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Malaria, Medicine, and Melanesians: Contested Hybrid Spaces in World War II

Judith A. Bennett


During the Pacific War malaria threatened the contending armies in western Melanesia, as they lacked immunity to the disease. These invaders created new hybrid spaces of interaction with the Melanesians who were hosts to the malarial parasites. They employed a variety of techniques to control the vector malaria mosquito and its habitat. The United States malarial experts also tried to control the Melanesian 'seedbed' of malaria parasites by regimes of drug suppression, a technique rejected by the Australians in New Guinea, because they believed suppressants could adversely affect native health. Despite this, within the hybrid spaces that the Americans shared with the New Guineans, the Australians were forced to comply with American preference since they were under United States' command. Despite the Australians' initial concerns about the consequences of this course of action, there was a failure to monitor the results for the health of the Melanesians who indeed deserved better.


From Bora Bora near Tahiti across to Buna in Papua, the war in the Pacific brought enormous, if transient, demographic change, as tens of thousands of Allied troops garrisoned the islands. In western Melanesia—in Papua, New Guinea and Solomons—the Allies confronted thousands of enemy Japanese.1 Long the home of perhaps 1.5 million people, these islands had only about 5000 scattered foreign inhabitants when war began in December 1941, and most fled.2 The troops occupied many areas that had never had substantial European or Asian populations. To wage their war, the newcomers rapidly created new hybrid spaces—alien but porous enclaves. The hybridity of these spaces was evident not only in the re-creation of foreign structures and routines, adapted to local conditions, but also in the intermingling of the invaders with the local people and the exchanges of ideas, objects, and organisms. While encompassing aspects of the cultural liminality of Homi Bhabha's 'third space,' a novel state emerging from interactions across dynamic cultures, my concerns are not with issues of identity, but with the materiality of hybrid spaces with regard to disease, its transmission, and habitat. Bhabha transferred the concept of hybridity from biological to cultural interactions.3 Here, I return to hybridity's biological connection, not in terms of miscegenation, but regarding organisms active in and among humans, while recognising cultural factors framing interventions in biological as well as epidemiological processes. 1
      Whilst they all fought the Japanese, the Allies in this region—consisting of Americans, Australians, and a small force of New Zealanders with Fijians—each did so in differing colonial contexts. In Papua and New Guinea (east New Guinea) the Australians found themselves in their dependencies, whereas the Americans like the enemy, were well beyond the limits of their prewar colonial possessions. This difference greatly influenced interactions within the hybrid spaces each created. Both United States and Australian commanders saw the Melanesians as assets, comprising labourers, guides, fighters, spies, and suppliers of resources, but soon realised that they were also a liability because of the enemy they carried within: the disease of malaria. Malaria and other endemic diseases came to the forefront of medical interest because they could make or break the war effort. However, because of their different relationships to this particular warzone, Australia's and the United States' strategies in dealing with this vital issue were not the same. The distinct approaches rested fundamentally on the knowledge that the Americans, once the war was over, would leave, whereas the Australians were in east New Guinea for the duration and into the foreseeable future. 2
      Mosquito-borne malaria was endemic in the Pacific in the zone west and north of Buxton's line—170 degrees east longitude and 20 degrees south latitude—including New Guinea, Solomons, and the New Hebrides.4 Malaria takes four forms, reflecting the effects of specific parasites in the blood: Plasmodium falciparum, P.vivax, P. malariae, and P. ovale. Of the four forms, only the first two were medically significant in this area. Vivax was formerly called benign tertian malaria, as fevers commonly recurred in a three-day cycle. In non-immunes, vivax malaria causes intermittent high fevers alternating with chills, profuse sweating, and severe headaches. Extreme weakness is a persistant feature, and there is also often abdominal pain and respiratory problems. It is a debilitating infection due to the destruction of red blood cells, and, even if treated, it commonly recurs. Untreated, falciparum malaria—formerly called malignant tertian—is more severe in non-immunes, and is usually fatal three to four weeks after the first infection.5 Female mosquitoes of the genus Anopheles transmit the plasmodium parasites from the infected to uninfected human host, by biting.6 3
      In their small, distinct communities Melanesians had learned to live with malaria. Adults, host to malarial parasites, had evolved or acquired a degree of immunity, apparently through gene mutation and a cluster of antigenic factors.7 In most coastal areas malaria was hyper-endemic. Those who lived above about 1500 metres had less immunity than coastal people, possibly because the intermediate populations were sparse and less able to maintain exposure to parasites that stimulated immune responses.8 Those who lacked such protection appear to have died early, reinforcing natural selection. Estimates of mortality from malaria in children under five ranged from 40 to 60 percent.9 Nonetheless, those who had become semi-immune or resistant to the parasites survived. Constant re-infection was needed to maintain this semi-immunity or 'premunition.' Adult Melanesians sometimes suffered bouts of fever and occasionally died of falciparum malaria but, compared to non-immunes from areas where Anopheles and malaria were not endemic, they were relatively free of malaria's worst effects. Some researchers also believed that the people within their specific locale had semi-immunity or 'communal premunition' to the localised strains of malaria, which was less effective elsewhere.10 4
      Prior to colonialism, in the varied ecological niches that Melanesians, Anopheles, and the malarial parasites occupied, the three had generally coexisted somewhat in a state of equilibrium; colonial intrusions in some areas had begun to disturb this. To make them easier to oversee, missionaries and administrators sometimes urged the replacement of more dispersed hamlets with consolidated coastal settlements. More significant was the temporary relocation of labourers to European plantations, mines, and Christian mission stations, the first long-term hybrid spaces in Melanesia.11 The Europeans soon observed that natives who were moved from inland areas to the coast became more susceptible to malaria.12 Such increased mobility in the post-European contact era also had begun to unsettle established patterns of limited interregional and intertribal contact determined by formidable geographic barriers and ancient enmities. Before the war came to their islands, however, the effects of these movement patterns were not yet too severe, with Melanesians still living much of their lives in their natal environments. 5
      To assert even a tenuous presence in this alien biological landscape, the early colonial Europeans in New Guinea had established several malaria-coping strategies including the use of quinine and mosquito nets; draining of their small settlements; distancing of themselves from native housing; and clearance of vegetation near residences, built to maximize sea breezes. A few seem to have developed semi-immunity. Malaria killed some and forced others to leave, while most sent their children overseas for education and safety.13 Colonial administrations before World War II undertook little research on malaria. Resources were devoted to establishing an administrative presence among the multitudinous small societies in the Australian territories of Papua and New Guinea, the British Solomon Islands, and the Anglo-French Condominium of the New Hebrides; and even for this, the available money was scarce. Australia in Papua and New Guinea saw little reason for a great deal of investment in this goal.14 It took on Papua as a Protectorate from Britain in 1906 and, after gaining the Mandate of New Guinea in 1920, Australia believed its vulnerable northern borders safe from unfriendly Europeans and the 'Yellow hordes' in Asia. Its occupation remained largely a strategic 'holding operation,' not a guarantor for some massive capitalist enterprise.15 Furthermore, Australia expected the dependencies to pay for themselves; the most ever spent in any one annual grant was £60,000, mainly in less-productive Papua.16 Though a good proportion of expenditure was allocated to health services, the Australian administrations could achieve little among a scattered population.17 They reduced tribal fighting and, when patrols came about once a year to villages, carried out basic medical procedures, as well as subsidising the medical efforts of the Christian missions. Much the same could be said of the administrations in the smaller Solomon Islands and the New Hebrides.18 With little background work on which to build, therefore, malaria proved to be an enormous challenge for the wartime entomologists and malariologists. Prior to the war, for example, visiting researchers had identified only thirty species of mosquito in the Solomon Islands; by the end of the war, United States entomologists had identified seventy on the island of Guadalcanal alone.19 6
   

Encountering malaria

 
To block the rapid Japanese expansion southward, the Americans sent forces to the New Hebrides and Guadalcanal. These went in ahead of malaria-control personnel who only began to be effectively centralised across the navy and army in late-1942.20 Initial ignorance at command level did not help. A commander on Efate, New Hebrides, confronted by a malaria specialist's directions, countered with, 'We are out here to fight troops, and to hell with mosquitoes.'21 Such views were tempered, however, when the scope of the problem emerged. On coastal Efate, one of the most malarious of the United States bases, rates in April 1942 reached over 2,600 cases per 1,000 per annum.22 A similar pattern was recorded on Guadalcanal in November when the first small group of malarial control personnel arrived, a few months after the United States established a beachhead.23 7
      The Australian forces were no better prepared, and initial infection rates among troops in Papua and New Guinea were high. When, for example, units of the Australian Imperial Force (AIF) landed at swampy Milne Bay, malaria-fighting equipment was lost. Control was minimal, with cases peaking at 1,000 a week in December 1942. With a shocking rate of 4,200 cases per 1,000 per annum, one-third of the AIF had been treated.24 8
      Australia's failure was partly due to a lack of supplies including various malarial suppressants, which control malaria symptoms, although do not eliminate the infection. A major source of quinine, derived from the bark of the cinchona tree, was no longer available since the loss of Java in Dutch East Indies to the Japanese, and the synthetic anti-malarial suppressants—atebrin25 (Atabrine) and plasmoquin—were hard to obtain and the optimum dosage regime and side effects were still uncertain. Futhermore, the European conflict was substantially advanced by 1942, so mosquito netting was scarce. So too, in the pre-DDT days before 1944, was the insecticide pyrethrum. Poor anti-malaria discipline among troops exacerbated the problems. The commander of the AIF, General Sir Thomas Blamey, aware of the worsening situation in 1942, advised the government to send a delegation, including Australian malariologist, Colonel Neil Fairley, to Washington and London to remedy supply problems. 9
      In the first eighteen months of the campaign, Australian scientists, led by Fairley, cooperated closely with American researchers headed in the United States by Dr. James A. Shannon and in New Guinea by Lt. Fred Bang. They learnt much about malaria's epidemiology and the most effective dosage of the malarial suppressant, atebrin, which had also become standard for the Australian forces in December 1942. In mid-1943, the Australian army established a research unit at Cairns where Fairley began experiments on army volunteers. Spurred on by E. Ford, assistant director of pathology in the Australian army, and by Fairley's work, General Blamey gave support by May 1943 to an intensified assault on malaria, as it was now a military problem. Malaria discipline became part of the Australian troops' routine orders, although the most effective dosage of atebrin remained unclear.26 At about the same time, the United States malaria field control organisation became fully operational, and enjoyed mixed results. In the South West Pacific command, divided medical authorities hindered effectiveness, whereas in the South Pacific the joint services' malarial organisation under one area commander—such that a Malaria Survey Detachment and Malaria Control Units worked with the support of the Construction Battalions (Seabees) and Army Engineers27—performed better.28 (See Map 1 for command regions.) Similar units were developed in the Australian forces in May1942.29 10

 
Map 1
    Map 1: South West and South Pacific commands. Map developed by Bill Mooney for author.
 
 
   

Multiplying malaria and counter attack

 
Prior to World War II, human mobility in western Melanesia had been confined to limited traditional trade interactions, a trickle of foreigners, and the circulation of several thousand local labourers. The war hugely magnified the scale and character of such movement. A deluge of incomers, intensified migrations of labourers, and the relocation of native communities in operational areas suddenly perturbed the islands. Hybrid spaces of encounter proliferated because of this movement of human hosts from the disparate coastal and inland societies, amid the progress of great armies across an extensive operational front. As ever, malarial parasites and vectors operated to delineate the biological landscape. 11
      Alteration of the environment by the military intensified the work already begun by early colonisers in destroying the ecological equilibrium between indigenous host humans, vector mosquito hosts, and malarial parasites in a number of ways. The presence of hundreds and often thousands of non-immunes among the Melanesians introduced a capacious source of blood meals for the vector mosquito and thus expansion in parasite numbers, even when the vector's numbers remained stable.30 Especially in the early campaigns, when troops did not take atebrin or took an insufficient dosage, the parasites in the blood were not fully controlled. The records are silent on the impact of higher parasite numbers among the Melanesians; but it is likely that they experienced more infection, and thus more chance of malarial symptoms breaking through their partial immunity. 12
      Military activity served up not only food but also an expanded habitat for Anopheles. An entomologist in the New Hebrides calculated that 90 percent of all mosquito breeding came from this.31 Site clearance and logging operations blocked streams, creating new breeding places, as mosquitoes need water in which to deposit their larvae.32 Shell craters, borrow pits, fox holes, slit trenches, and miles of ruts made by jeeps and heavy vehicles created perfect breeding conditions around bases, especially for the common carrier, Anopheles farauti. In New Guinea, clearance for camp construction, roads, and airfields expanded the habitat for the common vector Anopheles punctulatus, which likes sunlit breeding areas.33 More challenging for the control units was the discovery by entomologists that mosquitoes had adapted to their immediate environment: A. punctulatus on Guadalcanal thrived in conditions practically the reverse of those in New Guinea.34 13
      Units assigned to malaria control implemented several measures to counter mosquito-borne diseases, some involving environmental manipulation to control the vector's habitat. As soon as practicable after occupying a beachhead, the malaria units located camps as far from mosquito-breeding sites as possible. Yet in operational conditions this was often unrealistic. The strategy was to eliminate the mosquitoes' breeding habitat. Engineers advised on drainage systems and filled in swamps. Explosives unblocked waterways. Streams were dammed and then released to flush out stagnant waters. To sluice out coastal backwaters and lagoons with constant tidal flow, engineers installed flumes. The units cleaned weeds from the surface of sluggish water, an ideal habitat for certain species. Where standing water could not be dealt with using these methods, the units applied larvicides and insecticides to surfaces, in some areas by airplane. The fish minnow, Gambusia affinis, was introduced to prey on larvae.35 14
      Armed with posters, lectures, and films, malaria units conducted education campaigns to persuade the troops to adopt preventative measures against mospuito bites—they urged them to use mosquito nets, keep skin covered, and apply mosquito repellent. Military discipline reinforced education, and around camps the entomologists mapped 'hot spots.' To control 'man-made malaria,' units policed the disposal of cans and other receptacles that could hold water. Holes were filled and the miles of heavy vehicle ruts around camps, ammunition dumps, and fuel tanks farms were disc harrowed—although distant areas such as logging sites were often missed.36 15
      Coupled with this was the administration of regular malaria suppressants, which could hold the symptoms at bay. Many men believed, however, that atebrin lessened sexual potency, and others feared the yellowing of their skin from the dye indicated liver damage—neither of which was true—and in the early phases of the war many took the tablets but did not swallow them or otherwise avoided the dose. As epidemics hit different bases, officers were ordered to make sure men swallowed atebrin and outbreaks declined.37 16
   

Rearranging space: Seedbeds of infection

 
These strategies were not the total solution, however. For the military, the bodies of the native population also posed a dilemma. In their eyes, the local people were a major source of infection and this remained a dominant trope in all United States medical thinking.38 In the New Hebrides, Solomons, and New Guinea, it was reported, 'natives are ... to be feared as a seed bed of malaria.'39 Yet, the military needed their labour. The Americans calculated that to keep one soldier at the front, whether 'combatantly or logistically,' required ten behind the lines.40 Local substitutes reduced expenditure for transport, training, upkeep, and pensions. The Americans so needed labour that they worked hard to maintain amicable relations with the people and with the colonial administrations.41 17
      Before the war, such labour had been pivotal to the cash economy of these territories, and so some care had been taken to develop strategies for dealing with the malarial problem with respect to the local people. Plantation labourers were not dosed regularly with quinine, as were Europeans, but planters often treated labourers' severe, acute attacks. An established medical and lay opinion was that 'the quininisation of native people' would alter their natural partial immunity, rendering them liable to massive infection and symptoms.42 This principle, first enunciated in the 1920s, had been accepted by malariologists in Africa and Asia in the 1930s.43 Medical opinion also held that adult natives from the Highlands in New Guinea or inland hills in the New Hebrides were more likely to suffer severely from malaria if they came to the coast than would their 'salt water' neighbours.44 18
      During the war, one solution to the 'seedbed' problem that was in keeping with this prior thinking was to rearrange the hybrid space so that Melanesians were at a safe distance from the camps—beyond the mosquitoes' flight range—and to control native movements within that space. Another, however, was to attempt to reduce the parasitemia rate in Melanesians near camps by medication, and thus make them less infectious. These strategies took time. In September 1942 in the New Hebrides—where the United States bases at Efate and Espiritu Santo, established in early 1942, were to remain behind the lines for the duration—the Malaria Control Unit had been alarmed that native camps were scattered among military units at the beginning of the dry season. After surveys, malariologist James Sapero predicted that, when the rains came, 'these heavily infected natives will produce a malaria rate of alarming proportions.'45 His recommendations led those in charge at Espiritu Santo to implement the consolidation of labourers into three camps where they were supervised, tested for malaria, and put on a regime of suppressant atebrin.46 They were then sent home in early 1943.47 Santo thus escaped the high malaria infection rate that bases at Efate and Guadalcanal suffered. By early-1943 this regime was also being applied to nearby plantations where Melanesian and Tonkinese labourers were heavily infected. Native dwellings were sprayed regularly with insecticides, including DDT after its introduction in early 1944. From 1943, natives of forty villages in the extensive troop training areas were also dosed weekly with 0.6 grams of atebrin. Among the hundreds treated, a noticeable decrease was recorded in levels of the virulent Plasmodium falciparum parasite.48 19
      Near the front, the Americans found it more difficult to institute suppressive therapy. On Guadalcanal when they landed in August 1942, the commanders knew that the natives carried malaria parasites yet they judged the 'gravity of the tactical situation required all available troops on the firing line' and so, with British help, they recruited local labour for unskilled work.49 For over six months, operations caused
troop mobility and dispersion [to be] necessarily based on tactics and not on sanitary conditions; a great deal of vital nocturnal activity; difficult logistics ... enemy action ... , and combat tension when the chief concern is not malaria control but immediate life and death.50
 Even the Malaria Control Units in May 1943 had to concede, 'The natives are essential for labour and ... for the present ... they must be tolerated even though they are malaria carriers.'51		 20
      In April 1943, after the Japanese retreat, surveys had revealed 85 percent of native labour to have enlarged spleens and 14 percent, blood parasites; and so the Malaria Units began administering suppressant atebrin.52 In addition, entomologists had found that adjacent villagers were far more dangerous than labourers, as they had a much greater parasitemia rate. This rate reflected the higher incidence in infants and children than in adults, and the probable selectivity in hiring healthy men for the Labour Corps. The entomologists urged that these villages and the labour camps be moved away from the troops. Four camps were within one mile of 40,000 United States troops, and the American experts thought that Anopheles could fly that far.53 (See Map 2.) United States Service Command, however, wanted them near to save on transport—here and elsewhere the colonial authorities did not want the labour camps out of their sight. 21

 
Map 2
    Map 2: North coast of Guadalcanal, indicating Solomon Islands Labour Corps camp locations, 1943–4. Maps developed by Bill Mooney for author.
 
 
      Despite these protests, the Malaria Control Organization had the ear of the United States high command. Naval orders in July 1943 were explicit about rearranging space:
In every base consider the question of proximity to mosquito-breeding area. One mile is the minimum distance which is reasonably safe, two miles is preferable. Experience has shown that the same holds true for native villages ..., as these are prolific sources of infection. If the site of a native village is the only one suitable for the base, the village should be moved.54
 Although orders went out to remove the nearby camps in January 1944, however, flooding and costly road construction caused delays until August. So, for almost two years after the Americans had landed on Guadalcanal, though villagers initially had fled, the proximity of native labour meant the 'seedbed' was ever present. Here, as elsewhere, the main strategy was to confine natives to camp from sunset to sunrise, when the entomologists calculated Anopheles to be active, and when labourers worked at night they had to cover their skin.55 As an additional measure, while villages near camps were relocated, more distant which ones showed equally-high levels of infection also were placed on atebrin regimes. Villagers readily complied, probably because they saw the Americans, whom they admired,56 swallowing their own doses.57 It is worth noting here that, despite concerns with respect to their own troops about the toxicity of atebrin, and the medical profession's uncertainty about the dosage, the American malariologists did not consider how a suppressant regime might affect the long-term semi-immunity of the Melanesians.58		 22
      To summarise the course of the Americans' malarial experience in Melanesia: initially the Americans could not avoid being in close proximity to infected Melanesians, prisoners, and United States and Japanese troops at the front line; however, their management of the disease improved as the campaigns moved west from early 1943 in the Solomons to the Russell Islands and Munda. By the time the United States landed in the Northern Solomons in late 1943 and Manus in 1944 improved malaria control and medication, plus the absence, removal, or containment of Melanesians, meant the rate of malaria infection was far lower than initially on Guadalcanal.59 The British, for example, supervised the Solomon Islands Labour Corps camps on Hombu Hombu islet, off shore from the United States Munda base.60Those who worked for the Americans were ferried from Munda for the night and subjected to atebrin suppressants.61 Command had succeeded in managing the temporary hybrid space, with its threat from the 'seedbed,' by excluding Melanesians. 23
   

Contrary views: Reservoirs of pathology

 
The Australian wartime experience in Melanesia was necessarily quite different from the Americans'. While United States' occupation of western Melanesia was transient the Australians' military presence created more lasting hybrid spaces. Many of these would probably endure because New Guinea—on Australia's doorstep—had proved its strategic significance and would demand more administrative attention. Its wartime administration, the Australian New Guinea Administrative Unit (ANGAU), had the often-conflicting responsibility for organising civilians as well as labour for the Australian army and plantations. Most ANGAU officers had been members of the two prewar administrations and were now part of the AIF. Like their United States counterparts, they wanted to reduce the incidence of malaria by separating the 'natural reservoir of malaria'—the Melanesians—from the troops.62 Yet the AIF knew, 'No boong, no battle.'63 Many battlefields were located in mountainous terrain, accessible only by foot. As the AIF pushed north, native carriers could not be segregated, as they were moving in tandem with troops as escorts in a mobile hybrid space. Natives served alongside Australians in army units and as carriers, guides, intelligence agents, and 'coastwatchers.' Moreover, villagers regularly bartered fruit and curios with the soldiers.64 Rearranging space with quarantine zones would have been futile. Especially in 1942–3, when the outcome of the conflict hung in the balance, native assistants were a bonus because of their partial immunity to malaria since 'without taking any precautions they can go into highly malarious country that would destroy Australian, American or Japanese Forces under similar conditions.'65 24
      In contrast with the Americans' use of medicines along with segregation, ANGAU and the Australian military preferred to combat malaria primarily with environmental controls, and, when practicable, the semi-quarantine of infected natives.66 In early-1943, Col. Fairley fleetingly suggested that suppressant regimes could be tried on labourers, since 'all should be assumed to be infected'; but this did not eventuate. Instead ANGAU and the army used spatial segregation.67 After the AIF's initial advances, malarial discipline improved; but it was not until early-1943 that a push was made to separate army camps from labour camps and villages to obviate infection.68 Even so, as with the United States forces on Guadalcanal, '[h]ard and fast rules' could not always be adhered to, because carriers' camps needed to be near the units they were serving. For the Australian entomologists, a safe distance was at least a half a mile. The malaria units often found siting a new base difficult. As the Americans found in the Solomons, the best and healthiest places were already village sites.69 However, since ANGAU had 60,000 native refugees to keep away from battle zones, it had no hesitation in relocating villagers away from camps.70 25
      ANGAU also had enormous control over labour. So great was the Japanese threat that ANGAU conscripted tens of thousands of native labourers.71 Its officers' discourse reflected both control and responsibility. In this dual role, ANGAU was less fearful than the Americans of the disease threat of the labourers and villagers, but much more concerned about the effects of war-induced diseases among Melanesians with no loyalties to Australia.72 Army doctors with prewar experience in New Guinea also feared that the influx of non-immunes would induce a 'migrant malaria' epidemic in the population.73 Australian medical officers saw the native body as a 'reservoir' of pathology,74 and not a 'seedbed of infection' as did the Americans. This subtle difference suggests that the Americans perceived the native body as being a place where disease thrived, and possibly outside of their control; ANGAU saw the native body as a container of disease, which ANGAU did control because of its wide powers and experience.75 26
      ANGAU's experience, however, taught that control could not stem simply from force. War's needs gave its officers a singular opportunity to expand a skeletal medical system into a Health Directorate, with less regard for costs than in peacetime. To keep the labour force healthy, and meet the demands of a dysentery epidemic among villagers, ANGAU developed a core of medical officers; expanded teams of 'European' medical assistants and trained over two hundred men as native medical orderlies; established fifty-three district hospitals; and instigated basic medical intervention for thousands of Melanesians.76 ANGAU, in these novel hybrid spaces, saw Western medicine as a means of repaying the debt Australia owed the Melanesians, justifying the colonial presence, and winning allegiance.77 27
      Unlike the United States medical teams, ANGAU remained wedded to prewar practice, treating only acute cases and not administering suppressants:
This [disease] is almost universal and ... too much for this administration to eradicate. Natives as a rule do not suffer to the extent that whites do and they will be treated as their attacks arise.78
 		28
      The prewar administrations and ANGAU had to deal with logistical realities. Drug suppression of malaria was impossible among a dispersed and sometimes truculent population, a view shared by the League of Nations.79 More significantly, they were uncertain of the long-term effects, so followed the precautionary principle:
Natives, particularly native children, cannot be treated with continuous suppression by atebrin, partly because of administrative difficulties and partly because of the resulting interference with the development and maintenance of immunity that will result.80
 By 1945, the Australian army's routine orders were firm regarding the creation of dangerous hybrid spaces: 'Patrols should not camp in native villages as the primitive native sanitary arrangements will probably endanger the health of the troops.'81 ANGAU relocated villagers away from camps rather than administering suppressants.82 At Finschhafen, New Guinea, for example, native labourers were 'kept in a compound' four to five miles from the main camp while, as in many areas, villagers were moved inland.83		 29
      American and Australian malaria specialists met monthly in Port Moresby from February 1943, and so understood each other's practices.84 While ideas were shared, there was no recorded discussion of which approach (or combination of approaches) was better—segregation or suppressants. In spite of the Australian rationale for withholding suppressant regimes, ANGAU, when supplying labour for its United States ally, followed the practice of the Americans at base camps, most commonly where labour or villagers were less than a mile away. ANGAU's knowledge of local conditions was subsumed by more radical United States therapies because military hierarchies brooked few challenges: Australia's General Thomas Blamey, commanding land forces in New Guinea, was under the command of the often-hostile American, Douglas MacArthur, Supreme Commander of the Southwest Pacific. In spite of this fissure, ANGAU worked well with United States forces in the field, accepting the unity of command. The Americans valued its familiarity with the environment, ability to organise labour, and contribution to patrols. ANGAU admired and benefited from the Americans' supplies and equipment. Part of their cooperation meant ANGAU's acceptance of the malaria-suppressant medication given by the Americans to the labourers. The administrations of the New Hebrides and Solomon Islands also cooperated regarding their labour and adjacent villagers, as they were under the South Pacific Command in relation to military matters.85 30
      From the New Hebrides to New Guinea, the United States calculated that, in early 1944, at least 8,146 labourers and villagers were still living within a mile of their forces. All of these were on malaria suppression regimes.86 Where possible, the Americans, with their tendancy for extreme measures, also preferred their removal, especially with heavily-infected villagers. ANGAU removed the entire native population of Emirau Island, New Guinea for the Americans' occupation. When the Americans needed labour, ANGAU brought 180 natives from Mussau Island. It conformed to United States policy by taking only those whose blood tests showed neither malaria nor filariasis parasites, locating these people a mile from the camp, and dosing them weekly with 0.6 grams of atebrin.87 In other United States base camps in New Guinea, such as Milne Bay, the Americans tested the blood of the ANGAU labourers. Those infected had to take plasmoquin daily for a short period, as it could destroy the infectivity of the gametocytes (immature parasites)88 to the vector mosquito, thus breaking the cycle of transmission.89 31
      So enthusiastic were the American Malaria Control Units on Manus in 1944, that they recommended the relocation of a village of 245 people on Ponam islet because the Seabees were having malarial attacks. But ANGAU made a strong case against such action, with several compelling points: (1) The people were fishermen, and would starve if they were placed on the main island, (2) ANGAU could not find another site, and (3) Ponam was virtually mosquito-free. The Malaria Control Unit did find some Anopheles punctulatus, but was able to eradicate these with larvicides, and ANGAU's view prevailed. In the end it was discovered that, rather than these natives being the 'seedbed' for the troops, the reverse was in fact the case. Brought forward from other bases in the malaria zone, the Seabees were 'so highly seeded' with parasites that they were a threat to the natives until put on a strict regime of atebrin.90 Vanity had got the better of some of the men who, believing that they were about to be sent home, and not wanting yellow skin, had covertly taken themselves off atebrin.91 32
      This incident with the Seabees demonstrated that hybrid spaces of Melanesia created opportunities for the 'seedbed of infection' to encompass foreign troops. The American emphasis on separation plus the sanitisation of the native body with suppressants did not fully overcome the problem of malaria infection in its troops; yet this treatment policy was forced on natives controlled by ANGAU whenever they operated in the same spaces as the Americans. The Australian-preferred approach of non-medicalised intervention for the 'reservoir of malaria' was more protective of the long-term health of the Melanesians, but disregarded by the Americans who asserted military control of these hybrid spaces. 33
   

Pushing the malarial advantage

 
Beyond merely developing their anti-malarial techniques as survival strategies, the Allied forces aimed to maximise their malaria discipline to use the disease as a weapon against the enemy; malaria, as a consequence, contributed to the defeat of the Japanese. In spite of initial successes, the control of war's hybrid spaces in Melanesia by the Allies' enemy contracted rapidly. Although data are incomplete, surviving records documenting extremely high malaria rates among the Japanese, often resulting in death—especially in combination with other medical conditions—give some picture of what Allied observers witnessed. By February 1943, the Americans had driven the Japanese out of Guadalcanal, with 65 percent of Japanese having been lost. About 30 percent of those deaths were the result of malaria and other diseases, coupled with starvation.92 In the Bismarck Archipelago and the Solomons, the Japanese malaria rates in February 1943 reached 1,637 per 1,000 per annum and were still climbing; at Rabaul in the same month they reached 2,053 per 1,000. These rates were no greater than those suffered earlier by the AIF and the Americans, but the timing was of utmost significance. In 1943 and 1944, it was not only the failure of Japanese medical systems, when the Allies were consolidating theirs, but also the collapse of Japanese logistics that conspired with malaria so cruelly against the Allies' enemy. Few vessels reached the islands, leaving the Japanese lacking in medical supplies and suppressants.93 Moreover, they had relied more on quinine in combination with atebrin, than on atebrin alone.94 The Allies' loss of Java to the Japanese had been 'a blessing in disguise' because atebrin was far superior to quinine as an overall suppressant and, for much of the war, an eradicant for falciparum.95 In addition, the treating of associate natives with suppressants in the way that the Americans had, was never a possibility since the Japanese could not even cater for their own. This factor, too, had been highly significant, since the Japanese, far more than the Allies, had depended on local labour and produce, obtained in time by force. Taking none of this for granted, the vital role of the disease in their war in the Pacific was certainly not lost on the Allies:
Malarial discipline is an offensive weapon of great power. In exact proportion to the superiority of our troops' malarial discipline over the enemy's, so we decrease sickness and increase our reliable manpower and fire power. Malaria under these circumstances fights for us and against the enemy.96
 		34
      For United States and Australian forces, early infection rates had been high, but mortality rates were low. In the United States army alone, 219,937 cases of malaria were in the Pacific theatres—a huge loss of man-days—but they only suffered 157 deaths. The AIF mortality rate was 0.05 percent, and the New Zealanders recorded no deaths among their 11,000-strong force. The potential death rate for non-immunes can be gained by considering the fate of eight hundred malnourished Japanese prisoners taken from non-malarial Nauru and imprisoned at Fauro in the Shortland group: an epidemic of malaria carried off two hundred.97 The Japanese estimated that 10 percent of their men died of malaria in New Guinea.98 35
   

Miscalculating malaria

 
In spite of their superior approach, however, the Americans found their control was constrained by malaria's epidemiology. They were 'dealing with a dual ecological problem—with a parasite and its environment on the one hand and an insect and its environment on the other; and a knowledge of both is essential to a balanced, effective plan of control.'99 They understood how to modify the environment to make it unsuitable for mosquito breeding, but they needed to know how the drugs affected the human habitat of the parasites, and this was less clear in 1942–3. The Americans were unconcerned about the impact of atebrin on Melanesians, and so continued their regime of drug treatment for local populations; yet many believed that administration of the drug long term might be a danger to their own troops, and so eventually began to concentrate on perfecting environmental controls by manipulating military and hybrid spaces. 36
      One of their worst early miscalculations, however, was premature cessation of atebrin, or 'demalarialisation,' which was practised not only when units left the malaria zone,100 but also within that zone when malaria rates fell. As historian Benjamin Bacher has written,'[t]he results of this experiment were appalling.'101 On Efate, when rates fell from 2,600 per 1,000 per annum in April 1942 to 144 per 1,000 per annum, atebrin suppression was withdrawn; but the rate climbed to 521 per 1,000 per annum in November, so atebrin was reinstated.102 This demonstrated that atebrin could suppress P. vivax, but was no cure. By 1944, however, the malaria researchers had found that it did eliminate the most dangerous form of malaria, P. falciparum, provided there was no re-infection.103 For men returning home, P. vivax relapses were common. The disease often recurred for years, until treated with new, more effective drugs that eliminated the parasite.104 The immediate costs of this demalarialisation mistake for the Americans included over 295,000 lost man-days,105 however, the American Malaria Units failed to question how this process, without any medical monitoring, would affect the health of those Melanesians previously on a suppressant regime. 37
      The attempt to control contact with the 'seedbed of infection,' the Melanesians, had mixed outcomes. Certainly the hope had been to prevent initial infection of troops, but this was a virtual impossibility in operational zones. It was extremely difficult even where malaria control was efficient, as demalarialisation in malarial zones proved. Not only were bases surrounded by a huge natural environment buzzing with Anopheles, but also, against orders, troops sometimes visited outlying villages, just as infected natives covertly slipped into camps to trade curios and war surplus, demonstrating the porosity of these hybrid spaces. Moreover the dosing of labourers and villagers with atebrin suppressants was of limited value, because it did not act on the gametocytes of vivax.106 The gametocytes in humans are not affected by quinine or atebrin alone. Even if drugs destroy all the other stages of the parasite in the blood, falciparum gametocytes remain infectious to mosquitoes for several weeks. However, their infectiveness is destroyed by plasmoquin. This was a rationale for the Australians' continued plasmoquin use after the Americans stopped for fear of its toxicity.107 Atebrin relieved natives (as well as troops) of proneness to attacks of vivax malaria and falciparum and, by mid-1944, research had proved that it could eradicate the latter—but alone it did not stop the spread of falciparum. That would have required the elimination of all vector mosquitoes.108 In the early stages of the campaign, however, to control their potential infectiousness, the United States units gave thousands of natives mass loading dosages of atebrin (0.3 grams for seven days), followed by plasmoquin at the rate of 0.02 grams for five days, reducing the gametocytes dramatically. Although between 0.5 and 2.0 percent of these labourers still showed malaria parasites in blood smear tests, this compared favourably to between 7 and 11 percent before treatment. Their dosage then became a suppressant, at 0.1 grams daily of atebrin.109 It seems that thereafter only those who tested highly positive for malaria parasites in the blood were put on the atebrin/plasmoquin regime before the regular suppressant dose.110 Certainly among United States troops there had been adverse reactions because of the 'appreciable toxicity' of this combination.111 Melanesians suffered toxic reactions too though no specific records survive.112 While Melanesians on suppressants certainly felt better,113 at the time there was no research to show other effects of this therapy—notably on children.114 38
   

Conclusion

 
The war in the Pacific brought thousands of fighting men to western Melanesia where their installations, along with their need for native support, created a range of hybrid spaces—some fixed for the duration, others mobile and following operations. Both as locations of cultural exchanges and infective parasites, they provided unique milieux. Here the risk for Melanesians of increased infection by malarial parasites was significant, because military transformation of the environment gave Anopheles an expanded habitat and food supply, at least until control measures became regularised. Malaria, however, threatened non-immune troops far more than the semi-immune Melanesians. Since its vectors and carriers were initially concentrated within these hybrid spaces, malaria's debilitating effects on the fighting forces were soon manifest. The optimal dosage of atebrin as suppressant for the non-immune military finally emerged from Allied research. In controlling the effects of the malarial parasites in humans, this was responsible for saving thousands of Allied lives, and assisted in their victory. 39
      The impact of the research on the lives of those Melanesians sharing war's hybrid spaces was more equivocal. The Americans medicated the Melanesians—not for the Melanesians' benefit, but to better protect themselves from this 'seedbed of infection.' On this, the archives speak to us through their silences. Despite concerns about the effects of suppressants on their own non-immune troops, illustrated in 'demalarialisation' and cautious use of plasmoquin, the Americans never considered how their suppressant drug regimes might affect the long-term health of semi-immune Melanesians—though established medical opinion indicated possible harm. The Australians held that the administration of suppressants to native people was detrimental to long-term immunity, preferring to control the 'reservoir of malaria' by physical separation from new, non-immune hosts. Yet they conformed to United States practice wherever the Americans shared hybrid spaces with ANGAU-controlled natives. With no understanding of Western medicine, the Melanesians could not question this potentially-dangerous course of action. On the contrary, they rejoiced in the absence of low-level attacks of fever, especially in more-susceptible children, as much as they relished the goods given by generous Americans. Although in war's hybrid spaces the materiality of biological processes—wherein malarial infectiveness follows a predictable pattern—remained foundational, the cultural context influenced outcomes. The contest between the ANGAU and the Americans, and their preferred approaches to treating malaria's infectiveness in the hybrid spaces, reflected both their medical and political perspectives on the native body within the context of their postwar missions: a 'reservoir of malaria' as opposed to a 'seedbed of infection.' The Australians would continue to administer New Guinea, so had to consider the people's future. American operational goals were present-centred; commanders were not interested in postwar life in these islands. The focus was warfare, and welfare came second. Australian prewar experience and postwar aims were accordingly sacrificed to the wartime alliance and its demands on its junior partner.115 40
      The Allies preferred procedures to prevent initial infection of personnel. Their malaria units and engineers developed effective, if costly, methods for controlling the vector mosquito in the disturbed ecology of the hybrid spaces.116 In early 1944, as an aspiring regional power, Australia was promising that it would 'devote its best medical knowledge and services to the task of improving and maintaining the health of the native people.'117 Indeed, all postwar colonial administrations would not only spend millions of pounds on this, but they would also carry over many wartime techniques for environmental control to public health campaigns optimistically aimed at malaria eradication.118 Certainly the war had bequeathed a legacy of prevention methods, as well as research pertaining to malaria in non-immunes—but as the conflict ended a unique opportunity was missed. Had even some of the Melanesians from the war's hybrid spaces been observed for the effects of suppressant withdrawal, instead of being seen merely as a means to American and consequently Australian ends, something of benefit to them, and other semi-immunes in hyper-endemic areas, may have eventuated.119 The Allied forces and the colonial authorities failed to do this. More immediately, if Australian views on the likelihood of reduced immunity were correct, and these natives did suffer greater susceptibility to malaria as a consequence of suppressant regimes, then ANGAU's failure to monitor the impact constituted neglect. In a war not of their own making, these Melanesians had contributed significantly to Allied success by sharing the invaders' hybrid spaces. They deserved better from their colonial masters and erstwhile allies.
University of Otago
 		41
   

Acknowledgements

 
For their helpful comments on earlier drafts of this article, I thank: Tim Bayliss-Smith, Barbara Brookes, Ian Campbell, Murray Chapman, Tony Sweeney, and two anonymous reviewers. All errors and infelicities that persist are my own work, however. I thank Bill Mooney for his map-making and the University of Otago's Division of Humanities for research funds. 42


Notes

1. The western half of New Guinea was Dutch territory.

2. R.W. Robson, comp. and ed., Pacific Islands Year Book, 1942 (Sydney: Pacific Publications, 1942).

3. Jonathan Rutherford, "The Third Space: Interview with Homi Bhabha," in Identity, Community, Culture, Difference, edited by Jonathan Rutherford (London: Lawrence and Wishart, 1990), 211; Homi Bhabha, The Location of Culture (New York: Routledge, 1994).

4. P.A. Buxton, Researches in Polynesia and Melanesia: An Account of Investigations in Samoa, Tonga, the Ellice group, and the New Hebrides, in 1924, 1925, parts I–IV (London: London School of Hygiene and Tropical Medicine, 1927).

5. Robert H. Black, Malaria in the South-West Pacific (Noumea: South Pacific Commission, 1955), 18.

6. Socrates Litsios, The Tomorrow of Malaria (Wellington: Pacific Press, 1996), 30–1, 53.

7. J. Flint, et al., "High Frequencies of -thalassaemia are the Result of Natural Selection by Malaria," Nature 321 (19 June 1986): 743–50; Jeffrey T. Clark and Kevin M. Kelly, "Human Genetics, Paleoenvironments, and Malaria: Relationships and Implications for the Settlement of Oceania," American Anthropologist 95, no. 3 (1993): 612–30; Kevin Marsh, "Immunology of Malaria," in Essential Malariology, 4th ed., edited by David A. Warrell and Herbert M. Gilles (London, New York and New Delhi: Hodder Arnold, 2002), 252–65.

8. Margaret Spencer, "History of Malaria Control in the Southwest Pacific Region, with Particular Reference to Papua New Guinea and the Solomon Islands," Papua New Guinea Medical Journal 35 (1992): 33–66, 40–1.

9. Carl Gunther, Practical Malaria Control (New York: Philosophical Society, 1944), 12; Allan Walker, "Notes," c. 1943, 288, Series 5, AWM 75, Australian War Memorial (hereafter AWM), Canberra; R.F. Scragg, Depopulation in New Ireland: A Study of Demography and Fertility (Port Moresby: Administration of Papua and New Guinea, 1954), 47. See also Black, 21.

10. William H. Talliaferro, ed., Medicine and the War (Chicago: University of Chicago Press, 1944), 65–8; L.M. Groube, "Contradictions and Malaria in Melanesian and Australian Prehistory," in A Community of Culture: The People and Prehistory of the Pacific, edited by Matthew Spriggs et al. (Canberra: Australian National Museum, 1993), 164–86.

11. Spencer, "History of malaria control," 35–6; Judith A. Bennett, "Cross-cultural Influences on Village Re-location on the Weather Coast of Guadalcanal, Solomon Islands, c. 1870–1953" (MA thesis, University of Hawaii, 1974), 85–120, 142–58. See, for early example, Stewart Firth, New Guinea Under the Germans (Melbourne: Melbourne University Press, 1982), 114.

12. W. Tully, Draft Minute Paper, June 1931, Western Pacific High Commission New Hebrides Series (hereafter WPHC NH), MP 187/3/192, University of Auckland Archives, Auckland; Gunther, Practical Malaria Control, 14; Black, 26.

13. Nathaniel Crichlow, "The Climate and Health of the British Solomon Islands," Journal of Tropical Medicine and Hygiene 24 (15 October 1921): 268–9; Clifford S. James, Diseases Commonly Met with in Melanesia: Their Diagnosis, Prevention and Treatment (Sydney: Websdale Shoosmith, 1936); Judith A. Bennett, Pacific Forest: A History of Resource Control and Contest in Solomon Islands, c.1800–1997 (Cambridge and Leiden: White Horse Press and Brill, 2000), 56.

14. J.H.P. Murray, Papua or British New Guinea (New York: Charles Scribner's Sons, 1912; C.D. Rowley, The Australians in German New Guinea 1914–1921 (Melbourne: Melbourne University Press, 1958), 269–88.

15. Judith A. Bennett, "Holland, Britain and Germany in Melanesia," in Tides of History: The Pacific Islands in the Twentieth Century, edited by K.R Howe, Robert C. Kiste, and Brij V. Lal (St Leonards, NSW: Allen and Unwin, 1994), 40–70.

16. Brian Jinks, "Australia's Post-war Policy for New Guinea and Papua," Journal of Pacific History 17, nos 1–2 (1982): 86–100, 86; ANGAU, Report for February 1942–September 1944, A9373, Item 1, National Archives of Australia (hereafter NAA), Canberra; Lucy Mair, Australia in New Guinea (London: Christophers, 1948), 191; Robson, 241, 278.

17. Donald Denoon, Public Health in Papua New Guinea: Medical Possibility and Social Constraint, 1884–1984 (Cambridge: Cambridge University Press, 2002), 34–5, 41, 48–52.

18. Bennett, "Holland, Britain and Germany," 40–70; Judith A. Bennett, Wealth of the Solomons: A History of a Pacific Archipelago (Honolulu: University of Hawaii Press, 1987); Jeremy MacClancy, To Kill a Bird with Two Stones: A Short History of Vanuatu (Port Vila: Vanuatu Cultural Centre, 1980).

19. Ebbe Curtis Hoff, ed., Preventive Medicine in World War II , vol. VI (Washington DC: Office of the Surgeon General, Department of the Army, 1955), 472; Margaret Spencer, Malaria: The Australian Experience, 1943–1991 (Townsville: Australian College of Tropical Medicine, 1994), 42.

20. Hoff, 15–16.

21. D.W. Kralovec, "A Naval History of Espiritu Santo," New Hebrides, Shore Establishment, 1945, NRS II-231, microfilm at Naval Yards Library,Washington, DC, 430. See also, H.C.L. Merillat, Guadalcanal Remembered (New York: Dodd, Mead and Co., c. 1982), 255.

22. W. Tully, "Report on Malaria in the New Hebrides," 21 August 1931, WPHC NHBS MP 187/31, University of Auckland Archives, Auckland; "Base Malaria and Epidemic Control," 1945, Entry 183, Record Group (hereafter RG) 313, National Archives and Records Administration (hereafter NARA), College Park, US; Kralovec, 430.

23. "Organization of Armed Forces in South Pacific Area," c. 1945, Entry 1012, RG 112, NARA, College Park, US; W.G. Downs, P.A. Harper, and E.T. Lisansky, "Epidemiology of Insect Borne Diseases in Army Troops," Supplement to the American Journal of Tropical Medicine 27, no. 3 (1947): 69–89, 73.

24. Henry Bennett and R.H. Beckworth "The Influence of Medical Factors in Land Campaigns in the South and Southwest Pacific," 19 October 1944, Entry 1005, RG 52, NARA, College Park, US; Allan S. Walker, Clinical Problems of War (Canberra: Australian War Memorial, 1952, 3rd reprint 1962), 84–96.

25. Atebrin was also known as quinacrine and mepacrine.

26. Neil Fairley, "Malaria in the Western Pacific," 22 December 1942, Public Records Office 83/238/85448, Colonial Office, London; Tony Sweeney, Malaria Frontline: Australian Army Research During World War II (Melbourne: Melbourne University Press, 2003), 42–61. In late 1943, Fairley, through tests on Australian army volunteers, set the correct prophylactic dose of atebrin at 100 milligrams daily to prevent overt attacks of malaria. Hoff, 539–41, 564–5; Walker, Clinical Problems, 91–9, 104–7, 117–8; Sweeney, 27–35, 189, 239–41.

27. P. A. Harper, E.T. Lisansky, and B.E. Sasse, "General Aspects and Control Measures," Supplement to the American Journal of Tropical Medicine 27, no. 3 (1947): 1–68, 15–19.

28. Hoff, 1218; Robert J. T. Joy, "Malaria in American Troops on the South and Southwest Pacific in World War II," Medical History 43 (1999): 201.

29. Walker, Clinical Problems, 98–100, 107–9.

30. See, for example, Groube, Contradictions, 171.

31. "Supplement to August Report," 15 September 1943, RG 313, NARA, College Park, US; Richard H. Daggy, "The Biology and Seasonal Cycle of Anopheles farauti on Espiritu Santo, New Hebrides," Annals of the Entomological Society of America 38, no. 1 (1945): 1–13.

32. See, for example, Spencer, "History of Malaria Control," 36.

33. P.W. Oman and L.D. Christenson, "Entomology," Supplement to the American Journal of Tropical Medicine 27, no. 3 (1947): 91–117, 99; O.R. McCoy, "Malaria and the War," Science 100, no. 2607 (1944): 535–539, 538.

34. Walker, Clinical Problems, 146–7.

35. "Report, 3rd Malaria Control Detachment," 5 October 1945, Entry 54A, RG 112, NARA, College Park, US; "Report," Treasury Island, March 1944, RG 38, NARA, College Park, US; Harper, Lisansky, and Sasse, 42–56; Letter, Smith to Medical Officer and Enclosures, 5 January 1943, Entry 179, RG 313, NARA, College Park, US; 11 AMCU Report, Appendix 1, January 1944, PR 00525, AWM, Canberra.

36. "Base Malaria and Epidemic Control," New Hebrides, c. 1945, Entry 183, RG 313, NARA, College Park, US; Harper, Lisansky, and Sasse, 1–67; Walker, Clinical Problems, 107–9.

37. Jones, "A Volunteer's Story," MSS 1168, AWM, Canberra, 65.

38. This phrase appears constantly. See, Commander South Pacific to All Bases, 29 [month unclear] 1943, RG 313–58–3013, NARA, San Bruno (hereafter SB), US.

39. P. Harper, "Monthly Report for December," 31 December 1943, RG 313–58–3401, NARA, SB, US.

40. "'Operation Roll-Up': The History of Surplus Property Disposal in the Pacific Ocean," I–3, microfilm, Naval Yards Library, Washington, DC.

41. See, for example, Purviance, "History of US Advance Naval Base at Guadalcanal," c. September 1945, RG 313–58–3401, NARA, SB, US.

42. Raphael Cilento, cited in Spencer, Malaria: The Australian Experience, 29. See also W. Tully, Malaria Survey, Draft to June 1931, WPHC NH MP 187/3/192, University of Auckland Archives, Auckland; Black, 27; Carl Gunther, "New Conceptions of Malaria Control," Medical Journal of Australia (13 April 1946): 510–11.

43. William Hughes, "The Treatment of Malaria in a Hyperendemic Zone," Transactions of the Royal Society of Tropical Medicine and Hygiene 36, no. 2 (1942): 60–74, 60–1, 65.

44. W. Tully, Malaria Survey, Draft to June 1931, WPHC NH MP 187/3/192, University of Auckland Archives, Auckland; Gunther, Practical Malaria Control, 14; Black, 26.

45. Letter, James Sapero to Commanding General, 12 September 1942, Entry 179, RG 313, NARA, College Park, US; James J. Sapero, "Prevention of Malaria Infections by Drug Prophylaxis," in Malariology: A Comprehensive Survey of all Aspects of this Group of Diseases from A Global Standpoint, vol. 2, edited by Mark F. Boyd (Philadelphia and London: W.B. Saunders and Co., 1949): 1114–1132, 1130, 1132.

46. A "loading dose" of atebrin consisted of 4.5 grains (0.2916 grams) for five days, then three grains twice a week (0.3888 grams total). Officer in Charge, Resume of Malaria Control Activities at Base Button (Santo), 17 January 1943, Entry 179, RG 313, NARA, College Park, US.

47. Kralovec, 430.

48. James Sapero, "Malaria Hazard of Natives," 12 September 1942, Entry 179, RG 313, NARA, College Park, US; "Base and Epidemic Control," New Hebrides, c. 1945, Entry 183, RG 313, NARA, College Park, US; Letter, Curtin to Commanding General, 10 March 1943, RG 338, NARA, College Park, US; Malaria Control at Base Button 1942, 17 January 1943, Entry 179, RG 313, NARA, College Park, US; R.A. Mount, "Malaria Hazard of Tonkinese and Natives," 4 October 1943, Entry 179, RG 313, NARA, College Park, US; Harper, Lisansky, and Sasse, 39.

49. History of the Medical Department of the United States Navy in World War Two: A Narrative and Pictorial Volume, vol. 1 (Washington: United States Navy, 1953), 73.

50. Hoff, 5.

51. " Monthly Report," Guadalcanal, May 1943, RG 313–58–3401, NARA, SB, US.

52. Atebrin controlled malaria symptoms induced by P. vivax, but a form of the parasite, the gametocytes, remained in human blood. Even gametocytes of P. falciparum remained infectious for several weeks after treatment, although other stages of the parasite were destroyed. Thus there was still some potential for natives on atebrin alone to spread the malaria via the vector mosquito. See note 106.

53. Harper, "Monthly Report for December." See also L. Parks, "Monthly Malaria Reports," June 1943 and 8 July 1943, RG 313–58–3401, NARA, SB, US; Harper, Lisansky, and Sasse, 40.

54. "Manual for Advanced Base Development and Maintenance," July 1943, RG 313–58–3440, NARA, SB, US.

55. Letter, Poole to Secretary to the Government, 24 April 1944; Letter, Poole to Officer Commanding, 6 May 1944; Letter, Officer Commanding to SMO, 8 May 1944; Letter, Rutter to Secretary to the Government, 15 May 1944; Letter, Poole to CO, 19 June 1944; Letter, Bullen to Secretary to the Government, 22 June 1944, F 9/44 Part E, WPHC, University of Auckland Archives, Auckland; Letter, Homewood to Breene, 27 December 1942, Entry 44463, RG 338, NARA, College Park, US; Young, "British Solomon Islands," 4 December 1942, F 9/43, WPHC, University of Auckland Archives, Auckland; "Base Prevention Disease Officer," June 1944; "Malaria Control Report and Enclosures," February 1944; "Malaria Control Report," March 1944, RG 313–58–3013, NARA, SB, US.

56. United States servicemen were open-handed with payment for services and souvenirs, and their surplus goods such as clothing also found its way to Melanesians.

57. Harper, Lisansky, and Sasse, 40; Lamont Lindstrom and James Gwero, eds, Big Wok: Storian blong Wol Wo Tu long Vanuatu (Canterbury and Suva: Macmillan Brown Centre for Pacific Studies and Institute of Pacific Studies, 1998), 213–15.

58. See Sapero, "Prevention of Malaria," 1129–31.

59. Letter, J. Sapero to Commanding General, New Georgia, 9 August 1943, Entry 44463, RG 338, NARA, College Park, US; "Quarterly History of Medical Activities," Emirau, Gardiner, 12 October 1944, Entry 54A, RG 112, NARA, College Park, US; Letter, Officer in Charge, Manus to Commander, 5 May 1944, RG 313–58–3416, NARA, SB, US; Letter, Wainwright to Chief Engineer, 26 February 1944, Records of the Office of the Chief of Engineers, RG 77, NARA, College Park, US; "Malaria and Epidemic Disease Control," 6 June 1945, RG 313–50–3019, NARA, SB, US; Downs, Harper, and Lisansky, 76–80; Hoff, 400, 433.

60. "Sketch Map of Hombu Hombu," c. 1944, 1/111/14/19, Series British Solomon Islands Protectorate, WPHC, Honiara, Solomon Islands.

61. "Interview," Mikesell, May 1944, Entry 302, RG 112, NARA, College Park, US; Letter, Officer in Charge to Commanding General, 9 August 1943, Entry 44463, RG 338, NARA, College Park, US.

62. Walker, Clinical Problems, 13, 117–18.

63. Cited in Alan Powell, The Third Force: ANGAU's New Guinea War (Melbourne: Oxford University Press, 2003), 240.

64. Powell, The Third Force; Allan S. Walker, The Island Campaigns (Canberra: Australian War Memorial, 1957), 161, 164, 238–9.

65. "Malaria and its Military Implications in the SW Pacific," c. February 1943, 267/6/7, AWM 54, AWM, Canberra, 145.

66. See, for example, "Malaria in Base Areas in New Guinea," May 1944, Appendix C, 11/1/49, AWM 52, AWM, Canberra.

67. Neil Fairley, "Malaria in Papua," n.d., c. 1943, 481/1/16, AWM 54, AWM, Canberra.

68. Walker, Clinical Problems, 117–8.

69. "16th Meeting of Allied Malaria Control Conference," 1 September 1943; "Administrative Instruction," 3 November 1943; Letter, English to ADMS, 8 November 1943; "War Diary," 11/1/49, AWM 52, AWM, Canberra.

70. W.E.H. Stanner, "Appreciation of Current Situation and Problems of ANGAU," 80/8/17, AWM 54, AWM, Canberra.

71. Powell, 192–200.

72. "Epidemic Diseases in Natives," 2 March 1943, 481/12/205, AWM 54, AWM, Canberra; "Treatment of Natives," Appendix 42, September 1942, ANGAU War Diary, 1/10/1, AWM 51, AWM, Canberra; Letter, Morris to I. Mackay, 26 March 1943, 3 DRL 6850, AWM, Canberra.

73. Gunther, Practical Malaria Control, 12.

74. A. Walker, "Notes," 1945, AWM 75, 228, Series 5, AWM, Canberra; Gunther, Practical Malaria Control, 11.

75. Powell, The Third Force.

76. "Report on Activities to 31 Dec 1943," ANGAU War Diary, 1/10/1, AWM 52, AWM, Canberra; "Medical Administration, Report on Activities," 1944, ANGAU War Diary, 1/10/1, AWM 52, AWM, Canberra; Walker, The Island Campaigns, 44; Bryant J. Allen, "A Bomb or a Bullet or the Bloody Flux? Population Change in Aitape Inland, Papua New Guinea, 1941–1945," Journal of Pacific History 18, nos 3–4 (1983): 218–35; John Burton, "A Dysentery Epidemic in New Guinea and its Mortality," Journal of Pacific History 18, nos 3–4 (1983): 236–61. Compare with Denoon, 62.

77. Powell, 54, 55, 134–9, 253–5.

78. "Medical Appreciation, Month of May 1943," Appendix 117, ANGAU War Diary, 1/10/1, AWM 52, AWM, Canberra.

79. Sylvester M. Lambert, "Malaria Incidence in Australia and the South Pacific," in Malariology: A Comprehensive Survey of all Aspects of this Group of Diseases from a Global Standpoint Volume 2, edited by Mark F. Boyd (Philadelphia and London: Saunders, 1949), 1129.

80. "33rd Meeting of Allied Malaria Conference," 17 May 1944, 11/1/49, AWM 52, AWM, Canberra.

81. A.L. Benallack, "Routine Order Part 1," 16 April 1945, HQ and No. 1 Platoon, 2/2 Forestry Coy, 5/32/4, AWM 52, AWM, Canberra.

82. "16th Meeting of Allied Malaria Control Conference," 1 September 1943, Medical War Diary, 11/1/49, AWM 52, AWM, Canberra.

83. Donald Glover, "Interview Transcript," 14 August 1944, Entry 312, RG 112, NARA, College Park, US.

84. See 11/1/49, AWM 52, AWM, Canberra.

85. Powell, 172–7; Black, 30; Ronald H. Spector, The American War with Japan; Eagle Against the Sun (New York: The Free Press, 1985), 142–9, 232–3.

86. Harper, Lisansky, and Sasse, 39–40.

87. Norman D. Levine and Paul Harper, "Parasitological Observations on Malaria in Natives and Troops, and on Filariasis in Natives," Supplement to the American Journal of Tropical Medicine 27, no. 3 (1947): 119–128, 119–23; Ross, "Emirau," and enclosures, c. 1944, A. Walker's Records, 481/12/247, AWM 54, AWM, Canberra; N.G. Hairson, F.B. Bang, and J. Maier, "Malaria in the Natives of New Guinea," Transactions of the Royal Society of Tropical Medicine and Hygiene 40, no. 6 (1947): 795–807, 803.

88. 'Gametocytes' refer to a stage of the parasite in the blood that is taken up from humans by the mosquito to reproduce in the vector's body, in order for the parasite to be passed on to another human host.

89. Baldwin, "Native Labour Section Activities Ending 31 March 1944," ANGAU War Diary, 1/10/1, AWM 52, AWM, Canberra; "Allied Malaria Conference," 36th Meeting, 28 June 1944, 11/1/49, AWM 52, AWM, Canberra; Tony Sweeney, personal communication, 16 November 2005.

90. Base Prevention Disease Officer to Commander, 5 June 1944 and Minute, Malaria Officer to Officer in Charge, 20 July 1944 RG 313–58–3416, NARA, SB, US.

91. Letter, Base Prevention Disease Officer to Commander, 5 September 1944, RG 313–58–3416, NARA, SB, US.

92. Joy, 198; Stevenson, "Memo for Naval Attaché on Father D. Scanlon," 18 October 1942, Entry 183, RG 313, NARA, College Park, US; Henry Bennett and R.H. Beckworth, "The Influence of Medical Factors in Land Campaigns in the South and Southwest Pacific," 19 October 1944, Entry 1005, RG 52, NARA, College Park, US.

93. Harper, Lisansky, and Sasse, 4.

94. Steven Bullard, "'The Great Enemy of Humanity': Malaria and the Japanese Medical Corps in Papua, 1942–1943," Journal of Pacific History 39, no 2(2004): 203–220, 213–14.

95. Walker, Clinical Problems, 161. In time, and with inconsistent medication, malarial parasites developed resistance to atebrin. This occurred in the AIF's 6th Division in the Wewak-Aitape area in 1945. Sweeney, Malaria Frontline, 167–90.

96. "Report on Malaria Prevention," Dobadura-Buna area, 20 January 1943, War Diary, 11/1/49, AWM 52, AWM, Canberra.

97. "Appendix C, Quarterly Report 31 January 1946," ANGAU Medical Services, October–December 1945, 481/12/136, AWM 54, AWM, Canberra; Duncan M. Stout, War Surgery and Medicine (Wellington: New Zealand Government, 1954), 528–43; Walker, Clinical Problems, 127, 130, 154. This was certainly falciparum-caused malaria.

98. Spencer, Malaria: The Australian Experience, 72.

99. I. Mackerras, "Notes on Malaria for Medical Entomologists," c. 1943, 267/6/7, Part 145, AWM 54, AWM, Canberra.

100. See, for examples, Downs, Harper, and Lisansky, 81–3.

101. Benjamin Baker, "The Suppression of Malaria," in Internal Medicine in World War II, Vol II: Infectious Diseases, edited by John Boyd Coates (Washington DC: Office of the Surgeon General, Department of the Army, 1964), 468.

102. Harper, Lisansky, and Sasse, 59.

103. Walker, Clinical Problems, 118, 120–7; Alf S. Alving, "Clinical Treatment of Malaria," in Recent Advances in Medicine and Surgery, edited by Walter Reed (Washington: Army Institute of Research, 1955), 209.

104. J. D. Macgregor, "Malaria in the Island Territories of the South Pacific" (MD thesis, St Andrews University, Scotland, 1966), 60–4.

105. "Malaria and Epidemic Diseases control—South Pacific Area," c. 1944, Entry 1012, RG 112, NARA, College Park, US.

106. For both P. vivax and P. falciparum, merozoites released from blood schizonts may develop into trophozoites (to initiate another asexual cycle in the blood) or gametocytes (which are infectious to mosquitoes). Vivax gametocytes live for a few days only, but falciparum gametocytes can persist in the blood for several weeks and remain infectious to mosquitoes when drugs have eliminated the other blood stages. Tony Sweeney, personal communication, 17 November 2005.

107. Sweeney, Malaria Frontline, 151–5.

108. Prewar researchers understood the limitations of atebrin. See Arthur E. Horn, "The Control of Disease in Tropical Africa: Part II," Journal of the Royal African Society 32, no. 127 (1933): 126–7; P.H. Manson-Bahr and A.H. Walters, "Selective Action of Atebrin and Plasmoquin on the Subtertian Malaria Parasite," Lancet 226, no. 6 (1934): 15–16; W. Clark Cooper, "Summary of Antimalarial Drugs," Public Health Reports 64, no. 23 (1949): 717–21; E.A. Steck, The Chemotherapy of Protozoan Diseases (Washington DC: Walter Reed Institute of Research, 1972), 23,168–9.

109. "Malaria Control," Guadalcanal, Reports for December (31 December 1943), January (31 January 1944), RG 313–58–3401, NARA, SB, US; Harper, Lisansky, and Sasse, 41–2. Plasmoquin (also known as pamaquine and plasmochin) at this relatively high dosage, in association with atebrin, will destroy most vivax in the asexual stage (the liver cycle) as well as the gametocytes of falciparum (Cooper, 725–6). It seems that in 1942 the Americans tended to use only atebrin on natives, as was the case in the New Hebrides; but, by mid-1943, plasmoquin with or without atebrin was used when parasites were found in smears. Different regimes were tried—for example, at Milne Bay, in June–July 1943, the dosage for the native labourers was 0.02 grams of plasmoquin for three days. This was repeated every five weeks, "until their camps were removed 1 1/2 miles away" from the United States troops ("Allied Malaria Conference," 36th Meeting, 28 June 1944, 11/1/49, AWM 52, AWM, Canberra).

110. "Report for January 1944," Tulagi-Florida, RG 313–58–3401, NARA, SB, US; Levine and Harper, 119–23. See also for Papua, Walker, Clinical Problems, 94–5.

111. Steck, 23,169.

112. Sapero, "Prevention of Malaria Infections," 1130.

113. Lindstrom and Gwero, 212–15.

114. Black, 3, 18–19.

115. Only one malariologist, Margaret Spencer, hints that this was a cost to the people. Spencer, "History of Malaria Control," 39.

116. Martin D. Young, "Malaria During the Last Decade," American Journal of Tropical Medicine and Hygiene 2 (1953): 347–59; Spencer, "History of Malaria Control," 38–9.

117. H.V. Evatt, "Notes on Draft Agenda for the Use of Delegates at Australia and New Zealand Conference, January 1944," in The Australian-New Zealand Agreement 1944, edited by Robin Kay (Wellington: New Zealand Department of Internal Affairs, 1972), 90.

118. Spencer, "History of Malaria Control," 36–52; W. Peters, "A Critical Survey of the Results of Malaria-eradication and Control Programmes in the South West Pacific," Annals of Tropical Medicine and Parasitology 56, no. 1 (1962): 20–31; Macgregor, 69–78.

119. This question was raised but left unanswered. See Sapero, "Prevention of Malaria Infections," 1129–31.

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