Project description:Simultaneously controlling COVID-19 epidemics and limiting economic and societal impacts presents a difficult challenge, especially with limited public health budgets. Testing, contact tracing, and isolating/quarantining is a key strategy that has been used to reduce transmission of SARS-CoV-2, the virus that causes COVID-19 and other pathogens. However, manual contact tracing is a time-consuming process and as case numbers increase a smaller fraction of cases' contacts can be traced, leading to additional virus spread. Delays between symptom onset and being tested (and receiving results), and a low fraction of symptomatic cases being tested and traced can also reduce the impact of contact tracing on transmission. We examined the relationship between increasing cases and delays and the pathogen reproductive number Rt, and the implications for infection dynamics using deterministic and stochastic compartmental models of SARS-CoV-2. We found that Rt increased sigmoidally with the number of cases due to decreasing contact tracing efficacy. This relationship results in accelerating epidemics because Rt initially increases, rather than declines, as infections increase. Shifting contact tracers from locations with high and low case burdens relative to capacity to locations with intermediate case burdens maximizes their impact in reducing Rt (but minimizing total infections may be more complicated). Contact tracing efficacy decreased sharply with increasing delays between symptom onset and tracing and with lower fraction of symptomatic infections being tested. Finally, testing and tracing reductions in Rt can sometimes greatly delay epidemics due to the highly heterogeneous transmission dynamics of SARS-CoV-2. These results demonstrate the importance of having an expandable or mobile team of contact tracers that can be used to control surges in cases. They also highlight the synergistic value of high capacity, easy access testing and rapid turn-around of testing results, and outreach efforts to encourage symptomatic cases to be tested immediately after symptom onset.

Project description:The presence of heterogeneity in susceptibility, differences between hosts in their likelihood of becoming infected, can fundamentally alter disease dynamics and public health responses, for example, by changing the final epidemic size, the duration of an epidemic, and even the vaccination threshold required to achieve herd immunity. Yet, heterogeneity in susceptibility is notoriously difficult to detect and measure, especially early in an epidemic. Here we develop a method that can be used to detect and estimate heterogeneity in susceptibility given contact by using contact tracing data, which are typically collected early in the course of an outbreak. This approach provides the capability, given sufficient data, to estimate and account for the effects of this heterogeneity before they become apparent during an epidemic. It additionally provides the capability to analyze the wealth of contact tracing data available for previous epidemics and estimate heterogeneity in susceptibility for disease systems in which it has never been estimated previously. The premise of our approach is that highly susceptible individuals become infected more often than less susceptible individuals, and so individuals not infected after appearing in contact networks should be less susceptible than average. This change in susceptibility can be detected and quantified when individuals show up in a second contact network after not being infected in the first. To develop our method, we simulated contact tracing data from artificial populations with known levels of heterogeneity in susceptibility according to underlying discrete or continuous distributions of susceptibilities. We analyzed these data to determine the parameter space under which we are able to detect heterogeneity and the accuracy with which we are able to estimate it. We found that our power to detect heterogeneity increases with larger sample sizes, greater heterogeneity, and intermediate fractions of contacts becoming infected in the discrete case or greater fractions of contacts becoming infected in the continuous case. We also found that we are able to reliably estimate heterogeneity and disease dynamics. Ultimately, this means that contact tracing data alone are sufficient to detect and quantify heterogeneity in susceptibility.

Project description:The WHO recommended intervention of Directly Observed Treatment, Short-course (DOTS) appears to have been less successful than expected in reducing the burden of TB in some high prevalence settings. One strategy for enhancing DOTS is incorporating active case-finding through screening contacts of TB patients as widely used in low-prevalence settings. Predictive models that incorporate population-level effects on transmission provide one means of predicting impacts of such interventions. We aim to identify all TB transmission modelling studies addressing contact tracing and to describe and critically assess their modelling assumptions, parameter choices and relevance to policy. We searched MEDLINE, SCOPUS, COMPENDEX, Google Scholar and Web of Science databases for relevant English language publications up to February 2012. Of the 1285 studies identified, only 5 studies met our inclusion criteria of models of TB transmission dynamics in human populations designed to incorporate contact tracing as an intervention. Detailed implementation of contact processes was only present in two studies, while only one study presented a model for a high prevalence, developing world setting. Some use of relevant data for parameter estimation was made in each study however validation of the predicted impact of interventions was not attempted in any of the studies. Despite a large body of literature on TB transmission modelling, few published studies incorporate contact tracing. There is considerable scope for future analyses to make better use of data and to apply individual based models to facilitate more realistic patterns of infectious contact. Combined with a focus on high burden settings this would greatly increase the potential for models to inform the use of contract tracing as a TB control policy. Our findings highlight the potential for collaborative work between clinicians, epidemiologists and modellers to gather data required to enhance model development and validation and hence better inform future public health policy.

Project description:ObjectiveTo analyse the transmission dynamics of the monkeypox outbreak in the UK, declared a Public Health Emergency of International Concern in July 2022.DesignContact tracing study, linking data on case-contact pairs and on probable exposure dates.SettingCase questionnaires from the UK Health Security Agency (UKHSA), United Kingdom.Participants2746 people with polymerase chain reaction confirmed monkeypox virus in the UK between 6 May and 1 August 2022.Main outcome measuresThe incubation period and serial interval of a monkeypox infection using two bayesian time delay models-one corrected for interval censoring (ICC-interval censoring corrected) and one corrected for interval censoring, right truncation, and epidemic phase bias (ICRTC-interval censoring right truncation corrected). Growth rates of cases by reporting date, when monkeypox virus was confirmed and reported to UKHSA, were estimated using generalised additive models.ResultsThe mean age of participants was 37.8 years and 95% reported being gay, bisexual, and other men who have sex with men (1160 out of 1213 reporting). The mean incubation period was estimated to be 7.6 days (95% credible interval 6.5 to 9.9) using the ICC model and 7.8 days (6.6 to 9.2) using the ICRTC model. The estimated mean serial interval was 8.0 days (95% credible interval 6.5 to 9.8) using the ICC model and 9.5 days (7.4 to 12.3) using the ICRTC model. Although the mean serial interval was longer than the incubation period for both models, short serial intervals were more common than short incubation periods, with the 25th centile and the median of the serial interval shorter than the incubation period. For the ICC and ICRTC models, the corresponding estimates ranged from 1.8 days (95% credible interval 1.5 to 1.8) to 1.6 days (1.4 to 1.6) shorter at the 25th centile and 1.6 days (1.5 to 1.7) to 0.8 days (0.3 to 1.2) shorter at the median. 10 out of 13 linked patients had documented pre-symptomatic transmission. Doubling times of cases declined from 9.07 days (95% confidence interval 12.63 to 7.08) on the 6 May, when the first case of monkeypox was reported in the UK, to a halving time of 29 days (95% confidence interval 38.02 to 23.44) on 1 August.ConclusionsAnalysis of the instantaneous growth rate of monkeypox incidence indicates that the epidemic peaked in the UK as of 9 July and then started to decline. Short serial intervals were more common than short incubation periods suggesting considerable pre-symptomatic transmission, which was validated through linked patient level records. For patients who could be linked through personally identifiable data, four days was the maximum time that transmission was detected before symptoms manifested. An isolation period of 16 to 23 days would be required to detect 95% of people with a potential infection. The 95th centile of the serial interval was between 23 and 41 days, suggesting long infectious periods.

Dataset Information

Author Correction: Infectivity, susceptibility, and risk factors associated with SARS-CoV-2 transmission under intensive contact tracing in Hunan, China.

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