Journal articles: 'Malaria susceptibility'

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Haldar, Kasturi, and Narla Mohandas. "Malaria, erythrocytic infection, and anemia." Hematology 2009, no. 1 (January 1, 2009): 87–93. http://dx.doi.org/10.1182/asheducation-2009.1.87.

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Abstract Malaria is a major world health problem. It results from infection of parasites belonging to the genus Plasmodium. Plasmodium falciparum and Plasmodium vivax cause the major human malarias, with P falciparum being the more virulent. During their blood stages of infection, both P falciparum and P vivax induce anemia. Severe malarial anemia caused by P falciparum is responsible for approximately a third of the deaths associated with disease. Malarial anemia appears to be multi-factorial. It involves increased removal of circulating erythrocytes as well as decreased production of erythrocytes in the bone marrow. The molecular mechanisms underlying malarial anemia are largely unknown. Over the last five years, malaria parasite ligands have been investigated for their remodeling of erythrocytes and possible roles in destruction of mature erythrocytes. Polymorphisms in cytokines have been associated with susceptibility to severe malarial anemia: these cytokines and malaria “toxins” likely function by perturbing erythropoiesis. Finally a number of co-infections increase susceptibility to malarial anemia, likely because they exacerbate inflammation caused by malaria. Because of the complexities involved, the study of severe malarial anemia may need a “systems approach” to yield comprehensive understanding of defects in both erythropoiesis and immunity associated with disease. New and emerging tools such as (i) mathematical modeling of the dynamics of host control of malarial infection, (ii) ex vivo perfusion of human spleen to measure both infected and uninfected erythrocyte retention, and (iii) in vitro development of erythroid progenitors to dissect responsiveness to cytokine imbalance or malaria toxins, may be especially useful to develop integrated mechanistic insights and therapies to control this major and fatal disease pathology.

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Scanlon, Seth Thomas. "Variable malaria susceptibility." Science 372, no. 6544 (May 20, 2021): 804.1–805. http://dx.doi.org/10.1126/science.372.6544.804-a.

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Burhan, Hira, Askari Syed Hasan, Syed Mansur-ul-Haque, Ghazanfar Zaidi, Taha Shaikh, and Aisha Zia. "Association between blood group and susceptibility to malaria and its effects on platelets, TLC, and Hb." Journal of Infection in Developing Countries 10, no. 10 (October 31, 2016): 1124–28. http://dx.doi.org/10.3855/jidc.6828.

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Introduction: According to the World Health Organization, the estimated number of malaria cases in Pakistan is about 1.5 million. Hematological variables like platelets, total leukocyte count (TLC), and hemoglobin (Hb) need to be evaluated to diagnose malaria in suspects. This study aimed to investigate the association between blood group and susceptibility to malaria and effects on platelets, TLC, and Hb. Methodology: This was a case-control study with a sample size of 446, of which 224 were malarial cases and 222 were controls. A designated questionnaire was developed to know age, gender, malarial strain, Hb, TLC, platelets, and blood group. Results: Of 224 malarial cases, 213 were P. vivax, and 11 were P. falciparum. There were 58 patients with blood group A, 72 with group B, 69 were O and 23 were AB. There was no significant difference in the blood group of controls compared to malarial patients (p > 0.05). Mean Hb level was 11.5mg/dL in malaria patients and 12.5mg/dL in controls. There was significant difference (p<0.01) in the mean platelet count in malarial (11,7000/μL) and control (24,5000/μL) patients. All blood groups showed similar falls in Hb and platelet levels, showing no significant difference among blood groups (p = 0.79 and p = 0.52, respectively). TLC was not significant between malarial and control groups (p = 0.072). Males were two times susceptible to malaria. Conclusions: There was no significant association between the type of blood group and susceptibility to malaria or developing anemia or thrombocytopenia.

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ICHIMORI, Kazuyo. "Mosquito susceptibility to malaria." Medical Entomology and Zoology 40, no. 1 (1989): 1–12. http://dx.doi.org/10.7601/mez.40.1_1.

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Jha, Aditya Nath, Pandarisamy Sundaravadivel, Vipin Kumar Singh, Sudhanshu S. Pati, Pradeep K. Patra, Peter G. Kremsner, Thirumalaisamy P. Velavan, Lalji Singh, and Kumarasamy Thangaraj. "MBL2Variations and Malaria Susceptibility in Indian Populations." Infection and Immunity 82, no. 1 (October 14, 2013): 52–61. http://dx.doi.org/10.1128/iai.01041-13.

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ABSTRACTHuman mannose-binding lectin (MBL) encoded by theMBL2gene is a pattern recognition protein and has been associated with many infectious diseases, including malaria. We sought to investigate the contribution of functionalMBL2gene variations toPlasmodium falciparummalaria in well-defined cases and in matched controls. We resequenced the 8.7 kb of the entireMBL2gene in 434 individuals clinically classified with malaria from regions of India where malaria is endemic. The study cohort included 176 patients with severe malaria, 101 patients with mild malaria, and 157 ethnically matched asymptomatic individuals. In addition, 830 individuals from 32 socially, linguistically, and geographically diverse endogamous populations of India were investigated for the distribution of functionalMBL2variants. TheMBL2 −221C(X) allelic variant is associated with increased risk of malaria (mild malaria odds ratio [OR] = 1.9, correctedPvalue [PCorr] = 0.0036; severe malaria OR = 1.6,PCorr= 0.02). The exon1 variantsMBL2*B(severe malaria OR = 2.1,PCorr= 0.036; mild versus severe malaria OR = 2.5,PCorr= 0.039) andMBL2*C(mild versus severe malaria OR = 5.4,PCorr= 0.045) increased the odds of having malaria. The exon1MBL2*D/*B/*Cvariant increased the risk for severe malaria (OR = 3.4,PCorr= 0.000045). The frequencies of low MBL haplotypes were significantly higher in severe malaria (14.2%) compared to mild malaria (7.9%) and asymptomatic (3.8%). TheMBL2*LYPAhaplotypes confer protection, whereasMBL2*LXPAincreases the malaria risk. Our findings in Indian populations demonstrate thatMBL2functional variants are strongly associated with malaria and infection severity.

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Baliyan, Vinit, Jeyaseelan Nadarajah, Atin Kumar, and Zohra Ahmad. "Cerebral malaria: susceptibility weighted MRI." Asian Pacific Journal of Tropical Disease 5, no. 3 (March 2015): 239–41. http://dx.doi.org/10.1016/s2222-1808(14)60661-7.

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Aitman, Timothy J., Lisa D. Cooper, Penny J. Norsworthy, Faisal N. Wahid, Jennefer K. Gray, Brian R. Curtis, Paul M. McKeigue, et al. "Malaria susceptibility and CD36 mutation." Nature 405, no. 6790 (June 2000): 1015–16. http://dx.doi.org/10.1038/35016636.

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Hernandez-Valladares, Maria, Pascal Rihet, and Fuad A. Iraqi. "Host susceptibility to malaria in human and mice: compatible approaches to identify potential resistant genes." Physiological Genomics 46, no. 1 (January 1, 2014): 1–16. http://dx.doi.org/10.1152/physiolgenomics.00044.2013.

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There is growing evidence for human genetic factors controlling the outcome of malaria infection, while molecular basis of this genetic control is still poorly understood. Case-control and family-based studies have been carried out to identify genes underlying host susceptibility to malarial infection. Parasitemia and mild malaria have been genetically linked to human chromosomes 5q31-q33 and 6p21.3, and several immune genes located within those regions have been associated with malaria-related phenotypes. Association and linkage studies of resistance to malaria are not easy to carry out in human populations, because of the difficulty in surveying a significant number of families. Murine models have proven to be an excellent genetic tool for studying host response to malaria; their use allowed mapping 14 resistance loci, eight of them controlling parasitic levels and six controlling cerebral malaria. Once quantitative trait loci or genes have been identified, the human ortholog may then be identified. Comparative mapping studies showed that a couple of human and mouse might share similar genetically controlled mechanisms of resistance. In this way, char8, which controls parasitemia, was mapped on chromosome 11; char8 corresponds to human chromosome 5q31-q33 and contains immune genes, such as Il3, Il4, Il5, Il12b, Il13, Irf1, and Csf2. Nevertheless, part of the genetic factors controlling malaria traits might differ in both hosts because of specific host-pathogen interactions. Finally, novel genetic tools including animal models were recently developed and will offer new opportunities for identifying genetic factors underlying host phenotypic response to malaria, which will help in better therapeutic strategies including vaccine and drug development.

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Kwiatkowski, D. "Genetic susceptibility to malaria getting complex." Current Opinion in Genetics & Development 10, no. 3 (June 1, 2000): 320–24. http://dx.doi.org/10.1016/s0959-437x(00)00087-3.

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Bonn, Dorothy. "Susceptibility to malaria during pregnancy explained." Lancet 352, no. 9138 (October 1998): 1447. http://dx.doi.org/10.1016/s0140-6736(05)61271-8.

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Mutabingwa, Theonest K., Melissa C. Bolla, Jin-Long Li, Gonzalo J. Domingo, Xiaohong Li, Michal Fried, and Patrick E. Duffy. "Maternal Malaria and Gravidity Interact to Modify Infant Susceptibility to Malaria." PLoS Medicine 2, no. 12 (November 8, 2005): e407. http://dx.doi.org/10.1371/journal.pmed.0020407.

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Shah, Binal N., Philip E. Thuma, N. Scott Reading, Josef T. Prchal, and Victor R. Gordeuk. "Host Genetic Factors in Glucose-6-Phosphate Dehydrogenase and Cytochrome B5 Reductase 3 Affect the Susceptibility of Developing Severe Malarial Anemia." Blood 128, no. 22 (December 2, 2016): 2438. http://dx.doi.org/10.1182/blood.v128.22.2438.2438.

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Abstract Host genetic factors that influence the outcome of Plasmodium falciparum malaria infection are not fully understood. Glucose-6-phosphate dehydrogenase (G6PD), an X-linked gene, encodes the sole enzyme in red blood cells that produces NADPH for protection from reactive oxygen species. G6PD A+ (G6PD c. 376G) is an African specific polymorphism reported to have reduced activity1 but no apparent phenotype; G6PD A- (G6PD c 202A/376G) is a related polymorphism with decreased activity and increased risk for oxidant-induced hemolysis2. Previous investigators have reported that G6PD deficiency provides a protective effect from malaria3. A recent Malaria Genomic Epidemiology Network (MalariaGEN) study with almost 30,000 participants reported that G6PD A- increases the risk for severe malarial anemia4. Cytochrome b5 reductase 3 (CYB5R3) in red blood cells transfers electrons from NADH to cytochrome b5, which in turn converts methemoglobin to hemoglobin. The CYB5R3 T117S variant, an African-specific polymorphism with a prevalence higher than previously described African-specific polymorphisms (allele frequency .23)5, is not associated with methemoglobinemia. We hypothesized that CYB5R3 T117S may protect from severe malarial anemia, possibly by enhanced anti-oxidative potential of erythrocytes through higher NADH levels. We isolated DNA from dried blood spots from 133 children (age < 6 years) who presented to hospital in southern Zambia with clinical malaria. Sixty-seven had severe anemia (hematocrit <15%) and 66 had uncomplicated malaria (hematocrit ≥18%); all had normal coma scores. We determined G6PD A+, G6PD A- and CYB5R3 T117S by Taqman genotyping. We also isolated DNA from plasma samples and genotyped for CYB5R3 T117S. There was 97.7% agreement in the genotyping. The overall prevalence of G6PD A+ was 20.3% and of G6PD A- 12.0%. The gene frequency of CYB5R3 T117S was .31. We examined the association of these genotypes with severe malarial anemia in logistic regression models that adjusted for body weight, duration of febrile illness before presentation, and treatment with traditional herbal medicine or sulfadoxine-pyrimethamine before presentation6. In keeping with the MalariaGEN study, we found that G6PD A- increased the odds of severe malarial anemia (OR 8.2; 95% CI 1.6-42.7l; P=0.013), but we also observed a trend with G6PD A+ (OR 2.1, 95% CI 0.7-6.5; P=0.22). We therefore assessed the additive effect of these polymorphisms and observed a progressive increase in the risk with G6PD A+ and G6PD A- (OR 2.6, 95% CI 1.3-5.3). We added CYB5R3 T117S to this model and found a non-significant trend to a progressive reduction in the risk of severe anemia with heterozygosity and homozygosity for T117S (OR = 0.7, 95% CI 0.3-1.4; P=0.29). In further analysis, we observed an interaction between CYB5R3 T117S and G6PD genotype in the risk for severe anemia (P =0.092). We therefore stratified our analysis according to the presence or absence of G6PD variants. In the absence of G6PD A+ or A-, CYB5R3T117S offered protection against severe anemia (OR 0.3, 95% CI 0.1-0.9, P=0.035) in an additive model. In contrast, in the presence of G6PD A+ or G6PDA-, CYB5R3 T117S mutation tended to increase the odds of severe anemia in malaria (OR 3.1, 95% CI 0.6-15.9, P=0.18). In summary, 1) we confirm the association of G6PD A- with severe malarial anemia in southern Zambian children, 2) we observe an additive increased risk of severe malarial anemia with G6PD A+ and G6PD A-, and 3) we report heterogeneity of the effect of CYB5R3 T117S on the risk of severe anemia according to G6PD A+ and A- status. The observations with CYB5R3 T117S need to be confirmed in a larger cohort and the underlying mechanisms worked out through laboratory and translational research. We conclude that the combined effect of host genetic factors in two different red cell redox regulating enzymes may affect the outcome of P. falciparum infection. ReferencesGomez-Manzo, S. et al. International journal of molecular sciences16, 28657-28668 (2015).Luzzatto, L., Nannelli, C. & Notaro, R. Hematology/oncology clinics of North America30, 373-393 (2016).Ruwende, C. et al. Nature376, 246-249 (1995).Rockett, K. A. et al. Nature genetics46, 1197-1204 (2014).Jenkins, M. M. & Prchal, J. T. Hum Genet99, 248-250 (1997).Thuma, P. E. et al. J Infect Dis203, 211-219 (2011). Disclosures Thuma: Malaria Institute at Macha: Employment.

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Trovoada, Maria de Jesus, Madalena Martins, Riadh Ben Mansour, Maria do Rosário Sambo, Ana B. Fernandes, Lígia Antunes Gonçalves, Artur Borja, et al. "NOS2 Variants Reveal a Dual Genetic Control of Nitric Oxide Levels, Susceptibility to Plasmodium Infection, and Cerebral Malaria." Infection and Immunity 82, no. 3 (December 30, 2013): 1287–95. http://dx.doi.org/10.1128/iai.01070-13.

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ABSTRACTNitric oxide (NO) is a proposed component of malaria pathogenesis, and the inducible nitric oxide synthase gene (NOS2) has been associated to malaria susceptibility. We analyzed the role ofNOS2polymorphisms on NO bioavailability and on susceptibility to infection,Plasmodiumcarrier status and clinical malaria. Two distinct West African sample collections were studied: a population-based collection of 1,168 apparently healthy individuals from the Príncipe Island and a hospital-based cohort of 269 Angolan children. We found that twoNOS2promoter single-nucleotide polymorphism (SNP) alleles associated to low NO plasma levels in noninfected individuals were also associated to reduced risk of pre-erythrocytic infection as measured anti-CSP antibody levels (6.25E–04 <P< 7.57E–04). In contrast, three SNP alleles within theNOS2cistronic region conferring increased NO plasma levels in asymptomatic carriers were strongly associated to risk of parasite carriage (8.00E–05 <P< 7.90E–04). Notwithstanding, three SNP alleles in this region protected from cerebral malaria (7.90E–4 <P< 4.33E–02). Cohesively, the results revealed a dual regimen in the genetic control of NO bioavailability afforded byNOS2depending on the infection status.NOS2promoter variants operate in noninfected individuals to decrease both NO bioavailability and susceptibility to pre-erythrocytic infection. Conversely,NOS2cistronic variants (namely, rs6505469) operate in infected individuals to increase NO bioavailability and confer increased susceptibility to unapparent infection but protect from cerebral malaria. These findings corroborate the hypothesis that NO anti-inflammatory properties impact on different steps of malaria pathogenesis, explicitly by favoring infection susceptibility and deterring severe malaria syndromes.

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Sappenfield, Elisabeth, Denise J. Jamieson, and Athena P. Kourtis. "Pregnancy and Susceptibility to Infectious Diseases." Infectious Diseases in Obstetrics and Gynecology 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/752852.

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To summarize the literature regarding susceptibility of pregnant women to infectious diseases and severity of resulting disease, we conducted a review using a PubMed search and other strategies. Studies were included if they reported information on infection risk or disease outcome in pregnant women. In all, 1454 abstracts were reviewed, and a total of 85 studies were included. Data were extracted regarding number of cases in pregnant women, rates of infection, risk factors for disease severity or complications, and maternal outcomes. The evidence indicates that pregnancy is associated with increased severity of some infectious diseases, such as influenza, malaria, hepatitis E, and herpes simplex virus (HSV) infection (risk for dissemination/hepatitis); there is also some evidence for increased severity of measles and smallpox. Disease severity seems higher with advanced pregnancy. Pregnant women may be more susceptible to acquisition of malaria, HIV infection, and listeriosis, although the evidence is limited. These results reinforce the importance of infection prevention as well as of early identification and treatment of suspected influenza, malaria, hepatitis E, and HSV disease during pregnancy.

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CARPENTER, D., I. ROOTH, A. FARNERT, H. ABUSHAMA, R. QUINNELL, and M. SHAW. "Genetics of susceptibility to malaria related phenotypes." Infection, Genetics and Evolution 9, no. 1 (January 2009): 97–103. http://dx.doi.org/10.1016/j.meegid.2008.10.008.

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Carpenter, Danielle, Anna Färnert, Ingegerd Rooth, John A. L. Armour, and Marie-Anne Shaw. "CCL3L1 copy number and susceptibility to malaria." Infection, Genetics and Evolution 12, no. 5 (July 2012): 1147–54. http://dx.doi.org/10.1016/j.meegid.2012.03.021.

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BOUYOUAKOTET, M., A. ADEGNIKA, S. AGNANDJI, E. NGOUMILAMA, M. KOMBILA, P. KREMSNER, and E. MAVOUNGOU. "Cortisol and susceptibility to malaria during pregnancy." Microbes and Infection 7, no. 11-12 (August 2005): 1217–23. http://dx.doi.org/10.1016/j.micinf.2005.04.008.

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Kumar, C. Jairaj, Vijay Kumar Sharma, and Arunachalam Kumar. "Jet lag and enhanced susceptibility to malaria." Medical Hypotheses 66, no. 3 (January 2006): 671. http://dx.doi.org/10.1016/j.mehy.2005.10.002.

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Maurois, P., E. Gueux, and Y. Rayssiguier. "Magnesium deficiency affects malaria susceptibility in mice." Journal of the American College of Nutrition 12, no. 1 (February 1993): 21–25. http://dx.doi.org/10.1080/07315724.1993.10718277.

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Kursah, Matthew Biniyam. "Modelling malaria susceptibility using geographic information system." GeoJournal 82, no. 6 (July 18, 2016): 1101–11. http://dx.doi.org/10.1007/s10708-016-9732-0.

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Riley, E. M. "The role of MHC- and non-MHC-associated genes in determining the human immune response to malaria antigens." Parasitology 112, S1 (March 1996): S39—S51. http://dx.doi.org/10.1017/s0031182000076654.

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SUMMARYIndividual susceptibility to malaria infection, disease and death is influenced by host genotype, parasite virulence and a number of environmental factors including malaria-specific immunity. Immune responses are themselves determined by a combination of host genes and environmental effects. The extent to which host genotype limits the spectrum of possible immune responses may influence the outcome of infection and has consequences for vaccine design. Associations have been observed between human major histocompatibility complex (MHC) genotype and susceptibility to severe malaria, but no similar associations have been observed for mild malarial disease or for specific antibody responses to defined malaria antigens. Epidemiological studies have shown that, in practice, neither T helper cell nor antibody responses to malaria parasites are limited by host MHC genotype, but have revealed that genes lying outside the MHC may influence T cell proliferative responses. These genes have yet to be identified, but possible candidates include T cell receptor (TcR) genes, and genes involved in TcR gene rearrangements. More importantly, perhaps, longitudinal epidemiological studies have shown that the anti-malarial antibody repertoire is selective and becomes fixed in malaria-immune individuals, but is independent of host genotype. These findings suggest that the antibody repertoire may be determined, at least in part, by stochastic events. The first of these is the generation of the T and B cell repertoire, which results from random gene recombinations and somatic mutation and is thus partially independent of germline genes. Secondly, of the profusion of immunogenic peptides which are processed and presented by antigen presenting cells, a few will, by chance, interact with T and B cell surface antigen receptors of particularly high affinity. These T and B cell clones will be selected, will expand and may come to dominate the immune response, preventing the recognition of variant epitopes presented by subsequent infections - a process known as original antigenic sin or clonal imprinting. The immune response of an individual thus reflects the balance between genetic and stochastic effects. This may have important consequences for subunit vaccine development.

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K, Anju Viswan. "Density and Susceptibility Status of Malaria Vectors of Chilkuti Area, Bastar, Chhattisgarh." Journal of Communicable Diseases 51, no. 4 (February 24, 2020): 10–15. http://dx.doi.org/10.24321/0019.5138.201931.

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Kaur, Prabhjot, Arun Bhatia, Kanav Midha, and Mampi Debnath. "Malaria: A Cause of Anemia and Its Effect on Pregnancy." World Journal of Anemia 1, no. 2 (2017): 51–62. http://dx.doi.org/10.5005/jp-journals-10065-0012.

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ABSTRACT Malaria is one of the major health problems in the world. It remains an important cause of very high human morbidity and mortality, especially, among children and pregnant women. It results from the infection of parasites belonging to the genus Plasmodium. Plasmodium falciparum and Plasmodium vivax are the major pathogens responsible for causing human malaria. Approximately 75% of cases are caused by P. falciparum and associated with the mortality rate of approximately 0.5 to 1.0%. Both P. falciparum and P. vivax induce anemia during their erythrocytic stages of infection. Most of the malarial infections are related to some degree of anemia, the severity of which depends upon patient-specific characteristics (e.g., age, innate and acquired resistance, comorbid features, etc.) as well as parasite-specific characteristics (e.g., species, adhesive, and drug-resistant phenotype, etc.). Malarial anemia encompasses reduced production of erythrocytes as well as increased removal of circulating erythrocytes in the bone marrow. Susceptibility to severe malarial anemia is associated with the polymorphisms of the cytokines, which are likely to function by perturbing erythropoiesis. This article reviews the epidemiology, pathophysiology, clinical features, treatment, and various complications occurring due to malarial anemia. The second part of this article also focuses on the effect of malaria during pregnancy. Some significant effects of malaria during pregnancy include spontaneous abortion, preterm delivery, low birthweight, stillbirth, congenital infection, and maternal death. How to cite this article Saxena R, Bhatia A, Midha K, Debnath M, Kaur P. Malaria: A Cause of Anemia and Its Effect on Pregnancy. World J Anemia. 2017;1(2):51-62.

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Leke, Rose F. G., Rosine R. Djokam, Robinson Mbu, Robert J. Leke, Josephine Fogako, Rosette Megnekou, Simon Metenou, et al. "Detection of the Plasmodium falciparumAntigen Histidine-Rich Protein 2 in Blood of Pregnant Women: Implications for Diagnosing Placental Malaria." Journal of Clinical Microbiology 37, no. 9 (1999): 2992–96. http://dx.doi.org/10.1128/jcm.37.9.2992-2996.1999.

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Pregnant women have an increased susceptibility to infection byPlasmodium falciparum. Parasites may be present in the placenta yet not detectable in peripheral blood smears by routine light microscopy. In order to determine how frequently misdiagnosis occurs, peripheral blood and placental samples were collected from 1,077 Cameroonian women at the time of giving birth and examined for the presence of malarial parasites by using light microscopy. Results showed that 20.1% of the women who had placental malaria were peripheral blood smear negative. Thus, malarial infection was not detected by microscopic examination of peripheral blood smears from approximately one out of five malaria-infected women. Since P. falciparum parasites secrete histidine-rich protein 2 (HRP-2), we sought to determine if detecting HRP-2 in either peripheral plasma or whole blood might be used to diagnose the presence of parasites “hidden” in the placenta. Samples of peripheral plasma from 127 women with different levels of placental malarial infection were assayed by HRP-2-specific enzyme-linked immunosorbent assay. HRP-2 was detected in 88% of the women with placental malaria who tested negative by blood smear. Additionally, whole blood was obtained from 181 women and tested for HRP-2 with a rapid, chromatographic strip test (ICT). The ICT test accurately detected malarial infection in 89.1% ofP. falciparum-infected women. Furthermore, 94% of women with malaria were accurately diagnosed by using a combination of microscopy and the ICT test. Thus, detection of HRP-2 in conjunction with microscopy should improve diagnosis of malaria in pregnant women.

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Johnson, Jacob D., Richard A. Dennull, Lucia Gerena, Miriam Lopez-Sanchez, Norma E. Roncal, and Norman C. Waters. "Assessment and Continued Validation of the Malaria SYBR Green I-Based Fluorescence Assay for Use in Malaria Drug Screening." Antimicrobial Agents and Chemotherapy 51, no. 6 (March 19, 2007): 1926–33. http://dx.doi.org/10.1128/aac.01607-06.

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ABSTRACT Several new fluorescence malaria in vitro drug susceptibility microtiter plate assays that detect the presence of malarial DNA in infected erythrocytes have recently been reported, in contrast to traditional isotopic screens that involve radioactive substrate incorporation to measure in vitro malaria growth inhibition. We have assessed and further characterized the malaria SYBR Green I-based fluorescence (MSF) assay for its ability to monitor drug resistance. In order to use the MSF assay as a drug screen, all assay conditions must be thoroughly examined. In this study we expanded upon the capabilities of this assay by including antibiotics and antifolates in the drug panel and testing folic acid-free growth conditions. To do this, we evaluated a more expansive panel of antimalarials in combination with various drug assay culture conditions commonly used in drug sensitivity screening for their activity against Plasmodium falciparum strains D6 and W2. The detection and quantitation limits of the MSF assay were 0.04 to 0.08% and ∼0.5% parasitemia, respectively. The MSF assay quality was significantly robust, displaying a Z′ range of 0.73 to 0.95. The 50% inhibitory concentrations for each drug and culture condition combination were determined by using the MSF assay. Compared to the standard [3H]hypoxanthine assay, the MSF assay displayed the expected parasite drug resistance patterns with a high degree of global and phenotypic correlation (r 2 ≥ 0.9238), regardless of which culture condition combination was used. In conclusion, the MSF assay allows for reliable one-plate high-throughput, automated malaria in vitro susceptibility testing without the expense, time consumption, and hazard of other screening assays.

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Morenikeji, Olanrewaju B., Jessica L. Metelski, Megan E. Hawkes, Anna L. Capria, Brooke N. Seamans, Catherine O. Falade, Olusola Ojurongbe, and Bolaji N. Thomas. "CD209 and Not CD28 or STAT6 Polymorphism Mediates Clinical Malaria and Parasitemia among Children from Nigeria." Microorganisms 8, no. 2 (January 23, 2020): 158. http://dx.doi.org/10.3390/microorganisms8020158.

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Malaria remains a significant disease, causing epic health problems and challenges all over the world, especially in sub-Saharan Africa. CD209 and CD28 genes act as co-stimulators and regulators of the immune system, while the STAT6 gene has been reported to mediate cytokine-induced responses. Single nucleotide polymorphisms of these genes might lead to differential disease susceptibility among populations at risk for malaria, due to alterations in the immune response. We aim to identify key drivers of the immune response to malaria infection among the three SNPs: CD209 (rs4804803), CD28 (rs35593994) and STAT6 (rs3024974). After approval and informed consent, we genotyped blood samples from a total of 531 children recruited from Nigeria using the Taqman SNP genotyping assay and performed comparative analysis of clinical covariates among malaria-infected children. Our results reveal the CD209 (rs4804803) polymorphism as a susceptibility factor for malaria infection, significantly increasing the risk of disease among children, but not CD28 (rs35593994) or STAT6 (rs3024974) polymorphisms. Specifically, individuals with the homozygous mutant allele (rs4804803G/G) for the CD209 gene have a significantly greater susceptibility to malaria, and presented with higher mean parasitemia. This observation may be due to a defective antigen presentation and priming, leading to an ineffective downstream adaptive immune response needed to combat infection, as well as the resultant higher parasitemia and disease manifestation. We conclude that the CD209 gene is a critical driver of the immune response during malaria infection, and can serve as a predictor of disease susceptibility or a biomarker for disease diagnosis.

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Henry, Benoît, Camille Roussel, Papa Alioune Ndour, Mario Carucci, Julien Duez, Aurélie Fricot, Florentin Aussenac, et al. "Red Blood Cell Deformability, Age, Ethnicity and Susceptibility to Malaria in Africa." Blood 128, no. 22 (December 2, 2016): 2441. http://dx.doi.org/10.1182/blood.v128.22.2441.2441.

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Abstract Introduction: malaria is one of the most frequent hematological diseases worldwide. Because the malaria parasite Plasmodium falciparum develops mainly in red blood cells (RBC), splenic retention of infected and uninfected RBC is likely a key player in the variable susceptibility of humans to malaria. Age and ethnicity are important determinants of the manifestations of malaria in Africa (Reyburn JAMA 2005, Dolo Am J Trop Med Hyg 2005; Greenwood Ann Trop Med Parasitol 1987; Torcia PNAS 2008), Asia (Price Am J Trop Med Hyg 2001), and in travelers (Seringe Emerg Infect Dis 2011). We had speculated that variations in the splenic sensing of RBC contribute to the innate protection/susceptibility of infants against distinct forms of severe malaria and to the pathogenesis of chronic malaria (Buffet Curr Opin Hematol 2009; Buffet Blood 2011). Here, we explore the deformability and morphology of circulating RBC in populations living in a malaria-endemic area. Materials and methods: experiments were embedded in an integrated study driven by Institut de Recherche pour le Développement, which aims at the identification of genetic, epidemiologic and anthropologic determinants of susceptibility to malaria. IRB approval was obtained from Institut des Sciences Biomédicales Appliquées, Benin. Clinical and biological data were collected at the beginning of the rainy season from 627 individuals, belonging to 4 different ethnic groups living in sympatry in Atakora, North Benin and included age, gender, ethnicity, body temperature, presence and grade of splenomegaly, rapid diagnostic test for malaria (RDT), thick film and rapid hemoglobin determination with HemoCue©. Venous blood was collected for determination of RBC morphology and deformability. Using microsphiltration, a RBC filtering method that uses microsphere layers to mimic the mechanical retention of RBC in the splenic red pulp (Deplaine Blood 2011) we quantified the ability of a mix of labeled and non-labeled RBCs to squeeze between calibrated slits, results being expressed as retention or enrichment rates (RER) of subject's RBC compared to normal RBC (from a single French O-positive donor) stored in blood bank conditions. Microsphiltration has been adapted to high-throughput experimentation using microplates (Duez AAC 2015). Experiments were performed in a field laboratory established on site; microplates were prepared in Paris and brought to North Benin in luggage with constant care to avoid shocks during transportation. All RBC samples were filtered in triplicate less than 8 hours after blood collection. Up- and downstream samples were brought back to France at 4°C in sealed micro-well plates and analyzed for individual RER calculation in the next 2 weeks by flow cytometry. Results: over 10 days, 262 adults and 249 children were included, 31% Bariba, 17% Gando (genetically related to Bariba), 24% Otamari, 27% Peulhs. Prevalences of splenomegaly, positive RDT, and fever were 13%, 27%, and 2%, respectively. Of 629 blood samples collected, 511 could be analyzed. RER of controls remained stable with time and across 17 microfiltering plates, with a median (IQR) retention rate of 12% (5% - 21%). Ethnicity and age were the only two factors associated with statistically significant differences in RER (figures 1 and 2). Infants (less than 2 year-old) had a more important enrichment than older children and adults (median in 2 years old or less 287%; 3 to 5 years 103%; 6 to 10 years: 64%; more than ten years: 91%; p=0.0161). Peulhs and Otamari also had higher median enrichment rates than Bariba and Gando (RER: 122% and 118%, 75%, 64%, respectively; p=0.0246). Conversely, splenomegaly, gender, positivity of RDT or anemia at the time of sampling were not associated with RER. Discussion: higher averaged enrichment rates in specific ethnic subgroups, namely Peulhs and Otamari, likely result from a more stringent splenic retention, leaving more deformable RBC in circulation. An innate spleen-RBC interaction process was also observed in infants, which is consistent with the higher incidence of severe malarial anemia and splenomegaly observed in this population (Reyburn JAMA 2005; Price Am J Trop Med Hyg 2001). Our results show that innate factors (e.g. ethnicity and age) tend to influence the deformability of RBC, and therefore the phenotypic expression of malaria in Africa. Ongoing experiments aim at deciphering the mechanisms responsible for these differences. Disclosures No relevant conflicts of interest to declare.

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Sahu, Upasana, Biranchi N. Mohapatra, Shantanu K. Kar, and Manoranjan Ranjit. "Promoter Polymorphisms in the ATP Binding Cassette Transporter Gene Influence Production of Cell-Derived Microparticles and Are Highly Associated with Susceptibility to Severe Malaria in Humans." Infection and Immunity 81, no. 4 (February 4, 2013): 1287–94. http://dx.doi.org/10.1128/iai.01175-12.

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ABSTRACTMicroparticle (MP) efflux is known to be mediated by the ABCA1 protein, and the plasma level of these cell-derived MPs is elevated considerably during human malarial infection. Therefore, two polymorphisms at positions −477 and −320 in the promoter of the ABCA1 gene were genotyped and tested for association with the plasma MP level in four groups of malaria patients segregated according to the clinical severity, i.e., cerebral malaria (CM), multiorgan dysfunction (MOD), noncerebral severe malaria, and uncomplicated malaria (UM). The TruCount tube-based flow cytometric method was used for the exact quantification of different cell-derived MPs in patients. Polymorphisms in the ABCA1 gene promoter were analyzed by use of the PCR/two-primer-pair method, followed by restriction fragment length polymorphism, in 428 malaria patients. The level of circulating plasma MPs was significantly higher in febrile patients withPlasmodium falciparuminfection, especially in CM patients compared to healthy individuals. The homozygous wild-type −477 and −320 genotype was observed to be significantly higher in patients with severe malaria. These patients also showed marked increases in the plasma MP numbers compared to UM patients. We report here for the first time an association of ABCA1 promoter polymorphisms with susceptibility to severe malaria, especially to CM and MOD, indicating the protective effect of the mutant variant of the polymorphism. We hypothesize that the −477T and −320G polymorphisms affect the downregulation of MP efflux and may be a predictor of organ complication duringP. falciparummalarial infections.

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HARTGERS, FRANCA C., BENEDICTA B. OBENG, DANIEL BOAKYE, and MARIA YAZDANBAKHSH. "Immune responses during helminth-malaria co-infection: a pilot study in Ghanaian school children." Parasitology 135, no. 7 (May 12, 2008): 855–60. http://dx.doi.org/10.1017/s0031182008000401.

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SUMMARYMalaria and helminth infections have a shared geographical distribution and therefore co-infections are frequent in tropical areas of the world. Human populations of helminth and malaria co-infection have shown contradictory results for the course of malarial infection and disease, possibly depending on the type of helminth studied, the intensity of helminth infection and the age of the study population. Although immunological studies might clarify the underlying mechanisms of protection or increased susceptibility, there are very few studies that have looked at immunological parameters in helminth and malaria co-infection. After discussing the available immunological data on co-infection, we describe a pilot study performed in Ghanaian school children where we compare anti-malarial responses in children living in an urban area, where the prevalence of helminth andPlasmodium falciparuminfections was low, with that of children living in a rural area with high prevalence of helminth andPlasmodium falciparuminfections.

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Dembele, Laurent, Yaw Aniweh, Nouhoum Diallo, Fanta Sogore, Cheick Papa Oumar Sangare, Aboubecrin Sedhigh Haidara, Aliou Traore, et al. "Plasmodium malariae and Plasmodium falciparum comparative susceptibility to antimalarial drugs in Mali." Journal of Antimicrobial Chemotherapy 76, no. 8 (May 22, 2021): 2079–87. http://dx.doi.org/10.1093/jac/dkab133.

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Abstract Objectives To evaluate Plasmodium malariae susceptibility to current and lead candidate antimalarial drugs. Methods We conducted cross-sectional screening and detection of all Plasmodium species malaria cases, which were nested within a longitudinal prospective study, and an ex vivo assessment of efficacy of a panel of antimalarials against P. malariae and Plasmodium falciparum, both PCR-confirmed mono-infections. Reference compounds tested included chloroquine, lumefantrine, artemether and piperaquine, while candidate antimalarials included the imidazolopiperazine GNF179, a close analogue of KAF156, and the Plasmodium phosphatidylinositol-4-OH kinase (PI4K)-specific inhibitor KDU691. Results We report a high frequency (3%–15%) of P. malariae infections with a significant reduction in ex vivo susceptibility to chloroquine, lumefantrine and artemether, which are the current frontline drugs against P. malariae infections. Unlike these compounds, potent inhibition of P. malariae and P. falciparum was observed with piperaquine exposure. Furthermore, we evaluated advanced lead antimalarial compounds. In this regard, we identified strong inhibition of P. malariae using GNF179, a close analogue of KAF156 imidazolopiperazines, which is a novel class of antimalarial drug currently in clinical Phase IIb testing. Finally, in addition to GNF179, we demonstrated that the Plasmodium PI4K-specific inhibitor KDU691 is highly inhibitory against P. malariae and P. falciparum. Conclusions Our data indicated that chloroquine, lumefantrine and artemether may not be suitable for the treatment of P. malariae infections and the potential of piperaquine, as well as new antimalarials imidazolopiperazines and PI4K-specific inhibitor, for P. malariae cure.

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Mahkota, Renti, Fajaria Nurcandra, Fitria Dewi Puspita Anggraini, Annisa Ika Putri, and Bambang Wispriyono. "Risk of Agricultural Pesticide Exposure to Malaria Incidence and Anopheles Susceptibility at an Endemic Area in Central Java, Indonesia – A Case–control Study." Open Access Macedonian Journal of Medical Sciences 8, E (February 5, 2020): 52–59. http://dx.doi.org/10.3889/oamjms.2020.3024.

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BACKGROUND: Malaria is an infectious disease caused by Plasmodium sp. This disease often occurs in tropical countries and has sometimes been reported in agricultural countries. This vector-borne disease is associated with environmental factors and the presence of vectors. Some studies found that Anopheles is resistant to insecticide, and this topic was encouraged by the WHO for malaria control. AIM: This research aimed to explain the causal effects of agricultural pesticide exposure on malaria incidence and Anopheles susceptibility in an endemic area of Indonesia. METHODS: A case–control study was conducted between September and October 2016 in Purworejo, Central Java. The case group involved 131 individuals who had malaria in 2016 based on their medical records, whereas the control group comprised 131 individuals who were neighbors of the cases and never had a history of malaria. Cases were selected randomly from hospital medical records. Both case and control groups were interviewed using the same questionnaire, and data were analyzed using logistic regression. Insecticide susceptibility test was used to test the 80 mosquito samples collected from the neighborhood of recent malaria cases. RESULTS: The quantity of agricultural pesticide remains a potential health risk to malaria (odds ratio = 2.15; 95% confidence interval 1.000–4.638), which was adjusted by confounders (sex, resting place, and insecticide net). The susceptibility test indicated that Anopheles was resistant to both permethrin (86.25%) and bendiocarb (68.75%). CONCLUSIONS: The quantity of agricultural pesticide contributes as a risk factor to malaria incidences, and Anopheles was indicated to be resistant to bendiocarb in Purworejo, Central Java.

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Koch, Oliver, Agnes Awomoyi, Stanley Usen, Muminatou Jallow, Anna Richardson, Jeremy Hull, Margaret Pinder, Melanie Newport, and Dominic Kwiatkowski. "IFNGR1Gene Promoter Polymorphisms and Susceptibility to Cerebral Malaria." Journal of Infectious Diseases 185, no. 11 (June 2002): 1684–87. http://dx.doi.org/10.1086/340516.

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Wozniak, M. A. "Does apolipoprotein E polymorphism influence susceptibility to malaria?" Journal of Medical Genetics 40, no. 5 (May 1, 2003): 348–51. http://dx.doi.org/10.1136/jmg.40.5.348.

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Makgoba, MW. "Molecular basis of resistance and susceptibility to malaria." Lancet 350, no. 9079 (September 1997): 678–79. http://dx.doi.org/10.1016/s0140-6736(05)63507-6.

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Belnoue, Elodie, Michèle Kayibanda, Jean-Christophe Deschemin, Mireille Viguier, Matthias Mack, William A. Kuziel, and Laurent Rénia. "CCR5 deficiency decreases susceptibility to experimental cerebral malaria." Blood 101, no. 11 (June 1, 2003): 4253–59. http://dx.doi.org/10.1182/blood-2002-05-1493.

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Abstract Infection of susceptible mouse strains with Plasmodium berghei ANKA (PbA) is a valuable experimental model of cerebral malaria (CM). Two major pathologic features of CM are the intravascular sequestration of infected erythrocytes and leukocytes inside brain microvessels. We have recently shown that only the CD8+ T-cell subset of these brain-sequestered leukocytes is critical for progression to CM. Chemokine receptor–5 (CCR5) is an important regulator of leukocyte trafficking in the brain in response to fungal and viral infection. Therefore, we investigated whether CCR5 plays a role in the pathogenesis of experimental CM. Approximately 70% to 85% of wild-type and CCR5+/- mice infected with PbA developed CM, whereas only about 20% of PbA-infected CCR5-deficient mice exhibited the characteristic neurologic signs of CM. The brains of wild-type mice with CM showed significant increases in CCR5+ leukocytes, particularly CCR5+ CD8+ T cells, as well as increases in T-helper 1 (Th1) cytokine production. The few PbA-infected CCR5-deficient mice that developed CM exhibited a similar increase in CD8+ T cells. Significant leukocyte accumulation in the brain and Th1 cytokine production did not occur in PbA-infected CCR5-deficient mice that did not develop CM. Moreover, experiments using bone marrow (BM)–chimeric mice showed that a reduced but significant proportion of deficient mice grafted with CCR5+ BM develop CM, indicating that CCR5 expression on a radiation-resistant brain cell population is necessary for CM to occur. Taken together, these results suggest that CCR5 is an important factor in the development of experimental CM.

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KOSSODO, S., C. MONSO, P. JUILLARD, T. VELU, M. GOLDMAN, and G. E. GRAU. "Interleukin‐10 modulates susceptibility in experimental cerebral malaria." Immunology 91, no. 4 (August 1997): 536–40. http://dx.doi.org/10.1046/j.1365-2567.1997.00290.x.

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Valletta, John Joseph, John W. G. Addy, Adam J. Reid, Francis M. Ndungu, Yaw Bediako, Jedida Mwacharo, Khadija Said, et al. "Individual-level variations in malaria susceptibility and acquisition of clinical protection." Wellcome Open Research 6 (February 2, 2021): 22. http://dx.doi.org/10.12688/wellcomeopenres.16524.1.

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After decades of research, our understanding of when and why individuals infected with Plasmodium falciparum develop clinical malaria is still limited. Correlates of immune protection are often sought through prospective cohort studies, where measured host factors are correlated against the incidence of clinical disease over a set period of time. However, robustly inferring individual-level protection from these population-level findings has proved difficult due to small effect sizes and high levels of variance underlying such data. In order to better understand the nature of these inter-individual variations, we analysed the long-term malaria epidemiology of children ≤12 years old growing up under seasonal exposure to the parasite in the sub-location of Junju, Kenya. Despite the cohort’s limited geographic expanse (ca. 3km x 10km), our data reveal a high degree of spatial and temporal variability in malaria prevalence and incidence rates, causing individuals to experience varying levels of exposure to the parasite at different times during their life. Analysing individual-level infection histories further reveal an unexpectedly high variability in the rate at which children experience clinical malaria episodes. Besides exposure to the parasite, measured as disease prevalence in the surrounding area, we find that the birth time of year has an independent effect on the individual’s risk of experiencing a clinical episode. Furthermore, our analyses reveal that those children with a history of an above average number of episodes are more likely to experience further episodes during the upcoming transmission season. These findings are indicative of phenotypic differences in the rates by which children acquire clinical protection to malaria and offer important insights into the natural variability underlying malaria epidemiology.

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Valletta, John Joseph, John W. G. Addy, Adam J. Reid, Francis M. Ndungu, Yaw Bediako, Jedida Mwacharo, Khadija Said, et al. "Individual-level variations in malaria susceptibility and acquisition of clinical protection." Wellcome Open Research 6 (September 13, 2021): 22. http://dx.doi.org/10.12688/wellcomeopenres.16524.2.

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After decades of research, our understanding of when and why individuals infected with Plasmodium falciparum develop clinical malaria is still limited. Correlates of immune protection are often sought through prospective cohort studies, where measured host factors are correlated against the incidence of clinical disease over a set period of time. However, robustly inferring individual-level protection from these population-level findings has proved difficult due to small effect sizes and high levels of variance underlying such data. In order to better understand the nature of these inter-individual variations, we analysed the long-term malaria epidemiology of children ≤12 years old growing up under seasonal exposure to the parasite in the sub-location of Junju, Kenya. Despite the cohort’s limited geographic expanse (ca. 3km x 10km), our data reveal a high degree of spatial and temporal variability in malaria prevalence and incidence rates, causing individuals to experience varying levels of exposure to the parasite at different times during their life. Analysing individual-level infection histories further reveal an unexpectedly high variability in the rate at which children experience clinical malaria episodes. Besides exposure to the parasite, measured as disease prevalence in the surrounding area, we find that the birth time of year has an independent effect on the individual’s risk of experiencing a clinical episode. Furthermore, our analyses reveal that those children with a history of an above average number of episodes are more likely to experience further episodes during the upcoming transmission season. These findings are indicative of phenotypic differences in the rates by which children acquire clinical protection to malaria and offer important insights into the natural variability underlying malaria epidemiology.

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Tanomsing, Naowarat, Mallika Imwong, Sasithon Pukrittayakamee, Kesinee Chotivanich, Sornchai Looareesuwan, Mayfong Mayxay, Christiane Dolecek, et al. "Genetic Analysis of the Dihydrofolate Reductase-Thymidylate Synthase Gene from Geographically Diverse Isolates of Plasmodium malariae." Antimicrobial Agents and Chemotherapy 51, no. 10 (August 6, 2007): 3523–30. http://dx.doi.org/10.1128/aac.00234-07.

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ABSTRACT Plasmodium malariae, the parasite responsible for quartan malaria, is transmitted in most areas of malaria endemicity and is associated with significant morbidity. The sequence of the gene coding for the enzyme dihydrofolate reductase-thymidylate synthase (DHFR-TS) was obtained from field isolates of P. malariae and from the closely related simian parasite Plasmodium brasilianum. The two sequences were nearly 100% homologous, adding weight to the notion that they represent genetically distinct lines of the same species. A survey of polymorphisms of the dhfr sequences in 35 isolates of P. malariae collected from five countries in Asia and Africa revealed a low number of nonsynonymous mutations in five codons. In five of the isolates collected from southeast Asia, a nonsynonymous mutation was found at one of the three positions known to be associated with antifolate resistance in other Plasmodium species. Five isolates with the wild-type DHFR could be assayed for drug susceptibility in vitro and were found to be sensitive to pyrimethamine (mean 50% inhibitory concentration, 2.24 ng/ml [95% confidence interval, 0.4 to 3.1]).

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Patel, Sheral S., Rajeev K. Mehlotra, William Kastens, Charles S. Mgone, James W. Kazura, and Peter A. Zimmerman. "The association of the glycophorin C exon 3 deletion with ovalocytosis and malaria susceptibility in the Wosera, Papua New Guinea." Blood 98, no. 12 (December 1, 2001): 3489–91. http://dx.doi.org/10.1182/blood.v98.12.3489.

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Abstract Erythrocyte polymorphisms, including ovalocytosis, have been associated with protection against malaria. This study in the Wosera, a malaria holoendemic region of Papua New Guinea, examined the genetic basis of ovalocytosis and its influence on susceptibility to malaria infection. Whereas previous studies showed significant associations between Southeast Asian ovalocytosis (caused by a 27– base pair deletion in the anion exchanger 1 protein gene) and protection from cerebral malaria, this mutation was observed in only 1 of 1019 individuals in the Wosera. Polymerase chain reaction strategies were developed to genotype individuals for the glycophorin C exon 3 deletion associated with Melanesian Gerbich negativity (GPCΔex3). This polymorphism was commonly observed in the study population (GPCΔex3 frequency = 0.465, n = 742). Although GPCΔex3 was significantly associated with increased ovalocytosis, it was not associated with differences in either Plasmodium falciparumor P vivax infection measured over the 7-month study period. Future case-control studies will determine if GPCΔex3 reduces susceptibility to malaria morbidity.

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Garred, Peter, Morten A. Nielsen, Jørgen A. L. Kurtzhals, Rajneesh Malhotra, Hans O. Madsen, Bamenla Q. Goka, Bartholomew D. Akanmori, Robert B. Sim, and Lars Hviid. "Mannose-Binding Lectin Is a Disease Modifier in Clinical Malaria and May Function as Opsonin for Plasmodium falciparum- Infected Erythrocytes." Infection and Immunity 71, no. 9 (September 2003): 5245–53. http://dx.doi.org/10.1128/iai.71.9.5245-5253.2003.

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ABSTRACT Variant alleles in the mannose-binding lectin (MBL) gene (mbl2) causing low levels of functional MBL are associated with susceptibility to different infections and are common in areas where malaria is endemic. Therefore, we investigated whether MBL variant alleles in 551 children from Ghana were associated with the occurrence and outcome parameters of Plasmodium falciparum malaria and asked whether MBL may function as an opsonin for P. falciparum. No difference in MBL genotype frequency was observed between infected and noninfected children or between children with cerebral malaria and/or severe malarial anemia and children with uncomplicated malaria. However, patients with complicated malaria who were homozygous for MBL variant alleles had significantly higher parasite counts and lower blood glucose levels than their MBL-competent counterparts. Distinct calcium-dependent binding of MBL to the membrane of P. falciparum-infected erythrocytes, which could be inhibited by mannose, was observed. Further characterization revealed that MBL reacted with a P. falciparum glycoprotein identical to the 78-kDa glucose-regulated stress protein of P. falciparum. MBL seems to be a disease modifier in clinical malaria and to function as an opsonin for erythrocytes invaded by P. falciparum and may thus be involved in sequestration of the parasite, which in turn may explain the association between homozygosity for MBL variant alleles and high parasite counts.

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de Souza, J. Brian, James Todd, Gowdahalli Krishegowda, D. Channe Gowda, Dominic Kwiatkowski, and Eleanor M. Riley. "Prevalence and Boosting of Antibodies to Plasmodium falciparum Glycosylphosphatidylinositols and Evaluation of Their Association with Protection from Mild and Severe Clinical Malaria." Infection and Immunity 70, no. 9 (September 2002): 5045–51. http://dx.doi.org/10.1128/iai.70.9.5045-5051.2002.

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ABSTRACT Glycosylphosphatidylinositols (GPIs), the anchor molecules of some membrane proteins of Plasmodium species, have been implicated in the induction of immunopathology during malaria infections. Hence, neutralization of GPIs by antibodies may reduce the severity of clinical attacks of malaria. To test this hypothesis, we have assessed the levels of anti-GPI antibodies in plasma from children and adults living in areas of seasonal malaria transmission in The Gambia. In a prospective study of susceptibility to clinical or asymptomatic infection, the levels of anti-GPI antibodies were measured before and after the transmission season. Samples were also obtained from children recruited into a hospital-based study of severe malaria. We find that in malaria-exposed individuals both the prevalence and the concentration of anti-GPI antibodies increase with age and that antibody levels are significantly higher at the end of the malaria transmission season than at the start of the season. Antibody levels are also higher in children with asymptomatic infections (i.e., those with a degree of clinical immunity) than in children who developed clinical malaria and high parasitemia, although this difference is not statistically significant. Importantly, antibodies appear to be rapidly boosted by clinical malaria infection, but children under the age of two years are seronegative for anti-GPI antibodies, even during an acute infection. While GPIs may be involved in the pathogenesis of human malaria, the data from this study do not provide any strong evidence to support the notion that anti-GPI antibodies confer resistance to mild or severe malarial disease. Further case-control studies, ideally of a prospective nature, are required to elucidate the role of antiglycolipid antibodies in protection from severe malaria.

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Kabula, Bilali, Patrick Tungu, Johnson Matowo, Jovin Kitau, Clement Mweya, Basiliana Emidi, Denis Masue, et al. "Susceptibility status of malaria vectors to insecticides commonly used for malaria control in Tanzania." Tropical Medicine & International Health 17, no. 6 (April 23, 2012): 742–50. http://dx.doi.org/10.1111/j.1365-3156.2012.02986.x.

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Atkinson, C. T., K. L. Woods, R. J. Dusek, L. S. Sileo, and W. M. Iko. "Wildlife disease and conservation in Hawaii: Pathogenicity of avian malaria (Plasmodium relictum) in experimentally infected Iiwi (Vestiaria coccinea)." Parasitology 111, S1 (January 1995): S59—S69. http://dx.doi.org/10.1017/s003118200007582x.

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SUMMARYNative Hawaiian forest birds are facing a major extinction crisis with more than 75% of species recorded in historical times either extinct or endangered. Reasons for this catastrophe include habitat destruction, competition with non-native species, and introduction of predators and avian diseases. We tested susceptibility of Iiwi (Vestiaria coccinea), a declining native species, and Nutmeg Mannikins (Lonchura punctulata), a common non-native species, to an isolate ofPlasmodium relictumfrom the island of Hawaii. Food consumption, weight, and parasitaemia were monitored in juvenile Iiwi that were infected by either single (low-dose) or multiple (high-dose) mosquito bites. Mortality in both groups was significantly higher than in uninfected controls, reaching 100% of high-dose birds and 90% of low-dose birds. Significant declines in food consumption and a corresponding loss of body weight occurred in malaria-infected birds. Both sex and body weight had significant effects on survival time, with males more susceptible than females and birds with low initial weights more susceptible than those with higher initial weights. Gross and microscopic lesions in malaria fatalities included massive enlargement of the spleen and liver, hyperplasia of the reticuloendothelial system with extensive deposition of malarial pigment, and overwhelming anaemia in which over 30% of the circulating erythrocytes were parasitized. Nutmeg Mannikins, by contrast, were completely refractory to infection. Our findings support previous studies documenting high susceptibility of native Hawaiian forest birds to avian malaria. This disease continues to threaten remaining high elevation populations of endangered native birds.

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Mendonça, Vitor R. R., Nívea F. Luz, Nadja J. G. Santos, Valéria M. Borges, Marilda S. Gonçalves, Bruno B. Andrade, and Manoel Barral-Netto. "Association between the Haptoglobin and Heme Oxygenase 1 Genetic Profiles and Soluble CD163 in Susceptibility to and Severity of Human Malaria." Infection and Immunity 80, no. 4 (January 30, 2012): 1445–54. http://dx.doi.org/10.1128/iai.05933-11.

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ABSTRACTIntravascular hemolysis is a hallmark event in the immunopathology of malaria that results in increased systemic concentrations of free hemoglobin (Hb). The oxidation of Hb by free radicals causes the release of heme, which amplifies inflammation. To circumvent the detrimental effects of free heme, hosts have developed several homeostatic mechanisms, including the enzyme haptoglobin (Hp), which scavenges cell-free Hb, the monocyte receptor CD163, which binds to Hb-Hp complexes, and heme oxygenase-1 (HO-1), which degrades intracellular free heme. We tested the association between these three main components of the host response to hemolysis and susceptibility to malaria in a Brazilian population. The genetic profiles of theHMOX1andHpgenes and the plasma levels of a serum inflammatory marker, the soluble form of the CD163 receptor (sCD163), were studied in 264 subjects, including 78 individuals with symptomatic malaria, 106 individuals with asymptomatic malaria, and 80 uninfected individuals. We found that long (GT)nrepeats in the microsatellite polymorphism region of theHMOX1gene, theHp2allele, and theHp2.2genotype were associated with symptomatic malaria. Moreover, increased plasma concentrations of heme, Hp, HO-1, and sCD163 were associated with susceptibility to malaria. The validation of these results could support the development of targeted therapies and aid in reducing the severity of malaria.

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Nsanzabana, Christian. "Resistance to Artemisinin Combination Therapies (ACTs): Do Not Forget the Partner Drug!" Tropical Medicine and Infectious Disease 4, no. 1 (February 1, 2019): 26. http://dx.doi.org/10.3390/tropicalmed4010026.

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Artemisinin-based combination therapies (ACTs) have become the mainstay for malaria treatment in almost all malaria endemic settings. Artemisinin derivatives are highly potent and fast acting antimalarials; but they have a short half-life and need to be combined with partner drugs with a longer half-life to clear the remaining parasites after a standard 3-day ACT regimen. When introduced, ACTs were highly efficacious and contributed to the steep decrease of malaria over the last decades. However, parasites with decreased susceptibility to artemisinins have emerged in the Greater Mekong Subregion (GMS), followed by ACTs’ failure, due to both decreased susceptibility to artemisinin and partner drug resistance. Therefore, there is an urgent need to strengthen and expand current resistance surveillance systems beyond the GMS to track the emergence or spread of artemisinin resistance. Great attention has been paid to the spread of artemisinin resistance over the last five years, since molecular markers of decreased susceptibility to artemisinin in the GMS have been discovered. However, resistance to partner drugs is critical, as ACTs can still be effective against parasites with decreased susceptibility to artemisinins, when the latter are combined with a highly efficacious partner drug. This review outlines the different mechanisms of resistance and molecular markers associated with resistance to partner drugs for the currently used ACTs. Strategies to improve surveillance and potential solutions to extend the useful therapeutic lifespan of the currently available malaria medicines are proposed.

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Meira, Domingos Alves, Jordão Pellegrino Júnior, Jussara Marcondes-Machado, Kimiyoski Tsuji, Elinda Satie Matsuoka, Elizete Haida, and Albert Boutros El Khoury. "Frequency of human leukocyte antigen (hla) in patients with malaria and in the general population of Humaitá county, Amazonas state, Brazil." Revista da Sociedade Brasileira de Medicina Tropical 20, no. 3 (September 1987): 153–58. http://dx.doi.org/10.1590/s0037-86821987000300005.

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In August 1983,85 inhabitants of the municipality of Humaitá, Amazonas State, Brazil were studied to determine the prevalence of antigens to HLA-A, -B, -C and DR. Thirty-eight were sick with malaria due to Plasmodium falciparum. All subjects were examined for splenomegaly, blood parasitaemia and antibodies to malaria. They constituted three groups: 1) 25 subjects native to the Amazon region who had never had malaria; 2) 38 Amazonian subjects who had malaria in the past or currently had an infection; 3) 22 patients with malaria who had acquired the infection in the Amazon Region but came from other regions of Brazil. Blood was taken from each person, the lymphocytes were separated and typed by the test of microlymphocytotoxicity. There was a high frequency of antigens that could not be identified in the groups studied which suggests the existence of a homozygote or phenotype not identified in the population. There was a high frequency of the phenotype Ag(W24) (44.7%) in group 2 when compared with group 1 (32%) or group 3 (9%). Also the individuals in group 2 showed an elevated frequency of antigen DR(4)80%) when compared with group 1 (36.6%) or group 3 (16.6%). These observations suggest the possibility of a genetic susceptibility to malaria among Amazonian residents and indicate a necessity for more extensive studies of the frequency of HLA antigens among inhabitants of this endemic malarial zone.

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Min-Oo, Gundula, Anny Fortin, Giuseppina Pitari, Mifong Tam, Mary M. Stevenson, and Philippe Gros. "Complex genetic control of susceptibility to malaria: positional cloning of the Char9 locus." Journal of Experimental Medicine 204, no. 3 (February 20, 2007): 511–24. http://dx.doi.org/10.1084/jem.20061252.

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Mouse strains AcB55 and AcB61 are resistant to malaria by virtue of a mutation in erythrocyte pyruvate kinase (PklrI90N). Linkage analysis in [AcB55 × A/J] F2 mice detected a second locus (Char9; logarithm of odds = 4.74) that regulates the blood-stage replication of Plasmodium chabaudi AS independently of Pklr. We characterized the 77 genes of the Char9 locus for tissue-specific expression, strain-specific alterations in gene expression, and polymorphic variants that are possibly associated with differential susceptibility. We identified Vnn1/Vnn3 as the likely candidates responsible for Char9. Vnn3/Vnn1 map within a conserved haplotype block and show expression levels that are strictly cis-regulated by this haplotype. The absence of Vnn messenger RNA expression and lack of pantetheinase protein activity in tissues are associated with susceptibility to malaria and are linked to a complex rearrangement in the Vnn3 promoter region. The A/J strain also carries a unique nonsense mutation that leads to a truncated protein. Vanin genes code for a pantetheinase involved in the production of cysteamine, a key regulator of host responses to inflammatory stimuli. Administration of cystamine in vivo partially corrects susceptibility to malaria in A/J mice, as measured by reduced blood parasitemia and decreased mortality. These studies suggest that pantetheinase is critical for the host response to malaria.

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Nickerson, J. P., K. A. Tong, and R. Raghavan. "Imaging Cerebral Malaria with a Susceptibility-Weighted MR Sequence." American Journal of Neuroradiology 30, no. 6 (March 25, 2009): e85-e86. http://dx.doi.org/10.3174/ajnr.a1568.

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Diagne, Nafissatou, Christophe Rogier, Cheikh S. Sokhna, Adama Tall, Didier Fontenille, Christian Roussilhon, André Spiegel, and Jean-François Trape. "Increased Susceptibility to Malaria during the Early Postpartum Period." New England Journal of Medicine 343, no. 9 (August 31, 2000): 598–603. http://dx.doi.org/10.1056/nejm200008313430901.

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Journal articles on the topic 'Malaria susceptibility'

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