From heroin epidemics to methamphetamine epidemics: Modelling substance abuse in a South African province

The global rise in the use of methamphetamine has been documented to have reached epidemic proportions. Researchers have focussed on the social implications of the epidemic. A typical drug use cycle consists of concealed drugs use after initiation, addiction, treatment-recovery-relapse cycle, whose dynamics are not well understood. The model by White and Comiskey [41], on heroin epidemics, treatment and ODE modelling, is modified to model the dynamics of methamphetamine use in a South African province. The analysis of the model is presented in terms of the methamphetamine epidemic threshold R₀. It is shown that the model has multiple equilibria and using the center manifold theory, the model exhibits the phenomenon of backward bifurcation where a stable drug free equilibrium co-exists with a stable drug persistent equilibrium for a certain defined range of R₀. The stabilities of the model equilibria are ascertained and persistence conditions established. Furthermore, numerical simulations are performed; these include fitting the model to the available data on the number of patients with methamphetamine problems. The implications of the results to drug policy, treatment and prevention are discussed.     

Modeling the Impact of White-Plague Coral Disease in Climate Change Scenarios

Coral reefs are in global decline, with coral diseases increasing both in prevalence and in space, a situation that is expected only to worsen as future thermal stressors increase. Through intense surveillance, we have collected a unique and highly resolved dataset from the coral reef of Eilat (Israel, Red Sea), that documents the spatiotemporal dynamics of a White Plague Disease (WPD) outbreak over the course of a full season. Based on modern statistical methodologies, we develop a novel spatial epidemiological model that uses a maximum-likelihood procedure to fit the data and assess the transmission pattern of WPD. We link the model to sea surface temperature (SST) and test the possible effect of increasing temperatures on disease dynamics. Our results reveal that the likelihood of a susceptible coral to become infected is governed both by SST and by its spatial location relative to nearby infected corals. The model shows that the magnitude of WPD epidemics strongly depends on demographic circumstances; under one extreme, when recruitment is free-space regulated and coral density remains relatively constant, even an increase of only 0.5°C in SST can cause epidemics to double in magnitude. In reality, however, the spatial nature of transmission can effectively protect the community, restricting the magnitude of annual epidemics. This is because the probability of susceptible corals to become infected is negatively associated with coral density. Based on our findings, we expect that infectious diseases having a significant spatial component, such as Red-Sea WPD, will never lead to a complete destruction of the coral community under increased thermal stress. However, this also implies that signs of recovery of local coral communities may be misleading; indicative more of spatial dynamics than true rehabilitation of these communities. In contrast to earlier generic models, our approach captures dynamics of WPD both in space and time, accounting for the highly seasonal nature of annual WPD outbreaks.     

The uncertain burden of Plasmodium falciparum epidemics in Africa

Although the control of malaria epidemics has been a priority for the World Health Organization and other agencies for many years, surprisingly little is known about the public health burden of these epidemics. Here, we evaluate the available evidence of the morbidity and mortality impacts of individual epidemics in Africa and examine the problems associated with using these data to estimate the average annual burden of epidemics at national and continental scales. We argue that conventional approaches that are used to assess the burden of epidemics are inadequate, and outline the future steps that are required to produce estimates that are more accurate.     

Ethical problems in conducting research in acute epidemics: the Pfizer meningitis study in Nigeria as an illustration

The ethics of conducting research in epidemic situations have yet to account fully for differences in the proportion and acuteness of epidemics, among other factors. While epidemics most often arise from infectious diseases, not all infectious diseases are of epidemic proportions, and not all epidemics occur acutely. These and other variations constrain the generalization of ethical decision-making and impose ethical demands on the individual researcher in a way not previously highlighted. This paper discusses a number of such constraints and impositions. It applies the ethical principles enunciated by Emmanuel et al. ¹ to the controversial Pfizer study in Nigeria in order to highlight the particular ethical concerns of acute epidemic research, and suggest ways of meeting such challenges.
The paper recommends that research during epidemics should be partly evaluated on its own merits in order to determine its ethical appropriateness to the specific situation. Snap decisions to conduct research during acute epidemics should be resisted. Community engagement, public notification and good information management are needed to promote the ethics of conducting research during acute epidemics. Individual consent is most at risk of being compromised, and every effort should be made to ensure that it is maintained and valid. Use of data safety management boards should be routine. Acute epidemics also present opportunities to enhance the social value of research and maximize its benefits to communities.
Ethical research is possible in acute epidemics, if the potential challenges are thought of ahead of time and appropriate precautions taken.     

Variation in costs of parasite resistance among natural host populations

Organisms that can resist parasitic infection often have lower fitness in the absence of parasites. These costs of resistance can mediate host evolution during parasite epidemics. For example, large epidemics will select for increased host resistance. In contrast, small epidemics (or no disease) can select for increased host susceptibility when costly resistance allows more susceptible hosts to outcompete their resistant counterparts. Despite their importance for evolution in host populations, costs of resistance (which are also known as resistance trade‐offs) have mainly been examined in laboratory‐based host–parasite systems. Very few examples come from field‐collected hosts. Furthermore, little is known about how resistance trade‐offs vary across natural populations. We addressed these gaps using the freshwater crustacean Daphnia dentifera and its natural yeast parasite, Metschnikowia bicuspidata. We found a cost of resistance in two of the five populations we studied – those with the most genetic variation in resistance and the smallest epidemics in the previous year. However, yeast epidemics in the current year did not alter slopes of these trade‐offs before and after epidemics. In contrast, the no‐cost populations showed little variation in resistance, possibly because large yeast epidemics eroded that variation in the previous year. Consequently, our results demonstrate variation in costs of resistance in wild host populations. This variation has important implications for host evolution during epidemics in nature.     

The El Niño southern oscillation and malaria epidemics in South America

A better understanding of the relationship between the El Ni?o Southern Oscillation (ENSO), the climatic anomalies it engenders, and malaria epidemics could help mitigate the world-wide increase in incidence of this mosquito-transmitted disease. The purpose of this paper is to assess the possibility of using ENSO forecasts for improving malaria control. This paper analyses the relationship between ENSO events and malaria epidemics in a number of South American countries (Colombia, Ecuador, French Guiana, Guyana, Peru, Suriname, and Venezuela). A statistically significant relationship was found between El Ni?o and malaria epidemics in Colombia, Guyana, Peru, and Venezuela. We demonstrate that flooding engenders malaria epidemics in the dry coastal region of northern Peru, while droughts favor the development of epidemics in Colombia and Guyana, and epidemics lag a drought by 1 year in Venezuela. In Brazil, French Guiana, and Ecuador, where we did not detect an ENSO/malaria signal, non-climatic factors such as insecticide sprayings, variation in availability of anti-malaria drugs, and population migration are likely to play a stronger role in malaria epidemics than ENSO-generated climatic anomalies. In some South American countries, El Ni?o forecasts show strong potential for informing public health efforts to control malaria.     

Rapid evolution and ecological host-parasite dynamics

Traditionally, the termination of parasite epidemics has been attributed to ecological causes: namely, the depletion of susceptible hosts as a result of mortality or acquired immunity. Here, we suggest that epidemics can also end because of rapid host evolution. Focusing on a particular host–parasite system, Daphnia dentifera and its parasite Metschnikowia bicuspidata , we show that Daphnia from lakes with recent epidemics were more resistant to infection and had less variance in susceptibility than Daphnia from lakes without recent epidemics. However, our studies revealed little evidence for genetic variation in infectivity or virulence in Metschnikowia . Incorporating the observed genetic variation in host susceptibility into an epidemiological model parameterized for this system reveals that rapid evolution can explain the termination of epidemics on time scales matching what occurs in lake populations. Thus, not only does our study provide rare evidence for parasite-mediated selection in natural populations, it also suggests that rapid evolution has important effects on short-term host–parasite dynamics.     

以兽类为例探讨我国陆生野生动物疫病监管中面临的问题与对策

近年来, 新型冠状病毒、SARS病毒和鼠疫等新发和再发性动物源疫病多是由兽类及其媒介携带的病原生物直接或间接感染而引发的, 不仅对人类健康和生态系统平衡造成了重大威胁, 而且威胁全球公共卫生安全、粮食安全和生物安全。结合我国重要陆生兽类疫源疫病发生的新情况和新特点, 本文重点总结了我国以陆生野生及非野生兽类(家畜为主)为重点的24种重要人兽共患病的监管情况, 并对这些疫源疫病的监管空缺进行了分析。由于病原生物的种类多及其感染传播方式多样, 我国人间和动物间疫情呈现多发态势, 新发和再发疫病防控面临严峻挑战。从目前情况来看, 我国重要野生动物疫源疫病呈现为多部门、多层监管的局面。全球化贸易剧增、非法猎杀、非法交易、违法违规养殖、滥食野生动物陋习、检疫环节失察等导致了当前我国野生动物疫源疫病的传染源头和传播链错综复杂, 加剧了人类与野生动物所携带的病原接触、感染和传播的风险。极端气候或灾害事件频发以及对新发再发传染病的认知不足导致难以从源头做好疫病防控。针对上述问题, 本文提出了从源头加强基础研究和全链条监管来积极防范陆生野生动物疫病疫情的对策和建议。     

Quality matters: resource quality for hosts and the timing of epidemics

Epidemiologists increasingly realize that species interactions (e.g. selective predation) can determine when epidemics start and end. We hypothesize here that resource quality can also strongly influence disease dynamics: epidemics can be inhibited when resource quality for hosts is too poor and too good. In three lakes, resource quality for the zooplankton host ( Daphnia dentifera ) was poor when fungal epidemics ( Metschnikowia bicuspidata ) commenced and increased as epidemics waned. Experiments using variation in algal food showed that resource quality had conflicting effects on underlying epidemiology: high-quality food induced large production of infective propagules (spores) and high birth rate but also reduced transmission. A model then illustrated how these underlying correlations can inhibit the start of epidemics (when spore production/birth rate are too low) but also catalyse their end (when transmission becomes too low). This resource quality mechanism is likely to interface with other ones controlling disease dynamics and warrants closer evaluation.     

Epidemic outbreaks on structured populations

Our chances to halt epidemic outbreaks rely on how accurately we represent the population structure underlying the disease spread. When analysing global epidemics this force us to consider metapopulation models taking into account intra- and inter-community interactions. Here I introduce and analyze a metapopulation model which accounts for several features observed in real outbreaks. First, I demonstrate that depending on the intra-community expected outbreak size and the fraction of social bridges the epidemic outbreaks die out or there is a finite probability to observe a global epidemics. Second, I show that the global scenario is characterized by resurgent epidemics, their number increasing with increasing the intra-community average distance between individuals. Finally, I present empirical data for the AIDS epidemics supporting the model predictions.     

Epidemic size determines population-level effects of fungal parasites on Daphnia hosts

Parasites frequently reduce the fecundity, growth, and survival of individual hosts. How often do these virulent effects reduce the density of host populations? Spectacular examples show that recently invaded parasites can severely impact host populations—but what about parasites persisting long-term in host populations? We have addressed this issue using a zooplankton host (Daphnia dentifera) that becomes infected with a fungal microparasite (Metschnikowia bicuspidata). We combined observations of epidemics in nine lakes over 6 years, fine-scale sampling of three epidemics, and a mesocosm experiment. Most epidemics remained small (<10% maximum prevalence) and exerted little influence on host densities. However, larger epidemics more severely depressed the populations of their hosts. These large/severe epidemics started and peaked earlier than smaller/benign ones. The larger epidemics also exerted particularly negative effects on host densities at certain lags, reflecting the delayed consequences of infection on fecundity reduction and host mortality. Notably, negative effects on the juvenile stage class manifested later than those on the adult stage class. The results of the experiment further emphasized depression of host density by the fungus, especially on the density of the juvenile stage class. Consequently, this common parasite reduces the density of host populations when conditions foster larger outbreaks characterized by an earlier start and earlier peak. Given these considerable effects on host density seen in a number of large epidemics, parasitism may sometimes rank highly among other factors (predation, resource availability) driving the population dynamics of these hosts.     

A clonal analysis of Neisseria meningitidis serogroup A

A typing scheme has recently been developed for Neisseria meningitidis serogroup A based on the clonal population structure of these bacteria. An international strain collection consisting of 423 group A strains isolated from 23 epidemics or outbreaks since 1963, as well as from older epidemics and numerous non-epidemic situations was used in the analysis. Strains were first segregated into electrophoretic types, depending on the combined score for the electrophoretic mobilities of 7 cytoplasmic isoenzymes resolved by starch gel electrophoresis and of 2 outer membrane proteins resolved by sodium dodecyl sulphate polyacrylamide gel electrophoresis. The bacteria were subsequently assigned to one of 21 clones after numerical analysis of their electrophoretic types.The epidemiological value of the typing scheme was assessed by examining case and carrier strains isolated during (1982–83) and subsequent to (1984–85) an epidemic in the Gambia, West Africa. The case isolates, all of which were serogroup A, were of a single clonal type. All serogroup A carrier isolates were also of this clone, while carrier strains of other serogroups showed greater clonal diversity. These results indicate that case strains during an epidemic show little clonal diversity and thus that the typing scheme is of value in distinguishing the etiology of epidemics.A retrospective epidemiological analysis of the strains in the international collection showed that most serogroup A epidemics were associated with a single or predominant clone, although some epidemics were of mixed etiology. The survey included 256 isolates from 15 African epidemics since 1963, a period which covers 3 major epidemic waves (1960–63; 1967–73 and 1981–83), thus permitting a detailed epidemiological analysis of serogroup A epidemics in this continent.Epidemiological records indicate that seven clones have been responsible for sets of epidemics throughout the world since 1915 and that at least two of these sets can be considered to represent mutually exclusive pandemics, linking numerous epidemics between 1967–75 and 1973–83, respectively.     

A note on epidemics in heterogeneous populations.

Recent analysis has shown the importance of heterogeneity for understanding the course of epidemics. However, the results generally rely on computer models or the assumption that the population consists of internally homogeneous subgroups. This note presents some analytic results for the more general case, in which any distribution can characterize population heterogeneity in susceptibility under proportionate mixing. At any moment, epidemics in such a situation resemble classic epidemics, with rate of spread governed by the average susceptibility of those not yet infected. But, over time, this average susceptibility falls at a rate proportional to the dispersion of susceptibility among those not yet infected. The author concludes by noting some implications of heterogeneity for understanding epidemics.     

Length of intervals between epidemics: evaluating the influence of maternal transfer of immunity

The length of intervals between epidemic outbreaks of infectious diseases is critical in epidemiology. In several species of marine mammals and birds, it is pivotal to also consider the life history of the species of concern, as the contact rate between individuals can have a seasonal flux, for example, due to aggregations during the breeding season. Recently, particular interest has been given to the role of the dynamics of immunity in determining the intervals between epidemics in wild animal populations. One potentially powerful, but often neglected, process in this context is the maternal transfer of immunity. Here, we explore theoretically how the transfer of maternal antibodies can delay the recurrence of epidemics using Phocine Distemper in harbor seals as an example of a system in which epidemic outbreaks are followed by pathogen extinction. We show that the presence of temporarily protected newborns can significantly increase the predicted interval between epidemics, and this effect is strongly dependent on the degree of synchrony in the breeding season. Furthermore, we found that stochasticity in the onset of epidemics in combination with maternally acquired immunity increases the predicted intervals between epidemics even more. These effects arise because newborns with maternal antibodies temporarily boost population level immunity above the threshold of herd immunity, particularly when breeding is synchronous. Overall, our results show that maternal antibodies can have a profound influence on the dynamics of wildlife epidemics, notably in gregarious species such as many marine mammals and seabirds.     

the Influence of Epidemics on the Indian Populations and Cultures of Texas

Abstract

Historic records indicate that Indian tribes residing in Texas prior to 1820 suffered no fewer than 30 epidemics during the period of white contact prior to 1890. The cumulative effect of successive epidemics was a major factor in the extinction of some of these tribes, and in continued population decreases among the others. Most probably these epidemics also caused significant cultural changes among the Indians who survived them in such varied aspects of life as warfare, political and social organization, and religious beliefs and practices.     

A model of spatially evolving herpesvirus epidemics causing mass mortality in Australian pilchard Sardinops sagax

In 1995 mass mortality of pilchards Sardinops sagax occurred along >5000 km of Australian coast; similar events occurred in 1998/99. This mortality was closely associated with a herpesvirus. The pilchard is an important food source for larger animals and supports commercial fisheries. Both epidemics originated in South Australian waters and spread as waves with velocities of 10 to 40 km d(-1). Velocity was constant for a single wave, but varied between the epidemics and between the east- and west-bound waves in each epidemic. The pattern of mortality evolved from recurrent episodes to a single peak with distance from the origin. A 1-dimensional model of these epidemics has been developed. The host population is divided into susceptible, infected and latent, infected and infectious, and removed (recovered and dead) phases; the latent and infectious periods are of fixed duration. This model produces the mortality patterns observed locally and during the spread and evolution of the epidemic. It is consistent with evidence from pathology. The wave velocity is sensitive to diffusion coefficients, viral transmission rates and latent period. These parameters are constrained using the local and large-scale patterns of epidemic spread. The relative roles of these parameters in explaining differences between epidemics and between east- and west-bound waves within epidemics are discussed. The model predicts very high levels of infection, indicating that many surviving pilchards recovered following infection. Control appears impracticable once epidemics are initiated, but impact can be minimised by protecting juvenile stocks.     

Study of the effect of vaccination on periodic structures of measles epidemics in Japan

The purpose of this paper is to investigate the effect of vaccination on periodic structures of measles epidemics in Japan. We carried out spectral analysis for time series data of measles notifications collected in Japan. It was confirmed that the interepidemic period, which corresponds to the interval between major epidemics of measles, increases as the vaccination ratio increases. This result was supported by a theory based on a mathematical model for epidemics of infectious diseases. It was suggested that the interepidemic period is useful to estimate the effect of vaccination on measles incidences quantitatively.     

Interactions among symbionts operate across scales to influence parasite epidemics

Parasite epidemics may be influenced by interactions among symbionts, which can depend on past events at multiple spatial scales. Within host individuals, interactions can depend on the sequence in which symbionts infect a host, generating priority effects. Across host individuals, interactions can depend on parasite phenology. To test the roles of parasite interactions and phenology in epidemics, we embedded multiple cohorts of sentinel plants, grown from seeds with and without a vertically transmitted symbiont, into a wild host population, and tracked foliar infections caused by three common fungal parasites. Within hosts, parasite growth was influenced by coinfections, but coinfections were often prevented by priority effects among symbionts. Across hosts, parasite phenology altered host susceptibility to secondary infections, symbiont interactions and ultimately the magnitude of parasite epidemics. Together, these results indicate that parasite phenology can influence parasite epidemics by altering the sequence of infection and interactions among symbionts within host individuals.