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Popular writings often depict the infection enjoying an easy life of rich pickings from an unwitting host [2]. In truth, the immune responses of the host and the hurdles to transmission, impose severe selective pressures on the parasites. Thus, there are always strategies employed by the parasite to avoid the immune system, either through racing the production of immune effectors or avoiding them through cryptic or changing surfaces.

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This tends to generate two types of life histories: either short-lived rapid-reproduction parasites such as the simple viruses and bacteria e. Since the resolution of infection within the host destroys that population of infectious organisms, infectious diseases are in part subject to group selection. However, it should be remembered that the individual organism is also competing intra-specifically within the host and that future generations of infection will represent the genotypes of organisms that manage to transmit.

In any consideration of evolutionary strategies it is important to remember that evolution is blind. The flu virus does not consider the future problem of widespread immunity following an influenza pandemic and Neisseria meningitides does not consider its future success when it invades the host in a selective dead end, with catastrophic consequences for the host and itself.

What we observe in nature are either transient epidemics of infectious disease, which spread with short term success, but which will die out, or infectious diseases that have found a strategy to allow them to persist. In developing our understanding of the interaction between demography and infectious disease epidemiology, it is worth considering the type and quality of evidence available to us, and how we progress from anecdote to general rules and from speculation to theory.

A detailed knowledge of the natural history and transmissibility of infections from observational studies, allows us to speculate about how changes in host population structure may have influenced their epidemiology. Historical and archaeological records of population size and organisation, along with evidence of patterns of disease and death, provide examples of coincident changes, including the invasion of new pathogens as civilizations were formed, through to the reductions in disease associated with improved hygiene and living conditions [3].

Other ecological comparisons between populations are instructive, allowing us to compare the success of different types of organism in different locations [4]. In understanding the contribution of infections to demography, records of mortality and its causes are vital. However, in the frequent absence of detailed records we have to rely on theoretical estimates based on what we know of the distribution and consequences of particular infections. This is particularly true of the influence of infectious diseases on fertility where limited numbers of detailed studies have to be related to the global distribution of infections.

In studying both the impact of demography on infections and vice versa, general principles are derived from particular examples. However, the examples are never typical since it is specific pathogens such as bubonic plague, tuberculosis, malaria, influenza and HIV that dominate the relationship between infections and demography. Thus, throughout our discussion we have to relate to the particular characteristics of the key pathogens.

Three variables influence the potential for spread of an infection: the duration of infectiousness D ; the contact rate c ; and the likelihood of transmission if there is a contact p : the duration of infectiousness determines how long an infection stays prevalent to expose others; the contact rate and transmission probability are variables in the transmission from infectious to susceptible individuals [1]. Thus, the basic reproductive number has to be above one for there to be a risk of an infection spreading.

The influence of population size on the contact rate is central to the impact of population growth on infectious disease epidemiology. The Impact of Population Size and Density on Contact Patterns Whether the growth of a population influences the potential spread of an infectious disease depends upon how the number of individuals influences the patterns of contact and exposure.

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If population growth leads to greater crowding, more contaminated water supplies, or higher numbers of sexual contacts per person, then the contact rates allowing the transmission of many diseases will increase, making epidemics more likely. Alternatively, if expanding populations have additional geographic space, additional services and no change in sexual norms then the number of contacts can remain constant and no change in risk of epidemics occur. The two types of increase are illustrated in Fig.


With the transmission term above, the threshold population size for the inva- 30 G. Thus, the greater the transmission probability and duration of infection the smaller the population size in which an infection can invade. If population size does increase the contact rate, then growing populations will allow epidemics of organisms that have lower transmission probabilities and durations if they cross species barriers or evolve from other pathogenic or commensal organisms.

In reality it is likely that the relationship between population size and contacts will depend upon the local circumstances and the particular routes of transmission. However, growing populations place strains on the resources available; where these resources cannot keep pace, rates of contact and risks of epidemics will increase.

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  • If, with growing populations, individuals want to take the opportunity to mix in larger social groups or have more sexual partners then the infections which depend upon these forms of contact will thrive. It is likely therefore that growing populations do lead to a greater risk of infectious disease spread, but there are opportunities to combat this trend.

    The Supply of Susceptibles Through Birth and Immigration Analyses of the persistence of measles in cities and islands indicated that there was a threshold population size required for the persistence of the virus i. This was initially taken as evidence for a threshold population size for invasion and hence a density dependent transmission term.

    It also supported the belief that larger populations associated with the introduction of agriculture in early human history allowed for the invasion of directly transmitted simple viral infections such as measles and smallpox [10]. However, the ability of an infection to invade a population is not synonymous with the ability of an infection to persist [11]. Either through mortality decreasing population sizes or through inducing acquired immunity, infections are likely to reduce the numbers of susceptibles available to maintain chains of infection.

    New susceptibles are required to maintain an endemic infection and these susceptibles can be provided by loss of immunity, immigration or births. Thus, large populations and growing populations accrue susceptibles rapidly making it more likely that an infection will be able to persist [12]. A very rapid supply of susceptibles, as is the case for bacterial infections where recovery is back into a susceptible state or in the case of large growing populations, allows a continual high level of incidence. A slow supply of susceptibles is likely to lead to reductions in infection numbers or even stochastic fade out and elimination of the infection.

    Low numbers of infections will allow a build up of susceptible numbers in the population and new epidemics occur, leading to oscillation between epidemic and interepidemic periods. In a deterministic system we would expect to see damping of the oscillations over time, but epidemics continue because of seasonal variations in contact rates, as occurs with school attendance, and due to stochasticity [1].

    The faster the rate of resupply of susceptibles as a function of population size and population growth, the more frequent epidemics will be and the more stable with a regular endemic level of infection the system will be [12]. The need to maintain susceptibles applies in the case of both density dependent and frequency dependent transmission. In the former it is both the number and proportion of the population susceptible that matters. The effective reproductive Rt number is the number of new infections caused by a single infection at any given time and equals 1 at the endemic steady state. The effective reproductive number in a homogeneous population is simply the basic reproductive number times the proportion of the population susceptible.

    N Thus, at the endemic steady state the proportion of the population susceptible x is simply the inverse of the basic reproductive number. As the number of susceptibles increases, an epidemic becomes possible once the proportion susceptible exceeds this inverse of the basic reproductive number. If an infection causes mortality and drives down a population size, but does not induce acquired immunity, the recruitment of numbers to the population is what matters.


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    In the case of frequency dependent transmission a fatal infection that can spread has the potential to drive a population extinct if death rates exceed birth rates, unless something else reduces the spread of infection, such as behaviour change. The predicted changes of disease incidence have been observed in a detailed analysis of the spatial and temporal patterns of measles incidence within the UK [13]. Here, before the introduction of vaccination, epidemics of measles originated in the large cities of London and Manchester from which they spread as travelling waves.

    Vaccination when it is introduced greatly increases the time taken for sufficient numbers of susceptibles to accrue and thereby increases the interepidemic period [13]. Within this analysis, Liverpool, prior to vaccination, is particularly interesting since it had higher than average birth rates associated with a large immigrant, Catholic population and consequently had yearly epidemics of measles [12], as had New York [14]. Thus, large and growing populations are more likely to maintain an infection and suffer repeated epidemics prior to vaccination.

    The mean age of infection also depends upon the frequency of epidemics and the birth rate. A higher rate of births should lead to a higher reproductive number and thereby a lower age of infection. This has been observed in Guinea-Bissau where infection with measles amongst urban children occurred at a lower age than in their rural counterparts [15].

    Additionally, the high incidence of meningitis in West Africa reflects the high reproductive number of the bacterial infection in these communities [16].

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    In growing populations such as these the period between loss of maternally derived antibodies and infection is limited, leaving a limited period for vaccination as children age [17]. This led to efforts to develop a measles vaccine able to immunize children in the presence of maternally derived antibodies which unfortunately had to be withdrawn following observations of increased non-specific death rates associated with vaccination [18]. As vaccination becomes widespread, the mean age of infection increases, because susceptible individuals take longer to come into contact with infection, which should allow a greater window of opportunity to vaccinate.

    However, if there is poor vaccination coverage or efficacy, the growing population makes outbreaks more likely, since the speed of growth in susceptible numbers is greater and the critical number or proportion of the population susceptible is likely to be realised sooner. The increase in the mean age of infection that follows vaccination programmes can be problematic since for many infections severity increases with age. The Impact of Epidemic and Endemic Disease on Mortality There is no doubt that infectious diseases are a major cause of mortality in populations, which because of the young age of many of those infected and dying, can contribute to the loss of many life years.

    In healthy well nourished hosts the fatality rate the proportion of infections leading to death rather than recovery associated with the majority of infections is low. When health care provision and nourishment is adequate then mortality associated with infectious diseases is concentrated in those with underlying vulnerability, such as the elderly and immunocompromised, where rates of death from competing causes are high and the demographic impact of the infection is slight [23].

    In resource-poor settings deaths from respiratory and diarrhoeal diseases are common in infants and young children. Here it is estimated that measles, malaria, tuberculosis, and pneumococcal infections cause 5 million deaths each year, which is nearly a tenth of global deaths [23].

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    It is relatively rare for infections to be associated with death in young adults; and it is perhaps particularly their fatality rate in young adults that makes the bubonic plague, syphilis, Spanish flu and AIDS notable historic events [3]. The demographic impact of an infectious disease depends upon the incidence of infection, the fatality rate, the age at which deaths occur and how long lasting the pandemics are.

    Over the long term a relatively small but continuous increase in mortality rates has a greater effect than acute large scale mortality. This is illustrated in Fig. However, it was the repeated epidemics, which followed the first and kept returning into the fifteenth century that reduced the populations [25]. The virus is associated with an almost unprecedented high fatality rate, with seemingly all those infected dying eventually; and the infection is predominantly amongst young adults.

    This has to be balanced against the length of time it takes for HIV infection to progress to AIDS and death, and the low prevalence of the virus found in many populations. Thus, predicted negative population growths have not been observed in detailed studies. Furthermore, the observed prevalences are probably at the peak epidemic prevalence.

    As mortality due to AIDS increases then those initially most at risk of acquiring and transmitting infection are no longer present, and populations tend to reduce their risk behaviours [30, 31]. To maintain over time a given increase in death rates the prevalence of HIV would also have to be maintained. The AIDS epidemic is likely to reduce life expectancy and growth rates in many developing countries. However, if the death and disease associated with the virus undermines development and health it may delay or prevent the demographic transition and in the long run lead to larger rather than smaller populations.

    Gonorrhoea and chlamydia can cause pelvic inflammatory disease and lead to scarring of the fallopian tubes, causing sterility. Syphilis and HIV seem to reduce observed fertility in part due to early spontaneous abortions [32, 26]. The use of antenatal screening for syphilis and HIV allow for treatments to reduce neonatal syphilis and vertical transmission of HIV, but these are too late to prevent early foetal loss.

    The biological proximate determinants of fertility reduce population growth, as observed in Uganda and other African countries [33]. If they are removed, they are likely to be replaced by other proximate determinants limiting fertility, such as increased contraception and abortion [34]. As sexually transmitted infections STI are generally transmitted in a frequency dependent fashion i. However, there is some evidence of increased risk behaviour in urban populations and among migrant labourers [36]. This, along with the lack of access to timely and appropriate health care and the exchange of sex for material goods and money, would increase rates of sexual partner change and the incidence of STI.

    Thus if population growth is associated with worsening socio-economic conditions then it could increase infertility along with death rates.

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    The impact of STIs on fertility depends upon the incidence of infection, the rate of complications and infertility and the age of infection amongst women in relation to their childbearing years. A recent survey of data from sub-Saharan Africa suggested a population attributable decline in total fertility of 0. The high incidence of chlamydia in young women, which can lead to permanent primary or secondary sterility, means that it potentially has a major impact on birth rates. However, the actual rates of tubal occlusion are difficult to estimate since natural history studies are clearly unethical, and sterility can be difficult to detect especially if it follows earlier child birth.