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Christopher J. Duncan - One of the best experts on this subject based on the ideXlab platform.
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Modelling the Different Smallpox Epidemics in England
Philosophical transactions of the Royal Society of London. Series B Biological sciences, 1994Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Time series analysis has revealed two different patterns of Smallpox Epidemics in Britain in the seventeenth and eighteenth centuries: in large conurbations (exemplified by London) the disease was endemic whereas medium-sized rural towns (exemplified by Penrith, Cumbria) suffered from 5 year Epidemics with no cases of Smallpox in the inter-epidemic years. The oscillations (Epidemics) persisted for over 150 years and it is suggested that both systems were pumped up by regular fluctuations in susceptibility (delta beta). Modelling suggests that: (i) the natural frequency of oscillations in large cities is two years and the system is pumped up by a 1 year, seasonal input; (ii) it takes five years to build up a pool of susceptibles in medium-sized towns by new births and Epidemics are then triggered by a 5 year input. The equations represent a system that has two components, a basic linear element with the remainder of the system being nonlinear; modelling a progressive increase in delta beta in London illustrates theoretically how a predominantly linear response changes to a nonlinear response and ultimately to chaos. A variation in susceptibility is a theoretical condition for inducing chaos; the undriven system cannot become chaotic. Modelling populations of progressively increasing size/density and applying a 1 year or 5 year sinusoidal oscillation in delta beta illustrates the fundamental distinction in the response of medium-sized rural towns and large cities.
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Smallpox Epidemics In Cities In Britain
Journal of Interdisciplinary History, 1994Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:and was greatly feared from the time of the final visitation of bubonic plague in I666 until the end of the nineteenth century, when it ceased to be endemic in England. Relatively rare as a fatal disease in England until the I630s, after I666 it replaced plague as the most feared of diseases. Many accounts suggest that a particularly virulent strain began to afflict people of all ages in the middle and later decades of the seventeenth century, and the evidence points to a gradual but significant increase in the virulence and case fatality rate from the later sixteenth through to the end of the nineteenth century.1 By the first half of the eighteenth century, almost everyone had suffered at some time from the disease and it was thought to be directly, or indirectly, responsible for one death in every five. After 1750, inoculation or variolation began to be administered more widely among the educated and affluent, but there was a time lag of about ten to twenty years before the same degree of acceptance reached the northern counties of Cheshire, Cumberland, Lancashire, and Yorkshire. Although Smallpox remained unconquered, a rising proportion of the population had been
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The dynamics of Smallpox Epidemics in Britain, 1550-1800.
Demography, 1993Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Time-series analysis, a valuable tool in studying population dynamics, has been used to determine the periodicity of Smallpox Epidemics during the seventeenth and eighteenth centuries in two contrasting representative situations: 1) London, a large city where Smallpox was endemic, and 2) Penrith, a small rural town. The interepidemic period was found to be two years in London and five years in Penrith. Equations governing the dynamics of Epidemics predict 1) a two-year periodicity and 2) that oscillatory Epidemics die out quickly. It is suggested that Epidemics were maintained by a periodic variation in susceptibility linked either to a five-year cycle of malnutrition or to an annual cycle. Computer modeling shows how the very different patterns of Epidemics are related to population size and to the magnitude of the oscillation in susceptibility.
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An hypothesis for the periodicity of Smallpox Epidemics as revealed by time series analysis.
Journal of theoretical biology, 1993Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Parish registers have been studied by time series analysis to detect Smallpox Epidemics in England during 1600-1800. Confirmatory evidence was provided by the seasonality of child mortality. A 5-year cycle in Smallpox Epidemics was detected in medium-sized, rural towns. Consideration of the mathematics of the dynamics of viral diseases suggests that the true interepidemic period where Smallpox is endemic should be 2-3 years and it is concluded that, in the towns studied, the disease was not endemic but that the oscillations were established by 5-year cycles of periods of famine associated with high wheat prices. The cross-correlation function between the two cycles shows zero lag and the input-output function shows significant coherence. Another epidemic follows only when a sufficient density of susceptibles has been established by births, so that the cycles become phase-locked. It is predicted that Smallpox (i) was endemic in London and other large cities, with 2-3 year Epidemics, (ii) was epidemic with a 5-year oscillation in rural towns, (iii) did not reach epidemic proportions in scattered communities.
Susan Scott - One of the best experts on this subject based on the ideXlab platform.
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Modelling the Different Smallpox Epidemics in England
Philosophical transactions of the Royal Society of London. Series B Biological sciences, 1994Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Time series analysis has revealed two different patterns of Smallpox Epidemics in Britain in the seventeenth and eighteenth centuries: in large conurbations (exemplified by London) the disease was endemic whereas medium-sized rural towns (exemplified by Penrith, Cumbria) suffered from 5 year Epidemics with no cases of Smallpox in the inter-epidemic years. The oscillations (Epidemics) persisted for over 150 years and it is suggested that both systems were pumped up by regular fluctuations in susceptibility (delta beta). Modelling suggests that: (i) the natural frequency of oscillations in large cities is two years and the system is pumped up by a 1 year, seasonal input; (ii) it takes five years to build up a pool of susceptibles in medium-sized towns by new births and Epidemics are then triggered by a 5 year input. The equations represent a system that has two components, a basic linear element with the remainder of the system being nonlinear; modelling a progressive increase in delta beta in London illustrates theoretically how a predominantly linear response changes to a nonlinear response and ultimately to chaos. A variation in susceptibility is a theoretical condition for inducing chaos; the undriven system cannot become chaotic. Modelling populations of progressively increasing size/density and applying a 1 year or 5 year sinusoidal oscillation in delta beta illustrates the fundamental distinction in the response of medium-sized rural towns and large cities.
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Smallpox Epidemics In Cities In Britain
Journal of Interdisciplinary History, 1994Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:and was greatly feared from the time of the final visitation of bubonic plague in I666 until the end of the nineteenth century, when it ceased to be endemic in England. Relatively rare as a fatal disease in England until the I630s, after I666 it replaced plague as the most feared of diseases. Many accounts suggest that a particularly virulent strain began to afflict people of all ages in the middle and later decades of the seventeenth century, and the evidence points to a gradual but significant increase in the virulence and case fatality rate from the later sixteenth through to the end of the nineteenth century.1 By the first half of the eighteenth century, almost everyone had suffered at some time from the disease and it was thought to be directly, or indirectly, responsible for one death in every five. After 1750, inoculation or variolation began to be administered more widely among the educated and affluent, but there was a time lag of about ten to twenty years before the same degree of acceptance reached the northern counties of Cheshire, Cumberland, Lancashire, and Yorkshire. Although Smallpox remained unconquered, a rising proportion of the population had been
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The dynamics of Smallpox Epidemics in Britain, 1550–1800
Demography, 1993Co-Authors: S. R. Duncan, Susan Scott, C. J. DuncanAbstract:Time-series analysis, a valuable tool in studying population dynamics, has been used to determine the periodicity of Smallpox Epidemics during the seventeenth and eighteenth centuries in two contrasting representative situations: 1) London, a large city where Smallpox was endemic, and 2) Penrith, a small rural town. The interepidemic period was found to be two years in London and five years in Penrith. Equations governing the dynamics of Epidemics predict 1) a two-year periodicity and 2) that oscillatory Epidemics die out quickly. It is suggested that Epidemics were maintained by a periodic variation in susceptibility linked either to a five-year cycle of malnutrition or to an annual cycle. Computer modeling shows how the very different patterns of Epidemics are related to population size and to the magnitude of the oscillation in susceptibility.
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The dynamics of Smallpox Epidemics in Britain, 1550-1800.
Demography, 1993Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Time-series analysis, a valuable tool in studying population dynamics, has been used to determine the periodicity of Smallpox Epidemics during the seventeenth and eighteenth centuries in two contrasting representative situations: 1) London, a large city where Smallpox was endemic, and 2) Penrith, a small rural town. The interepidemic period was found to be two years in London and five years in Penrith. Equations governing the dynamics of Epidemics predict 1) a two-year periodicity and 2) that oscillatory Epidemics die out quickly. It is suggested that Epidemics were maintained by a periodic variation in susceptibility linked either to a five-year cycle of malnutrition or to an annual cycle. Computer modeling shows how the very different patterns of Epidemics are related to population size and to the magnitude of the oscillation in susceptibility.
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An hypothesis for the periodicity of Smallpox Epidemics as revealed by time series analysis.
Journal of theoretical biology, 1993Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Parish registers have been studied by time series analysis to detect Smallpox Epidemics in England during 1600-1800. Confirmatory evidence was provided by the seasonality of child mortality. A 5-year cycle in Smallpox Epidemics was detected in medium-sized, rural towns. Consideration of the mathematics of the dynamics of viral diseases suggests that the true interepidemic period where Smallpox is endemic should be 2-3 years and it is concluded that, in the towns studied, the disease was not endemic but that the oscillations were established by 5-year cycles of periods of famine associated with high wheat prices. The cross-correlation function between the two cycles shows zero lag and the input-output function shows significant coherence. Another epidemic follows only when a sufficient density of susceptibles has been established by births, so that the cycles become phase-locked. It is predicted that Smallpox (i) was endemic in London and other large cities, with 2-3 year Epidemics, (ii) was epidemic with a 5-year oscillation in rural towns, (iii) did not reach epidemic proportions in scattered communities.
Stephen R. Duncan - One of the best experts on this subject based on the ideXlab platform.
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Modelling the Different Smallpox Epidemics in England
Philosophical transactions of the Royal Society of London. Series B Biological sciences, 1994Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Time series analysis has revealed two different patterns of Smallpox Epidemics in Britain in the seventeenth and eighteenth centuries: in large conurbations (exemplified by London) the disease was endemic whereas medium-sized rural towns (exemplified by Penrith, Cumbria) suffered from 5 year Epidemics with no cases of Smallpox in the inter-epidemic years. The oscillations (Epidemics) persisted for over 150 years and it is suggested that both systems were pumped up by regular fluctuations in susceptibility (delta beta). Modelling suggests that: (i) the natural frequency of oscillations in large cities is two years and the system is pumped up by a 1 year, seasonal input; (ii) it takes five years to build up a pool of susceptibles in medium-sized towns by new births and Epidemics are then triggered by a 5 year input. The equations represent a system that has two components, a basic linear element with the remainder of the system being nonlinear; modelling a progressive increase in delta beta in London illustrates theoretically how a predominantly linear response changes to a nonlinear response and ultimately to chaos. A variation in susceptibility is a theoretical condition for inducing chaos; the undriven system cannot become chaotic. Modelling populations of progressively increasing size/density and applying a 1 year or 5 year sinusoidal oscillation in delta beta illustrates the fundamental distinction in the response of medium-sized rural towns and large cities.
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Smallpox Epidemics In Cities In Britain
Journal of Interdisciplinary History, 1994Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:and was greatly feared from the time of the final visitation of bubonic plague in I666 until the end of the nineteenth century, when it ceased to be endemic in England. Relatively rare as a fatal disease in England until the I630s, after I666 it replaced plague as the most feared of diseases. Many accounts suggest that a particularly virulent strain began to afflict people of all ages in the middle and later decades of the seventeenth century, and the evidence points to a gradual but significant increase in the virulence and case fatality rate from the later sixteenth through to the end of the nineteenth century.1 By the first half of the eighteenth century, almost everyone had suffered at some time from the disease and it was thought to be directly, or indirectly, responsible for one death in every five. After 1750, inoculation or variolation began to be administered more widely among the educated and affluent, but there was a time lag of about ten to twenty years before the same degree of acceptance reached the northern counties of Cheshire, Cumberland, Lancashire, and Yorkshire. Although Smallpox remained unconquered, a rising proportion of the population had been
-
The dynamics of Smallpox Epidemics in Britain, 1550-1800.
Demography, 1993Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Time-series analysis, a valuable tool in studying population dynamics, has been used to determine the periodicity of Smallpox Epidemics during the seventeenth and eighteenth centuries in two contrasting representative situations: 1) London, a large city where Smallpox was endemic, and 2) Penrith, a small rural town. The interepidemic period was found to be two years in London and five years in Penrith. Equations governing the dynamics of Epidemics predict 1) a two-year periodicity and 2) that oscillatory Epidemics die out quickly. It is suggested that Epidemics were maintained by a periodic variation in susceptibility linked either to a five-year cycle of malnutrition or to an annual cycle. Computer modeling shows how the very different patterns of Epidemics are related to population size and to the magnitude of the oscillation in susceptibility.
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An hypothesis for the periodicity of Smallpox Epidemics as revealed by time series analysis.
Journal of theoretical biology, 1993Co-Authors: Stephen R. Duncan, Susan Scott, Christopher J. DuncanAbstract:Parish registers have been studied by time series analysis to detect Smallpox Epidemics in England during 1600-1800. Confirmatory evidence was provided by the seasonality of child mortality. A 5-year cycle in Smallpox Epidemics was detected in medium-sized, rural towns. Consideration of the mathematics of the dynamics of viral diseases suggests that the true interepidemic period where Smallpox is endemic should be 2-3 years and it is concluded that, in the towns studied, the disease was not endemic but that the oscillations were established by 5-year cycles of periods of famine associated with high wheat prices. The cross-correlation function between the two cycles shows zero lag and the input-output function shows significant coherence. Another epidemic follows only when a sufficient density of susceptibles has been established by births, so that the cycles become phase-locked. It is predicted that Smallpox (i) was endemic in London and other large cities, with 2-3 year Epidemics, (ii) was epidemic with a 5-year oscillation in rural towns, (iii) did not reach epidemic proportions in scattered communities.
Brabin Bernard - One of the best experts on this subject based on the ideXlab platform.
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An Analysis of the United States and United Kingdom Smallpox Epidemics (1901-5) - The Special Relationship that Tested Public Health Strategies for Disease Control.
'Cambridge University Press (CUP)', 2020Co-Authors: Brabin BernardAbstract:At the end of the nineteenth century, the northern port of Liverpool had become the second largest in the United Kingdom. Fast transatlantic steamers to Boston and other American ports exploited this route, increasing the risk of maritime disease Epidemics. The 1901-3 epidemic in Liverpool was the last serious Smallpox outbreak in Liverpool and was probably seeded from these maritime contacts, which introduced a milder form of the disease that was more difficult to trace because of its long incubation period and occurrence of undiagnosed cases. The characteristics of these Epidemics in Boston and Liverpool are described and compared with outbreaks in New York, Glasgow and London between 1900 and 1903. Public health control strategies, notably medical inspection, quarantine and vaccination, differed between the two countries and in both settings were inconsistently applied, often for commercial reasons or due to public unpopularity. As a result, smaller Smallpox Epidemics spread out from Liverpool until 1905. This paper analyses factors that contributed to this last serious epidemic using the historical epidemiological data available at that time. Though imperfect, these early public health strategies paved the way for better prevention of imported maritime diseases
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An analysis of The United States and United Kingdom Smallpox Epidemics (1901 to 1905) – the special relationship that tested public health strategies for disease control
'Cambridge University Press (CUP)', 2020Co-Authors: Brabin BernardAbstract:Abstract: At the end of the nineteenth century the northern port of Liverpool had become the second largest in the United Kingdom. Fast transatlantic steamers to Boston and other American ports exploited this route, increasing the risk of maritime disease Epidemics. The 1901-1903 epidemic in Liverpool was the last serious Smallpox outbreak in Liverpool and was probably seeded from these maritime contacts, which introduced a milder form of the disease that was more difficult to trace because of its long incubation period and occurrence of undiagnosed cases. The characteristics of these Epidemics in Boston and Liverpool are described and compared with outbreaks in New York, Glasgow and London between 1900 and 1903. Public health control strategies, notably medical inspection, quarantine and vaccination differed between the two countries and in both settings, were inconsistently applied, often for commercial reasons or public unpopularity. As a result, smaller Smallpox Epidemics spread out from Liverpool until 1905. This paper analyses factors that contributed to this last serious epidemic using the historical epidemiological data available at that time. Though imperfect, these early public health strategies paved the way for better prevention of imported maritime diseases. Key words: Smallpox, maritime, epidemic, public health, Boston, Liverpool
A Lovenetski - One of the best experts on this subject based on the ideXlab platform.
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P1-S5.05 The emergence of HIV pandemic: who lifted the lid of the African SIV-HIV Pot? A hypothesis
Sexually Transmitted Infections, 2011Co-Authors: A LovenetskiAbstract:A series of studies established that HIV infection in humans originated from multiple episodes of zoonotic transmission of CD4 T cell-tropic lentiviruses infecting African monkey species—Simian Immunodeficiency Viruses (SIV). HIV-1 derives from the chimpanzee (Pan troglodytes)—SIVcpz, while HIV-2 derives from SIVsm, which naturally infects the Sooty mangabey (Cercocebus atys). Pan troglodytes is present across West Central Africa. Cercocebus atys have their natural habitat in West Africa (Guinea-Bissau to Cote d9Ivoire). Timing the emergence of HIV-1 in humans: four of the earliest known instances of HIV-1 infection are as follows: A plasma sample taken in 1959 from an adult male living in the Democratic Republic of the Congo. A lymph node sample taken in 1960 from an adult female, also from the Democratic Republic of the Congo. HIV-1 found in tissue samples from an American teenager who died in St. Louis in 1969. HIV-1 found in tissue samples from a Norwegian sailor who died around 1976. An 1998 analysis of the plasma sample dated 1959 suggested that HIV-1 was introduced into humans around the 1940s or the early 1950s. In 2000 the results of a new study suggested that HIV-1 infection occurred around 1931 in West Africa. However, a study in 2008 dated the origin of HIV to between 1884 and 1924. Timing the emergence of HIV-2 in human population: in 2003 molecular timing analysis of two subtypes of HIV-2 (A and B) and SIVsm samples led to conclusion that subtype A had passed into humans around 1940 and subtype B in 1945. The data evidence that Africa was the continent where the transfer of emerged HIV-1 and HIV-2 to humans first occurred. What caused the HIV epidemic to spread so suddenly from African pot in late 70s and early 80s? In this connection let9s recall the largest successful worldwide medical intervention in human history—the WHO Smallpox Eradication Programme (1967–1977). Smallpox Epidemics had inflicted mankind throughout history, and during 1967 some 10–15 million cases were occurring in 30 endemic countries. In WHO monograph Smallpox and Its Eradication “the chronology and precise timing of the Programme progress was well documented including Africa region: at the end of 1971 Smallpox was endemic in only three African countries and was completely eradicated by 1977. Can there be a possible link between the HIV-1/HIV-2 pandemic emergence from West and Central Africa and Smallpox eradication?. Smallpox was endemic for most of the countries of West and Central Africa where HIV9s originated. Smallpox may be fatal for the most of the HIV-infected immunocompromised persons resulting in interruption of HIV spread. Thus Smallpox could be considered as a natural barrier that limited prevalence of newly emerged HIV-1/HIV-2 in local human population. Smallpox eradication probably was the key factor which may contribute the widespread of HIV9s in the population of West and Central Africa and the subsequent HIV pandemic emergence”.