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.

Summary Points

• Thirty-one foodborne hazards caused 600 (95% uncertainty interval [UI] 420–960) million foodborne illnesses and 420,000 (95% UI 310,000–600,000) deaths in 2010.
• The global burden of FBD caused by the 31 hazards studied was 33 (95% UI 25–46) million DALYs in 2010.
• The most frequent causes of foodborne illness were diarrheal disease agents; particularly norovirus and Campylobacter spp.
• Foodborne diarrheal disease agents, particularly non-typhoidal Salmonella enterica, caused 230,000 (95% UI 160,000–320,000) deaths
• Other major causes of FBD deaths were Salmonella Typhi, Taenia solium, hepatitis A virus and aflatoxin.
• 40% of the FBD burden was among children under 5 years old.
• The African (AFR), South-East Asian (SEAR) and Eastern Mediterranean (EMR) D subregions had the highest FBD burden.
• Diarrheal disease agents were the leading cause of FBD burden in most subregions, and non-typhoidal Salmonella enterica caused an important burden in all subregions, particularly in the subregions in Africa.
• Other main causes of diarrheal FBD burden were enteropathogenic Escherichia coli, enterotoxigenic Escherichia coli and Vibrio cholerae in low-income subregions, and Campylobacter spp. in high-income subregions.
• The burden of aflatoxin was high in the AFR D, Western Pacific (WPR) B and SEAR B subregions, whereas dioxins caused the highest burden in SEAR D, EMR D and European (EUR) A and C subregions.
• In the South-East Asian subregions, there was a considerable burden of Salmonella Typhi; the burden of Opisthorchis spp. was concentrated in the SEAR B region, where the seafoodborne trematodes Paragonimus spp. and Clonorchis sinensis were also important.
• In Central and South American (AMR B and AMR D) subregions, T. solium and Toxoplasma gondii contributed significantly to the FBD burden.
• These estimates should inform policy development at national and international levels to improve food safety throughout the food chain.

     

A chromosome‐level genome assembly of the woolly apple aphid,Eriosoma lanigerum Hausmann (Hemiptera: Aphididae)

Woolly apple aphid (WAA, Eriosoma lanigerum Hausmann) (Hemiptera: Aphididae) is a major pest of apple trees (Malus domestica, order Rosales) and is critical to the economics of the apple industry in most parts of the world. Here, we generated a chromosome‐level genome assembly of WAA—representing the first genome sequence from the aphid subfamily Eriosomatinae—using a combination of 10X Genomics linked‐reads and in vivo Hi‐C data. The final genome assembly is 327 Mb, with 91% of the assembled sequences anchored into six chromosomes. The contig and scaffold N50 values are 158 kb and 71 Mb, respectively, and we predicted a total of 28,186 protein‐coding genes. The assembly is highly complete, including 97% of conserved arthropod single‐copy orthologues based on Benchmarking Universal Single‐Copy Orthologs (busco ) analysis. Phylogenomic analysis of WAA and nine previously published aphid genomes, spanning four aphid tribes and three subfamilies, reveals that the tribe Eriosomatini (represented by WAA) is recovered as a sister group to Aphidini + Macrosiphini (subfamily Aphidinae). We identified syntenic blocks of genes between our WAA assembly and the genomes of other aphid species and find that two WAA chromosomes (El5 and El6) map to the conserved Macrosiphini and Aphidini X chromosome. Our high‐quality WAA genome assembly and annotation provides a valuable resource for research in a broad range of areas such as comparative and population genomics, insect–plant interactions and pest resistance management.     

Transition in sexual system and sex chromosome evolution in the tadpole shrimp Triops cancriformis

Transitions in sexual system and reproductive mode may affect the course of sex chromosome evolution, for instance by altering the strength of sexually antagonistic selection. However, there have been few studies of sex chromosomes in systems where such transitions have been documented. The European tadpole shrimp, Triops cancriformis, has undergone a transition from dioecy to androdioecy (a sexual system where hermaphrodites and males coexist), offering an excellent opportunity to test the impact of this transition on the evolution of sex chromosomes. To identify sex-linked markers, to understand mechanisms of sex determination and to investigate differences between sexual systems, we carried out a genome-wide association study using restriction site-associated DNA sequencing (RAD-seq) of 47 males, females and hermaphrodites from one dioecious and one androdioecious population. We analysed 22.9 Gb of paired-end sequences and identified and scored >3000 high coverage novel genomic RAD markers. Presence–absence of markers, single-nucleotide polymorphism association and read depth identified 52 candidate sex-linked markers. We show that sex is genetically determined in T. cancriformis, with a ZW system conserved across dioecious and androdioecious populations and that hermaphrodites have likely evolved from females. We also show that the structure of the sex chromosomes differs strikingly, with a larger sex-linked region in the dioecious population compared with the androdioecious population.     

Development and validation of a standardized protocol to monitor human dietary exposure by metabolite fingerprinting of urine samples

Conventional tools for measuring dietary exposure have well recognized limitations. Measurement of food-derived metabolites in biofluids provides an alternative approach and our aim was to develop an experimental protocol which ensures that extraneous variability does not obscure metabolic signals from ingested foods. Healthy adults consumed a standardized meal in the evening before each test day and collected pooled overnight urine. On each test day of three different studies, urine was collected in the fasted state and at different time points after consumption of a standardized breakfast. Metabolite fingerprinting of samples using Flow Infusion Electrospray-Ionization Mass Spectrometry followed by multivariate data analysis showed strong discrimination between overnight, fasting and postprandial samples, in each study separately and when data from the three studies were pooled. Such differences were robust and highly reproducible within individuals on separate occasions. Urine volume was an efficient data normalization factor for metabolite fingerprinting data. Postprandial urines had a stable chemical composition over a period of 2–4 h after eating a standardized breakfast, suggesting that there is a flexible time window for urine collection. Fasting urine samples provided a stable baseline for universal comparisons with postprandial samples. A dietary exposure biomarker discovery protocol was validated by demonstrating that top-ranked signals discriminating between fasting and 2–4 h postprandial urine samples could be linked to metabolites abundant in some components of the standardized breakfast. We conclude that the protocol developed will have value in the search for biomarker leads of dietary exposure.     

Overview of genes, diet and cancer

Quantitative epidemiological analysis suggests that about one third of the variation in cancer risk can be attributed to variation in dietary exposure but it has proved difficult, using conventional epidemiological approaches, to identify which dietary components, in what amounts and over what time-scales are protective or potentially hazardous. Work in this area has been hampered by the lack of robust surrogate endpoints. However, the rapidly accumulating knowledge of the biological basis of cancer and the application of post-genomic technologies are helping the development of novel biomarkers of cancer risk. Genomic damage resulting in aberrant gene expression is the fundamental cause of all cancers. Such damage includes mutations, aberrant epigenetic marking, chromosomal damage and telomere shortening. Since both external agents and normal cell functions, such as mitosis, subject the genome to frequent and diverse insults, the human cell has evolved a battery of defence mechanisms which (a) attempt to minimize such damage (including inhibition of oxidative reactions by free radical scavenging and the detoxification of potential mutagens), (b) repair the damage or (c) remove severely damaged cells by shunting them into apoptosis. When such defences fail and a tumour becomes established, further genomic damage and further alterations in gene expression enable the tumour to grow, to cope with anoxia, to develop a novel blood supply (angiogenesis), to escape from the confines of its initiation site and to establish colonies elsewhere in the body (metastasis). All of these processes are potentially modifiable by food components and by nutritional status. In addition, interactions between dietary (and other environmental and lifestyle) factors and genetic make-up [seen principally in the assembly of single nucleotide polymorphisms (SNPs) which is unique to each individual] contributes to interindividual differences in cancer risk.     

Evidence that a polymorphism within the 3′UTR of glutathione peroxidase 4 is functional and is associated with susceptibility to colorectal cancer

Low selenium (Se) status has been associated with increased risk of colorectal cancer (CRC). Se is present as the amino acid selenocysteine in selenoproteins, such as the glutathione peroxidases. Se incorporation requires specific RNA structures in the 3' untranslated region (3'UTR) of the selenoprotein mRNAs. A single nucleotide polymorphism (SNP) occurs at nucleotide 718 (within the 3'UTR) in the glutathione peroxidase 4 gene. In the present study, Caco-2 cells were transfected with constructs in which type 1 iodothyronine deiodinase coding region was linked to the GPx4 3'UTR with either C or T variant at position 718. Higher reporter activity was observed in cells expressing the C variant compared to those expressing the T variant, under either Se-adequate or Se-deficient conditions. In addition, a disease association study was carried out in cohorts of patients with either adenomatous polyps, colorectal adenocarcinomas and in healthy controls. A higher proportion of individuals with CC genotype at the GPx4 T/C 718 SNP was present in the cancer group, but not in the polyp group, compared with the control group (P < 0.05). The present data demonstrate the functionality of the GPx4 T/C 718 SNP and suggest that T genotype is associated with lower risk of CRC.     

Walking performance and aerobic and anaerobic metabolism of Carcinus maenas (L.) in sea water at 15°C

Walking performance of the shore crab Carcinus maenas (L.) in sea water at 15 °C was assessed. In large crabs there was an inverse relationship between fatigue time and speed; crabs ran for $\text{\$}\text{?}$10 min at 3.2 m·min^?1 and for only 2 min at 14 m·min^?1. There were linear relationships between oxygen consumption and walking speeds for small and large animals walking at up to 4 m·min^?1 Estimates of maximum oxygen consumption were proportional to W^0.13 whereas inactive consumption is proportional to W^0.44 this resulted in aerobic scope (i.e. the difference between inactive and maximal rates of oxygen consumption) remaining almost constant across a weight range of animals whereas the aerobic expansibility (maximal rates/inactive rates) declined from 7- to 4-fold with increasing size. After a 12-h period without handling (settled animals) the animals could immediately become active and reach maximal rates of oxygen consumption similar to those of animals handled 1 h before the experiment. The aerobic expansibility of these settled animals could range from 21 to 8 times their inactive rates of oxygen consumption in small and large animals respectively. After 10 min of exercise oxygen consumption and whole body lactate levels returned to pre-exercise values within 5 to 25 min. The net oxygen debts range from 16 to 64% of the net oxygen consumption increase during exercise in small and large animals respectively.Calculations of the energy gained from lactate accumulation indicated that the net aerobic energy production during walking was supplemented from 4 to 71 % by anaerobic metabolism in small and large animals respectively. With increasing animal size the decline in aerobic expansibility was offset by an increased capacity for lactate production so that the overall maximum energy production during sustained activity remained almost constant at around seven times the inactive rate. The cost of transport (the net increase in oxygen consumption per g per m) falls with increased walking speed and increased animal size.