Niko Speybroeck

World Health Organization Global Estimates and Regional Comparisons of the Burden of Foodborne Disease in 2010

Illness and death from diseases caused by contaminated food are a constant threat to public health and a significant impediment to socio-economic development worldwide. To measure the global and regional burden of foodborne disease (FBD), the World Health Organization (WHO) established the Foodborne Disease Burden Epidemiology Reference Group (FERG), which here reports their first estimates of the incidence, mortality, and disease burden due to 31 foodborne hazards. We find that the global burden of FBD is comparable to those of the major infectious diseases, HIV/AIDS, malaria and tuberculosis. The most frequent causes of foodborne illness were diarrheal disease agents, particularly norovirus and Campylobacter spp. Diarrheal disease agents, especially non-typhoidal Salmonella enterica, were also responsible for the majority of deaths due to FBD. Other major causes of FBD deaths were Salmonella Typhi, Taenia solium and hepatitis A virus. The global burden of FBD caused by the 31 hazards in 2010 was 33 million Disability Adjusted Life Years (DALYs); children under five years old bore 40% of this burden. The 14 subregions, defined on the basis of child and adult mortality, had considerably different burdens of FBD, with the greatest falling on the subregions in Africa, followed by the subregions in South-East Asia and the Eastern Mediterranean D subregion. Some hazards, such as non-typhoidal S. enterica, were important causes of FBD in all regions of the world, whereas others, such as certain parasitic helminths, were highly localised. Thus, the burden of FBD is borne particularly by children under five years old–although they represent only 9% of the global population–and people living in low-income regions of the world. These estimates are conservative, i.e., underestimates rather than overestimates; further studies are needed to address the data gaps and limitations of the study. Nevertheless, all stakeholders can contribute to improvements in food safety throughout the food chain by incorporating these estimates into policy development at national and international levels.

Socioeconomic inequality in malnutrition in developing countries

OBJECTIVE The objectives of this study were to report on socioeconomic inequality in childhood malnutrition in the developing world, to provide evidence for an association between socioeconomic inequality and the average level of malnutrition, and to draw attention to different patterns of socioeconomic inequality in malnutrition. METHODS Both stunting and wasting were measured using new WHO child growth standards. Socioeconomic status was estimated by principal component analysis using a set of household assets and living conditions. Socioeconomic inequality was measured using an alternative concentration index that avoids problems with dependence on the mean level of malnutrition. FINDINGS In almost all countries investigated, stunting and wasting disproportionately affected the poor. However, socioeconomic inequality in wasting was limited and was not significant in about one third of countries. After correcting for the concentration indexs dependence on mean malnutrition, there was no clear association between average stunting and socioeconomic inequality. The latter showed different patterns, which were termed mass deprivation, queuing and exclusion. Although average levels of malnutrition were higher with the new WHO reference standards, estimates of socioeconomic inequality were largely unaffected by changing the growth standards. CONCLUSION Socioeconomic inequality in childhood malnutrition existed throughout the developing world, and was not related to the average malnutrition rate. Failure to tackle this inequality is a cause of social injustice. Moreover, reducing the overall rate of malnutrition does not necessarily lead to a reduction in inequality. Policies should, therefore, take into account the distribution of childhood malnutrition across all socioeconomic groups.

Disability weights for the Global Burden of Disease 2013 study

BACKGROUND The Global Burden of Disease (GBD) study assesses health losses from diseases, injuries, and risk factors using disability-adjusted life-years, which need a set of disability weights to quantify health levels associated with non-fatal outcomes. The objective of this study was to estimate disability weights for the GBD 2013 study. METHODS We analysed data from new web-based surveys of participants aged 18-65 years, completed in four European countries (Hungary, Italy, the Netherlands, and Sweden) between Sept 23, 2013, and Nov 11, 2013, combined with data previously collected in the GBD 2010 disability weights measurement study. Surveys used paired comparison questions for which respondents considered two hypothetical individuals with different health states and specified which person they deemed healthier than the other. These surveys covered 183 health states pertinent to GBD 2013; of these states, 30 were presented with descriptions revised from previous versions and 18 were new to GBD 2013. We analysed paired comparison data using probit regression analysis and rescaled results to disability weight units between 0 (no loss of health) and 1 (loss equivalent to death). We compared results with previous estimates, and an additional analysis examined sensitivity of paired comparison responses to duration of hypothetical health states. FINDINGS The total analysis sample consisted of 30 230 respondents from the GBD 2010 surveys and 30 660 from the new European surveys. For health states common to GBD 2010 and GBD 2013, results were highly correlated overall (Pearsons r 0·992 [95% uncertainty interval 0·989-0·994]). For health state descriptions that were revised for this study, resulting disability weights were substantially different for a subset of these weights, including those related to hearing loss (eg, complete hearing loss: GBD 2010 0·033 [0·020-0·052]; GBD 2013 0·215 [0·144-0·307]) and treated spinal cord lesions (below the neck: GBD 2010 0·047 [0·028-0·072]; GBD 2013 0·296 [0·198-0·414]; neck level: GBD 2010 0·369 [0·243-0·513]; GBD 2013 0·589 [0·415-0·748]). Survey responses to paired comparison questions were insensitive to whether the comparisons were framed in terms of temporary or chronic outcomes (Pearsons r 0·981 [0·973-0·987]). INTERPRETATION This study substantially expands the empirical basis for assessment of non-fatal outcomes in the GBD study. Findings from this study substantiate the notion that disability weights are sensitive to particular details in descriptions of health states, but robust to duration of outcomes. FUNDING European Centre for Disease Prevention and Control, Bill and Melinda Gates Foundation.

Long-term mortality and causes of death in isolated GHD, ISS, and SGA patients treated with recombinant growth hormone during childhood in Belgium, The Netherlands, and Sweden: preliminary report of 3 countries participating in the EU SAGhE study

CONTEXT The long-term mortality in adults treated with recombinant GH during childhood has been poorly investigated. Recently released data from the French part of the European Union Safety and Appropriateness of GH treatments in Europe (EU SAGhE) study have raised concerns on the long-term safety of GH treatment. OBJECTIVE To report preliminary data on long-term vital status and causes of death in patients with isolated GH deficiency or idiopathic short stature or born small for gestational age treated with GH during childhood, in Belgium, The Netherlands, and Sweden. DESIGN Data were retrieved from national registries of GH-treated patients and vital status from National Population Registries. Causes of death were retrieved from a National Cause of Death Register (Sweden), Federal and Regional Death Registries (Belgium), or individual patient records (The Netherlands). PATIENTS All patients diagnosed with isolated GH deficiency or idiopathic short stature or born small for gestational age started on recombinant GH during childhood from 1985-1997 and who had attained 18 yr of age by the end of 2010 were included. Vital status was available for approximately 98% of these 2,543 patients, corresponding to 46,556 person-years of observation. MAIN OUTCOME MEASURE Vital status, causes of death, age at death, year of death, duration of GH treatment, and mean GH dose during treatment were assessed. RESULTS Among 21 deaths identified, 12 were due to accidents, four were suicides, and one patient each died from pneumonia, endocrine dysfunction, primary cardiomyopathy, deficiency of humoral immunity, and coagulation defect. CONCLUSIONS In these cohorts, the majority of deaths (76%) were caused by accidents or suicides. Importantly, none of the patients died from cancer or from a cardiovascular disease.

The global burden of listeriosis: a systematic review and meta-analysis

BACKGROUND Listeriosis, caused by Listeria monocytogenes, is an important foodborne disease that can be difficult to control and commonly results in severe clinical outcomes. We aimed to provide the first estimates of global numbers of illnesses, deaths, and disability-adjusted life-years (DALYs) due to listeriosis, by synthesising information and knowledge through a systematic review. METHODS We retrieved data on listeriosis through a systematic review of peer-reviewed and grey literature (published in 1990-2012). We excluded incidence data from before 1990 from the analysis. We reviewed national surveillance data where available. We did a multilevel meta-analysis to impute missing country-specific listeriosis incidence rates. We used a meta-regression to calculate the proportions of health states, and a Monte Carlo simulation to generate DALYs by WHO subregion. FINDINGS We screened 11,722 references and identified 87 eligible studies containing listeriosis data for inclusion in the meta-analyses. We estimated that, in 2010, listeriosis resulted in 23,150 illnesses (95% credible interval 6061-91,247), 5463 deaths (1401-21,497), and 172,823 DALYs (44,079-676,465). The proportion of perinatal cases was 20·7% (SD 1·7). INTERPRETATION Our quantification of the global burden of listeriosis will enable international prioritisation exercises. The number of DALYs due to listeriosis was lower than those due to congenital toxoplasmosis but accords with those due to echinococcosis. Urgent efforts are needed to fill the missing data in developing countries. We were unable to identify incidence data for the AFRO, EMRO, and SEARO WHO regions. FUNDING WHO Foodborne Diseases Epidemiology Reference Group and the Université catholique de Louvain.

Weighing Risk Factors Associated With Bee Colony Collapse Disorder by Classification and Regression Tree Analysis

ABSTRACT Colony collapse disorder (CCD), a syndrome whose defining trait is the rapid loss of adult worker honey bees, Apis mellifera L., is thought to be responsible for a minority of the large overwintering losses experienced by U.S. beekeepers since the winter 2006–2007. Using the same data set developed to perform a monofactorial analysis (PloS ONE 4: e6481, 2009), we conducted a classification and regression tree (CART) analysis in an attempt to better understand the relative importance and interrelations among different risk variables in explaining CCD. Fifty-five exploratory variables were used to construct two CART models: one model with and one model without a cost of misclassifying a CCD-diagnosed colony as a non-CCD colony. The resulting model tree that permitted for misclassification had a sensitivity and specificity of 85 and 74%, respectively. Although factors measuring colony stress (e.g., adult bee physiological measures, such as fluctuating asymmetry or mass of head) were important discriminating values, six of the 19 variables having the greatest discriminatory value were pesticide levels in different hive matrices. Notably, coumaphos levels in brood (a miticide commonly used by beekeepers) had the highest discriminatory value and were highest in control (healthy) colonies. Our CART analysis provides evidence that CCD is probably the result of several factors acting in concert, making afflicted colonies more susceptible to disease. This analysis highlights several areas that warrant further attention, including the effect of sublethal pesticide exposure on pathogen prevalence and the role of variability in bee tolerance to pesticides on colony survivorship.

World Health Organization Estimates of the Global and Regional Disease Burden of 11 Foodborne Parasitic Diseases, 2010: A Data Synthesis.

Background Foodborne diseases are globally important, resulting in considerable morbidity and mortality. Parasitic diseases often result in high burdens of disease in low and middle income countries and are frequently transmitted to humans via contaminated food. This study presents the first estimates of the global and regional human disease burden of 10 helminth diseases and toxoplasmosis that may be attributed to contaminated food. Methods and Findings Data were abstracted from 16 systematic reviews or similar studies published between 2010 and 2015; from 5 disease data bases accessed in 2015; and from 79 reports, 73 of which have been published since 2000, 4 published between 1995 and 2000 and 2 published in 1986 and 1981. These included reports from national surveillance systems, journal articles, and national estimates of foodborne diseases. These data were used to estimate the number of infections, sequelae, deaths, and Disability Adjusted Life Years (DALYs), by age and region for 2010. These parasitic diseases, resulted in 48.4 million cases (95% Uncertainty intervals [UI] of 43.4–79.0 million) and 59,724 (95% UI 48,017–83,616) deaths annually resulting in 8.78 million (95% UI 7.62–12.51 million) DALYs. We estimated that 48% (95% UI 38%-56%) of cases of these parasitic diseases were foodborne, resulting in 76% (95% UI 65%-81%) of the DALYs attributable to these diseases. Overall, foodborne parasitic disease, excluding enteric protozoa, caused an estimated 23.2 million (95% UI 18.2–38.1 million) cases and 45,927 (95% UI 34,763–59,933) deaths annually resulting in an estimated 6.64 million (95% UI 5.61–8.41 million) DALYs. Foodborne Ascaris infection (12.3 million cases, 95% UI 8.29–22.0 million) and foodborne toxoplasmosis (10.3 million cases, 95% UI 7.40–14.9 million) were the most common foodborne parasitic diseases. Human cysticercosis with 2.78 million DALYs (95% UI 2.14–3.61 million), foodborne trematodosis with 2.02 million DALYs (95% UI 1.65–2.48 million) and foodborne toxoplasmosis with 825,000 DALYs (95% UI 561,000–1.26 million) resulted in the highest burdens in terms of DALYs, mainly due to years lived with disability. Foodborne enteric protozoa, reported elsewhere, resulted in an additional 67.2 million illnesses or 492,000 DALYs. Major limitations of our study include often substantial data gaps that had to be filled by imputation and suffer from the uncertainties that surround such models. Due to resource limitations it was also not possible to consider all potentially foodborne parasites (for example Trypanosoma cruzi). Conclusions Parasites are frequently transmitted to humans through contaminated food. These estimates represent an important step forward in understanding the impact of foodborne diseases globally and regionally. The disease burden due to most foodborne parasites is highly focal and results in significant morbidity and mortality among vulnerable populations.

Estimating Disease Prevalence in a Bayesian Framework Using Probabilistic Constraints

Studies sometimes estimate the prevalence of a disease from the results of one or more diagnostic tests that are applied to individuals of unknown disease status. This approach invariably means that, in the absence of a gold standard and without external constraints, more parameters must be estimated than the data permit. Two assumptions are regularly made in the literature, namely that the test characteristics (sensitivity and specificity) are constant over populations and the tests are conditionally independent given the true disease status. These assumptions have been criticized recently as being unrealistic. Nevertheless, to estimate the prevalence, some restrictions on the parameter estimates need to be imposed. We consider 2 types of restrictions: deterministic and probabilistic restrictions, the latter arising in a Bayesian framework when expert knowledge is available. Furthermore, we consider 2 possible parameterizations allowing incorporation of these restrictions. The first is an extension of the approach of Gardner et al and Dendukuri and Joseph to more than 2 diagnostic tests and assuming conditional dependence. We argue that this system of equations is difficult to combine with expert opinions. The second approach, based on conditional probabilities, looks more promising, and we develop this approach in a Bayesian context. To evaluate the combination of data with the (deterministic and probabilistic) constraints, we apply the recently developed Deviance Information Criterion and effective number of parameters estimated (pD) together with an appropriate Bayesian P value. We illustrate our approach using data collected in a study on the prevalence of porcine cysticercosis with verification from external data.

Prioritizing emerging zoonoses in The Netherlands.

Background To support the development of early warning and surveillance systems of emerging zoonoses, we present a general method to prioritize pathogens using a quantitative, stochastic multi-criteria model, parameterized for the Netherlands. Methodology/Principal Findings A risk score was based on seven criteria, reflecting assessments of the epidemiology and impact of these pathogens on society. Criteria were weighed, based on the preferences of a panel of judges with a background in infectious disease control. Conclusions/Significance Pathogens with the highest risk for the Netherlands included pathogens in the livestock reservoir with a high actual human disease burden (e.g. Campylobacter spp., Toxoplasma gondii, Coxiella burnetii) or a low current but higher historic burden (e.g. Mycobacterium bovis), rare zoonotic pathogens in domestic animals with severe disease manifestations in humans (e.g. BSE prion, Capnocytophaga canimorsus) as well as arthropod-borne and wildlife associated pathogens which may pose a severe risk in future (e.g. Japanese encephalitis virus and West-Nile virus). These agents are key targets for development of early warning and surveillance.

Multiple Insecticide Resistance: An Impediment to Insecticide-Based Malaria Vector Control Program

Background Indoor Residual Spraying (IRS), insecticide-treated nets (ITNs) and long-lasting insecticidal nets (LLINs) are key components in malaria prevention and control strategy. However, the development of resistance by mosquitoes to insecticides recommended for IRS and/or ITNs/LLINs would affect insecticide-based malaria vector control. We assessed the susceptibility levels of Anopheles arabiensis to insecticides used in malaria control, characterized basic mechanisms underlying resistance, and evaluated the role of public health use of insecticides in resistance selection. Methodology/Principal findings Susceptibility status of An. arabiensis was assessed using WHO bioassay tests to DDT, permethrin, deltamethrin, malathion and propoxur in Ethiopia from August to September 2009. Mosquito specimens were screened for knockdown resistance (kdr) and insensitive acetylcholinesterase (ace-1R) mutations using AS-PCR and PCR-RFLP, respectively. DDT residues level in soil from human dwellings and the surrounding environment were determined by Gas Chromatography with Electron Capture Detector. An. arabiensis was resistant to DDT, permethrin, deltamethrin and malathion, but susceptible to propoxur. The West African kdr allele was found in 280 specimens out of 284 with a frequency ranged from 95% to 100%. Ace-1R mutation was not detected in all specimens scored for the allele. Moreover, DDT residues were found in soil samples from human dwellings but not in the surrounding environment. Conclusion The observed multiple-resistance coupled with the occurrence of high kdr frequency in populations of An. arabiensis could profoundly affect the malaria vector control programme in Ethiopia. This needs an urgent call for implementing rational resistance management strategies and integrated vector control intervention.