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Understanding the links between environmental and wildlife elemental concentrations is key to help assess ecosystem functions and the potential effects of legacy pollutants. In this study, livers from 448 European badgers (Meles meles) collected across the English Midlands were used to investigate the relationship between elemental concentrations in topsoils and wildlife. Mean soil sample concentrations within 2 km of each badger, determined using data from the British Geological Survey's 'Geochemical Baseline Survey of the Environment', were compared to badger liver elemental concentrations, focusing primarily on Ag, As, Cd, Cr, Cu, K, Mn, Pb, Se, Zn. Generally, the badgers appeared to have elemental concentrations comparable with those published for other related animals, though Cu concentrations tended to be lower than expected. While there was no relationship between soil and badger liver concentrations for most biologically essential elements, biologically non-essential elements, specifically Pb, Cd, As, and Ag, were positively correlated between soil and badger livers. Lead and Cd, the elements with the strongest relationships between soils and badger livers, were primarily elevated in badgers collected in Derbyshire, a county with a millennia-long history of Pb mining and significant Pb and Cd soil pollution. Cadmium concentrations in badgers were also, on average, almost nine times higher than the local soil concentrations, likely due to Cd biomagnification in earthworms, a dietary staple of badgers. While badgers are good models for studying associations between soil and wildlife elemental concentrations, due to their diet, burrowing behaviours, and site fidelity, all flora and fauna local to human-modified environments could be exposed to and impacted by legacy pollutants.

This paper uses a robust method of spatial epidemiological analysis to assess the spatial growth rate of multiple lineages of SARS-CoV-2 in the local authority areas of England, September 2020–December 2021. Using the genomic surveillance records of the COVID-19 Genomics UK (COG-UK) Consortium, the analysis identifies a substantial (7.6-fold) difference in the average rate of spatial growth of 37 sample lineages, from the slowest (Delta AY.4.3) to the fastest (Omicron BA.1). Spatial growth of the Omicron (B.1.1.529 and BA) variant was found to be 2.81× faster than the Delta (B.1.617.2 and AY) variant and 3.76× faster than the Alpha (B.1.1.7 and Q) variant. In addition to AY.4.2 (a designated variant under investigation, VUI-21OCT-01), three Delta sublineages (AY.43, AY.98 and AY.120) were found to display a statistically faster rate of spatial growth than the parent lineage and would seem to merit further investigation. We suggest that the monitoring of spatial growth rates is a potentially valuable adjunct to outbreak response procedures for emerging SARS-CoV-2 variants in a defined population.

This paper presents the first systematic study of the spatial transmission of the 1929–33 epidemic of meningococcal meningitis and its association with local coal mining communities in three adjacent high incidence counties of England; Nottinghamshire, Derbyshire and the West Riding of Yorkshire. Drawing on a robust method of spatial epidemiological analysis (swash-backwash model), we demonstrate a gradient response with local levels of employment in coal mining for each of three key parameters of the epidemic wave: spatial velocity of transmission; duration of infectivity; and spatial reach. Partial least squares (PLS) regression analysis identifies the relatively young and fertile demographic of local mining communities as the principal determinant of the resulting epidemic burden. Other sociodemographic parameters, including established risk factors for invasive meningococcal disease (low social class, high residential density and overcrowding) are found to play little, or no, role in the spatial distribution of the disease. Our findings have importance for understanding the historic links between the coal mining industry and epidemic meningococcal meningitis, and point to possible present-day opportunities for intervention through the designation of coal mining communities as defined risk groups for meningococcal vaccines.

The Nazi ghetto system was one of the principal vehicles for the persecution of Jewish and other peoples in German-occupied Europe in World War II. Transport and confinement—twin pillars of the ghetto system—were intrinsically geographical matters that operated on scales from the international to the local and that shaped the demographic and epidemiological character of ghettos across Eastern Europe. This article uses geographical techniques of map-based visualization and spatial analysis to portray the demographic and epidemic history of the Nazi “model” camp-ghetto at Theresienstadt (Terezín) in the former German Protectorate of Bohemia and Moravia, 1941–45. Our study reconstructs the space-time pattern and demographic structure of transports of Jewish prisoners to the ghetto and their association with substantial outbreaks of communicable diseases in the ghetto. The study highlights the importance of a geographical approach to an understanding of the demographic and public health impacts of both the Holocaust and other genocidal events.

‘Global Origins and Dispersals’ addresses two key questions. First, how do epidemic diseases emerge and can their geographical origins be traced to any particular part of the world? Second, why do more infectious diseases appear to be emerging in recent decades and how far does this crudescence relate to the unprecedented changes in the global environment? The examination covers factors that, inter alia, have tended to increase the geographical scale of disease cycles, including the growth and relocation of the human population, globalization and the collapse of geographical space, and environmental changes associated with land use and climate change and variability. The origin and the spread of newly emerging infectious diseases are illustrated with reference to recent international epidemics of ‘bird flu’ associated with the avian influenza A (H5N1) virus, severe acute respiratory syndrome, and Ebola virus disease in West Africa (2013–16).

‘Epidemics in Small Communities’ develops an understanding of the ways in which an infection can achieve community circulation in small geographical areas. It begins by examining the local disease records of two doctors in general practice in the United Kingdom (William Pickles of Wensleydale and Edgar Hope-Simpson of Cirencester) to shed light on the processes whereby individual cases of diseases, such as measles and influenza, can develop into full-blown epidemics. The second half of the chapter focuses on Iceland as an island laboratory for the study of epidemic diffusion processes in the period 1902–1988. For this 87-year period, records of 131 discrete epidemic waves (with a recorded total of >0.5 million cases) of measles, influenza, and five other infectious diseases are examined in terms of wave spacing, wave velocity, and wave geography. These findings are related both to epidemiological theory and to aspects of the changing historical geography of the island.

‘Epidemics as Diffusion Waves’ establishes the parameters of the book. It begins by defining the basic building blocks of the study: infection, contagion, and disease. Key epidemiological concepts and terms are introduced and defined, and classic compartmental (susceptible → infective → recovered; SIR) approaches to epidemic modelling are outlined. Epidemic waves in the time domain are examined in terms of their shape (logistic model, Kendall waves), as repetitive wave trains (Bartlett threshold model), and as branching networks (Reed–Frost model). The second half of the chapter examines epidemic waves in the space domain. The swash–backwash model of the single epidemic wave introduces the concept of the spatial basic reproduction number R0A, the geographical analogue of the basic reproduction number R 0. Spatial simulations of diffusion waves are explored through the work of Torsten Hägerstrand. The chapter concludes with a consideration of dyadic (lag correlation and spatial interaction) approaches to epidemic modelling.

‘Infectious Disease Control’ examines the historical development of approaches to the geographical control, elimination, and eradication of infectious diseases. It begins at a local spatial scale, seven centuries ago, among the plague-ridden lazarettos of Venice. It ends at the global scale with twenty-first-century developments in the Internet-based monitoring and surveillance of infectious diseases. Basic spatial strategies for the control of infectious diseases (defensive isolation and offensive containment) are outlined, their historical development and application in the form of such measures as cordons sanitaires, isolation, and quarantine are reviewed, and their present-day forms highlighted. Vaccines and vaccination are reviewed as a second approach to disease control, alongside initiatives for the global eradication of infectious diseases such as smallpox and poliomyelitis. Disease surveillance continues to form a cornerstone of spatially focused control activities and, so, the chapter ends with a review of the evolution of disease intelligence systems down the centuries.

‘Pandemics, II: COVID-19’ explores the spatial and temporal patterns of infection, illness, and death due to the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19). It covers the period from the putative beginning of the COVID-19 pandemic in late 2019 to the turn of 2021. Consecutive sections review the basic epidemiological properties of the virus and the disease, the pattern of global dispersal, and the resulting patterns of reported disease activity in the United Kingdom and the United States. The swash–backwash model is used to analyse the spatial spread of the first wave of COVID-19 in England and to estimate the spatial velocity of wave expansion and retreat, January–June 2020. Approaches to the short- and longer-term forecasting of COVID-19 are illustrated with reference to sample states of the United States.

This paper uses a robust method of spatial epidemiological analysis to assess the spatial growth rate of multiple lineages of SARS-CoV-2 in the local authority areas of England, September 2020–December 2021. Using the genomic surveillance records of the COVID-19 Genomics UK (COG-UK) Consortium, the analysis identifies a substantial (7.6-fold) difference in the average rate of spatial growth of 37 sample lineages, from the slowest (Delta AY.4.3) to the fastest (Omicron BA.1). Spatial growth of the Omicron (B.1.1.529 and BA) variant was found to be 2.81× faster than the Delta (B.1.617.2 and AY) variant and 3.76× faster than the Alpha (B.1.1.7 and Q) variant. In addition to AY.4.2 (a designated variant under investigation, VUI-21OCT-01), three Delta sublineages (AY.43, AY.98 and AY.120) were found to display a statistically faster rate of spatial growth than the parent lineage and would seem to merit further investigation. We suggest that the monitoring of spatial growth rates is a potentially valuable adjunct to routine assessments of the growth of emerging SARS-CoV-2 lineages in a defined population.

Metapopulation dynamics play a critical role in driving endemic persistence and transmission of childhood infections. The endemic threshold concept, also referred to as critical community size (CCS), is a key example and is defined as the minimum population size required to sustain a continuous chain of infection transmission. The concept is fundamental to the implementation of effective vaccine-based disease control programmes. Vaccination serves to increase endemic threshold population size, promoting disease fadeout and eventual elimination of infection. To date, empirical investigations of the relationship between vaccination and endemic threshold population size have tended to focus on isolated populations in island communities. Very few studies have examined endemic threshold dynamics in 'mainland' regional populations with complex hierarchical spatial structures and varying levels of connectivity between subpopulations. The present paper provides the first spatially explicit analysis of the temporal changes in endemic threshold populations for one vaccine-preventable childhood infection (pertussis) in two dynamic regions of England and Wales: Lancashire and South Wales. Drawing upon weekly disease records of the Registrar-General of England and Wales over a 30-year period (January 1940-December 1969) regression techniques were used to estimate the endemic threshold size for pertussis in the two study regions. Survival analyses were performed to compare disease fadeout duration and probability for both regions in the pre-vaccine and vaccine eras, respectively. Our findings reveal the introduction of mass vaccination led to a considerable increase in threshold size for both Lancashire (~387,333) and South Wales (~1,460,667). Significant growth in fadeout duration was observed in the vaccine era for pertussis non-hotspots in both regions, consistent with geographical synchronisation of epidemic activity. Regional differences in endemic threshold populations reflect significant regional variations in spatial connectivity, population dispersion and level of geographical isolation.

This paper outlines the historical development of approaches to the geographical control of infectious diseases that have relevance today for interrupting the spatial transmission of COVID-19. Lockdown, isolation and social distancing have their origins in medieval Italy’s attempts to inhibit the spread of bubonic plague, whereas the practice of producing immunity by vaccination finds its early expression in the smallpox experiments of Edward Jenner in the 1790s. Since that time, vaccines have been used as a means of controlling the geographical spread of an expanding list of infectious diseases. Until a vaccine (or an effective treatment) is available, variants of the spatial control strategies that evolved in medieval Italy will remain the only means of controlling the COVID-19 pandemic.

The 1920–1935 epidemic of variola minor in England and Wales is a prime example of a major smallpox outbreak that spread in a national population with waning levels of vaccine-induced immunity. This paper examines the geographical course of the epidemic and the reasons why the disease was able to evade the (then) established protocols for smallpox control in many local government areas. The control issue is examined using archival records from the English county of Gloucestershire, where smallpox spread out of effective control in 1923. At the national level, our analysis demonstrates that the build-up (1920–1927) of the epidemic was characterised by a persistent core of reported cases of high intensity in the counties of central and northern England. Epidemic fade-out (1928–1935) was associated with an accelerated shift of disease activity to London and the southeast. Set against this national context, Gloucestershire represented a microcosm of the impediments to smallpox control in inter-war Britain. Here, a series of sociodemographic and administrative factors operated to impede disease control. Our study demonstrates the potential fragility of established disease control systems and the importance of professional and public cooperation, sometimes in the face of vehemently contested evidence over the nature of a disease and the means of its control, in attempts to limit the spread of epidemics.

The current epidemic of El Tor cholera in the Caribbean republic of Haiti is one of the largest single outbreaks of the disease ever recorded. The prospects are that the epidemic will continue to present challenges to workers in public health medicine, epidemiology and allied fields in the social sciences for years to come. This article introduces geographers to the environmental context of the Haiti cholera epidemic, the principal data sources available to analyze the occurrence of the epidemic, and evidence regarding its geographical origins and dispersal during the first thirty months of the epidemic, October 2010–March 2013. Using weekly case data collated by the Haitian Ministère de la Santé Publique et de la Population (MSPP), techniques of time series analysis are used to examine inter- and intra-departmental patterns of cholera activity. Our analysis demonstrates a pronounced lag structure to the spatial development of the epidemic (Artibonite and northern departments  Ouest and metropolitan Port-au-Prince  southern departments). Observed variations in levels of epidemiological integration, both within and between departments, provide new perspectives on the spatio-temporal evolution of the epidemic to its March 2013 pattern.

SUMMARYThe abrupt transition to heightened poliomyelitis epidemicity in England and Wales, 1947–1957, was associated with a profound change in the spatial dynamics of the disease. Drawing on the complete record of poliomyelitis notifications in England and Wales, we use a robust method of spatial epidemiological analysis (swash-backwash model) to evaluate the geographical rate of disease propagation in successive poliomyelitis seasons, 1940–1964. Comparisons with earlier and later time periods show that the period of heightened poliomyelitis epidemicity corresponded with a sudden and pronounced increase in the spatial rate of disease propagation. This change was observed for both urban and rural areas and points to an abrupt enhancement in the propensity for the geographical spread of polioviruses. Competing theories of the epidemic emergence of poliomyelitis in England and Wales should be assessed in the light of this evidence.

The 1947 epidemic of poliomyelitis was the largest and geographically most widespread outbreak of the disease ever recorded in England and Wales. As a transitional event in the history of poliomyelitis in the British Isles, the 1947 epidemic signalled the sudden onset of a sustained period of heightened epidemicity that continued until the introduction and mass administration of safe and effective poliovirus vaccines in the late 1950s. This paper explores the apparent shift in the spatial dynamics of poliovirus that underpinned the geographical spread of the 1947 epidemic in England and Wales. Drawing on a robust method of spatial epidemiological analysis (swash–backwash model), we demonstrate that the epidemic wave was associated with a pronounced acceleration in the rate of spatial propagation as compared to the preceding years. The velocity of spatial expansion and retreat and the duration of infectivity are shown to have varied by category of geographical area and by county of England and Wales. The weight of available evidence suggests that the so-called ‘hygiene model’ of the epidemic emergence of poliomyelitis, developed in the context of Western countries and generally assumed for England and Wales, does not adequately account for the events of 1947. Rather, we suggest that the features of the epidemic are consistent with the introduction and spread of one or more new strains of poliovirus in England and Wales in the summer of 1947. Possible connections to the epidemic occurrence of poliomyelitis in other European countries at about this time are considered.

The epidemic of cholera that spread through Egypt in the latter months of 1947 was one of the largest single outbreaks of the disease in the twentieth century. Using a swash–backwash model, this paper examines the geographical wave-like spread and subsequent retreat of the epidemic from an apparent origin in the settlements and prisoner-of-war camps of the Nile Delta area to reach its maximum geographical extent some six weeks later at Aswan (850 km away). Our results demonstrate the very rapid spatial advance of the epidemic wave through the provinces and governorates of Egypt, with an approximately linear sequence of progression up the Nile. Superimposed on this national pattern are pronounced differences in the rate of epidemic advance in the traditional geographical divisions of Lower and Upper Egypt. Alternative visualisations of the cholera spaces of Egypt, using techniques of multidimensional scaling (MDS) and cluster analysis, underscore the differential patterns of cholera transmission in these areas of the country. The patterns are interpreted in relation to a vigorous control effort that included restrictions on public transport, patient isolation, contact tracing and mass vaccination of the entire population exposed to risk of infection.

After the establishment of the first quarantine station in the Republic of Ragusa (modern-day Dubrovnik) in 1377, the states and principalities of Italy developed a sophisticated system of defensive quarantine in an attempt to protect themselves from the ravages of plague. Using largely unknown and unseen historical maps, this paper reconstructs the extent and operation of the system used. It is shown that a cordon sanitaire existed around the coast of Italy for several centuries, consisting of three elements: (i) an outer defensive ring of armed sailing boats in the Mediterranean and the Adriatic, (ii) a middle coastal ring of forts and observation towers, and (iii) an inner defensive ring of land-based cavalry. The principles established, although not especially successful at the time against a disease of (then) unknown aetiology, are still used today in attempts to control the spread of infections of animal and human populations.

The hypothesized role of deep coal mining in the development of community-based outbreaks of meningococcal meningitis has gone largely unexplored. Taking the coalfields of Britain as a historical testbed, techniques of linear and binomial logistic regression were used to assess the association between meningococcal meningitis rates and male occupation rates for coal mining in England and Wales during the national epidemic of 1931–32 and in its aftermath. Adjusting for the epidemiological effects of age, residential density, recent changes in the number of families, housing stock and low social class, the analysis yielded evidence of a significant and positive association between coal mining occupation rates and notified levels of meningitis activity in the epidemic period. Communities in areas of the world that currently maintain substantial deep coal extraction industries may be at increased risk for the epidemic transmission of meningococcal meningitis.

Summary The work of the Medical Research Council School Epidemics Committee—established in 1929 to undertake a study of ‘droplet infections’ in the ‘semi-isolated’ populations of England’s public schools—represents a little-known chapter in the historical development of applied medical statistics. Drawing on documents in the National Archives, London, we trace the original scheme for the Committee to Miss Ethel Newbold (1882–1933), a Fellow and Council member of the Royal Statistical Society and the first woman to be awarded the Society’s Guy Medal (1928, in silver). Using the Committee’s surviving records, databases of disease incidence are constructed for a multicentre cohort of 27 boarding schools, 1930–1939. Exploratory analysis of the data is illustrated by applying non-metric multi-dimensional scaling and Poisson regression to the themes of disease comorbidity and frequency of outbreak. Prompted by the emerging epidemiological concepts of pathogen–pathogen interaction and syndemicity, the multi-dimensional scaling analysis highlights the apparent epidemiological independence of common acute childhood infections (including chickenpox, measles, mumps, rubella, scarlet fever and whooping cough) in the disease system. Poisson regression reveals a complex pattern of controls on the frequency of school epidemics that vary by disease. The results that are obtained underscore the continuing relevance of the historical disease records of semi-isolated institutions, such as boarding schools, to an epidemiological understanding of common acute childhood infections and other ailments.

Iceland's centuries-long history of epidemics with its unusually complete disease records has attracted study from several disciplines. But detailed spatial data of particular interest to historical geographers date only from 1895 and were consistently maintained for about a century thereafter. Within this period, this paper concentrates on morbidity records of reported cases of infectious diseases for an 87-year window which was open between 1902 and 1988. In this time slice, spatially detailed data for seven demographically important infectious diseases allow the geography of 131 discrete epidemic waves with a recorded total of 529,000 cases to be tracked. Changes in the behaviour of the seven diseases over the period are analyzed and related to both epidemiological theory and to the changing historical geography of the island. The paper complements earlier Icelandic work by the authors on the historical geography of single diseases (measles, influenza and poliomyelitis) by extending the range of diseases, and by considering their common spatial behaviour and their interrelationships.

The World Health Organization (WHO) believes that the advent of highly pathogenic avian influenza A (H5N1) has moved the world closer to a further global pandemic of human influenza than at any time since the Hong Kong (H3N2) pandemic of 1968–1969. The immediacy of the perceived threat is underscored by the current classification of the world at Phase 3 of WHO's operative six-phase system of pandemic alert, with H5N1 having met all the prerequisites for the onset of a human pandemic but one: the efficient and sustained person-to-person transmission of the virus. With preparations for an anticipated pandemic now recognized as a global health priority, the purpose of this article is to provide a foundation for geographical research on avian influenza A (H5N1). The article introduces geographers to the complex nature and ecology of H5N1, the principal data sources available to analyze the global occurrence of the virus in birds and humans, and evidence regarding its geographical origins and international dis...

Background Historical data are necessary to establish long-term trends in disease incidence but pose analytical problems since their accuracy and reliability may be poorly specified. Methods A robust measure of the spatial velocity, R 0A , of epidemic waves from space-time series is proposed using binary data. The method was applied to the historical records of influenza morbidity for the island of Iceland over a 61-year period of influenza seasons from 1915-16 to 1975-76. Results The onset of influenza waves tended to speed up over the period studied and the three pandemic waves associated with viral shifts in influenza A [Spanish influenza H 1 N 1 (1918-19), Asian influenza H 2 N 2 (1957-58) and Hong Kong influenza H 3 N 2 (1968-69)] spread more rapidly around the island and struck earlier in the influenza season than did inter-pandemic waves, even when the latter were equally intensive as measured by total number of cases and case incidence. Discussion The potential for using R 0A in a real-time context is explored using French influenza data. Conclusions The new measure of wave velocity appears to be applicable to those historical time series where breakdown into regional or local areas is available. The study is being extended to (i) other countries where similar influenza time series are available and (ii) to other diseases within Iceland.

SUMMARYThis paper examines the geographical impact of the British Government's wartime evacuation scheme on notified rates of two common acute childhood diseases (scarlet fever and diphtheria) in the 1470 local government districts of England and Wales, 1939–1945. Drawing on the notifications of communicable diseases collated by the General Register Office (GRO), we establish pre-war (baseline) disease rates for the 1470 districts. For the war years, techniques of binary logistic regression analysis are used to assess the associations between (a) above-baseline (‘raised’) disease rates in evacuation, neutral and reception districts and (b) the major phases of the evacuation scheme. The analysis demonstrates that the evacuation was temporally associated with distinct national and regional effects on notified levels of disease activity. These effects were most pronounced in the early years of the dispersal (1939–1941) and corresponded with initial levels of evacuation-related population change at the regional and district scales.

SummaryThe great epidemic of poliomyelitis which swept New York City and surrounding territory in the summer of 1916 eclipsed all previous global experience of the disease. We draw on epidemiological information that is included in the seminal US Public Health Bulletin 91, ‘Epidemiologic studies of poliomyelitis in New York City and the northeastern United States during the year 1916’ (Washington DC, 1918), to re-examine the spatial structure of the epidemic. For the main phase of transmission of the epidemic, July–October 1916, it is shown that the maximum concentration of activity of poliomyelitis occurred within a 128-km radius of New York City. Although the integrity of the poliomyelitis cluster was maintained up to approximately 500 km from the metropolitan focus, the level and rate of propagation of disease declined with distance from the origin of the epidemic. Finally, it is shown that the geographical transmission of the epidemic in north-eastern USA probably followed a process of mixed contagious–hierarchical diffusion.

This article seeks to advance an understanding of the spatial dynamics of one of the great emergent viral diseases of the twentieth century—poliomyelitis. From an apparently rare clinical condition occurring only sporadically or in small outbreaks before the late nineteenth century, poliomyelitis had, by the early 1950s, developed into a globally distributed epidemic disease. But, from 1955, continued growth was suddenly and dramatically reversed by the mass administration of inactivated (killed) and live (attenuated) poliovirus vaccines. After almost half a century of vaccine control, the world now stands on the brink of the global eradication of the disease. Against this background, the article draws upon information included in the U.S. Public Health Service’s Public Health Reports and the U.S. Centers for Disease Control and Prevention’s Morbidity and Mortality Weekly Report to examine the spatial dynamics of poliomyelitis during the phases of epidemic emergence (1910–1955) and vaccine-induced retreat (1955–1971) in the United States. It is shown that epidemic emergence was accompanied by shifts in the spatial center of activity from early diffusion poles in the northeastern states, to the western seaboard, and then finally to cover all the states of the Union. This was accompanied by accelerating epidemic propagation. The introduction of mass vaccination from the mid-1950s realigned spatial transmission of the disease, producing increased spatial volatility in the geographical center of activity and heightened dependence of epidemic outbreaks upon endemic reservoirs in the most populous states. Finally, the empirical results are generalized to suggest that the emergence and reemergence of many infectious diseases is a distinctively geographical process.

The involvement of civilians, Boer women, children, and blacks is increasingly integrated within the military history of the South African War. This article assesses the disease history of the war in this context, collating data on mortality from various sources for the first time. Over 60 per cent of total deaths during the war were among civilians, shared among all ethnic groups (Boer, black, and white), and measles was probably the largest killer. Disaggregation by individual refugee camp shows: the rapidity of the epidemics; the early mortality peaks by July 1901; the varied timing and severity of disease by camp; and the importance of measles in explaining the very high mortality rates. At first sight, the decline in overall mortality appears to coincide with the 'magical effects' of the British commissions so often cited by historians. However, individual camp mortality curves do not support this historical explanation. We emphasize the epidemiological dynamics of measles, as well as the effects of local camp conditions of overcrowding and malnutrition. Providing a less dashing picture, the South African War is best characterized by measles as well as typhoid. The war shows the crossing in importance of a nineteenth-century military disease history represented by typhoid, and a refugee-civilian disease history that extends to the end of the twentieth century.

Wartime epidemics of infectious diseases have decimated the fighting strength of armies, caused the suspension and cancellation of military operations, and brought havoc to the civil populations of belligerent and nonbelligerent states. This article summarizes the principal factors that have contributed to the spread of infectious diseases in past wars and reviews the associated demographic losses in military and civil populations. Drawing on the detailed epidemiologic records for the United States Army, case studies of the spread of infectious diseases in relation to military mobilization are presented for the American Civil War, Spanish-American War,and World War I. The article concludes with a brief overview of infectious disease activity in high- and low-intensity conflicts of the late twentieth and early twenty-first centuries.

The epidemic of Asiatic cholera that decimated the commands of the British Army during the Crimean War (1853–56) spread as two discrete waves of infection. This paper presents a geographical examination of the diffusion of the first, and more severe, cholera wave (June 1854–February 1855) in the encampments of the British Army during the Bulgarian (1854) and the Crimean (1854–55) phases of the conflict. To these ends, we draw on the information included in the monumental report, The Medical and Surgical History of the British Army which Served in Turkey and the Crimea, prepared by the Army Medical Department and presented to Parliament in 1858. The History includes textual accounts of the progress of the epidemic wave, and numerical evidence regarding cholera-related morbidity and mortality in 66 regiments of the British Army. This information is first used to reconstruct the routes by which cholera spread in the British camp system of Bulgaria. Using techniques of multidimensional scaling, it is shown that the spread process was mediated through a camp connectivity space in which similarities in the regimental patterns of occupancy with two camps (Devna and Varna) were to govern the sequence of epidemic transmission. Within the Crimea, the magnitude and velocity of cholera transmission on the plateau before Sebastopol is shown to have been conditioned by a complex of factors relating to the size of incoming drafts, prior service in Bulgaria, and location within the siege camp.

The proposal to evacuate children from the large towns and cities of the United Kingdom during World War II caused much concern among wartime epidemiologists and public health officials. It was anticipated that dispersal on such an unprecedented scale might result in an unusually high incidence of epidemic disease amongst the native children of the reception areas. Although studies were carried out at the time, there was no general agreement about the actual extent to which the anticipated increase in disease activity occurred. The inconclusive nature of the findings has stimulated the present paper. We explore the temporal and spatial evidence for the raised incidence of three infectious diseases (scarlet fever, diphtheria and poliomyelitis) in the wake of the evacuation from the principal city affected (London) between 1939 and 1945. In so doing, we make allowance for the masking effect of the regular, background, pattern of disease activity on the pattern of disease associated with the evacuation. Isolation of the latter pattern indicates that the evacuation resulted in (i) a raised incidence of infectious disease in the reception areas to which the London evacuees were transferred and (ii) an associated increase in the epidemiological integration of London and the reception areas. Contrary to the expectation of wartime medical officers, Poisson probability mapping shows that, in general, evacuation-associated increases in disease activity were no more pronounced in rural than urban areas of the reception counties.

L'A. retrace un bref resume de la guerre franco-prussienne, les caracteristiques cliniques et epidemiologiques de la variole et les facteurs qui ont favorise sa diffusion geographique, particulierement la population militaire et les prisonniers dans les camps, ainsi que les centres urbains

Between 1902 and 1904 an epidemic of cholera, fuelled initially by the operations of the Philippine-American War (1899–1902), swept through the Philippine Islands in two waves. In earlier papers, the authors showed that spatially contagious spread dominated the waves at the geographical levels of province, island and nation (Smallman-Raynor and Cliff 1998a, b). To explore the visualization and analysis of epidemic transmission in an alternative metric, the present paper uses multidimensional scaling (MDS) to translate the spread corridors followed by the waves from conventional geographical space into non-Euclidean cholera spaces. The re-mapping confirms the importance of contagious diffusion in the spread of the epidemic, but also picks out the moments in time in which spread driven through the population hierarchy switched in. In addition, the analysis illustrates the utility of constructing non-Euclidean spaces to identify disease diffusion processes.

This article examines the geographical transmission of an epidemic disease in the makeshift encampments of a mobilized army. The choice of location (the southern and eastern United States), the time (an eight-month period of mobilization in the U.S. war with Spain, May to December 1898) and the epidemic disease (typhoid fever) are conditioned by the reports collated by three eminent figures in the history of medicine–Major Walter Reed, Major Victor C. Vaughan, and Major Edward O. Shakespeare–and published in the historic 1904 Report on the Origin and Spread of Typhoid Fever in U.S. Military Camps During the Spanish War of 1898. The Report includes information on the daily occurrence of some 19,000 cases of typhoid fever in 89 volunteer regiments of the U.S. Army. When geo-coded to the locations of army camps, this information is used (i) to reconstruct the spread of typhoid fever with the campwise movements of infected regiments and (ii) to model the diffusion process that drove the spread of the disease....

This paper presents a geographical examination of the impact of war and its aftermath upon the spread of an infectious disease in a civilian settlement system. The choice of area (the neighbouring provinces of Batangas and La Laguna, Philippine Islands), the time (a two year period in the closing stages and immediate aftermath of the war against US annexation, March 1902 - February 1904) and the epidemic (cholera) are conditioned by the detailed reports prepared by the chief quarantine officer 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 in Batangas and La Laguna, and numerical evidence regarding the weekly incidence of cholera in the settlements of the two provinces. Based on this information, a variety of geographical techniques (lag times, centroids, trend surfaces and autocorrelation on graphs) are introduced to reconstruct the spread of cholera, and to examine the diffusion processes that underpinned the spread patterns. It is demonstrated that the mass population movements associated with war had the effect of speeding up the geographical propagation of cholera as compared with peace, but did not destroy the basic channels of disease spread.

This paper examines the spatial transmission and rate of propagation of three infectious diseases (enteric fever, smallpox and yellow fever) in times of war and peace in Cuba between 1895 and 1898. For the three diseases studied, the analysis will demonstrate that, compared with peacetime, the Cuban Insurrection caused increased epidemiological integration of the settlement system of Cuba, acceleration of the spatial processes of disease transmission and a marked change in the geographical drift of infectious disease activity. While the first two findings may be attributed to the heightened levels of population mixing that accompanied the insurrection, the third implies that hostilities fundamentally altered the spatial courses of diseases. These changes transcended stark biases in the predisposition to infection among Spanish soldiers (to yellow fever) and Cuban civilians (to smallpox). Finally, it is shown that the military were the prime agents causing contrasts in the epidemiological experience of Cuba between war and peace.

This article examines temporal and spatial patterns in the relationship between provisional and amended reports for Hepatitis A and Hepatitis B received from each state by the Centers for Disease Control and Prevention through the U.S. National Notifiable Diseases Surveillance System from 1980 to 1992. It demonstrates that, as the 1980s unfolded, the preliminary disease reports became less representative markers of final disease counts. Practitioners at the state and community levels need to be aware of the temporal and spatial instabilities in such provisional data if they are used to provide early warning of contemporary health aberrations.

The environment plays an important part in the aetiology of atopic eczema, but specific causes are unknown. Exposure to hard water is thought to be a risk factor for eczema. We undertook an ecological study of the relation between domestic water hardness and the prevalence of eczema among Nottinghamshire schoolchildren.Questionnaire details of 1-year period and lifetime prevalence of eczema were obtained from parents of 4141 randomly selected primary-school children and 3499 secondary-school children in southern Nottinghamshire. Geographical information systems (GIS) were used to link the geographical distribution of eczema prevalence with domestic water-hardness data (four categories). Adjustment was made for potential confounding by sex, age, socioeconomic status, and access to health care.Among the primary-school children there was a significant direct relation between both 1-year period and lifetime prevalence of eczema and water hardness, both before and after adjustment for confounders. The 1-year period prevalence was 17.3% (261/1509) in the highest water-hardness category and 12.0% (94/786) in the lowest (adjusted odds ratio 1.54 [95% CI 1.19-1.99] p for trend0.001). The corresponding values for lifetime prevalence were 25.4% (384/1509) and 21.2% (167/786; adjusted odds ratio 1.28 [1.04-1.58], p for trend=0.02). Eczema prevalence trends in the secondary-school population were not significant (adjusted odds ratio for highest compared with lowest hardness category for 1-year prevalence 1.03 [0.79-1.33], p for trend=0.46; for lifetime prevalence 0.99 [0.83-1.23], p for trend=0.93). Eczema prevalence in primary-school children increased in relation to chlorine content of water, but the trend across four chlorine-content categories was not independently significant after adjustment for confounders.Exposure to hard water in the home may increase the risk of eczema in children of primary-school age.

The great epidemic of cholera which swept through the Philippine Islands in the immediate aftermath of the Philippine–American War (1899–1902) spread in two temporally distinct, but spatially concordant, waves of infection. Part I of this paper studied the first wave (wave I, March 1902 to February 1903). Here, in Part II, we explore the manner in which the second wave (wave II, May 1903 to February 1904) diffused through the same geographical areas. Using the cholera reports prepared by the Chief Quarantine Officer for the Philippine Islands and published weekly in the contemporary USPublic Health Reports, the diffusion of wave II is analysed at the geographical levels of province, island and nation. Comparison with wave I confirms that spatially contagious spread dominated in both waves at all spatial scales. However, it is shown that there were important differences between the waves in their intensity, speed of spread and resulting spatial patterns. Amelioration of the disruption brought about by the Philippine–American War may account for some of the observed differences between the two waves.

This, the first 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 1902–February 1903) and the epidemic (cholera) are conditioned by the detailed reports prepared by the Chief Quarantine Officer for the Philippine Islands, and published weekly in the contemporary USPublic 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 diffused through the archipelago and to model the diffusion 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 diffusion was generally found to be of only limited significance 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 theJournal, goes on to compare the spatial diffusion patterns described here with those found in a subsequent peacetime cholera wave in the Philippines (May 1903–February 1904). Results from both parts of the paper are used to assess the manner in which war can affect diffusion processes and the circumstances under which spread is likely to be dominated by contagious, hierarchical or mixed diffusion processes.