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Adv Parasitol. Author manuscript; available in PMC Dec 13, 2012.
Published in final edited form as:
PMCID: PMC3521063

The Changing Limits and Incidence of Malaria in Africa: 1939–2009


Understanding the historical, temporal changes of malaria risk following control efforts in Africa provides a unique insight into what has been and might be archived towards a long-term ambition of elimination on the continent. Here, we use archived published and unpublished material combined with biological constraints on transmission accompanied by a narrative on malaria control to document the changing incidence of malaria in Africa since earliest reports pre-second World War. One result is a more informed mapped definition of the changing margins of transmission in 1939, 1959, 1979, 1999 and 2009.


Africa is often called the “heartland” of malaria. Certainly, malaria has played a major role in shaping human evolution in Africa and remains a major public health threat and impediment to economic development. Although malaria in Africa is often spoken of as if it were a single well-characterized situation, in fact, the epidemiology and ecology of malaria are extremely heterogeneous. Over recent years, an increasingly accurate picture of the scale and heterogeneity of malaria in Africa has emerged. At the same time, there has been an increasing appreciation that the malaria situation is changing in many areas, with reports of falling transmission and disease burden in some but by no means all parts of the continent. It is assumed that many of these changes are related to deliberate intervention, and certainly, there has been a massive increase in investment in malaria control over the past 10 years, but it should not be forgotten that the ecology of malaria is shaped by many factors including climate, human settlement, human behaviours and factors that may affect vector populations, all of which are subject to changes for a multitude of reasons.

Today, there is an increasing emphasis on the concept of “shrinking the map” of malaria with the initial aim of local elimination and the long-term aim of global eradication. To shrink a map, one has to begin by knowing the map accurately and how it may have changed in the past. Several attempts have been made over the last 60 years to define the limits of malaria transmission using a variety of climate-driven constraints on parasite and vector survival and reported case incidence (Boyd, 1930; Craig et al., 1999; Dutta and Dutt, 1978; Guerra et al., 2006, 2008; Hay et al., 2009; Kiszewski et al., 2004; Le Lannou, 1936; Lysenko and Semashko, 1968; Macdonald, 1957; Manguin et al., 2008; Pampana and Russell, 1955; US War Department, 1944). These mapped products have been difficult to use sequentially to understand the changing margins and intensity of risk as each has used different methodologies and input data. We aim here to define the boundaries of malaria risk in Africa by reviewing available documented case data together with the application of biological and human settlement criteria to define malaria risk at its natural extent and record how this has changed over the last century. In doing this, we have brought together for the first time data relating to past attempts to control and eliminate malaria in different parts of Africa.


4.2.1. Pre-second world war

Following Sir Ronald Ross’s discovery of the role played by the mosquito in the transmission of malaria in 1897, he travelled widely, including Africa (Egypt, Mauritius, Nigeria, Ghana, Sierra Leone and Zimbabwe), to promote environmental sanitation using “mosquito brigades” (Nye and Gibson, 1997; Ross, 1902). Reference to Ross’s recommendations appear in many Colonial Administration Medical Department annual reports from 1900 and the reduction of larval breeding sites became a public health priority after the First World War for many of the rapidly expanding urban centres in Africa. The discovery by Alphonse Laveran of the blood stages of the malaria parasite in French Foreign Legion troops stationed in Algeria in 1880 (Bruce-Chwatt, 1981) and the effects of quinine as a therapeutic agent served as the second major approach to malaria prevention among Europeans in Africa, starting before the First World War (Shah, 2010). “Quininisation” was practiced as a means of personal prophylaxis or through mass drug administration, for example, in Dar es Salaam (Orenstein, 1914), the large towns of the Belgian Congo (Henrard and Van Hoof, 1933; Van den Branden and Van Hoof, 1923), Sudan (Henderson, 1934), Tunisia (Husson and Nicolle, 1907) and Algeria (Sergent and Sergent, 1928). The clinical and epidemiological link between sustained use of quinine, malaria and blackwater fever became a major cause for concern early in the twentieth century, and its use as a means of malaria prevention slowly declined through the 1950s (Foy and Kondi, 1950; Graham, 1912; Shah, 2010).

Despite an early recognition of the economic impact malaria had on productivity in the European colonies (League of Nations, 1933), a common epidemiological portrayal of malaria at the time was that “Africans” were immune, asymptomatic carriers of infection (Bagster-Wilson, 1939; Bagster-Wilson and Wilson, 1937; Christophers, 1924; Garnham, 1949; James, 1929) and that this posed “threats” to the transmission of the parasite to Europeans. Emphasis was on protecting European settlers and prevention recommendations included the spatial distances necessary for separate African housing to limit risks to Europeans in Sierra Leone (Christophers and Stephens, 1900) and Kenya (Paterson, 1928).

4.2.2. 1948–1960: The global malaria eradication programme (GMEP) in Africa

The Second World War marked a new era in drug discovery and the development of residual insecticides notably the 8-aminoquinolines such as chloroquine (Sweeney, 2000) and dichlorodiphenyltrichloroethane (DDT) (Russell, 1951). These new tools signalled a moment of great opportunity to tackle the public health burden posed by malaria, and importantly for the time, the economic growth of colonial Africa (Colbourne, 1966; Macdonald, 1950; WHO, 1948). A report presented to the World Health Organization (WHO) in 1948 states: “It is not enough to quote that about 3,000,000 deaths are caused yearly by malaria in the world, or that every year about 300,000,000 cases of malaria occur …… that malaria is prevalent in tropical and subtropical areas where food production and agricultural resources are potentially very high, and that, by affecting the mass of rural workers, it decreases their vitality and reduces their working capacity and thus hampers the exploitation of the natural resources of the country. At a time when the world is poor, it seems that control of malaria should be the first aim to achieve in order to increase agricultural output” (WHO, 1948).

Two years later at a conference in Kampala, the WHO recommended “to governments responsible for the administration of African territories that malaria should be controlled by modern methods as soon as feasible, whatever the degree of endemicity, and without awaiting the outcome of further experiments” (Dobson et al., 2000; Najera et al., 2011; WHO, 1950). Immediately after the Second World War, almost every country in Africa began using chloroquine and DDT. This varied in application and coverage but had become universal policy very quickly and adapted in different settings to achieve national ambitions of elimination or subnational pilot elimination projects. However, not long after the launch of the Global Malaria Eradication Programme (GMEP), it was decided that sub-Saharan Africa was not ready for elimination: “the prolonged period of the transmission season and the extremely high degree of malaria endemicity in the region …” combined with weak infrastructure “…are likely to form an effective barrier to a large-scale eradication programme” (WHO, 1954).

4.2.3. 1960–1999: Post GMEP

Across Africa, malaria programmes gradually returned to an objective of controlling, rather than eliminating risk and the GMEP defined control as “the reduction of the disease to a prevalence where it is no longer a major public health problem; the concept carries the implication that the programme will be unending, control having to be maintained by continuous active work” sometimes referred to as “pre-elimination” (WHO, 1957, 1961). Despite this conclusion, several countries maintained elimination ambitions through to the 1970s through the use chemoprophylaxis (Charmot, 1969; Hamon et al., 1963; Kouznetsov, 1979) and indoor residual house spraying (IRS) with sustained use of DDT and to a lesser degree other organochlorides such as benzene hexachloride (BHC), hexachlorocyclohexane (HCH), Gammexane and dieldrin, organophosphates (including malathion and fenitrothion) and carbamates (including propoxur) despite mounting threats of vector resistance to these insecticide classes (Hamon et al., 1963; Kouznetsov, 1976, 1977). Countries maintaining elimination strategies tended to be located at the margins of stable, endemic transmission in the northern and southern latitudes of Africa and the islands off the continental coast line. For the rest of central Africa, sustained control largely meant the treatment of febrile illness.

From the mid-1980s, trials began in Africa of a new approach to vector control based on the personal protection afforded by insecticide-treated bed nets (ITNs) (Lines et al., 1985; Ranque et al., 1984; Snow et al., 1987; 1988). By the mid-1990s, further large-scale trials across Africa had shown that ITN provided significant, cost-effective protection against child mortality (Lengeler, 2004). However, the community coverage of ITN by 2004 was minimal (Noor et al., 2009). By the late 1990s, the continent was gripped by a spiralling decline in chloroquine efficacy, leading to wide-spread treatment failures, evidence of increasing mortality (Snow et al., 2001; Trape, 2001) and hailed as a public health disaster (White et al., 1999). This promoted the accelerated development, registration and deployment of fast-acting artemisinin-based combination therapy (ACT) (White, 1999). However, in contrast to the rapid adoption after the Second World War of chloroquine, a drug that would be difficult to register with regulatory authorities today, protracted policy dialogue (Attaran et al., 2004, 2006), difficulties in manufacture and distribution and national procurement and regulation of ACTs have meant that these new medicines reached only a few people who needed them by 2009 (RBM, 2011).

4.2.4. 2000–2010: Roll Back Malaria

Following the recognition that malaria in Africa could not effectively be addressed by the GMEP, 40 years lapsed before malaria control in Africa became a significant part of international public health dialogue. A series of international meetings and declarations during the late 1990s (Greenwood et al., 2008; Kidson, 1992) led to launch of the Roll Back Malaria (RBM) movement in 1998 (Nabarro and Taylor, 1998). In April 2000, African leaders, meeting in Abuja, signed a declaration that said they would “Halve the malaria mortality for Africa’s people by 2010, through implementing the strategies and actions for Roll Back Malaria” (WHO, 2000). This was to be achieved by ensuring that at least 60% of at-risk populations were protected or treated with appropriate methods (WHO, 2000); subsequently redefined to 80% coverage by 2010 (WHO, 2005) and the bar raised even higher with the launch of the Global Malaria Action Plan (GMAP) in 2008 that called for universal coverage with some form of vector control (RBM, 2008). Where DDT and chloroquine were seen as the magic bullets for malaria elimination during the era of the GMEP, ITNs, ACTs and new rapid diagnostic tests were the exciting new tools during the RBM era. From its inception, RBM concentrated on “high-burden countries”, the result of which was that Africa was for the first time in malaria control history centre stage of an international effort to tackle malaria.

Underpinning the recent wave of international interest in malaria control has been a concerted effort to articulate the economic burden and inequities posed by malaria, creating a poverty trap (Gallup and Sachs, 2001; Sachs and Malaney, 2002; Sachs and McArthur, 2005). This evidence base increased the profile of malaria as a broad development issue, effectively levered support from key international partners (World Bank, 1993) and put malaria on the global development map articulated in the Millennium Development Goals (MDGs) (Sachs and McArthur, 2005). Despite the unquestionable health burden posed by malaria, making an economic argument for its control has been necessary during each wave of international interest in funding its control and elimination since the 1930s.

The Global Fund to fight AIDS, Tuberculosis and Malaria (GFATM) was established in 2002 to make available large-scale funding to help achieve health-related MDGs (Feachem and Sabot, 2006). In 1998, spending on malaria control globally was around 100 million USD (Narasimhan and Attaran, 2003). Between 2002 and 2009, the Global Fund had approved 5.6 billion USD for malaria grants to African countries. This has been accompanied by a significant increase in direct bilateral support for malaria (Snow et al., 2010a). The launch of the President’s Malaria Initiative (PMI) in 2006 massively changed the funding landscape in Africa (PMI, 2009). By 2009, 21 African countries had sufficient combined per capita annual donor assistance to meet the targets established at Abuja in 2000 (Snow et al., 2010a). In 2007, a commitment to a global eradication strategy re-emerged (BMGF, 2007; Feachem and Sabot, 2008; Roberts and Enserink, 2007) and the GMAP, launched in 2008 by the RBM partnership, reflected this renewed ambition—a malaria free world (RBM, 2008).


The territories and boundaries of nation states across Africa have changed considerably over the past 100 years through colonization by the Ottomans and Europeans, wars and struggles for independence. Throughout our descriptions of risk, we have regarded as separate nation states those that exist today (Fig. 4.1), but in reviewing reported intervention coverage, clinical evidence and changing risk, it is important to recognize the changing governance boundaries over the past century and where appropriate these are defined throughout.

The margins of stable P. falciparum transmission at its presumed natural extent (pre-1939). Dark grey representing no malaria risk; light grey biologically suitable transmission but population density less than 0.01 people per km2; green represents areas ...

4.3.1. Excluding malaria risk based on reported absence and population density

Plasmodium falciparum transmission probably reached its natural extent in Africa around 1900 (Carter and Mendis, 2002), and few African countries have been completely free from malaria transmission over the last 100 years. The Kingdom of Lesotho (Basutoland pre-1966) is the highest country in the world with 80% of the population living higher than 1800 m above sea level and has always been regarded as malaria free (Russell, 1956). The Islands of the Seychelles archipelago, Tromelin, Cargados Carajos, Agalega and Rodriguez, Saint Brandon and Chagos in the Mascarene archipelago were documented in the 1950s as being unable to support malaria transmission. Similarly, the island of St. Helena, in the Atlantic Ocean, regarded by the UN as part of Africa, has not supported malaria transmission (Russell, 1956). The Western Sahara is a barren, arid area that in 1956 was reported by the Spanish governing authorities to be completely free from transmission (WHO-Spanish Morocco, 1955). A careful assembly of historical evidence of risk in the Union of South Africa pre-1940s suggests that malaria was absent from large parts of the western part of the country (Sharp and Le Sueur, 1996) and the bordering southern areas of Namibia and Botswana (De Meillon, 1951; Franco de et al., 1984a; Ministry of Health, 2001; MoHSS, 1996). These sub-national limits of risk based on medical intelligence in Southern Africa have been digitized and excluded as part of the historical range of malaria transmission in Africa.

The presence of human hosts is clearly necessary to perpetuate transmission of the four malaria parasites that affect man in Africa. Earlier descriptions of malaria risk have applied the crude limits of unpopulated, barren areas across the Sahara desert and other low population density desert areas in southern Africa (Boyd, 1930; Lysenko and Semashko, 1968; Manguin et al., 2008; Pampana and Russell, 1955). More informed approaches to excluding human infection risks based on population density (≤1 person per km2) were implemented by Guerra and colleagues using global population surfaces developed by the Global Rural Urban Mapping Project (GRUMP) (Balk et al., 2006; Guerra et al., 2006). These masks were subsequently felt to be too imprecise due to the resolution and quality of the population input data used by GRUMP to describe the distribution of human settlement in Africa (Hay et al., 2009). A new human population settlement map has recently been developed employing considerably more input data at higher spatial and temporal resolutions that has substantially improved the modelled spatial predictions at 0.1×0.1 km resolutions of population density in Africa (Afripop, 2011). Here, we have used these spatial data, re-sampled to 5×5 km, to quantitatively define the spatial limits of parasite transmission based on a conservative definition ≤0.01 people per km2 (Fig. 4.1). This mask serves as a visual guide to the spatial limits of human malaria transmission and presumes that extremely sparsely populated areas of Africa today correspond to similar settlement patterns over the last century where transmission is biologically suitable.

4.3.2. The transmission limiting effects of temperature and aridity

Both altitude (a proxy for low ambient temperature) and deserts have been used to define the absence of malaria transmission in most previous iterations of global malaria maps (Boyd, 1930; Dutta and Dutt, 1978). Temperature plays a key role in determining the transmission of human malaria based on its relationship with the duration of sporogony and is particularly relevant to Plasmodium vivax and P. falciparum (Nikolaev, 1935). To provide a plausible mask to eliminate the possibility of transmission across Africa, we have used a recently developed temperature suitability index (TSI) (Gething et al., 2011). The TSI model uses a biological framework based on survival of vectors and the fluctuating monthly ambient temperature effects on the duration of sporogony that must be completed within the lifetime of a single generation of Anophelines. This was used to generate at each 1×1 km pixel periods of an average year when a vector’s lifespan would exceed the time required for sporogony, and hence when transmission was not precluded by temperature. If this time exceeded the maximum feasible vector lifespan, then the cohort was deemed unable to support transmission and the area classified as being at zero risk (Gething et al., 2011). Here, we have used a TSI value of zero for P. falciparum to represent no transmission and TSI values above zero as areas able to sustain some parasite transmission. The P. falciparum temperature mask highlights the highland areas and mountains of East Africa, the southern mountains of Tanzania, the mountains at the junction of Democratic Republic of Congo, Rwanda and Burundi, the highlands in Ethiopia, Mount Cameroun, the Shimbiris mountains in Somaliland, the Nyika Plateau in Malawi and Mount Nyangani in Eastern Zimbabwe (Fig. 4.1).

The second important environmental constraint on transmission is the effect of arid conditions on anopheline development and survival (Shililu et al., 2004). Limited surface water reduces the availability of sites suitable for oviposition and reduces the survival of vectors at all stages of their development through the process of desiccation (Gray and Bradley, 2005). The ability of adult vectors to survive long enough to contribute to parasite transmission and of pre-adult stages to ensure minimum population abundance thus depends on the levels of aridity and species-specific resilience to arid conditions. We have defined extreme aridity using the enhanced vegetation index (EVI) and used data from 12 monthly surfaces to classify into areas likely to support transmission, defined by an EVI of greater than 0.1 for any two consecutive months and areas without two or more consecutive months of an EVI>0.1 as unable to support transmission (Guerra et al., 2006, 2008). This aridity mask identifies small foci of risk across the Sahara that are likely to support transmission because of their proximity to oases and seasonal rivers while retaining a plausible mask of virtual zero transmission across the Sahara, in extremely arid areas that make up large areas of the Horn of Africa and in southern Africa through the aridity limiting effects of the Kalahari, the Sossusvlei and the Skeleton Coast (Fig. 4.1).

4.3.3. Defining transmission stability within the spatial margins of risk in relation to control and elimination

The stable–unstable classification was first introduced into malariology by Sir Ronald Ross (Ross, 1916) and adapted by George Macdonald for the measurement of malaria endemicity where stability was defined quantitatively by the average number of feeds that a mosquito takes on man during its life (Macdonald, 1952, 1957). The measurement of Macdonald’s stability index demands detailed entomological data that are rarely available. Qualitatively, stable malaria refers to situations that are relatively insensitive to natural and man-made changes and unstable malaria includes areas very sensitive to climatic aberrations and very amenable to control with ranges of intermediate stability between these extremes. These qualitative concepts of stability are still in use today.

Critical to the planning of malaria elimination during the GMEP was a quantitative description of risk for planning control and monitoring progress. During the preparatory phase, large-scale parasite prevalence surveys were undertaken to examine feasibility of elimination. During the attack phase, the aim was to reduce prevalence and incidence to interrupt transmission within 12–18 months and then remove the last reservoir of infections within a further 24–30 months. Towards the end of attack phase, parasite prevalence was deemed impractical to monitor effectively and malaria incidence became the key monitoring metric. It was suggested that when infection prevalence fell below 2%, national programmes should invest in combinations of passive, active and mass-blood survey surveillance of new infections, expressed as an annual parasite incidence (API) per 1000 people resident in a reporting administrative area. Additional measures have been variously included but not as regularly reported including average blood slide examination rates and slide positivity rates (Pampana, 1969; Pull, 1972; Ray and Beljaev, 1984; Yekutiel, 1960). When the API was less than 1 per 10,000, the consolidation phase started and comprehensive use of prevention was in theory stopped. API was originally set at 5 per 10,000, but experience showed that national programmes often overestimated the coverage and completeness of their surveillance. The consolidation phase maintained a targeted control component, guided by active case detection to eliminate residual foci of parasite reservoirs. The duration of the consolidation phase was highly variable (Russell, 1956), but migration to the maintenance phase was usually initiated after 3 years without local transmission. Theoretically, the maintenance phase included the introduction of measures to prevent the reintroduction of malaria.

Several authors have recently revisited the epidemiological definitions used to signal transitional points from sustained malaria control and a pathway towards elimination (Cohen et al., 2010; Feachem et al., 2010a,b; Hay et al., 2008, 2009). In practical terms, it has been generally considered that a parasite prevalence of less than 1% during peak transmission in a representative sample of the country, or lower administrative area, with prevalence in sub-populations of less than 5% (allowing for over-dispersion of risk) would constitute a situation referred to as low-stable endemicity and governments may elect to hold this line for disease control (Cohen et al., 2010). Conditions based on parasite prevalence lower than 1% become very difficult to measure and qualitatively represent unstable conditions. Hay and colleagues regard unstable transmission as represented by an API of less than 1 per 10,000, and this approach is used in current mapping of malaria risk worldwide (Guerra et al., 2008; Hay et al., 2009). There is also a growing recognition that zero transmission is both impossible to measure and too strict a definition in areas where vectors persist and immigration of infected hosts is high, especially in areas where the environmental criteria necessary to sustain further transmission exist. For example, the United States of America has experienced multiple autochthonous transmission events since it was declared malaria free in 1956 (Mali et al., 2009). As such elimination is presently regarded as a state where interventions have interrupted endemic transmission and limited onward transmission from imported infections below a threshold at which risk of reestablishment is minimized (Cohen et al., 2010). Throughout our current description of risk, we have used API as a measure of stability and reported documented presence and absence of transmission to define the margins of risk.


The fixed long-term average climatic conditions together with reported absence of transmission provide a natural maximal extent of possible malaria transmission in Africa (Fig. 4.1). However, these margins have changed over the past 100 years through systematic control, elimination and prevention of resurgent risks. We review the effects of scaled interventions that were mounted since the first reported efforts of aggressive control in North Africa, including the aberrant changes in the Republic of Djibouti, the islands of Africa in the Atlantic and Indian Oceans and countries in Southern Africa (South Africa, Botswana, Namibia, Zimbabwe and Swaziland). These countries represent the historical margins of Africa’s stable and unstable transmission, and it is important to define how these limits have contracted and expanded since 1900.

4.4.1. Changing boundaries and incidence of malaria in North Africa and Djibouti Morocco

Following the first world war, focal attempts at using biological control, a protracted period of quinine prophylaxis from 1929, followed by the use of atebrine+praequine (chloroquine-like drugs) in late 1930s and limited use of pyrethrum insecticides deployed in areas of agricultural significance were variously promoted to control malaria across the country (Gaud and Sicault, 1938; Vialatte, 1923). After the Second World War, Hoeul and Donadille (1953) mapped the extents of highest transmission along the coast from Tanger at the point of the Mediterranean to Casablanca further south on the Atlantic coast stretching inland along rivers and irrigation areas but declining in intensity towards the Atlas mountains and the desert fringe areas where foci were identified around oases. The main vectors were An. labrachiae in the north and central parts of Morocco, a vector refractory to P. falciparum and supports only P. vivax transmission (De Zulueta et al., 1975), and An. sergentii perpetuating both P. vivax and P. falciparum across the entire country (Guy and Holstein, 1968). In 1948, DDT had been introduced for IRS to supplement radical case treatment and control in 33 periurban areas and 28 rural zones augmenting special engineering projects combined with larviciding in irrigation areas. The case incidence declined significantly by the late 1950s; from this point, the Gharb region contributed more than a third of all cases; overall transmission had been reduced to only nine mapped focal areas (Houel, 1954; Hoeul and Donadille, 1953). By the early 1960s, 70% of clinical infections were caused by P. vivax (Guy, 1963). From 1968, a renewed effort was launched to eliminate malaria from the remaining foci which succeeded in reducing case incidence until a resurgent risk of malaria in the 1980s. At this time, all new cases were reported as vivax, and by 1974, it was assumed that the Kingdom of Morocco was falciparum free. Foci of vivax transmission continued to exist through the 1990s to 2000 in Al Hoecima, Chefchaouen, Taounate and Khouribga provinces. Chefchaouen, in the rice growing in the North West, 85 km south east of Tanger remained the last focus of P. vivax transmission by 2000 principally transmitted by An. labranchiae (Faraj et al., 2003, 2008, 2009). In 2004, the last case of locally acquired P. vivax infections was reported from this area and the Kingdom was certified malaria free in 2010. The longterm multiparasite case incidence data have been assembled from multiple sources and shown in Fig. 4.2.

Kingdom of Morocco. Annual malaria case incidence (both species) per 10,000 per annum 1928–1973 (left hand panel) and slide-confirmed P. vivax malaria 1974–2010 per 100,000 population (right hand panel). Last confirmed P. falciparum case ... Algeria

In 1904, the Antimalaria Department was established under the direction of the Institute Pasteur and headed by Etienne Sergeant (Dedet, 2008). Leading up to the First World War, environmental management dominated approaches to prevention around settler’s farms on the Mitidja plain and the railway. Between the World Wars, quinine prophylaxis was promoted for French settler populations and their work force with continued experimentation with environmental control (drainage, canalization, bush clearing and removal of permanent swamps) (Ciavaldini, 1917; Foley, 1923; Sergent and Sergent, 1928). These activities systematically expanded across the three Departments of Oran, Constantine and Algiers until the end of the Second World War. Between 1948 and 1953, an average of 5300 cases of malaria per year were reported in Algeria (WHO-Algeria, 1956). In 1948, DDT was introduced for IRS and became the mainstay of control with supporting larval control and use of atebrine and plasmochine as mass drug administration and prophylaxis (Parrot et al., 1946). The focus continued to be on the reduction of transmission in Oran, Constantine and Algiers to protect areas widely settled by French immigrants since the 1830s who were able to lobby political support through direct government representation in Paris (Guy and Gassabi, 1967). The bloody Algeria war ended 132 years of French rule in 1962 but delayed a declaration of malaria elimination ambitions until 1968 when there were over 95,000 cases reported per year (Fig. 4.3). The eradication programme in the newly independent Algeria was rapidly successful; by 1978, only 30 locally acquired cases of P. vivax were reported in foci in the middle of Algeria (Benzerrough and Janssens, 1985; Hammadi et al., 2009). Here, we assume that by 1978 P. falciparum and P. vivax had been eliminated in the northern territories, focal transmission occurred in the middle of the country and both P. falciparum and P. vivax remained through 1980 in the southern-most regions. In 1981, Khemis el Kechna represented nearly all of the autochthonous cases detected in Algeria that year (51 cases) and all were P. vivax (Benzeroug and Wery, 1985; Benzerrough, 1990). Between 1980 and 2007, only 300 confirmed, locally acquired cases were reported (Fig. 4.3). Importantly between 1985 and 2007, all cases were reported from the southern region among an average annual population of 100,000 residents and represented an average annualized incidence of less than 1 locally acquired P. falciparum case per 10,000 population at risk (Boubidi et al., 2010; Hammadi et al., 2009). Small residual foci of P. falciparum and P. vivax transmission continued to be reported at Tinzaouatine in the south between 2003 and 2007, thought to be a result of suitable local conditions for the vector An. sergentii, and the area is located on the trans-Saharan highway connecting Algeria to Mali and Niger (Boubidi et al., 2010). There were no locally acquired cases in 2009 and 2010 (Richard Cibulskis and Ryan O’Neil, Personal Communication).

Algeria: Annual malaria incidence per 10,000 population 1948–1954 (left hand side) and per 100,000 population 1977–2009 (right hand side). Annual malaria case data sourced from multiple sources: 1948–1953 (WHO-Algeria, 1956); 1954 ... Tunisia

Prior to the First World War larval control, environmental management and “quininization” were focused in areas of European settlement (Husson and Nicolle, 1907; Sergent and Sergent, 1906). Epidemics in 1911 and 1933 in Tunisia served as incentives for government responses and public health action. The epidemic of 1932–1933 doubled the case incidence in all provinces compared to 1927–1931 (Chadli et al., 1985) and resulted in 10,000 deaths in the lakeside area of Khelbia (WHO-Tunisia,1956). During the years 1934–1944, similar approaches to malaria control to those designed by Algeria were implemented including the use of larviciding and the mass chemoprophylaxis in the regions of Cap Bon and Gabès with prémaline (properties of primaquine/chloroquine) (Decourt et al., 1936; Wassilieff, 1938; WHO-Tunisia, 1956). Over 11 years after the Second World War, 1944–1954, an average of 6500 cases per year were reported in Tunisia among an average population of 3.8 million people, approximating to 17 cases per 10,000 population at risk (WHO-Tunisia, 1956; Fig. 4.4). By 1955, amodiaquine was the preferred drug for prophylaxis. The Tunisian Republic gained independence from France in 1957; between 1961 and 1966, an aggressive approach to malaria control was mounted using DDT and a malaria elimination campaign was announced by the Government of Tunisia in 1967. All of the Northern provinces, where the dominant vectors are An. labranchiae and An. multicolor, were malaria free by 1968 (Ambroise-Thomas et al., 1976). Between 1968 and 1977 activities included nationwide active case detection and radical treatment alongside focal IRS with DDT and larviciding. By 1972, Tunisia had entered the consolidation phase of elimination and the foci of remaining transmission were located in most southerly part of Sfax Governorate, and the three southern Governorates of Gafsa, Gabes and Medenine where transmission was predominantly by An. sergentii. The last three autochthonous P. vivax cases of malaria were officially recorded in 1979. A large-scale school-based serological survey was conducted between 1990 and 1991 across 20 Governorates including approximately 38,000 children none of whom were seropositive for P. falciparum or P. vivax. The 10 years after 1979 covered a maintenance phase that included active case detection in the “hot-spot” areas of southern Tunisia, nationwide passive case detection accompanied by health worker awareness and active follow-up of infected travellers.

Tunisia. Annual malaria case incidence per 10,000 1934–1969 (left hand panel) and slide confirmed, locally acquired case incidence per 100,000 1970–1995 (right hand panel). Case data from 1935–1938 to 1955–1978 (Chadli ... Libya

The Kingdom of Libya was historically characterized by very focal transmission around oases and settled farmlands in the southern region of Fezzan sustained by An. sergentii and An. multicolor (Ramsdale, 1990) and in the less arid areas to the West in Tripolitania maintained predominantly by An. multicolor. An. labranchaie is limited in its extent to a small coastal strip west of Tripoli (Manguin et al., 2008). Following the Italian occupation of Libya, between 82 and 300 cases of P. vivax were reported from Tripolitania (Anon, 1944-1950). In the south, it was presumed that P. falciparum was more significant compared to vivax (Gebreel, 1982). The densely populated Mediterranean coastal cities towards the East were not thought to sustain significant transmission (Gebreel, 1982). In 1954, the health and sanitation division of the United States Operation Mission (USOM) initiated a malaria control programme (Anon, 1957). The first campaign, using DDT and mass drug administration with Resochin (chloroquine), began in August 1955 covering 31 localities and reaching 51 localities by 1957 protecting approximately 23,300 people across the Fezzan Oases. In 1957, this was extended further to the Taourga Oases. The WHO then began a partnership with the Kingdom of Libya to launch a campaign of nationwide malaria elimination. Following on from the USOM collaboration, the renewed elimination campaign achieved rapid success with only 28 cases being reported by 1963 (Gebreel et al., 1985). No locally acquired P. falciparum or P. vivax cases were reported in the Eastern region of Cyrenaica or Tripolitania from 1963. Cases continued to be reported from Fezzan in the West including a resurgence of falciparum malaria between 1964–65 through to 1968 when King Idiris I was overthrown and the Libyan Arab Jamahiriya was established. Between 1968 and 1973, only 14 vivax autochthonous cases were documented in Fezzan (Gebreel et al., 1985). There were no locally acquired cases reported after 1973, and while the country was declared malaria free, in September 1980, an outbreak of vivax malaria, involving 18 subjects, occurred in Zuara, a coastal town surrounded by marshland 70 km east of the Tunisian border 120 km west of Tripoli and thought to have been introduced by migrant workers (Gebreel et al., 1985). Egypt

Across Egypt, both the extent and intensity of malaria risk have changed over the past 150 years. The building of the Suez Canal under French contract in 1869, the rapid irrigation of the Nile for agriculture including lucrative cotton farming during the 1870 s under Ismail Pasha’s rule to accelerate “modernization” and the building of the Aswan dam changed the ecology of malaria transmission in Egypt. Perhaps most notable was a rapidly changing epidemiology in the upper Nile region of Nubia where An. gambiae s.l. “invaded” in 1942 from North Sudan (Shousha, 1948).

Malaria control began as early as 1900 when Ronald Ross recommended environmental control methods at Ismailia near the recently completed Suez Canal where in that year 2234 malaria cases were reported, representing one-third of the town’s population (Bey and Hussein, 1928; Halawani and Shawarby, 1957). In 1916, the High Malaria Commission was established to develop a nation-wide malaria control effort and led to the establishment of the Malaria Control Centre at Khanka, north-west of Cairo. Between the two World Wars, activities focused on attacking breeding sites in major towns and oases in the Western Desert (Bey and Hussein, 1928). By the 1930s, An. pharoensis was thought to be the predominant vector across much of Egypt (Kirkpatrick, 1925). During the 1950s, An. pharoensis remained dominant in irrigated areas and banks of the River Nile while An. sergentii and An. multicolor were implicated as important vectors elsewhere (Kenawy, 1990; Madwar, 1938). The 1940s epidemic began in the south and eventually led to almost 38,000 cases reported during 1944 compared to an average of 15,000 during the 5 years 1939–1943 (WHO-Egypt, 1956;Fig. 4.5). The cause was the introduction of An. gambiae s.l. from Sudan. An aggressive gambiae elimination programme successfully eliminated the vector by 1948 (Shousha, 1948). This success encouraged further focal eradication projects at Kharga and Dhakla Oases south west of the Nile valley (Madwar and Shawarby, 1950). Prior to 1945, the principal vector control methods included larviciding using oiling, Malariol and Paris Green. From 1946, DDT was introduced first at the oases of Kharkla, Dhakla and Siwa with increased frequency and coverage through to 1952 and improved control with higher coverage by 1954 in Fayoum Governorate. Gammaxene and Octa-Klor were used as adjunct insecticides from late 1950s (Sobky, 1957). In 1940, approximately 50% of all malaria cases were due to P. falciparum in Lower Egypt and Fayoum Governorate and over 70% in the Oases; by 1953, only 6% of all clinical infections were due to P. falciparum and the main parasite had become P. vivax (Halawani and Shawarby, 1957). This change in species dominance coincided with a dramatic decline in incidence as defined by the slide positivity rates reported by endemic disease hospitals in Upper and Lower Egypt that declined from 31% in 1940 to 5.5% in Lower Egypt and 1.8% in Upper Egypt by 1953; with no cases or smear positives being recorded in the canal zone, Assiut, Girga, Kom Ombo, Aswan and Nubia regions (Halawani and Shawarby, 1957).

United Arab Republic of Egypt reported malaria case incidence 1939–1953 per 10,000 (left hand side) and 1979–2004 per 100,000 (right hand side). Annual reported malaria cases sourced for 1939–1953 (WHO-Egypt, 1956); 1979 (Anon, ...

The 1970s witnessed a series of epidemics across the country; however, from 1979, national case incidence had fallen to below 1 case per 10,000 population, and by 1987, it was reported that there were only 22 locally acquired cases with transmission predominantly in El Fayoum Governorate. Between 1982 and 1991, malaria cases were reported in seven governorates: Port Said, Suez, Shakira, Menofia, Beni Suef, Aswan and Fayoum; however, the cases in all governorates except Fayoum were very few (Hassan et al., 2003). It seems reasonable therefore to assume that P. falciparum and P. vivax incidence was unstable for six governorates between 1980 and 1990 and free of malaria from 1990; however, Fayoum Governorate remained a stable endemic focus of P. falciparum malaria through the 1980s to the 1990s with epidemics in 1989 and 1994–1995.

Fayoum is 1800 Km2 and has a unique ecology situated in an irrigated area fed by the Bahr Youssef tributary of the Nile that ends in the Kaun Lake and the area lies 20 m below sea level which combined provides very suitable conditions for An. sergentii (Kenawy et al., 1990; Morsy et al., 1995). Between 1991 and 1997, all locally acquired cases in Egypt came from Fayoum including an epidemic of 495 and 313 cases in 1994 and1995, respectively. Since 1998, there have been no officially reported autochthonous cases in this governorate or elsewhere in Egypt (Fig. 4.5). A serological screen of 2800 children aged 1–5 years living in 12 villages in Fayoum for the detection of specific IgG antibody against pan P. falciparum, P. vivax, P. malariae and P. ovale resulted in a seroprevalence of 0.7% but might have been due to cross-reactivity with non-malaria antigens (El Mohamady, 2010), and positives were later confirmed as seronegative in another laboratory (Hoda Atta, personal communication). We therefore assume that the United Arab Republic of Egypt had focal P. falciparum and P. vivax risks between 1980 and 1999 but that the entire country was malaria free from 1998 (Fig. 4.5) despite a high malariogenic potential in Fayoum and Aswan. Djibouti

The French governed territory of the Issa’s and Afar’s (French Somaliland) is likely to have experienced endemic transmission around Ambouli before 1910 (Bouffard, 1905); however, the entire territory was regarded as malaria free from 1910 up to 1973, 4 years before independence in 1977 (Carteron et al., 1978; Mohamed, 1990; Rodier et al., 1995; WHO-Djibouti, 1956). This small country borders the Danakil depression, one of the hottest places on earth, and large parts of the country are barren rocky deserts with erratic rainfall averaging 130 mm per year. Anopheles d’thali was thought to be the historical, potential vector; however during the early 1970s, an extensive entomological survey across the country could not identify any malaria vectors (Courtois and Mouchet, 1970). Sixty percent of the population of the Republic live in Djibouti ville, connected to Ethiopia by the Addis Abba–Dire Dawa–Djibouti Railway that during the 1970s served as a route for large refugee populations that expanded the outskirts of the city and led to urban informal agriculture.

From 1988, malaria epidemics from imported infections began to appear and led to onward transmission among local resident communities (Louis and Albert, 1988; Manguin et al., 2008; Rodier et al., 1995). An. arabiensis is now accepted as the dominant vector of P. falciparum around Djibouti city particularly among the wadis, agricultural areas and watering holes around the Ambouli region. Some have argued that both An. arabiensis and P. falciparum arrived by train from Ethiopia (Fox et al., 1991; Rogier et al., 2005). From all available evidence, the Republic of Djibouti was probably malaria free up to 1980; between 1988 and 2007, reported case incidence ranged between 60 and 120 cases per 10,000 population per year (Osman, 2008; PNLP-Djibouti, 2006, 2011). Since 2008, case incidence has begun to decline to levels of less than 1 case per 10,000 population in 2010 (Hawa Guessod, Personal Communication). This recent change is reflected in declining slide positivity at two hospitals in Djibouti ville (Ollivier et al., 2011). A seroprevalence survey in 2009 among 4687 people across Djibouti found 1.6% seropositives to P. falciparum AMA-1 and MSP16 antigens and not related to recent travel histories (Noor et al., 2011; PNLP-Djibouti, 2009) confirming an unstable endemicity where transmission is possible.

4.4.2. Changing boundaries and incidence of malaria on the islands of Africa Cape Verde

The Republic of Cape Verde is an archipelago of 10 (only 9 populated) volcanic islands in the Atlantic Ocean off the Coast of Senegal. The islands were uninhabited until used by Portuguese slavers in the fifteenth century. The Creole populations across the islands vary considerably in population density; 25% of the Republic’s population today live in the city of Praia on Santiago Island. The islands are grouped according to their windward position: the Barlavento Islands (Santo Antao, São Vicente, Sta Luzia, São Nicolau, Sal and Boavista) and the Sotavento Islands (Maio, Santiago Fogo and Brava). Independence from Portugal was achieved in 1975. Interest in the epidemiology and elimination of malaria by Portuguese malariologists dated back to the 1930s when extensive surveys of infection and disease prevalence were undertaken by members of the Permanent Mission in Cape Verde from the Instituto de Medicina Tropical, Lisbon (Cambournac and De Meira, 1952; De Meira 1954, 1964; Monteiro, 1952). Between 1938 and 1954, a total of 201,682 malaria cases were documented representing an average case incidence of 800 per 10,000 population (Fig. 4.6). Cases were both falciparum and vivax although predominantly falciparum and were reported from all of the inhabited Islands (WHO-Cape Verde, 1955). An. pretoriensis is a disputed vector on the islands (Joana Alves, personal communication) while An. arabiensis is the widely accepted vector with some doubt over its presence on São Nicolau (Cambournac et al., 1984; Ferriera, 1945; Joana Alves, personal communication).

Cape Verde: Annual slide-confirmed malaria case incidence per 10,000 population 1934–1963 (left hand side) and annual, locally acquired, slide-confirmed case incidence per 100,000 population 1964–2010. Data sources used include 1934–1952 ...

In 1948, a malaria elimination campaign was launched starting on the island of Sal using DDT, oiling of larval breeding sites and more latterly with the introduction of Gambusia affinis predatory fish. The campaign extended to other Islands throughout the 1950s. The campaign was successful and malaria was felt to have been eliminated through the removal of the vector in Sal (1950), São Vicente (1954), Boavista and Maio (1962) and Santiago (1968) (Cambournac et al., 1984; De Meira, 1963). Although claimed, malaria-free Santiago still had cases in 1973. Frequent population movements between the islands, mainland Africa and Brazil with increasing air travel always presented a threat to reintroduction of both vectors and parasites (Cambournac et al., 1984). With the exception of Santiago, no autochthonous cases were detected for many years on any of the islands since they were declared malaria free, despite imported cases being detected in almost all islands. In 1973 on the island of Santiago, 148 cases were reported leading to onward transmission of both P. vivax and P. falciparum (Fig. 4.6) and served as a stimulus to renewed application of DDT, use of Gambusia fish to supplement chemical larviciding and the use of chloroquine chemoprophylaxis under a new directorate, the Brigada de Luta contra o Paludismo in 1977.

In 1979, a further national elimination programme was launched and the focus was on Santiago with renewed efforts targeting the vector with DDT and larvicides (temephos). The entire archipelago was returned to zero incidence between 1983 and 1986. The following year transmission re-established itself on Santiago and heralded a period of annual cases being detected despite increased vigilance (Alves, 1994) through to 1995–1996 when an epidemic occurred in St. Catarina district on Santiago originating from sub-patent and chloroquine resistance asymptomatic carriers (Alves et al., 2006, 2009). Current approaches to eliminate malaria on Santiago include active case detection and case investigation, the use of artemether–lumefantrine for treatment (since 2008), mefloquine for prophylaxis for travellers, temephos for larviciding and very limited use of IRS (deltamethrin) for epidemic containment and ITN. Currently, locally acquired case incidence is below 1.0 per 10,000 on Santiago. On Boavista, four possible autochthonous cases were detected in 2003, the first since 1962, 10 cases in 2009 and three in 2010. The long-term case incidence data are shown in Fig. 4.6. São Tomé and Príncipe

The Democratic Republic of São Tomé and Príncipe is made up of two volcanic islands 140 km apart in the Gulf of Guinea, 250 km from Gabon on mainland Africa. Like the Cape Verdean islands, they were uninhabited before the Portuguese occupied them for trade in the 1470s. The volcano topography and plantation agricultural economy define the transmission of malaria on the two islands (Ceita, 1981). Sao Tomeans achieved independence from Portugal in 1975. Over 96% of the present population, of 162,000 people, lives on São Tomé.

Between 1942 and 1944, approximately 5000 cases were documented on São Tomé (Joaquim and de Mesquila, 1946); over the period 1946 and 1953 on both islands, an average of 10,000 cases were reported per year among a population of only 60,000 people, and 25–37% of slide examinations at dispensaries were positive for P. falciparum (WHO-São Tomé and Príncipe, 1955). In 1955, IRS using DDT and gammexane was limited to major settled, urban and peri-urban areas and larviciding was additionally used in the town of São Tomé. Over 20,000 people were protected with mass drug administration/intermittent treatment with chloroquine, atebrin, paludrine and camoquine (WHO-São Tomé and Príncipe, 1955).

During the late 1970s, a proposal for malaria elimination was redeveloped involving epidemiological surveillance with active and passive screening, radical treatment with chloroquine and primaquine recognizing the presence of P. vivax on the islands (Pinto et al., 2000a,b), weekly prophylaxis with chloroquine among selected groups, special screening at airports and the use of DDT for IRS (Ceita, 1981). By 1980, parasite prevalence on both Islands had declined to less than 5% (Ceita, 1986). Owing to a lack of financial support, the programme became less vigilant, chloroquine resistance emerged and doubts were raised about the susceptibility of the dominant vector An. gambiae s.s. to DDT (Ribeiro et al., 1988, 1992).

From 2004, a renewed effort at country-wide IRS using alphacypermethrin was implemented, managed by the Centro National de Endemias, augmented with the use of LLIN from 2005 and application of Bacillus thuringiensis israelensis (BTI) following larval mapping exercises and mass screening and treatment and use of artesunate–amodiaquine for treatment (CNE, 2006). On the smaller island of Príncipe, cases among a population of approximately 6500 declined from 2537 in 2003 to 51 in 2009 (75 per 10,000 population) (Lee et al., 2010). These successes were repeated with similar approaches on the island of São Tomé which achieved almost 100% coverage of the population with LLIN and IRS (Teklehaimanot et al., 2009; Tseng et al., 2008). On São Tomé, parasite prevalence declined from 30% to 2.1% by 2007 (Teklehaimanot et al., 2009), and by 2009, case incidence was 247 per 10,000 population at risk (WHO, 2010). Impressive reductions in infection prevalence, disease and mortality incidence have resulted from aggressive and comprehensive combinations of vector control, screening and treatment. The declining malaria mortality rates since 2000 are particularly impressive, yet it is notable that malaria mortality on the islands was probably at its peak during the early 2000s when compared to previous pre-elimination historical periods (Fig. 4.7). The recent scaled efforts and reductions in disease incidence are further notable as they have occurred during difficult periods in the islands’ history with two attempted military coups in 2003 and 2009. On both islands, malaria incidence reflects a stable transmission state by 2009 similar to the late 1970s, neither Island has ever reached a malaria free or unstable endemic status but the future cycle of investment in elimination may transform these islands to unstable or malaria-free conditions.

São Tomé and Príncipe. Annual malaria-specific mortality per 100,000 population. Mortality data sourced from several publications: 1948–1954 (WHO São Tomé and Príncipe, 1955); 1972–1979 ( ... Zanzibar

Zanzibar is composed of two large islands, Unguja (Zanzibar Island) and Pemba (40 km North-East of Zanzibar) and several smaller islands. The islands are only 25–50 km from mainland Tanzania. The islands were governed as part of the Omani Sultanate and as a British Protectorate (1890) until a brief independent Sultanate in 1963 followed by civil war and the overthrow of the Sultan in 1964. Zanzibar then became part of the United Republic of Tanzania while retaining its own parliamentary and governance system under the Revolutionary Government of Zanzibar. In terms of malaria control, it has always operated independent of mainland Tanzania, and therefore, we consider a separate territory. Between 1923 and 1933, an average of 6800 malaria cases were recorded per year across a combined Zanzibar and Pemba population of approximately 280,000 residents and accounted for over 25% of all clinic consultations (Zanzibar Protectorate, 1923-1966). A larval survey of the island of Zanzibar in 1919 identified An. gambiae and An. funestus as principal vectors (Mansfield-Aders, 1920), subsequent investigations have found An. merus on Pemba but not on Unguja (Schwartz et al., 1997). A detailed parasitological survey among children aged 1–6 years at 26 locations of the island of Zanzibar, including Tumbatu Island in the north, found an overall prevalence of 67% and noted the presence of both P. falciparum and P. vivax between 1923 and 1926 (Mansfield-Aders, 1927). Spleen rates among school children remained in excess of 50% on both Pemba and Zanzibar between 1930 and 1966 (Zanzibar Protectorate, 1923-1966). By 1953, only limited control was mounted involving larviciding of swamps with oil and use of Paris Green in “crab holes”. DDT was only used in private residences at a fee and free of charge at all government employees houses in Zanzibar town (WHO-Zanzibar, 1955).

During the 1960s, Zanzibar mounted a campaign of biannual cycles of IRS using DDT followed by mass drug administration with amodiaquine and primaquine and a combination of chloroquine and pyrimethamine (Delfini, 1969; Dola, 1974; ZMCP, 2009) with a view to interrupting transmission. The programme was successful, reducing parasite prevalence to 6.8% on Zanzibar and 0.8% on Pemba by 1967 (Delfini, 1969). Vigilance and interest in the final effort to eliminate transmission waned as malaria was perceived to no longer be a major public health burden (Schwartz et al., 1997). A second attempt to control, rather than eliminate, malaria was mounted by the Zanzibar Malaria Control Project (ZMCP) with funding from the United States in 1984 using two rounds of DDT house spraying each year by mobile malaria teams and improved use of chloroquine at dispensaries. However, by 1983, chloroquine resistance had begun to escalate (Schwartz et al., 1983), and between 1981 and 1987, mean mortalities of exposed An. gambiae s.l to DDT were less than 50% (Schwartz et al., 1997). The programme was abandoned in 1989 after failing to show any perceptible changes in parasite rates at clinics (Schwartz et al., 1997).

In 2001, the Ministry of Health and Social Welfare decided to adopt ACT, making it one of the first countries to do so in Africa and since 2002 secured substantial funding from the GFATM and US PMI to improve case management and expand coverage of ITN and IRS using lambdacyhalothrin. This programme did not anticipate elimination but followed international recommendations to halve the malaria burden. Coverage of vector control remained low by 2004. From 2005 onwards, this began to change with more than 70% of under-fives and pregnant women sleeping under an ITN and 96% of houses were covered with IRS by 2008. Parasite prevalence in young children sampled in the community in 2002 was 47% and declined to 0.9% by 2008 (ZMCP, 2009). From 2004, Zanzibar began to witness a precipitous decline in malaria incidence, hospitalizations and blood transfusions (Aregawi et al., 2011; Bhattarai et al., 2007; ZMCP, 2009). Between 1999 and 2003, there were between 15,000 and 18,500 confirmed cases of malaria each year; in 2005, this declined to 7600 cases. By 2010, 5000 parasitologically confirmed cases were identified through enhanced surveillance, and in two sentinel areas, community-based parasite prevalence remained below 1% (Abdullah Ali, personal communication). Using case incidence and parasite prevalence data, it is most reasonable to assume that the Zanzibari islands are in a state of low-stable endemic control and that at no time in the history of elimination efforts on the islands had they reached unstable conditions. Réunion

The island of Réunion is 200 km from Mauritius and 700 km from Madagascar in the Indian Ocean. This small island is only 63 by 45 km and is dominated by the Piton de la Fournaise (2631 m above sea level) and Piton des Neiges (3070 m above sea level) volcanoes. Réunion was colonized by the French in the 1600s and remains to this day an overseas department of France. Over the past two centuries, there have been large in-migrations from Africa, China, Malaysia, Vietnam and India. The island was thought to have been malaria free before a large epidemic, probably from imported infections from mainland Africa in 1868 that set in motion a cycle of frequent, high-burden epidemics (Julvez et al., 1990a). In 1949, malaria parasite rates in school children suggested a hypoendemic state (parasite prevalence <10%) across the island with transmission of both P. falciparum (28% of all infections) and P. vivax (66%) (Hamon and Dufour, 1954). Nevertheless malaria was a significant cause of morbidity and mortality: 17,459 clinical cases were confirmed in 1946 and 1779 deaths from malaria were recorded by the authorities in 1948 (WHO-Réunion, 1955). The mortality rate on the island among all age groups, 7.35 per 1000, was equivalent to the presumed malaria mortality in young children in Africa under stable, hyper-to holoendemic conditions (Rowe et al., 2006; Snow et al., 1999). Before 1949, larviciding and the presumptive treatment of school children using chloroquine were the only methods used to control malaria.

In 1949, an elimination strategy was launched (Hamon and Dufour, 1954). Following a detailed housing structure and breeding site census of the island, two divisions were created to stagger DDT house spraying that began in October 1949 in the first sectors (Sous-le-vent). A year later, it expanded to all areas on the island and continued annually through to 1953 accompanied by sustained use of chloroquine presumptive treatment to school attending children. Overall parasite prevalence declined from 2.9% in 1949 to 0.2% in 1952, and malaria mortality declined from 5.6 to 0.6 per 1000 population over the same period (Hamon and Dufour, 1954). After this initial attack phase, a period of consolidation of elimination efforts were mounted through larviciding of mapped breeding sites, restricted use of DDT in focal transmission areas and active case and entomological surveillance. Twenty-six locally acquired infections were identified between 1956 and 1967 (Denys and Isautier, 1991; Riff and Isautier, 1995). A mass screen of over 62,000 residents in 1966/1967 identified six possible autochthonous cases in the Mafate area and surveillance identified five possible cases in Saint-Paul in 1971 (Picot, 1976; Riff and Isautier, 1995). The WHO concluded that transmission had been interrupted in 1973 and certified Réunion malaria free in March 1979. Active surveillance since 1965 has included screening of immigrants and air travellers (Guihard, 2006), and there are on average 150 imported cases of malaria each year notably from neighbouring islands of Madagascar, Comoros and Mayotte. The dominant vector, An. arabiensis, remains wide spread and has not been eliminated (Girod et al., 1999; Morlais et al., 2005), and the 810,000 residents of the country remain vulnerable to imported malaria risks (D’Ortenzio et al., 2009; Denys and Isautier, 1991; Girod et al., 1995; Guihard, 2006; Julvez et al., 1982; Lassalle et al., 2000; Sissoko et al., 2006). Mauritius

The Republic of Mauritius includes the islands of Mauritius, Cargados Carajos, Rodrigues and Agalega. The archipelago is located in the south western part of the Indian Ocean 900 km east of Madagascar. Only the island of Mauritius has been identified as supporting malaria transmission. Mauritius was occupied first by the Dutch and French, who found the islands uninhabited. As with Réunion, it is likely that malaria was introduced onto the island of Mauritius in the mid-1860s by immigrant labour (Ross, 1908) and led to a large epidemic in 1867 (Balfour-Kirk, 1934; CDCU, MoH&QL, 2008). Ronald Ross completed an island-wide investigation of spleen rates in 1906 and found an overall rate of enlarged spleens of 48% and made recommendations for immediate sanitation to reduce vector breeding sites (Ross, 1908). In 1910, Smith, reporting to the Colonial Development Fund, estimated malaria death rates on the island to be in excess of 12 per 1000 population per year (Smith, 1911).

Before the Second World War, there was very little active prevention despite some reports of drainage of swamps and wide-spread use of quinine. Between 1942 and 1943, P. falciparum infection prevalence among children was 42%, P. vivax prevalence was 22% (Sippe and Twining, 1946) and An. funestus and An. gambiae s.l. were implicated as the sole vectors (Colony of Mauritius, 1950). Archived hospital and dispensary returns and census interpolations suggest that there were large between year variations in the annual incidence of malaria between 1930 and 1948, but most years showed more than 10% of the population suffering from a clinical attack (Fig. 4.8); the average malaria-specific mortality was 3.63 per 1000 per year among the entire population during this period (Colony of Mauritius, 1928–1972).

Mauritius. Annual malaria incidence per 10,000 population 1927–1962 (left hand side) and vivax incidence per 100,000 population 1963–2008 (right hand side). Annual malaria cases sourced from 1927–1971 (Colony of Mauritius, 1931–1972 ...

Immediately after the Second World War, the Ministry of Health began to implement some of the recommendations made by Ross 40 years earlier with major environmental works (canalization and cleaning of streams, drainage of marshes) and oiling of breeding sites. These efforts concentrated on the Central Plateau, the town of Port Louis and the drainage of two extensive marshes in Pamplemousses district. In 1948, to tackle the high incidence on the rest of the island, the Colonial Insecticide Committee proposed in conjunction with the Government of Mauritius a Malaria Eradication Scheme (Colony of Mauritius, 1950; Dowling, 1951a, b, 1952). In November 1948, a detailed housing census led to the creation of three zones for the attack phase of elimination: Zone 1 using DDT (80% pp in Kerosene); Zone 2 using DDT 50% Wettable Powder and Zone 3 using Gammexane 50% Wettable Powder. The first round of spraying began in January 1949. During the second spray round, the central area was extended and the “barrier” technique was adopted by spraying of the outskirts of the town of Port Louis and Mahebourg. The third spray round began in 1950 and covered over 720,000 rooms providing protection for over 614,000 people (Colony of Mauritius, 1950). Parasite prevalence surveys in school children showed a drop from 9.5% infection rates in 1948 to 0.4% in 1950 (Colony of Mauritius, 1950), and the effects on case incidence was immediate and dramatic (Fig. 4.8).

Between 1953 and 1956, case incidence was below 1 per 10,000 population per year. By the end of the attack phase, An. funestus was virtually extinct (Bryan and Gebert, 1976) while An. gambiae s.l. proved harder to control notably in the area of Flacq. This led to a more aggressive phase of breeding site identification and larval control. Between 1960 through to the early 1970s, mass IRS was replaced with targeted use of DDT accompanied by active surveillance to identify residual foci using mobile teams and screening of immigrants at ports. Apart from an excess of cases identified in 1960, malaria incidence continued to decline and it was assumed that local transmission had been interrupted in 1969, the year after independence from Britain (Fig. 4.8). In 1972, a serological survey among children living in Black River, high foci of previous transmission, showed that immunoflourescent antibodies to P. falciparum and P. vivax were present in less than 0.6% of children aged less than 5 years (Bruce-Chwatt et al., 1973). The WHO certified Mauritius malaria-free in 1973 which prompted what turned out to be a rather premature article hailing malaria as “dead as a dodo” (Bruce-Chwatt and Bruce-Chwatt, 1974). At this point, surveillance vigilance declined as the responsibility for malaria was absorbed into the wider health system (Tatarsky et al., 2011). In 1975, P. vivax transmission established itself in village close to Port Louis likely to have been imported from India. This initial importation event led to an increasing vivax transmission across the island peaking in the mid-1980s with over 500 cases each year (Fig. 4.8). Through the use of focal IRS (DDT), widespread larviciding (temephos), passenger screening and an up-regulated active case detection system, transmission was contained by 1990. With small vivax outbreaks in 1992 and 1996 (Fig. 4.8), the last indigenous case recorded in 1997. Since 1998, Mauritius has maintained the absence of local transmission. Mauritius therefore was able to eliminate P. falciparum and P. vivax transmission in 1969, witnessed re-emergence of P. vivax transmission in 1975 and achieved a second elimination in 1998. Comoros

Three islands formed the Federal Islamic Republic of Comoros at independence from France in 1975, Grand Comore (1024 km2, rising to 2361 m above sea level with the volcano of Karthala), Anjouan (424 km2 rising to 1578 m above sea level) and the lower altitude Mohéli island (374 km2) in the Comorian Archipelago. In 1997, Anjouan and Mohéli unsuccessfully sought independence from the union with Grand Comore. Under a new constitution in 2001, the islands form an unstable Union of the Comoros with each island having some political autonomy. The people of this archipelago, including Mayotte, have been part of the evolving Swahili corridor since the tenth century and comprise a mixture of Arab and Bantu people. Altitude, settlement patterns and agriculture determine the malaria risks across the three islands including malaria-free areas at high altitudes on Grand Comore.

The first recorded severe epidemics occurred in 1920 (Raynal, 1928a). An. gambiae and An. funestus are the dominant malaria vectors (Brunhes, 1977) of P. falciparum and the less commonly prevalent P. vivax (<1% parasite prevalence) (Blanchy et al., 1987, 1990). Between 1940 and 1943, reported case incidence was approximately 1555 per 10,000 population per year (WHO-Comoros, 1955). In June 1953, limited use of DDT was applied on the islands of Grand Comore and Mohéli, and there is a suggested use of chloroquine chemoprophylaxis in the 1950s (WHO-Comoros, 1955). No significant malaria prevention seems to have been reported up to the 1980s and transmission remained intense and stable. During 1987, 3370 clinical cases were detected on Grand Comores (population 223,600), 1788 on Anjouan (population 163,900) and 1294 on Mohéli (population 20,400); parasite prevalence among children 2–9 years during the same year was 51.4%, 23.3% and 44.6% on each of the islands, respectively (Blanchy et al., 1987). In January 1987, a campaign to control malaria and filariasis was mounted although details of precise activities and approaches are difficult to establish. In 1988, the Programme National de Lutte Contre le Paludisme (PNLP) was established. Between 1999 and 2001, case incidence remained high on all islands (Tchen et al., 2006), and in 2006, malaria accounted for 36% of all clinic consultations (PNLP-Comoros, 2009).

In 2007, a national plan of action was launched with the aim of preparing the Comoros for pre-elimination in 2014 and eventual Interruption of transmission. The new strategy focuses on the wide-scale distribution of ITN, IRS in selected areas with lambda-cyhalothrin, larval control with predatory guppies, intermittent presumptive treatment of pregnant women and enhanced clinical management using artemether–lumefantrine all implemented with funding from the Global Fund and some bilateral agency support (PNLP-Comoros, 2009). On the island of Mohéli, in collaboration with scientists from China, mass treatment of communities with artemisinin monotherapy (Artequick) and primaquine as a follow-up treatment began in October 2007 reducing infection prevalence from 23% in September 2007 to 1.4% by January 2008 and a further reduction to 0.4% by June 2009 (Anon, 2007; Bacar, 2010). Whether this was continued and scaled as an intervention to Grand Comore and Anjouan, despite WHO recommendations not to use artemisinin monotherapy (WHA, 2007), is unclear. By 2009, the PNLP had distributed almost 170,000 ITN across the three islands by 2009 (WHO, 2010), and during a mass-free distribution, campaign between November 2010 and January 2011 on Grand Comore and Anjouan distributed a further 255,000 ITN. Among the 640,000 residents in 2009, over 51,000 presumed cases of malaria were reported, of which only 10% were confirmed cases (WHO, 2010). Following the reduction of transmission on Mohéli as a result of mass drug administration, it is not possible to estimate the stability of endemicity due to the lack of corresponding case incidence data. For Grand Comore and Anjouan, clinical incidence has probably remained intense and stable over the past 100 years. Mayotte

The two islands that comprise Mayotte, Mahoré (352 km2) and Pamanzi (17 km2), are located within the Comorian Archipelago 320 km from Madagascar and 70 km from the Comorian island of Anjouan. The islands have been governed by France since 1841, and when the Federal Islamic Republic of Comoros secured independence from France in 1975, Mayotte elected to remain a French Territory Overseas. The majority of the population live in approximately 70 villages that surround the coastline of the island of Mahoré. Malaria has been intense and stable on the islands for many years, and the only parasite identified among clinical cases had been P. falciparum (Ali Halidi, 1995; Galtier and Blanchy, 1982); however, cases of vivax have more recently been identified (Loos et al., 2006; Solet et al., 2007). An. gambiae s.l. and An. funestus maintain transmission, although An. funestus plays a lesser role (Brunhes, 1977). Some limited use of dieldrin for IRS was applied in 1954, but there are few other records suggesting much aggressive control until the 1970s. Parasite prevalence was 36.5% among children living in villages on Pamanzi in 1972 (Galtier and Blanchy, 1982). A programme of chloroquine prophylaxis among school children was started on both islands in 1972 (Julvez et al., 1990b).

A joint effort to eliminate two, high morbidity burden vector-borne diseases, malaria and filariasis, was initiated in 1976. The malaria component included chloroquine prophylaxis to school children and preschool children attending dispensaries, IRS using DDT and malathion (subsequently, only malathion as culex vectors of filariasis was shown to be resistant to DDT) and larviciding with temephos (Galtier and Blanchy, 1982). By 1981, coverage was high with 91% of households sprayed and 60% of school children reached with chemoprophylaxis. Among sentinel villages, the overall parasite rate in all age groups was 25.5% in 1976 but declined to 0.9% by 1980 (Galtier and Blanchy, 1982). Between 1981 and 1983, it is likely that malaria transmission on the islands was unstable; however in 1984, early signs of reduced chloroquine efficacy were observed from Comorian immigrants, and in this year, there was an epidemic with 64 cases in May (Julvez et al., 1987) and 394 throughout 1984 (Julvez et al., 1990b). Parasite prevalence rose to 2.5%, and this prompted an emergency intervention with IRS using quarterly rounds of fenitrothion spraying, use of temephos and predator guppy fish (Lebistes reticulatus) in mapped larval areas and increased active and passive surveillance including serial, annual serological surveys (Julvez et al., 1986, 1987, 1990a,b). The use of chloroquine for chemoprophylaxis was stopped except for pregnant women. By 1985, parasite prevalence had declined to 0.3% and 75 clinical cases were reported for the year (Julvez et al., 1987, 1990b). For the three years 1986, 1987 and 1988, only 8, 44 and 8 cases, respectively, were detected (Julvez et al., 1990b), and it is reasonable to assume that the islands had returned to an unstable transmission state. Resurgent waves of transmission continued through the early 1990s as identified from age profiles of serological detection of falciparum-specific antibodies (Julvez, 1993). A large epidemic occurred in 1991 with 1724 cases detected through the active and passive surveillance system and parasite prevalence had increased to 1.3% (Receveur et al., 2004).

By 2001, malaria was the cause of over 1000 clinic presentations, 250 hospital admissions each year (Receveur et al., 2004; Tchen et al., 2006) and resistance to chloroquine and sulphadoxine–pyrimethamine had escalated (Roussin et al., 2002). In an attempt to tackle the high disease burden malaria control in the 2000s focussed on the distribution of ITN to pregnant women and newborn children, IRS using deltamethrin and the distribution of rapid diagnostic tests to all clinics (Receveur et al., 2004). Artesunate–mefloquine was recommended as first-line therapy in 2005 following documented high levels of resistance to chloroquine, pyrimethamine, amodiaquine and quinine (Pettinelli et al., 2004). By 2003, malaria incidence began to decline with a 25–40% reduction in cases detected compared to 1999–2002 (Tchen et al., 2006). Cases are more concentrated in the northern districts of the main island of Mahoré, most notably at Bandraboua (Solet et al., 2007) where re-emergence of An. funestus has been documented (Elissa and Karch, 2005). The complete interruption of transmission on the islands of Mayotte has never been achieved and the difficulties associated with elimination have been outlined by Receveur et al. (2004). Brief periods of unstable transmission have been experienced on the islands since 1939, and the changing status of risk since 1983 where data are available is shown in Fig. 4.9.

Mayotte malaria case incidence per 10,000 population 1983–2010. Annual malaria case data derived for period 1984–1988 (Julvez et al., 1990a); 1983, 1989–1994 (Ali Halidi, 1995); 1995–2004 (Tchen et al., 2006); 2005 and ... Madagascar

The Republic of Madagascar is the fourth largest island in the world and includes smaller islands located off its coastline including Nosy Be and Sainte-Marie. The central highland plateau rises to 1341 m above sea level, and this densely populated area is characterized by terraced, rice-growing valleys. It is likely that the first inhabitants arrived from Indonesia between 300 and 500 years BC followed in the first millennia by Bantu migrants crossing the Mozambique Channel. Immigrants from Arabia, India, China, East Africa and Europe have led to a diverse population. The island gained independence from France in 1960.

P. vivax has probably existed on the island for several centuries; however, it has been argued that P. falciparum was first introduced by the French Foreign Legion during the war with the Kingdom in 1878 leading to severe epidemics (Blanchy et al., 1993). For the past 100 years, the distribution and intensity of malaria have been governed by the diversity of ecology across the island, altitude, agriculture and changing human settlement patterns and population growth (Mouchet et al., 1993). In 1923, parasite prevalences in the northern part of Madagascar, Diego Suarez (Antsiranana), were in excess of 64% (Raynal, 1928b) and the spleen rate among children in the highlands, at Antananarivo, was over 77% in 1927 (Legendre, 1930). P. vivax was recorded in 20% of all malaria infections in 1927 (Legendre, 1930), but vivax now accounts for 6% of all infections and is concentrated in highlands and the western coastline (PNLP-Madagascar, 2007). An. gambiae s.s., An. arabiensis and An. funestus are reported as the most important vectors (Ayala et al., 2006; Bernard, 1954; Mouchet and Blanchy, 1995); however, their distribution and dominance in transmission have changed with time (Curtis, 2002; Joncour, 1956).

The antimalaria service of Madagascar was reorganized in 1927 (Legendre, 1930). Between the two world wars, control focused on limited drug prophylaxis, larval control using “stoxal”, Paris Green, Gambusia fish and drainage works (Bernard, 1950; Legrende, 1930). In 1948, DDT house spraying began and by 1949 covered almost 25,000 houses in Tananarive Province. This expanded in 1950 to approximately 46,000 houses in Tananarive (Antananarivo), Tamatave (Toamasina), Antsirabe, Diego Suarez (Antsiranana) and the island of Santa Marie (Bernard, 1950). By 1952, it was estimated that over 3 million people were protected through the spraying of 680,000 households (Bernard, 1954). In addition to IRS with DDT, the campaign included routine chemoprophylaxis with chloroquine administered to school children and younger children at dispensaries at a total of 4924 distribution sites (Bernard, 1954). Supplementary activities included larval control notably in rice irrigation areas including the use of Gambussia fish. Spleen rates declined from 40% in 1948 to 0.2% by 1953, and by 1952, parasite prevalence among 39,000 sampled children was 0.01% (Bernard, 1954). Crude mortality dropped by a half between 1948 and 1952 in the town of Tananarive from 21 per 1000 residents to 12.8 and malaria mortality declined from 6 per 1000 population at risk to 0.4 per 1000 over the same period with only 3.7% of all deaths attributed to malaria by 1952 (Bernard, 1954). IRS, chemoprophylaxis and larviciding continued through to 1955 when 50 of the 80 districts in Madagascar had become hypoendemic (<10% spleen rates in children aged 2–9 years) and 30 districts located largely on the West of the Island were mesoendemic, with spleen rates of 10-49% (Joncour, 1956; WHO-Madagascar, 1955). Transmission in the highland plateau districts was extremely low, An. funestus had largely disappeared and in Fianarantosa district zero infection prevalence was recorded in 1955. By 1957, the highland plateau was regarded as malaria free (Blanchy et al., 1993).

Continued efforts to maintain spraying were largely successful in maintaining low levels of case incidence through to 1975 in the highland plateau (Fig. 4.10; Blanchy et al., 1993; Bouma, 2003; Tchen et al., 2006). Chloroquine prophylaxis (Nivaquinization) was maintained reaching 35% of young children and school children between 1977 and 1978 (Laing, 1984) but ended in 1979 (Randrianarivelojosia et al., 2009). About this time, An. funestus reappeared in the highlands as a result of expanding rice cultivation (Blanchy et al., 1993). Reduced sensitivity to chloroquine was documented in 1981 (Le Bras et al., 1982) and became more wide-spread by 1983 (Deloron et al., 1984). Epidemics occurred in the highland plateau between 1985 and 1988 (Fig. 4.10). These epidemics had a devastating public health impact and are thought to have doubled malaria-specific mortality increasing during the late 1980s to over 1.9 per 1000 population (Mouchet and Baudon, 1988; Mouchet et al., 1998) and prompted the return to routine DDT use in 1993 (Blanchy et al., 1993; Jambou et al., 1998; Mouchet and Blanchy, 1995) accompanied by enhanced surveillance (Albonico et al., 1999; Romi et al., 2002). Despite focused intervention in the highlands, by 1999, the number of presumed malaria cases in Madagascar exceeded 1.4 million (Tchen et al., 2006). From 1998, the national malaria programme was reconfigured and began the promotion of ITN and continued house spraying with combinations of DDT and pyrethroids according to epidemiological stratification of the island. Malaria in the highlands once again began to decline (Jambou et al., 2001; Rabarijaona et al., 2006).

Antananarivo Province malaria case incidence per 10,000 population 1972–1989. Annual malaria case data derived for period between 1972–1974 and 1982–1983 where data presented only as incidence (Bouma, 2003); 1975–1989( ...

In 2004, it became policy to offer ITN free-of-charge across the island. Despite day 28 failure rates of over 50% to chloroquine by 2004 (Menard et al., 2008), home-based management of fevers was promoted using socially marketed pre-packaged chloroquine. In December 2005, the Ministry of Health adopted amodiaquine–artesunate as first-line treatment. In 2007, the Ministry launched a malaria elimination strategy that included a preparatory phase and attack phase by 2012, a consolidation phase to be completed by 2017 and maintenance malaria free-phase from 2018 (PNLP-Madagascar, 2007). Using funds from the GFATM, US PMI and other bilateral agencies, 6.2 million LLINs were distributed between 2007 and 2009, covering an estimated 57% of the population at risk and IRS protected 6.9 million people at risk in 2009. According to the WHO, from 2006 malaria admissions to hospitals declined rapidly through to 2009 and there were only 173 reported malaria deaths in 2009 (WHO, 2010). However, it is hard to interpret these data without knowing the location of the hospitals or the reliability of mortality reporting during the year when a coup d’état led to major civil disruption.

Despite remarkable, rapid achievements in reducing transmission in the Highland Plateau during the first malaria elimination campaign of 1948–1955, it is not clear from available evidence whether transmission had been interrupted, but it seems reasonable to assume that the area was rendered unstable through to 1980. The 1980s through to 2005 were periods when stable transmission and high disease burdens were reported in the Highland Plateau. P. falciparum risks were country wide, while evidence suggests that P. vivax transmission is concentrated in the Highland Plateau and Western districts (PNLP-Madagascar, 2007). Other than the small area of temperature limiting transmission in Antsirabe, Antanifotsy and Ambatolampy districts of Vakinankaratra province, at no time has any other location in Madagascar been strictly malaria free.

4.4.3. Changing boundaries of stable malaria risk and disease incidence in Southern Africa South Africa

Assembled historical data from a variety of government and research reports held at the Tzaneen National Institute of Tropical Diseases and the National Archives in Pretoria were used by various authors to define the limits of malaria transmission in 1938. Risks before expanded national control extended to within Durban’s city limits along the Indian Ocean, included Pretoria in the north and reached the railway crossing point at Ramatlabama on the Botswana border (Le Sueur et al., 1993; Sharp and Le Sueur, 1996; Strebel et al., 1988). Since the First World War, it is likely that malaria transmission has been concentrated in the extended Transvaal areas of the North-East and the wider Natal region in the South East.

Malaria impeded agricultural development from the turn of the last century in Northern and Eastern Transvaal. Anti-larval measures started in 1924 at irrigation sites south of the Hartbeespoort dam west of Pretoria. Epidemics in 1928 across the Transvaal prompted investigations (Swellengrebel, 1932) that led to the establishment of the Tzaneen Malaria Centre and extensive work on breeding site identification and reduction, education of farmers on personal protection, engaging the national railways to control vector breeding around stations and the promotion of the use of quinine through 200 “quinine distributors”. In 1944, a trial of larviciding combined with pyrethrum house spraying was undertaken at Springbok Flats. Only after the Second World War was progress made in shrinking the 1938 margins of transmission in the Transvaal using a strategy of focal elimination employing DDT IRS, continued targeted larviciding and expanded use of quinine treatment. In the Transvaal, 4439 malaria cases were detected in 1939–1940 and this declined to only 128 by 1949–1950, located along the river tributaries of the Limpopo and bordering the Kruger Game Reserve (Annecke, 1950). Attack and consolidation phases continued from Western to Central Transvaal through to the Lowveld from the 1950s and included a period from 1950 to 1969 when BHC was used in preference to DDT (Brink, 1958; Hansford, 1974, 1987). During the 1970s, annual and biannual rounds of DDT house spraying and active house-to-house surveillance in the Transvaal region focused on high-risk areas around the Limpopo, White and Crocodile River valleys, Bushbuckridge, Letaba valley up to Nelspruit (Hansford, 1972, 1974). A WHO sponsored study of intensive active surveillance and IRS was mounted in 1974 at Makonde that reduced autochthonous cases from 42 to 10 by 1976 (Smith et al., 1977). Progress across the province during the 1970s varied depending largely on aberrant rainfall patterns that led to epidemics. The apartheid era was a period when South Africa’s borders were rigorously policed, and very few imported cross-border infections were detected relative to locally acquired cases and imported infections came from bordering areas of Swaziland, Zimbabwe and Mozambique. Transvaal was divided in 1994 to Mpumalanga, Limpopo, Gauteng and North Western provinces. By the late 1980s, all local transmission was restricted to defined areas of Limpopo and Mpumalanga provinces. Malaria incidence began to rise during the late 1980s and early 1990s (Gerritsen et al., 2008). This increasing clinical burden was coincidental with rapidly changing cross-border human population movement from Zimbabwe and Mozambique, 5–10% of refugees from the civil war in Mozambique being asymptomatic carriers of infection in 1985 (Frank Hansford, personal communication), and emerging chloroquine resistance (Bac et al., 1985; Philip Kruger, personal communication).

Epidemics were common in KwaZulu-Natal at the turn of the last century. Hill and Haydon (1905) refer to the epidemic that caused 4177 clinical cases and 42 deaths in Durban in 1905. From 1910 screening of dwellings, use of bed nets and personal protection including the prophylactic use of quinine were recommended (Le Sueur et al., 1993). Severe epidemics occurred in 1929 and 1932 and over 22,000 malaria deaths were recorded by magistrates in 1932 (Le Sueur et al., 1993). Malaria Committees were formed from 1933 among sugar farmers who promoted larval control, environmental management and the planting of eucalyptus (De Meillon, 1936). In 1941/1942, experimental use of pyrethroids was used for weekly house spraying (Hansford, 1987). From 1945, DDT replaced pyrethrum and by 1956 had extended as far north as Ubombo and Ingwavuma districts. Malaria Committees began to be disbanded from 1952; by 1965, only 36 autochthonous were detected across the province and routine DDT spraying was discontinued. Case incidence and spatial extents continued to decline through the 1970s, although they varied depending on rainfall (Sharp et al., 1988). By the late 1980s, over 90% of cases were reported from the northern most districts of Ingwavuma and Ubombo (Craig et al., 2004; Kleinschmidt et al., 2001; Mnzava et al., 1998). Cases in KwaZulu-Natal started to increase in 1986–1987 and then began a dramatic rise from 1991 until over 40,000 cases were reported in 2000 (Fig. 4.11; Craig et al., 2004). The rise in case incidence followed the replacement of DDT with Deltamethrin for IRS, increasing clinical failures to chloroquine and rising malaria incidence in southern Mozambique. DDT was re-instated as the preferred insecticide for IRS in 2000 as resistance to pyrethroids was documented in KwaZulu-Natal among An. arabiensis close to Mozambique border (Maharaj et al., 2005). First-line treatment policy was changed in KwaZulu-Natal to ACT in 2001 (Barnes et al., 2005). Drug policy changes to ACT followed in 2002 in Mpumalanga and 2004 in Limpopo.

Annual malaria case incidence in KwaZulu-Natal Province per 10,000 population 1974–2009. Annual Malaria Cases for KwaZulu-Natal 1974–2005 (Craig et al., 2004; Marlies Craig, unpublished data); 2006 and 2007 (DoH South Africa, 2008); 2008 ...

By 2009/2010, less than 6000 cases were detected across South Africa reflecting a decline since 2000 but not a return to case incidence rates that prevailed in the 1970s (Fig. 4.12). The largest declines were witnessed in KwaZulu-Natal Province and less dramatic declines recorded in Limpopo and Mpumalanga Provinces. By 2010, case incidence was focal and unstable along a restricted margin from Zimbabwe running south through to the eastern river valleys in Inkumanze district in Mpumalanga (Aaron Mabuza, personal communication) and the districts Ingwavuma and Ubombo in KwaZulu-Natal. There remain practical difficulties in defining locally acquired versus imported cases across South Africa. Over the past 5 years, there have been increases in cross-border movement among the Gaza communities from Mozambique to Gaza settlements in South Africa across the Kruger National Park; increasing migration from Zimbabwe to Mutale sub-district in Limpopo and a more significant threat is posed by the massive immigration that occurs at Beitridge, Limpopo that has processed, without malaria screening, up to 300,000 economic and political migrants from central and horn of Africa in recent years (Philip Kruger, personal communication). Many of these migrants move rapidly to non-receptive areas of Gauteng Province but some remain in the more malaria receptive areas of Limpopo and Mpumalanga.

South Africa. Annual malaria case incidence per 10,000 population 1970/1971–2008/2009. Annual malaria incidence in 1970/1971 was 0.12 per 10,000 population—not visible on the graph. Malaria case data provided for period 1970/1971–1980/1981 ... Namibia

De Meillon conducted an opportunistic survey of communities across South-West Africa in 1950 and used information on vectors, spleen rates, parasite rates and reports from local school, railways and mission authorities to define four zones of transmission (De Meillon, 1951). Areas in the north including the Ovamboland, Bushmanland and Caprivi were regarded as intense, stable transmission, while the most southerly areas from Grootfontein and Franzfontein to the Orange River were likely to be free of transmission or very focal pockets of occasional transmission (De Meillon, 1951). The Ministry of Health and Social Services has always regarded the southern provinces of Karas and Hardap as malaria free (MoHSS, 1995, 1996) and supported De Meillon’s observations in the 1950s (De Meillon, 1951). It was not until 1965 that a campaign of IRS was launched using DDT and bendiocarb in urban residential houses in the North. A malaria public health specialist was provided by South Africa to establish a network of malaria health inspectors in the areas of Ovambo and Kavango along the Angolan border in the mid-1960s and this led to the rapid expansion of DDT house spraying across these areas with almost 1 million houses sprayed each year by 1970. This programme was managed from Windhoek with regional officers at Oshakati and Runtu; however, due to accessibility, the Caprivi area was managed directly from Pretoria and IRS was less complete in this region (Frank Hansford, personal communication; Hansford, 1990). Annual mass-blood surveys and treatment with Darachlor began in 1969; slides were read at Tzaneen in South Africa and results returned to guide the mapping of high-risk areas for the next annual spray rounds. Despite the war for independence mounted by SWAPO in the northern territories, which led to regular movement across Angola’s borders and periodic disruption of basic services, IRS control continued although costs and supply began to impact on coverage by the early 1990s. All Northern provinces have continued to support stable P. falciparum transmission since 1950, and following wide-scale use of DDT for IRS almost exclusively maintained by An. arabiensis. IRS was never mounted in the more southerly districts as parasite prevalence was intrinsically low.

Independence in 1990 unfortunately coincided with a large malaria epidemic. In 1991, the national malaria control programme was launched as part of the National Vector Diseases Control Programme. In 2004, chloroquine was replaced with artemether–lumefantrine following increasing chloroquine treatment failures and deltamethrin replaced bendiocarb for spraying of modern structures. With support from the Global Fund, distribution of ITNs began in 2000; by 2009, 22% of the population in the Northern provinces were sleeping under a treated net and 22% of households had been sprayed within the past year (MoHSS, 2010). Reliable health information on malaria diagnoses is not available for the years during German occupation or during subsequent Union of South Africa rule. A concerted effort to improve parasitologically diagnosed cases was mounted in 2004 and recent data are hard to interpret against changing diagnostic practices. Botswana

Malaria risk in the Republic of Botswana, formerly the British Protectorate of Bechuanaland until independence in 1966, is constrained by latitude and the Kalahari Desert that makes up 70% of the country’s land mass. In 1958, 98% of all malaria cases were reported from two districts, Ngamiland and Chobe in the North in areas surrounding the Okavango and Chobe swamps fed by the Zambezi River (Bechuanaland Protectorate, 1928-1963). Commenting on the combined parasitological data and clinic returns for the year 1960, the medical department regarded the southernmost districts of Tsabong through to Gaborone as malaria free but subject to introduced risks from neighbouring Transvaal (Bechuanaland Protectorate, 1928-1963). During a national parasitological survey in 1961–1962, no sampled infants were found to harbour infections in Tsha, Loda, Gaborone, Kanye, Moduchi, Tuli and Ghanzi areas (Franco de et al., 1984a).

Between 1958 and 1962, few cases were reported along the Limpopo River, and in 1959, discussions began with the Transvaal Medical Department of the Union of South Africa to start cross-border activities in support of malaria elimination. Malaria control focussed on larval reduction strategies and the use of DDT for house spraying in major towns before 1955 and was regarded as successful in reducing the case incidence in major towns such as Maun, Francistown, Mhalapye and Serowe by 1956 (WHO-Bechuanaland, 1955). The medical department of the Bechuanaland Protectorate undertook extensive reconnaissance of malaria risks through school-based parasitological surveys from 1959 to 1962 (Bechuanaland Protectorate, 1959-62). These mapped data were used to prepare a malaria elimination strategy with the WHO in January 1961. The use of DDT for IRS was irregular and incomplete between the 1950s and 1971, focussed largely in Ngamiland, Chobe and Francistown (Franco de et al., 1984a). In 1971/1972, fenitrothion was used briefly before being abandoned the following year (Franco de et al., 1984a; Mabaso et al., 2004). The Botswana National Malaria Control Programme was reorganized in 1980 with headquarters at Maun. Improved biannual IRS using DDT use was employed in the most malarious districts of Ngamiland, Chobe and Francistown (North-East) throughout the 1980s. There is reference made to weekly chloroquine prophylaxis for pregnant women and children below the age of 5 years in the mid-1980s (Franco de et al., 1984a). Between 1982 and 1984, over 94% of all cases were reported from Maun, Chobe and Tutume regions (Franco de et al., 1984a). Shortages of DDT in 1987 led to a failure to spray large parts of the endemic regions of Ngamiland and Tutume (Benthein, 1989).

In 1998, Botswana stopped using DDT and switched to the use of deltamethrin and lambda-cyhalothrin (MoH, 1999). ITN distribution began in 1997 but was only made free of charge through vaccine and antenatal clinics in the northern districts in 2008. Over 250,000 people were protected by IRS in 2009 and approximately 69,000 LLIN had been distributed since 2008. Following escalating treatment failures with chloroquine and sulphadoxine–pyrimethamine, Botswana switched to artemether–lumefantrine in 2007. Botswana experienced malaria epidemics in 1988, 1993, 1996 and 1997, but these may have occurred against a background of rising disease risk through the late 1980s to 2000 where after case incidence has declined (Fig. 4.13). In 2000, the National Malaria Control Programme assembled parasitological survey data from the 1990s and case-reporting data from the national health information system to confirm that the districts of Kgalagadi, Kweneng, Kgatleng, Gaborone, Southern (including Good Hope) and South East were for practical purposes malaria free but could be subject to localized epidemics following imported infections (MoH, 2001). Since 1990, case incidence, while probably focal in its extent and magnitude, remains above 1 per 10,000 population at risk in areas where transmission has been reported between 1990 and 2010 (Fig. 4.13). In September 2010, Botswana launched an elimination strategy with a renewed emphasis on the use of scaled annual spraying between October and December with DDT.

Botswana annual slide-confirmed malaria case incidence 1928–2010 per 10,000 population. Data sources used include 1928–1938 (Bechuanaland Protectorate, 1928–1938); 1945–1953 (WHO-Bechuanaland, 1955); 1954–1960 (Bechuanaland ... Zimbabwe

Malaria risks in Zimbabwe are determined by altitude and proximity to the river valleys of the Zambezi and Limpopo. During the 1920s, Thomson remarked on the high risks associated with low-lying areas in the river valleys of Shamva, Bindura, Sinoia, Gatooma and Victoria but describes Salisbury (Harare) and Bulawayo as urban centres ostensibly free from malaria (Thomson, 1929). It is often stated that the central ridge of mountains that bisects the country from Mutare to Bulawayo is largely free from malaria above 1200 m (Taylor, 1985; Taylor and Mutambu, 1986) although others have used 1500 m as the divide (Crees and Mhlanga, 1985). The medical department records of malaria start in the late 1800s but focus almost exclusively on the morbidity and mortality experiences of European settlers. What is clear is that annual hospital returns suggest some malaria risk across the entire country since the turn of the nineteenth century when the country was first colonized.

Malaria control began in earnest in 1949 in Mazoe Valley using HCH for IRS covering over 200,000 people (Alves, 1951; Alves and Blair, 1953; Blair, 1950) and increased across the lowveld areas through the early 1950s (Alves and Blair, 1955). In 1953, the programme expanded further to include areas of higher altitude to serve as a “buffer” for European communities, and by 1955, both lowveld and middleveld areas were “under control” (Alves and Blair, 1955). Between 1957 and 1991, DDT was the preferred residual insecticide. A number of experimental projects were also launched in reserve areas using enhanced surveillance (Wolfe, 1964) and mass drug administration with chloroquine among children or with amodiaquine and primaquine for immigrant labour (Alves, 1958; Reid, 1962). In 1942, malaria accounted for 10% of all hospitalizations, but by 1962, this had declined to only 0.3% of admissions (Taylor and Mutambu, 1986). The city limits of Bulawayo and Harare (previously Salisbury) were confirmed as malaria free from late 1970s by national malaria control agencies (NMCP Zimbabwe, 2008) and international travel advisories (IAMAT, 2004). The spatially restricted campaigns since the late 1940s were successful in reducing parasite prevalence and case incidence to a state of unstable transmission by 1959 and through to the late 1970s. It was hoped that malaria might be eliminated in the southern provinces during the 1960s although Rhodesia was never supported by the WHO beyond pre-eradication. Spraying activities continued throughout the civil war for independence during the 1970s although disruptions were inevitable.

Since independence in 1980, malaria control was re-energized, and in 1988, deltamethrin replaced DDT for IRS. The country witnessed a number of severe epidemics of increasing frequency from the mid-1980s with the most widespread and severe epidemics in 1988 and 1993 (Freeman, 1995; Fig. 4.14). From the first reported evaluation and documentation of chloroquine resistance in 1984, this spread across the country over the next 10 years (Makono and Sibanda, 1999). Zimbabwe changed its firstline treatment policy from chloroquine to a combination of chloroquine–sulphadoxine/pyrimethamine in 2004; by 2006, artemether-lumefantrine had become the recommended first-line treatment. Despite the continued disruption within the health sector wrought by political unrest (Tren et al., 2007), progress had been made in increasing coverage of ITN with 42% of children reported sleeping under a treated net the night before in a national sample survey of over 6000 households in 2008 (NMCP Zimbabwe, 2010). Coverage with DDT IRS, reintroduced in 2004 (NMCP Zimbabwe, 2008), was considerably lower in 2008 with only 15.5% of households reporting spraying in the last 12 months (NMCP Zimbabwe, 2010).

Zimbabwe: Annual malaria case incidence per 10,000 population 1980–2009. All case data combinations of slide confirmed and presumed cases. No data available for review for the years 2001–2003. Data 1980–1989 from Freeman (1995) ...

The various efforts to control and eradicate malaria over the years probably led to constrained areas of unstable transmission in the 1950s, and by 1979, the central districts were regarded as malaria free (Global Fund—Zimbabwe, 2010). Transmission today is largely supported only by An. arabiensis which has replaced the previously widespread presence of An. funestus reported in the 1950s (Reid and Woods, 1957). Epidemics continue to be common, but by 2009, there were 14 districts that were malaria free and part of elimination consolidation efforts (Fig. 4.20). The rise and fall of malaria between 1980 and 2009 is shown in Fig. 4.14, and it is important to recognize that Zimbabwe is yet to re-establish disease control to rates described in the early 1980s.

The changing margins and stability of P. falciparum transmission (A) 1959, (B) 1979, (C) 1999 and (D) 2009. Dark grey representing no malaria risk; light grey biologically suitable transmission but population density less than 0.01 person per km2; light ... Swaziland

The Kingdom of Swaziland is a landlocked country only 200 km by 130 km sharing borders with South Africa and Mozambique. In common with Zimbabwe, the ecology of malaria is divided along altitudinal lines with the lowveld (Bushveld) high-risk areas to the East, midveld and the highveld lower-risk areas to the mountainous regions in the West (Mastbaum, 1957a). Malaria epidemics in 1937 and 1945 highlight the severity of malaria in Swaziland; in 1937, hundreds of Swazis died of malaria (Packard, 1986); in 1945/1946, 6850 cases were reported (Fig. 4.15;Mastbaum, 1954). The only form of prevention prior to the end of the Second World War included very limited larval control measures as recommended by control agencies in the Union of South Africa. The first malaria control unit was established in 1945 and limited HCH house spraying began in 1949 (Mastbaum, 1954) which expanded through the lowveld during the 1950s and a subsequent switch to DDT until 1951 when BHC was used as a cheaper residual insecticide until 1961 (Mabaso et al., 2004). Dieldrin was also used experimentally in 1955–1956 in some areas and larviciding was maintained in Bremersdorp (Manzini) and Stegi (Siteki) (Mastbaum, 1957b). By 1955, all rural areas, sugar farms and irrigation schemes across the Kingdom were protected by IRS. Parasitological surveys were undertaken annually to monitor the impact of the control programme; in 1945/1946, parasite rates among infants were 37%, declining to 6% by 1952/1953, 1.2% by 1954/1955 and 0% by 1956 (Mastbaum, 1955, 1957a; WHO-Swaziland, 1955). In concert with Zimbabwe, Swaziland switched to a system of barrier control in 1958 with the highveld areas and an intensified buffer of 15 km from the Mozambique border in the Hhohho and Lubombo regions. An. funestus reduced significantly in numbers following the scaled IRS campaigns (Mastbaum, 1957b) and An. arabiensis predominates to this day. Spraying operations were systematically withdrawn from areas that reported no cases within a 2-year period and mass IRS was stopped in 1959. Between 1961 and 1967, focal IRS was maintained using both BHC and DDT. Between 1968 and 2000, DDT was used for rural IRS and cyfluthrin in houses with painted walls (Hansford, personal communication; Mabaso et al., 2004). One important threat to the success of control during the 1950s and 1960s was the rapid introduction of irrigation and imported labour for the Colonial Development Cooperation programme to stimulate sugar cane farming (Packard, 1986). This changed the landscape and risks of malaria including epidemics in 1966 and 1971 (Fig. 4.15). Between 1956 and 1975, malaria case incidence was less than 5 per 10,000 population per year with the exceptions of the epidemics in 1966 and 1971. By 1970, it is stated that the only cases were those imported from outside the country (MoHSW, 1999). At this point, malaria operations were drastically scaled down, funding withdrawn and the malaria department reduced from 36 staff to 7.

Kingdom of Swaziland. Annual malaria case incidence 1928/1929–2009/2010 per 10,000 populations. Total population of Swaziland used throughout to highlight changing national case incidence despite changing margins of risk. Case data derived for ...

During the early 1980s, large-scale population movements occurred as a result of refugees fleeing the civil war in Mozambique, for example, 24,000 were settled in Malindza and Ndzevane in 1983 alone (Hansford, 1994). In 1986/1987, spraying ceased due to lack of funding and declining government priority. This was followed by a resurgence of malaria risk until funding from South Africa restored control operations and led to a temporary decline, but malaria case incidence followed a pattern seen elsewhere in Southern Africa rising through to a peak in the late 1990s including a serious epidemic in 1996 that led to 125 malaria deaths (MoHSW, 1999). Between 1994 and 1999, 70% of cases came from Lubombo on the border with Mozambique (MoHSW, 1999). In 1999, Swaziland joined forces with KwaZulu-Natal Province in South Africa and Southern Mozambique to form the Lubombo Spatial Development Initiative (LSDI) to aggressively reduce transmission across borders (LSDI, 2007; Sharp et al., 2007). Global Fund external support increased the national capacity to fund IRS, ITN distribution, drugs and diagnostics and surveillance in 2003 and 2008. Up until 2009, the first-line treatment for malaria was chloroquine, and the Swazi Ministry of Health was the last to change to ACT in Africa in 2010. Case incidence began to decline from 2000, and for the three consecutive years 2006–2008, incidence was below 1 per 10,000 population (Fig. 4.15) and these areas of unstable risk are located in the Eastern regions of Lubombo and Hhohho. In 2008, the Kingdom of Swaziland launched a malaria elimination strategy (MoHSW, 2010).

Swaziland has probably witnessed several periods where it approached the elimination of P. falciparum resulting in unstable case incidence (late 1950s, early 1970s and late 2000s). These short-lived successes do not constitute sustained maintenance of unstable transmission. The recent declines in case incidence between 2006 and 2008 have resulted in less than 100 confirmed cases reported each year largely located in the Eastern regions; therefore, we have treated the mapped extent of the cases in the East of the country as unstable and the remaining areas are malaria free. In 2010, the number of reported confirmed cases increased to 253 (Simon Kunene, personal communication) highlighting the need for vigilance, cooperation with neighbouring Mozambique that provides seasonal labour and more aggressive containment of transmission if Swaziland aims to eliminate all local transmission.

4.4.4. Malaria control in Middle Africa: From GMEP pilots to RBM Before the Second World War

Before, and during, the Second World War, the control of malaria was largely focused on protecting Europeans settling in central African territories, military personnel or short-stay colonial administrators. Consequently, control was limited to urban administrative centres, ports and economic concessions such as mines and farming areas. Prior to the Second World War, attempts to reduce vector breeding sites were undertaken in a number of urban and economically important areas in the highly endemic countries of middle Africa under the colonial administration of Britain, France, Portugal, Belgium and Germany. Reference is made to environmental mapping of larval breeding sites and control, including in some cases penalties for infringement of “malaria legislation”, in Conakry, Guinea (Le Moal, 1906), Dakar, Senegal (Heckenroth, 1922), the “Dutton Scheme” in Bathurst (Banjul), The Gambia (Colony of The Gambia, 1917), Leopoldville (Kinshasa), Democratic Republic of Congo (Colonie du Congo Belge, 1931), Khartoum, Sudan (Balfour, 1913), Dar es Salaam (Colonial Development Fund, 1935; Mackay, 1938), Nairobi, Kisumu and Mombasa, Kenya (De Boer, 1930) and the use of oiling of breeding sites in large towns in Nigeria (Colony of Nigeria, 1927). Few data exist on the overall impact of these approaches; however, several examples are worth highlighting.

Nairobi was established as the administrative capital of Kenya in 1905, and although it is located at 1795 m above sea level, malaria was a significant problem for residents from 1911. Over 14,000 malaria cases were recorded in Nairobi in 1913, and malaria cases fluctuated between 2500 and 3600 per year between 1917 and 1919 (Symes, 1940). Three major epidemics occurred in 1926 (De Mello, 1947; Symes, 1940), 1935 and 1940 (De Mello, 1947; Haynes 1940). Following the 1926 epidemic, malaria was made a notifiable disease and renewed efforts were established, supported by legislation, to improve drainage and environmental management to reduce the larval breeding sites across the expanding city (De Mello, 1947; Nairobi Municipality, 1930-1969; Symes, 1940). Notifications showed a significant decrease of autochthonous malaria cases from an annual average of 1182 cases in the 1930s, to 317 cases in the 1940s to 250 in the 1950s and finally 49 cases in the 1960s during a period when the numbers of Nairobi residents had increased 35 times since the 1930s (Fig. 4.16; Mudhune et al., 2011). Attribution of declining risk to specific intervention approaches is difficult, but the data shown in Fig. 4.16 suggest that urban malaria control was successful in reducing vector breeding and locally acquired disease incidence before the Second World War.

Nairobi city malaria incidence per 10,000 population 1916–1969 (adapted from Mudhune et al., 2011). Annual malaria incidence in 1926 was 3649 per 10,000 populations and attenuated in graph. No data were reported in 1921–1925 and 1945. ...

During the 1920s in Sierra Leone, extensive drainage of wells and “canalization” were undertaken by the local colonial government’s Medical and Public Works Department to improve the malaria situation in the towns of Freetown, Kissy and Aberdeen and led to significant reductions in house resting An. gambiae by the early 1940s (Tredre, 1943; Turner and Walton, 1946). Detailed reconnaissance of local vector breeding and control continued throughout the Second World War as the port of Freetown was extensively used by the army (Tredre, 1943). In Northern Zambia, between 1929 and 1949, a comprehensive programme of vegetation clearance and drainage was mounted around the Roan Antelope copper mines, accompanied by provision of quinine and promotion of mosquito nets. Malaria mortality was reduced by 90% among European employees within 5 years of the programme starting (Utzinger et al., 2002). At Lagos in Nigeria, drainage of the swamps and provision of tide gates for the creeks during the Second World War were used to reduce malaria risks for the British Air Force who had built a base at Apapa and was thought to have been directly responsible for a reduction of malaria attack rates from 100 per 1000 to approximately 30 per 1000 stationed soldiers per year (Gilroy and Bruce-Chwatt, 1945). Throughout the twentieth century, urbanization has led to systematic declines in malaria risk across many parts of middle Africa. The changing epidemiology of malaria in rapidly growing urban centres in Africa is complex (Hay et al., 2005; Keiser et al., 2004; Robert et al., 2003); however, the effects of public heath engineering projects before the Second World War cannot be underestimated (Keiser et al., 2005; Utzinger et al., 2001, 2002). Vector control and pilot elimination projects post-Second World War

The 1948 WHO malaria meeting (WHO, 1948) sought to maximize the advances made in chemical discoveries for antimalarials and insecticides during the Second World War. Attempts to eliminate malaria in Africa were predominately located at the margins of stable transmission in the northern and southern latitudes or on islands. Far fewer national-level elimination efforts were reported in the countries and territories governed by colonial powers in Middle Africa. The coverage of malaria prevention in countries located in this subregion is best summarized from a review of reports presented to WHO regional meetings in 1955 and 1956 that brought together national malaria control programmes to review current progress toward elimination. The meetings were held in Lagos in August 1955 (WHO, 1955) covering most of the Middle African countries and in Athens in June 1956 where Sudan reported (WHO, 1956). The national summaries provided at these meetings allow some insight into the scope, scale, costs and impact of malaria control activities across the continent for the approximate reporting year of 1953. Across the Middle African countries, the reported information varied between countries in detail, completeness and the sources of data provided; three countries did not provide any information (Ethiopia, Italian Somalia and the British Cameroons). Nevertheless, the data generated for the year 1953 provide some estimate of IRS and chemoprophylaxis coverage. Most countries reported using some form of IRS with the exception of Guinea-Bissau and Uganda. The most widely reported insecticide used was DDT; however, countries also reported using in addition gammexane, BHC, dieldrin, malariol or hexastan. Overall among the 32 reporting countries, representing approximately 122.5 million people at risk, only 4.9% of the population was protected by preventative measures and most of the areas protected were either special projects or urban settings. In 1955, Russell estimated that in the combined territories of West, Central and Eastern Africa only 8.5% of people at risk of malaria were protected against infection (Russell, 1956). While it is hard to distinguish what constitutes middle, southern and northern Africa, it was estimated that by 1968 of the 214 million people living in the entire Africa region exposed to malaria, only 1.03 million (0.5%) were living in areas that had mounted consolidation or maintenance phases of elimination (Brown et al., 1976). By 1974, among the 240 million Africans living in potentially malarious areas, only 2.3% were protected under elimination campaigns, 5.9% were protected by vector control measures and 3.2% were protected by chemoprophylaxis; 89% remained unprotected by any form of vector control or chemoprophylaxis (Brown et al., 1976).

Pilot control and elimination projects across West, Central and Eastern Africa were in some cases highlighted in the WHO conferences in 1955 and 1956 others began after 1955. These were significant trials covering thousands of people. The trials provided important information on the impact on transmission and mortality of house spraying and drug-based regular prophylaxis or mass treatment. Between 1945 and 1979, IRS pilot projects were undertaken in Senegal (Locan and Michel, 1962), Sierra Leone (Davidson, 1947; Walton, 1947, 1949), Liberia (Guttuso, 1967), Ghana (Eddey, 1944), Nigeria (Bruce-Chwatt et al., 1955, 1957; Foll and Pant, 1966), Cameroon (Chastang, 1959), Togo (Bakri and Noguer, 1977), Democratic Republic of Congo (Davidson, 1950; Vincke, 1950), Rwanda-Burundi (Jadin et al., 1953), Tanzania (Draper and Smith, 1960; Smith, 1962; Smith and Draper, 1959), Kenya (Fontaine et al., 1975; Payne et al., 1976), Ethiopia (Chand, 1965), Republic of Sudan (BNHP, 1981; El Gaddal et al., 1985; Mirghani et al., 2010) and Mozambique (Soeiro, 1952, 1956); trials of combined IRS with mass drug administration or chemoprophylaxis in Nigeria (Molineaux and Gramiccia, 1980; Nájera et al., 1973), Cameroon (Cavalie and Mouchet, 1961), Burkina Faso (Escudie et al., 1961; Ricosse et al., 1959), Democratic Republic of Congo (Feuillat et al., 1954; Vincke, 1954), Kenya (Roberts, 1956, 1964a,b; Strangeways-Dixon, 1950) and Uganda (De Zulueta et al., 1964) and trials of drug-based control without IRS in Tanzania (Clyde, 1966, 1967), Ghana (Charles et al., 1962), Kenya (Avery-Jones, 1958), Uganda (Hall and Wilks, 1967) and Sudan (Omer, 1978). What is clear is that the escalation of IRS or mass drug administration across middle Africa failed and in most instances did not go beyond pilot projects. High costs of insecticides, fears of rapid escalation of vector resistance to insecticides and mixed results from malaria elimination pilot projects all contributed to a failure to expand vector control in Africa (Kouznetsov, 1977; Nájera, 1999; Nájera et al., 2011). Requirements for successful elimination programmes highlighted the need for strong and effective health systems and much of Africa neither had the resources nor was deemed prepared for the scaling up of attack phases (Cambournac, 1966; Gramiccia, 1966; Nájera, 1999; WHO AFRO, 1962). By the 1970s, malaria was seen as a health system problem for much of Africa and its control was integrated into strategies for the management of illness within the framework of Primary Health Care (Nájera, 1999).

The mounting fears of resistance to insecticides (notably at first dieldrin) highlighted the need to rapidly reduce transmission in order to mitigate the expected lost potency of insecticides in use (Bruce-Chwatt, 1956). This prompted early investigations into the combined effects of chemoprophylaxis in combination with IRS to escalate transmission reduction in highly endemic areas (Bruce-Chwatt, 1956; D’Alessandro and Buttiens, 2001; Dola, 1974; Kouznetsov, 1979). National programmes of chemoprophylaxis were beginning to be cited at the WHO Lagos conference in Kenya, Tanzania, Somaliland, Mozambique, Malawi and Angola; however, the details surrounding these programmes were limited. At the WHO regional conference in Yaoundé in 1962, it was stated that “The problem of collective drug administration for malaria control is of increased interest and importance in Africa. In a number of African countries where a malaria eradication programme cannot be put into immediate effect because of technical, administrative or financial obstacles, the responsible authorities are interested in the possibilities of malaria control through a large-scale administration of antimalarials either to the whole population or to selected and particularly vulnerable groups” (WHO AFRO, 1962).

From as early as the 1960s, chloroquine was widely available in clinics, shops and private pharmacies across Africa. Sixteen percent of children presenting to a clinic in Ibadan in 1959 had had some form of anti-malarial treatment at home before attending the clinic (Onuigbo, 1961). Throughout the 1960s and 1970s, there were reports of the use of chloroquine and pyrimethamine as a means of control as Mass Drug Administration in Middle Africa (von Seidlein and Greenwood, 2003), including school-based programmes referred to as the “Daraprim Parade” in Eastern Nigeria (Arthur, 1965), Western Nigeria (Fasan, 1971), Gabon (AFRO-WHO, 1962), Tanzania (Clyde, 1967) and Kenya (John Ouma, personal communication). The steady growth in the wide-spread use of chloroquine led to a situation following the end of the GMEP activities in Middle Africa, whereby all fevers were routinely treated with branded forms of chloroquine (AFRO WHO, 1962). At Saradidi in Western Kenya during the early 1980s, it was estimated that every person received on average 1.24 chloroquine exposures per year, and 13.4% of the population received five or more treatments per year (Spencer et al., 1987). With the scaled introduction of Primary Health Care and expanded availability of retail drugs (Foster, 1995; McCombie, 1996) during the 1970s and 1980s, the presumptive treatment of all fevers as malaria with chloroquine was widespread. The first confirmed case of chloroquine resistant malaria was reported in Kenya and Tanzania in the late 1970s (Campbell et al., 1979; Fogh et al., 1979) and spread westwards reaching a presumed complete incursion across all of Africa by 1989 (Bloland et al., 1993; D’Alessandro and Buttiens, 2001; Talisuna et al., 2004).

There are very few long time-series data on malaria incidence from Middle Africa, and this limits our ability to fully understand the changing clinical epidemiology of malaria in this region between 1950 and the 1990s. What has been suggested from the examination of cause-specific demographic surveillance studies across Middle Africa is that malaria-specific mortality in childhood reduced significantly following independence from colonial rule and remained at a lower incidence through to the 1990s where after it rose significantly as a cause of death against a continuing decline in all-cause mortality (Fig. 4.17; Snow et al., 2001). The rise in malaria mortality witnessed at surveillance sites during the 1990s coincided with established high levels of chloroquine resistance (Snow et al., 2001) and more temporally associated with documented drug resistance at Niakhar in Senegal (Fig. 4.18; Munier et al., 2009; Trape et al., 2012). These observations are further supported by longer-term data on malaria admissions at a Tea Estate population in Kenya which showed low incidence during the 1960s to early 1980s followed by a rise in malaria reaching peaks in the 1990s, of note in this series is the subsequent decline through to 2009 (Fig. 4.19; Shanks et al., 2002; Stern et al., 2011).

Annualized malaria-specific mortality in children aged 0–4 years old pre-1960; 1960–1989 and 1990–1999. Box plot showing median (central lines), 25%, 75% quartile ranges around the median (box width) and upper and lower limits ...
Niakhar, Senegal: Malaria-specific mortality per 1000 children 0–4 years 1984–2010 (adapted from Munier et al., 2009; Trape et al., 2012). Malaria defined in demographic surveillance of Naikhar population using verbal autopsies. In 1992, ...
Annual malaria admissions in Kericho Tea Estate population, Kenya 1966–2009 (adapted from Shanks et al., 2002; Stern et al., 2011).

The peak of malaria incidence since the end of the GMEP in Africa was probably somewhere between the early 1990s and early 2000s in many sites of Africa where first-line drugs were failing and the prevention of infection with vector control was minimal. This period coincides with resurgent risks described earlier for the Malagasy highlands (Fig. 4.10), malaria mortality in São Tomé and Príncipe (Fig. 4.7), Kingdom of Swaziland (Fig. 4.15), South Africa (Fig. 4.12) and Botswana (Fig. 4.13). The RBM era in middle Africa

The RBM initiative and the supporting financial structures provided by the Global Fund emerged at a time when Africa was facing a rapidly rising malaria disease burden. Both initiatives were slow to impact on the poor coverage of new efficacious tools such as ITN (Noor et al., 2009), removing failing monotherapies and supporting policy change in favour of ACTs (Attaran et al., 2006) and the funding necessary to implement aggressive control started reaching high-burden countries slowly (Narasimhan and Attaran, 2003; Teklehaimanot and Snow, 2002). The Scale-Up for Impact initiative was conceived to rapidly change the landscape of poor coverage across Africa and achieve near universal access and use of prevention and clinical care (Campbell and Steketee, 2011). By 2005, new international funding was translating into effective coverage of prevention (ITN, IRS and intermittent presumptive treatment of malaria in pregnancy) across middle Africa. Between 2008 and 2010, a total of about 254 million nets were supplied and delivered to sub-Saharan Africa, and approximately 34% of young children were sleeping under an ITN by 2010 (RBM, 2011). About 10% of Africans at risk of malaria were protected by IRS by 2010 (RBM, 2011) including more recent IRS policies and implementation in The Gambia, Senegal, Mali, Liberia, Ghana, Benin, Nigeria, Gabon, Angola, Democratic Republic of Congo, Zambia, Mozambique, Malawi, Uganda, Kenya, Tanzania, Rwanda, Burundi, Ethiopia and Eritrea. Although coverage was deliberately patchy, four countries achieved household coverage greater than 50% (RBM, 2011). Overall, IRS coverage estimates are considerably higher in 2010 than those reported during the 1950s and 1960s for Middle Africa. DDT is used for malaria control in 13 African countries.

Following growing concerns about chloroquine and sulphadoxine–pyrimethamine resistance and the lack of an international response (Attaran et al., 2006), remarkably rapid concerted action led to the policy changes to support novel ACTs as first-line therapies across Africa. In 2003, only four countries in Africa had adopted ACTs as their first-line therapy (Bosman and Mendis, 2007); by 2010, they were first-line treatment in every malaria endemic country in Africa. Despite rapid policy change, making sure clinical cases are treated with an ACT has so far proven to be the most elusive milestone of RBM success nationally and regionally. These drugs still reach only a fraction of people who need them. Most countries in Middle Africa, for which data are available, report that less than 20% of febrile children access an ACT (RBM, 2011). Not all fevers are malaria and the big-push is to now scale up parasitological diagnosis of malaria to improve case-management practices (D’Acremont et al., 2009).

RBM, the Global Fund and bilateral agencies supporting malaria control in Africa have all improved how we assess the impact of financial investments to support disease control and elimination efforts. However, while there has been a significant improvement in how partners measure financial investment and coverage of malaria control activities, far less attention has been given to the documented impact on disease incidence and death from malaria. Modelled expected impacts of reported intervention coverage form the main evidence base by which partners estimate deaths averted in Africa since 2000 (Eisele et al., 2009; 2010; Komatsu et al., 2010; RBM, 2011). These models predict that approximately 0.8 to 1.1 million deaths have been averted since the launch of RBM. Our only empirical evidence in Middle Africa comes from short-term temporal coincidence between increased access to effective interventions and the changing patterns of paediatric hospitalization with severe malaria since 1999 in Eritrea (Nyarango et al., 2006), Ethiopia (Graves et al., 2008; Otten et al., 2009), The Gambia (Ceesay et al., 2008; 2010); Gabon (Bouyou-Akotet et al., 2009), Rwanda (Otten et al., 2009; Sievers et al., 2008), Kenya (O’Meara et al., 2008; Okech et al., 2008; Okiro et al., 2007, 2009), Guinea-Bissau (Rodrigues et al., 2008), Senegal (Brasseur et al., 2011; Sarrassat et al., 2008), Tanzania (Mmbando et al., 2010) and Zambia (Chizema-Kawesha et al., 2010). These reports suggest a wide-spread effect of scaled intervention across middle Africa since 1999 and are consistent with declines seen in southern Africa and those island states pursuing elimination.

There is little doubt that the epidemiology of malaria is in transition across Africa, yet there are several important aspects of this change that need highlighting. Firstly, all is not equal and there are reports from some high transmission settings in Africa including Western Kenya, (Okiro et al., 2009), Uganda (Okiro et al., 2011) and Malawi (Roca-Feltrer et al., 2012); the clinical burden presenting to hospitals has increased since 1999. Most reports of declining malaria burdens are from settings where the initial transmission intensity was low to moderate (O’Meara et al., 2010). Secondly, progress in ensuring that the most vulnerable communities are protected across Middle Africa has been varied with some countries achieving more than others with similar levels of donor support (Flaxman et al., 2010; Hill and Kazembe, 2006; Noor et al., 2009; RBM, 2011; Van Eijk et al., 2010; WHO, 2010). There are very few published time-series data since 2000 from countries that have been slow to scale intervention coverage. Thirdly, the temporal association between scaled coverage of ITN, changing therapeutic policies and declining disease incidence is not always congruent. At several sites, malaria hospital admissions began to decline prior to significant coverage of prevention with ITN, IRS and effective access to ACT. Finally, where declining incidence of malaria has been documented, the decline has been dramatic; however, these declines were all reported from a baseline period towards the end of the 1990s and early 2000s when the malaria burden was at its recent peak.


4.5.1. Changing limits in North Africa

Using the narratives from published reports, mapped extents and descriptions on the locations and species of locally acquired infections, it is possible to combine historical medical intelligence with biological masks of temperature and aridity suitability for transmission and human population density to provide a sequence of spatial risks from 1939 (presumed natural extent; Fig. 4.1), 1959 (Fig. 4.20A), 1979 (Fig. 4.20B), 1999 (Fig. 4.20C) to 2009/2010 (Fig. 4.20D). The areas of biological suitability coincident with population densities greater than 0.01 per km2 are often oasis settlements across the Sahara. The focus here is on P. falciparum risks only, recognizing there were foci of P. vivax transmission in the Kingdom of Morocco after 1974 in Al Hoceima, Chefchaouen, Taounate and Khouribga provinces and from 2000 in Chefchaouen province until eliminated, and there was an outbreak of vivax malaria in 1981 Khemis el Khechna in the north of Algeria. In 1939, most of the populated areas of North Africa were exposed to stable transmission of both P. falciparum and P. vivax with the likely exception of the eastern coastal towns of Libya. By 1969, this spatial extent and the likely clinical incidence had reduced substantially as part of attack phases of national, post-independence elimination campaigns.

At the launch of the RBM initiative in 1999, almost all of the North African territories were P. falciparum free with the exception of the border area of Tinzaouatine in southern Algeria and Fayoum in the UAR Egypt. While difficult to establish with certainty, we have left the residual foci as unstable in southern Algeria by 2009, representing the last area of possible P. falciparum transmission. Figs. 4.2-4.4 demonstrate the rapid decline associated with aggressive adult vector control, reconnaissance of larval breeding sites and active case detection during the initial attack phases of elimination programmes in North Africa. It is, however, important to recognize that malaria control had a long history in North Africa dating back over many years prior to the GMEP, and the effects of larval reduction and mass drug administration on transmission in Morocco, Algeria, Tunisia and UAR Egypt are likely to have substantially reduced the endemicity prior to the launch of elimination campaigns. The natural barrier provided by the vast Saharan desert serves as a protection from the highly endemic regions of sub-Saharan Africa, thus reducing the risks of imported, cross-border malaria. Nevertheless, North Africa attracts many economic migrants from the south. Since 2002, in the Kingdom of Morocco, over 700 imported malaria cases have been detected (WHO-Morocco, 2010); between 1980 and 2009, 981 and 2466 imported cases have been detected in Tunisia (WHO-Tunisia, 2010) and Libya (WHO-Libya, 2010), respectively. Demonstrations in Tunisia in 2010 set off a wave of political unrest across North Africa and Arabian Peninsula known as the Arab Spring. It remains uncertain how the building and restructuring of Algeria, Tunisia, Libya and Egypt will affect the immediate vigilance required to maintain active detection of imported infections and the efforts required to contain onward transmission where vectors continue to provide areas of receptive risk.

4.5.2. The successes and failures of malaria elimination on Africa’s islands

Small island states are thought to represent unique opportunities to eliminate malaria (Kaneko et al., 2000), having identifiable vector ecologies and accessible populations isolated from neighbours harbouring continued transmission. All the self-governed African islands have attempted malaria elimination at some stage over the past 70 years. These islands share several common properties that distinguish them from mainland Africa. Human settlement was more recent and involved an ad-mixture of people from Asia and Africa resulting in significant proportions of the population having duffy-positive red cells and, combined with a history of trade outside Africa, receptive to the establishment of P. vivax transmission on all the islands in the Atlantic and Indian Oceans. P. vivax is usually the “last parasite standing” during elimination campaigns (Baird, 2010) and harder to prevent from reintroduction as witnessed in Mauritius. All the small islands have distinct agriculture-based ecologies and human settlement patterns allowing the relatively easy mapping of vector breeding sites, human risk and stratified spatial control. With the exception of Zanzibar, migration between mainland Africa and the islands is quantitatively limited through a sea buffer rather than a desert buffer for North Africa, with the high transmission countries of the continent. Increasing air travel has, however, transformed risks of imported malaria, and special screening and containment programmes at airports during consolidation phases of elimination in Cape Verde, Réunion, Mauritius and São Tomé and Príncipe have at some stage been implemented. Interestingly, the islands of Madagascar and the Union of Comoros pose the largest threats to the re-establishment of malaria in Réunion (Denys and Isautier, 1991). Although physically separated from one another, the islands of the Indian Ocean, therefore, require a subregional effort to reduce the risks of re-establishing transmission in island states with high malariogenic potential.

Only Réunion (1979) and Mauritius (1973 and 1998) have achieved malaria elimination since the launch of the GMEP. The Cape Verdean islands reduced the spatial extent considerably and much earlier, but local transmission continues on the islands of Santiago and Boavista. Zanzibar (three attempts), Mayotte (two attempts) and Madagascar (three attempts) have enjoyed varying degrees of success towards elimination over the past 50 years, often reducing transmission and disease incidence to extremely low levels but never interrupting transmission. On the islands of São Tomé and Príncipe and the Union of Comoros, far less was achieved before the launch of the RBM initiative. An important component of previous elimination efforts on the islands has been the combination of IRS with wide-scale use of anti-malarial drugs through mass drug administration, prophylaxis or screening and treatment. During periods when parasites were sensitive to chloroquine, this approach would have had a dramatic effect on the parasite reservoir. Resurgent interest in this approach has been adopted in Comoros; however, there remain concerns over the use of artemisinin monotherapy as resistance emerging to this important therapeutic agent would be a disaster on far more than a local scale.

A consistent theme throughout the combined histories of malaria elimination attempts across Africa’s islands is the impact of waning political support and financial commitments to maintaining prevention and surveillance when disease burdens are reduced to very low levels. Sustaining the malaria-fee status in Mauritius and the progressive effects of early elimination attempts in São Tomé and Príncipe, Zanzibar and Madagascar were all jeopardised by weakened enthusiasm and commitment to programme efforts. Failures were also attributed to emerging drug resistance (Cape Verde, Mayotte, Zanzibar and Madagascar), changing patterns of land use (Madagascar) and imported infections accompanied by declining surveillance efforts (Mauritius and Cape Verde). Anticipating a long game, demanding constant vigilance rather than a short-term win, is critical to sustaining success towards elimination.

All islands that have yet to interrupt transmission have witnessed dramatic reductions in the incidence and public health burden posed by malaria since 2005. This is coincident with the scaling up of replacement ACT first-line treatments, provision of free ITN and targeted IRS made possible following a massive increase in financial resources provided by the Global Fund and other international agencies. In addition to the independently governed islands, Bioko, one of the islands of Equatorial Guinea, saw a huge reduction in child mortality and malaria incidence following scaled IRS and ITN coverage since 2005 (Kleinschmidt et al., 2009). The disease reduction successes across high-burden islands have encouraged a renewed wave of enthusiasm for elimination: the Union of Comoros, Madagascar and São Tomé and Príncipe have all explicitly developed elimination attack, maintenance and consolidation strategies to achieve malaria-free status before 2020.

The Revolutionary Government of Zanzibar and its 1.2 million residents now face a difficult decision to either maintain aggressive control to sustain a very low prevalence and incidence of disease (low-stable endemic control) or embark on a pathway to elimination. An elimination feasibility study reviewed the risks posed by imported infections from travellers each year (between 10,000 and 25,000 air travellers per month), its close connectivity by ferry and boats to mainland Tanzania and the economic costs (ZMCP, 2009). The report concluded that the vulnerability posed by imported infections, high receptivity on the islands and the costs (US $1.88 per capita for sustained control versus US $2.87 per capita for elimination over 25 years) argued in favour of sustaining low-stable endemic control (ZMCP, 2009).

4.5.3. Elimination and control efforts in Southern Africa

Malaria control activities began as national campaigns from 1948 in South Africa, the Kingdom of Swaziland and Zimbabwe and the 1960s in Botswana and Namibia. Prior to 1948, malaria prevention was not wide-spread and tended to focus on the use of quinine prophylaxis among European settlers and limited vector control notably efforts to improve environmental sanitation, oiling and use of Paris Green. From the late 1940s, the wide-scale use of IRS programmes with a variety of residual insecticides, but mostly DDT, across many areas of Southern Africa was able to achieve rapid and substantial reductions in transmission and incident cases. None of the southern African countries have managed to substantially reduce the margins of transmission that prevailed in 1939 (Fig. 4.1), or completely interrupt transmission within the margins, but have enjoyed periods of low case incidence that would qualify as unstable transmission between the 1959 and 1979 (Fig. 4.20A and B) coincidental with periods of aggressive IRS campaigns (Mabaso et al., 2004; Mastbaum, 1965).

Resurgent risks began to emerge in the 1980s (Figs. 4.11-4.15) and have been variously attributed to large-scale population movements during the 1970s and 1980s due to regional conflicts, waning political commitment and funding, periodic interruption of IRS, emerging drug resistance and the HIV epidemic. The renewed political commitment to malaria control and elimination in the 2000s served to galvanize efforts in Southern Africa and have led to recent successes in reducing the burden of malaria in every country from its second peak. However, it is important to recognize that during the period when the international development lens was focussed elsewhere and malaria in Africa was not a priority, much of Southern Africa experienced a lower malaria incidence than they do presently following substantial investment and a renewed political interest.

There are a number of reasons why none of the Southern African countries have eliminated malaria. The dominant vectors, An. arabiensis and An. funestus, are considerably more efficient than their counterparts in North Africa and breeding sites harder to map than on islands. Insecticide resistance, behavioural adaptation and changing species dominance have posed challenges to IRS campaigns across the subregion (Enayati and Hemingway, 2010). Compared to North Africa, southern African countries have been considerably poorer and have realized independent governance representing the majority of the population much later. The continued presence of asymptomatic carriage among semi-immune residents and the constant introduction of new migrant infection render elimination particularly difficult even with the most aggressive combinations of active and passive surveillance. Towards the end of the attack phase of elimination, mass screening and active surveillance of populations who are likely to harbour infections asymptomatically through acquired anti-parasitic immunity is necessary. With the exception of South Africa, all other southern African countries have not mounted active surveillance since the 1960s, and the slide examination rates for presumed clinical cases have been poor. During a pilot approach to active screening in the southern part of Zimbabwe in the early 1960s, it was recognized that this is an expensive element of the attack phase of elimination, demanding skilled human resources and a carefully sensitized population (Wolfe, 1964). Prolific cross-border seasonal migration from neighbouring highly endemic countries such as Angola and Mozambique continues to pose a larger threat to interrupting transmission in Namibia and Swaziland and South Africa. In recognition of the subregional threats, initiatives have started across borders including the LSDI (Mozambique, Swaziland, South Africa) (LSDI, 2007; Sharp et al., 2007), Trans-Zambezi Malaria Initiative and the Trans-Kunene Initiative (SARN, 2011).

Recent progress in reducing case incidence has prompted the Ministers of Health in the subregion to launch the Africa Malaria Elimination Campaign supported by the African Union (AU) and the Southern Africa Development Community (SADC). The concept of the Malaria Elimination 8 (E8) was proposed and signed as the E8 Windhoek Agreement in 2009. The countries on mainland Africa that constitute the E8 include those regarded as having the greatest potential to eliminate malaria by 2015: Botswana, Namibia, South Africa and The Kingdom of Swaziland and second line neighbours Angola, Mozambique, Zambia and Zimbabwe (E8, 2010).

4.5.4. The double dip recession

Accounts of current emerging changes in the epidemiology of malaria sometimes give the impression that GMEP was an irrelevance to Africa and that the malaria situation was unchanged from the 1950s until the past few years. In fact, this was not the case; the 1950s, 1960s and 1970s saw dramatic successes in reducing the burden of malaria. These were most obvious at the limits of the malaria map, but declining child mortality (albeit from extremely high levels) and malaria-specific mortality in sites across sub-Saharan Africa in the post-colonial era suggests that a significant degree of control was achieved elsewhere.

The GMEP was a moment of tremendous expectation and brought into sharp relief the burden posed by malaria across Africa. Rapid adoption of IRS led to impressive declines in disease incidence in almost every area where this control approach was taken to scale in the North, the South and the islands of Africa. In addition to vector control, the wide-scale availability of and use of chloroquine were probably of major importance. The same was also true at sites where IRS and prophylaxis were introduced under pilot schemes in sub-Saharan Africa. What emerged was that despite huge reductions in disease burden, transmission in most settings was not interrupted within the few years that the GMEP had hoped to eliminate malaria. Against a waning enthusiasm for elimination in Africa, countries located at the margins, nonetheless, continued to pursue carefully coordinated elimination strategies after independence from colonial rule.

By 1979, no part of North Africa was considered to be subject to stable P. falciparum transmission, Réunion was certified malaria free in 1975, Mauritius was P. falciparum free (despite reintroduced P. vivax), malaria risks were exceptionally low on one remaining island of Cape Verde, Madagascar had achieved near interruption of transmission across the highland provinces and the spatial margins of stable risk had reduced significantly in Zimbabwe, South Africa and the Kingdom of Swaziland by 1979 (Fig. 4.20B). However around the late 1980s, things began to unravel. The years leading up to 1999 saw a precipitous rise in disease incidence in Southern Africa and the islands where P. falciparum transmission had been reduced to barely detectable levels in 1979 had returned to stable endemic levels (Fig. 4.20C). Because of pre-emptive, earlier elimination achievements, North Africa was largely protected from the re-expansion of stable transmission, although it is notable that the Kingdom of Morocco and Egypt witnessed resurgent P. vivax risks during the same period. Thus, rather than being the baseline against which we should measure what is happening now, the 1990s should probably be regarded as an exceptional period in which malaria was on the rise following a period of control, albeit limited, in many parts of Africa.

The reasons for this are probably multifactorial: because interest in malaria control had fallen off the international agenda since the late 1970s, effective new tools such as impregnated bed nets failed to be taken up. In areas that had enjoyed protracted periods of effective control populations were naive to the clinical consequences of infection having failed to develop collective immunity. In many areas, especially those where vector control had never been widely applied, the widespread use of chloroquine had probably played the major role in controlling morbidity and mortality which began to be lost with increasing drug failure. The result, beginning in the late 1980s and early 1990s, was a wave of increasing malaria incidence and deaths in many countries, including those located at the margins of stable transmission. A rise in incidence was seen across large parts of Southern Africa and the highland fringes of East Africa and Madagascar, and there was a stalling of progress towards elimination in North African countries yet to achieve a malaria-free status (Morocco, Egypt, Algeria). At the same time, malaria mortality was rising across many parts of sub-Saharan Africa and in some areas may have doubled. By 1999, the international community had recognized the need for global action with a focus on Africa, new funding was made available and the subsequent 10 years led to the re-establishment of effective control operations in Southern Africa and the African islands leading to a renewed contraction of stable endemicity by 2009 (Fig. 4.20D).

Thus, it seems plausible that the public health burden of malaria across much of Africa south of the Sahara witnessed a substantive decline following the Second World War. These achievements were probably sustained through the 1970s and early 1980s, and at some point towards the end of the 1980s into the 1990s, malaria incidence began to rise reaching, in some areas, pre-1940s levels by the late 1990s. Since 2000, evidence exists of a declining incidence of malaria in many (though by no means all) parts of Africa. It is reasonable to assume that the first “dip” in malaria in Africa was largely related to deliberate attempts at control; certainly, this was the case at the limits of transmission. Similarly, the massively increased investment in malaria control must be playing an important role in the second or “double dip” in malaria. However, it is also important to recognize that there may be other factors at play; in several areas, it is clear that the beginnings of the current decline in transmission considerably preceded the widespread application of new investments in control and that these are insufficient to explain the timing and degree of the changes. Many factors, including climatic, socioeconomic, and biological factors, could potentially be lending a hand to the undoubted effects of vector control and availability of effective drugs. Understanding these factors is important because whilst they seem to be moving in the right direction at the moment, there is no guarantee that this will always be the case.

4.5.5. The future

The past few years have seen renewed international commitment and investment in global malaria control. Its successes have led to a new optimism and a refocussing of the world’s attention on the importance of eradication as the long-term goal of our efforts. At the same time, there has been concern that Africa may once again be neglected and financial resources for a global programme diverted from high-burden countries to support shrinking the malaria map at the low-risk margins of the world outside Africa. Against this back ground, there are certainly many lessons to be drawn from the long experience in Africa of attempts at malaria control and elimination, and we have attempted to bring together for the first time in this review this accumulated experience in some depth. Although it is clear that the final steps to elimination, even in apparently favourable circumstances are difficult, prolonged and susceptible to setback from many causes, perhaps the most important point for the future is that reducing malaria to a minor problem in terms of disease or deaths is an inescapable point on the way to elimination. Here, the repeated lesson from control programmes around Africa is that this can be achieved remarkably quickly, and this should be the unremitting focus of African and international efforts until it is achieved.


This chapter is the result of funding provided by the Wellcome Trust, UK as part of fellowship support to RWS (079080) and AMN (095127) and the Wellcome Trust Core Grant to the Kenyan Major Overseas Programme (092654)

This review has only been possible with the gracious help and assistance provided by librarians and archivists in Europe and Africa particularly the library staff at The Wellcome Institute, London; the Institute Pasteur, Paris (Agés Raymond-Denise, Catherine Cecilio, Daniel Demellier and Dominique Dupenne); the Institute of Tropical Medicine, Antwerp (Dirk Schoonbaert); Sapienza—Università di Roma, Rome (Gilberto Corbellini, Mauro Capocci); Instituto Higiene Medicina Tropical, Project RIDES CPLP, Lisbon (Virgílio do Rosário, Susana Nery); the World Health Organization library in Geneva (Marie Sarah Villemin Partow), Sudan Civilization Institute, Khartoum (Jaffar Mirghani, Alaa Moawia); Wellcome Library, National Public Health Laboratory Service, Nairobi (Anne Mbeche); National Institutes for Health archives, Amani (William Kisinza, Jumanne Gwau, Japhet Kimbesa). Of additional note for acknowledgement are the invaluable on-line library resources provided by Armed Forces Pest Management Board Defense Pest Management Information Analysis Centre Literature Retrieval System—AFMIC Library: http://lrs.afpmb.org; the World Health Organizations malaria and country report repositories: http://whqlibdoc.who.int/malaria/; Inter-university health library, Paris, France: http://www.biusante.parisdescartes.fr/debut.htm; South African Medical journal archives: http://archive.samj.org.za/index.php and the Institute of Tropical Medicine, Antwerp, Belgium http://lib.itg.be. The authors are also indebted to malariologists, surveillance officers and malaria control programme managers from across Africa including; Joana Alves (Cape Verde), Rajae El Aouad (Morocco), Richard Kamwi and Benson Ntomwa (Namibia); Simon Kunene and Joseph Novotny (Swaziland); Philip Kruger, Aaron Mabuza, Marlies Craig, Rajendra Maharaj and Karen Barnes (South Africa); Abdulla Ali and Justin Cohen (Zanzibar); Jean-Francois Trape (Senegal); Richard Cibulskis and Ryan O’Neil (Algeria and Botswana); Hawa Guessod (Djibouti); Milijaona Randrianarivelojosia (Madagascar), Jean-Louis Solet (Mayotte and Réunion); Ghasem Zamani and Hoda Atta (Morocco and Egypt) and especially our gratitude to Frank Hansford for his detailed descriptions of malaria and its control in Namibia, Botswana, Swaziland and South Africa. Finally, we are grateful for the assistance provided by Clara Mundia for help with proof reading.


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