The distinctive role of membrane fibrinogen-like protein 2 in the liver stage of rodent malaria infections

Viral infection often induce the expression of murine fibrinogen-like protein 2 (mFGL2) triggering immune coagulation, which causes severe liver pathogenesis via increased fibrin deposition and thrombosis in the microvasculature. We aimed to investigate the role of mFGL2 in the liver stage of malaria infections. We reveal that infection with malaria sporozoites also induces increased expression of mFGL2 and that this expression is primarily located within the liver Kupffer and endothelial cells. In addition, we report that inhibition of FGL2 has no significant effect on immune coagulation but increases the expression of inflammatory cytokines in the livers of infected mice. Interestingly, FGL2 deficiency had no significant impact on the development of liver stage malaria parasites or the pathogenesis of the infected liver. In contrast to viral infections, we conclude that mFGL2 does not contribute to either parasite development or liver pathology during these infections, revealing the unique features of this protein in liver-stage malaria infections.     

Possible acute coinfections in Thai malaria patients

We conducted serodiagnostic testing for dengue virus infection, murine typhus, scrub typhus and leptospirosis in Plasmodium falciparum-infected individuals in Thailand. Sera from 194 malaria patients with a median age of 24 years were tested. No antibody titers diagnostic of dengue virus infection were demonstrated, but 29 (15%) of patients had serological evidence of scrub typhus, 45 (23.2 %) patients had evidence of murine typhus, and 15 (7.7%) sera tested positive for leptospirosis. Our serological results suggested that duel infections are not uncommon in malaria that is acquired in Thailand. However, our results must be confirmed by prospective studies aimed at describing the causative organisms. Mixed infections would have multiple implications for clinicians, including unexpected clinical findings and apparent poor responses to antimalarial treatment in patients thought only to have malaria.     

Angiotensin-converting enzyme 2: Possible role in hypertension and kidney disease

The discovery of angiotensin-converting enzyme (ACE) 2 adds a new level of complexity to the understanding of the renin-angiotensin system. The high catalytic efficiency of ACE2 for the generation of angiotensin (ANG)-1-7 from ANG II suggests an important role of ACE2 in preventing ANG II accumulation, while at the same time enhancing ANG-1-7 formation. ACE and ACE2 may have counterbalancing functions and a regulatory role in fine-tuning the rate at which ANG peptides are formed and degraded. By counterregulating the actions of ACE on ANG II formation, ACE2 may play a role in maintaining a balanced status of the renninangiotensin system. This review focuses on the function of ACE2 and its possible roles in kidney disease and hypertension. Studies using models of ACE2 ablation and the pharmacologic administration of an ACE2 inhibitor suggest that decreased ACE2 activity alone or in combination with increased ACE activity may play a role in both diseases.     

The role of entomology in malaria control

The significance of main parts of entological work in malaria epidemiology and control is discussed. The role of entomologists is very important, but the present-day entological services in Russia are almost destroyed. This situation is very dangerous in the context of malaria resurgence.     

Possible involvement of platelets in Plasmodium yoelii nigeriensis malaria infection in mice

The possible involvement of platelets in the pathogenesis of malaria was examined by monitoring the changes in platelet function (bleeding time [BT] and thrombin time [TT]) concomitantly with changes in packed cell volume (PCV) and erythrocyte infection rate (EIR) in Plasmodium yoelii nigeriensis infection in mice. In untreated plasmodium-infected mice, there was a progressive reduction (day 1-7) in BT from 120.0 +/- 12.6 s to 77.5 +/- 5.9 s (p less than 0.005), a reduction in TT from 26.8 +/- 1.2 s to 17.8 +/- 1.2 s (p less than 0.005), an increase in EIR from 0 to 64.6 +/- 6.3% and a reduction in PCV from 44.9 +/- 1.9% to 21.5 +/- 3.9% (p less than 0.001). Mortality on day 9 was 100%. Antiplatelet serum treatment of plasmodium-infected mice protected against malaria and there was a blunting of the malaria-induced changes in platelet function, EIR and PCV. The values obtained in these rats were significantly higher than those of the untreated malarious mice. The respective values obtained on day 1 were comparable to those of control mice. Data obtained on day 7 were: BT, 106.4 +/- 7.4 s (p less than 0.05), TT, 22.7 +/- 1.1 s (p less than 0.05), EIR, 45.7 +/- 3.2% (p less than 0.01) and PCV, 39.5 +/- 2.0% (p less than 0.01). Mortality on day 9 of infection was 60%. The protection by antiserum was not due to its thrombocytopenic response as busulphan-induced thrombocytopenia did not have the same effect. These results suggest that platelets play an important role in malaria infection as well as in the attendant coagulopathic complications.     

Eosinophilic response to falciparum malaria infections.

Eosinophilia was a frequently detected incidental finding during a prospective study of malaria seroepidemiology in Thailand. Blood eosinophil counts were performed every 3 months for a year in 823 Thai soldiers on border guard duty in a malaria endemic area. Soldiers developing malaria were admitted to hospital and more frequent eosinophil counts were done. P. falciparum parasitemia suppressed preexisting eosinophilia but eosinophilia returned following treatment. P. vivax and mixed infections had a similar but less marked effect on the peripheral blood eosinophil count. Eosinophilia in persons from a malaria endemic area may represent a normal late response to malaria infection.     

Asymptomatic malaria infections among foreign migrant workers in Thailand

ObjectiveTo determine the prevalence of malaria infections among foreign migrant workers in Thailand.MethodsGiemsa-stained thin and thick blood films were prepared from blood samples of 294 foreign migrant workers recruited in the study. Microscopic examination of these blood films was performed for malaria detection.ResultsBlood film examination revealed 1.36% malaria infections in these 294 subjects. All positive cases were male Myanmar workers in which their blood films only ring stage of Plasmodium spp. was found at low parasite density (mean= 144 parasites/μ L of blood). The prevalence of malaria infections was not significantly different among foreign migrant workers classified by age, gender, and resident province (P>0.05). Thin blood films of these workers also showed 78.91% hypochromic erythrocytes and 61.9% relative Eosinophilia.ConclusionsThese findings indicate a high risk of malaria transmission. Therefore active malaria surveillance by using molecular methods with more sensitive and specific than microscopy should be considered for malaria control in foreign migrant workers.     

Virulence and competitive ability in genetically diverse malaria infections

Explaining parasite virulence is a great challenge for evolutionary biology. Intuitively, parasites that depend on their hosts for their survival should be benign to their hosts, yet many parasites cause harm. One explanation for this is that within-host competition favors virulence, with more virulent strains having a competitive advantage in genetically diverse infections. This idea, which is well supported in theory, remains untested empirically. Here we provide evidence that within-host competition does indeed select for high parasite virulence. We examine the rodent malaria Plasmodium chabaudi in laboratory mice, a parasite-host system in which virulence can be easily monitored and competing strains quantified by using strain-specific real-time PCR. As predicted, we found a strong relationship between parasite virulence and competitive ability, so that more virulent strains have a competitive advantage in mixed-strain infections. In transmission experiments, we found that the strain composition of the parasite populations in mosquitoes was directly correlated with the composition of the blood-stage parasite population. Thus, the outcome of within-host competition determined relative transmission success. Our results imply that within-host competition is a major factor driving the evolution of virulence and can explain why many parasites harm their hosts.     

Formation and role of malaria pigment

Malaria pigment is most abundant and distinct in gametocytes. Trophozoites have variable amounts of pigment, depending on the species of Plasmodium and the stage of infection. In Plasmodium falciparum infection, blood smear preparations fall into two categories that are distinguishable at all levels of parasitemia; one type of preparation contains only pigment-deficient trophozoites, and the other type contains only pigment-rich trophozoites. Pigment accumulates in the residual body of the mature schizont and is lost upon rupture of the schizont. In contrast, pigment remains associated with the macrogametocyte and developing oocyst. Certain antimalarial drugs, such as chloroquine, have distinct effects on pigment clumping. These observations raise questions regarding the current idea of pigment as an inert excretory product of hemoglobin metabolism. It is suggested that pigment particles represent stacked utilizable intermediates of hemoglobin digestion that accumulate in the gametocyte to serve as a food reserve during the growth cycle in the mosquito.