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Ebook One health: The Human– Animal–Environment interfaces in emerging infectious diseases (Part 2)

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(BQ) Part 2 book “One health: The Human– Animal–Environment interfaces in emerging infectious diseases” has contents: Cost estimate of bovine tuberculosis to Ethiopia, Cysticercosis and Echinococcosis, H5N1 highly pathogenic avian influenza in Indonesia - retrospective considerations,… and other contents.

Part II Examples of Health approach to specific diseases from the field The Application of One Health Approaches to Henipavirus Research David T S Hayman, Emily S Gurley, Juliet R C Pulliam and Hume E Field Abstract Henipaviruses cause fatal infection in humans and domestic animals Transmission from fruit bats, the wildlife reservoirs of henipaviruses, is putatively driven (at least in part) by anthropogenic changes that alter host ecology Human and domestic animal fatalities occur regularly in Asia and Australia, but recent findings suggest henipaviruses are present in bats across the Old World tropics We review the application of the One Health approach to henipavirus research in three D T S Hayman (&) Department of Biology, Colorado State University, Fort Collins, CO 80523, USA e-mail: davidtshayman@gmail.com E S Gurley icddr, b (International Centre for Diarrheal Diseases Research, Bangladesh), 68 Shaheed Tajuddin Ahmed Sharani, Mohakhali, 1212 Dhaka, Bangladesh e-mail: egurley@icddrb.org D T S Hayman Á J R C Pulliam Department of Biology, University of Florida, Gainesville, FL 32611, USA e-mail: pulliam@ufl.edu J R C Pulliam Emerging Pathogens Institute University of Florida, Gainesville, FL 32611, USA J R C Pulliam Fogarty International Center, National Institutes of Health, Bethesda, MD, USA H E Field Queensland Centre for Emerging Infectious Diseases, Department of Agriculture, Fisheries & Forestry, 39 Kessels Rd, Brisbane, QLD 4108, Australia e-mail: Hume.Field@deedi.qld.gov.au Current Topics in Microbiology and Immunology (2012) 365: 155–170 DOI: 10.1007/82_2012_276 Ó Springer-Verlag Berlin Heidelberg 2013 Published Online: 17 November 2012 155 156 D T S Hayman et al locations: Australia, Malaysia and Bangladesh We propose that by recognising and addressing the complex interaction among human, domestic animal and wildlife systems, research within the One Health paradigm will be more successful in mitigating future human and domestic animal deaths from henipavirus infection than alternative single-discipline approaches Contents Introduction Hendra Virus in Australia Nipah Virus in Malaysia Nipah Virus in Bangladesh Expanding the One Health Paradigm for Henipavirus Research 5.1 Geographic Expansion 5.2 Disciplinary Expansion Conclusions References 156 157 161 162 164 164 166 167 167 Introduction Henipaviruses infect wildlife, domestic animals and humans and their emergence has been linked to anthropogenic activities Henipaviruses, therefore, provide a useful lens through which to view the development and implementation of the One Health paradigm, which strives for optimal human, animal and environmental health through collaborative multi-disciplinary work Furthermore, henipavirus outbreaks have occurred in countries as economically and culturally distinct as Australia and Bangladesh, providing opportunity for comparative approaches and cross-fertilisation of ideas that enhance understanding of the common processes that underlie cross-species transmission in these different settings To date, the One Health approach to henipavirus research has largely focused on integrating human and veterinary health; however, the continued transmission of Hendra virus (HeV) from bats to horse populations in Australia and Nipah virus (NiV) from bats to humans in Bangladesh indicates the challenges and complexity of preventing henipavirus spillover, and the need for further enhancement of the One Health approach In particular, additional integration of the social sciences to henipavirus research will be essential to identify locally acceptable and feasible interventions to promote behavioural changes to reduce the risk of cross-species infection Here, we review the history of henipavirus research since the first recognised outbreaks of HeV in Australia in 1994 We argue that the integration of human and veterinary medicine, ecology and epidemiology has been an important step in henipavirus control, but may prove inadequate in settings where ‘‘top-down’’ intervention, such as changes to policies and regulations, is less effective, as is The Application of One Health Approaches to Henipavirus Research 157 often the case when infrastructure and resources are limited, or where individuals not perceive themselves as being at risk (Spiegel et al 2011) Finally, we discuss recent findings from Africa that suggest henipaviruses are present in bats across the Old World tropics and how lessons from Australia and Asia can be applied to the development of a One Health approach to henipavirus research in other regions Hendra Virus in Australia HeV emergence, its zoonotic consequences, and identification of fruit bats as its reservoir prefaced the One Health approach to the investigation of emerging diseases associated with bats In September 1994, a gravely ill horse was stabled for veterinary care in the Brisbane suburb of Hendra, in the state of Queensland This action inadvertently precipitated the first recognised and single largest outbreak of HeV to date, resulting in 20 equine and two human cases (Fig 1a) Within 72 h of stabling the horse, two additional equine cases were evident and a cascade of cases followed Thirteen horses died or were euthanised, a case fatality of 65 % (Murray et al 1995) As the outbreak peaked, the treating veterinarian notified the state animal health authorities of the highly pathogenic novel syndrome, prompting quarantine declarations, horse movement restrictions, and cancellation of race meetings in southeast Queensland Exotic infectious agents (e.g African horse sickness) and toxins were considered differential diagnoses, but within days, both the Queensland Animal Research Institute and the CSIRO Australian Animal Health Laboratory (AAHL) had isolated HeV (initially called equine morbillivirus) AAHL subsequently conducted experimental infections in horses and was able to reproduce the disease and re-isolate the virus (Murray et al 1995), fulfilling Koch’s postulates Within a week of the first equine death, the horses’ trainer and a stable-hand became ill with an influenza-like illness The trainer in particular had direct and repeated contact with oro-nasal secretions as he endeavoured to force-feed the index case The stable-hand recovered, but the trainer’s condition deteriorated The differential diagnoses included glanders, the only known zoonotic equine disease (albeit exotic to Australia), indicating that medical authorities considered the possibility that the human cases were related to the equine outbreak (Selvey et al 1995) The trainer subsequently died, and HeV was isolated from kidney tissue Experimental studies later demonstrated HeV could infect multiple species including horses, cats, dogs, rabbits and laboratory rodents, although highly pathogenic disease was limited to horses and cats (Hooper et al 1997a, b; Westbury et al 1995, 1996; Williamson et al 1998) Subsequent retrospective investigations would show that the Brisbane outbreak did not mark the first emergence of HeV A month earlier and 800 km north, two horses on a stud farm near Mackay in Queensland died approximately a week apart after acute illness, characterised respectively by respiratory and neurological 158 Fig continued D T S Hayman et al The Application of One Health Approaches to Henipavirus Research 159 Fig The temporal pattern of the emergence of henipaviruses is shown for Hendra virus (HeV) in Australia (a) and Nipah virus (NiV) in Malaysia (b), Bangladesh (c) Arrows show which of the different disciplines required for a One Health approach are still being used; rectangles show studies that are not ongoing For brevity, disciplines such as microbiology, serology or the numerous branches of ecology are included in broad headings, such as veterinary (a focus on domestic animals), medical (a focus on humans), ecology (a focus on the host, host ecology and infection dynamics) and anthropology (a focus on human attitudes to disease, hosts and healthcare) Red–blue gradation indicates the extent to which the studies have been integrated Human and equine cases are given by H and EQ, respectively symptoms (Baldock et al 1996) (Fig 1a) The veterinarian owner, assisted by her husband, performed necropsies on both horses A definitive aetiology was not established The husband became ill shortly after with mild meningioencephalitis, but recovered after a short illness Cerebrospinal fluid analysis suggested a viral infection (Allworth et al 1995) Fourteen months later he developed severe encephalitis which resulted in his death (O’Sullivan et al 1997) HeV genome was retrospectively detected in samples from his initial illness and in samples from the relapsing illness, and matched sequences of HeV genome retrospectively detected in the two horses While the Brisbane outbreak precipitated an increased level of professional interaction between public and animal health authorities in Queensland, it was arguably the Mackay incident that heralded a lasting change in the frequency and 160 D T S Hayman et al nature of the inter-agency relationship Both authorities continued to operate as discrete agencies, but communication increased at the senior management, research and operational level (Fig 1a) When the next HeV incident occurred, strong cross-departmental linkages existed, facilitating communication and coordination of response activities The latter included case property visits, media communication and cross-agency briefings/de-briefings A manifestation of the cross-agency approach has been the formation of a HeV inter-agency technical working group whose role is to provide current, science based, best practice in relation to minimising HeV transmission that forms the basis of both animal and public health policy The inter-agency group includes public and animal health, workplace health and safety and industry representatives Information and risk management protocols targeted to horse owners, veterinarians and medical practitioners are readily available online (Anonymous 2011) The alignment of animal and public health authorities, however, represents a narrow definition of One Health, and the identification of fruit bats as the HeV reservoir promised a third perspective (Young et al 1996, Halpin et al 2000) As broader research increasingly identified the association between changes in land use practices and disease emergence from wildlife, an ecological perspective on the possible underlying drivers for HeV spillovers seemed relevant This occurred quite early at a research level, but involvement by environmental agencies at a broader level has been slower The reasons for this are unclear, but environmental agencies had a primary focus on wildlife management, and had limited expertise in relation to infectious diseases Thus, in an era of competing demands, an emerging zoonosis involving horses may not have been viewed as a priority However, it is now recognised by health authorities that consideration of ecological factors that contribute to HeV spillover events are fundamental to effective risk mitigation, and this perspective informs and complements the risk management and response perspectives of the other agencies Environmental agencies now contribute equally with animal and public health authorities at the policy and research levels, evident in the formation of an interstate and interagency Hendra Taskforce following 18 separate spillover incidents in 2011 The absence of human cases in 2011 suggests effective progress in risk communication; however, the unprecedented cluster of equine cases indicates that the drivers for HeV spillover are incompletely understood To minimise the risk to human and animal health, authorities have undertaken extensive interaction with key horse owner and veterinary stakeholders, fostering risk management strategies, proposing risk-mitigating on-farm animal and landscape management practices and supporting the development of an effective equine vaccine This combination of strategic policy and management at the government level and stakeholderimplemented mitigation efforts likely offers the most effective risk mitigation outcome Whichever approach or combination of approaches are applied, Australia, because of its advantageous socioeconomic status, is better positioned for success than countries that are less well resourced The Application of One Health Approaches to Henipavirus Research 161 Nipah Virus in Malaysia The second virus in the genus Henipavirus, NiV, was recognised about years after the discovery of HeV in Australia (Fig 1b) The first ProMED report on what was eventually recognised as an ongoing outbreak of NiV encephalitis in pigs and people in Malaysia was published on November 24, 1998, under the heading ‘‘Japanese encephalitis, suspected—Malaysia’’ (ProMed 1998) This report contained information on control measures taken at that time, which included vaccination of pig farm workers in Perak State against Japanese encephalitis virus (JEV) and insecticide fogging, intended to reduce mosquito populations, and therefore transmission of JEV via infected mosquitoes When these measures failed to contain the outbreak, pigs were also vaccinated against JEV Thus, from the outset—even before the correct aetiology of the disease was identified—efforts to control the outbreak of encephalitis in people took a multidisciplinary approach, coordinated jointly by the Ministry of Health and the Department of Veterinary Services in the Ministry of Agriculture, and drew from veterinary medicine and environmental health, as well as human medicine However, the lack of early collaboration with epidemiologists more experienced in detecting and managing epidemic JEV may have delayed the recognition that the outbreak was caused by a novel agent The discovery of a novel virus as the cause of the outbreak was made by a medical virologist working outside the scope of the main investigation and response, and by the time the finding was confirmed in March 1999 (Chua 2004; Chua et al 2000), the virus had spread to new areas and caused more than 130 cases in Malaysia and Singapore (Anonymous 1999) Once the cause of the outbreak was recognised as a novel paramyxovirus, and in particular a HeV-like agent, international involvement was requested World Health Organisation, Centers for Disease Control and Prevention and others sent teams to Malaysia that included experts in epidemiology, clinical microbiology, human and veterinary medicine, reservoir ecology, crisis management and logistics (Fig 1b) At this stage, the response to the NiV outbreak became recognisable as what would now be considered a One Health approach, which not only involved multiple disciplines but reflected a coordinated, collaborative effort working towards a common set of goals The outbreak was brought under control within a matter of weeks when the national government decided to cull infected and neighbouring pig farms, along with mandating increased used of personal protective equipment for those involved in the investigation and control efforts Epidemiological teams worked to identify factors that contributed to the spread of the outbreak as well as identify individual and farm-level risk factors for infection (Lam and Chua 2002; Parashar et al 2000) Due to its close relationship with HeV, once NiV was identified as the aetiological agent of the epidemic, pteropid bats were rapidly identified as the likely reservoir of the virus (Yob et al 2001) (Fig 1b) Investigations considered domestic animals (other than pigs) as potential intermediate hosts (Mills et al 2009), and retrospectively identified the occurrence of human cases on the outbreak’s index farm as early as January 1997 (Arif and 162 D T S Hayman et al Nipah Virus Study Group 1999) The practice of planting fruit trees adjacent to pigsties was identified as the epidemiological link between flying foxes and domestic pigs (Chua et al 2002) Further outbreaks have likely been prevented by a regulation made in 1999, prohibiting fruit trees being grown near livestock enclosures to prevent domestic animals having contact with potentially infectious bat fluids, such as urine or saliva on contaminated fruit Following the NiV outbreak in 1998–1999, there was substantial interest in the causes of viral emergence, which prompted a retrospective, multidisciplinary investigation to examine the process and drivers of emergence Serological surveillance of flying fox populations and characterisation of their movements within Malaysia through satellite tracking has indicated that the reservoir population is highly mobile and well connected, with near-ubiquitous presence of NiV antibodies (Epstein et al 2009; Pulliam et al 2012), providing evidence that the virus circulates widely Monitoring of captive bats has also highlighted difficulties of interpretation of serological data from the field and challenged assumptions relating to infection dynamics within the host (Rahman et al 2010; Sohayati et al 2011) The research team particularly focused on what factors influenced the timing and extent of the outbreak that triggered international attention This effort endeavoured to identify aspects of the emergence event that would inform prevention and surveillance efforts These investigations suggested that agricultural intensification was a major driver of emergence, both through the increased potential for ecological overlap between wildlife and domestic animals that resulted from dual-use agricultural practices, and through the intense management of commercial pig populations This intensive pig management ultimately allowed NiV to persist within the index farm (Pulliam et al 2012) Nipah Virus in Bangladesh Soon after the discovery of NiV in Malaysia, NiV was recognised as a cause of severe acute meningoencephalitis in Bangladesh in 2001 (Fig 1c) Much of what we know regarding NiV in Bangladesh comes from investigating and responding to outbreaks of human disease, including the risk factors for human disease, and local efforts to develop and implement public health interventions to prevent future outbreaks draw heavily from finding these investigations In contrast to HeV and NiV outbreaks in Australia, Malaysia and Singapore, human NiV infections in Bangladesh appear to result primarily from indirect bat-human contact, without an intermediate host, or through person-to-person transmission (Luby et al 2006, 2009) Thus, human health remains as the primary focus in Bangladesh Nevertheless, lessons learnt from Australia and Malaysia illustrated the importance of investigating NiV transmission across the human–animal interface, and a One Health approach has been used in Bangladesh since the first outbreak was identified (Fig 1c) The Application of One Health Approaches to Henipavirus Research 163 Currently, there are two passive and two active surveillance activities for outbreaks of NiV encephalitis in humans in Bangladesh First, physicians in Bangladesh are encouraged to report clusters of severe disease to the Institute of Epidemiology Disease Control and Research (IEDCR) at the Ministry of Health and Family Welfare Likewise, IEDCR reviews media reports on a daily basis to look for outbreaks suggestive of NiV In addition, active surveillance for clusters of encephalitis is conducted in six government hospitals Surveillance physicians list patients meeting an encephalitis case definition and determine whether or not they cluster in time and space with other admitted encephalitis cases In three of these hospitals, any patient admitted with encephalitis has serum collected for NiV antibody testing during the season (January–March) that NiV infections in humans have been most frequently identified Physicians in Bangladesh, particularly in the area where NiV infections commonly occur, have learned from government communication messages that humans are frequently infected through drinking date palm sap which has been contaminated by fruit bats Therefore, physicians in these parts of the country often investigate wildlife exposures among patients admitted with encephalitis and ask about date palm sap consumption Patients with encephalitis and a history of drinking date palm sap are considered likely to have NiV and physicians often notify local health authorities when any case meeting these criteria are identified Once a human case of NiV infection is reported, intensive investigations ensue to evaluate the role of livestock or wildlife in transmission The investigation team visits the locality where the cases reside and enquires about any recent animal illnesses or deaths Sick animals are examined by veterinarians and specimens are collected for laboratory diagnosis Recently, deceased animals may also be exhumed for examination and specimen collection Additionally, case-patient exposures to animals in the weeks prior to illness onset are systematically investigated through interviews with family members Due to the high case fatality of NiV ([70 %), most case-patients are not able to provide the information themselves Epidemiologic studies compare these exposures among cases to those of controls from the same neighbourhood to determine if contact with animals, or any animal in particular, is associated with having NiV infection Despite the direct relationship between a livestock outbreak and human illness in Malaysia and Singapore, a domestic or peri-domestic animal has never been identified with NiV infection during an outbreak in Bangladesh However, during two outbreaks in 2001 and 2003, epidemiologic studies showed that cases were more likely to have had contact with livestock than controls (Hsu et al 2004) In addition, one child with NiV reported exposure to goats who had died from apparent neurological illness, but these animals were not available for exam during the investigation (Luby et al 2009) Investigations into the role of wildlife during human outbreaks have focused on the local reservoir host, Pteropus giganteus Initial studies that sampled wildlife more broadly found no evidence of other wildlife infected, so investigations remain focused on Pteropus bats (icddr, b 2004) Wildlife ecologists and veterinarians working with the outbreak team routinely capture and collect specimens 346 J P Gonzalez et al 2.2 Retroviruses and Primates The old family affair with lentiviruses (see for review: Locatelli and Peeters 2012; Sharp and Hahn 2011) Lentiviruses of the Retroviridae family infect many mammalian species, including bovines, horses, felines, goats, sheep, and primates The great majority of lentiviruses are exogenous (i.e., transmitted horizontally), but they can also be integrated in the host genome (one of the main characteristics of retroviruses) and transmitted vertically through the germline, as reported in rabbits (RELIK) and lemurs (pSIV), in which the lentivirus became endogenous about 12 and million years ago, respectively (Katzourakis et al 2007; Gifford et al 2008; Sharp and Hahn 2011) As stated by Sharp and Hahn (2011) and from the estimated phylogenetic tree by Guindon and Gascuel (2003), such embedded viruses can be considered as ‘‘viral fossils’’ that demonstrate the ancient origin of retroviral infections in vertebrates and provide a direct evidence of the long coevolution of lentiviruses with their hosts Indeed, although molecular clock calculations based on Simian immunodeficiency virus (SIV) genomic sequences suggest that ancestral SIVs originated only few hundred years ago, the timescale of their evolution appears to be much longer (Holmes 2003) For instance, a study on SIV on Bioko Island, Equatorial Guinea, established that SIV is at least 32,000year/old (Worobey et al 2010) Although intraspecific transmission occurs more frequently, interspecific transmissions (i.e., crossing the barrier species) happen as well and they favor two types of SIV evolution: a long-term one, and a more recent diversification, possibly associated with recombination events between different lentiviruses (Souquiere et al 2001) During both types of evolution, SIV might have jumped the species barrier between humans and NHPs The circulation of primate immunodeficiency viruses Altogether, SIVs seem to have an ancient relationship with their hosts in Africa Indeed, more than 62 % of the known 73 African primate species harbor a specific SIV Moreover, CST among African primates has been documented in sympatric species (e.g., CST of SIVagm from African green monkeys to Patas monkeys) (Bibollet-Ruche et al 2004) along with coinfection and recombination (for instance, SIVmus2 is a recombinant lineage that includes SIVgsn and SIVmus sequences) In addition, exposure to blood or biological products from infected animals (through hunting, bushmeat butchering, bites, and scratches inflicted to humans by NHPs) might be the source of human infection by SIV, simian T cell lymphotropic virus (STLV) or simian foamy virus (SFV) African chimpanzees and gorillas are both infected by SIVs (SIVcpz and SIVgor, respectively) that have crossed the species barrier at least on four occasions, leading to the emergence of the human immunodeficiency virus type (HIV-1) groups M, N, O, and P (Gao et al 1999; Plantier et al 2009) The HIV-2 groups A to H resulted from at least eight independent CSTs of SIVs that infect sooty mangabeys (Hirsch et al 1989; Hahn et al 2000; Damond et al 2004) However, not all CSTs did have the same epidemic outcome Men, Primates, and Germs: An Ongoing Affair 347 In only one case (HIV-1 group M) these CSTs gave rise to a pandemic with almost 60 million human infections worldwide The HIV-1 group M epidemic illustrates the extraordinary social impact and consequences of a single zoonotic transmission HIV-1 group N appears to be derived from chimpanzee SIV and HIV-1 groups P and O from western lowland gorillas (Locatelli and Peeters 2012) Other retroviruses that infect several NHP species, particularly STLVs and SFV, are also of concern to humans Simian T cell lymphotropic viruses STLVs and Human T cell lymphotropic viruses (HTLVs) STLVs (type 1–5) could have been the progenitors of HTLVs (type 1–4) (Mahieux and Gessain 2011) and might have crossed the species barrier on multiple occasions causing HTLV infections that affect between 10 and 20 million people worldwide However, only % of the HTLV-infected human population develops serious health problems (Gessain 2011) The simian counterparts have been identified only for HTLV-1, HTLV-2, and HTLV-3, but not for the recently discovered HTLV-4 and also, no human counterpart has been found for the Asian STLV-5 from macaques Unlike the host-specific SIVs, STLVs present phylogenetic geographical clusters, suggesting that multiple CSTs occurred among NHPs and also from NHPs to humans (Locatelli and Peeters 2012) The simian foamy virus (SFV) is ubiquitous and highly prevalent among NHPs, including New World and Old World monkeys and apes, as well as prosimians It seems to have coevolved with its hosts for more than 30 million years (Switzer et al 2005) SFV infects humans more likely through primate bites; however, infected humans not present any clinical manifestation (Heneine et al 2003) No human foamy virus has been identified to date Human exposure to simian retroviruses appears heterogeneous across the surveyed African countries (Locatelli and Peeters 2012), probably due to the complexity of establishing infection after CTS between NHPs and humans, because the virus has to be ‘‘humanized’’ and, several requirements have to be met following exposure (‘‘first encounter’’), such as viral and host molecular characteristics and compatibility, host competency for viral replication and interspecies transmission 2.3 Plasmodium Parasites and Primates Plasmodium parasites and host biodiversity Malaria is caused by protozoan parasites that belong mainly to the genus Plasmodium More than 200 Plasmodium species have been identified that can infect mammals (more than 50 species), birds, or reptiles Among mammals, primates are by far the most common intermediate host for Plasmodium parasites From an evolutionary point of view, primate Plasmodium species form a paraphyletic clade (Martinsen et al 2008) subdivided in two subgenera: the subgenus Plasmodium that includes species infecting a large variety of primates in Africa, Asia (catarrhines), and South America (platyrrhines), and the subgenus Laverania with species that naturally infect only catarrhines (gorillas, chimpanzees, cercopithecidae 348 J P Gonzalez et al P reichenowi P falciparum P falciparum-like P falciparum-like P billcollinsi P gorB P gaboni P billbrayi P gorA L A V E R A N I A Human Pan sp Gorilla sp Hyobatidae African monkeys Asian monkeys American monkeys P ovale P malariae P brasilianum P gonderi P sp (DAJ) P knowlesi P cynomolgi P vivax P simium P inui P hylobati P fieldi P simiovale P L A S M O D I U M Rodents Fig Schematic representation of the phylogeny of the primate Plasmodium with the currently known categories of hosts Primate Plasmodium are subdivided in two subgenus: Laverania and Plasmodium and humans) Among these species, five infect humans: P falciparum, P vivax, P malariae, P ovale, and the most recently identified P knowlesi As shown in Fig 1, these five species are only remotely related to each other: four belong to the Plasmodium subgenus, but nevertheless constitute divergent lineages, and one is part of the Laverania subgenus This distribution suggests that adaptation to humans has occurred several times independently during the genus history In addition, the close relationships observed between human parasites and some phylogenetically distant nonhuman primates suggest that some of these species adopted humans as hosts following a lateral transfer This seems to be the case for the most virulent species of all: P falciparum Plasmodium falciparum: the quest for its origin Currently, P falciparum represents one of the biggest scourges of humanity Almost half a billion people are infected by this parasite and, despite the medical progress, one million of them still die every year, especially in Sub-Saharan Africa The origin of this disease has been the focus of much debate during the past 20 years Briefly, it was first hypothesized that P falciparum derived from a lateral transfer from birds (Waters et al 1991, 1993) or rodents, or coevolved with humans (Escalante and Ayala 1994) More recently a jump from chimpanzees (Rich et al 2009) or bonobos (Krief et al 2010) to humans (see, Prugnolle et al 2011b for review) was proposed Another hypothesis suggested a recent CST from gorillas (Liu et al 2010) based on the discovery of P falciparum-like pathogens that circulate naturally in wild populations of western gorillas (Liu et al 2010; Prugnolle et al 2010) Men, Primates, and Germs: An Ongoing Affair 349 The NHP origin The diversity of Laverania species infecting great apes in Africa was described for the first time at the beginning of the twentieth century (Coatney et al 1971) At that time, it was considered that only one sister lineage of P falciparum existed: P reichenowi, a chimpanzee parasite This notion persisted until the very recent development of non-invasive methods (Prugnolle et al 2010) and the use of molecular tools that allowed a complete reevaluation of the species diversity of African ape Plasmodium parasites (Kaiser et al 2010; Ollomo et al 2009; Rich et al 2009; Duval et al 2010; Krief et al 2010; Liu et al 2010; Prugnolle et al 2010) This led to the discovery that great apes in Africa are the hosts of a much larger number of Laverania species than previously thought In particular, these studies identified parasites that are very closely related to P falciparum and that infect only gorillas among all the wild populations of great apes (Liu et al 2010; Prugnolle et al 2010) Other P falciparum-like parasites were also identified in captive chimpanzees (Duval et al 2010) and bonobos (Krief et al 2010), but it was rapidly demonstrated that these parasites resulted from human-to-primate direct transfers The discovery of the culprit The discovery, in gorillas, of parasites that are genetically very close to P falciparum led to the hypothesis that gorillas could be the source of the human malaria parasite P falciparum (Liu et al 2010) The finding that the P falciparum-like parasites from gorillas display a large mitochondrial genetic diversity compared to the human P falciparum isolates, which form a monophyletic clade within the gorilla diversity, suggests that P falciparum appeared in humans following one single and recent CST event from gorillas (Liu et al 2010) Is this the final word on the origin of P falciparum in humans? Nothing is less sure Indeed, alternative scenarios could explain the genetic diversity profiles of P falciparum from humans and gorillas (e.g., multiple human to gorilla host switches during the history of the lineage) (Prugnolle et al 2011b) Moreover, it was recently discovered that P falciparum-like pathogens (the ones that infect gorillas in Central Africa) can also naturally infect monkeys in Africa (Prugnolle et al 2011c) This means that there might be other sylvatic reservoirs of P falciparum-like pathogens and all of them are as likely candidate sources of human P falciparum as the western gorillas (Prugnolle et al 2011a) Other human Plasmodium species The case of P falciparum is not isolated and the tight links between human and NHP Plasmodium parasites are numerous Several examples of transfer from primates to humans or vice versa are now well documented The case of P knowlesi is certainly the clearest It was considered to be exclusively a parasite of Asian macaques until it was recently identified as the cause of almost 70 % of human cases of malaria in some areas of South-East Asia It is now considered to be the ‘‘fifth human malaria parasite’’ (White 2008) It is still unclear whether P knowlesi infections are only due to primate-to-human CST or whether human-to-human transmission may occur as well; however, since 2004, reports on the incidence of this parasite among humans in various countries in South East Asia have been increasing P vivax has a similar history, but possibly much older This parasite belongs to a group of Plasmodium species that infect 350 J P Gonzalez et al monkeys in Asia (see Fig 1) and it might have emerged in humans following a transfer from macaques (Mu et al 2005) Some South American Plasmodium species that infect New World monkeys are also very closely related to human Plasmodium parasites For instance, P simium is very close genetically to P vivax and the closest relative of P brasilianum is P malariae (Tazi and Ayala 2010) If the hypothesis of an Asian origin of P vivax is true, the close phylogenetic relationship of P simium with P vivax could be interpreted as the result of an anthroponosis (i.e., host switching from humans to other animals) Concerning P brasilianum, while its close relationship with P malariae is suggestive of a host switch, the question of whether platyrrhines acquired it from or transferred it to humans remains unanswered (Tazi and Ayala 2010) The risk of emergence of new Plasmodium species in humans Should we fear the emergence of new zoonoses due to primate Plasmodium species? The answer is very likely yes Human populations are growing very rapidly and they are progressively colonizing areas where NHPs live, thus increasing the possibility that new species of Plasmodium might switch to humans This is all the more likely as some of these NHP pathogens are known to be able to infect humans For instance, P cynomolgi and P inui, two Plasmodium species that infect Asian macaques, have been implicated in symptomatic malaria in humans following experimental or accidental infection (Coatney et al 1971) The Future of Pathogen Circulation in a Changing world Environment Humans, NHPs and their microorganisms appear as a pathogenic complex that varies according to the population territories (environments) and their domain overlaps (not very clear) At any time and space, several pathogens are circulating among human and NHP populations, coinfecting them, spilling over from a species to another and expanding their endemic pattern Cross-Species Transmission appears as one of the major factor of evolution at the population level A successful species jump is achieved when the pathogen becomes transmissible between individuals of the new host population A successfully masterminded epidemic and the endemic maintenance of the pathogen in the new population require several human and non-human environmental factors (e.g., host receptiveness, proximity, population density, multiple passages, behavior, etc.) Zoonotic Risk Given the increasing exposure of humans to NHP pathogens through hunting and bushmeat butchering, it is likely that simian viruses are actually and constantly transmitted to human populations often without ‘‘success’’ and that only exceptionally they will give rise to EIDs Germ and host biodiversity appear to be the main EID and CST drivers by favoring the fittest ‘‘first encounter’’ between a parasite and a new host Host, parasite and environmental factors are all required for the optimal success of pathogen transmission; understanding the complexity of their interactions will lead to understanding infectious disease emergence and fulfill the One Health mission Men, Primates, and Germs: An Ongoing Affair 351 Sizing the risk Given that monkeys and apes often share parasites with humans, understanding the ecology of infectious diseases in NHPs is of paramount importance The zoonotic risk also depends on how environmental changes may promote contacts between primates and increase the possibility of sharing infectious diseases that are detrimental to humans and/or NHPs Indeed, 244 primate species have a genome that is genetically related to the human genome and could thus exchange parasites The ‘‘first encounter’’ of NHPs, humans and germs is driven by behavioral and environmental factors NHP-human transmission may occur both in domestic environments (pets, laboratory animals) and in the wild (Wolfe et al 2007) Protected areas, ecotourism, exotic pets, and animal farming may thus favor cross-species transmission, leading to 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Tuberculosis to Ethiopia Rea Tschopp, Jan Hattendorf, Felix Roth, Adnan Ali Khan Choudhury, Alexandra Shaw, Abraham Aseffa and Jakob Zinsstag Contents Erratum to: Cost Estimate of Bovine Tuberculosis to Ethiopia, doi: 10.1007/82_2012_245 DOI" Address="10.1007/82_2012_245"/> Erratum to: Cost Estimate of Bovine Tuberculosis to Ethiopia, doi: 10.1007/82_2012_245 It was noticed that one author’s name was spelled incorrect The correct name is Adnan Ali Khan Choudhury The online version of the original chapter can be found at 10.1007/82_2012_245 R Tschopp Á J Hattendorf Á F Roth Á J Zinsstag (&) Swiss Tropical and Public Health Institute, CH-4002 Basel, Switzerland e-mail: jakob.zinsstag@unibas.ch R Tschopp Á A Aseffa Armauer Hansen Research Institute, 1005 Addis Ababa, Ethiopia A A K Choudhury University of Queensland School of Public Health, Brisbane, QLD, Australia A Shaw AP Consultants, 22 Walworth Enterprise Centre, SP10 5AP Andover, UK R Tschopp Centre for Molecular Microbiology and Infection, Imperial College London, London, UK Current Topics in Microbiology and Immunology (2013) 365: 355–355 DOI: 10.1007/82_2013_318 Ó Springer-Verlag Berlin Heidelberg 2013 Published Online: 28 May 2013 355 Index A Acid rain, 103 Acute, 60 Acute diseases, 56 Acute infections, 51, 57, 59, 60 Adenoviridae, 51 Agriculture, 56, 58, 68, 71, 72 AIDS, Allocation of resources, 137, 145 American Veterinary Medical Association, Amphibians, 104 Ancient history, 59 Animal health, 203, 205, 233, 234, 297 Animal reservoirs, 58, 70 Animal sentinels, 18 Anthrax, 4, 67 Anthropozoonoses, 111 Antigenic cartography, 177 Antimicrobial resistance, 72 Arena viruses, 71 Avian influenza, 277 B Bacillus pertussis, 58, 60 Bacillus anthracis, 58 Bali, 169 Bangladesh, 94 Barriers to control of rabies, 188 Bat, 70, 71, 107 Bat colonization, 71 Batrachochytrium dendrobatidis, 104 Dr Beard, T C., 322 Biogeochemistry, 88 Biodiversity, 85 Biosecurity, 281, 282 Bird–release, 287 Black Death, 62, 63 Black rat, 62, 63 Bocavirus, 57 Bordetella bronchiseptica, 60 Bordetella pertussis, 57 Bovine spongiform encephalopathy, 69 Bovine Tuberculosis, 109 Bronze age, 59, 61 Brown rat, 63 Brucella abortus, 58, 108 Bubonic plague, 62 Burkholderia mallei, 58 Bush meat, 67, 68, 70, 107 C Caliciviruses, 57 Calvin Schwabe, Camelpox viruses, 57 Cattle, 245–249, 255–257, 259, 261, 262 Chimpanzee, 50, 53, 67, 68 Cholera, 61, 65, 94 Chronic, 53, 60, 71 Chronicity, 50 Chytrid fungus, 104 Clade 2.1, 174 Classic antiquity, 61 Climate, 72 Clinical practice, 16, 17, 19, 24 Clostridium difficile, 296–306 Co–evolution, 48, 53, 71 Colonization, 48, 61, 63, 64, 68, 71, 74 Commensal, 57–60, 62, 71, 94, 105, 297 Community ecology, 83 Complexity, 81 Contemporary History, 68 Coronavirus, 70 Corynebacterium diphtheriae, 57 Co–speciation, 50, 51 Current Topics in Microbiology and Immunology (2013) 365: 357–362 DOI: 10.1007/978–3–642–36889–9 Ó Springer-Verlag Berlin Heidelberg 2013 357 358 Cows, 56, 63 Cross–species transmission, 51, 152, 334, 346, 347 Crowd diseases, 56, 61 Crowd epidemics, 64 Culling, 117, 280, 281, 286 Cystic echinococcosis, control, 318 Cysticercosis, 313 Cysticercosis, control, 313 D Dichlorodiphenyltrichloroethane(DDT), 103 Definitive host, 312 Deforestation, 64 Demographic, 57, 59, 60, 67 Demographic changes, 56 Development Planning System, 245, 249 Diet, 50 Disease emergence, 129, 135, 141, 142, 144 DNA viruses, 50, 52 Dog, 55, 60, 64, 69 Domestic, 60, 65, 67, 68 Domestic animal, 67, 70 Domesticated, 54, 57–59, 68, 70 Domestic dogs, 54, 55, 62, 69 Domestic livestock, 57 Donor Support, 172 Drivers of disease emergence and persistence, 175 Duck, 64, 279, 282 E E coli O157:H7, 106 Ebola virus, 70, 114 Echinococcosis, 317 Echinococcus multilocularis, 71 Ecohealth, 82 Ecology, 82, 114 Ecology of infectious diseases, Economic efficiency, 125, 132–138, 140, 141, 144, 145 Economic evidence, 142, 144 Economics, 247, 252, 260, 261 Economic value, 129, 132, 133 Ecosystem ecology, 83 Ecosystem engineering, 89 Ecotourism, 110 Efficiency, 128, 129, 132, 134, 144, 145 EG95 vaccine, 324 Index Emergence, 127, 129–131, 135, 138, 139, 141, 142, 145 Emergence of infectious diseases, 141 Emerging disease, 16, 17 Emerging Infectious Diseases, 81, 100 Encephalitis, 190 Endocrine disruptors, 103 Endogenous retroviruses, 48, 52 Enteroviruses, 55 Environmental contamination, 299, 302, 305, 306 Environmental health, 2–8, 16, 17, 21, 24, 25 Environmental Indicators, 103 Environmental reservoirs, 60 Environmental Protection Agency (EPA), 103 Epidemic curve, 91 Epidemiology, Eradication, 73 Ethiopia, 245–248, 255, 260–262 Exotic pet, 69, 70 F Falciparum, 53 Food and Agriculture Organization (FAO), 255 Farmers, 56, 58, 59 Farming, 56, 58, 68, 69 Feline leukemia virus, 58 Filovirus, 70, 73 Flaviridae, 63 Flaviviridae, 52 Flaviviruses, 72 Fleas, 58, 62, 63 Food, 56, 57, 59, 64, 68, 72 Foot–and–mouth disease (FMD) virus, 67, 68, 108 Foodborne illnesses, 106 Food production, 56, 57 Food–web, 85 Fowl cholera, Furious rabies, 190 G GB viruses, 55 GBV–C viruses, 52 Geese, 282 Gene orthologs, 51 Genetic Characterization, 283 Geomyces destructans, 105 Index Gerbilpox viruses, 57 Globalization, 64, 68, 73 Global Viral Forecasting Initiative, Goats, 56, 63 Gorilla, 68 Guinea pig, 64 H H pylori, 55 H1N1 influenza, 266–268 H5N1 HPAI, 168 H5N1, 167, 277–280 Hantaviruses, 71 Heirloom, 50 Heirloom Pathogens, 48, 71 Helicobacter pylori, 54 Hendra virus, 71, 152, 153 Henipavirus, 71 Henri Toussaint, Hepadnaviridae, 52 Hepatitis A virus, 52 Hepatitis B virus, 52, 55 Hepatitis C, 52 Hepatitis C virus, 62 Hepatitis viruses, 55 Herpes–Papilloma and Polyomaviridae families, 50, 51 Herpes simplex viruses, 51 Herpesviruses, 50, 51 highly pathogenic Avian Influenza, 167 Highly pathogenic avian influenza A/H5N1, 115 HIV/AIDS, 67, 68, 102 Hominin, 49–53, 56 Hong Kong, 168, 277 Horses, 63, 71 Hotspot maps, 90 HTLV, 55 Human–animal interface, 53, 54 Human health, 201, 205, 234, 297, 306 Human immunodeficiency virus, 67 Human metapneumovirus, 65 Humans, 278 Human T lymphotropic, 54, 55 Hunter–Gatherers, 53, 54, 56, 58 I Iceland, 318 Indonesia, 167 359 Industrial, 64, 66, 68 Industrialization, 68, 72 Infectious disease emergence, 130 Influenza, 63, 65, 73 Influenza A (H5N1), 278 Influenza A viruses, 65 Influenza viruses, 65–67, 69, 72 Insect vectors, 58 Interdisciplinary, 138, 142, 143 Interdisciplinary approach, 125 Interdisciplinary partnerships, 134 Intermediate host, 312 International Task Force for Disease Eradication (ITFDE), 326 Intersectoral integration, 125, 144, 145 Interventions, 290 Iron Ages, 59 Isle Royal, 93 J Japanese encephalitis, 201, 202, 205 Java, 169 Justinian plague, 62 K Kalimantan, 169 KOMNAS FBPI, 170 L Laboratory Services, 172 Latent, 53 Leprosy, 61 Lice, 50, 55, 62, 63 Live poultry markets, 175, 280 Livestock, 59, 245–249, 252, 255–259, 261, 262 Livestock–Associated MRSA (LA–MRSA), 72 Llama/alpaca, 64 Louis Pasteur, M Malaria, 53, 58, 63, 65 Malaysia, 95 Malignant catarrhal fever, 108 Management of Wildlife Diseases, 117 Measles virus, 57, 59, 63 360 Measles, 61, 73, 74 Medical, 73 Medicine, 61, 64, 65, 72, 73 Metacestode, 312 Metapneumovirus, 65 Methicillinresistant Staphylococcus aureus (MRSA), 72 Mice, 58 Dr Michael Gemmell, 319 Middle Ages, 61, 62 Migrating birds, 115 Migration, 54, 55 Migratory, 59 Migratory wild birds, 287 Mitigation, 125 Modern History, 61, 63, 64, 69 Molecular epidemiological techniques, 173 Molluscum contagiosum, 51 Monkeypox, 102 Monkeypox virus, 70, 74 Morbilliviruses, 74 Mosquito–borne zoonotic disease, 233, 234 Mosquitoes, 58, 65, 72 Mosquito vectors, 72 M tuberculosis, 58 Mumps virus, 57 Mycobacterium, 58 Mycobacterium bovis, bovine tuberculosis, 246 Mycobacterium tuberculosis, 53 N Neolithic, 56–60, 65, 71 Neolithic farmers, 56 Network, 81 Neurocysticercosis, 313 New variant of Creutzfeldt Jacob disease, 69 New Zealand, 320 Nipah, 106 Nipah virus, 71, 94, 152, 157, 158 Nonhuman primates, 335, 344 O Ocupational health, 15, 16, 21, 22, 24, 25 OFFLU, 177 One Health, 1–4, 6–13, 81, 125, 127–129, 132–136, 138, 140–146, 152, 203, 234 One Health approach, 167, 168 One Health Commission, One Health practice, 24, 25 Index One Health risk mitigation, 128, 133, 135, 137 One Medicine, Orthomyxoviridae, 65 Oxfendazole, 314, 315 P Paleolithic and Mesolithic periods, 53 Pandemic, 266–271, 277, 278 Pandemic epicenter, 279 Papillomaviruses, 55 Paralytic rabies, 189, 190 Paramyxoviridae, 57, 65 Participatory disease surveillance and response (PDSR), 171 Parvovirus, 51, 57 Pathogens, 50 Perfluorinated chemicals, 103 Persistence, 50 Persistent, 60 Picornaviridae, 52, 55, 67 Pierre Galtier, Pig, 56, 57, 63, 71, 72, 300–305 Plague, 58, 62, 63 Plague of Athens, 61 Plasmodium, 53, 63 Plasmodium reichenowi, 53 Plasmodium vivax, Polio, 73 Population ecology, 83 Polyomaviruses, 55 Poultry, 65, 66, 69, 115, 277–280 Poultry production system, 175 Poxviridae, 51 Poxviruses, 51 Predation, 54 Prehistory, 49 Prevention, 19–22 Prey–predator life, 312 Primates, 335, 342–345, 347 Primate T lymphotropic viruses, 55 Prion, 69 Pseudomonas syringae, 58 Q Qinghai lake, 287 R Rabies, 3, 69, 73, 116, 182–185, 187–195 Rabies post–exposure prophylaxis, 190 Index Rabies vaccine, Rabies virus, 55 Rats, 58, 62, 63 Real–time PCR, 172 Reassortment, 283 Recombination, 51 Re–emergence, 129 Reservoir, 70 Resilience, 81 Resource allocation, 128, 132, 134, 137, 142 Retroviridae, 52, 55, 58, 67 Retroviruses, 67 Rhabdoviridae, 55 Rickettsia prowazekii, 63 Rickettsia typhi, 63 Rinderpest, 67, 73, 74 Rinderpest virus, 67, 108 Risk mitigation, 132, 139, 142–144 RNA viruses, 50, 52 Robert Koch, 2, Rodent, 58, 62, 63, 70, 71 Rotaviruses, 57 Rudolph Virchow, S Salmonella, 58, 69, 70 Salmonella enteric, 61 Sanitation, 60, 61 SARS, 73, 102, 277, 278, 286, 288 SARS coronavirus, 70, 73 Schistosoma, 55 Settlement, 56, 58 Severe acute respiratory syndrome (SARS), 70 Sheep, 56, 63 Simian foamy virus, 102 Simian immunodeficiency viruses (SIV), 67 Dr Sir Neil Begg, 320 Smallpox, 61, 67, 73 Smallpox virus, 57, 59, 63, 74 Sooty mangabeys, 68 Stone Age, 53, 56 Sumatera, 169 Superspreaders, 86 Surveillance, 277, 283, 291 Swine, 65, 66, 68, 69 Swine Flu, 266, 267, 271 T Taenia solium, control, 314 Tapeworms (Taenia spp.), 54, 57 361 Tasmania, 322 Ticks, 58 Toussaint, Trade, 48, 59–61, 63, 64, 69, 70 Trading systems, 72 Trading, 68–70 Transmission, 277, 280, 281, 284, 285 Transmission pathways, 113 Travel, 48, 72 Trichinella spiralis, 59 Trophic cascades, 87 Trypanosoma, 53 Trypanosoma brucei, 53 Trypanosomes, 53 TSOL18 vaccine, 316 Tuberculosis, 61, 65 Turkey, 64 Typhoid fever, 61, 62 Typhus, 63 U Urban, 60 Urbanization, 59, 61, 67, 68, 71, 72 Uruguay, 323 USAID PREDICT, 114 Usutu viruses, 72 V Vaccination, 2, 67, 73, 117, 177 Vaccine, 67, 285, 290 Value chains, 175 Vector control, 181, 182 Vectors of rabies, 184 Vector or reservoir, 61 Vibrio cholerae, 94 Viruses, 52 Virus reassortment, 271 Virus sharing, 176 W Waterbirds, 65 West Nile, 72 West Nile virus, Wet markets, 280 White–nose syndrome, 104 Whooping cough, 58, 60 Wildlife, 81, 99 Wildlife health, 117 Wildlife health surveillance, 112 362 Wildlife Trade, 101 William Osler, Y Y pestis, 62 Yellow fever, 5, 63 Yellow fever virus, 63 Yersinia pestis, 58 Index Z Zoonoses, 20, 101, 188 Zoonotic, 82 Zoonotic disease, 127, 128, 130, 131, 133, 134, 136, 137, 139–145 Zoonotic Disease Emergence, 130, 135, 139, 141, 145 Zoonotic disease risk mitigation, 135 ... comprehensive measures including the destruction of all poultry as outlined in the background section of this chapter The veterinary services in Indonesia, in the broadest sense including their relationships... understanding the H5N1 situation in Indonesia H5N1 Highly Pathogenic Avian Influenza in Indonesia 179 3.1 Understanding the Indonesian Poultry Production and Marketing Sector In a One Health... disease incidents or global pandemic situations 2.4 The Understanding of the Natural History of the H5N1 Virus in Indonesia that has Emerged The origin and route of introduction of the Indonesian

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