Basic Epidemiological Parameters at the end of the 5th month of the COVID-19 Outbreak

2020 ◽  
Vol 1 (1) ◽  
pp. 67-80
Author(s):  
Oktay Sarı ◽  
Tuğrul Hoşbul ◽  
Fatih Şahiner
2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
C. Höschl ◽  
P. Stopková

Both disorders are worldwide, lifelong, and recurrent illnesses with periods of exacerbation and partial or full remissions. Lifetime prevalence of schizophrenia and bipolar disorder type I is around 1%. Women and men are affected at proximately equal rates and the typical age of onset is similar. Both disorders also share risk factors showing evidence for impaired prenatal development, such as birth seasonality, abnormal dermatoglyphs and higher incidence of perinatal complications. However, there is evidence for differences in prevalence in geographical isolates, in presence of minor physical abnormalities and possibly also in influence of psychosocial factors, urbanicity and use of cannabis. However, based only on similar epidemiological parameters, it is not possible to assume any degree of continuity between bipolar disorder and schizophrenia. The main evidence for partially shared pathophysiology is given by genetic studies.


Nature ◽  
1988 ◽  
Vol 333 (6173) ◽  
pp. 514-519 ◽  
Author(s):  
Roy M. Andersen ◽  
Robert M. May

2007 ◽  
Vol 46 (01) ◽  
pp. 19-26 ◽  
Author(s):  
P. Crépey ◽  
M. Barthélemy ◽  
A.-J. Valleron ◽  
F.P. Alvarez

Summary Objectives: We present a simulation software which allows studying the dynamics of a hypothetic infectious disease within a network of connected people. The software is aimed to facilitate the discrimination of stochastic factors governing the evolution of an infection in a network. In order to do this it provides simple tools to create networks of individuals and to set the epidemiological parameters of the outbreaks. Methods: Three popular models of infectious disease can be used (SI, SIS, SIR). The simulated networks are either the algorithm-based included ones (scale free, small-world, and random homogeneous networks), or provided by third party software. Results: It allows the simulation of a single or many outbreaks over a network, or outbreaks over multiple networks (with identical properties). Standard outputs are the evolution of the prevalence of the disease, on a single outbreak basis or by averaging many outbreaks. The user can also obtain customized outputs which address in detail different possible epidemiological questions about the spread of an infectious agent in a community. Conclusions: The presented software introduces sources of stochasticity present in real epidemics by simulating outbreaks on contact networks of individuals. This approach may help to understand the paths followed by outbreaks in a given community and to design new strategies for preventing and controlling them.


1983 ◽  
Vol 90 (2) ◽  
pp. 259-325 ◽  
Author(s):  
R. M. Anderson ◽  
R. M. May

SUMMARYThis paper uses relatively simple and deterministic mathematical models to examine the impact that different immunization policies have on the age-specific incidence of rubella and measles. Following earlier work by Knox (1980) and others, we show that immunization programmes can, under some circumstances, increase the total number of cases among older age groups; the implications for the overall incidence of measles encephalitis and of congenital rubella syndrome are examined, paying attention both to the eventual equilibrium and to the short-term effect in the first few decades after immunization is initiated. Throughout, we use data (from the U.K., and U.S.A. and other countries) both in the estimation of the epidemiological parameters in our models, and in comparison between theoretical predictions and observed facts. The conclusions defy brief summary and are set out at the end of the paper.


Parasitology ◽  
1989 ◽  
Vol 99 (1) ◽  
pp. 47-56 ◽  
Author(s):  
M. E. J. Woolhouse

SUMMARYThe prevalence of schistosome infections in intermediate host snails varies with snail age. The relationship between age and prevalence, the age—prevalence curve, is complex and may vary in space and time, and among parasite—host species. Field studies show that the shape of the age—prevalence curve may be seasonally variable, and that at some times there may be a decline in prevalence among older snails. This paper attempts to explain these observations in terms of the underlying epidemiological processes. A discrete-time version of Muench's catalytic model for age-dependent infection is developed. Model simulations were carried out using life-history and epidemiological parameters derived from studies ofSchistosoma haematobium—Bulinus globususin Zimbabwe. Analysis of model behaviour identifies aspects of the schistosome— snail interaction that affect the shape of the age—prevalence curve. The following features can result in a decline in prevalence among older snails. (1) A decrease in the survival rate of patent infected snails with age. (2) A decrease in the force of infection with age. (3) A high rate of loss of infection. (4) A heterogeneity in the snail population such that the probability of infection is correlated with snail fecundity. (This would occur if there existed a spatial correlation between force of infection and fecundity, or if there were a correlation between fecundity and susceptibility.) The evidence for the occurrence of these features in the field is assessed. Survival rate is related more closely to the duration of patent infection than to ageper se. The evidence for age-dependent force of infection is equivocal. Significant loss-of-infection rates have yet to be demonstrated. Heterogeneities in force of infection and fecundity have been reported and, for the Zimbabwe data, this mechanism can explain seasonally in the age—prevalence curve as a function of known seasonal variation in the force of infection and snail fecundity.


2015 ◽  
Vol 11 (5) ◽  
pp. 20150131 ◽  
Author(s):  
Rony Izhar ◽  
Jarkko Routtu ◽  
Frida Ben-Ami

In many host populations, one of the most striking differences among hosts is their age. While parasite prevalence differences in relation to host age are well known, little is known on how host age impacts ecological and evolutionary dynamics of diseases. Using two clones of the water flea Daphnia magna and two clones of its bacterial parasite Pasteuria ramosa , we examined how host age at exposure influences within-host parasite competition and virulence. We found that multiply-exposed hosts were more susceptible to infection and suffered higher mortality than singly-exposed hosts. Hosts oldest at exposure were least often infected and vice versa. Furthermore, we found that in young multiply-exposed hosts competition was weak, allowing coexistence and transmission of both parasite clones, whereas in older multiply-exposed hosts competitive exclusion was observed. Thus, age-dependent parasite exposure and host demography (age structure) could together play an important role in mediating parasite evolution. At the individual level, our results demonstrate a previously unnoticed interaction of the host's immune system with host age, suggesting that the specificity of immune function changes as hosts mature. Therefore, evolutionary models of parasite virulence might benefit from incorporating age-dependent epidemiological parameters.


2020 ◽  
Vol 287 (1926) ◽  
pp. 20200062 ◽  
Author(s):  
Emily M. Hall ◽  
Jesse L. Brunner ◽  
Brandon Hutzenbiler ◽  
Erica J. Crespi

The stress-induced susceptibility hypothesis, which predicts chronic stress weakens immune defences, was proposed to explain increasing infectious disease-related mass mortality and population declines. Previous work characterized wetland salinization as a chronic stressor to larval amphibian populations. Thus, we combined field observations with experimental exposures quantifying epidemiological parameters to test the role of salinity stress in the occurrence of ranavirus-associated mass mortality events. Despite ubiquitous pathogen presence (94%), populations exposed to salt runoff had slightly more frequent ranavirus related mass mortality events, more lethal infections, and 117-times greater pathogen environmental DNA. Experimental exposure to chronic elevated salinity (0.8–1.6 g l −1 Cl − ) reduced tolerance to infection, causing greater mortality at lower doses. We found a strong negative relationship between splenocyte proliferation and corticosterone in ranavirus-infected larvae at a moderate elevation of salinity, supporting glucocorticoid-medicated immunosuppression, but not at high salinity. Salinity alone reduced proliferation further at similar corticosterone levels and infection intensities. Finally, larvae raised in elevated salinity had 10 times more intense infections and shed five times as much virus with similar viral decay rates, suggesting increased transmission. Our findings illustrate how a small change in habitat quality leads to more lethal infections and potentially greater transmission efficiency, increasing the severity of ranavirus epidemics.


Plant Disease ◽  
1998 ◽  
Vol 82 (10) ◽  
pp. 1142-1146 ◽  
Author(s):  
Cleide M. F. Pinto ◽  
Luiz A. Maffia ◽  
Richard D. Berger ◽  
Eduardo S. G. Mizubuti ◽  
Vicente W. D. Casali

In the region of Amarantina, Minas Gerais state, Brazil, four annual experiments with garlic (Allium sativum) were established in fields infested with Sclerotium cepivorum, causal agent of garlic white rot, to investigate the effect of time of planting on the day when disease was first noticed (tonset), incidence at harvest (yf), duration of epidemics (tf — tonset), and the response of five cultivars to white rot. Most epidemiological parameters were similar among cultivars. In 1986 to 1988, no white rot was observed on garlic planted during the warm temperatures in January. The average onset of white rot occurred at different times dependent on the day of planting as average temperatures decreased from January to May. That is, for February plantings, onset occurred after 93 to 140 days (between 1 June and 5 July); for March plantings, about 90 days (15 to 28 June); for mid-April plantings, about 77 days (1 July); and mid-May plantings, about 66 days (20 July). Because of these different times of onset, the average duration of epidemics was shorter for crops planted in February (30 days) compared to crops planted in March (48 days) or April to May (54 to 69 days). In general, most disease (highest incidence and longest duration) occurred on crops planted in March to May. Therefore, severe losses to white rot would be expected when garlic is planted at the traditional times (March and April) in areas infested with sclerotia of S. cepivorum. The early planting of garlic is recommended as an important management strategy to avoid white rot in areas with these infested soils.


2016 ◽  
Vol 13 (121) ◽  
pp. 20160288 ◽  
Author(s):  
Pieter Trapman ◽  
Frank Ball ◽  
Jean-Stéphane Dhersin ◽  
Viet Chi Tran ◽  
Jacco Wallinga ◽  
...  

When controlling an emerging outbreak of an infectious disease, it is essential to know the key epidemiological parameters, such as the basic reproduction number R 0 and the control effort required to prevent a large outbreak. These parameters are estimated from the observed incidence of new cases and information about the infectious contact structures of the population in which the disease spreads. However, the relevant infectious contact structures for new, emerging infections are often unknown or hard to obtain. Here, we show that, for many common true underlying heterogeneous contact structures, the simplification to neglect such structures and instead assume that all contacts are made homogeneously in the whole population results in conservative estimates for R 0 and the required control effort. This means that robust control policies can be planned during the early stages of an outbreak, using such conservative estimates of the required control effort.


2017 ◽  
Vol 372 (1721) ◽  
pp. 20160297 ◽  
Author(s):  
Cordelia E. M. Coltart ◽  
Benjamin Lindsey ◽  
Isaac Ghinai ◽  
Anne M. Johnson ◽  
David L. Heymann

Ebola virus causes a severe haemorrhagic fever in humans with high case fatality and significant epidemic potential. The 2013–2016 outbreak in West Africa was unprecedented in scale, being larger than all previous outbreaks combined, with 28 646 reported cases and 11 323 reported deaths. It was also unique in its geographical distribution and multicountry spread. It is vital that the lessons learned from the world's largest Ebola outbreak are not lost. This article aims to provide a detailed description of the evolution of the outbreak. We contextualize this outbreak in relation to previous Ebola outbreaks and outline the theories regarding its origins and emergence. The outbreak is described by country, in chronological order, including epidemiological parameters and implementation of outbreak containment strategies. We then summarize the factors that led to rapid and extensive propagation, as well as highlight the key successes, failures and lessons learned from this outbreak and the response. This article is part of the themed issue ‘The 2013–2016 West African Ebola epidemic: data, decision-making and disease control’.


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