MALARIA  

January 2006

Some Selected Abstracts:

1. 

Adam I, A-Elbasit IE, Idris SM, Malik EM, Elbashir MI.A comparison of the efficacy of artesunate plus sulfadoxine-pyrimethamine with that of sulfadoxine-pyrimethamine alone, in the treatment of uncomplicated, Plasmodium falciparum malaria in eastern Sudan. Ann Trop Med Parasitol. 2005 Jul;99(5):449-55.

New Halfa Teaching Hospital, Sudan. ishagadam@hotmail.com

In an open, randomized, clinical trial, conducted in New Halfa, eastern Sudan, in September-October 2004, the efficacies and adverse effects of artesunate plus sulfadoxine-pyrimethamine (SP), in the treatment of uncomplicated, Plasmodium falciparum malaria, were compared with those of SP alone. Patients were randomized to receive either artesunate (4 mg/kg. day) on days 0-2 plus SP (25 mg sulfadoxine/kg) on day 0 or the SP alone, and then followed-up for 28 days. Sixty patients completed follow-up. Compared with the 30 given artesunate plus SP (ASP), the 30 given SP alone were much more likely to be febrile (30% v. 3.3%; P=0.006) and parasitaemic (50% v. 6.7%; P<00001) on day 1. By day 3, 16.7% of the patients given SP alone were still febrile and 6.7% of them were still parasitaemic, although all the patients given ASP were then afebrile (P=0.02) and aparasitaemic (P=0.1). Five (16.7%) of the patients treated with SP alone but none of those given ASP appeared to be treatment failures (P<0.05). Parasite genotyping revealed that four of the five apparent treatment failures were true recrudescences but the other represented a re-infection detected on day 28. The true frequencies of cure by day 28 were therefore 100% for ASP and 86.7% for SP alone (P=0.02).Adverse effects of treatment (nausea, itching and giddiness) were observed with similar frequencies in the two treatment arms (10.0% of the patients given ASP v. 13.3% of the patients given SP alone; P>0.05). The frequencies of gametocytaemia during follow-up were, however, much lower in the ASP arm than in the SP-only (0.0% v. 23.3%; P=0.005).Thus, although the problems posed by adverse effects were similar in the two treatment arms, ASP appeared markedly better, in terms of fever- and parasite-clearance times and the prevalence of post-treatment gametocytaemia, than SP alone.

2.

Carter JY, Loolpapit MP, Lema OE, Tome JL, Nagelkerke NJ, Watkins WM.
Reduction of the efficacy of antifolate antimalarial therapy by folic acid supplementation. Am J Trop Med Hyg. 2005 Jul;73(1):166-70.

African Medical and Research Foundation, Nairobi, Kenya.

Malaria and anemia are common conditions in patients presenting to outpatient clinics in Kenya. Anemia is usually due to malaria infection with underlying micronutrient deficiency. Iron therapy has been shown to enhance recovery from anemia in children with malaria, without affecting malaria treatment. Iron and folic acid are often prescribed together for anemic individuals. Until recently in Kenya, the drug of first choice for non-severe malaria was sulfadoxine-pyrimethamine (SP), an antifolate antimalarial drug. In this study, 303 patients of all ages with anemia and uncomplicated Plasmodium falciparum malaria attending an outpatient clinic in an area of seasonal malaria were treated with SP and iron, and were randomized to receive folic acid. Parasite clearance rates were measured using a survival analysis plot for both parasitologic and clinical failure. There was a significant reduction in the efficacy of SP in patients taking standard therapeutic doses of folic acid using the survival curve for parasitologic failure (P < 0.0001), but no difference for clinical failure (P = 0.7008). Folic acid supplementation did not enhance recovery from anemia.

3.

Musumba CO, Griffiths KL, Ross A, Newton CR. Comparison of axillary, rectal and tympanic temperature measurements in children admitted with malaria. J Trop Pediatr. 2005 Aug;51(4):242-4.

Kenya Medical Research Institute (KEMRI) Centre for Geographic Medicine Research, Coast, Kilifi.

We compared axillary, rectal and tympanic temperatures in children admitted with severe malaria. The axillary temperatures were 0.74 degrees C (95% limits of agreement -0.85 to 2.33 degrees C) less than rectal temperatures and tympanic temperatures 0.42 degrees C (95% limits of agreement -0.16 to 2.44 degrees C) less than rectal temperatures. The difference was greater on admission than 24 hours later. These differences may be important in defining criteria for clinical syndromes.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:

13353.   Adam I, A-Elbasit IE, Idris SM, Malik EM, Elbashir MI. A comparison of the efficacy of artesunate plus sulfadoxine-pyrimethamine with that of sulfadoxine-pyrimethamine alone, in the treatment of uncomplicated, Plasmodium falciparum malaria in eastern Sudan. Ann Trop Med Parasitol. 2005 Jul;99(5):449-55.

13354.  Adegnika AA, Breitling LP, Agnandji ST, Chai SK, Schutte D, Oyakhirome S, Schwarz NG, Grobusch MP, Missinou MA, Ramharter M, Issifou S, Kremsner PG.  Effectiveness of quinine monotherapy for the treatment of Plasmodium falciparum infection in pregnant women in Lambarene, Gabon. Am J Trop Med Hyg. 2005 Aug;73(2):263-6.

13355.  Agnamey P, Brasseur P, Cisse M, Gaye O, Dumoulin J, Rigal J, Taylor WR, Olliaro P. Economic evaluation of a policy change from single-agent treatment for suspected malaria to artesunate-amodiaquine for microscopically confirmed uncomplicated falciparum malaria in the Oussouye District of south-western Senegal. Trop Med Int Health. 2005 Sep;10(9):926-33.

13356.  Amino R, Menard R, Frischknecht F. In vivo imaging of malaria parasites--recent advances and future directions. Curr Opin Microbiol. 2005 Aug;8(4):407-14. Review.

13357.  Bell DR, Wilson DW, Martin LB. False-positive results of a Plasmodium falciparum histidine-rich protein 2-detecting malaria rapid diagnostic test due to high sensitivity in a community with fluctuating low parasite density. Am J Trop Med Hyg. 2005 Jul;73(1):199-203.

13358.  Charrel RN, Brouqui P, Foucault C, de Lamballerie X. Concurrent dengue and malaria. Emerg Infect Dis. 2005 Jul;11(7):1153-4.

13359.  Mohire MD. Plasmodium falciparum delayed cerebellar ataxia and late cerebral malaria. Mov Disord. 2005 Aug;20(8):1087-8.

13360.  Musumba CO, Griffiths KL, Ross A, Newton CR. Comparison of axillary, rectal and tympanic temperature measurements in children admitted with malaria. J Trop Pediatr. 2005 Aug;51(4):242-4.

13361.  Mya MM, Saxena RK, Roy A. Seroepidemiological study of plasmodium falciparum antigens for detection of malaria. Indian J Biotechnol 2005, 4(1), 100-5.

13362.  Nahrevanian H. The penetration of Plasmodium into red blood cell is a protective mechanism of malaria parasite against high levels of accumulated nitric oxide in blood circulation. J Parasit Dis 2004, 28(2), 83-9.

13363.  Ravikumar K. Sudarshan KS. Clinical evaluation of a rapid diagnostic kit (Paracheck-pf) for diagnosis of Plasmodium falciparum in Karnataka state of India. Indian J Prev Soc Med 2004, 35(1-2), 10-14.

13364.  Sakai O, Barest GD. Diffusion-weighted imaging of cerebral malaria. J Neuroimaging. 2005 Jul;15(3):278-80.

13365.  Singh OP, Raghavendra K, Chandra D, Subbarao SK. An allele-specific polymerase chain reaction assay for the differentiation of members of the Anopheles culicifacies complex. J Biosci 2004, 29(1), 275-80.

13366.  White NJ, Silamut K. Postmortem brain smear assessment of fatal malaria. J Infect Dis. 2005 Aug 1;192(3):547;

13367.  Whitty CJ, Edmonds S, Mutabingwa TK. Malaria in pregnancy. BJOG. 2005 Sep;112(9):1189-95. Review.

Pathogenesis:

13368.   Gobbi F, Audagnotto S, Trentini L, Nkurunziza I, Corachan M, Di Perri G.  Blackwater fever in children, Burundi. Emerg Infect Dis. 2005 Jul;11(7):1118-20.

13369.  Kirchgatter K, Del Portillo HA. Clinical and molecular aspects of severe malaria. An Acad Bras Cienc. 2005 Sep;77(3):455-75.

13370.  Lipman HM. Preventing severe infection after splenectomy: risk of malaria and meningitis increases with asplenia. BMJ. 2005 Sep 10;331(7516):576.

Vaccines:

13371.   Butcher GA. The role of the spleen and immunization against malaria. Trends Parasitol. 2005 Aug;21(8):356-7.

13372.  Hviid L. Naturally acquired immunity to Plasmodium falciparum malaria in Africa. Acta Trop. 2005 Sep;95(3):270-5. Review.

Therapy:

13373.   Carter JY, Loolpapit MP, Lema OE, Tome JL, Nagelkerke NJ, Watkins WM.  Reduction of the efficacy of antifolate antimalarial therapy by folic acid supplementation. Am J Trop Med Hyg. 2005 Jul;73(1):166-70.

13374.  Croft AM, Beer MD, Herxheimer A. Effectiveness of antimalarial drugs. N Engl J Med. 2005 Jul 28;353(4):420-2;

13375.  Dondorp A, Nosten F, Stepniewska K, Day N, White N; South East Asian Quinine Artesunate Malaria Trial (SEAQUAMAT) group. Artesunate versus quinine for treatment of severe falciparum malaria: a randomised trial. Lancet. 2005 Aug 27-Sep 2;366(9487):717-25.

13376.  Druilhe P, Tall A, Sokhna C. Worms can worsen malaria: towards a new means to roll back malaria? Trends Parasitol. 2005 Aug;21(8):359-62. Review.

13377.   Jain SK, Persaud D, Perl TM, Pass MA, Murphy KM, Pisciotta JM, Scholl PF, Casella JF, Sullivan DJ. Nosocomial malaria and saline flush. Emerg Infect Dis. 2005 Jul;11(7):1097-9.

13378.  Magill A, Panosian C. Making antimalarial agents available in the United States. N Engl J Med. 2005 Jul 28;353(4):335-7.

13379.  Michel K, Kafatos FC. Mosquito immunity against Plasmodium. Insect Biochem Mol Biol. 2005 Jul;35(7):677-89.

13380.  Mutabingwa TK. Artemisinin-based combination therapies (ACTs): best hope for malaria treatment but inaccessible to the needy! Acta Trop. 2005 Sep;95(3):305-15. Review.

13381.  Nahlen BL, Korenromp EL, Miller JM, Shibuya K. Malaria risk: estimating clinical episodes of malaria. Nature. 2005 Sep 8;437(7056):E3; discussion E4-5.

13382.  Sharma P, Chhangani NP, Sharma KK. Gangrene in a child with Plasmodium falciparum malaria. J Trop Pediatr. 2005 Aug;51(4):252-3.

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April 2006

Some Selected Abstracts:

1. 

Balunas MJ, Kinghorn AD.  Drug discovery from medicinal plants. Life Sci. 2005 Dec 22;78(5):431-41.  Review.

Program for Collaborative Research in the Pharmaceutical Sciences, Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, 833 South Wood Street, University of Illinois at Chicago, Chicago, IL 60612, USA.

Current research in drug discovery from medicinal plants involves a multifaceted approach combining botanical, phytochemical, biological, and molecular techniques. Medicinal plant drug discovery continues to provide new and important leads against various pharmacological targets including cancer, HIV/AIDS, Alzheimer's, malaria, and pain. Several natural product drugs of plant origin have either recently been introduced to the United States market, including arteether, galantamine, nitisinone, and tiotropium, or are currently involved in late-phase clinical trials. As part of our National Cooperative Drug Discovery Group (NCDDG) research project, numerous compounds from tropical rainforest plant species with potential anticancer activity have been identified. Our group has also isolated several compounds, mainly from edible plant species or plants used as dietary supplements, that may act as chemopreventive agents. Although drug discovery from medicinal plants continues to provide an important source of new drug leads, numerous challenges are encountered including the procurement of plant materials, the selection and implementation of appropriate high-throughput screening bioassays, and the scale-up of active compounds.

2.

Barennes H, Valea I, Nagot N, Van de Perre P, Pussard E. Sublingual sugar administration as an alternative to intravenous dextrose administration to correct hypoglycemia among children in the tropics.Pediatrics. 2005 Nov;116(5):e648-53.

Centre Muraz, Bobo-Dioulasso, Burkina Faso, France. hubert.barennes@avf.org

BACKGROUND: Hypoglycemia is a common determining factor of poor prognosis for children with severe malaria in sub-Saharan Africa. Intravenous dextrose administration is rarely available. Oral mucosal delivery may be an alternative to parenteral administration. A randomized, clinical trial was performed in Burkina Faso among moderately hypoglycemic children, comparing sublingual sugar administration with oral water, oral sugar, and dextrose infusion administrations. METHODS: Sixty-nine children with glucose concentrations of < 0.8 g/L were assigned randomly to 1 of 4 methods of administration, 1 with 3 different doses of sugar, as follows: oral group (OG) (n = 15): 2.5 g of sugar; sublingual group (SG) (n = 27): 2.5 g of sugar under the tongue, with 3 treatment subgroups, ie, 0.1 g/kg, 0.15 g/kg, and 0.2 g/kg; intravenous group (IG) (n = 8): 8 mL of 30% dextrose in a single bolus; water group (n = 11). Eight children received sublingual sugar twice, ie, 0.1 g/kg at baseline and 20 minutes later. Blood glucose concentrations were measured every 20 minutes for 80 minutes. Treatment failures, peak glucose concentrations, times to glucose concentration normalization, and kinetic profiles were evaluated. RESULTS: No treatment failures were observed in the SG and IG, compared with 8 (53%) and 9 (81.8%) failures in the OG and water group, respectively. SG children exhibited glucose kinetic profiles and bioavailabilities (77%, 99%, and 81% in the 3 SG groups) similar to those of IG children. Bioavailabilities were 84% and 38% in the SG and OG, respectively. Children > 7 years of age required repeated sublingual administrations to maintain normoglycemia. CONCLUSIONS: The sublingual administration of sugar proved to be effective among moderately hypoglycemic children. It is a simple and promising method to control hypoglycemia among children in both developing and developed countries. This pediatric practice should be investigated in more detail among children with severe malaria.

3.

Lemnge MM, Ali AS, Malecela EK, Sambu E, Abdulla R, Juma MS, Fakih K, Abdulla KH, Njau RJ. Therapeutic efficacy of sulfadoxine-pyrimethamine and amodiaquine among children with uncomplicated Plasmodium falciparum malaria in Zanzibar, Tanzania. Am J Trop Med Hyg. 2005 Oct;73(4):681-5.

National Institute for Medical Research, Amani Medical Research Centre, Amani, Tanga, Tanzania. mlemnge@amani.mimcom.net

The efficacy of sulfadoxine-pyrimethamine (SP) and amodiaquine (AQ) was assessed at Kivunge and Micheweni in Zanzibar, Tanzania, in 2001. The main objective was to obtain baseline data after observations of high levels of chloroquine treatment failures. Children (6-59 months) were randomized to receive either drug. At Kivunge, SP and AQ were given to 64 and 63 cases, while for Micheweni, 61 and 70 cases were treated. Main findings were overall high rates (> 90%) of adequate clinical response (ACR) with AQ. A lower ACR was seen in the SP group at Kivunge (87.1%) compared with Micheweni (94.8%). Furthermore, in the ACR group, 16.7% AQ parasitological resistance (RI-RIII) was encountered at Kivunge. Most of the cases of SP parasitological resistance (14.5%; RI/RII) were seen at Micheweni. Notwithstanding this, the overall treatment failure was only 9.2% with SP and 5.5% with AQ. The Zanzibar Ministry of Health has since reviewed its antimalarial drug policy.

4.

Mehta M, Sonawat HM, Sharma S. Malaria parasite-infected erythrocytes inhibit glucose utilization in uninfected red cells. FEBS Lett. 2005 Nov 7;579(27):6151-8. 

Department of Biological Sciences, Tata Institute of Fundamental Research, Mumbai 400 005, India.

The erythrocytic stages of the malaria parasite depend on anaerobic glycolysis for energy. Using [2-13C]glucose and nuclear magnetic resonance, the glucose utilization rate and 2,3-diphosphoglycerate (2,3-DPG) level produced in normal RBCs and Plasmodium falciparum infected red blood cell populations (IRBCs, with <4% parasite infected red cells), were measured. The glucose flux in IRBCs was several-folds greater, was proportional to parasitemia, and maximal at trophozoite stage. The 2,3-DPG levels were disproportionately lower in IRBCs, indicating a downregulation of 2,3-DPG flux in non-parasitized RBCs. This may be due to lowered pH leading to selective differential inhibition of the regulatory glycolytic enzyme phosphofructokinase. This downregulation of the glucose utilization rate in the majority (>96%) of uninfected RBCs in an IRBC population may have physiological implications in malaria patients.

5.

Richer J, Chudley AE. The hemoglobinopathies and malaria. Clin Genet. 2005 Oct;68(4):332-6. Review.

Department of Pediatrics and Child Health, Program in Genetics and Metabolism, Children's Hospital, University of Manitoba, Winnipeg, Manitoba, Canada.

With philatelic illustrations, we review sickle cell anemia, some of the common hemoglobinopathies, and their relevance to malaria. We discuss the mechanism by which hemoglobinopathies arise, the progress made with pre-natal screening, as well as innovative therapies. We review recent developments in the pathophysiology of malaria and discuss innovations in the effort against this parasite.

6.

Williams TN, Mwangi TW, Wambua S, Peto TE, Weatherall DJ, Gupta S, Recker M, Penman BS, Uyoga S, Macharia A, Mwacharo JK, Snow RW, Marsh K. Negative epistasis between the malaria-protective effects of alpha+-thalassemia and the sickle cell trait. Nat Genet. 2005 Nov;37(11):1253-7. 

Kenya Medical Research Institute/Wellcome Trust Programme, Centre for Geographic Medicine Research, Coast, PO Box 230, Kilifi District Hospital, Kilifi, Kenya. twilliams@kilifi.mimcom.net

The hemoglobinopathies, disorders of hemoglobin structure and production, protect against death from malaria. In sub-Saharan Africa, two such conditions occur at particularly high frequencies: presence of the structural variant hemoglobin S and alpha(+)-thalassemia, a condition characterized by reduced production of the normal alpha-globin component of hemoglobin. Individually, each is protective against severe Plasmodium falciparum malaria, but little is known about their malaria-protective effects when inherited in combination. We investigated this question by studying a population on the coast of Kenya and found that the protection afforded by each condition inherited alone was lost when the two conditions were inherited together, to such a degree that the incidence of both uncomplicated and severe P. falciparum malaria was close to baseline in children heterozygous with respect to the mutation underlying the hemoglobin S variant and homozygous with respect to the mutation underlying alpha(+)-thalassemia. Negative epistasis could explain the failure of alpha(+)-thalassemia to reach fixation in any population in sub-Saharan Africa.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:

13919.   Afenyadu GY, Agyepong IA, Barnish G, Adjei S. Improving access to early treatment of malaria: a trial with primary school teachers as care providers. Trop Med Int Health. 2005 Oct;10(10):1065-72.

13920.   Ashley EA, White NJ. Artemisinin-based combinations. Curr Opin Infect Dis. 2005 Dec;18(6):531-6. Review.

13921.   Chung WY, Gardiner DL, Hyland C, Gatton M, Kemp DJ, Trenholme KR. Enhanced invasion of blood group A1 erythrocytes by Plasmodium falciparum. Mol Biochem Parasitol. 2005 Nov;144(1):128-30.

13922.   Ginsburg H. Should chloroquine be laid to rest? Acta Trop. 2005 Oct;96(1):16-23. Review.

13923.   Heppner DG Jr, Walsh DS, Uthaimongkol N, Tang DB, Tulyayon S, Permpanich B, Wimonwattrawatee T, Chuanak N, Laoboonchai A, Sookto P, Brewer TG, McDaniel P, Eamsila C, Yongvanitchit K, Uhl K, Kyle DE, Keep LW, Miller RE, Wongsrichanalai C. Randomized, controlled, double-blind trial of daily oral azithromycin in adults for the prophylaxis of Plasmodium vivax malaria in Western Thailand. Am J Trop Med Hyg. 2005 Nov;73(5):842-9.

13924.   Kundu R, Ganguly N, Ghosh TK, Choudhury P, Shah RC. Diagnosis and management of malaria in children: recommendations and IAP plan of action. Indian Pediatr. 2005 Nov;42(11):1101-14.

13925.   Lesho EP, George S, Wortmann G. Fever in a returned traveler. Cleve Clin J Med. 2005 Oct;72(10):921-7. Review.

13926.  Okocha E C, Ibeh C C, Ele P U, Ibeh N C. The prevalence of malariaparasitaemia in blood donors in a Nigerian teaching hospital. Jvector borne Dis 2005; 42(1): 21-4.

13927.  Villamor E, Msamanga G, Aboud S, Urassa W, Hunter DJ, Fawzi WW.   Adverse perinatal outcomes of HIV-1-infected women in relation to malaria parasitemia in maternal and umbilical cord blood. Am J Trop Med Hyg. 2005 Oct;73(4):694-7.

Pathogenesis:

13928.  Adam I, Elbashir MI. Comments on "Risk factors for malaria infection and anemia for pregnant women in the Sahel area of Bandiagara, Mali" by A. Dicko et al. [Acta Trop. 89 (2003) 17-23]. Acta Trop. 2005 Oct;96(1):60-1.

Therapy:

13929.     Boctor FN. Red blood cell exchange transfusion as an adjunct treatment for severe pediatric falciparum malaria, using automated or manual procedures. Pediatrics. 2005 Oct;116(4):e592-5. 

13930   Dunavan CP. Tackling malaria. Sci Am. 2005 Dec;293(6):76-83.

13931.  Hutchinson OC, Cunningham AA. Benefits and risks in malaria control. Science. 2005 Oct 7;310(5745):49-51; author reply 49-51.

13932.  Khan MA, Mekan SF, Abbas Z, Smego RA Jr. Concurrent malaria and enteric fever in Pakistan. Singapore Med J. 2005 Nov;46(11):635-8.

13933.  Okie S. Betting on a malaria vaccine. N Engl J Med. 2005 Nov 3;353(18):1877-81.

13934.   The Lancet. Support for antimalaria efforts will depend on results. Lancet. 2005 Dec 3;366(9501):1904.

13935.  Vogel G.  Infectious diseases. Cracks in the first line of defense. Science. 2005 Dec 9;310(5754):1607.

13936.  Ward MD, Selgrade MK. Benefits and risks in malaria control. Science. 2005 Oct 7;310(5745):49-51; author reply 49-51.

13937.   Zarocostas J. Health experts gather to step up fight against malaria. BMJ. 2005 Oct 29;331(7523):986. 

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July 2006

Some selected abstracts:

1. 

Baspinar O, Bayraktaroglu Z, Karsligil T, Bayram A, Coskun Y. A rare cause of anemia and thrombocytopenia in a newborn: congenital malaria. Turk J Pediatr. 2006 Jan-Mar;48(1):63-5.

Department of Pediatrics, Gaziantep University Faculty of Medicine, Gaziantep, Turkey.

A newborn with fever and jaundice was referred to our hospital with anemia and thrombocytopenia of unknown origin. The patient's mother suffered from malaria infection during the third trimester of her pregnancy, but she did not accept medical therapy. On physical examination the newborn showed mild splenomegaly and jaundice. Laboratory tests revealed marked anemia with a hemoglobin value of 7.7 g/L and thrombocytopenia with platelet numbers of 17,000/mm3. Plasmodium vivax was detected in blood smear. Oral therapy with chloroquine and primaquine was started. This patient is the second case of congenital malaria reported from Turkey, and shows that the diagnosis of congenital  malaria should be considered in infants with suspected congenital infection who are born to mothers with a history of malarial disease. We emphasize the importance of adequate antenatal medical therapy during pregnancy.

2.

Mendiratta DK, Bhutada K, Narang R, Narang P. Evaluation of different methods for diagnosis of P. falciparum malaria. Indian J Med Microbiol. 2006 Jan;24(1):49-51.

Department of Microbiology, Mahatma Gandhi Institute of Medical Sciences, Sevagram - 442 102, Maharashtra, India. dkmendiratta@rediffmail.com

Rapid diagnosis is a prerequisite for institution of effective treatment and reducing the mortality and morbidity of falciparum malaria. This study was taken up to compare the efficacy of various rapid methods viz, acridine orange, Plasmodium falciparum histidine rich protein II antigen detection and Field's stain with traditional microscopy i.e, Leishman stain for diagnosing falciparum malaria. Thick and thin blood films of 443 consecutive patients with history of fever with chills and rigors were examined by Leishman and Field's method. Acridine orange stained wet mounts of blood were examined under fluorescence microscopy. All films were examined by two independent microbiologists. Plasmodium falciparum histidine rich protein II antigen was detected using commercially available kit, Paracheck Pf. Out of the 443 subjects examined for P.falciparum 18.28% were detected by Leishman stain, 6.32% by Field's stain, 18.28% by acridine orange and 18.1% by antigen based technique. Field's stain missed 53 (65.4%), while Paracheck Pf was negative in 6(7.4%) of the Leishman positive samples. All Field's stain and acridine orange positives were positive by Leishman, but five Paracheck Pf positives were negative. Leishman stain is cost effective but if facilities are available one should use acridine orange for screening. The antigen detection kits are rapid, simple and are useful but to rule out false negatives in clinically suspected cases, Leishman stain is reliable.

3.

Miller RS, Wongsrichanalai C, Buathong N, McDaniel P, Walsh DS, Knirsch C, Ohrt C. Effective treatment of uncomplicated Plasmodium falciparum malaria with azithromycin- quinine combinations: a randomized, dose-ranging study. Am J Trop Med Hyg. 2006
Mar;74(3):401-6.

Department of Immunology and Medicine, Armed Forces Research Institute of Medical Sciences, Bangkok, Thailand. robert.s.miller@us.army.ml

Azithromycin, the most potent antimalarial macrolide antibiotic, is synergistic with quinine against Plasmodium falciparum in vitro. We assessed combinations of azithromycin and quinine against uncomplicated P. falciparum malaria at the Armed Forces Research Institute of Medical Sciences-Kwai River Clinical Center along the Thailand-Myanmar border, an area with a high prevalence of multidrug-resistant P. falciparum. Four regimens were assessed in an open-label dose-ranging design involving 61 volunteers. All received oral quinine (Q; 30 mg/kg/day divided every 8 hours for 3 days) with oral azithromycin (Az; 500 mg twice a day for 3 days, 500 mg twice a day for 5 days, or 500 mg three times a day for 3 days). A comparator group received quinine and doxycycline (Dx; 100 mg twice a day for 7 days). Study observation was 28 days per protocol. Sixty volunteers completed the study. Seven days of QDx cured 100% of the volunteers. One failure occurred in the lowest QAz regimen (on day 28) and none occurred in either of the two higher Az regimens. Cinchonism occurred in nearly all subjects. Overall, the azithromycin regimens were well tolerated, and no volunteers discontinued therapy. Three- and five-day azithromycin-quinine combination therapy appears safe, well tolerated, and effective in curing drug-resistant P. falciparum malaria. Further evaluation, especially in pediatric and obstetric populations, is warranted.

4.

Planche T, Krishna S. Severe malaria: metabolic complications. Curr Mol Med. 2006 Mar;6(2):141-53.

Division of Cellular and Molecular Medicine, Centre for Infection, St. George's University of London, London SW17 0RE, UK. tim@planche.demon.co.uk

Metabolic complications of severe malaria are some of the most important and potentially treatable manifestations of this deadly disease. The commonest metabolic complications (lactic acidosis and hypoglycaemia) arise from increased host anaerobic metabolism probably due to a mismatch between tissue oxygen supply and requirement. Optimising treatments for these complications should be guided by detailed understanding of their underlying pathophysiology, and may help to reduce the intolerably high case fatality rate of severe malaria.

5.

Rodriguez-Morales AJ, Sanchez E, Vargas M, Piccolo C, Colina R, Arria M. Anemia and thrombocytopenia in children with Plasmodium vivax malaria. J Trop Pediatr. 2006 Feb;52(1):49-51.

Environmental Health (Regional Malariology Office), Ministry of Health, Sucre, Venezuela. Clinico-epidemiological features of pediatric patients with malaria due Plasmodium vivax that developed anemia and thrombocytopenia requiring hospitalization are herein reported. Over a 3-year period, 78 children with P. vivax infection were admitted to our Hospital in Sucre, Venezuela. Clinical manifestations at admission were 93.59 per cent fever, 41.03 per cent chills and 14.10 per cent headache, among others. On paraclinical evaluations 94.87 percent presented with anemia (10.26 per cent severe), 25.64 percent with malnutrition, and 10.26 percent had intestinal parasitosis. The mean hemoglobin levels on admission were 8.09 g/dl and mean platelet counts 127 402 cells/mm3. Among these patients 58.97 per cent developed thrombocytopenia (24.36 per cent severe) requiring transfusion in 25.64 per cent of patients. After antimalarial treatment with chloroquine and primaquine and supportive care all patients were successfully discharged. No deaths or further complications were seen, except for persistent mild thrombocytopenia in 17.95 per cent of the patients.

6.

Schofield L, Mueller I. Clinical immunity to malaria. Curr Mol Med. 2006 Mar;6(2):205-21.

The Walter and Eliza Hall Institute of Medical Research, 1G, Royal Parade, Parkville, Victoria 3050, Australia. schofield@wehi.edu.au

Under appropriate conditions of transmission intensity, functional immunity to malaria appears to be acquired in distinct stages. The first phase reduces the likelihood of severe or fatal disease; the second phase limits the clinical impact of 'mild' malaria; and the third provides partial but incomplete protection against pathogen burden. These findings suggest clinical immunity to mortality and morbidity is acquired earlier, with greater ease, and via distinct mechanisms as compared to anti-parasite immunity, which is more difficult to achieve, takes longer and is only ever partially efficacious. The implications of this view are significant in that current vaccination strategies aim predominantly to achieve anti-parasite immunity, although imparting clinical immunity is the public health objective. Despite enormous relevance for global public health, the mechanisms governing these processes remain obscure. Four candidate mechanisms might mediate clinical immunity, namely immunity to cytoadherence determinants, tolerance to toxins, acquired immunity to toxins, and immunoregulation. This review addresses the targets and determinants of clinical immunity, and considers the implications for vaccine development.

Diagnosis, Diagnostics, Immunodiagnosis & Immunodiagnostics:

14404. Brent AJ, Oundo JO, Mwangi I, Ochola L, Lowe B, Berkley JA. Salmonella bacteremia in Kenyan children. Pediatr Infect Dis J. 2006 Mar;25(3):230-6.

14405. Gockel HR, Heidemann J, Lorenz D, Gockel I. Spontaneous splenic rupture, in tertian malaria. Infection. 2006 Feb;34(1):43-5.

14406. Gogtay NJ, Kamtekar KD, Dalvi SS, Mehta SS, Chogle AR, Aigal U, Kshirsagar NA. A randomized, parallel study of the safety and efficacy of 45 mg primaquine versus 75 mg bulaquine as gametocytocidal agents in adults with blood schizonticide-responsive uncomplicated falciparum malaria [ISCRTN50134587].. BMC Infect Dis. 2006 Feb 1;6:16.

14407. Hill DR. The burden of illness in international travelers. N Engl J Med. 2006 Jan 12;354(2):115-7.

14408. Karplus R, Johnston SP. Images in clinical medicine. Plasmodium vivax microgametes. N Engl J Med. 2006 Mar 9;354(10):1064.

14409. Karunajeewa HA, Reeder J, Lorry K, Dabod E, Hamzah J, Page-Sharp M, Chiswell GM, Ilett KF, Davis TM. Artesunate suppositories versus intramuscular artemether for treatment of severe malaria in children in Papua New Guinea. Antimicrob Agents Chemother. 2006 Mar;50(3):968-74.

14410. Kitchen AD, Chiodini PL. Malaria and blood transfusion. Vox Sang. 2006 Feb;90(2):77-84. Review.

14411. Lathia T, Kalantri SP. Malaria masquerading as HELLP. J Mahatma Gandhi Inst Med Sci. 2004;9(1):51.

14412. Murray S. Taking away the sting of malaria. CMAJ. 2006 Jan 17;174(2):161-2.

14413. Sharma YD. Genetic alteration in drug resistance markers of Plasmodiumfalciparum. Indian J med Res 2005, 121(1), 13-22.

14414. Woodrow CJ, Planche T, Krishna S. Artesunate versus quinine for severe falciparum malaria. Lancet. 2006 Jan 14;367(9505):110-1.

   Vaccines:

14415. Guinovart C, Navia MM, Tanner M, Alonso PL. Malaria: burden of disease. Curr Mol Med. 2006 Mar;6(2):137-40. Review.

14416. Marsh K, Kinyanjui S. Immune effector mechanisms in malaria. Parasite Immunol. 2006 Jan-Feb;28(1-2):51-60. Review.

14417. Stevenson MM, Zavala F. Immunology of malaria infections. Parasite Immunol. 2006 Jan-Feb;28(1-2):1-4.

   Therapy:

14418. Barat LM. Four malaria success stories: how malaria burden was successfully reduced in Brazil, Eritrea, India, and Vietnam. Am J Trop Med Hyg. 2006 Jan;74(1):12-6.

14419. Bhattacharya N. A preliminary study of placental umbilical cord whole blood transfusion in under resourced patients with malaria in the background of anaemia. Malar J. 2006 Mar 23;5:20.

14420. Burns M, Baker J, Auliff AM, Gatton ML, Edstein MD, Cheng Q. Efficacy of sulfadoxine-pyrimethamine in the treatment of uncomplicated Plasmodium falciparum malaria in East Timor. Am J Trop Med Hyg. 2006 Mar;74(3):361-6.

14421. Casals-Pascual C, Roberts DJ. Severe malarial anaemia. Curr Mol Med. 2006 Mar;6(2):155-68. Review.

14422. de Benoist B, Darnton-Hill I, Lynch S, Allen L, Savioli L. Zinc and iron supplementation trials in Nepal and Tanzania. Lancet. 2006 Mar 11;367(9513):816.

14423. Hentschel C, Moree M. Malaria research. Lancet Infect Dis. 2006 Mar;6(3):123.

14424. McGready R, Ashley EA, Tan SO, Brabin B, Nosten F. Re: Malaria in pregnancy. BJOG. 2006 Feb;113(2):246.

14425. Mohamed AO, Eltaib EH, Ahmed OA, Elamin SB, Malik EM. The efficacies of artesunate-sulfadoxine-pyrimethamine and artemether-lumefantrine in the treatment of uncomplicated, Plasmodium falciparum malaria, in an area of low transmission in central Sudan. Ann Trop Med Parasitol. 2006 Jan;100(1):5-10.

14426. Mordmuller B, Kremsner PG. Malarial parasites vs. antimalarials: never-ending rumble in the jungle. Curr Mol Med. 2006 Mar;6(2):247-51. Review.

14427. Njau JD, Goodman C, Kachur SP, Palmer N, Khatib RA, Abdulla S, Mills A, Bloland P. Fever treatment and household wealth: the challenge posed for rolling out combination therapy for malaria. Trop Med Int Health. 2006 Mar;11(3):299-313.

14428. Raju TN. Hot brains: manipulating body heat to save the brain. Pediatrics. 2006 Feb;117(2):e320-1.

14429. Schellenberg D, Abdulla S, Roper C. Current issues for anti-malarial drugs to control P. falciparum malaria. Curr Mol Med. 2006 Mar;6(2):253-60. Review.

14430. Sun HY, Fang CT, Wang JT, Kuo PH, Chen YC, Chang SC. Successful treatment of imported cerebral malaria with artesunate-mefloquine combination therapy. J Formos Med Assoc. 2006 Jan;105(1):86-9.

14431. Toovey S. Artesunate versus quinine for severe falciparum malaria. Lancet. 2006 Jan 14;367(9505):111-2.

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October 2006

 

Some selected abstracts:

1

Barennes H, Balima-Koussoube T, Nagot N, Charpentier JC, Pussard E. Safety and efficacy of rectal compared with intramuscular quinine for the early treatment of moderately severe malaria in children: randomised clinical trial. BMJ. 2006 May 6;332(7549):1055-9.
Centre MURAZ, 01BP390 Bobo-Dioulasso, Burkina Faso. hubert.barennes@auf.org
OBJECTIVE: To compare the safety and efficacy of quinine given by the rectal route with quinine given by the intramuscular route in children with moderately severe Plasmodium falciparum malaria. DESIGN: Randomised, open, clinical trial. SETTING: Health centre in Burkina Faso. PARTICIPANTS: 898 children with moderately severe P falciparum malaria who were unable to take oral treatment. INTERVENTION: Rectal quinine (20 mg/kg diluted to 30 mg/ml in water solution) or intramuscular quinine (12.5 mg/kg) every 12 hours until oral quinine could be taken. MAIN OUTCOME MEASURES: Primary safety outcome was the presence of blood in stools and secondary safety outcome was diarrhoea. Primary efficacy outcome was early treatment failure and secondary efficacy outcomes were late clinical and parasitological failures, fever clearance time, and time to oral intake. RESULTS: Blood in stools and diarrhoea were more common in children given quinine by the rectal route than by the intramuscular route (blood in stools: 5% v 1%, absolute difference 3.9%, 95% confidence interval 1.8% to 6.1%; diarrhoea: 5% v 1%, 3.5%, 1.3% to 5.7%). On anoscopy, inflammatory lesions (9/248, 3%) were associated with bloody striations in stools. Side effects of rectal quinine were rare and transitory. Local pain (90%), inflammation (79%), and transient impairment of mobility (15%) were observed with intramuscular quinine. Early treatment failure was higher in the rectal group (6% v 3%, absolute difference 3.0%, 95% confidence interval 0.2% to 5.9%). All except two children in each group had negative blood slide results at day 5. Fever recurrence at day 7 was higher in the intramuscular group (37/375 v 18/395, absolute difference 5.3%, 1.6% to 8.9%). Other efficacy outcomes (late clinical failure, late parasitological failure, fever clearance time, time to starting oral intake and rate of deterioration to severe malaria) did not differ. CONCLUSION: Quinine given by the rectal route has an acceptable safety profile and could be used in the early management of moderately severe malaria in children in sub-Saharan Africa, halting progression to severe disease.
 

2

Gimnig JE, MacArthur JR, M'bang'ombe M, Kramer MH, Chizani N, Stern RS, Mkandala C, Newman RD, Steketee RW, Campbell CH. Severe cutaneous reactions to sulfadoxine-pyrimethamine and trimethoprim-sulfamethoxazole in Blantyre District, Malawi. Am J Trop Med Hyg. 2006 May;74(5):738-43.

Division of Parasitic Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30341, USA. hzg1@cdc.gov

We estimated the frequency of clinically diagnosed Stevens-Johnson syndrome and toxic epidermal necrolysis associated with sulfadoxine-pyrimethamine (SP) and trimethoprim-sulfamethoxazole (CTX) in Blantyre District, Malawi. Cases were detected by passive surveillance at 22 health centers from March 2001 through September 2002. Denominators were estimated from the Malawi national census for Blantyre District and the frequency of SP and CTX use reported in five household surveys. Crude rates of adverse reactions were estimated to be 1.2 per 100,000 exposures for SP and 1.5 per 100,000 exposures for CTX. Rates were higher in adults (1.7 cases per 100,000 SP exposures and 2.6 cases per 100,000 CTX exposures) and in persons positive for human immunodeficiency virus (4.9 cases per 100,000 SP exposures and 8.4 cases per 100,000 CTX exposures). Infrequent treatment doses with SP are associated with a low risk of an adverse cutaneous reaction, and SP can be recommended for treatment of malaria in areas where P. falciparum is susceptible.

 

3

Kalanda GC, Hill J, Verhoeff FH, Brabin BJ. Comparative efficacy of chloroquine and sulphadoxine--pyrimethamine in pregnant women and children: a meta-analysis. Trop Med Int Health. 2006 May;11(5):569-77.
Child and Reproductive Health Group, Liverpool School of Tropical Medicine, and Royal Liverpool Children's Hospital NHS Trust, UK.
OBJECTIVE: To compare the efficacy of chloroquine and sulphadoxine-pyremethamine against Plasmodium falciparum infection in pregnant women and in children from the same endemic areas of Africa, with the aim of determining the level of correspondence in efficacy determinations in these two risk groups. METHODS: Meta-analysis of nine published and unpublished in vivo antimalarial efficacy studies in pregnant women and in children across five African countries. RESULTS: Pregnant women (all gravidae) were more likely to be sensitive than children to both chloroquine (odds ratio: 2.07; 95% confidence interval: 1.5, 2.9) and sulphadoxine-pyrimethamine (odds ratio: 2.66; 95% confidence interval: 11.1, 6.7). Pregnant women demonstrated an almost uniform increased sensitivity for peripheral parasite clearance at day 14 compared with children. This finding was consistent across a wide range of drug sensitivities. Primigravidae at day 14 showed lower clearance to antimalarial drugs than multigravidae (P<0.05). There was no significant difference between parasite clearance in primigravidae and in children. CONCLUSION: The greater drug sensitivity in pregnant women probably indicates differences in host susceptibility rather than parasite resistance. Parasite sensitivity patterns in children may be a suitable guide to antimalarial policy in pregnant women.
 

4

Lopansri BK, Anstey NM, Stoddard GJ, Mwaikambo ED, Boutlis CS, Tjitra E, Maniboey H, Hobbs MR, Levesque MC, Weinberg JB, Granger DL. Elevated plasma phenylalanine in severe malaria and implications for pathophysiology of neurological complications. Infect Immun. 2006 Jun;74(6):3355-9.
Division of Infectious Diseases, VA and University of Utah School of Medicine, Salt Lake City, Utah 84132, USA. bert.lopansri@hsc.utah.edu
Cerebral malaria is associated with decreased production of nitric oxide and decreased levels of its precursor, l-arginine. Abnormal amino acid metabolism may thus be an important factor in malaria pathogenesis. We sought to determine if other amino acid abnormalities are associated with disease severity in falciparum malaria. Subjects were enrolled in Dar es Salaam, Tanzania (children) (n = 126), and Papua, Indonesia (adults) (n = 156), in two separate studies. Plasma samples were collected from subjects with WHO-defined cerebral malaria (children), all forms of severe malaria (adults), and uncomplicated malaria (children and adults). Healthy children and adults without fever or illness served as controls. Plasma amino acids were measured using reverse-phase high-performance liquid chromatography with fluorescence detection. Several plasma amino acids were significantly lower in the clinical malaria groups than in healthy controls. Despite the differences, phenylalanine was the only amino acid with mean levels outside the normal range (40 to 84 microM) and was markedly elevated in children with cerebral malaria (median [95% confidence interval], 163 [134 to 193] microM; P < 0.0001) and adults with all forms of severe malaria (median [95% confidence interval], 129 [111 to 155] microM; P < 0.0001). In adults who survived severe malaria, phenylalanine levels returned to normal, with clinical improvement (P = 0.0002). Maintenance of plasma phenylalanine homeostasis is disrupted in severe malaria, leading to significant hyperphenylalaninemia. This is likely a result of an acquired abnormality in the function of the liver enzyme phenylalanine hydroxylase. Determination of the mechanism of this abnormality may contribute to the understanding of neurological complications in malaria.
 

5

Omari AA, Gamble C, Garner P. Artemether-lumefantrine (four-dose regimen) for treating uncomplicated falciparum malaria. Cochrane Database Syst Rev. 2006 Apr 19;(2):CD005965. Review.
Countess of Chester Hospital, NHS Foundation Trust, Paediatric Department, Countess of Chester Health Park, Liverpool Road, Chester, Cheshire, UK, CH2 1UL. aika@omari1677.freeserve.co.uk
BACKGROUND: The World Health Organization recommends artemether-lumefantrine, an expensive drug, as a treatment for uncomplicated malaria. We sought evidence of the superiority of the four-dose regimen over existing treatments. OBJECTIVES: To evaluate the four-dose regimen of artemether-lumefantrine for treating uncomplicated falciparum malaria. SEARCH STRATEGY: We searched the Cochrane Infectious Diseases Group Specialized Register (October 2005), CENTRAL (The Cochrane Library 2005, Issue 3), MEDLINE (1966 to October 2005), EMBASE (1988 to October 2005), LILACS (1982 to October 2005), conference proceedings, and reference lists of articles. We also contacted experts in malaria research and the pharmaceutical company that manufactures artemether-lumefantrine. SELECTION CRITERIA: Randomized controlled trials comparing four doses of artemether-lumefantrine with standard treatment regimens (single drug or combination), or six doses of artemether-lumefantrine, for treating uncomplicated falciparum malaria. DATA COLLECTION AND ANALYSIS: Two authors independently applied inclusion criteria to potentially relevant trials, assessed trial quality, and extracted data, including adverse events. Total failure by day 28 (day 42 for sulfadoxine-pyrimethamine and day 63 for mefloquine) was the primary outcome. MAIN RESULTS: Seven trials (2057 participants) tested a four-dose regimen. More people tended to fail treatment with artemether-lumefantrine than with other drugs, including sulfadoxine-pyrimethamine (247 participants, 1 trial), halofantrine (86 participants, 1 trial), and mefloquine (233 participants, 1 trial; difference statistically significant for mefloquine). When compared with chloroquine, artemether-lumefantrine was better in two trials (378 participants), but over 50% of the participants treated with chloroquine had total failure by day 28. Fewer people failed treatment with the six-dose regimen compared to the four-dose regimen (RR 7.71, 95% CI 2.99 to 19.88; 306 participants, 1 trial). AUTHORS' CONCLUSIONS: The four-dose regimen of artemether-lumefantrine seems to be less effective than regimens against which it has been tested. The six-dose regimen is superior to four-dose regimen.
 

6

Owens S, Harper G, Amuasi J, Offei-Larbi G, Ordi J, Brabin BJ.  Placental malaria and immunity to infant measles. Arch Dis Child. 2006 Jun;91(6):507-8.
MRC Laboratories, Atlantic Road, Fajara, The Gambia.
The efficiency of transplacental transfer of measles specific antibody was assessed in relation to placental malaria. Infection at delivery was associated with a 30% decrease in expected cord measles antibody titres. Uninfected women who received anti-malarial drugs during pregnancy transmitted 30% more antibody than those who received no antimalarial drugs.
 

Diagnosis , Dignostics, Immunodiagnosis & Immunodignostics:

14756.  Allan PJ, Tahir HI. How easily malaria can be missed. J R Soc Med. 2006 Apr;99(4):201-2.

14757.  Cunha BA. Typhoid fever: the temporal relations of key clinical diagnostic points. Lancet Infect Dis. 2006 Jun;6(6):318-20; author reply 320-1.

14758.  Donati D, Espmark E, Kironde F, Mbidde EK, Kamya M, Lundkvist A, Wahlgren M, Bejarano MT, Falk KI. Clearance of circulating Epstein-Barr virus DNA in children with acute malaria after antimalaria treatment. J Infect Dis. 2006 Apr 1;193(7):971-7.

14759.  Tumwline J, Luboobi LS, Mugisha J T. Modelling the effect of treatment and mosquito control onmalaria transmission. Int J Mgmt Systems 2005, 21(2), 107-124.

14760.  Jorgensen P, Chanthap L, Rebueno A, Tsuyuoka R, Bell D. Malaria rapid diagnostic tests in tropical climates: the need for a cool chain. Am J Trop Med Hyg. 2006 May;74(5):750-4.

Pathogenesis:                  

14761.  Keller CC, Davenport GC, Dickman KR, Hittner JB, Kaplan SS, Weinberg JB, Kremsner PG, Perkins DJ. Suppression of prostaglandin E2 by malaria parasite products and antipyretics promotes overproduction of tumor necrosis factor-alpha: association with the pathogenesis of childhood malarial anemia. J Infect Dis. 2006 May 15;193(10):1384-93.

14762.  McDevitt MA, Xie J, Shanmugasundaram G, Griffith J, Liu A, McDonald C, Thuma P, Gordeuk VR, Metz CN, Mitchell R, Keefer J, David J, Leng L, Bucala R. A critical role for the host mediator macrophage migration inhibitory factor in the pathogenesis of malarial anemia. J Exp Med. 2006 May 15;203(5):1185-96.

Therapy:

14763.  A-Elbasit IE, Elbashir MI, Khalil IF, Alifrangis M, Giha HA. The efficacy of sulfadoxine-pyrimethamine alone and in combination with chloroquine for malaria treatment in rural Eastern Sudan: the interrelation between resistance, age and gametocytogenesis. Trop Med Int Health. 2006 May;11(5):604-12.

14764.  Bar-Zeev N, White N. Evidence behind the WHO guidelines: Hospital Care for Children: efficacy and safety of artemisinin derivatives in children with malaria. J Trop Pediatr. 2006 Apr;52(2):78-82.    Review.

14765.  Fried M, Domingo GJ, Gowda CD, Mutabingwa TK, Duffy PE.  Plasmodium falciparum: chondroitin sulfate A is the major receptor for adhesion of parasitized erythrocytes in the placenta. Exp Parasitol. 2006 May;113(1):36-42.

14766.  Fanello CI, Karema C, van Doren W, Rwagacondo CE, D'Alessandro U. Tolerability of amodiaquine and sulphadoxine-pyrimethamine, alone or in combination for the treatment of uncomplicated Plasmodium falciparum malaria in Rwandan adults. Trop Med Int Health. 2006 May;11(5):589-96.

14767.  Hale VG.  Supporting the use of artemisinin in combination. Nature. 2006 May 18;441(7091):282.

14768.  Hopkin M. World Bank defends efforts to curb malaria. Nature. 2006 Apr 27;440(7088):1096-7. 

14769.  Padhan P. Rectal quinine for malaria: risk of hypoglycaemia may be higher by rectal route. BMJ. 2006 May 20;332(7551):1216; author reply 1216.

14770.  Rehwagen C. WHO ultimatum on artemisinin monotherapy is showing results. BMJ. 2006 May 20;332(7551):1176.

14771.  Sowunmi A, Fateye BA, Adedeji AA, Gbotosho GO, Happi TC, Bamgboye AE, Bolaji OM, Oduola AM. Predictors of the failure of treatment with pyrimethamine-sulfadoxine in children with uncomplicated falciparum malaria. Acta Trop. 2006 Apr;98(1):6-14.

14772.  Towie N.  Malaria breakthrough raises spectre of drug resistance. Nature. 2006 Apr 13;440(7086):852-3.

14773.  White NJ.  Developing drugs for neglected diseases. Trop Med Int Health. 2006 Apr;11(4):383-4.

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