Outbreaks of Rift Valley fever have devastating impacts on ruminants, humans, as well as on regional and national economies. Although numerous studies on the impact and outbreak of Rift Valley fever exist, relatively little is known about the role of environmental factors, especially soil, on the aestivation of the virus. This study thus selected 22 sites for study in central South Africa, known to be the recurrent epicenter of widespread Rift Valley fever outbreaks in Southern Africa. Soils were described, sampled and analyzed in detail at each site. Of all the soil variables analyzed for, only eight (cation exchange capacity, exchangeable Ca2+, exchangeable K+, exchangeable Mg2+, soluble Ca2+, medium sand, As, and Br) were statistically identified to be potential indicators of sites with reported Rift Valley fever mortalities, as reported for the 2009–2010 Rift Valley fever outbreak. Four soil characteristics (exchangeable K+, exchangeable Mg2+, medium sand, and Br) were subsequently included in a discriminant function that could potentially be used to predict sites that had reported Rift Valley fever-associated mortalities in livestock. This study therefore constitutes an initial attempt to predict sites prone to Rift Valley fever livestock mortality from soil properties and thus serves as a basis for broader research on the interaction between soil, mosquitoes and Rift Valley fever virus. Future research should include other environmental components such as vegetation, climate, and water properties as well as correlating soil properties with floodwater Aedes spp. abundance and Rift Valley fever virus prevalence.
Several human and animal Ebola outbreaks have occurred over the past 4 years in Gabon and the Republic of Congo. The human outbreaks consisted of multiple simultaneous epidemics caused by different viral strains, and each epidemic resulted from the handling of a distinct gorilla, chimpanzee, or duiker carcass. These animal populations declined markedly during human Ebola outbreaks, apparently as a result of Ebola infection. Recovered carcasses were infected by a variety of Ebola strains, suggesting that Ebola outbreaks in great apes result from multiple virus introductions from the natural host. Surveillance of animal mortality may help to predict and prevent human Ebola outbreaks.
Infectious diseases have caused die-offs in both free-ranging gorillas and chimpanzees. Understanding pathogen diversity and disease ecology is therefore critical for conserving these endangered animals. To determine viral diversity in free-ranging, non-habituated gorillas and chimpanzees in the Republic of Congo, genetic testing was performed on great-ape fecal samples collected near Odzala-Kokoua National Park. Samples were analyzed to determine ape species, identify individuals in the population, and to test for the presence of herpesviruses, adenoviruses, poxviruses, bocaviruses, flaviviruses, paramyxoviruses, coronaviruses, filoviruses, and simian immunodeficiency virus (SIV). We identified 19 DNA viruses representing two viral families, Herpesviridae and Adenoviridae, of which three herpesviruses had not been previously described. Co-detections of multiple herpesviruses and/or adenoviruses were present in both gorillas and chimpanzees. Cytomegalovirus (CMV) and lymphocryptovirus (LCV) were found primarily in the context of co-association with each other and adenoviruses. Using viral discovery curves for herpesviruses and adenoviruses, the total viral richness in the sample population of gorillas and chimpanzees was estimated to be a minimum of 23 viruses, corresponding to a detection rate of 83%. These findings represent the first description of DNA viral diversity in feces from free-ranging gorillas and chimpanzees in or near the Odzala-Kokoua National Park and form a basis for understanding the types of viruses circulating among great apes in this region.
In his article “Evidence points to migratory birds in H5N1 spread” (3 Mar., p. [1225][1]), D. Normile reports that “increasingly, scientists are attributing this remarkably fast spread [of H5N1] to migratory birds, but dissenters remain.” All agreed that wild birds have a role, but attributing the spread of HPAI H5N1 entirely to migratory birds overlooks evidence that is inconsistent with this conclusion.
One cannot ignore the apparent lack of previous outbreaks along migratory pathways. Birds have been migrating along these same routes annually since this genotype of HPAI H5N1 was first identified in Asia in 1997, yet there was no spread of disease to Eurasia or Europe in the interim years. Although fewer than 0.05% of more than 13,000 healthy waterfowl tested ([1][2]) were positive for HPAI H5N1, billions of birds have traveled to Eurasia and Europe for 8 years. It seems suspicious that none has managed to transmit this highly pathogenic virus until now. The introduction of HPAI H5N1 onto the continent of Africa, as well as the earlier outbreaks in poultry, notably in Russia and Turkey, could have been as easily accommodated by the movement of infected poultry, poultry products, or contaminated fomites as suggested for migratory bird routes. Meanwhile, Japan, with strong controls on poultry imports, has remained H5N1-free since early 2004, when infected poultry flocks were destroyed, despite the annual arrival of large migratory bird populations from areas with known H5N1 outbreaks.
Four pathways are most likely involved in the movement of HPAI H5N1: poultry shipments; the movement of contaminated equipment, materials, and waste products; migratory birds; and the wild bird trade. At most, the evidence suggests that wild birds may be responsible for short-distance, secondary movement of HPAI H5N1. Ornithologists, virologists, veterinarians, and others must work together, sharing their specialized knowledge to understand more thoroughly the movement of this virus.
1. 1.[↵][3]1. H. Chen 2. et al.
, Proc. Natl. Acad. Sci. U.S.A. 103, 2845 (2006).
[OpenUrl][4][Abstract/FREE Full Text][5]
[1]: /lookup/doi/10.1126/science.311.5765.1225
[2]: #ref-1
[3]: #xref-ref-1-1 View reference 1. in text
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Mongolia combines a near absence of domestic poultry, with an abundance of migratory waterbirds, to create an ideal location to study the epidemiology of highly pathogenic avian influenza virus (HPAIV) in a purely wild bird system. Here we present the findings of active and passive surveillance for HPAIV subtype H5N1 in Mongolia from 2005–2011, together with the results of five outbreak investigations. In total eight HPAIV outbreaks were confirmed in Mongolia during this period. Of these, one was detected during active surveillance employed by this project, three by active surveillance performed by Mongolian government agencies, and four through passive surveillance. A further three outbreaks were recorded in the neighbouring Tyva Republic of Russia on a lake that bisects the international border. No HPAIV was isolated (cultured) from 7,855 environmental fecal samples (primarily from ducks), or from 2,765 live, clinically healthy birds captured during active surveillance (primarily shelducks, geese and swans), while four HPAIVs were isolated from 141 clinically ill or dead birds located through active surveillance. Two low pathogenic avian influenza viruses (LPAIV) were cultured from ill or dead birds during active surveillance, while environmental feces and live healthy birds yielded 56 and 1 LPAIV respectively. All Mongolian outbreaks occurred in 2005 and 2006 (clade 2.2), or 2009 and 2010 (clade 2.3.2.1); all years in which spring HPAIV outbreaks were reported in Tibet and/or Qinghai provinces in China. The occurrence of outbreaks in areas deficient in domestic poultry is strong evidence that wild birds can carry HPAIV over at least moderate distances. However, failure to detect further outbreaks of clade 2.2 after June 2006, and clade 2.3.2.1 after June 2010 suggests that wild birds migrating to and from Mongolia may not be competent as indefinite reservoirs of HPAIV, or that HPAIV did not reach susceptible populations during our study.
The global wildlife trade network is a massive system that has been shown to threaten biodiversity, introduce non-native species and pathogens, and cause chronic animal welfare concerns. Despite its scale and impact, comprehensive characterization of the global wildlife trade is hampered by data that are limited in their temporal or taxonomic scope and detail. To help fill this gap, we present data on 15 years of the importation of wildlife and their derived products into the United States (2000-2014), originally collected by the United States Fish and Wildlife Service. We curated and cleaned the data and added taxonomic information to improve data usability. These data include >2 million wildlife or wildlife product shipments, representing >60 biological classes and >3.2 billion live organisms. Further, the majority of species in the dataset are not currently reported on by CITES parties. These data will be broadly useful to both scientists and policymakers seeking to better understand the volume, sources, biological composition, and potential risks of the global wildlife trade.
The United Nations (UN) launched the 2030 Agenda for Sustainable Development to address an ongoing crisis: human pressure leading to unprecedented environmental degradation, climatic change, social inequality, and other negative planet-wide consequences. This crisis stems from a dramatic increase in human appropriation of natural resources to keep pace with rapid population growth, dietary shifts toward higher consumption of animal products, and higher demand for energy (1, 2). There is an increased recognition that Sustainable Development Goals (SDGs) are linked to one another (3, 4), and priorities such as food production, biodiversity conservation, and climate change mitigation cannot be considered in isolation (5⇓⇓–8). Hence, understanding those dynamics is central to achieving the vision of the UN 2030 Agenda.
Infectious zoonotic diseases typically emerge as a result of complex interactions between humans and wild and/or domestic animals. Image credit: Pixabay/sasint.
But environmental change also has direct human health outcomes via infectious disease emergence, and this link is not customarily integrated into planning for sustainable development. Currently, 65 countries are engaged in the Global Health Security Agenda (GHSA) and are finalizing a strategic plan for the next five years (the GHSA 2024 Roadmap) to better prevent, detect, and respond to infectious disease outbreaks in alignment with SDGs 2 and 3 on food security and human health. Without an integrated approach to mitigating the disease emergence consequences of environmental change, countries’ abilities to achieve SDGs and GHSA targets will be compromised.
Emerging infectious diseases (EIDs) such as Ebola, influenza, SARS, MERS, and, most recently, coronavirus (2019-nCoV) cause large-scale mortality and morbidity, disrupt trade and travel networks, and stimulate civil unrest (9). When local emergence leads to regional outbreaks or global pandemics, the economic impacts can be devastating: The SARS outbreak in 2003, the H1N1 pandemic in 2009, and …
[↵][1]1To whom correspondence may be addressed. Email: moreno.dimarco{at}uniroma1.it.
[1]: #xref-corresp-1-1
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