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The duck (Anas platyrhynchos) is one of the economically important poultry species as a source of meat, eggs and feathers. Ducks harbour most of the hemagglutinin (HA) and neuraminidase (NA) subtypes of avian influenza viruses that are currently known [2, 3] and serve as the principal natural reservoir host for influenza A viruses [2, 4–6]. Influenza A viruses maintained in wild aquatic birds have been associated with stable host switch events to novel hosts including mammals and domestic gallinaceous poultry leading to the emergence of novel influenza A viruses [7, 8].
To control the outbreaks of emerging or re-emerging viral diseases and prevent the transmission of viruses from the reservoir host, monitoring the virome status in the reservoir hosts is essential. Further, understanding the viral diversity in the poultry gut will improve the knowledge of enteric disease syndromes and the feed conversion efficiency of the poultry species. In recent years, next generation sequencing technology based viral metagenomics has provided a powerful tool for large-scale detection of known and unknown viruses existing in the reservoir host [11, 12]. Using this approach, known and novel viruses have been characterized from the enteric tract of turkey, bats, pigs, rodents, pigeon, ducks and ferrets. To obtain an unbiased measure of the viral diversity in the enteric tract of ducks, we deep sequenced viral nucleic acid isolated from cloacal swabs of 23 ducks collected from Bhoj wetland of Bhopal, the capital of the central Indian state of Madhya Pradesh. The present study revealed that the duck gut virome contained sequences related to a wide range of animal, insect, plant, and bacterial viruses. This study increases our understanding of the viral diversity present in the enteric tract of ducks. Further, this virome dataset provide a baseline faecal virome of the ducks and will be used as reference for identification of future changes in its virome composition, which may be associated with disease outbreaks or environmental changes.
Circoviruses are non-enveloped DNA viruses belonging to the genus Circovirus of the family Circoviridae, and contain a small circular, single stranded ~2 kb DNA genome1. This genus harbors viruses that infect domestic and wildlife animal species, including porcine circoviruses (PCV-1 and -2), canary circovirus (CaCV) and beak and feather disease virus (BFDV) of birds2–5. Next generation sequencing (NGS) has recently allowed the discovery of additional mammalian circoviruses including PCV-3 in pigs6 and canine circovirus-1 (CanineCV-1) in dogs1. Infection with CanineCV-1, recently re-classified as ‘CanineCV’7, has been associated with several disease entities accompanied by manifestations like vasculitis, hemorrhages, thrombocytopenia, neutropenia and diarrhea2,7–9, although it is also detected in healthy dogs1,8,10. Interestingly, dogs infected with CanineCV are often co-infected with other enteric or respiratory pathogens2,7,10,11. Therefore, the pathogenic role of CanineCV is not clear. To date, CanineCV-infected dogs have been documented in several countries including the USA1,8,11, Italy9, Germany7, China (GenBank accession number: KT946839) and Taiwan2.
Besides genetic mutation, recombination is a driver of circovirus evolution, as several previous studies have shown genetic recombination within the Circoviridae family. These include BFDV12, Torque teno virus13 and PCV-214–17, and have contributed to genetic diversity of these viruses. Types of recombination mechanisms include homologous recombination in which homologous sequences are exchanged, non-homologous recombination in which genome regions are rearranged, deleted, duplicated or inserted into the host genome and reassortment in which whole genome components of the virus get exchanged between strains and species18. In homologous recombination, any interruption during replication, such as the encounter of strand break sites or clashes between replication and transcription complexes, can create temporary detachment of the replication enzyme. The enzyme can then use another similar template to reinitiate replication, thus generating a recombinant genome18. Thus far, genetic recombination of CanineCV genomes has not been documented. In the present study, we have molecularly characterized CanineCV strains from Thai dogs by next generation sequencing with special emphasis on the occurrence of genetic recombination.
Influenza A virus (IAV) has caused significant morbidity and mortality globally in humans, with an estimated 14 pandemics that have occurred since the 1500s.1 Wild aquatic birds are well known to be the natural reservoirs for IAV subtypes harbouring H1–H16 subtypes,2, 3, 4 with the exception of H17 and H18 subtypes that were recently discovered in bats.5, 6 The phylogenetic relationships of all IAV subtypes are displayed in Fig. 1. In addition to its natural reservoir species, influenza viruses infect a wide range of hosts including canids, equids, humans and swine.2 IAVs’ ability to generate novel gene constellations through reassortment between subtypes poses a risk for immune escape in these new hosts.7 Furthermore, IAV undergoes rapid genetic and antigenic evolution, which makes vaccination control difficult in humans and other domestic species.
In addition to human pandemics that have emerged from avian and swine hosts, there are also repeated spillover events from domesticated animals, primarily poultry and swine, that pose a significant threat to human health.8, 9, 10, 11, 12, 13, 14 Direct transmission of IAV from a wild avian source to humans is rare, as there has only been a single report of laboratory‐confirmed human infection with H5N1 contracted through close contact with dead and infected wild swan in Azerbaijan.15 However, there is serological evidence of H5N1 infection among Alaskan hunters who handled dead wild avian species,16 indicating that exposure to IAVs from wild birds through close contact can potentially cause infection. More notably, viral genes that are similar to the 1918‐like H1N1 avian virus were recently detected in the influenza gene pools of wild birds, raising the potential for the re‐emergence of a 1918‐like pandemic virus.17 Furthermore, due to increasing human encroachment of wildlife habitats, the potential of a wild‐source threat becomes more relevant, as is seen with the emergence of other pathogens such as human immunodeficiency virus (HIV), severe acute respiratory syndrome coronavirus and the more recent Zaire‐variant Ebola virus in Western Africa.18, 19, 20, 21
In this review, we discuss the current knowledge of ecological and molecular determinants responsible for interspecies transmission of IAV, with specific focus on avian‐derived influenza subtypes involved in zoonotic and epizootic transmission to other hosts (see Fig. 2).
Canine enteritis can be caused by a number of viral, bacterial or parasitic agents. The most common viral entero-pathogens are canine parvovirus (CPV) and coronavirus (CCoV),, although other agents, such as canine adenovirus (CAdV) type 1, canine distemper virus (CDV), rotaviruses, reoviruses, and caliciviruses, have been associated with enteric disease in dogs. In recent years, novel viruses have been discovered from dogs with enteritis, namely noroviruses, sapoviruses, astroviruses, and kobuviruses,.
More recently, a dog circovirus (DogCV) was detected in dogs with vasculitis and/or hemorrhagic diarrhoea in the US (13). Circoviruses (family Circoviridae, genus Circovirus) are non-enveloped, spherical viruses with a small monomeric single-strand circular DNA genome of about 2 kb in length. According to the most recent release of the Universal Virus Database of the International Committee on Taxonomy of Viruses, the genus Circovirus consists of eleven recognized species, including Porcine circovirus 1 (PCV-1), Porcine circovirus 2 (PCV-2), Canary circovirus (CaCV), Beak and feather disease virus (BFDV), and other viruses of domestic and wild birds (http://ictvdb.bio-mirror.cn/Ictv/fs_circo.htm). Porcine and avian circovirus infections are characterized by clinical courses that may vary from asymptomatic infections to lethal disease.
Two independent studies have shown that, similar to other animal circoviruses, DogCV possesses an ambisense genomic organization with 2 major inversely arranged ORFs encoding for the replicase and capsid proteins, respectively,. The canine virus, firstly detected in serum samples, was later recognized as causative agent of necrotizing vasculitis and granulomatous lymphadenitis.
The aim of this paper is to report the detection and molecular characterisation of DogCV in dogs with acute gastroenteritis in Italy. The full-length genome of the Italian prototype strain was determined and analyzed in comparison with American strains and other circoviruses.
Gastrointestinal disorders are one of the most common diseases reported in companion animal clinics. They can be caused by a number of viral, bacterial and parasitic pathogens. The most common viral gastrointestinal-pathogens are canine parvovirus [1, 2] and coronavirus. However, other agents, such as dog circovirus (DogCV), have recently been considered to be related to enteric disorders in dogs [3, 4]. DogCV was first identified in dogs with vasculitis and/or hemorrhagic gastroenteritis in the United States in 2012. DogCV is a non-enveloped, circular, single-stranded DNA virus containing a circular genome approximately 2 kb in length. It belongs to the genus Circovirus, together with porcine circovirus type 1 (PCV1), porcine circovirus type 2 (PCV2), canary circovirus, beak and feather disease virus and other viruses of domestic and wild birds.
PCV2 causes clinical conditions including systemic, lung, enteric, reproductive and skin diseases. In recent years, a possible association between DogCV and canine enteritis has been suggested [3, 4]. DogCV has also been reported to cause necrotizing lymphadenitis and vasculitis, which are also caused by porcine circovirus type 2 infections in pigs. Previous studies have shown that DogCV is associated with hemorrhagic enteritis in dogs [3, 4], however, limited information is available to determine the direct correlation between the severity of diarrhea and DogCV infections.
DogCV has only been detected in the US [4, 6], Italy, Germany (GeneBank accession number: KF887949) and China (GeneBank accession number: KT946839). In the present study, we determined the previously unidentified DogCV and its prevalence in Taiwanese household dogs and clarified the correlation between diarrhea and DogCV infection.
About 70% of microbial agents causing outbreaks of emerging infectious diseases in humans originate directly from animals. Among respiratory virus infections, the influenza A viruses H5N1 and H7N9 from avian species, and the severe acute respiratory syndrome coronavirus from bats have caused large epidemics–. Atypical bacterial pathogens causing community-acquired pneumonia include Chlamydophila psittaci from psittacine birds and Coxiella burnetti from livestock and other animals. However, human outbreaks due to zoonotic bacteria associated with the emergence of a novel animal virus in the animal host were not previously documented.
In November 2012, an outbreak of human psittacosis affecting six staff members occurred at the New Territories North Animal Management Centre (NTNAMC) in Hong Kong. The human outbreak was preceded by an outbreak of avian chlamydiosis among the detained Mealy Parrots (Amazona farinose). Although birds in the tropical and sub-tropical areas are commonly infected with C. psittaci, most infected birds are asymptomatic,. Large human outbreaks are rare even among bird handlers. Although co-infection of C. psittaci and viruses has been reported in outbreaks of avian species–, no virus-bacterium co-infection of implicated avian species has ever been reported in outbreaks of human psittacosis. In this study, we sought to investigate viruses that cause avian co-infection, which may have led to this outbreak of psittacosis.
Proventricular dilatation disease (PDD) is considered by many to be the greatest threat to aviculture of psittacine birds (parrots). This disease has been documented in multiple continents in over 50 different species of psittacines as well as captive and free-ranging species in at least 5 other orders of birds. Most, if not all major psittacine collections throughout the world have experienced cases of PDD. It has been particularly devastating in countries like Canada and northern areas of the United States where parrots are housed primarily indoors. However, it is also problematic in warmer regions where birds are typically bred in outdoor aviaries. Moreover, captive breeding efforts for at least one psittacine which is thought to be extinct in the wild, the Spix's macaw (Cyanopsitta spixii), have been severely impacted by PDD.
PDD is an inflammatory disease of birds, first described in the 1970s as Macaw Wasting Disease during an outbreak among macaws (reviewed in). PDD primarily affects the autonomic nerves of the upper and middle digestive tract, including the esophagus, crop, proventriculus, ventriculus, and duodenum. Microscopically, the disease is recognized by the presence of lymphoplasmacytic infiltrates within myenteric ganglia and nerves. Similar infiltrates may also be present in the brain, spinal cord, peripheral nerves, conductive tissue of the heart, smooth and cardiac muscle, and adrenal glands. Non-suppurative leiomyositis and/or myocarditis may accompany the neural lesions. Clinically, PDD cases present with GI tract dysfunction (dysphagia, regurgitation, and passage of undigested food in feces), neurologic symptoms (e.g. ataxia, abnormal gait, proprioceptive defects), or both. Although the clinical course of the disease can vary, it is generally fatal in untreated animals.
The cause of PDD is unknown, but several studies have raised the possibility that PDD may be caused by a viral pathogen. Evidence for an infectious etiology stems from the initial outbreaks of Macaw Wasting Disease, and other subsequent outbreaks of PDD. Reports of pleomorphic virus-like particles of variable size (30–250 nm) observed in tissues of PDD affected birds led to the proposal that paramyxovirus (PMV) may cause the disease; however, serological data has shown that PDD affected birds lack detectable antibodies against PMV of serotypes 1–4, 6, and 7, as well as against avian herpes viruses, polyomavirus, and avian encephalitis virus. Similarly, a proposed role for equine encephalitis virus in PDD has been ruled out. Enveloped virus-like particles of approximately 80 nm in diameter derived from the feces of affected birds have been shown to produce cytopathic effect in monolayers of macaw embryonic cells, but to date no reports confirming these results or identifying this possible agent have been published. Likewise, adeno-like viruses, enteroviruses, coronaviruses and reoviruses have also been sporadically documented in tissues or excretions of affected birds yet in each case, follow-up evidence for reproducible isolation specifically from PDD cases or identification of these candidate agents has not been reported. Thus, the etiology of PDD has remained an open question.
To address this question, we have turned to a comprehensive, high throughput strategy to test for the presence of known or novel viruses in PDD affected birds. We employed the Virus chip, a DNA microarray containing representation of all viral taxonomy to interrogate 2 PDD case/control series independently collected on two different continents for the presence of viral pathogens. We report here the detection of a novel bornavirus signature in 62.5% of the PDD cases and none of the controls. These bornavirus-positive samples were confirmed by virus-specific PCR testing, and the complete genome sequence has been recovered by ultra-high throughput sequencing combined with conventional PCR-based cloning.
Bornaviruses are a family of negative strand RNA viruses whose prototype member is Borna Disease Virus (BDV), an agent of encephalitis whose natural reservoir is primarily horses and sheep. Although experimental transmission of BDV to many species (including chicks) has been described, there is little information on natural avian infection, and existing BDV isolates are remarkable for their relative sequence homogeneity. The agent reported here, which we designate avian bornavirus (ABV) is highly diverged from all previously identified members of the Bornaviridae family and represents the first full-length bornavirus genome cloned directly from avian tissue. Subsequent PCR screening for similar ABVs confirmed a detection rate of approximately 70% among PDD cases and none among the controls. Sequence analysis of a single complete genome and all of the additional partial sequences that we have recovered directly from the PDD case specimens suggests that the viruses detected in cases of PDD form a new, genetically diverse clade of the Bornaviridae.
A case was defined as a staff member working at the NTNAMC who was hospitalized for respiratory tract infection between November 1 and November 30, 2012, and confirmed to have C. psittaci infection by polymerase chain reaction (PCR) and/or a four-fold rise in serum microimmunofluorescent antibody titer against C. psittaci (Focus Diagnostics, Cypress, California, USA).
Vesicular stomatitis is a viral disease which primarily affects cattle, horses, and swine. It occurs in enzootic and epizootic forms in the tropical and subtropical areas. The disease is rarely life-threatening but can have a significant financial impact on the horse industry. Vesicular stomatitis virus (VSV) is the prototype of the genus Vesiculovirus in family Rhabdoviridae. The virus has two serologically distinct serotypes, VSV-New Jersey (NJ) and VSV-Indiana (IND). The neutralizing antibodies generated by these two serotypes are not cross-reactive. The IND serogroup has three subtypes IND-1 (classical IND) IND-2 (cocal virus) and IND-3 (alagoas virus) The virus is endemic in South America, Central America, Southern Mexico, Venezuela, Colombia, Ecuador and Peru but the disease has been reported in South Africa in 1886 and 1897 and France in years 1915 and 1917.
The disease has been reported across continents in Belize, Bolivia, Brazil, Colombia, Costa Rica, Ecuador, El Salvador, Guatemala, Honduras, Mexico, Nicaragua, Pakistan, Panama, Peru, USA and Venezuela [91, 92]. Outbreaks historically occurred in all regions of the USA but have been limited to western states in 1995, 1997, 1998, 2004, 2005, 2006, 2009, 2010, and 2012 [93, 94]. While VS has been reported in horses at about 800 premises in eight states. VSV spread to Europe during the First World War and periodically appears in South Africa. The Chandipura virus, a Vesiculovirus caused encephalitis outbreaks in different states of India leading to mortalities in children. Isfahan another virus in this genus is endemic in Iran [89, 97]. The countries with incidence/serological evidence of vesicular stomatitis are presented in Fig. (2).
Clinical disease has been observed in cattle, horses, pigs and camels whereas sheep, goats and llamas tend to be resistant. White-tailed deer and numerous species of small mammals in the tropics are considered as wild hosts. Many species, including cervids, nonhuman primates, rodents, birds, dogs, antelope, and bats have shown serological evidence of infection. Experimentally different animals like mice, rats, guinea-pig, deer, raccoons, bobcats, and monkeys can be infected.
The virus is zoonotic and causes flu-like symptoms characterized by fever, chills, nausea, vomiting, headache, retrobulbar pain, myalgia, sub-sternal pain, malaise, pharyngitis, conjunctivitis, and lymphadenitis in humans. Vesicular lesions may be present in the pharynx, buccal mucosa, or tongue. Encephalitis is rare but may occur in children [107, 108].
The transmission is more likely by trans-cutaneous or transmucosal route. The virus can be transmitted through direct contact with infected animals having lesions of the disease or by blood-feeding insects. In endemic areas, Lutzomyia sp. (sand fly) is proven biologic vectors. Black flies (Simulidae) are the most likely biologic insect vector in USA. Other insects may also act as mechanical vectors. Saliva, exudates and epithelium from open vesicles are sources of virus. Plants and soil are also suspected as the source of virus.
Horses of all ages appear equally susceptible but lesions do not appear in all susceptible horses. The lesions of the disease resemble foot-and-mouth disease in cattle and the other viral vesicular diseases in pigs. The horses are resistant to foot and mouth disease and susceptible to VS. VSV is the only viral vesicular disease of livestock that infects horses. VSV is also the most important of these four viruses as a zoonotic agent for humans. When vesicular stomatitis occurs in horses, blanched raised or broken vesicles or blister-like lesions develop on the tongue, mouth lining, nose and lips. In some cases, lesions also develop on the udder or sheath or the coronary bands of horses. Animals may become anorectic, lethargic and have pyrexia. One of the most obvious clinical signs is drooling of saliva or frothing at the mouth. The rupture of the blisters creates painful ulcers in the mouth. The surface of the tongue may slough. Excessive salivation is often mistaken as a dental problem or colic. There may be weight loss due to mouth ulcers as animal finds it too painful to eat. The lesions around the coronary band may cause lameness and laminitis. In severe cases, the lesions on the coronary band may cause the hoof to slough. Animals usually recover completely within two weeks. Morbidity rates vary between 5 and 70% but mortality is rare. Vesicular stomatitis like disease disabled 4000 horses during the Civil War in 1862. Major epidemics in the US occurred in 1889, 1906, 1916, 1926, 1937, 1949, 1963, 1982, and 1995, with minor outbreaks during many other years. No specific treatment is available for the disease. Anti-inflammatory medications as supportive care help to minimize swelling and pain. Dressing the lesions with mild antiseptics may help avoid secondary bacterial infections. If fever, swelling, inflammation or pus develops around the sores, treatment with antibiotics may be required. The animals should be quarantined at least for 21 days after recovery of the last case before moving to other places. Vaccines for livestock are available in some Latin American countries.
Some populations of geese and swans in Europe and North America have undergone dramatic growth during recent decades and they are now larger than any time in known history.[1,2] At the same time, outside the breeding season these birds have increasingly abandoned their natural foraging habitats in favour of croplands, meadows and turfs. This and a generally reduced level of fearfulness have resulted in there now being more geese, close to more people, than ever before over large and densely populated areas in the Northern Hemisphere. This, in turn, has sparked conflicts with respect to crop damage, bird strikes at airports, fouling of drinking and recreational waters, eutrophication of wetlands, and degradation of natural vegetation. Although there are well-described local cases for most of these conflicts, their prevalence and consequences over larger spatial and temporal scales have only recently been reviewed comprehensively and critically.[3–5]
A recurring issue in this context is geese and other waterfowl as sources of infections (e.g.). This is true for agriculture and food production, but also for human health via transmission of zoonotic diseases. Interestingly, this is a rather recent concern, illustrated by it not even being mentioned in the influential monograph Man and Wildfowl by Janet Kear that was published in 1990. Still, such worries are understandable, as it is commonplace to observe large flocks of geese and swans grazing and defecating in pastures and in fields producing food for livestock and humans. This behaviour brings these birds physically close to livestock during parts of the year, sometimes also close to poultry. Another concern is that large goose flocks for prolonged periods roost on lakes and wetlands where livestock drink and humans extract drinking water and swim. On top of this, most goose populations are highly mobile, on a daily as well as a seasonal basis, making them potential disease vectors at short and medium spatial scales. Most species and populations are migratory, in many cases performing long-distance migration from tundra and high boreal areas in N and NE Europe, to wintering areas in W and C Europe. Consequently, geese and swans comprise an excellent model to study aspects of zoonotic diseases and disease transmission between wild and domestic animals. In this review, we apply a One Health perspective to tackle this question, reflecting the multifaceted disciplines involved in the study of diseases shared by several species.
The aim of the One Health initiative is to create common ground for several disciplines in order to establish more holistic approaches to diseases shared by more than one species. Several major organizations, such as the World Health Organization (WHO), Food and Agriculture Organization of the United Nations (FAO), and World Organisation for Animal Health (OIE), are proponents of One Health, and the central disciplines are human medicine, veterinary medicine, and biology. The One Health approach in the present paper is to combine findings about diseases and disease transmission in veterinary and human medicine with insights from ecology and management of waterfowl.
The overall number of pathogens found in wildlife is staggering, and so is the scientific literature on the topic. Partly as a consequence of this, most textbooks and reviews provide information with insufficient detail for practical management of more restricted taxonomic groups and geographical areas (e.g.), for example in goose management in Europe. Another challenge is the rapid development of disease surveillance technologies, such as sequence and genome-based methods for detection and characterization of pathogenic microorganisms. Importantly, these methods open new avenues to differentiate between strains of pathogens, and thus to understand disease dynamics and effects better. Such information needs to be condensed and synthesized and put in more lucid writing before it can be used by managers and decision-makers.
Rapidly increasing goose numbers, goose–man conflicts, and increased knowledge about pathogens together call for an up-to-date review of the role of geese and swans as reservoirs, spill-over hosts and vectors of pathogens of known or suspected zoonotic potential. Wild herbivorous waterfowl can act both as biological vectors, i.e. harbouring an active infection where the pathogen develops and multiplies, and as mechanical vectors (containers, dispersers), i.e. physically dispersing pathogens from one site to another without being essential to the life cycle of the pathogen. Here we provide a comprehensive review of the scientific literature on the likely risk of disease transmission from wild herbivorous geese and swans to livestock, poultry and humans. We also discuss the implications of these patterns and identify knowledge gaps for management of and research about these birds and their habitats.
Increasing morbidity from zoonoses is a significant problem in terms of global health, and they are currently considered exotic in Europe. Zoonoses are infectious or parasitic diseases transmitted by animals to humans (Spahr et al. 2018). These infections as aetiological factors can develop in humans in several ways:
by the digestive tract, where the microorganism gets into the body via infected feed (meat) or water, which is quite often in large-scale farming. Therefore, Escherichia and Salmonella transmission to people occurs mainly through ingestion or frequent contact with infected birds. The above microorganisms can live in the external environment for a long period of time without damage to the pathogenic properties.by skin laceration; a break in the continuity of the skin promotes infection by pathogens of the staphylococci and streptococci families. In addition, the infection is intensified by the release of toxins into the host system.by the respiratory system (by inhalation of dust in which the pathogens are raised); infection occurs through direct contact of a healthy individual with contaminated excretion or through indirect contact (low hygiene at the slaughterhouse) with contaminated faeces and secretion on bird feathers (Hugh-Jones and de Vos 2002).
Humans are more susceptible to zoonoses carried by mammals than birds, and they share more diseases with them. This sharing is due to a higher degree of similarity between the intracellular environment of mammals (to which they belong), rather than birds. Many microorganisms need proper conditions and parameters to determine their host, for example, the presence of its receptor on the surface of the cells. These receptors can serve as a site for attachment and penetration into cells, which provides a pathway for the development of infection. The above situation determines the susceptibility of one animal species to a pathogen and resistance of another species. Vectors, such as insects, are also involved in the transmission of various pathogens, which may have an effect on the immune system. In the case of infecting a human with an avian zoonosis, the course of the disease is usually severe with general life-threatening symptoms. People who have been infected with an avian zoonosis require in-hospital treatment in isolation. Avian zoonoses in humans may end in death or a chronic disease requiring prolonged administration of antibiotics (Hugh-Jones and de Vos 2002).
Hence, the aim of this work is to present the aetiological factors of bird zoonoses, which are currently the most threatening to the European population. In addition, the epidemiological and economic analysis of the above infections in humans is presented. In general, zoonoses from birds can be divided by the type of the infectious agent: bacterial, viral and fungal.
Eastern equine encephalitis (EEE) commonly called triple E or, sleeping sickness is a rare but serious viral disease affecting horses and man. The disease is transmitted through mosquitoes and man and horses are dead-end hosts.
EEEV belongs to the genus Alphavirus of the family Togaviridae. It is closely related to Venezuelan equine encephalitis (VEE) virus and Western equine encephalitis (WEE) virus. This virus has North American and South American variants. The North American variant is more pathogenic. EEE is capable of infecting a wide range of animals including mammals, birds, reptiles and amphibians. The virus has been reported to cause disease in poultry, game birds and ratites. The disease has also been reported to occur in cattle, sheep, pigs, deer, and dogs though sporadically. The disease is present in North, Central and South America and the Caribbean. EEE was first recognized in the USA in 1831 from an outbreak where 75 horses died of encephalitic illness and EEE virus (EEEV) was first isolated from infection horse brain in 1933. The serological evidence and outbreaks of the disease have also been reported from horses in Canada and Brazil [119, 120]. Countries with incidence/serological evidence are presented in Fig. (3). EEEV infection in horses is often fatal. The human cases were identified first time in 1938 in the north-eastern United States. Thirty children died of encephalitis in this outbreak. The fatality rate in humans was 35%. The outbreaks of the disease also occurred in horses simultaneously in the same regions. A total of 19 human cases of the disease were reported in children between 1970-2010 in Massachusetts and New Hampshire. As per the CDC reports 220 confirmed human cases of the disease occurred in the U.S. from 1964 to 2004. In 2007, a citizen of Livingston, West Lothian, Scotland became the first European victim of this disease after infected with EEEV from New Hampshire. EEE has been diagnosed in Canada, the United States of America (USA), the Caribbean Islands and Mexico [122, 123]. Eighteen cases of Eastern equine encephalomyelitis occurred in six Brazilian states between 2005 and 2009.
Alternate infection of birds and mosquitoes maintains these viruses in nature. Culiseta melanura and Cs. morsitans species are primarily involved. Transmission of EEEV to mammals occurs via other mosquitoes which are primarily mammalian feeders and called as bridge vectors. Infected mammals do not circulate enough viruses in their blood to infect additional mosquitoes. The virus is introduced by mosquitoes, but feather picking and cannibalism also contribute towards the transmission of the disease within the flocks. Most people bitten by an infected mosquito do not develop any symptoms. The symptoms generally appear 3 to 10 days after the bite of an infected mosquito. The clinically affected patients may have pyrexia, muscle pains, headache, photophobia, and seizures. EEEV is one of the potential biological weapons. The disease in horses is characterized by fever, anorexia, and severe depression. Symptoms appear one to three weeks post-infection, and begin with a fever that may be as high as 106ºF. The fever usually lasts for 24–48 hours. In severe cases, the disease in horses progresses to hyper-excitability, blindness, ataxia, severe mental depression, recumbency, convulsions, and death. The nervous symptoms may appear due to brain lesions. This may be followed by paralysis, causing the horse to have difficulty raising its head. The horses usually suffer complete paralysis and die two to four days after symptoms appear. Mortality rates among horses range from 70 to 90%.
There is no cure for EEE. Severe illnesses are treated by supportive therapy consisting of corticosteroids, anticonvulsants, intravenous fluids, tracheal intubation, and antipyretics. Vaccines containing killed virus are used for prevention of the disease. These vaccinations are usually given as combination vaccines, most commonly with WEE, VEE, and tetanus. Elimination of mosquito breeding sites and use of insect repellents may help in control of the disease.
A novel avian-origin influenza A (H7N9) virus has caused severe disease in humans in China since February 2013. The high number of new cases within a short period and the high-case death rate have caused public panic and attracted global attention. Some patient's families undertook large medical costs. According to the literature, exposure to live poultry could be an important risk factor for human infection with H7N9.1–5 As a result, closing down the live poultry markets and slaughtering the poultry were the main interventional measures in the affected areas of China. These interventions not only played an important role in disease prevention but also caused serious losses to the poultry industry.
The introduction of the novel virus led to numerous investigations of its origin, its genes, clinical symptoms, laboratory testing, treatment and transmission6–8; however, the burden of human infection with H7N9 has not yet been measured. It is important to estimate the overall burden of disease (BOD) due to H7N9 in China because this virus is new to humans and could cause a global pandemic in the future. The Global Burden of Disease (GBD) 2010 study presents a comprehensive methodological framework for death and disability loss estimation and has had a pronounced impact on the BOD estimate.9
10 In this study, we identified the main drivers of economic loss and summarised the direct and indirect costs of human H7N9 infection. We present an accurate and operable approach for estimating the overall burden of emerging infectious diseases and provide evidence on the cost-effectiveness of H7N9 prevention and control. We also set up a BOD estimate example for any animal-borne infectious disease, particularly with the introduction of modern medical devices.
The evolution of emerging diseases is associated with factors embedded in the concept “host-agent-environment triangle” (1). To infect the host and cause disease, the pathogen needs to evade host defenses, which may occur through single point mutations, genome rearrangements, recombination and/or translocation (2). Genetic uniformity generated through genetic selection of the host (3) and the fact that demographic changes, intensification of farming, and international commerce have occurred markedly over the last decades, must be also considered as essential factors for the development of emerging diseases (4–6).
As well as in humans, emerging diseases drastically affect animal populations, especially food-producing animals. Livestock production in large communities (i.e., pig farms or poultry flocks) represents an excellent environment to facilitate the transmission and maintenance of huge viral populations, contributing to the pathogen evolution (through mutation, recombination and reassortment, followed by natural selection) (7–9). The intensification of livestock during the last four decades has probably been one of the main factors that contributed to the emergence of new pathogens and/or pathogen variants, leading to changes in the epidemiology and presentation of diseases (10).
The number of viral infectious diseases in swine has significantly increased in the last 30 years. Several important worldwide distributed viruses have been reported in this period, including Porcine reproductive and respiratory syndrome virus (PRRSV, family Arteriviridae), Porcine circovirus 2 (PCV-2, family Circoviridae) and Porcine epidemic diarrhea virus (PEDV, family Coronaviridae). In addition to those worldwide widespread viruses, an important number of novel swine pathogens causing different types of diseases has been described (11, 12). Although their economic impact might be variable, they are considered significant infection agents and their monitoring is nowadays performed in some parts of the world. Among others, relevant examples are Porcine deltacoronavirus (associated with diarrhea) (12), Senecavirus A (causing a vesicular disease and increased pre-weaning mortality) (11), Porcine sapelovirus (found in cases of polioencephalomyelitis) (13), Porcine orthoreovirus (assumed to cause diarrhea) (14), Atypical porcine pestivirus (cause of congenital tremors type II) (15) and HKU2-related coronavirus of bat origin (associated with a fatal swine acute diarrhea syndrome) (16).
Besides overt emerging diseases of swine, many other novel infectious agents have been detected in both healthy and diseased animals, and their importance is under discussion. This group of agents is mainly represented by Torque teno sus viruses, Porcine bocavirus, Porcine torovirus and Porcine kobuvirus, which are thought to cause subclinical infections with no defined impact on production (13, 17, 18). An exception may be represented by Hepatitis E virus (HEV); although it seems fairly innocuous for pigs, it is considered an important zoonotic agent (19, 20). Recently, a novel member of the Circoviridae family named Porcine circovirus 3 (PCV- 3), with unknown effects on pigs, has been discovered (21, 22).
Porcine circovirus 3 (PCV-3) was first described in 2015 in North Carolina (USA) in a farm that experienced increased mortality and a decrease in the conception rate (21). Sows presented clinical signs compatible with porcine dermatitis and nephropathy syndrome (PDNS) and reproductive failure. In order to identify the etiological pathogen, aborted fetuses and organs from the affected sows were collected for further analyses. Whilst histological results were consistent with PCV-2-systemic disease, both immunohistochemistry (IHC) and quantitative PCR (qPCR) methods to detect PCV-2 yielded negative results. Samples were also negative for PRRSV and Influenza A virus. Homogenized tissues from sows with PDNS-like lesions and three fetuses were tested through metagenomic analysis, revealing the presence of an uncharacterized virus (21). Further analyses using rolling circle amplification (RCA) followed by Sanger sequencing showed a circular genome of 2,000 nucleotides. Palinski et al. (21) also performed a brief retrospective study through qPCR on serum samples from animals clinically affected by PDNS-like lesions (but negative for PCV-2 by IHC) and pigs with porcine respiratory diseases. Results revealed PCV-3 qPCR positivity in 93.75 and 12.5% of the analyzed samples, respectively (21).
Interestingly, almost concomitantly, another research group from the USA reported a clinical picture pathologically characterized by multi-systemic and cardiac inflammation of unknown etiology in three pigs of different ages ranging between 3 and 9 week-old (22). Several tissues from these animals were tested by next-generation sequencing (NGS) methods and PCV-3 genome was found. Beyond NGS, in situ hybridization was performed in one out of these three pigs, confirming PCV-3 mRNA in the myocardium (cytoplasm of myocardiocytes and inflammatory cells mainly, although to a very low frequency).
Based on these two initial works, the name PCV-3 was proposed as the third species of circoviruses affecting pigs, since pairwise analysis demonstrated significant divergence with the existing PCVs. The novel sequences showed < 70% of identity in the predicted whole genome and capsid protein amino acid (aa) sequence compared to the other members of the Circovirus genus (22). Taking into account the economic importance and the well-known effects of PCV-2 on the swine industry, a new member of the same family like PCV-3 should not be neglected. Studies on epidemiology, pathogenesis, immunity and diagnosis are guaranteed in the next few years, but the scientific community is still in its very beginning on the knowledge of this new infectious agent. Therefore, the objective of the present review is to update the current knowledge and forecast future trends on PCV-3.
The confirmed human H7N9 infections were divided into mild and severe cases based on the ‘Diagnostic and treatment protocol for human infections with avian influenza A (H7N9) (2nd edition, 2013)’.11 Mild cases presented with influenza-like illness, whereas severe cases developed quickly and presented with severe pneumonia, usually accompanied by severe complications and organ failure. Severe illness was divided into ‘severe without death’ and ‘severe with death’. The 11 H7N9 cases of unknown status were classified as ‘unknown without death’.
Pigeon circovirus (PiCV) is classified in the genus Circovirus of the Circoviridae family. It is a small non-enveloped single-stranded circular DNA virus with approximately 2030 base pairs (bp) ambisense genome. The genome of PiCV contains at least two major open reading frames (ORFs). Located on the virion sense strand ORF, V1, encodes the replicase protein (Rep protein) which is involved in rolling circle PiCV DNA replication. Located on the complementary sense strand ORF, C1, encodes the viral capsid protein (Cap protein, CP) [1, 2]. The CP of circoviruses has been documented to exhibit antigenic properties, as confirmed in the case of porcine circovirus genotype 2 (PCV2), psittacine circovirus, and pigeon circovirus [3–5].
Like other circoviruses, PiCV is an immunosuppressive factor. Infection with this virus leads to the atrophy of the immune system organs and to lymphocyte apoptosis [6–8]. Pigeons immunosuppressed by PiCV infection are predisposed to concomitant infections with other viruses (pigeon herpesvirus) or bacteria, like Escherichia (E.) coli and Chlamydia (C.) psittaci [9–11]. The combination of various immunosuppressive factors (PiCV infection and stress associated with trainings and racing of young pigeons) with accompanying infections leads to a clinical complex disease called young pigeon disease syndrome (YPDS) [9, 12, 13]. The type and intensity of clinical symptoms of YPDS are correlated with the type of the confounding factor. Initial symptoms are relatively non-specific, but after 2–3 days increased thirst and regurgitation from the crop is usually noticed. Crops are often filled with large volumes of water combined with mucus and refluxed duodenal contents. Other symptoms include diarrhea, apathy, feather ruffling or reluctance to training. Those birds are disqualified from racing. For the reason of a very high global prevalence of PiCV infections approximating 70%, the YPDS is currently the biggest health issue in pigeon breeding [10, 12, 14, 15]. The global spreading of PiCV infections in pigeon population is probably due to pigeon racing and intercontinental trade.
The asymptomatic infections with this virus are quite common and approximate 40% [10, 16–19]. Their high prevalence in reproductive pigeons poses problems with disease control. The laboratory diagnosis is limited only to screening for PiCV genetic material with molecular methods. The possibility of detecting anti-PiCV antibodies in subclinically infected pigeons has been described as well. Because the laboratory culture of PiCV has so far proved unsuccessful, a scientific project was designed to develop an alternative method for obtaining an antigen which is recombinant capsid protein of pigeon circovirus (PiCV rCP). This protein could be used as an antigen in a sub-unit vaccine against this virus. A previous study has revealed PiCV rCP to be immunogenic to pigeons and to stimulate both cell-mediated and humoral immunity. Due to high prevalence of PiCV asymptomatic infections [18, 19], it is very likely that the subclinically infected pigeons will be vaccinated in practice. Bearing in mind the potential immunosuppressive effect of PiCV, it is important to compare the immune response to PiCV rCP in pigeons asymptomatically infected with PiCV (natural infection) to that in the uninfected pigeons, before the protectivity of the vaccine is tested. The aim of this study was, therefore, to answer a question if subclinically infected with PiCV pigeons would develop a similar immune response to PiCV rCP to that developed by the uninfected birds.
Viruses are obligatory cellular parasites, developing with their hosts since the dawn of life. Coevolution, when the virus and the host reciprocally affect each other’s evolution, is often detected. According to the Red Queen Hypothesis, both the parasite and the host are perpetually struggling to maintain a constant fitness level (McLaughlin and Malik 2017). This long-term evolutionary pressure gave rise to some surprising consequences for the entire tree of life.
With all the probabilities calculated already, we can calculate the total probability of entry of the disease j from the country i to the European Union, taking into account all the routes of entry already evaluated(PIij).
To do this, we calculate the probability of occurrence of the opposite case, the probability of no introduction of the j disease by any of the routes of entry, using the following formula:
With the same type of formula, it is estimated the likelihood of entry of a disease j in the European Union.
A high, moderate and low risk of introduction of infectious diseases from different countries has been estimated based on a 75 and 90-percentile (P75 and P90) over the final results of probability of each route of entry. Therefore, the results that are over the 75-percentile and 90-percentile are classified as moderate and high risk of entry.
Avian species serve as hosts for a diversity of viruses that pose both biosecurity and zoonotic risks. Numerous outbreaks of disease in collections of caged birds and commercial domestic poultry have been attributed to viruses introduced by direct or indirect contact with wild birds [1–7]. Some avian viruses can also cause disease in humans [8–14]. As such, understanding the viruses present in wild birds is important for managing potential risks to human and animal health, and for understanding the biology of these viruses in their natural hosts. Studying viruses in wild birds can be challenging as gaining access to these birds for the purpose of sample collection can be difficult, and their capture may be a cause of stress or injury. Collecting and testing samples from avian patients presenting to veterinary hospitals can be a convenient and useful approach to detecting and studying avian viruses. Importantly this approach does not involve additional capturing or handling of birds, and allows the risks to staff and other avian patients/collections within the facility to be more accurately assessed, since the species from which the samples are collected reflects the species being handled at the participating facility. This approach has been successful in previous studies utilizing veterinary hospitals and wildlife rescue centres in several countries including Australia, the United Kingdom, France and Belgium [15–18].
In Australia, the Australian Wildlife Health Centre (AWHC) at Zoos Victoria’s Healesville Sanctuary functions as a large primary care and referral centre for sick, injured and orphaned native wildlife, including providing veterinary care for approximately 700–900 wild birds each year, as well as Healesville Sanctuary’s collection of captive animals. Patients may be presented to the AWHC by members of the public, wildlife carers, keepers, government wildlife officers or by referral from other veterinary clinics for veterinary diagnosis and treatment. During this period in captivity there is an elevated risk of stress-induced shedding of pathogens, presenting a risk for both the veterinary staff and other animals in care, including the Sanctuary’s collection animals and captive breeding programs. Close contact between infected and susceptible animals can facilitate the transmission of pathogens between species, particularly when the hosts are taxonomically related. The large number of avian patients passing through the AWHC provides an opportunity to study the viruses present in Australian birds and better understand the potential risks these viruses present.
Of particular importance and conservation value at Healesville Sanctuary are the captive breeding and insurance programs for threatened species. This includes a captive breeding program for the critically endangered orange-bellied parrot (Neophema chrysogaster), which is facing imminent extinction in the wild. The orange-bellied parrot is arguably the most threatened parrot species in the world, with the wild-bred population declining to only three females and 13 male birds in the 2016/2017 breeding season. Infectious diseases, including viral diseases, are a recognized threat to this and other threatened bird species both within Australia and around the world. Beak and feather disease virus (BFDV), a circovirus, is of particular concern. Our past work has shown that BFDV is prevalent in both psittacine and non-psittacine birds presenting to the AWHC, and has revealed that non-psittacine birds may represent a previously unrecognized risk for spreading BFDV infection. Other viruses are also a potential threat to Psittaciformes in Australia. Psittacid alphaherpesvirus 1 (PsHV1) is the aetiologic agent of both Pacheco’s disease and mucosal papillomas in Psittaciformes. PsHV1 has not been reported in wild Psittaciformes in Australia, but has been detected in Australia in captive green-winged macaws (Ara chloropterus) imported from the United Kingdom in the 1990s [23, 24]. It is not known how far the virus has been transmitted from these birds but it is likely to be present in at least some avicultural collections in Australia. The inadvertent introduction of such a virus into the remaining population of a threatened avian species, such as through the Neophema chrysogaster recovery program, would be potentially devastating. Avian paramyxoviruses (APMVs) also pose a threat to Australian Psittaciformes. Avian avulavirus 3 (previously avian paryamyxovirus serotype 3, APMV-3) has been documented causing mortality rates of up to 70% in captive collections of Neophema species and other Australian psittacines overseas [25–28]. APMV-3 strains have been isolated from a diversity of avian species in different parts of the world, but has not yet been reported in Australia [25–31]. However we do know that the Australian parrot genus Neophema is highly susceptible to APMV-3, with infection frequently resulting in fatal neurological disease [26, 28]. Another avian paramyxovirus, Avian avulavirus 5 (avian paramyxovirus 5, APMV-5) has caused outbreaks of severe disease with up to 100% mortality in captive budgerigars (Melopsittacus undulatus), including an outbreak in a captive budgerigar flock in Queensland in 1972 [25, 32–34].
Few avian viruses represent a risk to veterinary staff and others handling birds, but avian influenza viruses (AIVs) can threaten human health [8, 9, 11–13]. Wild birds, particularly waterfowl, waders and sea birds, are the natural reservoirs of low pathogenicity avian influenza (LPAI) viruses and play important roles in the circulation of AIVs [35–38], with potential for transmission of AIVs both to and from poultry and the potential for mutation to generate highly pathogenic avian influenza (HPAI) viruses [6, 7, 39]. Some AIVs can be transmitted from poultry to humans, and some have caused severe disease or even death in humans [8, 9, 11–13, 40, 41]. Transmission of AIVs from wild birds to commercial poultry has occurred recently in Australia in Victoria, New South Wales and Queensland [10, 42–45]. The Australian National Avian Influenza Wild Bird Surveillance Program has been in place since 2006 but primarily targets Anseriformes (ducks, swans, geese) and Charadriiformes (gulls, terns and shorebirds) [46, 47]. The prevalence of AIV infection in birds presenting to veterinary care facilities, such as the AWHC, has not been as comprehensively studied. In Australia, avian coronaviruses (AvCoVs) are also of particular interest in wild birds because of the presence of variant forms of the poultry pathogen infectious bronchitis virus (IBV) in Australian commercial poultry [48–50]. It is suspected that the variant IBV strains contain genetic material derived from AvCoVs hosted by wild birds, but this requires further investigation.
This study aimed to collect samples from birds presenting to the AWHC and use them for the molecular detection and characterization of viruses with potential significance to biosecurity, human health or animal health. Four virus families were targeted in this study: avian influenza viruses, herpesviruses, paramyxoviruses and coronaviruses. Samples were screened using a combination of genus- or family-wide polymerase chain reaction methods coupled with sequencing and phylogenetic analyses for detection and identification of both known and novel viruses. Two novel viruses were detected in this study, hence contributing to our knowledge of avian virodiversity, while the overall low level of virus detection adds to our understanding about the presence or absence of viruses of birds in Australia and their potential risk to avian and human health.
In 2008, avian bornavirus (ABV) was discovered to be the causative agent of Parrot bornavirus syndrome (PaBVs), formerly known as macaw wasting disease, proventricular dilatation disease or PDD, enteric ganglioneuritis and encephalitis, and avian ganglioneuritis.1–3 Since then, multiple ABV genotypes have been recognized in over 80 different species such as psittaciformes, passeriformes, and waterfowls.4 Diagnosis of PaBVs includes clinical signs and radiological changes, detection of viral antigen, viral RNA or ABV antibodies, gross pathology, and histopatholgy.5–8 Sampling for histopathology and tissue immunoassays, especially of nervous tissues, is not practical in living birds, thus these tests are more commonly used in post-mortem diagnosis. Reverse transcriptase polymerase chain reaction (RT-PCR) can utilize less invasive samples such as feather follicles, feces/urine, and cloacal swabs,5,7,9–13 however sensitivity will vary due to intermittent viral shedding.13–15
Immunologic testing comparing ABV specific antigens found that the viral nucleoprotein is immunodominant and hence the best antigen to use in a microtiter plate ELISA and in fluorescent antibody assays.9,16 A mixed anti-avian species IgY secondary antibody is often used in ABV serologic tests.8,9,17–20 The anti-bird secondary antibody, produced in goats using immunoglobulins from the White-crowned sparrow, Ringed turtle dove, domestic chicken, and Muscovy duck,a has been used in other ELISAs for the detection of arboviruses, flaviviruses, alpha-viruses, and poxviruses.21–24 The advantage of an anti-bird secondary antibody is the range of species that can be tested. This anti-bird secondary antibody has been used in serologic tests for the detection of antibodies in psittacine birds, even though the immunogen used to stimulate this secondary antibody did not contain antibodies from psittaciformes. Anti-passerine IgY secondary antibody produces better results than the anti-bird IgY secondary antibody or the anti-chicken IgY secondary antibody for serologic assays on passerine birds.25 This suggests that species-specific secondary antibodies may provide more sensitive results in immunologic assays than commercially available mixed species anti-bird secondary antibody. In assays that employ short antigen-antibody incubation times, such as dot-blot or lateral flow ELISAs, a species-specific secondary antibody may be more useful when testing psittacine birds. Additionally due to the large variety of avian species susceptible to ABV infection, a low affinity of the secondary antibody could result in erroneous test results. The goal of this study was to evaluate the specificity of different avian secondary antibodies used in Western blot and dot-blot ELISA to detect ABV antibodies in the plasma of Blue and gold macaw (Ara ararauna), Cockatiel (Nymphicus hollandicus), Monk parakeet (Myiopsitta monachus), and Mallard (Anas platyrhynchos).
Coronaviruses (CoVs) are enveloped, single-stranded, positive-sense RNA viruses that can infect and cause diseases in avian and mammal species, including humans. CoVs contain the largest known RNA genomes and can be genetically divided into four genera; namely, Alphacoronavirus, Betacoronavirus, Gammacoronavirus, and Deltacoronavirus. Deltacoronavirus (DCoV) genus was mainly discovered in a variety of avian species and pigs. Porcine DCoV (PDCoV) was first detected in pigs during a molecular surveillance of CoVs in mammals and birds in Hong Kong in 2012, while the first PDCoV outbreak in swine herds was reported in 2014 in the United States. Thereafter, PDCoV was rapidly identified in many countries, including China, Canada, South Korea, Lao People’s Democratic Republic, Thailand, and Vietnam. PDCoV can cause severe diarrhoea, vomiting, and dehydration in suckling and nursing piglets, and the clinical symptoms are indistinguishable from those caused by porcine epidemic diarrhoea virus (PEDV) and transmissible gastroenteritis virus (TGEV). PDCoV has caused serious economic losses for the pig industries. However, there are no effective reagents and vaccines to control PDCoV.
The host range of CoVs is expanding from wildlife to humans; generally, mammals are thought to be the host for Alphacoronavirus and Betacoronavirus, while avian is considered to be the host for Gammacoronavirus and DCoV. Some CoVs can be transmitted to different animal species, and subsequently adapt to the new host, even to humans. Examples include the severe acute respiratory syndrome CoV (SARS-CoV) and middle east respiratory syndrome CoV (MERS-CoV), which were transmitted by civet cats and camels, respectively, to humans, and caused great harm to humans. The novel swine acute diarrhoea syndrome coronavirus (SADS-CoV) was also verified to be a bat-related CoV that was 98.48% identical in genome sequence to the bat HKU2-CoV, which originated from the same genus of horseshoe bats as SARS-CoV. However, little was known about the natural reservoir of these CoVs. DCoVs have been mainly found in wild birds in early research, but recent findings suggested that DCoVs are also present in mammals. With the detection of PDCoV in pig herds, it was confirmed that PDCoV had a close relation to birds’ DCoV, especially with sparrow CoV HKU17, which suggested there might exist bird-to-mammal transmission of PDCoV. Meanwhile, DCoVs were detected previously in some small wild mammals, such as Asian leopard cats and Chinese ferret badgers. The S genes of the DCoVs isolated from these mammals were closely related to those of PDCoV identified in pigs, with the nucleotide similarity over 99.8%. On the basis of these findings, we deduce that the potential interspecies transmission of PDCoV may exist between these wild small mammals and pigs, as well as between domestic pigs and birds/avian.
To date, the origin of the novel PDCoV is still unknown. It was reported that PDCoV can infect 3- to 7-day-old gnotobiotic (Gn) calves with a high level of viral RNA titer in feces and specific IgG antibody in sera, but did not show any clinical symptoms and histological lesions. Recently reports showed that PDCoV could infect human and chicken cells in vitro, indicating that PDCoV has the potential to infect chickens and humans to some extent. Given the broad host ranges of PDCoV, we speculate that PDCoV may infect other mammalian and avian species.
Whether the PDCoV really has the ability to infect chickens in vivo, and the exact mechanisms of the interspecies transmission and the pathogenicity of this novel virus, is largely unknown. Thus, in our study, the chicken embryos and specific pathogen free (SPF) chickens were used to evaluate the PDCoV infection. Our data indicated that PDCoV can infect three lines of chicken embryos, including White-feather Broiler, Hyline Layer, and SPF chicken embryos, and PDCoV can be passaged on these chicken embryos. Furthermore, we investigated the susceptibility of chickens to PDCoV infection. The PDCoV-inoculated chickens showed mild diarrhea symptoms; positive PDCoV RNA in feces and multiple organs; and mild histology lesions in the lung, kidney, and intestinal tissues. Our data suggested that chickens are susceptible to PDCoV infection, indicating that PDCoV may have the potential for cross-species transmission between pigs and chickens.
During the last two decades, scientists have grown increasingly aware that viruses are emerging from the human–animal interface. In order to combat this increasingly complex problem, the One Health approach or initiative has been proposed as a way of working across disciplines to incorporate human, animal, and environmental health. Of particular concern are emerging respiratory virus infections; in a recent seminar given by the National Institute of Health on emerging and re-emerging pathogens, nearly 18% were respiratory viruses (1). Among the recently emerged respiratory pathogens contributing to the high burden of respiratory tract infection-related morbidity and mortality, displayed graphically in Figure 1, are influenza viruses, coronaviruses, enteroviruses (EVs), and adenoviruses (Ads). In this report, we summarize the emerging threat characteristics of these four groups of viruses.
For the validation of the model, historic data has been used to relate the obtained results with the historic events. The information available in the OIE database WAHIS INTERFACE (20) has been used to the extraction of the data referring to the exceptional epidemiological events in the European Union countries during the last 2 years (2017 and 2018).
The economic impact of enteric virus infections on the poultry industry has been evaluated and ranges from insignificant economic effects to those that are severe and cause devastating losses. Enteric diseases tend to predominantly affect young birds; however, the disease may occur in all age groups, which increases susceptibility to other diseases, decreases feed conversion efficiency, and prolongs the time to market [1, 2]. At present, no specific treatment exists, and commercially available vaccines have not yet been developed for any of the viruses that are involved in this disease.
Enteric disease was induced by experimental infection in one-day-old broiler chicks with intestinal content from a broiler flock which has presented enteric problems such as diarrhea, poor performance, and mortality [3, 4] or with preparations from the intestinal contents of affected birds that did not contain bacteria or protozoa [3, 5]. However, experimental attempts to reproduce this disease following inoculation with a single pathogen were unsuccessful. Under field conditions, these intestinal infections are usually complicated by interactions with other infectious agents or by the age, nutrition, and immune status of the birds as well as the management and environmental conditions, which complicated the evaluation of the role of these viruses in the enteric diseases manifestation [6–8]. Enteric diseases related to viruses were firstly reported in the late 1970s and is characterized by growth deficiency, retarded feather development, diarrhea, and other abnormalities [9–11]. Although several clinical cases of enteric disease have been observed in several regions of Brazil, there is no extensive research on this syndrome, except for studies on the detection of some atypical rotaviruses in broiler chickens with enteritis [12, 13] rotavirus, reovirus, and picobirnavirus using the polyacrylamide gel electrophoresis (PAGE) technique.
In the past, enteric disease has been called the pale bird syndrome and helicopter wing disease and was characterized by poor growth and retarded feather development. These symptoms are observed consistently along with the other less frequent clinical signs including diarrhea, increased mortality, and pancreatic and lymphoid atrophy [6, 15]. Enteric diseases seem to be the most acceptable name for this clinical manifestation because it most appropriately reflects the consistency of the clinical findings and indicates that these cases are probably caused by the same infectious agents.
In this study, we screened seven related viruses as potential agents of enteric disease in chickens to investigate the highest number of agents and their emergence in the Brazilian poultry production.
Multisystemic inflammation and myocarditis were initially linked with the presence of PCV-3 (22). One single study described PCV-3 in weaned pigs that suffered from gastro-intestinal disorders (diarrhea), showing higher prevalence in pigs with clinical signs (17.14%, 6 out of 35) compared to those with non-diarrhea signs (2.86%; 1 out of 35) (87). In another report, animals with congenital tremors were analyzed and PCV-3 was the only pathogen found in the brain, with high amount of viral DNA (101).