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Ebola virus disease (EVD) is a complex zoonosis that is highly virulent in humans. The largest recorded outbreak of EVD is ongoing in West Africa, outside of its previously reported and predicted niche. We assembled location data on all recorded zoonotic transmission to humans and Ebola virus infection in bats and primates (1976–2014). Using species distribution models, these occurrence data were paired with environmental covariates to predict a zoonotic transmission niche covering 22 countries across Central and West Africa. Vegetation, elevation, temperature, evapotranspiration, and suspected reservoir bat distributions define this relationship. At-risk areas are inhabited by 22 million people; however, the rarity of human outbreaks emphasises the very low probability of transmission to humans. Increasing population sizes and international connectivity by air since the first detection of EVD in 1976 suggest that the dynamics of human-to-human secondary transmission in contemporary outbreaks will be very different to those of the past. Since the first outbreaks of Ebola virus disease in 1976, there have been numerous other outbreaks in humans across Africa with fatality rates ranging from 50% to 90%. Humans can become infected with the Ebola virus after direct contact with blood or bodily fluids from an infected person or animal. The virus also infects and kills other primates—such as chimpanzees or gorillas—though Old World fruit bats are suspected to be the most likely carriers of the virus in the wild. The largest recorded outbreak of Ebola virus disease is ongoing in West Africa: more people have been infected in this current outbreak than in all previous outbreaks combined. The current outbreak is also the first to occur in West Africa—which is outside the previously known range of the Ebola virus. Pigott et al. have now updated predictions about where in Africa wild animals may harbour the virus and where the transmission of the virus from these animals to humans is possible. As such, the map identifies the regions that are most at risk of a future Ebola outbreak. The data behind these new maps include the locations of all recorded primary cases of Ebola in human populations—the ‘index’ cases—many of which have been linked to animal sources. The data also include the locations of recorded cases of Ebola virus infections in wild bats and primates from the last forty years. The maps, which were modelled using more flexible methods than previous predictions, also include new information—collected using satellites—about environmental factors and new predictions of the range of wild fruit bats. Pigott et al. report that the transmission of Ebola virus from animals to humans is possible in 22 countries across Central and West Africa—and that 22 million people live in the areas at risk. However, outbreaks in human populations are rare and the likelihood of a human getting the disease from an infected animal still remains very low. The updated map does not include data about how infections spread from one person to another, so the next challenge is to use existing data on human-to-human transmission to better understand the likely size and extent of current and future outbreaks. As more people live in, and travel to and from, the at-risk regions than ever before, Pigott et al. note that new outbreaks of Ebola virus disease are likely to be very different to those of the past.

São Paulo, a densely inhabited state in southeast Brazil that contains the fourth most populated city in the world, recently experienced its largest yellow fever virus (YFV) outbreak in decades. YFV does not normally circulate extensively in São Paulo, so most people were unvaccinated when the outbreak began. Surveillance in non-human primates (NHPs) is important for determining the magnitude and geographic extent of an epizootic, thereby helping to evaluate the risk of YFV spillover to humans. Data from infected NHPs can give more accurate insights into YFV spread than when using data from human cases alone. To contextualise human cases, identify epizootic foci and uncover the rate and direction of YFV spread in São Paulo, we generated and analysed virus genomic data and epizootic case data from NHPs in São Paulo. We report the occurrence of three spatiotemporally distinct phases of the outbreak in São Paulo prior to February 2018. We generated 51 new virus genomes from YFV positive cases identified in 23 different municipalities in São Paulo, mostly sampled from NHPs between October 2016 and January 2018. Although we observe substantial heterogeneity in lineage dispersal velocities between phylogenetic branches, continuous phylogeographic analyses of generated YFV genomes suggest that YFV lineages spread in São Paulo at a mean rate of approximately 1km per day during all phases of the outbreak. Viral lineages from the first epizootic phase in northern São Paulo subsequently dispersed towards the south of the state to cause the second and third epizootic phases there. This alters our understanding of how YFV was introduced into the densely populated south of São Paulo state. Our results shed light on the sylvatic transmission of YFV in highly fragmented forested regions in São Paulo state and highlight the importance of continued surveillance of zoonotic pathogens in sentinel species.

The bacterium Treponema pallidum pertenue causes yaws in humans and nonhuman primates. We describe 33% T. pallidum pertenue seropositivity in 9 species of nonhuman primates in Uganda and Rwanda, seroconversion during a lethal outbreak and a novel bacterial genomic lineage. Yaws may threaten both public health and conservation in the region.

Zoonotic disease dynamics in wildlife hosts are rarely quantified at macroecological scales due to the lack of systematic surveys. Non-human primates (NHPs) host Plasmodium knowlesi, a zoonotic malaria of public health concern and the main barrier to malaria elimination in Southeast Asia. Understanding of regional P. knowlesi infection dynamics in wildlife is limited. Here, we systematically assemble reports of NHP P. knowlesi and investigate geographic determinants of prevalence in reservoir species. Meta-analysis of 6322 NHPs from 148 sites reveals that prevalence is heterogeneous across Southeast Asia, with low overall prevalence and high estimates for Malaysian Borneo. We find that regions exhibiting higher prevalence in NHPs overlap with human infection hotspots. In wildlife and humans, parasite transmission is linked to land conversion and fragmentation. By assembling remote sensing data and fitting statistical models to prevalence at multiple spatial scales, we identify novel relationships between P. knowlesi in NHPs and forest fragmentation. This suggests that higher prevalence may be contingent on habitat complexity, which would begin to explain observed geographic variation in parasite burden. These findings address critical gaps in understanding regional P. knowlesi epidemiology and indicate that prevalence in simian reservoirs may be a key spatial driver of human spillover risk. Zoonotic diseases are infectious diseases that are transmitted from animals to humans. For example, the malaria-causing parasite Plasmodium knowlesi can be transmitted from monkeys to humans through mosquitos that have previously fed on infected monkeys. In Malaysia, progress towards eliminating malaria is being undermined by the rise of human incidences of ‘monkey malaria’, which has been declared a public health threat by The World Health Organisation. In humans, cases of monkey malaria are higher in areas of recent deforestation. Changes in habitat may affect how monkeys, insects and humans interact, making it easier for diseases like malaria to pass between them. Deforestation could also change the behaviour of wildlife, which could lead to an increase in infection rates. For example, reduced living space increases contact between monkeys, or it may prevent behaviours that help animals to avoid parasites. Johnson et al. wanted to investigate how the prevalence of malaria in monkeys varies across Southeast Asia to see whether an increase of Plasmodium knowlesi in primates is linked to changes in the landscape. They merged the results of 23 existing studies, including data from 148 sites and 6322 monkeys to see how environmental factors like deforestation influenced the amount of disease in different places. Many previous studies have assumed that disease prevalence is high across all macaques, monkey species that are considered pests, and in all places. But Johnson et al. found that disease rates vary widely across different regions. Overall disease rates in monkeys are lower than expected (only 12%), but in regions with less forest or more ‘fragmented’ forest areas, malaria rates are higher. Areas with a high disease rate in monkeys tend to further coincide with infection hotspots for humans. This suggests that deforestation may be driving malaria infection in monkeys, which could be part of the reason for increased human infection rates. Johnsons et al.’s study has provided an important step towards better understanding the link between deforestation and the levels of monkey malaria in humans living nearby. Their study provides important insights into how we might find ways of managing the landscape better to reduce health risks from wildlife infection.

Many emerging zoonotic viruses pose major risks to animal and human health, with most recent epidemics of viral origin. This review focuses on encephalomyocarditis virus (EMCV), a member of the Picornaviridae family and the Cardiovirus genus with significant but largely underrecognized zoonotic potential. While EMCV has not yet caused major public health crises, its broad host range and rodent reservoir suggest a wider ecological impact. It is typically detected only during high-fatality outbreaks, particularly in domestic animals and non-human primates (NHPs), which are among the most vulnerable hosts. Multiple fatal outbreaks in captive and semi-captive NHPs have been documented. Human infections appear rare, yet the prevalence of antibodies suggests widespread exposure. EMCV remains largely absent from diagnostic panels and its epidemiology is poorly understood. We argue that EMCV warrants much closer attention due to its ability to cause severe disease in NHPs and its potential risk to humans. This review synthesizes current knowledge on the biology, epidemiology, pathogenicity, diagnosis, and prevention of EMCV in primates.

The 2008 Reston ebolavirus infection event in domestic pigs has triggered continuing epidemiologic investigations among Philippine health and veterinary agencies in collaboration with international filovirus experts. Prior to this, there were only 3 known and documented Reston ebolavirus outbreaks in nonhuman primates in the world, all traced back to a single geographic source in the Philippines in a monkey breeding/export facility. The first one in 1989 was the first-ever Ebola virus that emerged outside of Africa and was also the first known natural infection of Ebola virus in nonhuman primates. When it was first discovered among laboratory monkeys in the United States, the source was immediately traced back to the farm located in the Philippines. The second outbreak was in 1992-93. The third episode in 1996 was the last known outbreak before Reston ebolavirus reemerged in pigs in 2008. The isolated outbreaks involving 2 animal species bring forth issues requiring further investigations, and highlight the significance of intersectoral collaboration to effectively address zoonoses prevention and control/response in the interest of minimizing public health risk.

Monkeypox, a vesiculo-pustular rash illness, was initially discovered to cause human infection in 1970 through the World Health Organization (WHO)-sponsored efforts of the Commission to Certify Smallpox Eradication in Western Africa and the Congo Basin. The virus had been discovered to cause a nonhuman primate rash illness in 1958, and was thus named monkeypox. The causative agents of monkeypox and smallpox diseases both are species of Orthopoxvirus. Orthopoxvirus monkeypox, when it infects humans as an epizootic, produces a similar clinical picture to that of ordinary human smallpox. Since 1970, extensive epidemiology, virology, ecology and public health research has enabled better characterization of monkeypox virus and the associated human disease. This work reviews the progress in this body of research, and reviews studies of this “newly” emerging zoonotic disease.

Dengue virus (DENV) circulates in two distinct transmission cycles: one, termed the sylvatic cycle, is enzootic to canopy-living hosts, including non-human primates and primatophilic mosquitoes, and the other, initiated by spillover from the sylvatic cycle, is endemic to humans and anthropophilic mosquitoes. Transmission dynamics of sylvatic DENV in non-human hosts has not been well characterized, and the identity of reservoir and amplification hosts is still to be determined. We investigated the role of the three common species of monkeys in the Kédougou region of Senegal in the sylvatic transmission cycle of DENV. Longitudinal surveillance of primatophilic mosquitoes in this region dating back to the 1970s revealed that sylvatic DENV-2, the only one of the four DENV serotypes found to circulate in a sylvatic transmission in West Africa, is amplified cyclically at intervals of approximately eight years based on the isolation of the virus from mosquitoes. Subsequent to the detection of DENV-2 in primatophilic mosquitoes in Kédougou in 2008, 737 monkeys, including 3 species: Chlorocebus sabaeus (n = 219), Erythrocebus patas (n = 78), and Papio papio (n = 440) were captured from 2010 to 2012 for the current study. Their age was determined using dentition and other morphological measurements. Evidence of DENV-2 infection was detected via neutralizing antibody in sera, and the annual hazard of DENV-2 infection was estimated per species using catalytic models. These analyses revealed annual hazard ranging from 0.09 to 0.42 across the three species, consistent with high levels of transmission in these populations. Furthermore, seroprevalence was moderate in individuals under one year of age, despite the lack of detection of DENV-2 in primatophilic mosquitoes for up to three years prior, suggesting that non-primate hosts contributed to the maintenance of sylvatic DENV in this region.

The 2017-2018 yellow fever virus (YFV) outbreak in southeastern Brazil marked a reemergence of YFV in urban states that had been YFV-free for nearly a century. Unlike earlier urban YFV transmission, this epidemic was driven by forest mosquitoes. The objective of this study was to evaluate environmental drivers of this outbreak. Using surveillance data from the Brazilian Ministry of Health on human and non-human primate (NHP) cases of YFV, we traced the spatiotemporal progression of the outbreak. We then assessed the epidemic timing in relation to drought using a monthly Standardized Precipitation Evapotranspiration Index (SPEI) and evaluated demographic risk factors for rural or outdoor exposure amongst YFV cases. Finally, we developed a mechanistic framework to map the relationship between drought and YFV. Both human and NHP cases were first identified in a hot, dry, rural area in northern Minas Gerais before spreading southeast into the more cool, wet urban states. Outbreaks coincided with drought in all four southeastern states of Brazil and an extreme drought in Minas Gerais. Confirmed YFV cases had an increased odds of being male (OR 2.6; 95% CI 2.2-3.0), working age (OR: 1.8; 95% CI: 1.5-2.1), and reporting any recent travel (OR: 2.8; 95% CI: 2.3-3.3). Based on this data as well as mosquito and non-human primate biology, we created the \"Mono-DrY\" mechanistic framework showing how an unusual drought in this region could have amplified YFV transmission at the rural-urban interface and sparked the spread of this epidemic. The 2017-2018 YFV epidemic in Brazil originated in hot, dry rural areas of Minas Gerais before expanding south into urban centers. An unusually severe drought in this region may have created environmental pressures that sparked the reemergence of YFV in Brazil's southeastern cities.

Currently, there is limited available information on the epidemiology of parasitic infections in captive non-human primates (NHPs) and their zoonotic potential. However, numerous cases of helminth infections in NHPs have been documented in several zoos around the world, with one of the most prevalent being those of the genus Trichuris. The main objective of this study is to investigate the occurrence of infection by Trichuris spp. in primates from zoological gardens in Spain and to ascertain, at the species level, the specific Trichuris species harbored by these hosts by using mitochondrial and ribosomal markers. A total of 315 stools collected from NPHs (n = 47) in the 13 zoological gardens analyzed yielded a prevalence rate of 19.05%. Nevertheless, not all the zoos exhibited parasitic infections; this was observed in only 53.85% of the zoos. Moreover, 15 host groups of 12 different species were found to be infected by Trichuris species, among which the identified species included Trichuris trichiura, Trichuris colobae, and Trichuris sp. Our findings suggest a substantial exposure of primates to zoonotic Trichuris species, suggesting that NHPs could potentially act as reservoirs capable of transmitting this parasite to humans. Hence, it is crucial to implement additional control and prevention measures and explore ways to eradicate parasitic infections in these areas. Further examination is warranted to minimize the risk of spreading drug-resistant parasite strains.