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Administración masiva de fármacos para el paludismo

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Referencias

References to studies included in this review

Archibald 1960 NGA {published data only}

Archibald HM. Field trials of mass administration of antimalarial drugs in Northern Nigeria. World Health Organization 1960, (262):1‐11.

Cáceres Garcia 2008 VEN {published data only}

Cáceres Garcia JL. Eficacia de la cura radical masiva en la incidencia malárica del Municipio Mariño, Estado Sucre. Boletin de Malariologia y Salud Ambiental 2004;44(1):45‐9.
Cáceres Garcia JL. Estado Sucre: El éxito antimalárico de Venezuela en el año 2003. Boletin de Malariologia y Salud Ambiental 2004;44(1):51‐5.
Cáceres Garcia JL. Malaria antes y después de la cura radical masiva en el estado Sucre Venezuela. Boletin de Malariologia y Salud Ambiental 2008;48(1):83‐90.
Cáceres Garcia JL, Nelsón P, Franklin VA, Pérez W, Rojas JG, Mora JD, et al. Impacto de la Cura Radical Masiva sobre la incidencia malárica del estado Sucre, Venezuela. Boletin de Malariologia y Salud Ambiental 2005;45(1):27‐36.

Cavalie 1962 CMR {published data only}

Cavalie Ph, Mouchet J. Les Campagnes Experimentales d'eradication du paludisme dans le nord de la Republique du Cameroun. Medicine Tropicale 1962;22(1):95‐118.

Comer 1971 PAN {published data only}

Comer RD, Young MD, Johnson CM, Babione RW. Mass drug trial of pyrimethamine and primaquine for the eradication of malaria in Sambu, Republic of Panama. Boletin de la Oficina Sanitaria Panamericana 1971;70(3):226‐33.

De Zulueta 1961 UGA {published data only}

De Zulueta J, Kafuko GW, Cullen JR, Pedersen CK. The results of the first year of a malaria eradication pilot project in Northern Kigezi (Uganda). East African Medical Journal 1961;38(1):1‐26.

De Zulueta 1964 UGA {published data only}

De Zulueta J, Kafuko GW, McCrae AWR, Cullen JR, Pedersen CK, Wasswa DFB. A malaria eradication experiment in the highlands of Kigezi (Uganda). East African Medical Journal 1964;41(3):102‐20.

Escudie 1962 BFA {published data only}

Escudie A, Hamon J, Schneider J. Results of mass antimalarial chemoprophylaxis with a combination of 4‐aminoquinoline and 8‐aminoquinoline under rural African conditions in the region of Bobo‐Dioulasso (Upper Volta) 1960. Comparative study in a zone treated with DDT and outside this zone. Medecine Tropicale 1962;22(2):268‐305.

Gabaldon 1959 VEN {published data only}

Gabaldon A, Guerrero L. An attempt to eradicate malaria by the weekly administration of pyrimethamine in areas of out‐of‐doors transmission in Venezuela. American Journal of Tropical Medicine and Hygiene 1959;8(4):433‐9.

Garfield 1983 NIC {published data only}

Bruce‐Chwatt LJ, Bruce‐Chwatt LJ. Mass drug administration for control of malaria. The Lancet 1983;2(8351):688.
Foll C, Foll C. Mass drug administration for control of malaria. The Lancet 1983;2(8357):1022.
Garfield R. Malaria control in Nicaragua: social and political influences on disease transmission and control activities. The Lancet 1999;354:414‐8.
Garfield RM, Vermund SH. Malaria in Nicaragua: an update. The Lancet 1984;1(8386):1125.
Garfield RM, Vermund SH, Garfield RM, Vermund SH. Changes in malaria incidence after mass drug administration in Nicaragua. Lancet 1983;2(8348):500‐3.
Garfield RM, Vermund SH, Garfield RM, Vermund SH. Health education and community participation in mass drug administration for malaria in Nicaragua. Social Science & Medicine 1986;22(8):869‐77.

Gaud 1953 MAR {published data only}

Gaud J, Houel G. Individual and mass treatment of malaria by a single dose of Flavoquine (amodiaqulne). Bulletin de la Societe de Pathologie Exotique 1953;46(4):565‐71.

Hii 1987 MYS {published data only}

Hii JL, Vun YS, Chin KF, Chua R, Tambakau S, Binisol ES, et al. The influence of permethrin‐impregnated bednets and mass drug administration on the incidence of Plasmodium falciparum malaria in children in Sabah, Malaysia. Medical and Veterinary Entomology 1987;1(4):397‐407.

Houel 1954 MAR {published data only}

Houel G. A note on the treatment of epidemic‐malaria with a single dose of pyrimethamine [Note sur le traitement du paludisme épidémique par une dose unique de pyriméthamine]. Bulletin de la Societe de Pathologie Exotique 1954;47(2):262‐4.

Jones 1954 KEN {published data only}

Jones SA, Jones SA. Resistance of P. falciparum and P. malariae to pyrimethamine (daraprim) following mass treatment with this drug; a preliminary note. East African Medical Journal 1954;31(2):47‐9.

Jones 1958 KEN {published data only}

Jones SA, Jones SA. Mass treatment with pyrimethamine; a study of resistance and cross resistance resulting from a field trial in the hyperendemic malarious area of Makueni, Kenya. September 1952‐September 1953. Transactions of the Royal Society of Tropical Medicine & Hygiene 1958;52(6):547‐61.

Kaneko 2000 VUT {published data only}

Kaneko A, Taleo G, Kalkoa M, Yamar S, Kobayakawa T, Bjorkman A. Malaria eradication on islands. Lancet 2000;356(9241):1560‐4.
Kaneko A, Taleo GK, Rieckmann KH. Island malaria control in eastern Melanesia: 1. Malaria eliminated from a small island by 9‐week mass drug administration and impregnated bednets. Japanese Journal of Parasitology 1994;43(5):358‐70.

Kligler 1931 PSE {published data only}

Kligler IJ, Mer G. Periodic intermittent treatment with Chinoplasmine as a measure of malaria control in a hyperendemic area. Rivista di Malariologia 1931;10(4):425‐438.

Kondrashin 1985 IND {published data only}

Kondrashin AV, Sanyal MC, Kondrashin AV, Sanyal MC. Mass drug administration in Andhra Pradesh in areas under Plasmodium falciparum containment programme. Journal of Communicable Diseases 1985;17(4):293‐9.

Malaria_Taiwan 1991 TWN {published data only}

Department of Health, The Executive Yuan Republic of China. Malaria eradication in Lanyu. Malaria Eradication in Taiwan. 1991:245‐62.

Metselaar 1961 PNG {published data only}

Metselaar D. Seven years' malaria research and residual house spraying in Netherlands New Guinea. The American Journal of Tropical Medicine and Hygiene 1961;10(3):327‐34.

Molineaux 1980 NGA {published data only}

Cornille Brogger R, Mathews HM, Storey J, Ashkar TS, Brogger S, Molineaux L. Changing patterns in the humoral immune response to malaria before, during and after the application of control measures: a longitudinal study in the West African savanna. Bulletin of the World Health Organization 1978;56(4):579‐600.
Molineaux L, Cornille‐Brogger R, Mathews HM, Storey J, Ashkar TS. Longitudinal serological study of malaria in infants in the West African savanna. Comparisons in infants exposed to, or protected from, transmission from birth. Bulletin of the World Health Organisation 1978;56(4):573‐8.
Molineaux L, Gramiccia G. The Garki Project. Research on the epidemiology and control of malaria in the Sudan Savanna of West Africa. Geneva: World Health Organization, 1980.
Molineaux L, Storey J, Cohen JE, Thomas A. A longitudinal study of human malaria in the West African savanna in the absence of control measures: relationships between different Plasmodium species, in particular P. falciparum and P. malariae . The American Journal of Tropical Medicine and Hygiene 1980;29(5):725‐37.

Najera 1973 NGA {published data only}

Najera JA, Shidrawi GR, Storey J, Lietaert PEA. Mass drug administration and DDT indoor‐spraying as antimalarial measures in the northern savanna of Nigeria. World Health Organization 1973;73(817):1‐34.

Paik 1974a SLB {published data only}

Paik. Focus on malaria. Papua New Guinea Medical Journal 1974;17(1):1‐115.

Paik 1974b SLB {published data only}

Paik. Focus on Malaria. Papua New Guinea Medical Journal 1974;17(1):1‐115.

Ricosse 1959 BFA {published data only}

Ricosse J, Bailly‐Choumara H, Adam JP, Hamon J. Results of pyrimethamine chemoprophylaxis in a pilot antimalarial prevention study in Bobo‐Dioulasso [Resultats d'une experimentation de chimioprophylaxie par la pyrimethamine dans la zone pilote de lutte antipaludique de Bobo‐Diolasso]. Bulletin de la Societe de Pathologie Exotique 1959;52:516‐35.

Roberts 1964 KEN {published data only}

Roberts JMD. Pyrimethamine (Daraprim) in the control of epidemic malaria. The American Journal of Tropical Medicine and Hygiene 1956;59:201‐8.
Roberts JMD. The control of epidemic malaria in the highlands of Western Kenya. Part I. Before the campaign. The American Journal of Tropical Medicine and Hygiene 1964;67(7):161‐8.
Roberts JMD. The control of epidemic malaria in the highlands of Western Kenya. Part II. The campaign. The American Journal of Tropical Medicine and Hygiene 1964;67(8):191‐9.
Roberts JMD. The control of epidemic malaria in the highlands of Western Kenya. Part III. After the campaign. The American Journal of Tropical Medicine and Hygiene 1964;67(9):230‐37.

Schneider 1961 BFA {published data only}

Schneider J, Escudie A, Hamon J. Eradication of malaria and chemotherapy. Results obtained with the association amino‐4 quinoline + amino‐8 quinoline in the pilot area of Bobo‐Dioulasso (Haute‐ Volta) [Eradication du paludisme et chimiotherapie resultats d'un essai de l'association: <<amino‐4 quinoleine>>/<<amino‐8 quinoleine>> dans la <<zone pilote>> de Bobo‐Dioulasso (Haute Volta)]. Bulletin de la Societe de Pathologie Exotique 1961;54(5):1012‐25.

Shekalaghe 2011 TZA {published data only}

Shekalaghe SA, Drakeley C, van den Bosch S, ter Braak R, van den Bikilaardt W, Mwanziva C, et al. A cluster‐randomized trial of mass drug administration with a gametocytocidal drug combination to interrupt malaria transmission in a low endemic area in Tanzania. Malaria Journal 2011;10:247.
Shekalaghe SA, ter Braak R, Daou M, Kavishe R, van den Bijilaardt W, van den Bosch S, et al. In Tanzania, hemolysis after a single dose of primaquine coadministered with an artemisinin is not restricted to glucose‐6‐phosphate dehydrogenase‐deficient (G6PD A) individuals. Antimicrobial Agents and Chemotherapy 2010;54(5):1762‐8.

Simeons 1938 IND {published data only}

Simeons ATW. Follow‐up of a mass treatment with injectable atebrin. Indian Medical Gazette 1938;73(12):713‐5.
Simeons ATW. Mass treatment with injectable atebrin. Indian Medical Gazette 1936;71(3):132‐7.

Singh 1953 IND {published data only}

Singh J, Misra BG, Ray AP. Suppressive treatment with amodlaquln. Indian Journal of Malariology 1953;7(1):27‐31.

Song 2010 KHM {published data only}

Song J, Socheat D, Tan B, Dara P, Deng C, Sokynthea S, et al. Rapid and effective malaria control in Cambodia through mass administration of artemisinin‐piperaquine. Malaria Journal 2010;9:57.

van Dijk 1961 PNG {published data only}

van Dijk W, van Dijk W. Mass treatment of malaria with chloroquine. Results of a trial in Inanwatan. Tropical & Geographical Medicine 1961;13:351‐6.

von Seidlein 2003 GMB {published data only}

De Martin S, von Seidlein L, Deen JL, Pinder M, Walraven G, Greenwood B, et al. Community perceptions of a mass administration of an antimalarial drug combination in The Gambia. Tropical Medicine & International Health 2001;6(6):442‐8.
von Seidlein L, Walraven G, Milligan PJ, Alexander N, Manneh F, Deen JL, et al. The effect of mass administration of sulfadoxine‐pyrimethamine combined with artesunate on malaria incidence: a double‐blind, community‐randomized, placebo‐controlled trial in The Gambia. Transactions of the Royal Society of Tropical Medicine & Hygiene 2003;97(2):217‐25.

References to studies excluded from this review

Abraham 1944 {published data only}

Abraham AC, Samuels RD. Epidemiology of malaria in the Nizam‐ sagar Ayacut Area, Niz'amabad District, Hyderabad State. Journal of the Malaria Institute of India 1944;5(3):305‐18.

Afridi 1959 {published data only}

Afridi MK, Rahim A. Further observation on the interruption of malaria transmission with single dose of pyrimethamine (Daraprim). Rivista di Parassitologia 1959;20(4):229‐42.

Ahorlu 2009 {published data only}

Ahorlu CK, Koram KA, Seakey AK, Weiss MG, Ahorlu Collins K, Koram Kwadwo A, et al. Effectiveness of combined intermittent preventive treatment for children and timely home treatment for malaria control. Malaria Journal 2009;8:292.

Ahorlu 2011 {published data only}

Ahorlu CK, Koram KA, Seake‐Kwawu A, Weiss MG. Two‐year evaluation of intermittent preventive treatment for children (IPTc) combined with timely home treatment for malaria control in Ghana. Malaria Journal 2011;10:127.

Aikins 1993 {published data only}

Aikins MK, Pickering H, Alonso PL, D'Alessandro U, Lindsay SW, Todd J, Greenwood BM. A malarial control trial using insecticide‐treated bed nets and targeted chemoprophylaxis in a rural area of The Gambia, West Africa. 4. Perceptions of the causes of malaria and of its treatment and prevention in the study area. Transactions of the Royal Society of Tropical Medicine and Hygiene 1993;87(Supplement 3):25‐30.

Alicata 1955 {published data only}

Alicata JE, Dajani S W. Observation of pyrimethamine (Daraprim) as a suppressant of malaria in a small village in Jordan. The American Journal of Tropical Medicine and Hygiene 1955;4(6):1006‐8.

Aliev 2000 {published data only}

Aliev SP, Aliev SP. Malaria in the Republic of Tajikistan. Meditsinskaia Parazitologiia i Parazitarnye Bolezni 2000, (2):27‐9.

Aliev 2001 {published data only}

Aliev S, Saparova N, Aliev S, Saparova N. Current malaria situation and its control in Tadjikistan. Meditsinskaia Parazitologiia i Parazitarnye Bolezni 2001, (1):35‐7.

Allen 1990 {published data only}

Allen SJ, Otoo LN, Cooke G, O'Donnell A, Greenwood BM. Sensitivity of Plasmodium falciparum to Maloprim after five years of targeted chemoprophylaxis in a rural area of The Gambia. Transactions of the Royal Society of Tropical Medicine and Hygiene 1990;84(5):666‐7.

Alonso 1993a {published data only}

Alonso PL, Lindsay SW, Armstrong Schellenberg JRM, Konteh M, Keita K, Marshall C, et al. A malaria control trial using insecticide‐treated bed nets and targeted chemoprophylaxis in a rural area of The Gambia, West Africa. 5. Design and implementation of the trial. Transactions of the Royal Society of Tropical Medicine and Hygiene 1993;87(Supplement 2):31‐6.

Alonso 1993b {published data only}

Alonso PL, Lindsay SW, Armstrong Schellenberg JRM, Keita K, Gomez P, Shenton FC, et al. A malaria control trial using insecticide‐treated bed nets and targeted chemoprophylaxis in a rural area of The Gambia, West Africa. 6. The impact of the interventions on mortality and morbidity from malaria. Transactions of the Royal Society of Tropical Medicine and Hygiene 1993;87(Supplement 2):37‐44.

Alving 1952 {published data only}

Alving AS, Arnold J, Robinson DH, Alving AS, Arnold J, Robinson DH. Mass therapy of subclinical vivax malaria with primaquine. Journal of the American Medical Association 1952;149(17):1558‐62.

Amangel'diev 2001 {published data only}

Amangel'diev KA, Amangel'diev KA. Current malaria situation in Turkmenistan. Meditsinskaia Parazitologiia i Parazitarnye Bolezni 2001, (1):37‐9.

Annual Report 1932 {published data only}

Annual Report of the Institute for Medical Research for the Year 1932. Kuala Lumpur: Govt. Press. Kuala Lumpur : Govt. Press, 1933:100.

Archambeault 1954 {published data only}

Archambeault CP. Mass antimalarial therapy in veterans returning from Korea. JAMA 1954;154(17):1411‐5.

Archibald 1956 {published data only}

Archibald HM, Bruce‐Chwatt LJ. Suppression of malaria with pyrimethamine in Nigerian schoolchildren. Bulletin World Health Organization 1956;15:775‐84.

Babione 1966 {published data only}

Babione RW. Epidemiology of malaria eradication. II. Epidemiology of malaria eradication in Central America: A study of technical problems. American Journal of Public Health 1966;56(1):76‐90.

Banerjea 1949 {published data only}

Banerjea R. The control of malaria in a rural area of West Bengal. Indian Journal of Malariology 1949;3(4):371‐86.

Barber 1932 {published data only}

Barber MA, Rice JB, Brown JY. Malaria studies on the firestone rubber plantation in Liberia, West Africa. The American Journal of Hygiene 1932;15(3):601‐33.

Barger 2009 {published data only}

Barger B, Maiga H, Traore OB, Tekete M, Tembine I, Dara A, et al. Intermittent preventive treatment using artemisinin‐based combination therapy reduces malaria morbidity among school‐aged children in Mali. Tropical Medicine & International Health 2009;14(7):784‐91.

Baukapur 1984 {published data only}

Baukapur SN, Babu CJ. A focal outbreak of malaria in Valsad District, Gujarat State. Journal of Communicable Diseases 1984;16(4):268‐72.

Berberian 1948 {published data only}

Berberian DA, Dennis EW. Field experiments with chloroquine diphosphate. American Journal of Tropical Medicine 1948;28(6):755‐76.

Berny 1936 {published data only}

Berny P, Nicolas L. Prophylaxis of malaria with Quinacrine and Rhodoquine in French Guiana. Bulletin de la Societe de Pathologie Exotique 1936;29(8):870‐2.

Bloch 1982 {published data only}

Bloch M. Teachings of the antimalarial campaign in El Salvador, Central America. Revista del Instituto de Investigaciones Medicas1982; Vol. 11, issue 2:119‐24.

Bojang 2009 {published data only}

Bojang KA, Sesay S, Sowe M, Conway D, Milligan P, Greenwood B. A study of intermittent preventive treatment and home based management of malaria in a rural area of The Gambia. The American Journal of Tropical Medicine and Hygiene 2009;81(5 SUPPL. 1):145.

Bojang 2010 {published data only}

Bojang K, Akor F, Bittaye O, Conway D, Bottomley C, Milligan P, et al. A randomised trial to compare the safety, tolerability and efficacy of three drug combinations for intermittent preventive treatment in children. PLoS One 2010;5(6):e11225.

Bojang 2011 {published data only}

Bojang KA, Akor F, Conteh L, Webb E, Bittaye O, Conway DJ. Two strategies for the delivery of IPTc in an area of seasonal malaria transmission in the Gambia: a randomised controlled trial. PLoS Medicine 2011;8(2):e1000409.

Boulanger 2009 {published data only}

Boulanger D, Sarr JB, Fillol F, Cisse B, Sokhna C, Riveau G, et al. Intermittent preventive treatment of malaria decreases the anti‐Plasmodium schizont antibody response of Senegalese children. Tropical Medicine and International Health 2009;14(suppl. 4):31.

Boulanger 2010 {published data only}

Boulanger DJ, Sarr JB, Fillol F, Sokhna C, Cisse B, Schacht AM, et al. Immunological consequences of intermittent preventive treatment in Senegalese preschool children. Malaria Journal 2010;9(363).

Brink 1958 {published data only}

Brink CJH. Malaria control in the Northern Transvaal. South African Medical Journal 1958;32(32):800‐9.

Butler 1943 {published data only}

Butler FA. Malaria control program on a South Pacific base. Naval Medical Bulletin 1943;41(6):1603‐12.

Canet 1936 {published data only}

Canet J. Prevention of malaria by the administration of synthetic drugs in the rubber plantations [Prophylaxie collective par medicaments synthetiques sur les plantation des terres rouges (1934‐1936)]. 1936.

Canet 1939 {published data only}

Canet J. Results of four years mass prophylaxis with synthetic drugs in plantations in North Cochin‐China. Bulletin de la Societe de Pathologie Exotique 1939;32(1):58‐69.

Canet 1949 {published data only}

Canet J. First trials in southern Indo‐China of mass prophylaxis of malaria with Nivaquine B (resoqulne) and with Paludrine. Bulletin de la Societe de Pathologie Exotique 1949;42(5/6):165‐8.

Canet 1952 {published data only}

Canet J, Farinaud E. First trials of mass prophylaxis of malaria in Indo‐China by Daraprim. Bulletin de la Societe de Pathologie Exotique 1952;45(5):645‐52.

Canet 1953 {published data only}

Canet J. Proguanil resistance during mass prophylaxis of hyperendemic P. falciparum malaria in Indo‐China. Bulletin de la Societe de Pathologie Exotique 1953;46(2):230‐45.

Capponi 1953 {published data only}

Capponi M. Note on malaria In Douala. Medecine Tropicale 1953;13(3):361‐4.

Celli 1914 {published data only}

Celli A. [English title not available]. Ann. d'Igiene 1914;24(2):177‐243.

Charles 1958 {published data only}

Charles LJ. Comparative assessment of chloroquine and amodiaquine as malaria suppressive in Nigeria. Annals of Tropical Medicine and Parasitology 1958;52(67):55‐67.

Charles 1960 {published data only}

Charles LJ. Aftermath of a field trial in self‐administered pyrimethamine in a Ghanian community: the appearance of P. falciparum resistance. World Health Organization1960; Vol. WHO/Mal/260.

Charles 1962 {published data only}

Charles LJ, Van Der Kaay HJ, Vincke IH, Brady J. The appearance of pyrimethamine resistance in Plasmodium falciparum following self‐medication by a rural community in Ghana. Bulletin of the World Health Organization 1962;26(1):103‐8.

Chaudhuri 1950 {published data only}

Chaudhuri RN. Suppressive treatment of malaria, with statistical analysis by S. J. POTI. Indian Journal of Malariology 1950;4(2):115‐33.

Chen 1999 {published data only}

Chen W, Wu K, Lin M, Tang L, Gu Z, Wang S, et al. A pilot study on malaria control by using a new strategy of combining strengthening infection source treatment and health education in mountainous areas of Hainan province. Chinese Journal of Parasitology & Parasitic Diseases 1999;17(1):1‐4.

Cisse 2006 {published data only}

Cisse B, Sokhna C, Boulanger D, Milet J, Ba el H, Richardson K, et al. Seasonal intermittent preventive treatment with artesunate and sulfadoxine‐pyrimethamine for prevention of malaria in Senegalese children: a randomised, placebo‐controlled, double‐blind trial. The Lancet 2006;367(9511):659‐67.

Cisse 2009 {published data only}

Cisse B, Cairns M, Faye E, NDiaye O, Faye B, Cames C, et al. Randomized trial of piperaquine with sulfadoxine‐pyrimethamine or dihydroartemisinin for malaria intermittent preventive treatment in children. PLoS ONE [Electronic Resource] 2009;4(9):e7164.

Ciuca 1937 {published data only}

Ciuca M, Balteanu I, Alexa I. Experimental control of malaria with synthetic drugs. Archives Roumaines de Pathologie Experimentale et de Microbiologie 1937;10(3):295‐306.

Clark 1942 {published data only}

Clark HC, Komp WHW, Jobbins DM. A tenth year's observations on malaria in Panama, with reference to the occurrence of variations in the parasite index, during continued treatment with atabrine and plasmochine. American Journal of Tropical Medicine 1942;22:191‐216.

Clarke 2008 {published data only}

Clarke SE, Jukes MC, Njagi JK, Khasakhala L, Cundill B, Otido J, et al. Effect of intermittent preventive treatment of malaria on health and education in schoolchildren: a cluster‐randomised, double‐blind, placebo‐controlled trial. The Lancet 2008;372(9633):127‐38.

Clyde 1958 {published data only}

Clyde DF, Webbe G, Shute GT. Single dose pyrimethamine treatment of Africans during a malaria epidemic in Tanganyika. East African Medical Journal 1958;35(1):23‐9.

Clyde 1961a {published data only}

Clyde DF. Malaria control in Tanganyika under the German administration. Part I. East African Medical Journal 1961;38(1):27‐42.

Clyde 1961b {published data only}

Clyde DF. Malaria control in Tanganyika under the German administration. Part II. Mass chemoprophylaxis in Dar es Salaam. East African Medical Journal 1961;38(2):69‐82.

Clyde 1962 {published data only}

Clyde DF. Mass administration of an antimalarial drug combining 4‐aminoquinoline and 8‐aminoquinoline in Tanganyika. Bulletin of the World Health Organization 1962;27(2):203‐12.

Coutinho 1962 {published data only}

Coutinho Da Costa F, Viana De Meira L. Malaria and anti‐malarial campaign in Bissau. Boletim Cultural da Guine Portuguesa 1962;17(65):119‐165.

D'Anfreville 1930 {published data only}

D'Anfreville De La Salle L. A method of dealing with malaria in Morocco. Bulletin de la Societe de Pathologie Exotique 1930;23(1):53‐8.

Danquah 2009 {published data only}

Danquah I, Dietz E, Zanger P, Reither K, Ziniel P, Bienzle U, et al. Reduced efficacy of intermittent preventive treatment of malaria in malnourished children. Antimicrobial Agents & Chemotherapy 2009;53(5):1753‐9.

Dapeng 1996 {published data only}

Dapeng L, Leyuan S, Xili L, Xiance Y. A successful control programme for falciparum malaria in Xinyang, China. Transactions of the Royal Society of Tropical Medicine and Hygiene 1996;90:100‐2.

Decourt 1935 {published data only}

Decourt P. Mixed drug prophylaxis in Malaria. Bulletin de la Societe de Pathologie Exotique 1935;28(4):255‐61.

Decourt 1936 {published data only}

Decourt Ph, Dupoux R, Belfort, Henry Ch. Mass prophylaxis of malaria in Tunisia. Bulletin de la Societe de Pathologie Exotique 1936;29(5):487‐93.

Delmont 1981 {published data only}

Delmont J, Ranque P, Balique H, Tounkara A, Soula G, Quilici M, et al. Influence of antimalarial chemoprophylaxis on the health status of a rural community in West Africa. Preliminary results. Bulletin de la Societe de Pathologie Exotique 1981;74(6):600‐10.

de Mello 1938 {published data only}

de Mello IF. Anti‐malaria measures in rural areas of Portuguese India. Rivista di Malariologia 1938;17(3):208‐24.

Desowitz 1987 {published data only}

Desowitz RS, Spark RA. Malaria in the Maprik area of the Sepik region, Papua New Guinea: 1957‐1984. Transactions of the Royal Society of Tropical Medicine and Hygiene 1987;81(1):175‐6.

Diallo 1977 {published data only}

Diallo S, Coulibaly A, Konate M, Samba O. Chloroquine prophylaxis and the prevalence of malaria. Medecine d'Afrique Noire 1977;24(2):117‐25.

Diallo 1983 {published data only}

Diallo S, Diouf F, Bah IB, N'Dir O, Victorius A. Clinical consequences of chloroquine prophylaxis and of its discontinuation in an hyperendemic malarial region. Dakar Medical 1983;28(1):43‐65.

Dicko 2008 {published data only}

Dicko A, Sagara I, Sissoko MS, Guindo O, Diallo AI, Kone M, et al. Impact of intermittent preventive treatment with sulphadoxine‐pyrimethamine targeting the transmission season on the incidence of clinical malaria in children in Mali. Malaria Journal 2008;7:123.

Dicko 2011 {published data only}

Dicko A, Diallo AI, Tembine I, Dicko Y, Dara N, Sidibe Y, et al. Intermittent preventive treatment of malaria provides substantial protection against malaria in children already protected by an insecticide‐treated bednet in Mali: a randomised, double‐blind, placebo‐controlled trial. PLoS Medicine 2011;8(2):e1000407.

Dixon 1950 {published data only}

Dixon DS. Paludrine (Proguanil) as a malarial prophylactic amongst African labour in Kenya. East African Medical Journal 1950;27(3):127‐30.

Doi 1989 {published data only}

Doi H, Kaneko A, Panjaitan W, Ishii A. Chemotherapeutic malaria control operation by single dose of Fandisar plus Primaquine in North Sumatra, Indonesia. Southeast Asian Journal of Tropical Medicine and Public Health 1989;20(3):341‐9.

Dola 1974 {published data only}

Dola SK, Dola SK. Mass drug administration as a supplementary attack measure in malaria eradication programme. East African Medical Journal 1974;51(7):529‐31.

Doucet 1947 {published data only}

Doucet G. Preliminary note on the use of S.N. 7618 (Chloroquine) in a hyperendemic malarial locality. Annales de la Societe Belge de Medecine Tropicale 1947;27(4):341‐6.

Downs 1946 {published data only}

Downs WG. Results in an infantry regiment of several plans of treatment for vivax malaria. American Journal of Tropical Medicine 1946;26(1):67‐86.

Dupoux 1937 {published data only}

Dupoux R, Marini C, Barthas R. Mass prophylaxis of malaria in Tunis. Bulletin De l'Academie Nationale de Medecine 1937;118(35):368‐72.

Dupoux 1939 {published data only}

Dupoux R, Barthas R, Antoine A, Garali TM. Recent results of experiment in collective antimalarial prophylaxis in Tunis. Bulletin De l'Academie Nationale de Medecine 1939;121(15):591‐5.

Edeson 1957 {published data only}

Edeson JFB, Wharton RH, Wilson T, Reid JA. An experiment in the control of rural malaria in Malaya. The Medical Journal of Malaya 1957;12(1):319‐47.

Farinaud 1934 {published data only}

Farinaud M. [English title not available] [Essai de prophylaxie rationnelle du paludisme en milieu infantile a Tri‐Cu (Tonkin)]. Bulletin de la Societe de Pathologie Exotique 1934;27(6):568‐75.

Farinaud 1950 {published data only}

Farinaud ME, Choumara R. Malarial infestation and demography of the mountain population of Southern Indo‐China (P.M.S.I.). First Part: Malaria among the P.M.S.I; chemoprophylaxis and DDT dusting. Bull. Econ. Indochine 1950;22:5‐22.

Gaud 1949 {published data only}

Gaud J, Schneider J, Mechali D. Comparative efficacy of nivaquine and chloriguane in mass prophylaxis of Malaria. Bull. Inst. Hyg. Maroc. 1949;9(1/2):121‐9.

Gilroy 1952 {published data only}

Gilroy AB. Proguanil‐resistant Plasmodium falciparum in Assam. Annals of Tropical Medicine and Parasitology 1952;46(2):121‐6.

Gomez Mendoza 1960 {published data only}

Gomez Mendoza I. Observations on the programme for the employment of antimalarial drugs in the malaria eradication campaign in Venezuela. CNEP Boletin 1960;4(2):74‐81.

Gribben 1933 {published data only}

Gribben GR. Mass treatment with plasmoquine. The British Medical Journal 1933, (3802):919‐20.

Gruer 1962 {published data only}

Gruer N, Ousset JH, Lopez Manan CE. Special problems in the malaria eradication campaign. Anales del Instituto Nacional de Microbiologia 1962;1:127‐31.

Gunther 1951 {published data only}

Gunther CE. Proguanil hydrochloride (paludrine) in the prevention and treatment of malaria in New Guinea. Transactions of the Royal Society of Tropical Medicine and Hygiene 1951;44(4):473‐8.

Gunther 1952 {published data only}

Gunther CEM, Fraser NM, Wright WG. Proguanil and malaria among non‐tolerant New Guinea natives. Transactions of the Royal Society of Tropical Medicine and Hygiene 1952;46(2):185‐200.

Gusmao 1970 {published data only}

Gusmao HH, Juarez E. A trial of CI‐564 (Dapolar(r)), a repository antimalarial for prophylaxis in Amapá, Brazil. The American Journal of Tropical Medicine and Hygiene 1970;19(3):394‐400.

Han 2006 {published data only}

Han ET, Lee DH, Park KD, Seok WS, Kim YS, Tsuboi T, et al. Reemerging vivax malaria: changing patterns of annual incidence and control programs in the Republic of Korea. Korean Journal of Parasitology 2006;44(4):285‐94.

Harwin 1973 {published data only}

Harwin RM. A field trial of the effectiveness of cycloguanil pamoate in Rhodesia. Central African Journal of Medicine 1973;19(1):9‐12.

Henderson 1934 {published data only}

Henderson LH. Prophylaxis of malaria in the Sudan, with special reference to the use of plasmoqulne. Transactions of the Royal Society of Tropical Medicine and Hygiene 1934;28(2):157‐164.

Ho 1965 {published data only}

Ho C. Studies on malaria in new China. Chinese Medical Journal 1965;84(8):491‐7.

Houel 1954b {published data only}

Houel G, Van Goor WT. Chemoprophylaxis of malaria with monthly doses of chloroquine and amodiaquine. Bulletin de la Societe de Pathologie Exotique 1954;47(2):254‐60.

Huehne 1971 {published data only}

Huehne WH. Experience with an insecticide/drug combination and observations on suppressive chloroquine/pyrimethamine treatment. The American Journal of Tropical Medicine and Hygiene 1971;74(5):110‐6.

Janssens 1950 {published data only}

Janssens PG, Verstraete N, Sieniawski J. Trials of collective antimalaria drug prophylaxis among children of mine workers at Kilo. Annales de la Societe Belge de Medecine Tropicale 1950;30(2/3):257‐86; 449‐78.

Joncour 1956 {published data only}

Joncour G. La lutte contre le paludisme A Madagascar. Bulletin World Health Organization 1956;15:711‐23.

Kaneko 2010 {published data only}

Kaneko A. A community‐directed strategy for sustainable malaria elimination on islands: short‐term MDA integrated with ITNs and robust surveillance. Acta Tropica 2010;114(3):177‐83.

Karimov 2008 {published data only}

Karimov SS, Kadamov DS, Murodova NKh, Karimov SS, Kadamov DS, Murodova NKh. The current malaria situation in Tadjikistan. Meditsinskaia Parazitologiia i Parazitarnye Bolezni 2008, (1):33‐6.

Kingsbury 1931 {published data only}

Kingsbury AN, Amies CR. A field experiment on the value of plasmoquine in the prophylaxis of malaria. Transactions of the Royal Society of Tropical Medicine and Hygiene 1931;25(3):159‐172.

Klopfer 1949 {published data only}

Klopfer S. The suppressive sction of paludrine in benign tertian (vivax) malaria. Documenta Neerlandica et Indonesica de Morbis Tropicis 1949;1(1):50‐4.

Komp 1935 {published data only}

Komp WHW, Clark HC. A fourth year's observations on malaria in Panama, with reference to control with atabrine and plasmochin. American Journal of Tropical Medicine 1935;15(2):131‐54.

Konate 2011 {published data only}

Konate AT, Yaro JB, Ouedraogo AZ, Diarra A, Gansane A, Soulama I, et al. Intermittent preventive treatment of malaria provides substantial protection against malaria in children already protected by an insecticide‐treated bednet in Burkina Faso: a randomised, double‐blind, placebo‐controlled trial. PLoS Medicine 2011;8(2):e1000408.

Kweku 2008 {published data only}

Kweku M, Liu D, Adjuik M, Binka F, Seidu M, Greenwood B, et al. Seasonal intermittent preventive treatment for the prevention of anaemia and malaria in Ghanaian children: a randomized, placebo controlled trial. PLoS ONE [Electronic Resource] 2008;3(12):e4000.

Kweku 2009 {published data only}

Kweku M, Webster J, Adjuik M, Abudey S, Greenwood B, Chandramohan D, et al. Options for the delivery of intermittent preventive treatment for malaria to children: a community randomised trial. PLoS ONE [Electronic Resource] 2009;4(9):e7256.

Lacroix 1952 {published data only}

Lacroix M, Mazzuca M, Bonnet M. Proguanil and malaria prophylaxis in two Algerian villages. Bulletin de la Societe de Pathologie Exotique 1952;45(4):460‐4.

Lahon 1960 {published data only}

Lahon H, De Smet M, Boets L. Results of 5 years of mass chemoprophylaxis with pyrimethamine in Yangambi, Congo. Annales de la Societe Belge de Medecine Tropicale 1960;40(4):651‐73.

Laing 1970 {published data only}

Laing AB. Malaria suppression with fortnightly doses of pyrimethamine with sulfadoxine in the Gambia. Bulletin of the World Health Organization 1970;43:513‐20.

Laing 1984 {published data only}

Laing ABG. The impact of malaria chemoprophylaxis in Africa with special reference to Madagascar, Cameroon, and Senegal. Bulletin of the World Health Organization 1984;62(Suppl.):41‐8.

Lakshmanacharyulu 1968 {published data only}

Lakshmanacharyulu T, Guha AK, Kache SR. Control of malaria epidemics in a river valley project. Bulletin of the Indian Society for Malaria and Other Communicable Diseases 1968;5(1‐2):312‐22.

Levenson 1943 {published data only}

Levenson ED, Fastorskaya EI, Khovanskaya AI, Duk‐Hanina NN. Experiences in the control of a malarial focus in the north (Arehangel Région) by mass chemoprophylaxis and systematic treatment of malaria patients (Russian). Meditsinskaya Parazitologiya i Parazitarnye Bolezni 1943;12(Pt. 1):23‐38.

Liljander 2010 {published data only}

Liljander A, Chandramohan D, Kweku M, Olsson D, Montgomery SM, Greenwood B, et al. Influences of intermittent preventive treatment and persistent multiclonal Plasmodium falciparum infections on clinical malaria risk. PLoS ONE [Electronic Resource] 2010;5(10):e13649.

Lui 1986 {published data only}

Liu YL, Wu KS, Jia JX. Integrated approach in malaria control including environmental management to reduce man‐mosquito contact and reduction of infection source in Huanghuai Plain. Journal of Parasitology and Parasitic Diseases 1986;4(4):246‐50.

Lysenko 1960 {published data only}

Lysenko AY. Use of quinocide in treatment and prophylaxis of vivax malaria. Bulletin of the World Health Organization 1960;22:641‐62.

MacCormack 1983 {published data only}

MacCormack CP, Lwihula G. Failure to participate in a malaria chemosuppression programme: North Mara, Tanzania. Journal of Tropical Medicine and Hygiene 1983;86(3):99‐107.

Mackerras 1954 {published data only}

Mackerras MJ, Saxdars DF. Malaria in the Torres Straits Islands. South Pacific Comission Technical Paper No. 681954:vi + 27 pp.

Maiga 2009 {published data only}

Maiga H, Barger B, Traore OB, Tekete M, Timbine A, Dara A, et al. Intermittent preventive treatment using artemisinin‐based combination therapy reduces malaria morbidity among school‐aged children in Mali. The American Journal of Tropical Medicine and Hygiene 2009;81(5 SUPPL. 1):42.

Malaria_Army 1934 {published data only}

Malaria in the army in India. The Lancet 1934;223:802.

Mason 1973 {published data only}

Mason J, Hobbs JH. A study of the epidemiology of malaria in a high‐incidence coastal area of El Salvador, C. A. Revista del Instituto de Investigaciones Medicas 1973;2(1):51‐7.

Mason 1977 {published data only}

Mason J, Hobbs J. Malaria field studies in a high‐incidence coastal area of El Salvador, C.A. Bulletin of the Pan American Health Organization 1977;11(1):17‐30.

Mastbaum 1957a {published data only}

Mastbaum O. Past and present position of malaria in Swaziland. Journal of Tropical Medicine and Hygiene 1957;60(5):119‐27.

Mastbaum 1957b {published data only}

Mastbaum O. Malaria control in Swaziland. Some observations during the first year of partial discontinuation of insecticides. Journal of Tropical Medicine and Hygiene 1957;60(8):190‐2.

McGregor 1966 {published data only}

McGregor LA, Williams K, Walker GH, Rahman AK. Cycloguanil pamoate in the treatment and suppression of malaria in the Gambia, West Africa. British Medical Journal 1966;1:695‐701.

Melik‐Adamian 1938 {published data only}

Melik‐Adamian SS. Acriquine in the mass treatment of malarious children. Meditsinskaya Parazitologiya i Parazitarnye Bolezni 1938;7(2):178‐91.

Mendez Galvan 1984 {published data only}

Mendez Galvan JF, Guerrero Alvarado J, Gonzalez Mora M, Perez Landa M, Quintero Cabanillas R. Evaluation of alternative scheme of treatment for malaria control. Salud Publica de Mexico 1984;26(6):561‐72.

Mercier 1953 {published data only}

Mercier S. Epidemiologlcal and demographic results of malaria control in Tananarive in 1951. Revue du Paludisme et de Medicine Tropicale 1953;11(104):26‐36.

Merle 1955 {published data only}

Merle F, Maillot L. [English title not available] [Problemas actuales del control y erradicacion de la malaria en America Latina]. Bulletin de la Societe de Pathologie Exotique 1955;48(2):242‐69.

Mezincesco 1935 {published data only}

Mezincesco D, Cornelson DA. The prophylactic treatment of malaria with atebrin and with quinine. Archives Roumaines de Pathologie Experimentale et de Microbiologie 1935;8(4):449‐70.

Miller 1955 {published data only}

Miller M. Suppression of malaria by monthly drug administration. The American Journal of Tropical Medicine and Hygiene 1955;4:790‐9.

Monteny 1960 {published data only}

Monteny VAR. Comparative efficacy of chloroquine and pyrimethamine as prophylactics against malaria. Annales de la Societe Belge de Medecine Tropicale 1960;40(3):511‐6.

Mühlens 1913 {published data only}

MüHlens. Report of a malaria expedition to Jerusalem. Zentralblatt fur Bakteriologie, Parasitenkunde, Infektionskrankheiten und Hygiene 1913;69(1‐2):41‐85.

Nakibuuka 2009 {published data only}

Nakibuuka V, Ndeezi G, Nakiboneka D, Ndugwa CM, Tumwine JK, Nakibuuka Victoria, et al. Presumptive treatment with sulphadoxine‐pyrimethamine versus weekly chloroquine for malaria prophylaxis in children with sickle cell anaemia in Uganda: a randomized controlled trial. Malaria Journal 2009;8:237.

Nankabirwa 2010 {published data only}

Nankabirwa J, Cundill B, Clarke S, Kabatereine N, Rosenthal PJ, Dorsey G, et al. Efficacy, safety, and tolerability of three regimens for prevention of malaria: a randomized, placebo‐controlled trial in Ugandan schoolchildren. PLoS ONE [Electronic Resource] 2010;5(10):e13438.

Nave 1973 {published data only}

Nave Rebollo O, Parada E, Guerra A. Malaria in El Salvador. Control and eradication campaign analysis. Revista del Instituto de Investigaciones Medicas 1973;2(1):31‐9, 3‐30.

Norman 1952 {published data only}

Norman T. An investigation of the failure of proguanil prophylaxis. Transactions of the Royal Society of Tropical Medicine and Hygiene 1952;46(6):653‐5.

Ntab 2007 {published data only}

Ntab B, Cisse B, Boulanger D, Sokhna C, Targett G, Lines J, et al. Impact of intermittent preventive anti‐malarial treatment on the growth and nutritional status of preschool children in rural Senegal (west Africa). The American Journal of Tropical Medicine & Hygiene 2007;77(3):411‐7.

Omer 1978 {published data only}

Omer AHS. Species prevalence of malaria in northern and southern Sudan, and control by mass chemoprophylaxis. The American Journal of Tropical Medicine and Hygiene 1978;27(5):858‐63.

Onori 1972 {published data only}

Onori E, Onori E. Experience with mass drug administration as a supplementary attack measure in areas of vivax malaria. Bulletin of the World Health Organization 1972;47(5):543‐8.

Ossi 1967 {published data only}

Ossi GT. An epidemic in the life of a malaria eradication programme. Bulletin of Endemic Diseases 1967;9(1/4):5‐18.

Ouedraogo 2010 {published data only}

Ouedraogo A, Tiono AB, Diarra A, Nebie IO, Konate AT, Sirima SB. The effects of a pre‐season treatment with effective antimalarials on subsequent malaria morbidity in under five‐year‐old children living in high and seasonal malaria transmission area of Burkina Faso. Tropical Medicine and International Health 2010;15(11):1315‐21.

Parrot 1937 {published data only}

Parrot L, Catanei A, Ambialet R. Comparative experiments in mass prophylaxis of malaria by means of quinine and of synthetic drugs (Quinacrine and Praequine). Bulletin Health Organisation (League of Nations) 1937;6(5):683‐765.

Parrot 1943 {published data only}

Parrot L, Catanei A, Collignon E, Ambialet R. New trial of synthetic drugs for collective prophylaxis of malaria. Archives de l'Institut Pasteur d'Algerie 1943;21(3):131‐79.

Parrot 1944 {published data only}

Parrot L, Catanei A, Collignon E. New trials of mass prophylaxis of malaria with synthetic drugs. Archives de l'Institut Pasteur d'Algerie 1944;22(3):179‐246.

Parrot 1946 {published data only}

Parrot L, Catanei A, Collignon E. Further trials of mass prophylaxis of malaria with synthetic drugs. Archives de l'Institut Pasteur d'Algerie 1946;24(3/4):205‐78.

Peters 1962 {published data only}

Peters W. A critical survey of the results of malaria‐eradication and control programmes in the south‐west Pacific. Annals of Tropical Medicine and Parasitology 1962;56(1):20‐32.

Phillips 1954 {published data only}

Phillips Mary G. Malaria prophylaxis. The British Medical Journal 1954;1(4854):155.

Pikul 1934 {published data only}

Pikul J, Serguiev P, Tibourskaya N. Experiment on the prophylactic use of plasmocide in Daghestan with observations on the mosquito infection rate. Meditsinskaya Parazitologiya i Parazitarnye Bolezni 1934;3(4):322‐9.

Pribadi 1986 {published data only}

Pribadi W, Muzaham F, Santoso T, Rasidi R, Rukmono B, Soeharto, et al. The implementation of community participation in the control of malaria in rural Tanjung Pinang, Indonesia. Southeast Asian Journal of Tropical Medicine & Public Health 1986;17(3):371‐8.

Prokopenko 1945 {published data only}

Prokopenko LI. An analysis of the causes of the severe epidemic of malaria in 1942 in the Urgut district of the province of Samarkand and measures to prevent an increase in malaria morbidity in 1943. Medical Parasitology 1945;14(3):15‐33.

Rachou 1965 {published data only}

Rachou RG, Lyons G, Moura‐Lima M, Kerr JA. Synoptic epidemiológical studies of Malaria in El Salvador. The American Journal of Tropical Medicine and Hygiene 1965;14(1):1‐62.

Rafi 1951 {published data only}

Rafi SM, Shah IA. Paludrine as a causal prophylactic in hyperendemic areas. Pakistan Journal of Health 1951;1(1):42‐6.

Ray 1948 {published data only}

Ray AP. Prophylactic use of paludrine in a tea estate. Indian Journal of Malariology 1948;2:35‐66.

Robin 1946 {published data only}

Robin C, Brochen L. Malaria in Dakar. Results of the therapeutic and prophylactic administration of synthetic drugs in a native population. Bulletin Medical de l'Afrique‐Occidentale Francaise 1946;3(1):97‐108.

Rodríguez 1994 {published data only}

Rodríguez López MH, Loyola Elizondo EG, Betanzos Reyes AF, Villareal Treviño C, Nielsen Bown D. Control focal del paludismo: tratamiento focal usando quimioprofilaxis y rociado intradomiciliar con insecticida para el control del paludismo en el sur de México. Gaceta Medica De Mexico 1994;130(5):313‐9.

Rohner 2010 {published data only}

Rohner F, Zimmermann MB, Amon RJ, Vounatsou P, Tschannen AB, N'Goran E K, et al. In a randomized controlled trial of iron fortification, anthelmintic treatment, and intermittent preventive treatment of malaria for anemia control in Ivorian children, only anthelmintic treatment shows modest benefit. Journal of Nutrition 2010;140(3):635‐41.

Saarinen 1987 {published data only}

Saarinen M, Iyambo N, Shinyafa L, Paajanen H, Indongo I, Thoren E, et al. Mass proguanil prophylaxis. The Lancet 1987;1(8539):985‐6.

Salako 1990 {published data only}

Salako LA, Ajayi FO, Sowunmi A, Walker O, Salako LA, Ajayi FO, et al. Malaria in Nigeria: a revisit. Annals of Tropical Medicine & Parasitology 1990;84(5):435‐45.

Salihu 2000 {published data only}

Salihu HM, Tchuinguem G, Ratard R. Effect of chloroquine prophylaxis on birthweight and malaria parasite load among pregnant women delivering in a regional hospital in Cameroon. The West Indian Medical Journal 2000;49(2):143‐7.

Santos 1993 {published data only}

Santos JB, Prata A, Wanssa E. Quimioprofilaxia da malária com mefloquina na amazônia brasileira. Revista da Sociedade Brasileira de Medicina Tropical 1993;26(3):157‐62.

Schliessmann 1973 {published data only}

Schliessmann DJ, Joseph VR, Solis M, Carmichael GT. Drainage and larviciding for control of a malaria focus in Haiti. Mosquito News 1973;33(3):371‐8.

Schneider 1948a {published data only}

Schneider J, Dignat M, Voron, Sfar M. Mass prophylaxis of malaria with premaline in the Gabes Area, May to November, 1946. Bulletin de la Societe de Pathologie Exotique 1948;41(3/4):104‐8.

Schneider 1948b {published data only}

Schneider J, Larabi M, Balti M. Mass prophylaxis of Malaria with Nivaquine; Results of experience in Ghardimaou, Tunisia. Bulletin de la Societe de Pathologie Exotique 1948;41(3/4):188‐94.

Schneider 1958 {published data only}

Schneider J, Languillon J, Delas A. Chloroquine‐pyrimethamine combination in the prophylaxis of Malaria. Results after 22 months of treatment [Association chloroquine‐pyrimethamine dans la chimioprophylaxie du paludisme resultats apres 22 mois de traitement ‐ 2e note]. Bulletin de la Societe de Pathologie Exotique 1958;51(3):316‐9.

Schneider 1962 {published data only}

Schneider J, Escudie A, Ouedraogo A, Sales P. Chimoprophylaxie du paludisme par distributions hebdomadaires de chloroquine ou d'une association chloroquine‐primaquine‐pyrimethamine. Bulletin de la Societe de Pathologie Exotique 1962;2:280‐90.

Seckinger 1935 {published data only}

Seckinger DL. Atabrine and plasmochin in the treatment and control of Malaria. American Journal of Tropical Medicine 1935;15(6):631‐49.

Sehgal 1968 {published data only}

Sehgal JK. Progress of malaria eradication in Orissa State during 1965‐66. Bulletin of the Indian Society for Malaria and Other Communicable Diseases 1968;5(1‐2):88‐93.

Sergent 1913 {published data only}

Sergent Edm, Sergent Et. [Etudes epidemiologiques et prophylactiques du paludisme: neuvieme et dixieme campagnes en Algerie, en 1910 et 1911]. Annales De l'Institut Pasteur 1912;27(5):373‐90.

Sesay 2011 {published data only}

Sesay S, Milligan P, Touray E, Sowe M, Webb EL, Greenwood BM, et al. A trial of intermittent preventive treatment and home‐based management of malaria in a rural area of The Gambia. Malaria Journal 2011;10(2).

Shanks 1992 {published data only}

Shanks GD, Edstien MD, Suriyamongkol V, Timsaad S, Webster HK. Malaria chemoprophylaxis using proguanil/dapsone combinations on the Thai‐Cambodian border. American Journal of Tropical Medicine and Hygiene 1992;46(6):643‐8.

Shanks 1993 {published data only}

Shanks GD, Edstien MD, Kereu RK, Spicer PE, Rieckmann KH. Postexposure administration of halofantrine for the prevention of malaria. Clinical Infectious Diseases 1993;17:628‐31.

Shanks 1995a {published data only}

Shanks GD, Roessler P. Doxycycline for malaria prophylaxis in Australian soldiers deployed to United Nations missions in Somalia and Cambodia. Military Medicine 1995;160(9):443‐5.

Shanks 1995b {published data only}

Shanks DG, Barnett A, Edstein MD, Rieckmann KH. Effectiveness of doxycycline combined with primaquine for malaria prophylaxis. The Medical Journal of Australia 1995;162:306‐10.

Sheinker 1945 {published data only}

Sheinker KP. An experiment in epidemiological chemical Prophylaxis at a site of new construction in central Asia. Medical Parasitology 1945;14(4):56‐62.

Singh 1968 {published data only}

Singh MV, Agarwala RS, Singh KN. Epidemiological study of focal outbreak of malaria in consolidation phase area and evaluation of remedial measures in Uttar Pradesh (India). Bulletin of the Indian Society for Malaria and Other Communicable Diseases 1968;5(1/2):207‐20.

Snowden 2006 {published data only}

Snowden FM. Conquest of malaria: Italy, 1900‐1962. New Haven: Yale University Press, 2006.

Sokhna 2008 {published data only}

Sokhna C, Cisse B, Ba el H, Milligan P, Hallett R, Sutherland C, et al. A trial of the efficacy, safety and impact on drug resistance of four drug regimens for seasonal intermittent preventive treatment for malaria in Senegalese children. PLoS ONE [Electronic Resource] 2008;3(1):e1471.

Sorel 1913 {published data only}

Sorel F. Hygiene in Bassam in 1912. Bulletin de la Societe de Pathologie Exotique 1913;6(9):645‐53.

Srivastava 1950 {published data only}

Srivastava R S. Malaria control measures in the Tarai area under the Tarai Colonization Scheme, KIchha, District Naini Tal : September 1947 to December 1948. First Report. Indian Journal of Malariology 1950;4(2):151‐65.

Strangeways‐Dixon 1950 {published data only}

Strangeways Dixon D. Paludrine (Proguanil) as a malarial prophylactic amongst African labour in Kenya. The East African Medical Journal 1950;28:127‐30.

Strickland 1986 {published data only}

Strickland GT, Khaliq AA, Sarwar M, Hassan H, Pervez M, Fox E. Effects of Fansidar on chloroquine‐resistant Plasmodium falciparum in Pakistan. The American Journal of Tropical Medicine and Hygiene 1986;35(1):61‐5.

Swellengrebel 1931 {published data only}

Swellengrebel NH. Report on investigation into malaria in the union of South Africa, 1930‐31. Journal of the Medical Association of South Africa 1931;5(13):409‐24.

Tagbor 2011 {published data only}

Tagbor H, Cairns M, Nakwa E, Browne E, Sarkodie B, Counihan H, et al. The clinical impact of combining intermittent preventive treatment with home management of malaria in children aged below 5 years: cluster randomised trial. Tropical Medicine & International Health 2011;16(3):280‐9.

Tine 2011 {published data only}

Tine RCK, Faye B, Ndour CT, Ndiaye JL, Ndiaye M, Bassene C, Magnussen P, Bygbjerg IC, Sylla K, Ndour JD, Gaye O. Impact of combining intermittent preventive treatment with home management of malaria in children less than 10 years in a rural area of Senegal: a cluster randomized trial. Malaria Journal 2011;10:358.

Turner 1977 {published data only}

Turner DA. A review of the malaria eradication programme in the Solomon Islands 1975‐1976. Papua New Guinea Medical Journal 1977;20(4):188‐97.

Usenbaev 2006 {published data only}

Usenbaev NT, Ezhov MN, Zvantsov AB, Annarbaev A, Zhoroev AA, Almerekov KSh. An outbreak of Plasmodium vivax in malaria in Kyrghyzstan. Meditsinskaia Parazitologiia I Parazitarnye Bolezni 2006;1:17‐20.

Usenbaev 2008 {published data only}

Usenbaev NT, Baranova AM, Anarbaev AA, Almerekov K. Experience in sanitizing an urban focus of vivax malaria (Tashkumyr, Kyrghyzstan). Meditsinskaia Parazitologiia I Parazitarnye Bolezni 2008;3:45‐6.

Van Dijk 1958 {published data only}

Van Dijk WJOM. Mass chemoprophylaxis with chloroquine additional to DDT indoor spraying. Tropical and Geographical Medicine 1958;10(4):379‐84.

Van Goor 1950 {published data only}

Van Goor WT, Lodens JG. Clinical malaria prophylaxis with proguanil. Documenta Neerlandica et Indonesica de Morbis Tropicis 1950;2(1):62‐81.

Verhoef 2002 {published data only}

Verhoef H, West CE, Nzyuko SM, de Vogel S, van der Valk R, Wanga MA, et al. Intermittent administration of iron and sulfadoxine‐pyrimethamine to control anaemia in Kenyan children: a randomised controlled trial.[Erratum appears in Lancet 2002 Oct 19;360(9341):1256]. Lancet 2002;360(9337):908‐14.

Villegas 2010 {published data only}

Villegas L, Cairo H, Huur A, Vinisi H, Pereira H, Jozuazoon N, et al. Mass screening and treatment for malaria among gold miners in Suriname. International Journal of Infectious Diseases 2010;14:e435.

Wallace 1936 {published data only}

Wallace RB. Mass treatment with atebrin and plasmochin simplex, 1933. Malayan Medical Journal 1934;9(1):33‐7.
Wallace RB. The control of malaria on estates by mass treatment with atebrin. Malayan Medical Journal 1936;11(4):187‐213.

Wallace 1954 {published data only}

Wallace MF. Resochin; single dose therapy and mass suppression. The Medical Journal of Malaya 1954;8(3):251‐9.

Watkins 1987 {published data only}

Watkins WM, Oloo AJ, Gilles HM, Brandling‐Bennett AD, Howells RE, Koech DK. Inadequacy of chloroproguanil 20 mg per week as chemoprophylaxis for falciparum malaria in Kenya. The Lancet 1987;1(8525):125‐8.

White 1934 {published data only}

White R Senior, Adhikari A K. Anti‐gametoeyte treatment combined with anti‐larval malaria control. Records of the Malaria Survey of India 1934;4(2):77‐94.

White 1937 {published data only}

White R Senior, Adhikari A K. Anti‐gametocyte treatment combined with anti‐larval malaria control. Part II. Records of the Malaria Survey of India 1937;7(4):221‐31.

Winter 1934 {published data only}

Winter HG. Malaria control in Bengal. Journal of the Royal Army Medical Corps 1934;63(4):238‐46.

Wone 1967 {published data only}

Wone I, Michel R. Bilan de la chimioprophylaxie systematique par chloroquine au Senegal, 1963‐1966. Medecine d'Afrique Noire 1967;14(6):249‐322.

Yip 1998 {published data only}

Yip K, Yip K. Antimalarial work in China: a historical perspective. Parasitologia 1998;40(1‐2):29‐38.

Additional references

Edwards 2000

Edwards IR, Aronson JK. Adverse drug reactions: definitions, diagnosis, and management. The Lancet Oct 7 2000;356(9237):1255‐9.

Feachem 2009

Feachem RGA, Philips AA, Targett GA (eds). Shrinking the Malaria Map: A Prospectus on Malaria Elimination. The Global Health Group, Global Health Sciences, University of California, San Francisco2009.

Greenwood 2004

Greenwood B. The use of anti‐malarial drugs to prevent malaria in the population of malaria‐endemic areas. American Journal of Tropical Medicine and Hygiene 2004;70(1):1‐7.

Hay 2008

Hay SI, Smith DL, Snow RW. Measuring malaria endemicity from intense to interrupted transmission. Lancet Infectious Diseases 2008;8(6):9–378.

Higgins 2011

Higgins JPT, Green S (editors). Cochrane Handbook of Systematic Reviews of Interventions Version 5.1.0. The Cochrane Collaboration. The Cochrane, 2011.

Hotez 2009

Hotez PJ. Mass drug administration and integrated control for the world's high‐prevalence neglected tropical diseases. Clinical Pharmacology & Therapeutics 2009;85(6):659‐64.

Maude 2012

Maude RJ, Socheat D, Nguon C, Saroth P, Dara P, Li G, et al. Optimising strategies for Plasmodium falciparum malaria elimination in Cambodia: primaquine, mass drug administration and artemisinin resistance. PloS One 2012;7(5):e37166.

Okell 2011

Okell LC, Griffin JT, Kleinschmidt I, Hollingsworth TD, Churcher TS, White MJ, et al. The potential contribution of mass treatment to the control of Plasmodium falciparum malaria. PLoS ONE 2011;6(5):1‐11.

Shanks 2012

Shanks GD. Control and elimination of Plasmodium vivax.. Advances in Parasitology 2012;80:301‐41.

von Seidlein 2003

von Seidlein L, Greenwood BM. Mass administration of antimalaria drugs. Trends in Parasitology 2003;19(10):452‐60.

WHO 1951

World Health Organization. Report on the malaria conference in equatorial Africa, technical report series, No. 38. World Health Organization1951; Vol. 8, issue 7:1‐72.

WHO 1963

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World Health Organization. Malaria Elimination: A field manual for low and moderate endemic countries. World Health Organization2007.

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World Health Organization. Guidelines for the treatment of malaria ‐ 2nd Edition. World Health Organization2010.

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World Health Organization. World Malaria Report 2012. World Health Organization2012.

Characteristics of studies

Characteristics of included studies [ordered by study ID]

Archibald 1960 NGA

Methods

Dates of study: 1957‐1959

Location of study: Nigeria

Malaria endemicity (prevalence): Intervention group 1 (Arugungu ‐ June 1958): 28% in children 1‐10 years; 29% in children 0‐15 years [Moderate]. Intervention group 1 (Gulmare and Koei ‐ October 1957): 64% in children 1‐10 years; 58.3% in children 0‐15 years [High].

Transmission season: June to October

Malaria species: P. falciparum, P. malariae

Vector species: A. gambiae, A. funestus

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 10,000

Intervention group 2 (mean): 1300

Interventions

Intervention group 1 (Arugungu): MDA to all persons with chloroquine 600 mg and pyrimethamine 25 mg given monthly from June to October 1958. Coverage not specified. Co‐intervention with IRS.

Intervention group 2 (Gulmare and Koei): MDA to all persons with chloroquine 600 mg and pyrimethamine 25 mg given every six months (November 1957, May 1958, November 1958 and March 1959). Coverage not specified. Co‐intervention with IRS.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

No adverse event surveillance conducted

Adverse events reported: "There were substantial difficulties with toddlers taking chloroquine and a number of them vomited that drug."

Notes

MDA added to IRS programme. The outcomes for intervention groups 1 and 2 were assessed in a sub‐sample of the treated population. A third intervention group received only pyrimethamine 25 mg but was not included in the meta‐analysis due to reports of rapid development of resistance.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

The highest number of confirmed absentees reported by the investigators in September 1958 in Argungu was only 625 (6%).

Selective reporting (reporting bias)

High risk

The number of children examined varied greatly between surveys without any explanation and a very small number of children were examined in Arugungu.

Other bias

High risk

Anecdotes of ill effects began to circulate and there was evidence of 'palming' of tablets.

Cavalie 1962 CMR

Methods

Dates of study: 1960‐1961

Location of study: Cameroon

Malaria endemicity (prevalence): Intervention group 1: 20% in children 2‐9 years [Moderate]; 13% in all ages. Intervention group 2: 76% in children 2‐9 years; 65% in all ages [High].

Transmission season: May to June, November to December

Malaria species: P. falciparum, P. malariae

Vector species: A. gambiae, A. funestus

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: Ages > 3 months

Sample size

Intervention group 1 (mean): 22,500

Intervention group 2 (mean): 7000

Interventions

Intervention group 1 (Secteur Sud): MDA administered to all persons aged > 3 months with chloroquine 600 mg and pyrimethamine 50 mg once for two rounds in July and November 1960. Coverage 76‐92%. Co‐intervention with IRS using DDT.

Intervention group 2 (Secteur Nord): MDA administered to all persons aged > 3 months with chloroquine 600 mg and pyrimethamine 50 mg once for one round in November 1960. Coverage approximately 100%. Co‐intervention with IRS using DDT.

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Data presented in Table XV was used in the meta‐analysis. Parasitaemia prevalence results only presented for children > 3 months to 9 years of age; meta‐analysis includes only first round data. Only 13 mixed infections of P. falciparum and P. malariae were found. The remaining were P. falciparum infections only.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

Insufficient reporting of attrition/exclusions to permit judgement. No reasons for missing data provided.

Selective reporting (reporting bias)

Unclear risk

Insufficient information to permit judgement

Other bias

Low risk

No other bias detected

Comer 1971 PAN

Methods

Dates of study: 1965‐1968

Location of study: Panama

Malaria endemicity (prevalence): 17.4% in all ages [Moderate]

Transmission season: Rainy season late May to late December

Malaria species: P. falciparum, P. vivax

Vector species: Not specified

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: Ages > 6 months

Sample size

Intervention group 1 mean (range): 1709 (1548 ‐ 1908)

Interventions

Intervention group 1 (Valle del Rio Sambu): MDA to all persons aged > 6 months with pyrimethamine 50 mg (cycles 1‐25)/ 75 mg (cycles 26‐49) and primaquine 40 mg given every 2 weeks for 2 years from August 1966 to April 1968. Coverage 61‐87%. No co‐interventions.

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

Adverse events reported: The acceptance of drugs by the population was excellent. Complaints of nausea and headache were reported, but no other serious side effects were described. None of the people who complained of headaches or nausea refused to take the medicine in subsequent cycles. The number of people who refused to take the medicine was < 1% of the population covered by the programme.

Notes

No post‐intervention data

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Coupon system used to track patients; all persons included in the surveys.

Selective reporting (reporting bias)

Low risk

All intended outcomes reported

Other bias

Low risk

No other bias detected

Cáceres Garcia 2008 VEN

Methods

Dates of study: 2002‐2007

Location of study: Venezuela

Malaria endemicity (incidence): 22/1000 monthly incidence in all ages

Transmission season: November

Malaria species: P. vivax

Vector species: Not specified

Study design: Uncontrolled before‐and‐after study

Evaluation design: Passive surveillance

Participants

Age groups included: Ages > 6 months; non‐pregnant

Sample size

Intervention group 1: 25,722

Interventions

Intervention group 1 (6 municipalities in Estado Sucre): MDA to all non‐pregnant persons aged >6 months with chloroquine 25 mg/kg administered over 3 days and primaquine 3.5 mg/kg administered over 7 days in November 2002. Coverage 77% (of census)/ 86% (of included). No co‐intervention specified.

Outcomes

Parasitaemia incidence

No adverse event surveillance conducted

No adverse events reported

Notes

MDA done in setting of an outbreak

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Passive surveillance of large municipalities after one round of treatment

Selective reporting (reporting bias)

Low risk

No evidence of selective reporting

Other bias

Low risk

No other bias detected

De Zulueta 1961 UGA

Methods

Dates of study: 1959‐1960

Location of study: Uganda

Malaria endemicity (prevalence): 34% in children 2‐9 years; 17% in all ages [Moderate]

Transmission season: Rainy season April to May, August to November

Malaria species: P. falciparum, P. malariae

Vector species: A. gambiae, A. funestus

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 mean (range): 30,384 (10,303 ‐ 59,605)

Interventions

Intervention group 1 (North Kigezi): MDA administered to all persons with chloroquine 600 mg and pyrimethamine 50 mg every three months for four rounds at the time of IRS application from May 1959 to May 1960. Coverage 80%. Co‐intervention with IRS.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Outcomes assessed in a sub‐sample of the treated population.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Cooperation of the local inhabitants was remarkably good and not a single dwelling was left unsprayed

Selective reporting (reporting bias)

Low risk

Increased number of samples from hyperendemic areas in the post‐intervention survey

Other bias

Low risk

No other bias detected

De Zulueta 1964 UGA

Methods

Dates of study: 1960

Location of study: Uganda

Malaria endemicity (prevalence): 23% in children 2‐9 years; 21% in all ages [Moderate]

Transmission season: Rainy season April to May, August to November

Malaria species: P. falciparum, P. malariae

Vector species: A. gambiae

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: Ages > 3 months

Sample size

Intervention group 1 (mean): 16,000

Interventions

Intervention group 1 (Lake Bunyonyi): MDA to all persons aged > 3 months with chloroquine 600 mg and pyrimethamine 50 mg once per round for two rounds (April to May 1960 and September to October 1960). Coverage approximately 50% in the first round. Co‐intervention with IRS.

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Outcomes assessed in a sub‐sample of the treated population. A. funestus disappeared after one year of spraying and no new malaria cases were noted two years later.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

Insufficient detail, but the total number surveyed differs greatly between surveys

Selective reporting (reporting bias)

Low risk

All relevant outcomes were measured

Other bias

High risk

Only about half of the population was given MDA during the first round

Escudie 1962 BFA

Methods

Dates of study: 1960‐1961

Location of study: Burkina Faso

Malaria endemicity (prevalence): Comparison group 1: 56.1% in children 0‐10 years [High]

Transmission season: June to December

Malaria species: P. falciparum, P. ovale, P. malariae

Vector species: A. gambiae, A. funestus, A. nili

Study design: Non‐randomized controlled study

Evaluation design: Cross‐sectional surveys

Participants

Age group included: All ages

Sample size

Intervention group 1 (mean): 1890

Intervention group 2 (mean): 2560

Intervention group 3 (mean): 5400

Intervention group 4 (mean): 3490

Comparison group 1 (mean): Not described

Comparison group 2 (mean): Not described

Interventions

Intervention group 1: MDA to all persons with a single dose of either chloroquine‐primaquine (600 mg/15 mg) or amodiaquine‐primaquine (600 mg/15 mg) every 28 days from June to December 1960. Coverage 75.2 to 91.2%. No co‐interventions.

Intervention group 2: MDA to all persons with a single dose of either chloroquine‐primaquine (600 mg/15 mg) or amodiaquine‐primaquine (600 mg/15 mg) every 14 days from June to December 1960. Coverage 84.1 to 96.5%. No co‐interventions.

Intervention group 3: MDA to all persons with a single dose of either chloroquine‐primaquine (600 mg/15 mg) or amodiaquine‐primaquine (600 mg/15 mg) every 28 days from June to December 1960. Coverage 80.9 to 91.8%. Co‐intervention with IRS using DDT annually.

Intervention group 4: MDA to all persons with a single dose of either chloroquine‐primaquine (600 mg/15 mg) or amodiaquine‐primaquine (600 mg/15 mg) every 14 days from June to December 1960. Coverage 82.1 to 93.8%. Co‐intervention with IRS using DDT annually.

Comparison group 1: Control villages. No co‐interventions.

Comparison group 2: Villages sprayed with IRS using DDT annually. No other co‐interventions.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Outcomes assessed in a sub‐sample of the treated population (children 0‐10 years). Baseline data from June 1960 survey. Ninety percent of cases are P. falciparum infections; P. ovale is rare and P. malariae is very rare.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

Assignment to MDA was not randomized although drug assignment was randomized

Allocation concealment (selection bias)

High risk

Non‐randomized controlled study

Baseline imbalance (selection bias)

High risk

Baseline parasitaemia estimates are not balanced between the intervention groups and the comparison groups. Also, there was large variability in endemicity between comparison group 1 villages.

Contamination protection

Unclear risk

Insufficient information to permit judgement

Blinding of participants and personnel (performance bias)
All outcomes

Unclear risk

Participants and personnel aware of treatment, but unclear if this impacted outcomes

Blinding of outcome assessment (detection bias)
All outcomes

Unclear risk

Not blinded, but unclear if this impacted outcomes

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Adults included in MDA, but not in the evaluation. Only children 0‐10 years of age were examined in the malaria surveys before, during and after MDA.

Selective reporting (reporting bias)

Low risk

All pre‐specified outcomes of interest are reported

Other bias

Unclear risk

Atypical seasonal changes experienced in 1959‐1960, but it is unclear if these changes impacted outcomes.

Gabaldon 1959 VEN

Methods

Dates of study: 1956‐1957

Location of study: Venezuela

Malaria endemicity (incidence): 0.4/1000 baseline monthly incidence

Transmission season: May to November

Malaria species: P. vivax

Vector species: A. aquasalis, A. nuneztovari

Study design: Uncontrolled before‐and‐after study

Evaluation design: Active and passive surveillance

Participants

Age groups included: Ages > 1 month

Sample size

Intervention group 1 (mean): 111,995

Interventions

Intervention group 1: Eastern Venezuela (174 localities, 3084 houses, 16,416 persons) and Western Venezuela (735 localities, 17,638 houses, 95,579 persons): MDA to all persons aged > 1 month with pyrimethamine 50 mg per week for 24 weeks from July 1957 to December 1957. Coverage not specified. Co‐intervention with IRS.

Outcomes

Parasitaemia incidence

No adverse event surveillance conducted

No adverse events reported

Notes

MDA added to IRS program

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

All houses numbered. Envelope system for drug dispensers and slide collectors. Cooperation of the people was excellent. Active search for all infections and passive search at all medical dispensaries in the area.

Selective reporting (reporting bias)

Low risk

Most persons received more than 19 treatments; however, the actual figures are not reported due to "lack of mechanical tabulation of the data". The number of persons with relapses who had less than 19 treatments demonstrated similar trends to those who received 19 or more treatments.

Other bias

Low risk

No other bias detected

Garfield 1983 NIC

Methods

Dates of study: 1981‐1982

Location of study: Nicaragua

Malaria endemicity (incidence): 0.4/1000 baseline monthly incidence

Transmission season: November to March

Malaria species: P. falciparum, P. vivax

Vector species: A. albimanus

Study design: Uncontrolled before‐and‐after study

Evaluation design: Passive surveillance

Participants

Age groups included: Ages > 1 year

Sample size

Intervention group 1 (mean): 2,300,000

Interventions

Intervention group 1: MDA administered to all persons aged > 1 year with chloroquine 1500 mg and primaquine 45 mg over three days given once to the entire population of Nicaragua in November 1981. Coverage 70‐80%. Co‐intervention with larviciding using large scale application of temephos to peridomiciliary breeding sites targeting Aedes aegypti, but likely to have an effect on anophelines.

Outcomes

Parasitaemia incidence

No adverse event surveillance conducted

Adverse events reported: Common side effects included dizziness, nausea, vomiting and diarrhoea. Occasional cases of psychomotor disturbance, temporary psychological abnormalities and haemolysis.

Notes

Data used in the meta‐analysis was extrapolated from graphs presented in the text; baseline MDA estimates were determined using monthly surveillance data from 1974‐1981.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Single treatment episode after conducting a census, door‐to‐door education and promotion of community participation.

Selective reporting (reporting bias)

Low risk

National passive surveillance

Other bias

Low risk

No other bias detected

Gaud 1953 MAR

Methods

Dates of study: 1952

Location of study: Morocco

Malaria endemicity (prevalence): 41.5% in all ages (baseline) [High]

Transmission season: June to October

Malaria species: P. falciparum, P. vivax

Vector species: Not specified

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size:

Intervention group 1 (mean): 3000

Interventions

Intervention group 1: MDA administered to all persons with amodiaquine 600 mg given once in the summer of 1952. Coverage not specified. No co‐interventions.

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

Insufficient information to permit judgement

Selective reporting (reporting bias)

Unclear risk

Insufficient information to permit judgement

Other bias

Low risk

No other bias detected

Hii 1987 MYS

Methods

Dates of study: 1984‐1985

Location of study: Malaysia

Malaria endemicity (prevalence): Intervention group 1 (December 1984 baseline survey): 46.3% in children 0‐8 years [High]; Intervention group 2 (December 1984 baseline survey): 55.6% in children 0‐8 years [High]

Transmission season: Perennial

Malaria species: P. falciparum, P. malariae, P. vivax

Vector species: A. balabacensis

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys and active surveillance

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 754

Intervention group 2 (mean): 148

Interventions

Intervention group 1: MDA administered to all persons (139 households in five villages) with sulfadoxine‐pyrimethamine (1500 mg/75 mg) and primaquine 30 mg once in December 1984 to January 1985. Coverage 87%. Co‐intervention with permethrin‐impregnated bed nets to all households.

Intervention group 2: MDA administered to all persons (nine households in one village) with sulfadoxine‐pyrimethamine (1500 mg/75 mg) and primaquine 30 mg once in December 1984 to January 1985. Coverage 76%. No co‐interventions.

Outcomes

Parasitaemia prevalence

Parasitaemia incidence

Gametocytaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Though the entire population was treated, thick and thin blood films were collected during eight surveys on a population of 286 children aged 0‐8 years. Only data for these children were reported and therefore used in the meta‐analysis. Furthermore, because the study design included a comparison group that received MDA, the intervention and comparison groups will be treated as two intervention groups and each intervention group will be analyzed in the meta‐analysis as a separate uncontrolled before‐and‐after study. Lastly, due to insufficient information to extract incidence data, parasitaemia incidence was not included as an outcome in the meta‐analysis.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

High risk

Though the entire population was treated, thick and thin blood films were collected during eight surveys on a population of 286 children aged 0‐8 years. Only 29.7% of children were present at every one of the eight sessions.

Selective reporting (reporting bias)

High risk

The study report fails to include results on P. vivax infections that would be expected to have been reported for such a study. The study methods indicate that thick blood films will be classified as "positive or negative for asexual and/or sexual parasites of either P. falciparum, P. vivax, P. malariae, or mixed infections". Only parasitological findings for P. falciparum are described and presented in detail.

Other bias

Low risk

With the exception of two study villages, which are both intervention group 1 sites, the study villages are "well separated and demarcated". Therefore, it is unlikely that contamination between sites occurred. All villages also received the same treatment dose and schedule. However, it should be noted that in the meta‐analysis, the two interventions were analyzed as two separate uncontrolled before‐and‐after studies.

Houel 1954 MAR

Methods

Dates of study: 1953

Location of study: Morocco

Malaria endemicity (prevalence): 14.3%, children only (August 1953 baseline survey) [Moderate]

Transmission season: July to November

Malaria species: P. falciparum, P. malariae, P. vivax

Vector species: Not specified

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 9999

Interventions

Intervention group 1: MDA administered to all persons with pyrimethamine 100 mg once in June 1953 to September 1953. Coverage not specified. Co‐intervention with IRS prior to MDA.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Only results from the 147 children examined were included in the meta‐analysis.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

High risk

While adults were included in MDA, only a subset of children were included in the evaluation.

Selective reporting (reporting bias)

Unclear risk

Insufficient information to permit judgement

Other bias

High risk

No data on coverage of intervention

Jones 1954 KEN

Methods

Dates of study: 1952‐1953

Location of study: Kenya

Malaria endemicity (prevalence): 34.8% (baseline survey in a random sample of adults and infants); 32.6% (baseline survey in school children) [Moderate]

Transmission season: January to March, May to August

Malaria species: P. falciparum, P. malariae

Vector species: A. gambiae, A. funestus

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 3721 (including 297 school children)

Interventions

Intervention group 1: MDA administered to all persons in Makueni with pyrimethamine 100 mg once for three rounds in September 1952, March 1953 and September 1953. Coverage not specified. No co‐interventions.

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Following the first MDA round, blood smears were taken from random samples of the adult and infant (< 5 years) population and from all school children for a year. Due to the high degree of resistance that developed following two MDA rounds, parasitaemia prevalence results in the meta‐analysis reflect only first round MDA results for infants and adults.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Individual data kept of all school children and of all subjects with malaria attending the dispensary

Selective reporting (reporting bias)

Low risk

Blood smears collected from random samples of adults and infants and of all school children monthly for a year following the first MDA round. All pre‐specified outcomes have been reported.

Other bias

High risk

Complicated by resistance

Jones 1958 KEN

Methods

Dates of study: 1952‐1953

Location of study: Kenya

Malaria endemicity (prevalence): Intervention group 1 (September 1952): 60% in school‐age children; Comparison group 1 (September 1953): 34% in school‐age children [Moderate]

Transmission season: January to March, May to August

Malaria species: P. falciparum, P. malariae, P. vivax

Vector species: A. gambiae, A. funestus

Study design: Non‐randomized controlled study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages; school‐age children

Sample size

Intervention group 1 (range): 3721‐4500

Comparison group 1: Not specified

Interventions

Intervention group 1: MDA administered to all school children in Makueni with pyrimethamine 100 mg for three rounds in September 1952, March 1953 and September 1953. Coverage not specified. No co‐interventions.

Comparison group 1: School children in Okia used as a comparison arm. No co‐interventions.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Outcome data for the intervention group is a subset of the Jones 1954 KEN study. The meta‐analysis only included first‐round results. Gametocytaemia prevalence data is forP. falciparum only.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

Non‐randomized controlled study

Allocation concealment (selection bias)

High risk

Non‐randomized controlled study

Baseline imbalance (selection bias)

High risk

Baseline parasitaemia estimates are not balanced between the intervention group and the comparison group.

Contamination protection

Unclear risk

Although the comparison group site was 13 miles from the intervention group site, there is no indication whether the control group was adequately protected against contamination. It is quite possible that the control group received the intervention.

Blinding of participants and personnel (performance bias)
All outcomes

Unclear risk

Participants and personnel aware of treatment, but unclear if this impacted outcomes

Blinding of outcome assessment (detection bias)
All outcomes

Unclear risk

Not blinded, but unclear if this impacted outcomes

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Individual data kept of all school‐age children and of all subjects with malaria attending the dispensary. No antimalarials were sold in local shops. At the end of the 12th month of evaluation, 221 children remained out of the original 297 children.

Selective reporting (reporting bias)

Low risk

Blood smears from random samples and all school‐age children. Over the course of the study, the school population rose by 178 children. To avoid confusion, the investigators excluded these additional children from the figures used to compile prevalence and only reported data from the original 297 children.

Other bias

High risk

Complicated by drug resistance

Kaneko 2000 VUT

Methods

Dates of study: 1991‐1999

Location of study: Vanuatu

Malaria endemicity (prevalence): Intervention group 1 (January ‐ September 1991): 15.7% in all ages; Comparison group 1 (May 1990): 28.8% in all ages [Moderate].

Transmission season: December to April

Malaria species:P. falciparum, P. vivax

Vector species: A. farauti

Study design: Non‐randomized controlled study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 718

Comparison group 1 (mean): 19,289

Interventions

Intervention group 1: MDA administered to all persons in Aneityum weekly for nine weeks with chloroquine 600 mg and sulfadoxine‐pyrimethamine 1500 mg/75 mg and primaquine 45 mg once a week in weeks 1, 5, and 9; chloroquine 300 mg and primaquine 45 mg once a week in weeks 2, 3, 4, 6, 7, and 8 in September 1991 to November 1991. Coverage 79 to 92%. Co‐intervention with larvivorous fish in several identified breeding sites and universal coverage with insecticide treated bed nets (about 0.94 nets per villager).

Comparison group 1: Persons living in Malakula Island. Co‐intervention with bed nets (approximately 20% coverage).

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

Adverse events reported: Some villagers reported vomiting after taking the tablets.

Notes

Another village on Futana island was included in the study for comparison; however, because no parasitaemia was detected in the two surveys on Futuna, it was excluded from the meta‐analysis. The meta‐analysis only included data from Aneityum for the months of January and September 1991 (before MDA) and March 1998 (post‐MDA).

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

Non‐randomized controlled study

Allocation concealment (selection bias)

High risk

Non‐randomized controlled study

Baseline imbalance (selection bias)

Low risk

According to investigators, "the parasite rates were initially similar on Aneityum and Malakula islands and in general, decreased with age".

Contamination protection

Low risk

The comparison group was a village from Malakula, an adjacent island; therefore, it is unlikely that the comparison group received the intervention.

Blinding of participants and personnel (performance bias)
All outcomes

Unclear risk

Not blinded, but unclear if this impacted outcomes

Blinding of outcome assessment (detection bias)
All outcomes

Unclear risk

Not blinded, but unclear if this impacted outcomes

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Only 7.9% of doses unable to be administered and only 3.8% doses were not properly reported and could not be confirmed. The overall calculated compliance rate of the remaining doses was 88.3%.

Selective reporting (reporting bias)

High risk

Of the 13 surveys, two covered only school children whereas the other 11 surveys covered the entire population of Aneityum.

Other bias

Low risk

No other bias detected

Kligler 1931 PSE

Methods

Dates of study: 1930

Location of study: Palestine (known as British Mandate Palestine at the time of the study's publication)

Malaria endemicity (prevalence): 35% in all ages; 67% in children 2‐10 years [High]

Transmission season: October to December

Malaria species:P. falciparum, P. malariae, P. vivax

Vector species: A. elutus

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys and active surveillance

Participants

Age groups included: All ages

Sample size

Intervention group 1 mean (range): 953 (899‐993)

Interventions

Intervention group 1: MDA administered to all persons in five selected villages with plasmochine 30 mg plus quinine 900 mg twice daily for five days every three weeks for three rounds between September and November 1930. Coverage 78.8%. No co‐interventions.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

Adverse event surveillance conducted (active during the course of the treatment)

Adverse events reported: No ill results were noted during the entire course of treatment.

Notes

Noted that repeated treatments tended to increase resistance.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

High risk

There was a large drop in the number of villages surveyed from baseline to post‐survey without any explanation.

Selective reporting (reporting bias)

High risk

Five villages were treated but only select villages reported outcome data.

Other bias

Low risk

No other bias detected

Kondrashin 1985 IND

Methods

Dates of study: 1981

Location of study: India

Malaria endemicity (incidence): 4/1000 baseline monthly incidence

Transmission season; April to August

Malaria species: P. falciparum, P. vivax

Vector species: Not specified

Study design: Uncontrolled before‐and‐after study

Evaluation design: Passive surveillance

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 51,325

Interventions

Intervention group 1: MDA administered to all persons with chloroquine 600 mg (plus primaquine 45 mg in falciparum areas only) for one round in March to May 1981 in four primary health centres and two rounds in February to March 1981 and June to September 1981 in four other primary health centres. Coverage 85%. Co‐intervention with IRS.

Outcomes

Parasitaemia incidence

No adverse event surveillance conducted

No adverse events reported

Notes

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Only 1 or 2 rounds of treatment with 85% coverage

Selective reporting (reporting bias)

Unclear risk

No mention of the thoroughness of passive surveillance

Other bias

High risk

A likely increase inP. falciparum due to labour movement into treated area

Malaria_Taiwan 1991 TWN

Methods

Dates of study: 1955

Location of study: Taiwan

Malaria endemicity (prevalence): 4.12% in all ages (May 1955 survey); 2.93% in all ages (November 1955) [Low]

Transmission season: Not described

Malaria species: P. falciparum, P. malariae, P. vivax

Vector species: A. maculatus, A. minimus, A. sinensis

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys and passive surveillance

Participants

Age groups included: All ages, except infants

Sample size

Intervention group 1 mean (range): 1520 (1502‐1537)

Interventions

Intervention group 1: MDA administered to all persons, except infants, in Lanyu with a single dose of chloroquine (12 mg/kg) in November 1955. Coverage not specified. Co‐intervention with IRS using DDT.

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Post‐MDA (> 12 months) estimated using survey data from April‐May 1957 and April 1960

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

Insufficient reporting of attrition/exclusions to permit judgement

Selective reporting (reporting bias)

Low risk

The first three malariometric baseline surveys reported consisted of only a portion of the entire population on the island. Subsequent surveys examined all inhabitants. While these disproportionate samples could result in a certain bias when compared to the remaining surveys that comprised the entire population, the investigators weighted the first three surveys according to the natural distribution of the population.

Other bias

Low risk

No other bias detected

Metselaar 1961 PNG

Methods

Dates of study: 1958‐1959

Location of study: Papua New Guinea

Malaria endemicity (prevalence): 46‐80% in children 2‐11 years; 46% in all ages before spraying [High]; During spraying 13‐21% in children 2‐11 years; 12% in all ages [Moderate]

Transmission season: Not described

Malaria species: P. falciparum, P. malariae, P. vivax

Vector species: A. punctulatus, A. farauti, A. koliensis

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 2500

Interventions

Intervention group 1 (Sentani): MDA administered to all persons in sprayed areas with chloroquine 450 mg plus pyrimethamine 50 mg at weekly intervals for five rounds in 1958 and for one round in 1959. Two villages with high absolute parasite rates received an additional round of treatment in 1959. In addition, during all rounds, positives received chloroquine for an additional three successive days, completing a full course (1350 mg base for adults). Coverage 90%. Co‐intervention with IRS.

Outcomes

Parasite prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Baseline data from 1958 survey

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

90% coverage, but no further description

Selective reporting (reporting bias)

Unclear risk

Selection for inclusion in surveys not described

Other bias

Low risk

No other bias detected

Molineaux 1980 NGA

Methods

Dates of study: 1970‐1975

Location of study: Nigeria

Malaria endemicity (prevalence): 46% in all ages [High]

Transmission season: April to October

Malaria species: P. falciparum, P. malariae, P. ovale

Vector species: A. gambiae, A. funestus

Study design: Non‐randomized controlled study

Evaluation design: Cross‐sectional surveys and active surveillance

Participants

Age groups included: All ages, but infants not included in MDA until their first malaria episode.

Sample size

Intervention group 1 (mean): 14,129

Intervention group 2 (mean): 1810

Comparison group 1 (mean): 32,828

Comparison group 2 (mean): ND

Interventions

Intervention group 1 (Low frequency MDA+IRS group): MDA administered to all ages, except for infants who have not had their first malaria episode, with sulfalene‐pyrimethamine 500 mg/25 mg every 10 weeks from April 1972 to October 1973. Coverage 85%. Co‐intervention with IRS using propoxur 3‐4 rounds per year.

Intervention group 2 (High frequency MDA+IRS group): MDA administered to all ages, except for infants who have not had their first malaria episode, with sulfalene‐pyrimethamine 500 mg/25 mg every two weeks during the wet season and every 10 weeks during the dry season from April 1972 to October 1973. Coverage 85%. Co‐intervention with IRS using propoxur 3‐4 rounds per year.

Comparison group 1: IRS using propoxur 3‐4 rounds per year.

Comparison group 2: No interventions.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

Mortality

No adverse event surveillance conducted

No adverse events reported

Notes

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

Non‐randomized controlled study

Allocation concealment (selection bias)

High risk

Non‐randomized controlled study

Baseline imbalance (selection bias)

Low risk

Similiar malaria characteristics between groups

Contamination protection

Low risk

It was desirable to allocate contiguous areas to the same treatment and also to reduce the effect of migrations by having similarly treated buffer zones around the evaluation villages.

Blinding of participants and personnel (performance bias)
All outcomes

Unclear risk

Not mentioned but unclear if this impacted outcomes

Blinding of outcome assessment (detection bias)
All outcomes

Low risk

Independent reexamination of slides

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Operation aimed for total coverage

Selective reporting (reporting bias)

Low risk

The surveys covered the total de facto population of selected village clusters and all possible outcomes measured and reported.

Other bias

Low risk

No other bias detected

Najera 1973 NGA

Methods

Dates of study: 1966‐1968

Location of study: Nigeria

Malaria endemicity (prevalence): Comparison group 1: 28.9% in all ages [Moderate]

Transmission season: May to September

Malaria species: P. falciparum

Vector species: A. gambiae, A. funestus

Study design: Non‐randomized controlled study (no post‐intervention measurements)

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: Ages > 3 months

Sample size

Intervention 1 mean (range): 52,000 (52,060 to 53,897)

Comparison 1 mean: 11,500

Interventions

Intervention group 1: MDA administered to all persons aged > 3 months with chloroquine 450 mg and pyrimethamine 45 mg every 60 days for 11 rounds from November 1966 to August 1968. Coverage 78 to 92%. Co‐intervention with IRS.

Comparison group 1: Co‐intervention with IRS only. Coverage not described.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

Active adverse event surveillance conducted

Adverse events reported: Direct observation of 5003 treatments during MDA rounds 9 and 10 revealed 2% vomiting immediately after taking the drug. When a subset of the population was asked about vomiting, 9% reported this symptom.

Notes

Data collected during rounds 2 to 11 are summarized as during MDA results. This is problematic as the initial decline and later rise of cases during the two years of drug administration is aggregated. Evaluation conducted in a subset of treated population.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

Non‐randomized controlled study

Allocation concealment (selection bias)

High risk

Non‐randomized controlled study

Baseline imbalance (selection bias)

High risk

The comparison area was not comparable to the intervention area in terms of entomologic or parasitological parameters.

Contamination protection

Low risk

Treated large peripheral zone, but evaluation done in central zone only

Blinding of participants and personnel (performance bias)
All outcomes

Unclear risk

Not blinded, but unclear if this impacted outcomes

Blinding of outcome assessment (detection bias)
All outcomes

Unclear risk

Not mentioned, but unclear if this impacted outcomes

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Recorded census and population movement without large loss to follow‐up

Selective reporting (reporting bias)

Low risk

Random sampling of clusters of 200 people for the parasitological surveys

Other bias

Low risk

No other bias detected

Paik 1974a SLB

Methods

Dates of study: 1972

Location of study: Solomon Islands (known as British Solomon Islands at the time of the study's publication)

Malaria endemicity (prevalence): 27.8% all ages (May 1972 survey) [Moderate]

Transmission season: Rainy season December to April

Malaria species: P. falciparum, P. vivax

Vector species:A. farauti

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys, passive surveillance and active surveillance

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): Not specified

Interventions

Intervention group 1 (Nggela archipelago): MDA administered to all persons with chloroquine 600 mg and pyrimethamine 50 mg monthly for four months from July to October 1972. Coverage 90%. Co‐intervention with IRS.

Outcomes

Parasitaemia prevalence (includes both passive and active case detection for the period during and after the intervention)

Parasitaemia incidence (population size not given)

No adverse event surveillance conducted

No adverse events reported

Notes

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

Insufficient reporting of attrition/exclusions to permit judgement

Selective reporting (reporting bias)

High risk

Only 50% of children 2‐9 years old included in the pre‐MDA and post‐MDA household surveys

Other bias

High risk

Baseline surveillance did not include active case detection

Paik 1974b SLB

Methods

Dates of study: 1972‐1973

Location of study: Solomon Islands (known as British Solomon Islands at the time of the study's publication)

Malaria endemicity (incidence): 15/1000 baseline monthly incidence

Transmission season: Rainy season December to April

Malaria species: P. vivax, P. malariae

Vector species: A. farauti

Study design: Uncontrolled before‐and‐after study

Evaluation design: Passive surveillance

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 1200

Interventions

Intervention group 1 (Wagina and Shortland): MDA administered to all persons with chloroquine 1500 mg and primaquine 75 mg over five days every three months for three rounds from October 1972 to March 1973. Coverage 90%. No co‐interventions.

Outcomes

Parasitaemia incidence

No adverse event surveillance conducted

No adverse events reported

Notes

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Unclear risk

Insufficient information to permit judgement

Selective reporting (reporting bias)

Unclear risk

Insufficient information to permit judgement

Other bias

Low risk

No other bias detected

Ricosse 1959 BFA

Methods

Dates of study: 1958‐1959

Location of study: Burkina Faso

Malaria endemicity (prevalence): Intervention group 1 (March‐May 1958 baseline survey): 15.3% in children 0‐9 years [Moderate]; Intervention group 2 (March to May 1958 baseline survey): 56.0% in children 0‐9 years [High]

Transmission season: June to October

Malaria species: P. falciparum, P. malariae

Vector species: A. gambiae, A. funestus

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 5000

Intervention group 2 (mean): 3000

Interventions

Intervention group 1 (Zone A): MDA administered to all persons with pyrimethamine 50 mg every two weeks for eight rounds in June to September 1958. Coverage 82‐91%. Co‐intervention with IRS using DDT.

Intervention group 2 (Zone B): MDA administered to all persons with pyrimethamine 50 mg every two weeks for eight rounds in June to September 1958. Coverage 82‐91%. No co‐interventions.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Outcomes assessed in sub‐sample of treated population (0‐9 years). Data presented in Table 1 was used in the meta‐analysis.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

High risk

In Zone B, pyrimethamine distribution stopped on September 20th and resumed in October, so the study was unable to follow the entire evolution of resistance that apparently began during the fourth month of distribution. Also, the method of selection of children 2‐9 years is unclear. They took monthly blood samples in all children 0‐23 months, but due to the large sample size selected only a proportion of children 2‐9 years to examine.

Selective reporting (reporting bias)

Unclear risk

Insufficient information to permit judgement

Other bias

High risk

Complicated by resistance in the fourth month of MDA

Roberts 1964 KEN

Methods

Dates of study: 1953‐1954

Location of study: Kenya

Malaria endemicity (prevalence): 28% in 1953 [Moderate] and 22% in 1954 [Moderate] in all ages in Tiriki

Transmission season: May to July

Malaria species:P. falciparum, P. malariae

Vector species: A. gambiae, A. funestus

Study design: Non‐randomized controlled study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 101,000

Intervention group 2 (mean): 99,000

Comparison group 1 (mean): Not specified

Comparison group 2 (mean): Not specified

Interventions

Intervention group 1 (Nandi District 1953): MDA administered to all persons with pyrimethamine 50 mg once in May 1953. Coverage 95%. No co‐intervention.

Intervention group 2 (Nandi District 1954): MDA administered to all persons with pyrimethamine 50 mg once in May 1954. Coverage 95%. No co‐intervention.

Comparison group 1 (Tiriki control area 1953): No interventions

Comparison group 2 (Tiriki control area 1954): No interventions

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Intended to control epidemics.

In the methods, it states: "one hundred thick blood films were taken in treated and untreated areas from persons in each of the age groups 0‐10 years, 11‐20 years, and 21 years and older". Therefore, we assumed that the number of total patients examined was 300 for both intervention and comparison groups to determine the number of cases identified in our calculations for parasitaemia prevalence.

Outcomes were assessed in a sub‐sample of the treated population.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

Non‐randomized controlled study

Allocation concealment (selection bias)

High risk

Non‐randomized controlled study

Baseline imbalance (selection bias)

High risk

Higher baseline parasitaemia in the control area

Contamination protection

Low risk

Not described but trial area was very large

Blinding of participants and personnel (performance bias)
All outcomes

Unclear risk

Not blinded but unclear if this impacted outcomes

Blinding of outcome assessment (detection bias)
All outcomes

Unclear risk

Not mentioned but unclear if this impacted outcomes

Incomplete outcome data (attrition bias)
All outcomes

Low risk

All inhabitants living in the selected area received treatment

Selective reporting (reporting bias)

Unclear risk

Unclear who or how many were included in the malaria surveys

Other bias

Low risk

No other bias detected

Schneider 1961 BFA

Methods

Dates of study: 1960‐1961

Location of study: Burkina Faso

Malaria endemicity (prevalence): Comparison group 1 (baseline survey): 59.4% in children 2‐9 years [High]

Transmission season: August to September

Malaria species: P. falciparum, P. vivax

Vector species: Not described

Study design: Non‐randomized controlled study (no pre‐intervention measurements)

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 2500

Intervention group 2 (mean): 3535

Comparison group 1 (mean): Not specified

Interventions

Intervention group 1: MDA administered to all persons with a combination of 600 mg base chloroquine or amodiaquine and 15 mg base primaquine every 14 days in June to December 1960 for 15 rounds. No co‐intervention. Coverage 90%.

Intervention group 2: MDA administered to all persons with 600 mg base amodiaquine and 15 mg base primaquine every 14 days in June to December 1960 for eight rounds. Coverage not specified. Co‐intervention with IRS using DDT once a year in May 1960.

Comparison group 1: Control zone free of any intervention (house spraying or treatment). Coverage not specified.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Data on children 0‐9 years were reported; however, data could only be abstracted for 2‐9 years to draw appropriate comparisons. In addition, data for during MDA for the intervention groups were estimated using only October 1960 survey data; during MDA data for the comparison group was only provided for October 1960.

Intervention sample size is based on the 2500 inhabitants of the three villages surveyed; half were randomized to receive amodiaquine and primaquine while the other half received chloroquine and primaquine.

A third intervention group was treated with a combination of 600 mg base chloroquine or amodiaquine and 15 mg base primaquine every 14 days in June to December 1960; however, due to lack of detailed data presented, this group was not included in the meta‐analysis.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

Non‐randomized controlled study

Allocation concealment (selection bias)

High risk

Non‐randomized controlled study

Baseline imbalance (selection bias)

Low risk

Patient outcomes were measured prior to the intervention. According to investigators, no important differences were present across study groups.

Contamination protection

Unclear risk

Insufficient information to permit judgement

Blinding of participants and personnel (performance bias)
All outcomes

Unclear risk

Insufficient information to permit judgement

Blinding of outcome assessment (detection bias)
All outcomes

Unclear risk

Insufficient information to permit judgement

Incomplete outcome data (attrition bias)
All outcomes

High risk

Adults were treated during MDA, but were not included in the evaluation.

Selective reporting (reporting bias)

High risk

A monthly distribution schedule was also administered in the study; however due to the poor quality data, minimal results were described.

Other bias

Unclear risk

Insufficient information to permit judgement

Shekalaghe 2011 TZA

Methods

Dates of study: 2008

Location of study: Tanzania

Malaria endemicity (prevalence): 0% in all ages [Low]

Transmission season: March to May, October to November

Malaria species: P. falciparum

Vector species: Not described

Study design: Cluster‐randomized trial

Unit of randomization: Geographical clusters of households

Adjusted analyses for clustering: Yes

Adjustment method: Generalized estimating equations

ICC: Not described

Numbers of clusters: 16

Number of people: 3457

Average cluster size: 216

Evaluation design: Cross‐sectional surveys, passive surveillance and active surveillance in children

Participants

Age groups included: Ages > 1 year, but individuals who had received a full dose of ACT in the two weeks before the intervention were excluded.

Sample size

Intervention group 1 (mean): 1110

Comparison group 1 (mean): 2347

Interventions

Intervention group 1: MDA administered to all persons in eight clusters in four villages in Lower Moshi with sulphadoxine‐pyrimethamine (25 mg + 1.25 mg/kg as a single dose on the first day) plus artesunate (4 mg/kg/day for three days) plus primaquine (0.75 mg/kg as a single dose on the third day). Pregnant women received sulphadoxine‐pyrimethamine (25 mg + 1.25 mg/kg 25 mg + 1.25 mg/kg as a single dose on the first day) plus amodiaquine (10 mg/kg once daily for three days). Anaemic individuals received sulphadoxine‐pyrimethamine (25 mg + 1.25 mg/kg 25 mg + 1.25 mg/kg as a single dose on the first day) plus artesunate (4 mg/kg/day for three days). Coverage 93%. Co‐intervention with background bed net use (25.1% to 36.1%) and a single treatment campaign for trachoma with azithromycin was undertaken by a non‐governmental organisation.

Comparison group 1: Placebo administered to all persons in eight clusters once daily over three days. Coverage not described. Co‐intervention with background bed net use (25.1% to 36.1%) and a single treatment campaign for trachoma with azithromycin was undertaken by a non‐governmental organisation.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

Active adverse event surveillance with haemoglobin monitoring conducted in a subset of the population

Adverse events reported: One individual was diagnosed with a severe skin reaction in the week following MDA. Upon review, it was determined that the event was drug related. A second individual presented with skin hyperpigmentation on the face, which was determined unrelated to drug treatment. Both individuals were treated with steroids and monitored until symptoms disappeared. In those given primaquine, moderate anaemia (Hb level of <8 g/dL) was observed in 40% (6/15 individuals) of the G6PD A‐, 11.1% (3/27 individuals) of the G6PD A, and 4.5% (18/399 individuals) of the G6PD B individuals; one case of severe anaemia (Hb level of <5 g/dL) was observed.

Notes

The prevalence outcomes were assessed in a sub‐sample of the treated population.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Low risk

Randomized using computer generated randomization tables

Allocation concealment (selection bias)

Low risk

Not described, but low risk with the randomization of a small number of clusters presumably by the investigator

Baseline imbalance (selection bias)

Low risk

Baseline demographic and malaria characteristics were similar

Contamination protection

Low risk

Households that were located between clusters (ie within 1 km distance from the boundary of intervention and/or control clusters) were considered as buffer zones. Members of these households received the intervention in order to minimize contamination.

Blinding of participants and personnel (performance bias)
All outcomes

Low risk

Placebo was used in the comparison arm

Blinding of outcome assessment (detection bias)
All outcomes

Low risk

The measurement of outcomes for intervention and comparison arms were identical.

Incomplete outcome data (attrition bias)
All outcomes

Low risk

High coverage of intervention and population movement monitored

Selective reporting (reporting bias)

Low risk

For each cross‐sectional survey, individuals were randomly selected from computer‐generated random tables. All planned outcome measures were reported.

Other bias

Low risk

No other bias detected

Simeons 1938 IND

Methods

Dates of study: 1935

Location of study: India

Malaria endemicity (incidence): 156 cases/1000 baseline monthly incidence in all age groups

Transmission season: March to August

Malaria species: P. vivax

Vector species: A. culicifacies

Study design: Uncontrolled before‐and‐after study

Evaluation design: Passive surveillance

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 5650

Interventions

Intervention group 1 (Mill Area): MDA administered to all persons with atebrin intramuscular 300 mg daily for 2 days and plasmochin simplex 60 mg daily for three days once in May to June 1935. Coverage 100%. Co‐intervention with oiling for larval control after MDA.

Outcomes

Parasitaemia incidence

Passive event surveillance conducted

Adverse events reported: Haemoglobinuria occurred in 4 cases (2 severe and died; 2 mild); three of the cases were from the same household and all were taking treatment for syphilis. Fatal cases known to have syphilis and unlikely to be associated with atebrin; although potentially associated with plasmochin. Abcesses reported in 49 small children and weak adults. "Giddiness" reported with atebrin.

Notes

Baseline monthly incidence was estimated using survey data from May 1934 to April 1935 prior to MDA. Data used in the meta‐analysis was extrapolated from graphs presented in the text.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

Low risk

Every person in the Mill Area was treated; extensive propaganda was carried out to bring every fever case to the doctor.

Selective reporting (reporting bias)

Low risk

Passive surveillance data for the entire population was reported

Other bias

Low risk

No other bias detected

Singh 1953 IND

Methods

Dates of study: 1952‐1953

Location of study: India

Malaria endemicity (prevalence): 22% in all ages [Moderate]

Transmission season: September to November

Malaria species: P. falciparum

Vector species: Not described

Study design: Non‐randomized controlled study

Evaluation design: Cross‐sectional surveys and active surveillance

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 125

Comparison group 1 (mean): 55

Comparison group 2 (mean): 121

Interventions

Intervention group 1: MDA administered to all persons with amodiaquine 600 mg every two weeks for ten weeks starting in September 1952. Coverage not specified. No co‐interventions.

Comparison group 1 (comparison groups 1 and 2 combined): Neighboring control area. No co‐interventions.

Outcomes

Parasitaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

Non‐randomized controlled study

Allocation concealment (selection bias)

High risk

Non‐randomized controlled study; selection of villages were made after initial survey. Communication facilities were taken into place to decide on the intervention.

Baseline imbalance (selection bias)

High risk

Baseline malaria characteristics were similar to comparison group 2 but not to comparison group 1.

Contamination protection

High risk

Incidence of malaria was so high that every week large numbers of labourers were being repatriated to their own villages.

Blinding of participants and personnel (performance bias)
All outcomes

Unclear risk

Not blinded, but unclear if this impacted outcomes

Blinding of outcome assessment (detection bias)
All outcomes

Unclear risk

Not blinded, but unclear if this impacted outcomes

Incomplete outcome data (attrition bias)
All outcomes

High risk

No description of intervention coverage

Selective reporting (reporting bias)

Low risk

Entire population surveyed

Other bias

Low risk

No other bias detected

Song 2010 KHM

Methods

Dates of study: 2003‐2006

Location of study: Cambodia

Malaria endemicity (prevalence): 55.8% in children < 16 years; 52.3% in all ages [High]

Transmission season: Not described

Malaria species: P. falciparum, P. malariae, P. vivax

Vector species: Not described

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 3653

Intervention group 2 (mean): 2387

Interventions

Intervention group 1 (Kampong Speu, 17 villages, single round): MDA administered to all ages with artesunate 125 mg daily for two days, piperaquine 750 mg daily for two days and primaquine 9 mg every 10 days for six months starting in December 2003. Coverage not specified. No co‐interventions.

Intervention group 2 (Kampot, nine villages, two rounds on days 0 and 42): MDA administered to all ages with artesunate 125 mg daily for two days and piperaquine 750 mg daily for two days given on days 0 and 42 and primaquine 9 mg every 10 days for six months starting in December 2003 . Coverage not specified. No co‐interventions.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

Passive event surveillance conducted

Adverse events reported: No adverse reactions reported to village malaria volunteers.

Notes

Kampot data was not included in meta‐analysis as the denominator of children for the outcome data was not provided.

The outcomes were assessed in a sub‐sample of the treated population.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

High risk

One village missing data from one year

Selective reporting (reporting bias)

High risk

Monitoring was different for the different villages. Some villages had missing data.

Other bias

Low risk

No other bias detected

van Dijk 1961 PNG

Methods

Dates of study: 1960

Location of study: Papua New Guinea

Malaria endemicity (prevalence): 38.6% in children 2‐9 years (1959 survey); 18% in all ages (1959 and 1960 surveys) [Moderate]

Transmission season: Not described

Malaria species:P. falciparum, P. malariae, P. vivax

Vector species: A. farauti

Study design: Uncontrolled before‐and‐after study

Evaluation design: Cross‐sectional surveys

Participants

Age groups included: All ages

Sample size

Intervention group 1 (mean): 1250

Interventions

Intervention group 1: MDA administered to all persons with chloroquine (450 mg) once every four weeks for 11 rounds. Coverage 97.2% (range 93.1% to 100%). Co‐intervention with mass treatment of filariasis with diethylcarbamazine.

Outcomes

Parasitaemia prevalence

Gametocytaemia prevalence

No adverse event surveillance conducted

No adverse events reported

Notes

Before MDA estimates include data from June 1959 and January 1960 surveys (Tables I and II). For intervention group 1, outcome estimates come from Table V.

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

High risk

No comparison group

Allocation concealment (selection bias)

High risk

No comparison group

Baseline imbalance (selection bias)

High risk

No comparison group

Contamination protection

High risk

No comparison group

Blinding of participants and personnel (performance bias)
All outcomes

High risk

No comparison group

Blinding of outcome assessment (detection bias)
All outcomes

High risk

No comparison group

Incomplete outcome data (attrition bias)
All outcomes

High risk

Nine positives were not included in the 0‐1 month post‐MDA survey; they were not present during the last distribution.

Selective reporting (reporting bias)

Low risk

All pre‐specified outcomes of interest have been reported

Other bias

Unclear risk

Visitors to the village were also treated with the group to which they were most closely related. Persons who stayed only a few days were not treated. However, it is unclear whether this introduced bias.

von Seidlein 2003 GMB

Methods

Dates of study: 1999

Location of study: Gambia

Malaria endemicity: 42.9% in children ≤ 5 years [High]; describes 17‐19% in all ages but this data was not from this study.

Transmission season: June to December

Malaria species: P. falciparum

Vector species: Not described

Study design: Cluster‐randomized trial

Unit of randomization: Villages

Adjusted analyses for clustering: Yes

Adjustment method: Poisson regression model adjusting for population size

ICC: Not described

Number of clusters: 18 villages

Number of people: 3655

Average cluster size: 203

Feature: Matched villages

Evaluation design: Cross‐sectional surveys, active surveillance and passive surveillance

Participants

Age groups included: Ages > 6 months old; non‐pregnant

A total of 16,442 people, of which 14,017 people (85%) where treated (placebo or MDA) including the buffer zone

Sample size (of number evaluated)

Intervention group 1 (mean): 1969

Comparison group 1 (mean): 1686

Interventions

Intervention group 1: MDA administered to all non‐pregnant persons aged > 6 months with sulfadoxine‐pyrimethamine 1500 mg/75 mg and artesunate 200 mg once in June 1999. Coverage 89% in total population (90.8% in evaluated group). No co‐interventions.

Comparison group 1: Placebo administered to all non‐pregnant persons aged > 6 months once in June 1999. Coverage 89% in total population (89.6% in evaluated group). No co‐interventions.

Outcomes

Parasitaemia prevalence

Parasitaemia incidence

Gametocytaemia prevalence

Anaemia prevalence (defined as hematocrit < 33%)

Mortality

Passive and active adverse event surveillance conducted

Adverse events reported (passive surveillance system): 1 episode of pruritus

Adverse events reported (active surveillance system): 25 of 75 individuals remembered one or more complaints within 2 days of taking the drug including dizziness (13), fever (6), diarrhoea (5), vomiting (5) and itching (4).

Notes

Incidence, gametocyte prevalence, anaemia prevalence and mortality reported for children only

Risk of bias

Bias

Authors' judgement

Support for judgement

Random sequence generation (selection bias)

Low risk

While the study is a cluster‐randomized, double blind, placebo‐controlled trial, the method of randomization is not described. Author correspondence revealed that randomization was computer generated.

Allocation concealment (selection bias)

Low risk

Drugs allocated to each of the 18 study villages were delivered to the study site in identical containers. One nurse was aware of the identity of the drugs, administered the drugs in the study villages and then left the study area.

Baseline imbalance (selection bias)

Low risk

Intervention and control villages did not differ appreciably in the demographic of malaria transmission characteristics.

Contamination protection

Low risk

All inhabitants of the non‐randomized controlled villages in the study area were treated, to minimize possible dilution of the effect of the intervention.

Blinding of participants and personnel (performance bias)
All outcomes

Low risk

Cluster‐randomized, double blind, placebo‐controlled trial; neither study personnel nor the study population were aware of which villages received placebo.

Blinding of outcome assessment (detection bias)
All outcomes

Low risk

Cluster‐randomized, double blind, placebo‐controlled trial

Incomplete outcome data (attrition bias)
All outcomes

Low risk

All children in the surveillance villages were visited weekly; all 18 study villages that were randomized were analyzed.

Selective reporting (reporting bias)

Low risk

All primary and secondary endpoints reported

Other bias

Low risk

No other bias detected

Characteristics of excluded studies [ordered by study ID]

Study

Reason for exclusion

Abraham 1944

Inadequate treatment dose

Afridi 1959

Inadequate treatment dose

Ahorlu 2009

Treatment not administered to entire population; intermittent preventive treatment for children (IPTc) study

Ahorlu 2011

Treatment not administered to entire population; intermittent preventive treatment for children (IPTc) study

Aikins 1993

Inadequate treatment dose; knowledge, attitudes, and prevention component of an individually randomized study

Alicata 1955

Inadequate treatment dose; individually randomized study

Aliev 2000

Inadequate treatment dose

Aliev 2001

Inadequate treatment dose

Allen 1990

Inadequate treatment dose

Alonso 1993a

Inadequate treatment dose; individually randomized study

Alonso 1993b

Inadequate treatment dose; individually randomized study

Alving 1952

Individually randomized study; study participants did not remain in endemic area

Amangel'diev 2001

Inadequate treatment dose; testing conducted prior to treatment; insufficient information on drug administration

Annual Report 1932

Inadequate treatment dose

Archambeault 1954

Study participants did not remain in endemic area

Archibald 1956

Individually randomized study

Babione 1966

Insufficient information on drug administration

Banerjea 1949

Inadequate treatment dose

Barber 1932

Inadequate treatment dose

Barger 2009

Individually randomized study

Baukapur 1984

Insufficient information on drug administration

Berberian 1948

Testing conducted prior to treatment

Berny 1936

Inadequate treatment dose

Bloch 1982

Insufficient information on drug administration

Bojang 2009

Insufficient information on outcomes reported

Bojang 2010

Individually randomized study

Bojang 2011

Insufficient information on outcomes reported

Boulanger 2009

Individually randomized study

Boulanger 2010

Individually randomized study

Brink 1958

Inadequate treatment dose

Butler 1943

Insufficient information on drug administration

Canet 1936

Inadequate treatment dose

Canet 1939

Insufficient information on outcomes reported

Canet 1949

Insufficient information on drug administration; insufficient information on outcomes reported (no outcome of interest reported)

Canet 1952

Inadequate treatment dose

Canet 1953

Inadequate treatment dose

Capponi 1953

Inadequate treatment dose

Celli 1914

Insufficient information on drug administration

Charles 1958

Individually randomized study; testing conducted prior to treatment

Charles 1960

Inadequate treatment dose

Charles 1962

Inadequate treatment dose

Chaudhuri 1950

Inadequate treatment dose

Chen 1999

Insufficient information on outcomes reported; treatment not administered to entire population

Cisse 2006

Individually randomized study

Cisse 2009

Treatment not administered to entire population; intermittent preventive treatment for children (IPTc) study

Ciuca 1937

Mixed curative and prophylactic dosing

Clark 1942

Testing conducted prior to treatment

Clarke 2008

Treatment not administered to entire population; intermittent preventive treatment for children (IPTc) study

Clyde 1958

Insufficient information on drug administration

Clyde 1961a

Insufficient information on outcomes reported

Clyde 1961b

Insufficient information on outcomes reported

Clyde 1962

Inadequate treatment dose

Coutinho 1962

Inadequate treatment dose

D'Anfreville 1930

Insufficient information on drug administration; insufficient information on outcomes reported (no outcome of interest reported)

Danquah 2009

Individually randomized study

Dapeng 1996

Insufficient information on drug administration; insufficient information on outcomes reported

de Mello 1938

Inadequate treatment dose

Decourt 1935

Inadequate treatment dose; individually randomized study

Decourt 1936

Inadequate treatment dose

Delmont 1981

Inadequate treatment dose; individually randomized study

Desowitz 1987

Insufficient information on drug administration

Diallo 1977

Inadequate treatment dose

Diallo 1983

Treatment not administered to entire population; intermittent preventive treatment in children (IPTc) study

Dicko 2008

Individually randomized study; testing conducted prior to treatment

Dicko 2011

Individually randomized study

Dixon 1950

Inadeqaute treatment dose

Doi 1989

Individually randomized study; testing conducted prior to treatment

Dola 1974

Inadequate treatment dose

Doucet 1947

Inadequate treatment dose

Downs 1946

Study participants did not remain in endemic area

Dupoux 1937

Insufficient information on outcomes reported

Dupoux 1939

Inadequate treatment dose

Edeson 1957

Inadequate treatment dose

Farinaud 1934

Insufficient information on drug administration

Farinaud 1950

Inadequate treatment dose

Gaud 1949

Inadequate treatment dose

Gilroy 1952

Inadequate treatment dose

Gomez Mendoza 1960

Insufficient information on outcomes reported

Gribben 1933

Inadequate treatment dose

Gruer 1962

Insufficient information on drug administration; insufficient information on outcomes of interest

Gunther 1951

Inadequate treatment dose

Gunther 1952

Mixed curative and prophylactic dosing

Gusmao 1970

Inadequate treatment dose; individually randomized study

Han 2006

Inadequate treatment dose

Harwin 1973

Individually randomized study

Henderson 1934

Mixed curative and prophylactic dosing

Ho 1965

Insufficient information on outcomes reported (no outcome of interest reported)

Houel 1954b

Treatment not administered to entire population (children only)

Huehne 1971

Post‐only outcomes reported

Janssens 1950

Inadequate treatment dose

Joncour 1956

Inadequate treatment dose

Kaneko 2010

Insufficient information on drug administration; insufficient information on outcomes reported.

Karimov 2008

Inadequate treatment dose

Kingsbury 1931

Inadequate treatment dose

Klopfer 1949

Inadequate treatment dose

Komp 1935

Testing conducted prior to treatment

Konate 2011

Individually randomized study

Kweku 2008

Individually randomized study

Kweku 2009

Insufficient information on outcomes reported; comparison of delivery strategies; treatment not administered to entire population (both arms included intermittent preventive treatment in children (IPTc))

Lacroix 1952

Inadequate treatment dose

Lahon 1960

Inadequate treatment dose

Laing 1970

Testing conducted prior to treatment

Laing 1984

Inadequate treatment dose

Lakshmanacharyulu 1968

Insufficient information on drug administration

Levenson 1943

Mixed curative and prophylactic dosing

Liljander 2010

Individually randomized study

Lui 1986

Mixed curative and prophylactic dosing

Lysenko 1960

Mixed curative and prophylactic dosing

MacCormack 1983

Inadequate treatment dose

Mackerras 1954

Inadequate treatment dose

Maiga 2009

Individually randomized study

Malaria_Army 1934

Inadequate treatment dose; insufficient information on outcomes reported

Mason 1973

Insufficient information on drug administration

Mason 1977

Insufficient information on drug administration

Mastbaum 1957a

Inadequate treatment dose

Mastbaum 1957b

Inadequate treatment dose

McGregor 1966

Individually randomized study; testing conducted prior to treatment

Melik‐Adamian 1938

Testing conducted prior to treatment

Mendez Galvan 1984

Insufficient information on drug administration; insufficient information on outcomes reported

Mercier 1953

Inadequate treatment dose

Merle 1955

Inadequate treatment dose; treatment not administered to entire population (eg intermittent preventive treatment for children (IPTc))

Mezincesco 1935

Inadequate treatment dose

Miller 1955

Inadequate treatment dose; individually randomized study; treatment not administered to entire population

Monteny 1960

Inadequate treatment dose

Mühlens 1913

Insufficient information on drug administration; insufficient information on outcomes of interest

Nakibuuka 2009

Individually randomized study; testing conducted prior to treatment

Nankabirwa 2010

Individually randomized study

Nave 1973

Insufficient information on outcomes reported

Norman 1952

Inadequate treatment dose; insufficient information on outcomes of interest

Ntab 2007

Individually randomized study; insufficient information on outcomes reported

Omer 1978

Inadequate treatment dose

Onori 1972

Inadequate treatment dose

Ossi 1967

Insufficient information on outcomes reported

Ouedraogo 2010

Individually randomized study

Parrot 1937

Inadequate treatment dose

Parrot 1943

Inadequate treatment dose

Parrot 1944

Inadequate treatment dose

Parrot 1946

Inadequate treatment dose

Peters 1962

Inadequate treatment dose

Phillips 1954

Inadequate treatment dose

Pikul 1934

Insufficient information on outcomes reported

Pribadi 1986

Inadequate treatment dose

Prokopenko 1945

Inadequate treatment dose

Rachou 1965

Inadequate treatment dose

Rafi 1951

Inadequate treatment dose

Ray 1948

Inadequate treatment dose

Robin 1946

Testing conducted prior to treatment

Rodríguez 1994

Testing conducted prior to treatment

Rohner 2010

Individually randomized study

Saarinen 1987

Mixed curative and prophylactic dosing

Salako 1990

Individually randomized study; testing conducted prior to treatment

Salihu 2000

Inadequate treatment dose

Santos 1993

Inadequate treatment dose

Schliessmann 1973

Insufficient information on outcomes reported

Schneider 1948a

Inadequate treatment dose

Schneider 1948b

Inadequate treatment dose

Schneider 1958

Inadequate treatment dose

Schneider 1962

Individually randomized study; treatment not administered to entire population (eg intermittent preventive treatment for children (IPTc))

Seckinger 1935

Inadequate treatment dose

Sehgal 1968

Insufficient information on drug administration

Sergent 1913

Inadequate treatment dose; insufficient information on outcomes reported

Sesay 2011

Individually randomized study

Shanks 1992

Inadequate treatment dose; individually randomized study; testing conducted prior to treatment

Shanks 1993

Individually randomized study; study participants did not remain in endemic area

Shanks 1995a

Inadequate treatment dose; study participants did not remain in endemic area

Shanks 1995b

Study participants did not remain in endemic area

Sheinker 1945

Testing conducted prior to treatment

Singh 1968

Insufficient information on outcomes reported

Snowden 2006

Insufficient information on drug administration; insufficient information on outcomes reported

Sokhna 2008

Individually randomized study

Sorel 1913

Insufficient information on drug administration

Srivastava 1950

Inadequate treatment dose

Strangeways‐Dixon 1950

Inadequate treatment dose

Strickland 1986

Testing conducted prior to treatment

Swellengrebel 1931

Inadequate treatment dose

Tagbor 2011

Treatment not administered to entire population; intermittent preventive treatment for children (IPTc) study

Tine 2011

Treatment not administered to entire population; intermittent preventive treatment for children (IPTc) study

Turner 1977

Insufficient information on outcomes reported

Usenbaev 2006

Insufficient information on drug administration

Usenbaev 2008

Insufficient information on drug administration

Van Dijk 1958

Inadequate treatment dose

Van Goor 1950

Inadequate treatment dose

Verhoef 2002

Individually randomized study

Villegas 2010

Testing conducted prior to treatment

Wallace 1936

Mixed curative and prophylactic dosing

Wallace 1954

Insufficient information on drug administration

Watkins 1987

Individually randomized; mixed curative and prophylactic dosing

White 1934

Inadequate treatment dose

White 1937

Mixed curative and prophylactic dosing

Winter 1934

Insufficient information on outcomes reported

Wone 1967

Inadequate treatment dose

Yip 1998

Insufficient information on outcomes reported

Data and analyses

Open in table viewer
Comparison 1. MDA versus no MDA in areas of low endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 1.1

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Cluster‐randomized trials.

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Cluster‐randomized trials.

1.1 At baseline

1

496

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

1.2 <1 month post MDA

1

484

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

1.3 1‐3 months post MDA

1

794

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

1.4 4‐6 months post MDA

1

660

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 1.2

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

2.1 <1 month post MDA

1

3039

Risk Ratio (M‐H, Random, 95% CI)

0.27 [0.14, 0.50]

2.2 >12 months post MDA

1

3509

Risk Ratio (M‐H, Random, 95% CI)

0.02 [0.00, 0.12]

3 Gametocytaemia Prevalence: Cluster randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 1.3

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Cluster randomized trials.

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Cluster randomized trials.

3.1 At baseline

1

496

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

3.2 < 1 month post MDA

1

484

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

3.3 1‐3 months post MDA

1

794

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

3.4 4‐6 months post MDA

1

660

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

Open in table viewer
Comparison 2. MDA versus no MDA in areas of moderate endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Non‐randomized controlled studies Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 2.1

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

1.1 At baseline

4

3123

Risk Ratio (M‐H, Random, 95% CI)

0.73 [0.43, 1.24]

1.2 During MDA

1

47014

Risk Ratio (M‐H, Random, 95% CI)

0.27 [0.25, 0.28]

1.3 < 1 month post MDA

3

1934

Risk Ratio (M‐H, Random, 95% CI)

0.03 [0.01, 0.08]

1.4 1‐3 months post MDA

2

1557

Risk Ratio (M‐H, Random, 95% CI)

0.15 [0.10, 0.23]

1.5 4‐6 months post MDA

2

1610

Risk Ratio (M‐H, Random, 95% CI)

0.18 [0.10, 0.33]

1.6 7‐12 months post MDA

1

600

Risk Ratio (M‐H, Random, 95% CI)

0.19 [0.11, 0.33]

2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

7

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 2.2

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

2.1 During MDA

2

7965

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.02, 1.47]

2.2 <1 month post MDA

3

3096

Risk Ratio (M‐H, Random, 95% CI)

0.29 [0.17, 0.48]

2.3 1‐3 months post MDA

4

7925

Risk Ratio (M‐H, Random, 95% CI)

0.16 [0.08, 0.31]

2.4 4‐6 months post MDA

2

3797

Risk Ratio (M‐H, Random, 95% CI)

1.75 [0.41, 7.41]

3 Gametocytaemia Prevalence: Non‐randomized controlled studies Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 2.3

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Non‐randomized controlled studies.

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Non‐randomized controlled studies.

3.1 At baseline

2

1622

Risk Ratio (M‐H, Random, 95% CI)

1.40 [0.76, 2.57]

3.2 During MDA

1

47014

Risk Ratio (M‐H, Random, 95% CI)

0.48 [0.42, 0.54]

3.3 <1 month post MDA

1

433

Risk Ratio (M‐H, Random, 95% CI)

0.28 [0.10, 0.82]

3.4 1‐3 months post MDA

1

357

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.03, 0.86]

3.5 4‐6 months post MDA

1

410

Risk Ratio (M‐H, Random, 95% CI)

0.52 [0.24, 1.11]

4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 2.4

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

4.1 <1 month post MDA

3

3096

Risk Ratio (M‐H, Random, 95% CI)

0.47 [0.25, 0.87]

4.2 1‐3 months post MDA

1

294

Risk Ratio (M‐H, Random, 95% CI)

0.36 [0.12, 1.12]

4.3 4‐6 months post MDA

1

204

Risk Ratio (M‐H, Random, 95% CI)

0.35 [0.12, 1.01]

Open in table viewer
Comparison 3. MDA versus no MDA in areas of high endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 3.1

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Cluster‐randomized trials.

1.1 At baseline

1

1376

Risk Ratio (M‐H, Random, 95% CI)

0.97 [0.86, 1.10]

1.2 1‐3 months post MDA

1

1800

Risk Ratio (M‐H, Random, 95% CI)

0.82 [0.67, 1.01]

1.3 4‐6 months post MDA

1

1089

Risk Ratio (M‐H, Random, 95% CI)

1.16 [0.93, 1.44]

2 Parasitaemia Prevalence: Non‐randomized controlled studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 3.2

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Non‐randomized controlled studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Non‐randomized controlled studies.

2.1 At baseline

3

9395

Risk Ratio (M‐H, Random, 95% CI)

0.84 [0.70, 1.00]

2.2 During MDA

3

12561

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.11, 0.27]

2.3 1‐3 months post MDA

2

7197

Risk Ratio (M‐H, Random, 95% CI)

0.52 [0.33, 0.81]

3 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

7

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 3.3

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 3 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 3 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

3.1 During MDA

2

2011

Risk Ratio (M‐H, Random, 95% CI)

0.10 [0.03, 0.34]

3.2 <1 month post MDA

4

3863

Risk Ratio (M‐H, Random, 95% CI)

0.37 [0.28, 0.49]

3.3 1‐3 months post MDA

4

5132

Risk Ratio (M‐H, Random, 95% CI)

0.35 [0.15, 0.84]

3.4 4‐6 months post MDA

3

2979

Risk Ratio (M‐H, Random, 95% CI)

0.41 [0.24, 0.72]

3.5 7‐12 months post MDA

1

75

Risk Ratio (M‐H, Random, 95% CI)

0.72 [0.43, 1.20]

3.6 >12 months post MDA

1

2375

Risk Ratio (M‐H, Random, 95% CI)

0.10 [0.07, 0.12]

4 Parasitaemia Incidence: Cluster‐randomized trials Show forest plot

1

Rate Ratio (Random, 95% CI)

0.84 [0.53, 1.32]

Analysis 3.4

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 4 Parasitaemia Incidence: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 4 Parasitaemia Incidence: Cluster‐randomized trials.

4.1 < 1 month post MDA

1

Rate Ratio (Random, 95% CI)

0.41 [0.23, 0.74]

4.2 1‐3 months post MDA

1

Rate Ratio (Random, 95% CI)

1.03 [0.75, 1.41]

4.3 4‐6 months post MDA

1

Rate Ratio (Random, 95% CI)

1.11 [0.84, 1.45]

5 Gametocytaemia Prevalence: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 3.5

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 5 Gametocytaemia Prevalence: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 5 Gametocytaemia Prevalence: Cluster‐randomized trials.

5.1 At baseline

1

1376

Risk Ratio (M‐H, Random, 95% CI)

0.66 [0.33, 1.29]

5.2 4‐6 months post MDA

1

1414

Risk Ratio (M‐H, Random, 95% CI)

1.07 [0.62, 1.85]

6 Gametocytaemia Prevalence: Non‐randomized controlled studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 3.6

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 6 Gametocytaemia Prevalence: Non‐randomized controlled studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 6 Gametocytaemia Prevalence: Non‐randomized controlled studies.

6.1 At baseline

3

9395

Risk Ratio (M‐H, Random, 95% CI)

0.72 [0.55, 0.95]

6.2 During MDA

3

12561

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.10, 0.28]

6.3 1‐3 months post MDA

2

7197

Risk Ratio (M‐H, Random, 95% CI)

0.55 [0.28, 1.07]

7 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

5

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 3.7

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 7 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 7 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

7.1 During MDA

2

2011

Risk Ratio (M‐H, Random, 95% CI)

0.35 [0.09, 1.40]

7.2 <1 month post MDA

3

2582

Risk Ratio (M‐H, Random, 95% CI)

0.38 [0.13, 1.08]

7.3 1‐3 months post MDA

2

1199

Risk Ratio (M‐H, Random, 95% CI)

1.14 [0.64, 2.01]

7.4 4‐6 months post MDA

2

2789

Risk Ratio (M‐H, Random, 95% CI)

0.35 [0.10, 1.28]

7.5 7‐12 months post MDA

1

75

Risk Ratio (M‐H, Random, 95% CI)

0.86 [0.41, 1.79]

7.6 >12 months post MDA

1

2269

Risk Ratio (M‐H, Random, 95% CI)

0.09 [0.05, 0.15]

8 Anaemia Prevalence: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 3.8

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 8 Anaemia Prevalence: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 8 Anaemia Prevalence: Cluster‐randomized trials.

8.1 4‐6 months post MDA

1

1414

Risk Ratio (M‐H, Random, 95% CI)

0.84 [0.75, 0.93]

9 Mortality: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 3.9

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 9 Mortality: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 9 Mortality: Cluster‐randomized trials.

9.1 4‐6 months post MDA

1

3655

Risk Ratio (M‐H, Random, 95% CI)

1.43 [0.34, 5.96]

Open in table viewer
Comparison 4. MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Non‐randomized controlled studies Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 4.1

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

1.1 At baseline

1

1080

Risk Ratio (M‐H, Random, 95% CI)

2.09 [1.48, 2.98]

1.2 >12 months post MDA

1

1331

Risk Ratio (M‐H, Random, 95% CI)

0.10 [0.05, 0.20]

2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 4.2

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

2.1 During MDA

2

2336

Risk Ratio (M‐H, Random, 95% CI)

0.12 [0.02, 0.62]

2.2 <1 month post MDA

3

5006

Risk Ratio (M‐H, Random, 95% CI)

0.06 [0.01, 0.33]

2.3 1‐3 months post MDA

3

4724

Risk Ratio (M‐H, Random, 95% CI)

0.14 [0.04, 0.57]

2.4 4‐6 months post MDA

1

939

Risk Ratio (M‐H, Random, 95% CI)

0.57 [0.39, 0.85]

2.5 >12 months post MDA

1

1758

Risk Ratio (M‐H, Random, 95% CI)

0.00 [0.00, 0.03]

3 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 4.3

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

3.1 During MDA

2

4425

Risk Ratio (M‐H, Random, 95% CI)

0.13 [0.06, 0.27]

3.2 < 1 month post MDA

1

1907

Risk Ratio (M‐H, Random, 95% CI)

0.01 [0.00, 0.16]

3.3 1‐3 months post MDA

1

1941

Risk Ratio (M‐H, Random, 95% CI)

0.22 [0.11, 0.41]

Open in table viewer
Comparison 5. MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Non‐randomized controlled studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 5.1

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

1.1 At baseline

3

8042

Risk Ratio (M‐H, Random, 95% CI)

0.56 [0.37, 0.84]

1.2 During MDA

3

9493

Risk Ratio (M‐H, Random, 95% CI)

0.10 [0.06, 0.16]

1.3 1‐3 months post MDA

2

4455

Risk Ratio (M‐H, Random, 95% CI)

0.12 [0.06, 0.23]

1.4 7‐12 months post MDA

1

3154

Risk Ratio (M‐H, Random, 95% CI)

0.60 [0.55, 0.67]

1.5 >12 months post MDA

1

3261

Risk Ratio (M‐H, Random, 95% CI)

0.77 [0.70, 0.84]

2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 5.2

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

2.1 During MDA

2

5437

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.09, 0.31]

2.2 1‐3 months post MDA

2

5440

Risk Ratio (M‐H, Random, 95% CI)

0.13 [0.01, 2.51]

2.3 4‐6 months post MDA

1

415

Risk Ratio (M‐H, Random, 95% CI)

0.83 [0.66, 1.04]

2.4 7‐12 months post MDA

1

412

Risk Ratio (M‐H, Random, 95% CI)

0.93 [0.75, 1.16]

3 Gametocytaemia Prevalence: Non‐randomized controlled studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 5.3

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Non‐randomized controlled studies.

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Non‐randomized controlled studies.

3.1 At baseline

3

8042

Risk Ratio (M‐H, Random, 95% CI)

0.53 [0.31, 0.90]

3.2 During MDA

3

9493

Risk Ratio (M‐H, Random, 95% CI)

0.08 [0.03, 0.20]

3.3 1‐3 months post MDA

2

4455

Risk Ratio (M‐H, Random, 95% CI)

0.08 [0.05, 0.14]

3.4 7‐12 months post MDA

1

3154

Risk Ratio (M‐H, Random, 95% CI)

0.87 [0.73, 1.05]

3.5 > 12 months post MDA

1

3261

Risk Ratio (M‐H, Random, 95% CI)

0.96 [0.81, 1.14]

4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 5.4

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

4.1 During MDA

1

437

Risk Ratio (M‐H, Random, 95% CI)

0.29 [0.17, 0.50]

4.2 1‐3 months post MDA

1

440

Risk Ratio (M‐H, Random, 95% CI)

0.52 [0.34, 0.80]

4.3 4‐6 months post MDA

1

415

Risk Ratio (M‐H, Random, 95% CI)

0.76 [0.52, 1.12]

4.4 7‐12 months post MDA

1

412

Risk Ratio (M‐H, Random, 95% CI)

0.93 [0.65, 1.33]

Open in table viewer
Comparison 6. Parasitaemia Incidence studies

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 MDA versus no MDA: Uncontrolled before‐and‐after studies Show forest plot

4

Rate Ratio (Random, 95% CI)

Subtotals only

Analysis 6.1

Comparison 6 Parasitaemia Incidence studies, Outcome 1 MDA versus no MDA: Uncontrolled before‐and‐after studies.

Comparison 6 Parasitaemia Incidence studies, Outcome 1 MDA versus no MDA: Uncontrolled before‐and‐after studies.

1.1 During MDA

3

Rate Ratio (Random, 95% CI)

0.29 [0.07, 1.14]

1.2 < 1 month post MDA

4

Rate Ratio (Random, 95% CI)

0.21 [0.05, 0.84]

1.3 1‐3 months post MDA

4

Rate Ratio (Random, 95% CI)

0.61 [0.26, 1.40]

1.4 4‐6 months post MDA

1

Rate Ratio (Random, 95% CI)

0.65 [0.41, 1.02]

1.5 7‐12 months post MDA

1

Rate Ratio (Random, 95% CI)

0.15 [0.07, 0.34]

1.6 >12 months post MDA

1

Rate Ratio (Random, 95% CI)

0.48 [0.42, 0.55]

2 MDA + vector control versus no MDA: Uncontrolled before‐and‐after studies Show forest plot

2

Rate Ratio (Random, 95% CI)

Subtotals only

Analysis 6.2

Comparison 6 Parasitaemia Incidence studies, Outcome 2 MDA + vector control versus no MDA: Uncontrolled before‐and‐after studies.

Comparison 6 Parasitaemia Incidence studies, Outcome 2 MDA + vector control versus no MDA: Uncontrolled before‐and‐after studies.

2.1 During MDA

2

Rate Ratio (Random, 95% CI)

0.92 [0.49, 1.75]

2.2 < 1 month post MDA

2

Rate Ratio (Random, 95% CI)

0.04 [0.00, 1.54]

2.3 1‐3 months post MDA

2

Rate Ratio (Random, 95% CI)

0.08 [0.01, 0.98]

2.4 4‐6 months post MDA

2

Rate Ratio (Random, 95% CI)

0.11 [0.01, 1.97]

2.5 7‐12 months post MDA

2

Rate Ratio (Random, 95% CI)

0.16 [0.01, 3.10]

2.6 > 12 months post MDA

1

Rate Ratio (Random, 95% CI)

0.04 [0.03, 0.07]

Open in table viewer
Comparison 7. MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence during MDA Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 7.1

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 1 Parasitaemia Prevalence during MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 1 Parasitaemia Prevalence during MDA.

1.1 Non‐randomized controlled studies ‐ with 8‐aminoquinoline

2

6634

Risk Ratio (M‐H, Random, 95% CI)

0.20 [0.12, 0.32]

1.2 Non‐randomized controlled studies ‐ without 8‐aminoquinoline

2

52941

Risk Ratio (M‐H, Random, 95% CI)

0.16 [0.08, 0.31]

2 Parasitaemia Prevalence 1‐3 months post MDA Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 7.2

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 2 Parasitaemia Prevalence 1‐3 months post MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 2 Parasitaemia Prevalence 1‐3 months post MDA.

2.1 Non‐randomized controlled studies ‐ with 8‐aminoquinoline

2

7197

Risk Ratio (M‐H, Random, 95% CI)

0.52 [0.33, 0.81]

2.2 Non‐randomized controlled studies ‐ without 8‐aminoquinoline

2

1557

Risk Ratio (M‐H, Random, 95% CI)

0.15 [0.10, 0.23]

3 Parasitaemia Prevalence during MDA Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 7.3

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 3 Parasitaemia Prevalence during MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 3 Parasitaemia Prevalence during MDA.

3.1 Uncontrolled before‐and‐after studies ‐ with 8‐aminoquinoline

1

2965

Risk Ratio (M‐H, Random, 95% CI)

0.06 [0.03, 0.10]

3.2 Uncontrolled before‐and‐after studies ‐ without 8‐aminoquinoline

3

7011

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.06, 0.51]

4 Parasitaemia Prevalence <1 month post MDA Show forest plot

7

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 7.4

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 4 Parasitaemia Prevalence <1 month post MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 4 Parasitaemia Prevalence <1 month post MDA.

4.1 Uncontrolled before‐and‐after studies ‐ with 8‐aminoquinoline

3

2650

Risk Ratio (M‐H, Random, 95% CI)

0.42 [0.29, 0.61]

4.2 Uncontrolled before‐and‐after studies ‐ without 8‐aminoquinoline

4

4309

Risk Ratio (M‐H, Random, 95% CI)

0.29 [0.22, 0.38]

5 Parasitaemia Prevalence 1‐3 months post MDA Show forest plot

7

Risk Ratio (M‐H, Fixed, 95% CI)

Subtotals only

Analysis 7.5

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 5 Parasitaemia Prevalence 1‐3 months post MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 5 Parasitaemia Prevalence 1‐3 months post MDA.

5.1 Uncontrolled before‐and‐after studies ‐ with 8‐aminoquinoline

1

98

Risk Ratio (M‐H, Fixed, 95% CI)

0.65 [0.41, 1.01]

5.2 Uncontrolled before‐and‐after studies ‐ without 8‐aminoquinoline

6

12959

Risk Ratio (M‐H, Fixed, 95% CI)

0.32 [0.29, 0.34]

6 Parasitaemia Prevalence 4‐6 months post MDA Show forest plot

5

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 7.6

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 6 Parasitaemia Prevalence 4‐6 months post MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 6 Parasitaemia Prevalence 4‐6 months post MDA.

6.1 Uncontrolled before‐and‐after studies ‐ with 8‐aminoquinoline

3

2979

Risk Ratio (M‐H, Random, 95% CI)

0.41 [0.24, 0.72]

6.2 Uncontrolled before‐and‐after studies ‐ without 8‐aminoquinoline

2

3797

Risk Ratio (M‐H, Random, 95% CI)

1.75 [0.41, 7.41]

Open in table viewer
Comparison 8. MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence at baseline Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 8.1

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 1 Parasitaemia Prevalence at baseline.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 1 Parasitaemia Prevalence at baseline.

1.1 Non‐randomized controlled studies ‐ falciparum

2

1537

Risk Ratio (M‐H, Random, 95% CI)

1.34 [1.03, 1.74]

1.2 Non‐randomized controlled studies ‐ vivax

2

1537

Risk Ratio (M‐H, Random, 95% CI)

3.84 [1.33, 11.04]

2 Parasitaemia Prevalence during MDA Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 8.2

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 2 Parasitaemia Prevalence during MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 2 Parasitaemia Prevalence during MDA.

2.1 Uncontrolled before‐and‐after studies ‐ falciparum

2

5561

Risk Ratio (M‐H, Random, 95% CI)

0.40 [0.08, 1.97]

2.2 Uncontrolled before‐and‐after studies ‐ vivax

2

5561

Risk Ratio (M‐H, Random, 95% CI)

0.60 [0.40, 0.90]

3 Parasitaemia Prevalence <1 month post MDA Show forest plot

5

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 8.3

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 3 Parasitaemia Prevalence <1 month post MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 3 Parasitaemia Prevalence <1 month post MDA.

3.1 Non‐randomized controlled studies ‐ falciparum

1

433

Risk Ratio (M‐H, Random, 95% CI)

0.02 [0.00, 0.08]

3.2 Non‐randomized controlled studies ‐ vivax

1

433

Risk Ratio (M‐H, Random, 95% CI)

0.05 [0.00, 0.82]

3.3 Uncontrolled before‐and‐after studies ‐ falciparum

4

7367

Risk Ratio (M‐H, Random, 95% CI)

0.22 [0.18, 0.29]

3.4 Uncontrolled before‐and‐after studies ‐ vivax

4

7367

Risk Ratio (M‐H, Random, 95% CI)

0.50 [0.41, 0.61]

4 Parasitaemia Prevalence 1‐3 months post MDA Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 8.4

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 4 Parasitaemia Prevalence 1‐3 months post MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 4 Parasitaemia Prevalence 1‐3 months post MDA.

4.1 Non‐randomized controlled studies ‐ falciparum

1

357

Risk Ratio (M‐H, Random, 95% CI)

0.03 [0.01, 0.12]

4.2 Non‐randomized controlled studies ‐ vivax

1

357

Risk Ratio (M‐H, Random, 95% CI)

1.37 [0.46, 4.11]

4.3 Uncontrolled before‐and‐after studies ‐ falciparum

2

5754

Risk Ratio (M‐H, Random, 95% CI)

0.22 [0.09, 0.51]

4.4 Uncontrolled before‐and‐after studies ‐ vivax

2

5754

Risk Ratio (M‐H, Random, 95% CI)

0.49 [0.32, 0.76]

5 Parasitaemia Prevalence 4‐6 months post MDA Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 8.5

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 5 Parasitaemia Prevalence 4‐6 months post MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 5 Parasitaemia Prevalence 4‐6 months post MDA.

5.1 Non‐randomized controlled studies ‐ falciparum

1

410

Risk Ratio (M‐H, Random, 95% CI)

0.22 [0.14, 0.33]

5.2 Non‐randomized controlled studies ‐ vivax

1

410

Risk Ratio (M‐H, Random, 95% CI)

0.81 [0.31, 2.08]

5.3 Uncontrolled before‐and‐after studies ‐ falciparum

2

3642

Risk Ratio (M‐H, Random, 95% CI)

0.40 [0.13, 1.23]

5.4 Uncontrolled before‐and‐after studies ‐ vivax

2

3642

Risk Ratio (M‐H, Random, 95% CI)

0.31 [0.24, 0.39]

6 Parasitaemia Prevalence >12 months post MDA Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

Analysis 8.6

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 6 Parasitaemia Prevalence >12 months post MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 6 Parasitaemia Prevalence >12 months post MDA.

6.1 Non‐randomized controlled studies ‐ falciparum

1

1331

Risk Ratio (M‐H, Random, 95% CI)

0.01 [0.00, 0.13]

6.2 Non‐randomized controlled studies ‐ vivax

1

1331

Risk Ratio (M‐H, Random, 95% CI)

0.36 [0.15, 0.86]

6.3 Uncontrolled before‐and‐after studies ‐ falciparum

2

5884

Risk Ratio (M‐H, Random, 95% CI)

0.06 [0.04, 0.09]

6.4 Uncontrolled before‐and‐after studies ‐ vivax

2

5884

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.12, 0.24]

Study flow diagram.
Figuras y tablas -
Figure 1

Study flow diagram.

Risk of bias summary: review authors' judgements about each risk of bias item for each included study.
Figuras y tablas -
Figure 2

Risk of bias summary: review authors' judgements about each risk of bias item for each included study.

Risk of bias graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.
Figuras y tablas -
Figure 3

Risk of bias graph: review authors' judgements about each risk of bias item presented as percentages across all included studies.

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Cluster‐randomized trials.
Figuras y tablas -
Analysis 1.1

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Cluster‐randomized trials.

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 1.2

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Cluster randomized trials.
Figuras y tablas -
Analysis 1.3

Comparison 1 MDA versus no MDA in areas of low endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Cluster randomized trials.

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.
Figuras y tablas -
Analysis 2.1

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 2.2

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Non‐randomized controlled studies.
Figuras y tablas -
Analysis 2.3

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Non‐randomized controlled studies.

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 2.4

Comparison 2 MDA versus no MDA in areas of moderate endemicity (Stratified by study design), Outcome 4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Cluster‐randomized trials.
Figuras y tablas -
Analysis 3.1

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Non‐randomized controlled studies.
Figuras y tablas -
Analysis 3.2

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Non‐randomized controlled studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 3 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 3.3

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 3 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 4 Parasitaemia Incidence: Cluster‐randomized trials.
Figuras y tablas -
Analysis 3.4

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 4 Parasitaemia Incidence: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 5 Gametocytaemia Prevalence: Cluster‐randomized trials.
Figuras y tablas -
Analysis 3.5

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 5 Gametocytaemia Prevalence: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 6 Gametocytaemia Prevalence: Non‐randomized controlled studies.
Figuras y tablas -
Analysis 3.6

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 6 Gametocytaemia Prevalence: Non‐randomized controlled studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 7 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 3.7

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 7 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 8 Anaemia Prevalence: Cluster‐randomized trials.
Figuras y tablas -
Analysis 3.8

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 8 Anaemia Prevalence: Cluster‐randomized trials.

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 9 Mortality: Cluster‐randomized trials.
Figuras y tablas -
Analysis 3.9

Comparison 3 MDA versus no MDA in areas of high endemicity (Stratified by study design), Outcome 9 Mortality: Cluster‐randomized trials.

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.
Figuras y tablas -
Analysis 4.1

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 4.2

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 4.3

Comparison 4 MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.
Figuras y tablas -
Analysis 5.1

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 1 Parasitaemia Prevalence: Non‐randomized controlled studies.

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 5.2

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Non‐randomized controlled studies.
Figuras y tablas -
Analysis 5.3

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 3 Gametocytaemia Prevalence: Non‐randomized controlled studies.

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 5.4

Comparison 5 MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design), Outcome 4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies.

Comparison 6 Parasitaemia Incidence studies, Outcome 1 MDA versus no MDA: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 6.1

Comparison 6 Parasitaemia Incidence studies, Outcome 1 MDA versus no MDA: Uncontrolled before‐and‐after studies.

Comparison 6 Parasitaemia Incidence studies, Outcome 2 MDA + vector control versus no MDA: Uncontrolled before‐and‐after studies.
Figuras y tablas -
Analysis 6.2

Comparison 6 Parasitaemia Incidence studies, Outcome 2 MDA + vector control versus no MDA: Uncontrolled before‐and‐after studies.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 1 Parasitaemia Prevalence during MDA.
Figuras y tablas -
Analysis 7.1

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 1 Parasitaemia Prevalence during MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 2 Parasitaemia Prevalence 1‐3 months post MDA.
Figuras y tablas -
Analysis 7.2

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 2 Parasitaemia Prevalence 1‐3 months post MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 3 Parasitaemia Prevalence during MDA.
Figuras y tablas -
Analysis 7.3

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 3 Parasitaemia Prevalence during MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 4 Parasitaemia Prevalence <1 month post MDA.
Figuras y tablas -
Analysis 7.4

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 4 Parasitaemia Prevalence <1 month post MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 5 Parasitaemia Prevalence 1‐3 months post MDA.
Figuras y tablas -
Analysis 7.5

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 5 Parasitaemia Prevalence 1‐3 months post MDA.

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 6 Parasitaemia Prevalence 4‐6 months post MDA.
Figuras y tablas -
Analysis 7.6

Comparison 7 MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline), Outcome 6 Parasitaemia Prevalence 4‐6 months post MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 1 Parasitaemia Prevalence at baseline.
Figuras y tablas -
Analysis 8.1

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 1 Parasitaemia Prevalence at baseline.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 2 Parasitaemia Prevalence during MDA.
Figuras y tablas -
Analysis 8.2

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 2 Parasitaemia Prevalence during MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 3 Parasitaemia Prevalence <1 month post MDA.
Figuras y tablas -
Analysis 8.3

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 3 Parasitaemia Prevalence <1 month post MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 4 Parasitaemia Prevalence 1‐3 months post MDA.
Figuras y tablas -
Analysis 8.4

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 4 Parasitaemia Prevalence 1‐3 months post MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 5 Parasitaemia Prevalence 4‐6 months post MDA.
Figuras y tablas -
Analysis 8.5

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 5 Parasitaemia Prevalence 4‐6 months post MDA.

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 6 Parasitaemia Prevalence >12 months post MDA.
Figuras y tablas -
Analysis 8.6

Comparison 8 MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species), Outcome 6 Parasitaemia Prevalence >12 months post MDA.

Table 1. Overview of studies conducted in areas of low endemicity

Study ID

Design

Country

Year

Endemicity

MDA group

Control group/

Baseline

Drug (dose)

Interval

No. of rounds

Population
targeted

Coverage

Co‐intervention

Shekalaghe 2011

CRT

Tanzania

2008

0%*

AS (4 mg/kg/day for 3 days) +SP (25 mg/1.25 mg on day 1) +PQ (0.75 mg on day 3)

1

1110

93%

Background ITN use

Placebo + Background ITN use

Malaria_Taiwan 1991

BAS

Taiwan

1955

3‐4%*

CQ (12 mg/kg)

1

1520

ND

IRS

IRS

CRT = Cluster‐randomized trial; BAS = Uncontrolled before‐and‐after study; AS = Artesunate; SP = Sulfadoxine‐Pyrimethamine; PQ = Primaquine; CQ = Chloroquine; ND = Not described; IRS = Indoor Residual Spraying.

*In all ages

Figuras y tablas -
Table 1. Overview of studies conducted in areas of low endemicity
Table 2. Overview of studies conducted in areas of moderate endemicity

Study ID

Design

Country

Year

Endemicity

MDA group

Control group/baseline

Drug (dose)

Interval

No. of rounds

Population
targeted

Coverage

Co‐intervention

Najera 1973

N‐RCS

Nigeria

1966‐68

29%*

CQ (450 mg) + Pyr (45 mg)

2 months

11

52,000

78‐92%

IRS

IRS alone

Singh 1953

N‐RCS

India

1952‐53

22%*

AQ (600 mg)

2 weeks

5

125

ND

None

No intervention

Jones 1958

N‐RCS

Kenya

1952‐53

34%†

Pyr (100 mg)

6 months

3

3721‐4500

ND

None

No intervention

Roberts 1964

N‐RCS

Kenya

1953

28%*

Pyr (50 mg)

1

101,000

95%

None

No intervention

N‐RCS

Kenya

1954

22%*

Pyr (50 mg)

1

99,000

95%

None

No intervention

Archibald 1960

BAS

Nigeria

1958

29%†

CQ (600 mg) + Pyr (25 mg)

1 month

5

10,000

ND

IRS

IRS

Cavalie 1962

BAS

Cameroon

1960‐61

20%†

CQ (600 mg) + Pyr (50 mg)

4 months

2

22,500

76‐92%

IRS

IRS

Houel 1954

BAS

Morocco

1953

14%†

Pyr (100 mg)

1

9999

ND

IRS

IRS

Metselaar 1961

BAS

New Guinea

1958‐59

13‐21%†

CQ (450 mg) +Pyr (50 mg)

1 week

6

2500

90%

IRS

IRS

Jones 1954

BAS

Kenya

1952‐53

35%†

Pyr (100 mg)

6 months

3

3721

ND

None

van Dijk 1961

BAS

Papua New Guinea

1960

39%†

CQ (450 mg)

4 weeks

11

1250

97%

None

Comer 1971

BAS

Panama

1965‐68

17%*

Pyr (50 mg / 75 mg) + PQ (40 mg)

2 weeks

49

1709

61‐87%

None

N‐RCS = Non‐randomized controlled study; BAS = Uncontrolled before‐and‐after study; AQ = Amodiaquine; Pyr = Pyrimethamine; CQ = Chloroquine; PQ = Primaquine; ND = Not described; IRS = Indoor Residual Spraying.

*In all ages

†Amongst children only

Figuras y tablas -
Table 2. Overview of studies conducted in areas of moderate endemicity
Table 3. Overview of studies conducted in areas of high endemicity

Study ID

Design

Country

Year

Endemicity

MDA group

Control group

Drug (dose)

Interval

No. of rounds

Population
targeted

Coverage

Co‐intervention

Von Seidlein 2003

CRT

Gambia

1999

43%†

AS (4 mg/kg/day for 3 days) +SP (25 mg/1.25 mg on day 1)

1

1969

89%

None

Placebo

Molineaux 1980

N‐RCS

Nigeria

1970‐75

46%*

SP (500 mg/25 mg)

10 weeks

9‡

14,129

85%

IRS

IRS alone

SP (500 mg/25 mg)

2‐10 weeks

23‡

1810

85%

IRS

IRS alone

Escudie 1962

N‐RCS

Burkina Faso

1960‐61

56.1%†

CQ (600 mg)/AQ (600 mg) +PQ (15 mg)

1 month

8

1890

75‐92%

None

No intervention

CQ (600 mg)/AQ (600 mg) +PQ (15 mg)

2 weeks

15

2560

84‐97%

None

No intervention

CQ (600 mg)/AQ (600 mg) +PQ (15 mg)

1 month

8

5400

81‐92%

IRS

IRS alone‐

CQ (600 mg)/AQ (600 mg) +PQ (15 mg)

2 weeks

15

3490

82‐94%

IRS

IRS alone‐

Schneider 1961

N‐RCS

Burkina Faso

1960‐61

59%†

CQ (600 mg)/AQ (600 mg) +PQ (15 mg)

2 weeks

15

2500

90%

None

No intervention

Archibald 1960

BAS

Nigeria

1957‐59

64%†

CQ (600 mg) +Pyr (25 mg)

6 months

4

1300

ND

IRS

IRS‐

Cavalie 1962

BAS

Cameroon

1960‐61

65%*

CQ (600 mg) +Pyr (50 mg)

1

7000

100%

IRS

IRS

Gaud 1953

BAS

Morocco

1952

42%*

AQ (600 mg)

1

3000

ND

None

Ricosse 1959

BAS

Burkina Faso

1958‐59

56%†

Pyr (50 mg)

2 weeks

8

3000

82‐91%

None

Song 2010

BAS

Cambodia

2003‐06

56%†

AS (125 mg/day for 2 days) + PIP (750 mg/day for 2 days) + PQ (9 mg every 10 days)

1

3653

ND

None

Hii 1987

BAS

Malaysia

1984‐85

56%†

SP (1500 mg / 75 mg) + PQ (30 mg)

1

148

76%

None

Kligler 1931

BAS

Palestine

1930

67%†

Plas (30 mg) + Q (900 mg) twice daily for 5 days

3 weeks

3

953

79%

None

CRT= Cluster‐randomized trial; N‐RCS = Non‐randomized controlled study; BAS = Uncontrolled before‐and‐after study; AS = Artesunate; SP = Sulfadoxine (or sulfalene)‐Pyrimethamine; Pyr = Pyrimethamine; CQ = Chloroquine; AQ = Amodiaquine; PQ = Primaquine; Pip = Piperaquine; Plas = Plasmochin; Q = Quinine; ND = Not described; IRS = Indoor Residual Spraying.

*In all ages

†Amongst children only

‡Estimated from the data provided

Figuras y tablas -
Table 3. Overview of studies conducted in areas of high endemicity
Table 4. Overview of studies comparing MDA + vector control versus no intervention

Study ID

Design

Country

Year

Endemicity

MDA group

Control group/ baseline

Drug (dose)

Interval

No. of rounds

Population
targeted

Coverage

Co‐intervention

Moderate Endemicity

Kaneko 2000

N‐RCS

Vanuatu

1991‐99

29%*

CQ (600 mg) + SP (1500 mg/75 mg) + PQ (45 mg) weeks 1, 5, and 9;

CQ (300 mg) + PQ (45 mg) weeks 2, 3, 4, 6, 7, and 8

1 week

9

718

79‐92%

ITN + larvivorous fish

low baseline coverage of ITNs

Ricosse 1959

BAS

Burkina Faso

1958‐59

15%†

Pyr (50 mg)

2 weeks

8

5000

82‐91%

IRS

None

De Zulueta 1961

BAS

Uganda

1959‐60

34%†

CQ (600 mg) + Pyr (50 mg)

3 months

4

30,384

80%

IRS

None

De Zulueta 1964

BAS

Uganda

1960

23%†

CQ (600 mg) + Pyr (50 mg)

5 months

2

16,000

50%

IRS

None

Paik 1974a

BAS

Solomon Islands

1972

28%*

CQ (600 mg) +Pyr (50 mg)

1 month

4

ND

90%

IRS

None

High Endemicity

Molineaux 1980

N‐RCS

Nigeria

1970‐75

46%*

SP (500 mg/25 mg)

10 weeks

9‡

14,129

85%

IRS

None

SP (500 mg/25 mg)

2‐10 weeks

23‡

1810

85%

IRS

None

Escudie 1962

N‐RCS

Burkina Faso

1960‐61

56.1%†

CQ (600 mg) /AQ (600 mg) + PQ (15 mg)

1 month

8

5400

81‐92%

IRS

None

CQ (600 mg)/AQ (600 mg) + PQ (15 mg)

2 weeks

15

3490

82‐94%

IRS

None

Schneider 1961

N‐RCS

Burkina Faso

1960‐61

59%†

AQ (600 mg) + PQ (15 mg)

2 weeks

8

3525

ND

IRS

None

Metselaar 1961

BAS

New Guinea

1958‐59

46%*

CQ (450 mg) +Pyr (50 mg)

1 week

6

2500

90%

IRS

None

Hii 1987

BAS

Malaysia

1984‐85

46%†

SP (1500 mg / 75 mg) + PQ (30 mg)

1

754

87%

ITN

None

N‐RCS = Non‐randomized controlled study; BAS = Uncontrolled before‐and‐after study; AQ = Amodiaquine; Pyr = Pyrimethamine; CQ = Chloroquine; SP = Sulfadoxine (or sulfalene)‐Pyrimethamine; PQ = Primaquine; ND = Not described; IRS = Indoor Residual Spraying; ITN = Insecticide Treated Net.

*In all ages

†Amongst children only

‡Estimated from the data provided

Figuras y tablas -
Table 4. Overview of studies comparing MDA + vector control versus no intervention
Table 5. Overview of studies assessing parasitaemia incidence only

Study ID

Design

Country

Year

Baseline Incidence

MDA group

Baseline

Drug (dose)

Interval

No. of rounds

Population
targeted

Coverage

Co‐intervention

Garfield 1983

BAS

Nicaragua

1981‐82

0.4/1000

CQ (500 mg/day for 3 days) + PQ (15 mg/day for 3 days)

1

2,300,000

70‐80%

Larval control

None

Simeons 1938

BAS

India

1935

156/1000

Ate (300 mg) + Plas (60 mg)

1

5650

100%

Larval control

None

Gabaldon 1959

BAS

Venezuela

1956‐57

0.4/1000

Pyr (50 mg)

1 week

24

111,995

ND

IRS

IRS

Kondrashin 1985

BAS

India

1981

4/1000

CQ (600 mg) + PQ (45 mg)

6 months

2

51,325

85%

IRS

IRS

Paik 1974b

BAS

Solomon Islands

1972‐73

15/1000

CQ (300 mg/day for 5 days) + PQ (15 mg/day for 5 days)

3 months

3

1200

90%

None

Cáceres Garcia 2008

BAS

Venezuela

2002‐07

22/1000

CQ (25 mg/kg over 3 days) +PQ (3.5 mg/kg over 7 days)

1

22,941

77%

None

BAS = Uncontrolled before‐and‐after study; PQ = Primaquine; CQ = Chloroquine; Pyr = Pyrimethamine; Plas = Plasmochin; Ate = Atebrin; ND = Not described; IRS = Indoor Residual Spraying.

†Amongst children only

Figuras y tablas -
Table 5. Overview of studies assessing parasitaemia incidence only
Table 6. Summary of findings table: Mass drug administration in areas of low endemicity (≤5%)

Mass drug administration in areas of low endemicity

Patient or population: People living in malaria endemic areas
Settings: Areas with low (≤5%) endemicity
Intervention: Mass drug administration (any regimen)
Comparison: Placebo or no intervention (or baseline data in before‐and‐after studies)

Timepoint
post MDA

Outcomes

Study design

Illustrative comparative risks* (95% CI)

Relative effect
(95% CI)

No of
studies

Quality of the evidence
(GRADE)

Assumed risk

Corresponding risk

Control

MDA

<1 month

Parasite
prevalence

Before‐and‐after

50 per 10001

14 per 1000
(7 to 25)

RR 0.27
(0.14 to 0.50)

1 study

⊕⊝⊝⊝
very low2,3,4,5

Parasite
incidence

0 studies

Gametocyte
prevalence

0 studies2

12 months

Parasite
prevalence

Before‐and‐after

50 per 10001

1 per 1000
(0 to 6)

RR 0.02
(0 to 0.12)

1 study

⊕⊝⊝⊝
very low2,3,4,5

Parasite
incidence

0 studies

Gametocyte
prevalence

0 studies2

The assumed risk has been set at 5%. The corresponding risk (and its 95% CI) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI).
CI: Confidence interval; RR: Risk Ratio.

GRADE Working Group grades of evidence
High quality: Further research is very unlikely to change our confidence in the estimate of effect.
Moderate quality: Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
Low quality: Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
Very low quality: We are very uncertain about the estimate.

1 For illustrative purposes the control group prevalence has been set at 5%.
2 Only one cluster‐randomized trial from Tanzania has evaluated MDA in a setting of low endemicity and this study recorded no episodes of parasitaemia or gametocytaemia at baseline or throughout six months follow‐up in either the control or intervention groups.
3 Downgrade by 1 for serious risk of bias: This study is uncontrolled, and so at very high risk of confounding.
4 Downgraded by 1 for serious indirectness: This singe study from Taiwan reported the effects of MDA administered as a single dose of chloroquine (12 mg/kg). Further trials are needed from a variety of settings to have confidence in the results.
5 Compared to baseline data a large reduction in parasite prevalence was seen at 1 month and 12 months post‐MDA.

Figuras y tablas -
Table 6. Summary of findings table: Mass drug administration in areas of low endemicity (≤5%)
Table 7. Summary of findings table: Mass drug administration in areas of moderate endemicity (6 to 39%)

Mass drug administration in areas of moderate endemicity

Patient or population: People living in malaria endemic areas
Settings: Areas with moderate malaria endemicity (6‐39%)
Intervention: Mass drug administration (any regimen)
Comparison: No intervention (or baseline data in before‐and‐after studies)

Timepoint post MDA

Outcomes

Study design

Illustrative comparative risks* (95% CI)

Relative effect
(95% CI)

No of studies

Quality of the evidence
(GRADE)

Assumed risk

Corresponding risk

Control

MDA

<1 month

Parasitaemia
prevalence

Non‐randomized

250 per 1000

5 per 1000
(3 to 15)

RR 0.03
(0.01 to 0.08)

3 studies

⊕⊕⊕⊝
moderate1,2,3,4

Before‐and‐after

250 per 1000

73 per 1000
(43 to 120)

RR 0.29
(0.17 to 0.48)

3 studies

⊕⊕⊝⊝
low5,3,6

Parasitaemia
incidence

0 studies

Gametocytaemia
prevalence

Non‐randomized

100 per 1000

28 per 1000
(10 to 82)

RR 0.28
(0.1 to 0.82)

1 study

⊕⊝⊝⊝
very low1,7

Before‐and‐after

100 per 1000

47 per 1000
(25 to 87)

RR 0.47
(0.25 to 0.87)

3 studies

⊕⊕⊝⊝
low5,6,8

4‐6 months

Parasitaemia
prevalence

Non‐randomized

250 per 1000

70 per 1000
(53 to 95)

RR 0.18
(0.10 to 0.33)

2 studies

⊕⊕⊝⊝
low1,3,9

Before‐and‐after

250 per 1000

438 per 1000
(103 to 1000)

RR 1.75
(0.41 to 7.41)

2 studies

⊕⊝⊝⊝
very low5,10,11

Parasitaemia
incidence

0 studies

Gametocytaemia
prevalence

Non‐randomized

100 per 1000

52 per 1000
(24 to 111)

RR 0.52
(0.24 to 1.11)

1 study

⊕⊝⊝⊝
very low12

Before‐and‐after

100 per 1000

35 per 1000
(12 to 101)

RR 0.35
(0.12 to 1.01)

1 study

⊕⊝⊝⊝
very low12

The assumed risk for parasitaemia prevalence has been set at 25%. Gametocytaemia prevalence was generally lower in the included studies and the assumed risk has therefore been set at 10%.

The corresponding risk (and its 95% CI) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI).
CI: Confidence interval; RR: Risk Ratio.

GRADE Working Group grades of evidence
High quality: Further research is very unlikely to change our confidence in the estimate of effect.
Moderate quality: Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
Low quality: Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
Very low quality: We are very uncertain about the estimate.

1 No serious risk of bias: Although there were some differences in prevalence at baseline, these were much smaller in size than the large effects seen post‐intervention.
2 No serious indirectness: These three studies were conducted in Kenya in 1953 and 1954 (pyrimethamine administered every six months for three rounds), and in India in 1953 (amodiaquine administered every two weeks for five rounds). A fourth study from Nigeria in 1973 reported a similar reduction in prevalence during an ongoing MDA program. Although these studies are old, similar effects might be expected today with effective anti‐malarials.
3 No serious inconsistency: Consistent and large reductions were seen in these studies.
4 Upgraded by 1 for large effect size: Very large effects were seen consistently across both controlled and uncontrolled studies.
5 No serious risk of bias: These studies are uncontrolled, and so are at very high risk of confounding. However, as the GRADE approach automatically downgrades non‐randomized controlled studies by two levels for risk of bias we did not further downgrade.
6 No serious indirectness: These three studies were conducted between 1953 and 1961, and administered MDA as: Pyrimethamine once only (Morocco), chloroquine plus pyrimethamine every month for five rounds (Nigeria) and chloroquine every four weeks for 11 rounds (Papua New Guinea). Although these studies are old, similar effects might be expected today with effective anti‐malarials.
7 Downgraded by 1 for serious indirectness: This single trial in Kenya gave pyrimethamine every six months for three rounds. Different regimens may have different effects and primaquine, a drug with gametocytocidal properties, was not given. One further trial from Nigeria in the 1960s, which only reported on prevalence during an ongoing MDA programme, also administered MDA without primaquine.
8 No serious inconsistency: Gametocyte prevalence was lower post‐intervention in all four trials, however there was variation in the size of this effect.
9 No serious indirectness: These two studies are both from Kenya in the 1950s, and both administer MDA as pyrimethamine alone. One study continued follow‐up for > 6 months when an effect was still present.
10 No serious indirectness: These two studies were conducted between 1959 and 1961, and administered MDA as: chloroquine plus pyrimethamine every four months for two rounds (Cameroon), chloroquine plus pyrimethamine every month for five rounds (Nigeria).
11 Downgraded by 1 for serious inconsistency: At this time point results were mixed. One study found a higher prevalence at this time point and one found no difference.
12 Downgraded by 1 for serious indirectness: This single trial found no substantial difference between groups at 4‐6 months. Modern trials with different regimens may have different effects. This study did not administer primaquine as part of MDA.

Figuras y tablas -
Table 7. Summary of findings table: Mass drug administration in areas of moderate endemicity (6 to 39%)
Table 8. Summary of findings table: Mass drug administration in areas of high endemicity (≥40%)

Mass drug administration in areas of high endemicity

Patient or population: People living in malaria endemic areas
Settings: Areas with high malaria endemicity (≥ 40%)
Intervention: Mass drug administration (any regimen)
Comparison: No intervention (or baseline data in before‐and‐after studies)

Timepoint post MDA

Outcomes

Study design

Illustrative comparative risks* (95% CI)

Relative effect
(95% CI)

No of studies

Quality of the evidence
(GRADE)

Assumed risk

Corresponding risk

Control

MDA

< 1 month

Parasitaemia
prevalence

Cluster‐randomized

500 per 1000

410 per 1000
(335 to 505)

RR 0.82
(0.67 to 1.01)

1 study

⊕⊕⊝⊝
low1,2,3

Non‐randomized

500 per 1000

85 per 1000
(50 to 140)

RR 0.17
(0.10 to 0.28)

3 studies

⊕⊕⊕⊝
moderate4,5,6,7

Before‐and‐after

500 per 1000

185 per 1000
(140 to 245)

RR 0.37
(0.28 to 0.49)

4 studies

⊕⊕⊝⊝
low8,9,10

Parasitaemia
incidence

Cluster‐randomized

60 per 1000

25 per 1000
(14 to 44)

RR 0.41
(0.23 to 0.73)

1 study

⊕⊕⊕⊝
moderate1,2,11

Gametocytaemia
prevalence

Non‐randomized

100 per 1000

16 per 1000
(8 to 30)

RR 0.16
(0.08 to 0.30)

3 studies

⊕⊕⊕⊝
moderate4,5,6,7

Before‐and‐after

100 per 1000

38 per 1000
(13 to 108)

RR 0.38
(0.13 to 1.08)

3 studies

⊕⊕⊝⊝
low8,12

4‐6 months

Parasitaemia
prevalence

Cluster‐randomized

500 per 1000

580 per 1000
(465 to 720)

RR 1.16
(0.93 to 1.44)

1 study

⊕⊕⊕⊝
moderate1,2,13

Non‐randomized

0 studies

Before‐and‐after

500 per 1000

205 per 1000
(120 to 360)

RR 0.41
(0.24 to 0.72)

3 studies

⊕⊕⊝⊝
low8,14

Parasitaemia
incidence

Cluster‐randomized

60 per 1000

67 per 1000
(52 to 85)

RR 1.11
(0.87 to 1.41)

1 study

⊕⊕⊕⊝
moderate1,2,13

Gametocytaemia
prevalence

Cluster‐randomized

100 per 1000

107 per 1000
(62 to 185)

RR 1.07
(0.62 to 1.85)

1 study

⊕⊕⊝⊝
low1,2,3

Non‐randomized

0 studies

Before‐and‐after

100 per 1000

35 per 1000
(10 to 128)

RR 0.35
(0.10 to 1.28)

2 studies

⊕⊝⊝⊝
very low8,15

The assumed risk for parasitaemia prevalence has been set at 50%. Gametocytaemia prevalence was generally lower in the included studies and the assumed risk has therefore been set at 10%. The assumed risk for parasitaemia incidence is taken from the control group of the single trial.

The corresponding risk (and its 95% CI) is based on the assumed risk in the comparison group and the relative effect of the intervention (and its 95% CI).
CI: Confidence interval; RR: Risk ratio.

GRADE Working Group grades of evidence
High quality: Further research is very unlikely to change our confidence in the estimate of effect.
Moderate quality: Further research is likely to have an important impact on our confidence in the estimate of effect and may change the estimate.
Low quality: Further research is very likely to have an important impact on our confidence in the estimate of effect and is likely to change the estimate.
Very low quality: We are very uncertain about the estimate.

1 No serious risk of bias: This cluster‐randomized trial was at low risk of bias.
2 Downgraded by 1 for serious indirectness: This single study from the Gambia in 1999 administered MDA as AS+SP. The findings may not be easily generalized to other settings, or to alternative MDA regimens. The first time point measured post‐MDA was 1‐3 months.
3 Downgraded by 1 for serious imprecision: The result was not statistically significant but the 95% CI is wide and includes important effects.
4 No serious risk of bias: Although there was some evidence of baseline imbalance between the intervention and control areas, these were generally of smaller magnitude than the effects seen.
5 No serious indirectness: The data presented here were measured during ongoing multiple‐round MDA programmes, not at one month post‐intervention. The studies were conducted in Burkina Faso in 1961 (CQ or AQ plus PQ every two to four weeks), and Nigeria in 1975 (SP given every two weeks or every 10 weeks). Although these studies are old, similar effects might be expected today with effective anti‐malarials.
6 No serious inconsistency: The observed effects were consistently large in all three trials.
7 Upgraded by 1 for the large effect size: Large effects seen in all trials.
8 No serious risk of bias: These studies are uncontrolled, and so are at very high risk of confounding. However, as the GRADE approach automatically downgrades non‐randomized controlled studies by two levels for risk of bias we did not further downgrade.
9 No serious indirectness: These four studies were conducted in Palestine in 1930 (plasmoquine plus quinine every three weeks for three rounds), Burkina Faso in 1959 (pyrimethamine every two weeks), in Malaysia in 1985 (SP + PQ once only), and Cambodia in 2006 (AS + piperaquine once only plus PQ every 10 days).
10 No serious inconsistency: Three studies observed large effects, while one small study found no effect.
11 No serious imprecision: The result is statistically significant.
12 No serious indirectness: Two large studies found large effects in Burkina Faso in the 1950s (pyrimethamine every 2 weeks for 8 rounds), and Palestine in the 1930s (plasmoquine plus quinine every three weeks for three rounds). One small study from Malaysia in the 1980s found no effect.
13 No serious imprecision: The 95% CI excludes clinically important reductions at this time point.
14 No serious inconsistency: The two large studies from Palestine and Cambodia still demonstrated a large reduction at 4‐6 months while the small study from Malaysia found no difference
15 Downgraded by 1 for serious indirectness: Benefits beyond three months have only been demonstrated in this single study from Cambodia. MDA was administered as artesunate plus piperaquine once only followed by primaquine every 10 days for six months.

Figuras y tablas -
Table 8. Summary of findings table: Mass drug administration in areas of high endemicity (≥40%)
Comparison 1. MDA versus no MDA in areas of low endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

1.1 At baseline

1

496

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

1.2 <1 month post MDA

1

484

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

1.3 1‐3 months post MDA

1

794

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

1.4 4‐6 months post MDA

1

660

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

2.1 <1 month post MDA

1

3039

Risk Ratio (M‐H, Random, 95% CI)

0.27 [0.14, 0.50]

2.2 >12 months post MDA

1

3509

Risk Ratio (M‐H, Random, 95% CI)

0.02 [0.00, 0.12]

3 Gametocytaemia Prevalence: Cluster randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

3.1 At baseline

1

496

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

3.2 < 1 month post MDA

1

484

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

3.3 1‐3 months post MDA

1

794

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

3.4 4‐6 months post MDA

1

660

Risk Ratio (M‐H, Random, 95% CI)

0.0 [0.0, 0.0]

Figuras y tablas -
Comparison 1. MDA versus no MDA in areas of low endemicity (Stratified by study design)
Comparison 2. MDA versus no MDA in areas of moderate endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Non‐randomized controlled studies Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

1.1 At baseline

4

3123

Risk Ratio (M‐H, Random, 95% CI)

0.73 [0.43, 1.24]

1.2 During MDA

1

47014

Risk Ratio (M‐H, Random, 95% CI)

0.27 [0.25, 0.28]

1.3 < 1 month post MDA

3

1934

Risk Ratio (M‐H, Random, 95% CI)

0.03 [0.01, 0.08]

1.4 1‐3 months post MDA

2

1557

Risk Ratio (M‐H, Random, 95% CI)

0.15 [0.10, 0.23]

1.5 4‐6 months post MDA

2

1610

Risk Ratio (M‐H, Random, 95% CI)

0.18 [0.10, 0.33]

1.6 7‐12 months post MDA

1

600

Risk Ratio (M‐H, Random, 95% CI)

0.19 [0.11, 0.33]

2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

7

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

2.1 During MDA

2

7965

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.02, 1.47]

2.2 <1 month post MDA

3

3096

Risk Ratio (M‐H, Random, 95% CI)

0.29 [0.17, 0.48]

2.3 1‐3 months post MDA

4

7925

Risk Ratio (M‐H, Random, 95% CI)

0.16 [0.08, 0.31]

2.4 4‐6 months post MDA

2

3797

Risk Ratio (M‐H, Random, 95% CI)

1.75 [0.41, 7.41]

3 Gametocytaemia Prevalence: Non‐randomized controlled studies Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

3.1 At baseline

2

1622

Risk Ratio (M‐H, Random, 95% CI)

1.40 [0.76, 2.57]

3.2 During MDA

1

47014

Risk Ratio (M‐H, Random, 95% CI)

0.48 [0.42, 0.54]

3.3 <1 month post MDA

1

433

Risk Ratio (M‐H, Random, 95% CI)

0.28 [0.10, 0.82]

3.4 1‐3 months post MDA

1

357

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.03, 0.86]

3.5 4‐6 months post MDA

1

410

Risk Ratio (M‐H, Random, 95% CI)

0.52 [0.24, 1.11]

4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

4.1 <1 month post MDA

3

3096

Risk Ratio (M‐H, Random, 95% CI)

0.47 [0.25, 0.87]

4.2 1‐3 months post MDA

1

294

Risk Ratio (M‐H, Random, 95% CI)

0.36 [0.12, 1.12]

4.3 4‐6 months post MDA

1

204

Risk Ratio (M‐H, Random, 95% CI)

0.35 [0.12, 1.01]

Figuras y tablas -
Comparison 2. MDA versus no MDA in areas of moderate endemicity (Stratified by study design)
Comparison 3. MDA versus no MDA in areas of high endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

1.1 At baseline

1

1376

Risk Ratio (M‐H, Random, 95% CI)

0.97 [0.86, 1.10]

1.2 1‐3 months post MDA

1

1800

Risk Ratio (M‐H, Random, 95% CI)

0.82 [0.67, 1.01]

1.3 4‐6 months post MDA

1

1089

Risk Ratio (M‐H, Random, 95% CI)

1.16 [0.93, 1.44]

2 Parasitaemia Prevalence: Non‐randomized controlled studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

2.1 At baseline

3

9395

Risk Ratio (M‐H, Random, 95% CI)

0.84 [0.70, 1.00]

2.2 During MDA

3

12561

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.11, 0.27]

2.3 1‐3 months post MDA

2

7197

Risk Ratio (M‐H, Random, 95% CI)

0.52 [0.33, 0.81]

3 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

7

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

3.1 During MDA

2

2011

Risk Ratio (M‐H, Random, 95% CI)

0.10 [0.03, 0.34]

3.2 <1 month post MDA

4

3863

Risk Ratio (M‐H, Random, 95% CI)

0.37 [0.28, 0.49]

3.3 1‐3 months post MDA

4

5132

Risk Ratio (M‐H, Random, 95% CI)

0.35 [0.15, 0.84]

3.4 4‐6 months post MDA

3

2979

Risk Ratio (M‐H, Random, 95% CI)

0.41 [0.24, 0.72]

3.5 7‐12 months post MDA

1

75

Risk Ratio (M‐H, Random, 95% CI)

0.72 [0.43, 1.20]

3.6 >12 months post MDA

1

2375

Risk Ratio (M‐H, Random, 95% CI)

0.10 [0.07, 0.12]

4 Parasitaemia Incidence: Cluster‐randomized trials Show forest plot

1

Rate Ratio (Random, 95% CI)

0.84 [0.53, 1.32]

4.1 < 1 month post MDA

1

Rate Ratio (Random, 95% CI)

0.41 [0.23, 0.74]

4.2 1‐3 months post MDA

1

Rate Ratio (Random, 95% CI)

1.03 [0.75, 1.41]

4.3 4‐6 months post MDA

1

Rate Ratio (Random, 95% CI)

1.11 [0.84, 1.45]

5 Gametocytaemia Prevalence: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

5.1 At baseline

1

1376

Risk Ratio (M‐H, Random, 95% CI)

0.66 [0.33, 1.29]

5.2 4‐6 months post MDA

1

1414

Risk Ratio (M‐H, Random, 95% CI)

1.07 [0.62, 1.85]

6 Gametocytaemia Prevalence: Non‐randomized controlled studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

6.1 At baseline

3

9395

Risk Ratio (M‐H, Random, 95% CI)

0.72 [0.55, 0.95]

6.2 During MDA

3

12561

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.10, 0.28]

6.3 1‐3 months post MDA

2

7197

Risk Ratio (M‐H, Random, 95% CI)

0.55 [0.28, 1.07]

7 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

5

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

7.1 During MDA

2

2011

Risk Ratio (M‐H, Random, 95% CI)

0.35 [0.09, 1.40]

7.2 <1 month post MDA

3

2582

Risk Ratio (M‐H, Random, 95% CI)

0.38 [0.13, 1.08]

7.3 1‐3 months post MDA

2

1199

Risk Ratio (M‐H, Random, 95% CI)

1.14 [0.64, 2.01]

7.4 4‐6 months post MDA

2

2789

Risk Ratio (M‐H, Random, 95% CI)

0.35 [0.10, 1.28]

7.5 7‐12 months post MDA

1

75

Risk Ratio (M‐H, Random, 95% CI)

0.86 [0.41, 1.79]

7.6 >12 months post MDA

1

2269

Risk Ratio (M‐H, Random, 95% CI)

0.09 [0.05, 0.15]

8 Anaemia Prevalence: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

8.1 4‐6 months post MDA

1

1414

Risk Ratio (M‐H, Random, 95% CI)

0.84 [0.75, 0.93]

9 Mortality: Cluster‐randomized trials Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

9.1 4‐6 months post MDA

1

3655

Risk Ratio (M‐H, Random, 95% CI)

1.43 [0.34, 5.96]

Figuras y tablas -
Comparison 3. MDA versus no MDA in areas of high endemicity (Stratified by study design)
Comparison 4. MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Non‐randomized controlled studies Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

1.1 At baseline

1

1080

Risk Ratio (M‐H, Random, 95% CI)

2.09 [1.48, 2.98]

1.2 >12 months post MDA

1

1331

Risk Ratio (M‐H, Random, 95% CI)

0.10 [0.05, 0.20]

2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

2.1 During MDA

2

2336

Risk Ratio (M‐H, Random, 95% CI)

0.12 [0.02, 0.62]

2.2 <1 month post MDA

3

5006

Risk Ratio (M‐H, Random, 95% CI)

0.06 [0.01, 0.33]

2.3 1‐3 months post MDA

3

4724

Risk Ratio (M‐H, Random, 95% CI)

0.14 [0.04, 0.57]

2.4 4‐6 months post MDA

1

939

Risk Ratio (M‐H, Random, 95% CI)

0.57 [0.39, 0.85]

2.5 >12 months post MDA

1

1758

Risk Ratio (M‐H, Random, 95% CI)

0.00 [0.00, 0.03]

3 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

3.1 During MDA

2

4425

Risk Ratio (M‐H, Random, 95% CI)

0.13 [0.06, 0.27]

3.2 < 1 month post MDA

1

1907

Risk Ratio (M‐H, Random, 95% CI)

0.01 [0.00, 0.16]

3.3 1‐3 months post MDA

1

1941

Risk Ratio (M‐H, Random, 95% CI)

0.22 [0.11, 0.41]

Figuras y tablas -
Comparison 4. MDA + vector control versus no intervention in areas of moderate endemicity (Stratified by study design)
Comparison 5. MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence: Non‐randomized controlled studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

1.1 At baseline

3

8042

Risk Ratio (M‐H, Random, 95% CI)

0.56 [0.37, 0.84]

1.2 During MDA

3

9493

Risk Ratio (M‐H, Random, 95% CI)

0.10 [0.06, 0.16]

1.3 1‐3 months post MDA

2

4455

Risk Ratio (M‐H, Random, 95% CI)

0.12 [0.06, 0.23]

1.4 7‐12 months post MDA

1

3154

Risk Ratio (M‐H, Random, 95% CI)

0.60 [0.55, 0.67]

1.5 >12 months post MDA

1

3261

Risk Ratio (M‐H, Random, 95% CI)

0.77 [0.70, 0.84]

2 Parasitaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

2.1 During MDA

2

5437

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.09, 0.31]

2.2 1‐3 months post MDA

2

5440

Risk Ratio (M‐H, Random, 95% CI)

0.13 [0.01, 2.51]

2.3 4‐6 months post MDA

1

415

Risk Ratio (M‐H, Random, 95% CI)

0.83 [0.66, 1.04]

2.4 7‐12 months post MDA

1

412

Risk Ratio (M‐H, Random, 95% CI)

0.93 [0.75, 1.16]

3 Gametocytaemia Prevalence: Non‐randomized controlled studies Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

3.1 At baseline

3

8042

Risk Ratio (M‐H, Random, 95% CI)

0.53 [0.31, 0.90]

3.2 During MDA

3

9493

Risk Ratio (M‐H, Random, 95% CI)

0.08 [0.03, 0.20]

3.3 1‐3 months post MDA

2

4455

Risk Ratio (M‐H, Random, 95% CI)

0.08 [0.05, 0.14]

3.4 7‐12 months post MDA

1

3154

Risk Ratio (M‐H, Random, 95% CI)

0.87 [0.73, 1.05]

3.5 > 12 months post MDA

1

3261

Risk Ratio (M‐H, Random, 95% CI)

0.96 [0.81, 1.14]

4 Gametocytaemia Prevalence: Uncontrolled before‐and‐after studies Show forest plot

1

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

4.1 During MDA

1

437

Risk Ratio (M‐H, Random, 95% CI)

0.29 [0.17, 0.50]

4.2 1‐3 months post MDA

1

440

Risk Ratio (M‐H, Random, 95% CI)

0.52 [0.34, 0.80]

4.3 4‐6 months post MDA

1

415

Risk Ratio (M‐H, Random, 95% CI)

0.76 [0.52, 1.12]

4.4 7‐12 months post MDA

1

412

Risk Ratio (M‐H, Random, 95% CI)

0.93 [0.65, 1.33]

Figuras y tablas -
Comparison 5. MDA + vector control versus no intervention in areas of high endemicity (Stratified by study design)
Comparison 6. Parasitaemia Incidence studies

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 MDA versus no MDA: Uncontrolled before‐and‐after studies Show forest plot

4

Rate Ratio (Random, 95% CI)

Subtotals only

1.1 During MDA

3

Rate Ratio (Random, 95% CI)

0.29 [0.07, 1.14]

1.2 < 1 month post MDA

4

Rate Ratio (Random, 95% CI)

0.21 [0.05, 0.84]

1.3 1‐3 months post MDA

4

Rate Ratio (Random, 95% CI)

0.61 [0.26, 1.40]

1.4 4‐6 months post MDA

1

Rate Ratio (Random, 95% CI)

0.65 [0.41, 1.02]

1.5 7‐12 months post MDA

1

Rate Ratio (Random, 95% CI)

0.15 [0.07, 0.34]

1.6 >12 months post MDA

1

Rate Ratio (Random, 95% CI)

0.48 [0.42, 0.55]

2 MDA + vector control versus no MDA: Uncontrolled before‐and‐after studies Show forest plot

2

Rate Ratio (Random, 95% CI)

Subtotals only

2.1 During MDA

2

Rate Ratio (Random, 95% CI)

0.92 [0.49, 1.75]

2.2 < 1 month post MDA

2

Rate Ratio (Random, 95% CI)

0.04 [0.00, 1.54]

2.3 1‐3 months post MDA

2

Rate Ratio (Random, 95% CI)

0.08 [0.01, 0.98]

2.4 4‐6 months post MDA

2

Rate Ratio (Random, 95% CI)

0.11 [0.01, 1.97]

2.5 7‐12 months post MDA

2

Rate Ratio (Random, 95% CI)

0.16 [0.01, 3.10]

2.6 > 12 months post MDA

1

Rate Ratio (Random, 95% CI)

0.04 [0.03, 0.07]

Figuras y tablas -
Comparison 6. Parasitaemia Incidence studies
Comparison 7. MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence during MDA Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

1.1 Non‐randomized controlled studies ‐ with 8‐aminoquinoline

2

6634

Risk Ratio (M‐H, Random, 95% CI)

0.20 [0.12, 0.32]

1.2 Non‐randomized controlled studies ‐ without 8‐aminoquinoline

2

52941

Risk Ratio (M‐H, Random, 95% CI)

0.16 [0.08, 0.31]

2 Parasitaemia Prevalence 1‐3 months post MDA Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

2.1 Non‐randomized controlled studies ‐ with 8‐aminoquinoline

2

7197

Risk Ratio (M‐H, Random, 95% CI)

0.52 [0.33, 0.81]

2.2 Non‐randomized controlled studies ‐ without 8‐aminoquinoline

2

1557

Risk Ratio (M‐H, Random, 95% CI)

0.15 [0.10, 0.23]

3 Parasitaemia Prevalence during MDA Show forest plot

4

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

3.1 Uncontrolled before‐and‐after studies ‐ with 8‐aminoquinoline

1

2965

Risk Ratio (M‐H, Random, 95% CI)

0.06 [0.03, 0.10]

3.2 Uncontrolled before‐and‐after studies ‐ without 8‐aminoquinoline

3

7011

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.06, 0.51]

4 Parasitaemia Prevalence <1 month post MDA Show forest plot

7

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

4.1 Uncontrolled before‐and‐after studies ‐ with 8‐aminoquinoline

3

2650

Risk Ratio (M‐H, Random, 95% CI)

0.42 [0.29, 0.61]

4.2 Uncontrolled before‐and‐after studies ‐ without 8‐aminoquinoline

4

4309

Risk Ratio (M‐H, Random, 95% CI)

0.29 [0.22, 0.38]

5 Parasitaemia Prevalence 1‐3 months post MDA Show forest plot

7

Risk Ratio (M‐H, Fixed, 95% CI)

Subtotals only

5.1 Uncontrolled before‐and‐after studies ‐ with 8‐aminoquinoline

1

98

Risk Ratio (M‐H, Fixed, 95% CI)

0.65 [0.41, 1.01]

5.2 Uncontrolled before‐and‐after studies ‐ without 8‐aminoquinoline

6

12959

Risk Ratio (M‐H, Fixed, 95% CI)

0.32 [0.29, 0.34]

6 Parasitaemia Prevalence 4‐6 months post MDA Show forest plot

5

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

6.1 Uncontrolled before‐and‐after studies ‐ with 8‐aminoquinoline

3

2979

Risk Ratio (M‐H, Random, 95% CI)

0.41 [0.24, 0.72]

6.2 Uncontrolled before‐and‐after studies ‐ without 8‐aminoquinoline

2

3797

Risk Ratio (M‐H, Random, 95% CI)

1.75 [0.41, 7.41]

Figuras y tablas -
Comparison 7. MDA versus no MDA in areas of moderate and high endemicity (Stratified by study design; subgrouped by 8‐aminoquinoline)
Comparison 8. MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species)

Outcome or subgroup title

No. of studies

No. of participants

Statistical method

Effect size

1 Parasitaemia Prevalence at baseline Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

1.1 Non‐randomized controlled studies ‐ falciparum

2

1537

Risk Ratio (M‐H, Random, 95% CI)

1.34 [1.03, 1.74]

1.2 Non‐randomized controlled studies ‐ vivax

2

1537

Risk Ratio (M‐H, Random, 95% CI)

3.84 [1.33, 11.04]

2 Parasitaemia Prevalence during MDA Show forest plot

2

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

2.1 Uncontrolled before‐and‐after studies ‐ falciparum

2

5561

Risk Ratio (M‐H, Random, 95% CI)

0.40 [0.08, 1.97]

2.2 Uncontrolled before‐and‐after studies ‐ vivax

2

5561

Risk Ratio (M‐H, Random, 95% CI)

0.60 [0.40, 0.90]

3 Parasitaemia Prevalence <1 month post MDA Show forest plot

5

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

3.1 Non‐randomized controlled studies ‐ falciparum

1

433

Risk Ratio (M‐H, Random, 95% CI)

0.02 [0.00, 0.08]

3.2 Non‐randomized controlled studies ‐ vivax

1

433

Risk Ratio (M‐H, Random, 95% CI)

0.05 [0.00, 0.82]

3.3 Uncontrolled before‐and‐after studies ‐ falciparum

4

7367

Risk Ratio (M‐H, Random, 95% CI)

0.22 [0.18, 0.29]

3.4 Uncontrolled before‐and‐after studies ‐ vivax

4

7367

Risk Ratio (M‐H, Random, 95% CI)

0.50 [0.41, 0.61]

4 Parasitaemia Prevalence 1‐3 months post MDA Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

4.1 Non‐randomized controlled studies ‐ falciparum

1

357

Risk Ratio (M‐H, Random, 95% CI)

0.03 [0.01, 0.12]

4.2 Non‐randomized controlled studies ‐ vivax

1

357

Risk Ratio (M‐H, Random, 95% CI)

1.37 [0.46, 4.11]

4.3 Uncontrolled before‐and‐after studies ‐ falciparum

2

5754

Risk Ratio (M‐H, Random, 95% CI)

0.22 [0.09, 0.51]

4.4 Uncontrolled before‐and‐after studies ‐ vivax

2

5754

Risk Ratio (M‐H, Random, 95% CI)

0.49 [0.32, 0.76]

5 Parasitaemia Prevalence 4‐6 months post MDA Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

5.1 Non‐randomized controlled studies ‐ falciparum

1

410

Risk Ratio (M‐H, Random, 95% CI)

0.22 [0.14, 0.33]

5.2 Non‐randomized controlled studies ‐ vivax

1

410

Risk Ratio (M‐H, Random, 95% CI)

0.81 [0.31, 2.08]

5.3 Uncontrolled before‐and‐after studies ‐ falciparum

2

3642

Risk Ratio (M‐H, Random, 95% CI)

0.40 [0.13, 1.23]

5.4 Uncontrolled before‐and‐after studies ‐ vivax

2

3642

Risk Ratio (M‐H, Random, 95% CI)

0.31 [0.24, 0.39]

6 Parasitaemia Prevalence >12 months post MDA Show forest plot

3

Risk Ratio (M‐H, Random, 95% CI)

Subtotals only

6.1 Non‐randomized controlled studies ‐ falciparum

1

1331

Risk Ratio (M‐H, Random, 95% CI)

0.01 [0.00, 0.13]

6.2 Non‐randomized controlled studies ‐ vivax

1

1331

Risk Ratio (M‐H, Random, 95% CI)

0.36 [0.15, 0.86]

6.3 Uncontrolled before‐and‐after studies ‐ falciparum

2

5884

Risk Ratio (M‐H, Random, 95% CI)

0.06 [0.04, 0.09]

6.4 Uncontrolled before‐and‐after studies ‐ vivax

2

5884

Risk Ratio (M‐H, Random, 95% CI)

0.17 [0.12, 0.24]

Figuras y tablas -
Comparison 8. MDA versus no MDA for all endemicity levels (Stratified by study design; subgrouped by plasmodium species)