine-resistant Plasmodium vivax malaria in Indonesian adults with limited immunity [2].
• The observation that none of the four test subjects in this study had relapses has not previously been published and may have important implications for the evaluation of other 8-aminoquinoline compounds against relapsing vivax malaria [3].
• Infectivity enhancing effects of up to 12-fold were demonstrated when a transmission blocking monoclonal antibody and immune human sera were diluted, in some undiluted immune human sera, and in the sera of vivax malaria patients during convalescence after drug cure [4].
• Toxicity related to chloroquine treatment of resistant vivax malaria [5].

High impact information on Malaria, Vivax

• Frequency of relapse and primaquine resistance in Southeast Asian vivax malaria [6].
• Landmark article July 20, 1946: Chloroquine for treatment of acute attacks of vivax malaria. By Harry Most, Irving M. London, Charles A. Kane, Paul H. Lavietes, Edmund F. Schroeder and Joseph M. Hayman, Jr [7].
• Cloning of glycoprotein D cDNA, which encodes the major subunit of the Duffy blood group system and the receptor for the Plasmodium vivax malaria parasite [8].
• We have measured the changing levels of serum tumor necrosis factor (TNF) during paroxysms in non-immune patients infected with P. vivax malaria [9].
• In the present study, we show that HNE can degrade the major circumsporozoite protein of the infective (sporozoite) stage of Plasmodium vivax malaria, and that this enzyme can also interfere with the cytoadherence of human E infected with Plasmodium falciparum (strain K+ FMG-FCR3) (IE) [10].

Chemical compound and disease context of Malaria, Vivax

• There were no significant differences in the times taken for vivax malaria reappearance among the different groups except for those given mefloquine and chloroquine, in which all vivax malaria reappearances developed >28 days after treatment, suggesting suppression of the first relapse by these slowly eliminated drugs [11].
• Intrinsic efficacy of proguanil against falciparum and vivax malaria independent of the metabolite cycloguanil [12].
• Following a preliminary study of CQ plus sulfadoxine-pyrimethamine (CQ-SP) for the treatment of Plasmodium vivax infection, we used modified World Health Organization criteria to evaluate the efficacy of ART-SP for the treatment of vivax malaria in Papua [13].
• This information, together with its known potent antimalarial activity, portends well for the application of tafenoquine as a useful prophylactic drug or for short-term radical treatment of vivax malaria [14].
• However, proguanil/dapsone was more effective than pyrimethamine/dapsone in preventing vivax malaria (1.6% versus 12.4%) [15].

Biological context of Malaria, Vivax

• Population pharmacokinetics of piperaquine in adults and children with uncomplicated falciparum or vivax malaria [16].
• Macrophage activation in vivax malaria: fever is associated with increased levels of neopterin and interferon-gamma [17].
• Lipid peroxidation was assessed by measuring malondialdehyde (MDA) in 30 patients with falciparum malaria and 20 controls (10 healthy adults and 10 patients of vivax malaria) [18].
• The in vitro sensitivity of 39 P. vivax isolates was assessed: the mean IC50 and IC90 were 189 ng/ml and 698 ng/ml blood respectively; for in vivo testing, all 39 vivax malaria patients were treated with a standard regimen of chloroquine and followed-up at 28 days: the mean parasite clearance time was 67.2 +/- 22.5 hours [19].
• Serum total cholesterol, HDL and LDL cholesterols, triglycerides, lipid peroxidation level and platelet counts were determined in 60 patients with vivax malaria and compared with 50 healthy individuals [20].

Anatomical context of Malaria, Vivax

• The elevation of serum TM levels suggests that endothelial cell damage occurs in the acute phase of vivax malaria [21].
• Because of the potential for the elimination of lymphocytes through anti-lymphocytotoxic antibodies we examined individual sera of patients infected with falciparum or vivax malaria for the presence of antibodies against normal peripheral blood mononuclear cells [22].

Gene context of Malaria, Vivax

• Serum TM, ICAM-1, VCAM-1, E-selectin, and creatinine levels were determined in six Japanese patients in the acute phase of vivax malaria and in seven healthy Japanese controls [21].
• Serum cytokine (TNF) levels and killing effects on blood stage malaria parasites were lower in patients who were exposed to endemic P. vivax malaria who had partial clinical immunity, than in non-immune patients [23].
• Pharmacokinetics of primaquine in G6PD deficient and G6PD normal patients with vivax malaria [24].
• Functional polymorphisms in the dhfr gene of P. vivax (pvdhfr) were assessed by PCR-restriction fragment length polymorphism using blood samples taken from 125 patients with acute vivax malaria from three widely separated locations, Thailand (n = 100), India (n = 16), and Madagascar and the Comoros Islands (n = 9) [25].
• Evolution of the levels of soluble interleukin-2 receptors during Plasmodium falciparum and P. vivax malaria [26].

Analytical, diagnostic and therapeutic context of Malaria, Vivax

• Eighteen patients with Plasmodium vivax malaria were prospectively evaluated to assess the time of onset and extent of upper gastrointestinal mucosal injury caused by oral administration of four tablets (600-mg base) of chloroquine [27].
• Group 2: 60 men receiving doxycycline (no control group) were all protected against falciparum malaria but two developed vivax malaria [28].
• As the most intense reactions observed were those between the IgG from the malaria sera and the recombinant MSP, the latter antigen may be useful in diagnostic tests and as a component of any vaccine used to protect against P. vivax malaria [29].
• The significant reduction of vivax malaria in study subjects (compared to background incidence) implied good compliance with self administration of chloroquine in the intervening weeks between scheduled appointments [30].

References