Journal of Historical Geography, 24, 1 (1998) 6989

The Philippines insurrection and the 19024 cholera epidemic: Part IEpidemiological diffusion processes in war
Matthew Smallman-Raynor and Andrew D. Cliff

This, the rst of a two-part paper, presents an historical case study of the impact of war and its aftermath upon the spread of an infectious disease, cholera. The choice of area (Philippine Islands), the time (a year-long period in the immediate aftermath of the Insurrection against US annexation, March 1902February 1903) and the epidemic (cholera) are conditioned by the detailed reports prepared by the Chief Quarantine Ocer for the Philippine Islands, and published weekly in the contemporary US Public Health Reports. The reports include textual accounts of the progress of the epidemic, and numerical evidence regarding the weekly incidence of cholera in over 440 settlements. This information is used to reconstruct the routes by which cholera diused through the archipelago and to model the diusion process on the geographical levels of province, island and nation. It is shown that a spatially contagious component dominated the spread of cholera in many geographical areas and at all spatial levels. In contrast, hierarchical diusion was generally found to be of only limited signicance in the transmission process. These results correlate with the lack of a well-developed urban hierarchy in many parts of the Philippines. Part II of the paper, to be published in Vol. 24, Number 2 (April 1998) of the Journal, goes on to compare the spatial diusion patterns described here with those found in a subsequent peacetime cholera wave in the Philippines (May 1903February 1904). Results from both parts of the paper are used to assess the manner in which war can aect diusion processes and the circumstances under which spread is likely to be dominated by contagious, hierarchical or mixed diusion processes. 1998 Academic Press Limited

Introduction
War provides an environment ripe for the rapid spread of infectious diseases. With war comes the increased mobility, mixing and congregation of both military and civilian populations. The combatants may be drawn from very dierent epidemiological environments, they may possess dierent patterns of disease immunity, and their resistance to infection may be compromised by mental and physical stress, trauma and nutritional deprivation. Unsanitary conditions and the collapse of normal rules of social behaviour further compound the epidemiological unhealthiness of war.[1] Historically, cholera ranks as one of the great war pestilences.[2] For example, in his
Reprint requests to Matthew Smallman-Raynor.

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M. SMALLMAN-RAYNOR AND A. D. CLIFF

classic book, Epidemics Resulting From Wars, Friedrich Prinzing notes that the French Army lost 1015 per cent of its eective strength to morbidity and mortality from cholera in the rst year of the Crimean War (18546).[3] A similar proportion of the Prussian Army succumbed to cholera in the AustroPrussian War of 1866.[4] But the highest death tolls are usually associated with the spread of cholera among civilian populations, often in the immediate aftermath of war. The cholera epidemic that struck the Philippine Islands between 1902 and 1904 began just as the three-year war (18991902) against American annexation was drawing to a close. The war had already claimed up to 800 000 Filipino lives, and this in a population of less than eight million. The cholera epidemic that followed the war spread across the archipelago and left another 200 000 dead.[5] Despite the historical association of cholera and war, geographical studies of the disease have tended to focus on epidemic spread in peacetime.[6] As a consequence, relatively little is known of the diusion of cholera as a sequel to armed conict. To redress this imbalance, we present here a geographical analysis of the cholera epidemic which followed in the wake of the PhilippineAmerican War. The social and political context of this epidemic has been outlined in a number of recent studies.[7] In this paper, we add a spatial dimension by examining the processes by which the epidemic diused on dierent geographical levels in the course of its rst year, March 1902February 1903. To these ends, we make use of a novel archival source in epidemiological studies: the sanitary dispatches prepared by the Chief Quarantine Ocer for the Philippine Islands and reprinted in the US Public Health Services Public Health Reports.[8] For the period covered by this paper, the post of Chief Quarantine Ocer was held by J. C. Perry, a Passed Assistant Surgeon of the US Marine Hospital Service;[9] we examine Perrys textual accounts and numerical summaries of the cholera epidemic in subsequent sections. The present study is part of an ongoing project concerned with the use of island communities as laboratories for disease diusion analyses.[10] We begin with a brief description of the Philippine Islands, the nature of cholera and the wartime legacies that inuenced its spread. In the second part, we outline the nature and sources of the cholera data contained in the Public Health Reports. Then, we use qualitative evidence contained in the Reports to reconstruct the routes by which cholera diused through the Philippines archipelago. Finally, we turn to the quantitative evidence contained in the Reports to identify the diusion processes operating at the geographical scales of nation, island and province.

Background to the epidemic The study site

The Philippines archipelago consists of some 7100 islands strewn over half a million square miles of ocean (Figure 1). At about the time of the epidemic, in 1903, some ve per cent of the islands were inhabited by a population totalling 7 635 000.[11] Almost half resided on the northern island of Luzon; only seven other islands (Bohol, Cebu, Leyte, Mindanao, Negros, Panay and Samar) recorded populations in excess of 100 000. Manila City, situated on the west coast of Luzon, was the largest settlement (1903 population 220 000), chief port and trading centre. Elsewhere, the settlement pattern was characterized by scattered villages and towns of less than 40 000 inhabitants.[12] As a country of oceanic islands, settlements in the Philippines were doubly isolated

DIFFUSION PROCESSES AND WAR IN THE PHILIPPINES

71

Figure 1. The Philippine Islands.

externally from the rest of the world, and internally from each other. Internal isolation was not only by way of the sea, from one island to another, but also, because of the rugged and mountainous nature of much of the terrain, from settlement to settlement on a single island.[13] The profound epidemiological consequences of such isolation have been reviewed at length elsewhere[14] but, in essence, natural isolation served as an eective barrier to the spread of infectious diseases.

The war context

The PhilippineAmerican War gravely impaired the epidemiological protection aorded by natural isolation. Contributory factors have been outlined in other sources.[15] The

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M. SMALLMAN-RAYNOR AND A. D. CLIFF

war began on 4 February 1899 and ocially ended some 40 months later in July 1902. During this period, over 100 000 US troops were deployed to combat the rural guerrilla forces. Many of the troops were stationed in an interconnected network of some 500 garrison towns, and these towns became the focus for migrants seeking protection from the war in the countryside. Large-scale population movements and congregation were further fuelled by agricultural dislocation, the disruption of food supply lines and the US strategy of forced population concentration to combat the guerrilla ghting. Thus, when cholera appeared in the archipelago in the penultimate month of ghting, March 1902, the isolation of many settlements had been eroded by three years of military occupation, conict, population displacement and congregation. The situation was compounded by population dispersal in the immediate aftermath of the war. Recent histories of the 19024 cholera epidemic on the Philippine Islands have ascribed only a limited role to American military personnel in the carriage of the disease.[16] A number of American soldiers were certainly aicted in the early stages of the epidemic, although instances in which they were directly implicated in the spread of cholera are few.[17] Troopships, in particular, were a potentially ecient mechanism for the carriage of the disease from port to port. But, with one critical exception in the very early stages of the epidemic, quarantine appears to have contained the spread of cholera by this route.[18] Rather, the inuence of war on the spread of cholera rested with the social and environmental conditions created by the hostilities[19] and the military-style approach to disease control.[20] The social and environmental aftermath of the PhilippineAmerican War is well illustrated by the experience of the provinces of Batangas and La Laguna, Luzon Island[21] (Figure 1). Batangas and La Laguna had been the scene of intense ghting during the war and, as late as December 1901, population reconcentration was undertaken by the American administration as part of its strategy nally to quash the rebel insurgents. Such were the cramped and unsanitary conditions endured by the reconcentrated populations that, by April 1902, dysentery and malaria were rife. Health problems were exacerbated by food shortages which were, in large measure, attributable to the destruction of local agricultural infrastructure earlier in the war. Thus, when cholera reached Batangas and La Laguna in late April 1902, it spread rapidly through the dense, unsanitary and physically weakened populations. The signicance of these conditions was not lost on contemporary observers; one US military report attributed the very high cholera mortality in the two provinces to the demoralising and debilitating inuences of war.[22] Moreover, food shortages fuelled an illicit movement of people and produce that military restrictions and quarantine cordons were powerless to stop. These local population movements gave rise to some well-documented episodes in the diusion of the epidemic[23] and, doubtless, countless others.

The nature of cholera

Classic Asiatic cholera which caused the epidemic is a severe, often rapidly fatal, disease produced by the bacterium, vibrio cholerae. Transmission of the bacterium usually occurs via the ingestion of faecally contaminated water and, less commonly, food. As regards its clinical course, an incubation period of two to ve days is usually followed by the sudden onset of diarrhoea and vomiting, giving rise to massive uid loss and dehydration. Consequent symptoms include cramps, a reduction in body temperature and blood pressure leading to shock and, ultimately, death within a few hours or days of symptom onset. Mortality is typically witnessed in 4060 per cent of untreated cases.[24]

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73

At least until the beginning of the present century, the Philippine Islands lacked the conditions necessary to maintain cholera in endemic form. So, for each of the six epidemics to strike the country by 1904, rst in 1820 and then in the 1840s, 1860s, twice in the 1880s and nally in 1902, an external source of the vibrio is either known or strongly suspected.[25] As a consequence, each epidemic had a discrete and denable starting point in the archipelago and each event was separated by an extended diseasefree period.[26]

The data Sources of data

One legacy of the American annexation of the Philippine Islands is the detailed sanitary reports from the period. Ocers of the United States Public Health Service (USPHS), stationed in the Philippines, were directed to submit reports of the progress of the cholera epidemic to the USPHS Surgeon-General in Washington, DC. These reports were published in the weekly Public Health Reports, the US equivalent of England and Wales Weekly Returns of the Registrar-General.[27] The information contained in the Public Health Reports forms part of the original material on which the annual reports of the Chief Quarantine Ocer for the Philippine Islands, published in the widely used Annual Report of the Philippines Commission, were based.[28] In this paper, we use the epidemiological information contained in the weekly volumes of the Public Health Reports to reconstruct the spread of the epidemic. These data are supplemented by demographic information from the 1903 Census of the Philippine Islands.[29] For the purposes of enumeration under the 1903 census, the Philippines was organized into some 1000 municipalities.[30] Municipalities were commensurate with settlements and ranged in size from small villages to large towns. Each municipality was allocated to one of 51 provinces or comandancias (military districts) and these, in turn, to the major island groupings of the Philippines archipelago.[31] All epidemiological information included in the Public Health Reports is coded according to these standard geographical divisions of municipality, province/comandancia and island. It is convenient to divide the information in the Public Health Reports into two categories: numerical evidence; and textual accounts. Numerical evidence. The cholera epidemic began on, or about, 20 March 1902 and persisted for 99 weeks until the beginning of February 1904. For each of these 99 weeks, the Public Health Reports record the number of cholera cases and deaths registered in infected municipalities. Textual accounts. The numerical reports of morbidity and mortality were usually accompanied by textual accounts of the development of the epidemic. These were prepared by the Chief Quarantine Ocer for the Philippines from reports led by US ocials in the various provinces. The accounts contain details of the factors that inuenced the size and severity of the epidemic, and measures adopted to combat its spread. In addition, and crucially from a geographical point of view, the accounts record the geographical source of cholera in various locations.

Selection of time period

The textual accounts of the 19024 cholera epidemic describe how it passed through the Philippine Islands as two temporally distinct, but spatially concordant, waves of

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M. SMALLMAN-RAYNOR AND A. D. CLIFF

Wave I (weeks 150) 9000 8000 7000 Wave II (weeks 6199)

Cholera incidence

6000 5000 4000 3000 2000 1000 0 1 50 Week 61 99

Figure 2. National series of cholera cases (histograms) and deaths (line traces) by week, Philippine Islands, March 1902February 1903. The series are based on the weekly counts of morbidity and mortality recorded in the Public Health Reports for 570 infected municipalities. The horizontal axis has been formed by coding the rst week of the epidemic (ending 22 March 1902) week 1, with subsequent weeks numbered sequentially thereafter up to, and including, week 99 (ending 6 February 1904). The graph denes two waves of infection; summary details of each wave are given in Table 1. The present analysis is restricted to the diusion of wave I (weeks 150). T 1 Summary details of infection Waves I and II associated with the 19024 cholera epidemic in the Philippine Islands Wave 1 Start End Duration (weeks) Cases Deaths Epidemic peak 22 March 1902 (week 1) 28 February 1903 (week 50) 50 71 221 47 548 4 October 1902 (week 29) Wave 2 16 May 1903 (week 61) 6 February 1904 (week 99) 39 26 267 19 896 22 August 1903 (week 75)

Date given as the last day of the calendar week. The week number, coded sequentially from the rst week of the epidemic (22 March 1902, week 1), is given in parentheses. Epidemic peak is dened as the week in which the maximum number of cases was reported, with the date given here as the last day of that calendar week.

infection. Figure 2, which is based on the numerical information contained in the Public Health Reports, plots the national series of cholera morbidity and mortality on a weekly basis, March 1902February 1904.[32] The two infection waves identied in Figure 2 formed discrete diusion events.[33] As Table 1 shows, wave I began in the third week of March 1902 (week 1) and persisted for 50 weeks, ending in the last week of February 1903 (week 50). It reached a peak

DIFFUSION PROCESSES AND WAR IN THE PHILIPPINES

75

in early October (week 29) and was associated with a reported total of 71 221 cases and 47 548 deaths. The rather less severe wave II began in late May 1903 (week 61), lasted 39 weeks to early February 1904 (week 99) and is documented to have claimed some 20 000 lives. In this paper, we analyse the diusion of the more severe wave I. The diusion of wave II is examined elsewhere.[34]

Database formation
The numerical and textual information contained in the Public Health Reports was used to form two databases relating to the occurrence of wave I: Database 1: numerical evidence. The number of infected municipalities documented in the Public Health Reports varies on a weekly basis, but a total of n=441 dierent municipalities (including Manila City) were included at some stage during the t=50 weeks duration of wave I.[35] These municipalities were located in 39 provinces on 13 islands; the assignment of municipalities to provinces and islands is shown in Table 2.[36] For each infected municipality, the weekly disease counts were abstracted to form (44150) spacetime matrices of (1) cholera morbidity, and (2) cholera mortality. Further n50 matrices, at the spatial levels of province and island, were then formed by dividing the 44150 matrices into the constituent municipalities of individual provinces and islands. The total number of cases and deaths recorded nationally, and by island and province, is shown in Table 2. Database 2: textual accounts. All information on inter-area linkages in the spread of cholera was abstracted from the Public Health Reports, and organized to form a timesequenced account of the diusion of wave I. First the textual accounts in database 2 are used to reconstruct the broad routes by which wave I spread through the archipelago. We then turn to the numerical evidence in database 1 to examine the processes by which the wave spread at the geographical levels of province, island and nation.

Textual accounts: reconstruction of national diffusion routes

In a period of less than 12 months, wave I of the cholera epidemic (March 1902February 1903) had been introduced to the Philippines, spread hundreds of kilometres from its point of introduction to reach the most remote islands of the archipelago, and faded away. A telegram dated 24 March 1902 provided the rst evidence of cholera in the islands. The informant was the Chief Quarantine Ocer for the Philippines, J. C. Perry, and the message was unequivocal: Cholera is now present at Manila; 18 cases.[37] In fact, the rst cases had appeared a few days earlier, on 20 March, in the Farola district of the city.[38] It is unlikely that the ultimate source of cholera in Manila will ever be known, although contemporary accounts speculated on its importation with fresh vegetables from Canton, China, where cholera had been present for some time.[39] Whatever the source of the disease, emergency measures were immediately invoked in the city. Public health surveillance was intensied, all suspicious cases were admitted to hospital, contacts were sent to the citys detention camp, infected houses were cleansed and placed under guard, all green vegetables were destroyed, wells and cisterns were closed and distilled water stations established. To prevent onwards spread from Manila to the provinces, a cordon was thrown around the city; ferry boat and rail trac was halted and a permit system was introduced to control the movements of individuals.[40]

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M. SMALLMAN-RAYNOR AND A. D. CLIFF

T 2 Number of cholera cases and deaths recorded by island and province in the Public Health Reports for wave I of the epidemic, 22 March 190228 February 1903 Island Basilan Bohol Cebu Leyte Luzon Province Basilan Bohol Cebu Leyte Albay Bataan Batangas Benguet Bulacaan Cagayan Camarines Cavite Ilocos Norte Ilocos Sur Isabela La Laguna La Union Manila Nueva Ecija Pampanga Pangasinan Rizal Sorsogon Tarlac Tayabas Zambales Marinduque Masbate Misamis Surigao Zamboanga Mindoro Negros Occidental Negros Oriental Panay Antique Capiz Ilolo Romblon Samar Number of municipalities 1 11 18 9 264 2 8 14 1 22 2 23 14 1 16 1 23 13 1 17 21 30 17 3 8 9 18 2 4 20 18 1 1 4 30 20 10 72 12 23 37 1 5 441 Cases 0 1911 2288 569 30 271 264 1204 3080 4 1427 50 1490 884 360 1306 24 2619 3661 4621 1346 1044 4163 715 225 312 223 1249 246 188 2271 1883 198 190 283 5011 4212 (000) (7098) (3500) (1463) (8411) (1103) (26657) (11951) (4362) (6390) (350) (6382) (6559) (2036) (7514) (344) (17624) (28649) (21011) (10120) (4689) (10552) (4815) (1868) (2337) (1484) (12320) (4761) (4305) (8890) (13899) (1994) (9182) (8757) (10257) (13871) Deaths 3 1274 1323 396 22 517 190 861 2527 2 960 33 1041 606 279 864 14 2227 2819 3487 1119 753 3036 470 87 217 170 755 168 116 1137 953 86 98 262 3328 2694 (2253) (4732) (2024) (1018) (6257) (794) (19063) (9805) (2181) (4299) (231) (4459) (4496) (1578) (4971) (201) (14986) (22060) (15855) (8414) (3382) (7696) (3165) (722) (1625) (1131) (7447) (3251) (2656) (4451) (7035) (866) (4736) (8107) (6814) (8872)

Marinduque Masbate Mindanao

Mindoro Negros

Romblon Samar Total

799 (4322) 27 713 (35068) 782 (5958) 2984 (11698) 23 947 (59285) 200 (3784) 270 (1017) 71 221 (9327)

634 (3429) 16 691 (21121) 538 (4099) 1937 (7593) 14 216 (35194) 74 (1400) 259 (975) 47 548 (6227)

Rates per 10 000 population (1903 census) are shown in parentheses. Sub-province of Tayabas.

DIFFUSION PROCESSES AND WAR IN THE PHILIPPINES

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 Manila, 20 March 1902 ' 19 April 1902 Orion, Hagonoy, 19 April 1902 ' Nueva Caceres, 19 April 1902 Calamba, 19 April 1902 ~ Binan, 26 April 1902 Santa Cruz, 3 May 1902 Tacloban, 10 May 1902 Batangas, 17 May 1902 Tayabas 17 May 1902 Pangasinan 24 May 1902 Sumar, 31 May June 1902 ' 14 June 1902 Calapan, Carigara, 28 June 1902 ' Boac, 5 July 1902 ' 12 July 1902 Cebu, ' Catmon, 23 August 1902 Iloilo, 23 August 1902 Surigao, 16 September 1902 Misamis, 31 January 1903 Tobogan

77

China Sea

Pacific Ocean

11

3 2

7 6 5 9 13

10 4 15

18 21 17 16

12 8 14

19

20

Figure 3. Diusion of wave I of the cholera epidemic, Philippine Islands, March 1902February 1903. The reconstruction is based on the textual accounts of the Chief Quarantine Ocer for the Philippine Islands. Vectors show the spatial links in the transmission of cholera; the date and time of appearance of cholera in various municipalities and provinces is indicated. Source: Public Health Reports.

By mid-April it had become evident that these eorts to quarantine Manila from the rest of the archipelago had failed (Figure 3). The dispatches from the Chief Quarantine Ocer recount how the disease was rst carried to two towns on Manila Bay, Orion and Hagonoy, by escapees aboard local bancas (a type of native sailing vessel).[41] Further localized spread from Manila occurred down the Pasig River and into lake Laguna de Bay, with the lakeside towns of Calamba, Binan and Santa Cruz infected by early May. From La Laguna province, the bacterium spread overland to Batangas with onwards carriage to Calapan on the adjacent island of Mindoro.[42] From Mindoro,

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M. SMALLMAN-RAYNOR AND A. D. CLIFF

the bacterium was carried by banca to the island of Marinduque in July.[43] Meanwhile, northwards spread from Manila occurred along the Pangasinan railway, eventually reaching La Union province by June.[44] To set against this contagious wave-like expansion outwards from Manila, as early as April 1902 we obtain the rst impression of long-distance carriage of the bacterium by the United States Army. A dispatch from the Chief Quarantine Ocer recounts how a troopship, headed from Manila, carried the bacterium to the port city of Nueva Caceres, south-eastern Luzon, in mid-April.[45] This establishment of Nueva Caceres as an epidemic bridgehead was to play a pivotal role in the subsequent appearance of the disease in the southern islands. By early May, the bacterium had appeared in Tacloban, Leyte Island, with Nueva Caceres the suspected source.[46] From here, the disease spread rapidly to the adjacent islands, the arrival of the disease in the island of Cebu in August 1902 having been documented in particular detail:
a banca arrived at Tobogan (sic.), on this island [Cebu], with a dead Filipino on board from Carigara, Leyte, and requested permission to enter that port and to inter the dead man. This was refused by the presidente. . . . [T]he banca had gone, after this refusal, ` to Catmon, where it was allowed to land and the body buried. Following this, within a few days (the exact time not known), several cases of death occurred preceded by vomiting and diarrhea.[47]

Although no source is reported for Negros Island, some link to the outbreak in the adjacent Cebu must be suspected. But, once in Negros, the disease spread by native sailing vessel to the populous island of Panay by late August 1902[48] and Misamis province on the far southern island of Mindanao by January of the following year.[49]

Numerical evidence: diffusion processes at different spatial scales

The textual record takes us thus far in unravelling the diusion of wave I. In this section, we turn to the numerical evidence in database 1 to see what further information about the diusion process can be gleaned from it. The analysis begins with a comment on the quality of the numerical evidence contained in the Public Health Reports. Then, after a brief review of diusion processes, complementary statistical techniques are applied to identify the manner in which cholera spread on the spatial levels of nation, island and province. Data completeness. Some idea of the completeness of the statistical data included in the Public Health Reports can be gained from the reports of J. C. Perry, the Chief Quarantine Ocer. For example, in his dispatch of 2 August 1902, Perry estimated the reporting completeness for cholera at 80 per cent.[50] Six weeks later, he revised his estimate down to 70 per cent, only to raise it to 75 per cent at the end of the year.[51] Certainly, the dispatches recount the logistical diculties encountered in the surveillance programme, particularly in the provinces. For example, the breakdown in telecommunications between Manila and the rest of the archipelago in the early weeks of November 1902 prompted Perry to warn that the reported data was . . . not a true index of the prevalence of cholera outside of Manila.[52] Rather less optimistic estimates of statistical completeness are gained when the data in the Public Health Reports are compared with mortality counts included in Volume III of the 1903 census. The latter source registered a national total of 137 505 cholera deaths for the year 1902.[53] A total of 45 625 cholera deaths were recorded in the Public

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Health Reports for the same period, representing a statistical completeness of about 33 per cent for cholera mortality. Because of these uncertainties about the accuracy of the absolute disease counts, the n50 spacetime matrices in database 1 were reduced to a binary basis, recording 1 if a case or death occurred at a given spacetime location and 0 otherwise. All the analysis described in this paper is based on these binary matrices of disease presence/absence. Diffusion processes. Accounts of the spread of an infectious disease usually recognize three main types of diusion process.[54] A contagious process describes the situation in which the disease moves from its centre of introduction to its physically nearest neighbouring centres. These, in their turn, transmit the disease to their geographically nearest neighbours, and so on. In this manner, the disease spreads in a wave-like manner outwards from its point of introduction. Alternatively, a hierarchical process describes the situation in which the disease moves progressively through the urban hierarchy. Typically, the initial point of introduction of a disease is the largest urban centre. Then, urban centres next in size follow, and so on, through to the smallest settlements. Finally, a mixed process describes the situation in which the spread pattern contains components of both contagious and hierarchical diusion. A number of methods have been developed for the identication and analysis of these diusion processes.[55] In this paper, two complementary statistical methods are applied to the Philippines data: (1) multiple regression analysis; and (2) spatial autocorrelation. Regression analysis: diffusion patterns in space Method. In this approach, the time-ordered sequence of appearance of a disease in the settlements of an urban system is modelled as a function of: (1) urban population size, representing the hierarchical component in the spread process; and (2) geographical distance from the settlement of initial introduction, representing the contagious component.[56] Specically, for a given geographical area of the Philippines (nation, island or province), the rst week in which cholera was recorded is coded as week 1, and for municipality i, the week in which the disease was rst reported in that municipality is coded as week 2, or 3, or 4, etc. This week is denoted as t i . Then, the regression model loge(t di )+ei i )=b0+bi loge(Pi )+b2 loge( (1)

was postulated. Here, Pi is the population of municipality i in 1903, di is the straight-line distance (in kilometres) of that municipality from the municipality in which cholera was rst reported and ei is an error term. For many areas of the Philippines, the independent variables, Pi and di, can be shown to display a double-logarithmic relationship with t i ; the logarithmic transformations in equation (1) serve to linearize these. The regression model in equation (1) was tted to each of the n (municipality)50 (weeks) spacetime matrices of cholera morbidity at the spatial levels of nation, island and province. Model tting was by ordinary least squares using a stepwise algorithm. Because of the small sample sizes (less than eight infected municipalities) in some provinces and islands, analysis was restricted to 32 areas (24 provinces, seven islands and the nation). Where more than one municipality was recorded as the point of introduction for a given area, di was estimated as the average distance di of municipality i from the introduction points. Finally, one potential complication in the regression procedure is possible co-linearity between population size and distance. In particular,

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4.0

M. SMALLMAN-RAYNOR AND A. D. CLIFF

4.0 (b)

(a)

Loge(time)

3.0

3.0

2.0

2.0

1.0

1 Loge(distance)

1.0

11 Loge(population)

Figure 4. Spread processes on the national level, cholera wave I. (a) Relationship between the time of rst appearance of cholera in each of 440 municipalities and distance from epidemic origin. (b) Relationship between the date of rst appearance of cholera in each of 440 municipalities and population size. All variables have been logarithmically transformed. Superimposed on each graph is a trend line tted to the data by ordinary least squares.

a decrease in municipality size with increasing distance would hinder separation of the contagious and hierarchical components in the model. Consequently, Pearsons r correlation coecient was used to assess the level of correlation between the independent variables in each model. Results. The application of regression analysis to the diusion problem is illustrated graphically for the Philippine Islands as a whole in Figure 4, although the index settlement (Manila) has been omitted. A striking feature of Figure 4 is the positive association between distance and time to infection [Fig. 4(a)]. Generally, municipalities proximal to the point of introduction of cholera (Manila) were infected rst, with more distant centres infected at increasingly later dates. Such a pattern accords with the operation of a spatially contagious component in the diusion process. However, only very weak evidence exists for the operation of a hierarchical component [Fig. 4(b)]. Under this process, an inverse association between the {loge(Pi )} and the {loge(t i )} (that is, the larger the municipality, the shorter the time to infection) would be expected. The low association is indicated by the near-horizontal regression line in Figure 4(b). Table 3 examines the spread process using the framework of the multiple regression model dened in equation (1). National level. Model 1 shows that time to infection is positively associated with the distance variable and negatively associated with the population variable; although just statistically signicant, the low and positive correlation (rPd=+014; 95 per cent condence interval +005 to +023) between the independent variables suggests that the modelling procedure was reasonably successful in separating the hierarchical and contagious components. As would be expected from the simple regressions in Figure 4, however, the relative importance of the distance variable is underscored by its entry in step 1 of the model. Taken together, these results indicate that wave I of the cholera epidemic spread through the archipelago as a mixed diusion process with a dominant contagious component. Islands and provinces Models 232 in Table 3 summarize the results of the analysis at the ner geographical levels of island and province. For each model, only those

T 3 Results of stepwise multiple regression analysis to identify diffusion processes at the levels of nation, island and province
Independent variable, slope coecient (t-statistic) r2(F )
1

Model rPd Step 1 (500) Step 2

Area (NATION, ISLAND, Province)

Process

(t-statistic)

(259) (242)

055 091 091 075 075 058 058 028 056 048 058 058 041

(26900) (1379) (1379) (4190) (4190) (826) (826) (5011) (752) (1018) (1256) (2914) (833)

DIFFUSION PROCESSES AND WAR IN THE PHILIPPINES

(235) (239)

032 044 063 064 036 024

(314) (867) (1108) (1594) (1533) (484)

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 22 16 17 18 19 20 21 23 24 25 26 27 28 29 30 31 32 060 025 057 035 043 034 073 031 (2418) (497) (3488) (985) (612) (3546) (2179) (890)

NATION BOHOL Bohol CEBU Cebu LEYTE Leyte LUZON Bataan Batangas Bulacaan Camarines Cavite Ilocos Sur La Laguna La Unio n Nueva Ecija Pampanga Pangasinan Rizal Tarlac Tayabas Zambales MINDANAO Misamis NEGROS Negros Occidental Negros Oriental PANAY Antique Capiz Ilolo

440 11 11 16 16 8 8 263 8 13 21 23 14 15 23 13 16 21 29 17 8 9 17 18 17 28 20 10 72 10 22 36

Loge(di ), 039 (2316) Loge(Pi ), 000 Loge( di ), 007 (371) Loge( di ), 007 (371) di ), 013 (647) Loge( Loge(di ), 013 (647) Loge(di ), 022 (287) Loge(di ), 022 (287) Loge( di ), 029 (994) Loge(Pi ), 010 Loge(di ), 037 (274) Loge(Pi ), 014 (319) Loge(di ), 055 (420) Loge(Pi ), 031 Loge( di ), 088 (540) di ), 075 (289) Loge( No signicant regressor Loge(Pi ), 029 (314) Loge( di ), 031 (294) Loge( di ), 022 (367) Loge(Pi ), 026 di ), 067 (499) Loge(Pi ), 045 Loge( Loge( di ), 012 (391) Loge(Pi ), 019 (220) No signicant regressor No signicant regressor No signicant regressor Loge( di ), 003 (492) Loge( di ), 010 (223) Loge(di ), 009 (591) di ), 008 (314) Loge( Loge( di ), 008 (247) Loge( di ), 011 (596) Loge(di ), 020 (467) Loge( di ), 014 (298) No signicant regressor Mixed Contagious Contagious Contagious Contagious Contagious Contagious Mixed Contagious Hierarchical Mixed Contagious Contagious Hierarchical Contagious Mixed Mixed Contagious Hierarchical Contagious Contagious Contagious Contagious Contagious Contagious Contagious Contagious

014 034 034 004 004 019 019 015 038 053 008 036 026 030 015 019 015 005 026 006 040 012 032 016 071 011 009 044 020 015 041 031

035 (8559) 034 (2495) 034 (2495) 049 (2654) 049 (2654) 038 (957) 038 (957) 039 (7891) not calculated 079 (1018) 040 (2998) 046 (681) 027 (620) 044 (1391) 056 (2442) 027 (807) 040 (1978) 035 (1016) 042 (1854) 056 (1063) 034 (490) 023 (1487) Not calculated 049 (1419) 049 (509) 025 (1379) 025 (936) 029 (1506) 037 (1875) 031 (530) 038 (522) 042 (1418)

81

Signicant at the p=005 level (two-tailed test). One extreme outlier omitted. Two extreme outliers omitted. Insucient municipalities above the national average size for the computation of

82

M. SMALLMAN-RAYNOR AND A. D. CLIFF

independent variables which made a statistically signicant contribution to the model are shown. In some areas, one or more municipalities served as extreme outliers that inuenced the parameters of the regression model. All results relate to models with extreme outliers omitted; these are indicated in Table 3. The most striking feature of models 232 is the importance they attach to the distance variable. All seven islands and two-thirds of the provinces display a positive association between loge(t di ). The distance variable was entered as step 1 in 23 areas i ) and loge( (seven islands and 16 provinces) and formed the sole signicant regressor in 19 models (six islands and 13 provinces). Only eight areas (one island and seven provinces) displayed a negative association between loge(ti) and loge(Pi ), with the population variable entered as step 1 in just three models. Both independent variables failed to make a signicant contribution to ve models. Finally, it is noteworthy that only two areas displayed evidence of a statistically signicant correlation between the independent variables. These results conrm the importance of a distance-dominated diusion process in many geographical areas and on all spatial scales. Three-quarters of the areas displayed either a purely contagious process (six islands and 13 provinces) or a mixed process with a dominant contagious element (one island, three provinces and the nation). Only three areas (provinces) displayed a purely hierarchical process. Rank size rule. The structure of an urban system may inuence the type of transmission process in operation.[57] In particular, the operation of a hierarchical diusion process is, inter alia, dependent on a well-developed settlement hierarchy.[58] It is instructive, therefore, to examine the results of the regression analysis in Table 3 in the context of urban size structure via the ranksize rule.[59] Let Pk be the population of the kth municipality in the series k=1, 2, 3, . . ., n in which all municipalities are arranged in descending order by population. Then, the ranksize rule can be written as log(Pk)=log 0 1(logk)+ek (2)

where 0 and 1 are constants to be estimated and ek is an error term. Full details of the model are given elsewhere,[60] but larger (negative) values of 2 mark larger (relative) dierences in municipality size. Equation (2) was tted to each area in Table 3 by ordinary least squares. Because of the complications encountered in the tting of the ranksize rule to the lower limb of the size hierarchy,[61] analysis was restricted to municipalities with populations in excess of the national average municipality size (that is, 6846 in 1903). An expectation of the ranksize analysis is that large (negative) values of 1, which identify more pronounced dierences in urban size structure, are more likely to be associated with the operation of a hierarchical diusion process. Conversely, low values of 1 mark less pronounced dierences in size structure and therefore are less likely to be associated with a hierarchical diusion process. The results of the present analysis conrm this expectation. As Table 3 shows, the largest (negative) values of 1 (less than 05) are found in the three areas (Batangas, La Laguna and Rizal provinces) for which a purely hierarchical diusion process was identied. Moreover, when areas are grouped by diusion process, the average values of 1 (that is, 1) reduce systematically from 064 (purely hierarchical) to 038 (mixed contagioushierarchical) and to 035 (purely contagious).

Spatial autocorrelation analysis: diffusion patterns in time

Although regression analysis provides an insight into the processes by which cholera rst spread to each municipality in a given area, an alternative approach is required

DIFFUSION PROCESSES AND WAR IN THE PHILIPPINES

83

to determine the changing role of contagious and hierarchical components as the epidemic unfolded over time. One way to assess this temporal variability is by the application of spatial autocorrelation analysis. Method. The application of spatial autocorrelation analysis to epidemiological diusion studies is described by Cli et al.[62] In brief, the area of the Philippines (province, island and nation) over which the spread is occurring is treated as a graph consisting of a set of nodes (municipalities) and the links between them. These links can be formed to give a graph which corresponds closely to a hypothetical diusion process. For the purposes of the present analysis, each of the 32 areas (the nation, seven islands, 24 provinces) in Table 3 was reduced to two graphs. (1) Minimum spanning tree (MST).[63] This denes the area such that all municipalities are joined to their geographically nearest neighbouring municipalities. This network implies a highly localized, contagious, spread process. (2) Urban population hierarchy. This denes the area such that all municipalities are joined to their next largest, and next smallest, municipalities in terms of the rank order of the population size in 1903. This network implies a strict hierarchical diusion process. To discriminate between the two graphs, for each of the 32 geographical areas a binary outbreak/no outbreak map was drawn for each of the 50 weekly periods of the epidemic. Vertices (municipalities) on each graph so dened were coded black (B ) for cases of cholera or white (W ) for no cases, and the BW join-count statistic under non-free sampling was computed for each to measure the degree of contagion present.[64] The BW statistic is dened as BW=1 2

 w (x x )
ij i j n=1 n=1

(3)

irj

where wij=1 if a link existed between the vertices i and j on the graph in question and wij=0 otherwise; xi=1 if vertex i was colour-coded B and xi=0 if the vertex was coded W. In the present analysis, the sampling distribution of BW under the null hypothesis of no contagion in outbreaks was assumed to be normally distributed for graphs with 20 or more vertices; BW may be tested for signicant departure from its null value as a standardized normal (z) score.[65] This standardized score marks the degree of correspondence between any graph and the transmission path followed by the diusion wave: the larger (negative) the standardized score for BW, the greater the correspondence between the hypothetical and the actual diusion paths. For graphs with less than 20 vertices, the approximation for BW joins described in Cli and Ord was applied.[66] Results. The national level results are illustrated in Figure 5. Figure 5(a) plots the weekly number of cholera cases recorded; the vertical peaked line drawn at week 29 marks the peak week of the infection wave. Figure 5(b) and (c) give the autocorrelation results in the corresponding weeks of the epidemic for the MST graph and the hierarchy graph, respectively. For each weekly period, the vertical axes plot the z-scores [x (1) for plotting convenience] evaluated for the BW statistic of equation (3). Note that, due to the connement of cholera to Manila during the rst four weeks of the observation period, the results are illustrated for weeks 550 only. The horizontal lines drawn at

84
10 000 8000 6000 4000 2000 0 7 6 5 4
z (x-1)

M. SMALLMAN-RAYNOR AND A. D. CLIFF

Pre-peak (a) Post-peak

Cases

(b)

3 2 1.65 1 0 1 2 5 (c)

z (x-1)

1.65 0 5 10 15 20 25 30 Week 35 40 45 50

Figure 5. Join-count statistics for cholera diusion at the national level, Philippine Islands. (a) Weekly count of cholera cases, weeks 550. The remaining charts plot weekly values of the BW join-count statistic as a z-score (x1, for convenience in plotting) on a minimum spanning tree (MST) graph (b) and an urban population hierarchy graph (c). The solid horizontal line at z= 165 marks the P=005 signicance level in a one-tailed test for positive spatial autocorrelation; statistically signicant scores are identifed by the shaded bars. For reference, the vertical dashed line marks the peak week of the epidemic.

z=1.65 mark statistically signicant standard. Normal deviates ( =0.05 level, onetailed test); bars above this value have been shaded. Figure 5(b) shows that the MST graph is important throughout the course of the infection wave; strong and positive spatial autocorrelation is recorded for 41 of the 46 weekly periods. Although a reduction in z-scores can be identied over time (indicative of a weakening in the contagious component during the course of the infection wave), scores remain very high until week 50. In contrast, Figure 5(c) shows that the urban hierarchy graph is important for only a seven-week period leading to the epidemic peak. These ndings suggest a transmission process which started through localized spread to nearest neighbour settlements. This contagious process was bolstered by hierarchical spread as the epidemic developed to its peak, reverting to a purely contagious process during epidemic fade-out. Such an interpretation accords with the mixed diusion process identied by multiple regression analysis in model 1 of Table 3.

DIFFUSION PROCESSES AND WAR IN THE PHILIPPINES

Number of significant BW scores

85

14 12 10 8 6 4 2 0

Number of significant BW scores

(a)

14 12 10 8 6 4 2 0

(b)

Number of significant BW scores

14 12 10 8 6 4 2

Number of significant BW scores

(c)

14 12 10 8 6 4 2

(d)

0 10 8 6 4 2 0 2 4 6 Pre-peak Post-peak

8 10

0 10 8 6 4 2 0 2 4 6 Pre-peak Post-peak

8 10

Figure 6. Join-count statistics for cholera diusion at the levels of province and island, Philippine Islands. The charts plot the number of times a signicant BW statistic was obtained for various weekly periods. The results are shown at the p=01 signicance level (bars) and the p=005 signicance level (line trace) in a one-tailed test for positive spatial autocorrelation. (a) Minimum spanning tree (MST) graph, provinces. (b) Urban population hierarchy graph, provinces. (c) MST graph, islands. (d) Urban population hierarchy graph, islands. Vertical pecked lines indicate epidemic peaks, denoted at week 0 on the horizontal axis. The time scale on the horizontal axes is in weeks either side of the epidemic peaks. The maximum possible scores in a given week are 24 for provinces in (a) and (b) and seven for islands in (c) and (d).

Islands and provinces. As judged by the number of signicant counts in Figure 6, the spatial levels of province and island have three features in common: (1) from the start of each local epidemic wave until shortly after the peak week, spatially contagious spread was more important than hierarchical spread; (2) contagious spread was most important around the peak week; (3) hierarchical spread was generally most important from two or three weeks before epidemic peaks to six or seven weeks after. These island and province ndings are broadly similar to those for the national level illustrated in Figure 5; at these scales, the transmission process also started as localized spread among nearest neighbour settlements, and this contagious spread was joined by a hierarchical component in the immediate build-up to epidemic peaks. However, unlike the national spread process, there is no evidence of reversion to purely contagious spread in the fade-out phase of the epidemic. Finally, Figure 6 also shows that diusion patterns were much more strongly developed at the provincial- than the island-level scale.

86

M. SMALLMAN-RAYNOR AND A. D. CLIFF

Conclusion
Recent research into the 19024 cholera epidemic in the Philippine Islands has emphasized its link to the social and political upheavals of war and annexation.[67] This paper has sought to add a further, spatial, dimension to the story by exploring the diusion of the epidemic during its rst year, March 1902 to February 1903. The analysis has been facilitated by the richness of the information contained in a littleused archival source in historical epidemiological studies, namely the international sanitary reports published weekly in the contemporary US Public Health Reports. The reconstruction of the nation-wide spread of cholera (Figure 3) has revealed several key features in the spatial development of the epidemic. First, it has highlighted the role of localized, or spatially contagious, diusion as the epidemic spread wavelike from its point of introduction in Manila City. Here, the locally intense nature of native river and sea trac played a central role, and this was bolstered by overland spread along the Luzon railway. Second, it has illustrated the importance of militaryassociated events in epidemic development. In particular, the long-distance carriage of cholera by troopship from Manila to Nueva Caceres formed a critical link in the subsequent diusion of cholera to the more southerly islands. Finally, the reconstruction has underlined the ineectual nature of many of the early counter-measures taken to control the diusion process. The statistical techniques of multiple regression analysis and spatial autocorrelation analysis have thrown further light on the nature of the cholera diusion process, and at geographical scales for which textual evidence is fragmentary or absent. The analyses have revealed that the disease spread with a dominant contagious component in many geographical areas, on all spatial scales and throughout the duration of the infection wave. In contrast, evidence for the operation of a hierarchical component was statistically weaker, geographically far more limited and temporally restricted to the late build-up and/or fade-out stages of the wave. The lack of a well-developed urban hierarchy in many areas of the Philippines would limit the operation of a strong hierarchical component in the spread process.[68] If we set our ndings alongside those described in other diusion studies for both cholera and other transmissible diseases, then some general principles emerge. (1) Where a well-developed ranksize distribution exists, hierarchical rather than distance eects are likely to dominate the diusion process; in other circumstances, as in the Philippines, contagious diusion will be the norm. In his classic account of the geographical propagation of cholera in the United States in the three great epidemics of 1832, 18489 and 1866, Pyle[69] found that the diusion process switched from distance dominated in the rst epidemic, through a mixed hierarchical/ contagious process in the second, to a purely hierarchical process in the third. He showed that this switch occurred as the urban hierarchy emerged in the United States over the course of the nineteenth century. Working with US and British cities, Cli et al.[70] found, for six diseases (diphtheria, enteric fever, measles, scarlet fever, tuberculosis and whooping cough) in the period, 18871912, when a fully developed size hierarchy existed, that geographical spread of these diseases occurred primarily through the urban system rather than among neighbouring cities. (2) Distance eects are most sharply dened around epidemic peaks. The autocorrelation results of Cli et al. (inuenza and measles in Iceland)[71], and of Haggett (measles in Cornwall, UK)[72] support our ndings in this regard for cholera in the Philippines. (3) War does not appear to change the fundamental structure of the diusion process. Since the other studies referred to above examine data from times of peace and

DIFFUSION PROCESSES AND WAR IN THE PHILIPPINES

87

war (the second US cholera epidemic occurred immediately after the War Between the States), we may hypothesize, given the analyses presented in this paper, that war may not materially alter the geographical engines driving diusion processes, although it may substantially change timings. This speculation requires systematic investigation. Department of Geography, University of Nottingham, University Park, Nottingham, NG7 2RD, UK Department of Geography, University of Cambridge, Downing Place, Cambridge, CB2 3EN, UK.

Acknowledgement
The work described has been undertaken as part of a ve-year programme of research entitled Disease in War, 18501990: geographical patterns, spread and demographic impact, funded by the Leverhulme Trust. Their nancial support is gratefully acknowledged.

Notes
[1] R. M. Gareld and A. I. Neugat, Epidemiologic analysis of warfare: a historical review, Journal of the American Medical Association 266 (1991) 68892; H. O. Lancaster, Expectations of Life: A Study in Demography, Statistics, and History of World Mortality (New York 1990) 31440. [2] F. Prinzing, Epidemics Resulting from Wars (Oxford 1916); S. Dumas and K. O. VedelPetersen, Losses of Life Caused by War (Oxford 1923). [3] F. Prinzing, op. cit., 171. [4] Ibid., 186. [5] K. de Bevoise, Agents of Apocalypse: Epidemic Disease in the Colonial Philippines (Princeton 1995). [6] See, for example: G. F. Pyle, Diusion of cholera in the United States, Geographical Analysis 1 (1969) 5975; A. D. Cli, P. Haggett, J. K. Ord and G. R. Versey, Spatial Diffusion: An Historical Geography of Epidemics in an Island Community (Cambridge 1981) 2732; R. F. Stock, Cholera in Africa: Diffusion of the Disease 19701975 with Particular Emphasis on West Africa (London 1976); K. D. Patterson, Cholera diusion in Russia, 18231923, Social Science and Medicine 38 (1995) 117191. [7] R. C. Ileto, Cholera and the origins of the American sanitary order in the Philippines, in D. Arnold (Ed.), Imperial Medicine and Indigenous Societies (Manchester 1988) 12548; R. Sullivan, Cholera and colonialism in the Philippines, 18991903, in R. MacLeod and M. Lewis (Eds), Disease, Medicine and Empire: Perspectives on Western Medicine and the Experience of European Expansion (London 1988) 284300; de Bevoise, op. cit. [8] United States Public Health Service, Public Health Reports (Washington, D.C.). [9] J. C. Perry was appointed to the post of Chief Quarantine Ocer in January 1900. He retained this position until March 1903, when he was succeeded by Victor G. Heiser. [10] The role of islands as laboratories for the study of epidemiological diusion processes is discussed in: Cli, Haggett, Ord and Versey, op. cit.; A. D. Cli, P. Haggett and R. Graham, Reconstruction of diusion processes at dierent geographical scales: the 1904 measles epidemic in northwest Iceland, Journal of Historical Geography 9 (1983) 2946; A. D. Cli and P. Haggett, The epidemiological signicance of islands, Health and Place 1 (1995) 199209. [11] United States Bureau of the Census, Census of the Philippine Islands (Volumes IIV) (Washington D.C., 1905). [12] Ibid. [13] de Bevoise, op. cit., 18. [14] See note 9. [15] See note 7.

88 [16] [17] [18] [19] [20] [21] [22] [23] [24] [25] [26] [27]

M. SMALLMAN-RAYNOR AND A. D. CLIFF de Bevoise, op. cit.; Ileto, op. cit. United States Public Health Service, op cit. XVII (1902) 1759. Ibid., 2131. de Bevoise, op. cit., 178. Sullivan, op. cit. Ileto, op. cit., 1289; de Bevoise, op. cit., 1789. Chief Surgeons Report, Third Separate Brigade, quoted in Ileto, op. cit., 129. See, for example, de Bevoise, op. cit., 1789. R. S. Speck, Cholera, in K. F. Kiple (Ed.), The Cambridge World History of Human Disease (Cambridge 1993) 6429. The geographical dispersion of the various nineteenth-century global pandemics of Asiatic cholera is mapped in A. D. Cli and P. Haggett, Atlas of Disease Distributions: Analytic Approaches to Epidemiological Data (Blackwell 1988) 5. de Bevoise, op. cit. United States Public Health Service, op. cit. The nature and scope of the information included in the Public Health Reports is reviewed in: A. D. Cli, P. Haggett, M. SmallmanRaynor, et al., The importance of long-term records in public health surveillance: the US weekly sanitation reports, 18881912, revisited, Journal of Public Health Medicine 19 (1987) 7684; A. D. Cli, P. Haggett and M. Smallman-Raynor, Deciphering Global Epidemics. Analytical Approaches to the Disease Records of World Cities, 18881912 (Cambridge 1998). See, for example, Annual Report of the Philippines Commission, 1903 (Part II, Appendix B) (Washington D.C. 1904). United States Bureau of the Census, op. cit. Ibid. Ibid. The national series in Figure 2 have been formed by summing the weekly counts of cholera cases, and cholera deaths, recorded in the Public Health Reports for each of 570 infected municipalities, March 1902February 1904. Waves I and II were formally dened by reducing the national series of cholera cases in Figure 2 to standard normal score form. A sustained weekly score of less than 05 standard deviations below the zero mean was identied between week 51 (7 March 1903) and week 60 (9 May 1903). In this manner, wave I was dened as weeks 150 (22 March 190228 February 1903) and wave II as weeks 61103 (16 May 19036 February 1904). M. Smallman-Raynor and A. D. Cli, The Philippines Insurrection and the 19024 cholera epidemic II: diusion patterns in war and peace, Journal of Historical Geography 24, 2 (1997) (in press). Only those areas classied as municipalities under the 1903 census were included in the present analysis. Marinduque, a sub-province of Tayabas, was classied as a separate province for the purposes of the present analysis. United States Public Health Service, op. cit., XVII (1902) 716. Ibid., 1090. Speculation concerning the importation of cholera with fresh vegetables rested with the traditional use of human manure by Chinese farmers; see Sullivan, op. cit. In his dispatch of 30 March 1902, the Chief Quarantine Ocer explained that Manila was the greatest vegetable market in the Orient, as nothing of that character is produced here, all such supplies have to be imported, and all green vegetables such as cabbage, celery, lettuce, and cauliower have come from the Canton districts [United States Public Health Service, op. cit., XVII (1902) 108990]. In a later communication, the Quarantine Ocer dismissed speculation concerning another possible source of the disease (Hong Kong) on the grounds of available epidemiological evidence (Ibid., 1531). United States Public Health Service, op. cit., XVII (1902) 1090. Ibid., 132930. Ibid., 1759. Ibid., 21302. Ibid. Ibid. See also Ileto, op. cit. United States Public Health Service, op. cit., XVII (1902) 132931. Ibid., 20745.

[28] [29] [30] [31] [32] [33]

[34] [35] [36] [37] [38] [39]

[40] [41] [42] [43] [44] [45] [46] [47]

DIFFUSION PROCESSES AND WAR IN THE PHILIPPINES [48] [49] [50] [51] [52] [53] [54] [55] [56] [57] [58] [59] [60] [61] [62] [63] [64] [65] [66] [67] [68] [69] [70] [71] [72]

89

Ibid., 2483. Ibid., 2771. Ibid., 22401. Ibid., 2488; United States Public Health Service, op. cit., XVIII (1903) 1089. Ibid., 46. United States Bureau of the Census, op. cit., Volume III, 47. Cli and Haggett, op. cit. Ibid. See Pyle, loc. cit. for a graphical approach to the problem. Pyles analysis is reworked within a multiple regression framework in Cli, Haggett, Ord and Versey, op. cit., 2732. P. Haggett, A. D. Cli and A. Frey, Locational Analysis in Human Geography (London 1977) 132. See, for example Pyle, loc. cit. Haggett, Cli and Frey, op. cit., 11026. Ibid. Ibid. Cli, Haggett, Ord and Versey, op. cit., 99102. A. D. Cli, P. Haggett and J. K. Ord, Spatial Aspects of Inuenza Epidemics (London 1986) 1825. For a formal denition of the minimum spanning tree, see Haggett, Cli and Frey, op. cit., 82. The BW join-count statistic is described in A. D. Cli and J. K. Ord, Spatial Autocorrelation (London 1973) 47. The expectation and variance of BW under H0 is described in Cli and Ord, Ibid. Ibid., 48. In all instances, evaluation was for positive spatial autocorrelation under nonfree sampling. See note 7 for examples of this work. Cli, Haggett and Frey, op. cit., 132. Pyle, op. cit. Cli, Haggett and Smallman-Raynor (1997), op. cit., Chapter 6. A. D. Cli, P. Haggett and J. K. Ord, op. cit., 1825. P. Haggett, Hybridizing alternative models of an epidemic diusion process, Economic Geography 52 (1976) 13646.