Dataset: 11.1K articles from the COVID-19 Open Research Dataset (PMC Open Access subset)
All articles are made available under a Creative Commons or similar license. Specific licensing information for individual articles can be found in the PMC source and CORD-19 metadata.
More datasets: Wikipedia | CORD-19
Deep Learning Technology: Sebastian Arnold, Betty van Aken, Paul Grundmann, Felix A. Gers and Alexander Löser. Learning Contextualized Document Representations for Healthcare Answer Retrieval. The Web Conference 2020 (WWW'20)
Funded by The Federal Ministry for Economic Affairs and Energy; Grant: 01MD19013D, Smart-MD Project, Digital Technologies
The porcine hemagglutinating encephalomyelitis virus (PHEV) is the causative agent of neurological and/or digestive disease in pigs. PHEV was one of the first swine coronaviruses identified and isolated, and the only known neurotropic virus that affects pigs. However, PHEV remains among the least studied of the swine coronaviruses because of its low clinical prevalence reported in the swine industry worldwide. PHEV can infect naïve pigs of any age, but clinical disease is age-dependent. Clinical manifestations, including vomiting and wasting and/or neurological signs, are age-related, and generally reported only in piglets under 4 weeks old. Subclinical circulation of PHEV has been reported nearly worldwide in association with a high seroprevalence in swine herds. Protection from the disease could be provided through lactogenic immunity transferred from PHEV seropositive sows to their offspring in enzootically infected herds. However, PHEV still constitutes a potential threat to herds of high-health gilts, as evidenced by different outbreaks of vomiting and wasting syndrome and encephalomyelitis reported in neonatal pigs born from naïve sows, with mortality rates reaching 100%. In absence of effective vaccine, the best practice for preventing clinical disease in suckling piglets could be ensuring that gilts and sows are PHEV seropositive prior to farrowing.
PHEV can infect naïve pigs of any age, but clinical disease is variable and dependent on age, possible differences in virus virulence (74), and the course of viral pathogenesis. In growing pigs and adults, PHEV infection is subclinical, and animals develop a robust humoral immune response against the virus (66, 75). Exceptionally, transient anorexia (1–2 days) was reported in PHEV-infected sows in absence of other clinical signs (55). An experimental study performed on 7 weeks old pigs reported transient mild neuromotor signs, including tremor and generalized muscle fasciculation in 17% (2/12) of pigs between 4 and 6 days after oronasal inoculation (75). Acute outbreaks of VWD and encephalomyelitis have been reported in piglets under 3–4 weeks of age born from naïve sows, with mortality rates reaching 100%. The first signs of infection are generally non-specific and may include sneezing and/or coughing because of virus replication primarily occur in the upper respiratory tract; followed by transient fever that may last for 1–2 days. More specific clinical manifestations may appear between 4 and 7 days after infection and are characterized by (1) VWD and (2) neurological signs including tremor, recumbency, padding opisthotonus, and finally death. Both clinical forms can be observed concurrently in the same herd during an acute outbreak. More recently, PHEV was associated with a case of influenza-like respiratory illness in a swine exhibition in Michigan, USA, in 2015 (76). Although PEHV can replicate in the respiratory epithelium, the role of PHEV as respiratory pathogen has not yet been confirmed and needs further investigation.
The VWD was experimentally reproduced and reported for the first time in 1974 (59) in colostrum-deprived (CD) pigs by oronasal and intracranial inoculation. Mengeling et al. (74) experimentally reproduced both clinical forms of the disease in neonatal pigs inoculated with a field virus isolate. Later, Andries et al. (77) evaluated the clinical and pathogenic outcomes with different routes of inoculation. In this experiment, all piglets inoculated oronasally or via the infraorbital nerve showed signs of VWD 5 days after the inoculation. However, a high percentage of animals inoculated through the stomach wall, intramuscularly, and intracerebrally showed VWD signs 3 days after inoculation. Pigs inoculated intravenously, intraperitoneal or in the stomach lumen did not show PHEV-associated VDW signs.
Suckling piglets experiencing PHEV-associated VWD show repeated retching and vomiting, which could be centrally induced (4, 49, 59, 73). The persistent vomiting and decreased food intake result in dehydration, constipation, and therefore a rapid loss of body condition. PHEV-infected neonates become severely dehydrated after few days, exhibit dyspnea, cyanosis, lapse into a coma, and die. During the acute stage of VWD outbreaks, some pigs may also display neurologic signs, including muscle tremors, hyperesthesia, excess physical sensitivity, incoordination, paddling, paralysis, and dullness (68). When the infection occurs in older pigs, there is anorexia followed by emaciation (Figure 1). They continue to vomit, although less frequently than in the acute stage. After the acute stage, animals start showing emaciation (“wasting disease”) and often present distension of the cranial abdomen. This “wasting” state may persist for several weeks after weaning, which in most cases requires euthanasia.
Pre-weaning morbidity varies depending on the immune status of neonatal litters at the time of PHEV infection (4, 74). In piglets without lactogenic immunity against PHEV, morbidity is litter-dependent and may approach 100% when the infection occurs near birth. Overall, morbidity decreases markedly as the pig's age increases at the time of PHEV infection. Mortality is variable, reaching up to 100% in neonatal litters born from PHEV naïve dams. However, a different epidemiological picture was observed in the outbreak reported during the winter of 2006 in Argentina (66) where only suckling pigs born from an isolated pool of non-immune gilts were affected. The severity of the main clinical signs reported, including vomiting, emaciation, wasting, and death was unexpected according to previous reports in the field (73). The morbidity was 27.6% in 1 week old pigs and declined to 1.6% in 3 weeks old pigs. After weaning, 15–40% of the pigs coming from affected farrowing units showed wasting disease. An estimated 12.6% (3,683) pigs died or were euthanized (66).
The first clinical signs observed during neurological PHEV outbreaks include sneezing, coughing, and vomiting 4–7 days after birth, with a morbidity rate of approximately 100% (4, 78, 79). Mild vomiting may continue intermittently for 1–2 days. In some outbreaks, the first sign is acute depression and huddling. After 1–3 days, pigs exhibit various combinations of neurological disorders. Generalized muscle tremors and hyperesthesia are common. Pigs may have a jerky gait and walk backwards, ending in a dog-sitting position. They become weak and unable to rise, and they paddle their limbs. Blindness, opisthotonus, and nystagmus may also occur. Finally, the animals become dyspneic and lie in lateral recumbency. In most cases, coma precedes death, with a mortality rate of 100% in neonatal pigs (4). Older pigs show mild transient neurological signs, including generalized muscle fasciculation and posterior paralysis. Outbreaks described in Taiwan (65) in 30–50 days old pigs were characterized by fever, constipation, hyperesthesia, muscular tremor, progressive anterior paresis, posterior paresis, prostration, recumbency, and paddling movements with a morbidity of 4% and a mortality of 100% at 4–5 days after the onset of clinical signs.
In non-swine species, PHEV-related disease only has been induced experimentally. It was also demonstrated that suckling mice (3 days old) were susceptible in a dose- and age-dependent manner to PHEV infection through intracranial inoculation, showing neurological signs and dying (80).
Porcine reproductive and respiratory syndrome virus (PRRSV), an enveloped and positive-stranded RNA virus of Arteriviridae family, causes porcine reproductive and respiratory syndrome (PRRS). PRRS is responsible for over one billion dollar loss per year through direct and indirect costs in the US swine industry. Two entirely distinct genotypes of PRRSV circulate in European (genotype 1/PRRSV 1) and North American countries (genotype 2/PRRSV 2) and cause tremendous economic loss. PRRSV is transmitted through oral-nasal secretions and semen. The clinical signs include fever, anorexia, mild to severe respiratory problems, abortion and reproductive failures. It is the most common pathogen associated with porcine respiratory disease complex (PRDC).
Swine influenza (flu) constitutes another persistent health challenge to the global pig industry. Flu infection is caused by influenza A virus of Orthomyxoviridae family which has negative-sense, single-stranded, segmented RNA genome. Influenza virus is transmitted through direct contact with infected animals or contaminated fomites, aerosols and large droplets. The clinical signs of influenza infection include fever, anorexia, loss of weight gain and respiratory problems. Influenza associated economic losses are due to morbidity, loss of body weight gain, increased time to market, secondary infections, medication and veterinary expenses. Influenza of swine origin occasionally infect humans and can even lead to pandemics as of 2009.
Porcine epidemic diarrhea virus (PEDV), transmissible gastroenteritis virus (TGEV) and porcine deltacoronavirus (PDCoV) are enteric pathogens of young pigs. These viruses belong to Coronaviridae family and have positive-sense, single-stranded RNA genome. TGEV did serious economic damage to the swine industry in 1990s but with the advent of vaccines it has been largely controlled. PEDV still results in high morbidity and mortality in neonatal piglets with clinical signs like severe diarrhea, vomiting, dehydration and death. In 2013/14, PEDV outbreak in the US led to over a billion-dollar loss. Rotaviruses are double-stranded RNA viruses of Reoviridae family, cause enteric infections in pigs. Rotavirus of groups A, B, C, E and H are involved in porcine enteric infections. Some of these porcine rotaviruses also have zoonotic potential.
Foot and mouth disease (FMD) is another highly contagious, acute viral disease in pigs. The etiologic agent, FMD virus (FMDV), is a positive-sense, single-stranded RNA virus of Picornaviridae family. FMDV is transmitted through direct contact with infected animals or contaminated sources. Clinical signs include high fever, appearance of vesicular lesions on the extremities, salivation, lameness and death. FMDV causes frequent epizootics in many parts of the world resulting in severe economic loss, food insecurity and trade restrictions.
Classical swine fever (CSF) or hog cholera can result in high morbidity and mortality in pigs. It is caused by CSF virus (CSFV), an enveloped, positive-sense, single-stranded virus of Flaviviridae family. Transmission of CSFV occurs through oral-nasal routes after contact with infected pigs or contaminated resources and even vertically from infected sows to piglets. Clinical signs include fever, anorexia, respiratory problems, neurological disorders, reproductive failures and death. CSF is a notifiable disease to World Organization for Animal Health (OIE). The economic losses are associated with production loss, trade limitations and tremendous expenditures in eradication programs. For example, the 1997/98 outbreak of CSFV in the Netherland resulted in death of 9 million pigs and economic losses of 2.3 billion dollars. United States is free of CSFV; however, this virus is endemic in many parts of the world including Central and South America, Africa and Asia.
The burden of viral disease is a global concern. Due to their unique properties, viruses have a particular relevance when analyzing the interaction among humans, animals, and the environment. Viruses are small compared to other pathogens, facilitating transport in the environment. Moreover, their resistance to disinfection and ability to survive for prolonged periods in water and solids make their transmission from the environment to suitable hosts likely. This is compounded by their low infectious dose, inability to be treated by antibiotics, and their proclivity for adaptive mutation. Additionally, viruses do not replicate outside their host cells, therefore detection in environmental samples can be directly related to the human or animal population that excreted these viruses.
Fig. 1 summarizes viral exposure pathways and the relevance of the One-Health approach. One-Health is a relatively new approach to the solving of global health challenges. Formally put forth by the One Health Commission in 2007, the concept is defined as “the collaborative effort of multiple disciplines – working locally, nationally, and globally – to attain optimal health for people, animals and our environment.” Consequently, a key component to the One-Health approach is the notion that human health, animal health, and environmental health are all innately interrelated. The quality and well-being of one group can directly and indirectly impact the quality of the other two groups. By taking all three aspects of health into account, solutions can be generated that not only address the health problems of a specific group but mitigate the source of those problems as well.
Much of the current work using the One-Health approach is focused upon the exposure pathway between humans and animals, while the water-related exposure pathway has not been thoroughly investigated from a One-Health perspective. The purpose of this paper is to explore water-related exposure pathways as they relate to human, animal, and environmental health, to explore the possibility of surveillance of water and wastewater systems as means of identification of endemic disease and potential outbreaks at a population level, and to develop a framework with which to apply the One-Health methodology for early detection and management of water-related viral outbreaks.
The Iberian lynx (Lynx pardinus) is an endangered wild feline endemic to the Iberian Peninsula, located in the southwest corner of Europe. The Iberian lynx population suffered a dramatic reduction in size during the 20th century. From 2002 to 2015 it was considered the world’s most endangered wild feline species. Recently, the Iberian lynx has been reclassified from a critically endangered to an endangered species. The population was 406 at the 2015 census. Iberian lynxes predominantly prey on wild rabbits (Oryctolagus cuniculus), although they alternatively may prey on small mammals, juvenile ungulates, partridges, other birds, reptiles and insects. Moreover, Iberian lynxes occasionally consume wild boar as prey and as carrion, which puts them at risk for pseudorabies infection. The species is highly solitary and territorial, although family groups have occasionally been detected. The Iberian lynx is found in areas of Mediterranean scrub and in habitats of open forests and thickets with high rabbit abundance. The small population and low genetic diversity of the Iberian lynx make this species especially vulnerable to bacterial and viral infections. A number of infectious agents have been detected in Iberian lynxes, including a variety of feline viral and bacterial pathogens [8, 9].
The causative agent of Aujeszky’s disease (AD) is Suid Herpesvirus 1 (SuHV1), which is also known as pseudorabies virus (PRV). This virus is a member of the genus Varicellovirus belonging to the subfamily Alphaherpesvirinae of the family Herpesviridae that can infect a wide range of species, though it is does not affect the higher primates. Pseudorabies is a viral disease which was first reported in dogs in 1902, and is prevalent throughout the world. The only natural hosts of PRV are domestic and wild suids (Sus scrofa scrofa) and their hybrids. Symptoms of AD depend on the age of the animal, and can include respiratory, reproductive and nervous signs. PRV is a neurotropic virus which replicates in the nasopharyngeal mucosa, before taking a number of nervous pathways to reach the central nervous system (CNS). It results in a non-suppurative meningoencephalitis which is frequently fatal in piglets [14–17]. PRV seroprevalence in European wild boar varies considerably between different geographic regions. The highest seroprevalences were described in Mediterranean countries including Spain (up to 100%) [5, 12, 18–24]. In both domestic pigs and wild boar, the disease is usually subclinical because of the virus-host adaptation; however, in piglets, the infection is commonly fatal [15–17]. Like other herpesviruses, PRV usually produces latent infections in the host. PRV can infect the neurons and glial cells of apparently healthy swine over long periods. These latent infections can be reactivated, which means PRV can spread to other susceptible animals, mainly mammals, such as carnivores [14, 25], although humans seem insusceptible. Species other than suids can be considered dead-end hosts because the disease is generally fatal before the virus is excreted. In these mammals, including carnivores, PRV infections usually result in very severe neurological symptoms which often involve localised pruritus, resulting in death within hours after appearance of the first symptoms. There are considerable implications for conservation, as cases have been reported in endangered carnivores such as the Florida panther, the wolf and captive brown bears after consumption of PRV-contaminated meat. No seropositive lynxes have ever been found, nor has PRV been detected in dead Iberian lynxes to date.
This article is the first reported case of pseudorabies in an Iberian lynx. We describe the second reported case of pseudorabies in a wild feline considering that PRV infection has only been previously reported once in a Florida panther in 1994.
PRV infection was suspected in this lynx based on histopathological findings, and because PRV infections in wild boar are endemic in SW Spain. Infection was confirmed with immunohistochemistry, PCR, and sequence analysis.
Swine influenza A viruses (SIVs) are enzootic in most European pig populations. The SIV H1N1 and H3N2 subtypes have been circulating for more than 30 years, and the SIV subtype H1N2 has been circulating since it was first isolated in Great Britain in 1994 [2, 3]. In April 2009, a new influenza A virus of subtype H1N1 emerged in the human population in Mexico and the United States. This was a multiple reassortant virus containing genes from North American and Eurasian lineages [4, 5]. The virus spread rapidly across the world by human-to-human transmission. Human-to-pig transmission was first reported in Canada in late April 2009, then in European pig population in early September 2009, and has since been reported in several countries all over the world [6–9]. In October 2009, SIV was reported for the first time in Norway when an integrated pig herd tested positive for pandemic (H1N1) 2009 virus after showing mild clinical signs of respiratory disease.
The clinical picture of pandemic (H1N1) 2009 infections in experimentally and naturally infected pigs was described as mild respiratory illness, increased temperature, and decreased appetite [6, 11, 12]. In some infected herds, clinical signs were not detected. Studies have shown that immunological naïve pigs experimentally infected with pandemic (H1N1) 2009 virus could transmit the virus efficiently to other naïve pigs [11, 14, 15]. Although pandemic (H1N1) 2009 virus contains gene segment genetically related to other swine influenza virus strains circulating in Europe and North America, it shows antigenetic differences in the major glycoproteins of the virus. However, it has been shown that pigs infected or vaccinated with H1N1 European avian-like swine influenza virus could produce cross-reactive antibodies against pandemic (H1N1) 2009 virus which protected pigs against the infection of pandemic (H1N1) 2009 virus [13, 16].
The pig production in Norway consists of approximately 2500 herds, mainly small family farms, with about 1.5 million slaughtered pigs in 2010. National surveillance and control program shows that the pig population is free for Aujeszky's disease (AD), transmissible gastroenteritis (TGE), porcine respiratory corona virus (PRCV), porcine reproductive and respiratory syndrome (PRRS), and Mycoplasma hyopneumoniae [17, 18]. The Norwegian Food Safety Authority has been running annual surveillance programs to document the status since 1994. SIV was added to the program in 1997. Under the surveillance, blood samples from about 500 randomly selected herds are collected annually for specific disease surveillance. The surveillance has never detected SIV infection in Norway until October 2009, except for pigs in one herd that tested seropositive for subtype H3N2 in 1998 without showing clinical signs or further spread of the infection.
This paper consists of studies that describe the initial spread of pandemic (H1N1) 2009 virus amongst Norwegian pig herds, the control measures initiated, and the infection status 20 months after the introduction. The paper also discusses the manifestation of the infection in the Norwegian pigs given that they had no prior immunity to any influenza A viruses and are free from most other viral respiratory diseases.
As can be seen by a graph depicting the number of PubMed citations per year, advances in virology and prion studies are accelerating at a pace that makes it difficult for any individual to remain informed in areas outside one’s specialty (Figure 1). In addition, scientific meetings are continuing to focus on specific areas to maximize dissemination of information to select groups while general meetings that cover multiple fields are typically too large to permit prolonged informal discussion, especially with students and early-stage investigators. With these facts in mind, the Rocky Mountain Virology Association (RMVA) was formed to provide a venue that permitted formal presentations of current research in multiple areas of virology and prion biology in a venue that is sufficiently removed from major cities to ensure extended informal discussions and opportunities to establish/strengthen collaborations. Professional child daycare was provided to help enable attendance by individuals with young children, which provided an educational opportunity through the children’s participation in a virus and prion themed performance during the formal poster session. Taken together, the 17th annual RMVA meeting (Figure 2) upheld the tradition of presenting novel findings, summarized below, that spanned the fields of bio-informatics, host-pathogen interactions, immunology, therapeutics, replication of DNA and RNA viruses along with prion detection and disease propagation.
Two features of human behavior throughout history are striking. The first has been the domestication of numerous animals for food production, as working animals for activities such as transport, and for hunting purposes. They are also, particularly in modern times, used as a source of companionship, and in the USA alone there are estimated to be over 77 million dogs.1 The second feature is our propensity to travel. This trait has accelerated in the modern age through technical innovations such as the motor car, air travel, and international shipping.2 Human travel through migration, leisure, or business continues to increase in parallel with a population increase and the spread of affluence. This provides opportunities for pathogens to move to new areas and cause outbreaks of disease. Commercial air travel has been particularly effective at transporting pathogens such as SARS coronavirus and influenza viruses.3 It is also contributing to the spread of disease vectors and the diseases they transmit.4 As we travel, we take animals with us either through trade in livestock or in the movement of companion animals.
In Europe, the free movement of people within the continent has been enabled by the formation of the European Union (EU) and liberalization of border controls. This was formalized by the Schengen Agreement signed by member states in 1985 and implemented in 1995. This created the Schengen Area that reduced border controls between member states and allowed free movement of people between countries. Some countries, including the UK and Ireland, have in the past, agreed opt-outs that retain limitations of movement into those countries.
When humans travel, they often take their companion animals, particularly dogs, and these in turn can relocate the pathogens and vectors they harbor. Canine parvovirus emerged in 1978 as a new disease in dogs causing hemorrhagic enteritis. Retrospective serology suggested that the disease appeared in Europe in 1976 and spread throughout the world by 1978.5 The mechanism that enabled global dissemination of the virus has been attributed to contaminated footwear. There are numerous canine-associated diseases but relatively few are significant zoonoses. However, of these, a number are fatal to humans and control is essential to protect public health. Globally, the most significant is the rabies virus. Infection leads to fatal encephalitis, for which there is no treatment.6,7 Pre-exposure vaccination protects against the disease in mammals, and due to the extended incubation period between contact with a rabid animal and development of disease, often measured in months, timely post-exposure vaccination is also effective in humans.8 The dog is the most important reservoir for the virus, and contact with dogs is responsible for virtually all human cases of the disease. Where efforts have been concentrated on controlling dog rabies, the reduction in human cases of disease has been dramatic.9 Dog rabies has been virtually eliminated from Europe, although there are examples of reintroduction10,11 and cross-border movement of rabid animals.12
Alveolar echinococcosis is caused by the tapeworm Echinococcus multilocularis. It is a fatal condition that is relatively rare in Europe although there are clear areas of endemicity, resulting in human infections in an area of Europe ranging from France in the west to Austria in the east.13 The disease manifests as a tumor-like growth of cysts containing the larval stage of the parasite in organs such as the liver. Detection of cysts often occurs many years after initial infection, and without intervention such as surgery to remove the cyst(s), the disease is fatal. Dogs act as the definitive host for the adult form of the parasite and movement of infected dogs can lead to the spread of tapeworm eggs and introduction of the disease into new areas. As the adult worm is very small (less than 5 mm) and does not cause clinical signs in the definitive host, spreading of eggs and human infection can remain undetected until clinical symptoms develop.
Leishmaniasis is caused by protozoa belonging to the genus Leishmania. Two forms are recognized, ie, cutaneous leishmaniasis causing skin lesions and the more serious visceral disease involving multiple organs. Natural transmission is through the bite of phlebotomine sandflies belonging to the genera Phlebotomus in the Old World.14 Distribution of leishmaniasis is limited by the presence of the vector. In Europe, the vector is indigenous to those countries around the Mediterranean Sea. The major mammalian reservoir is the domestic dog. Estimates of autochthonous human cases in Europe are approximately 700 a year.15 Numbers of cases in Turkey are higher, with over 3,000 annually. Non-endemic countries in Europe do encounter cases of canine leishmaniasis as a result of pet movements.16
In the absence of border restrictions, it is difficult to establish the true extent of regional movement of animals either for trade or through holiday travel. Monitoring of dogs and cats entering the UK through its pet travel scheme indicated that almost 100,000 animals entered the country annually (Table 1). A similar situation is likely to exist for most EU member states. In addition to this, there is the problem of illegal movement of animals either by organized groups for commercial purposes or inadvertent contraventions of legal requirements by holidaymakers through importation of their animals. Quantification of this is by its very nature difficult, but detection of noncompliance with legislation or deliberately smuggled animals is a regular occurrence,17 and the incidence of disease often highlights this activity.
The following sections review important zoonotic diseases of pet origin and the policies currently in place to control zoonotic diseases of companion animals and their limitations, concluding with recommendations on what more could be done.
Since its emergence in the late 1980s, the porcine reproductive and respiratory syndrome virus (PRRSv) has posed a significant challenge to the pig industry worldwide. Even though PRRS is a relatively new disease affecting swine, its rapid worldwide spread, the lack of efficient control tools in the first years after its discovery, and its complex epidemiology and pathogenesis resulted in a number of published scientific papers comparable to that published during a longer period for other swine diseases. However, despite substantial efforts and resources invested by researchers worldwide, there are still many important gaps in our understanding of critical aspects of its epidemiology. Those unknowns include, for instance, an updated knowledge of regional PRRSv dynamics in endemically infected areas, full quantification of its impact on production (particularly in subclinically affected herds), and development of improved tools for assessing the relation between PRRSv strains with a close genetic relatedness and linked epidemiologically at a local level. There are, nevertheless, new opportunities to address those problems thanks to the increasing awareness of the value of sharing information to improve disease management at a supra-farm level, the extended use of production management software that allows recording and storage of large datasets over long periods of time, development of standardized and optimized cost-effective diagnostic systems for surveillance that may be linked with production data [3, 4], and the increasing availability of molecular tools. This changing reality is expected to lead to the generation of information that may be then combined with novel analytical tools to gain new insights on the epidemiology of PRRS. The objective of the paper here is to summarize the work that has been done to provide answers to some of those pending questions on PRRS epidemiology with a focus on studies performed in the U.S., where the predominant PRRSv type is type 2. We initially focus on PRRSv control at the regional level, then we review the use of routinely collected production data to evaluate the impact of PRRS at the system or farm level, and finally we introduce the potential application of molecular tools to the near real time surveillance of virus spread. The review here will help to understand how quantitative analysis of routinely collected data may help to design effective strategies to support PRRS control at the regional and local levels, and ultimately, improve health status in swine farms and systems.
Respiratory illness is traditionally regarded as the disease of the growing pig, and has historically been associated with bacterial infections such as Mycoplasma hyopneumoniae [1–3] and Actinobacillus pleuropneumoniae [4–6]. These bacteria still are of great importance, but the continuously increasing herd sizes have complicated the clinical picture. As the number of transmission events between pigs in a population is equal to the number of pigs multiplied with the number of pigs minus one [x = n * (n − 1)], they will escalate as the herd size increase. Thus, the number of transmission events between pigs will increase with a factor of around four if a population is doubled and with a factor of around 100 if a population is enlarged ten times.
The increased number of transmissions between pigs may increase the influence of other microbes. M. hyopneumoniae and A. pleuropneumoniae are important pathogenic microbes, but co-infections may intensify or prolong clinical signs of respiratory disease [8–11]. It has also been observed that the incidence of respiratory illness may vary with season. Therefore, infections in the respiratory tract of grower pigs have become regarded as a syndrome rather than linked to single microorganisms [11, 13, 14]. This syndrome is referred to as the porcine respiratory disease complex (PRDC). As stated above PRDC is regarded to be dominated by bacterial species, and important primarily pathogenic bacterial species include M. hyopneumoniae [1–3] and A. pleuropneumoniae [4–6]. The frequent demonstration of interferon-α in serum in growers during the first week after arrival to fattening herds [15, 16] suggest that PRDC can be associated with viral infections, and that PRDC can also include the influence of secondary invaders such as Pasteurella spp [17, 18].
When Sweden in 1986 as the first country in the world banned the use of low dose antibiotics in animal feed for growth promotion, some introductory health disturbances were recorded. As a consequence, a strict age segregated rearing from birth to slaughter was implemented in a large scale, which improved health as well as productivity [19, 20]. As seen in Fig. 1, the incidence of recorded pathogenic lesions in the respiratory tract at slaughter decreased during the last decade of the twentieth century. The registrations of pneumonia at slaughter has remained stable at that level since then. In contrast, the incidence of recorded pleuritis at slaughter has continuously increased since the year 2000, as has the clinical evidence of actinobacillosis. Discussions concerning the reason for this increase has included suggestions of introduction of new strains, or mutation of existing strains of A. pleuropneumoniae. However, acute actinobacillosis has in Sweden historically been dominated by serotype 2, and is still dominated by that serotype. Further, Pulse Field Gel Electrophoreses has revealed that strains isolated in the twenty-first century were identical to strains isolated in the 1970s and 1980s. As a consequence, the increase of actinobacillosis and pleuritic recordings at slaughter has merely been linked to the continuously increasing herd sizes with increasing number of transmissions of microbes between pigs, within and between units.
The aim of this study was to validate the presence of A. pleuropneumoniae and M. hyopneumoniae, as well as the secondary invaders P. multocida and Streptococcus suis in pig herds with a high incidence of pleuritic lesions at slaughter.
Environmental factors, specifically climate conditions, are the seasonal drivers that have received the most attention. This may be because they often covary with seasonal disease incidence. Environmental drivers are abiotic conditions that influence transmission via their effects on hosts and/or parasites; classic examples are temperature and rainfall, which influence a variety of infectious diseases, but other examples include seasonal nonclimatic abiotic environmental conditions, such as water salinity, which may impact water-borne pathogens. Environmental factors can impact pathogen survival during transitions between hosts. Transitions can take place during short time windows (e.g., for droplet-transmitted infections) or long time windows (e.g., for parasites with environmental life stages). In addition to their impact on pathogens, environmental drivers can also influence host susceptibility to infection or vector population dynamics.
As for host susceptibility, environmental conditions can impact the host immune response and increase cells' susceptibility to infection or pose seasonal challenges (such as food limitations) that leave hosts vulnerable to infection or pathology, which has been proposed to influence disease progression in individuals infected with HIV. For directly transmitted infections, environmental conditions can be major drivers of cycles in incidence, with influenza and cholera transmission being notable examples (e.g., see [3, 80]). The effects of climate on flu transmission have been studied using population-level data coupled with transmission models, as well as empirical animal studies, to demonstrate the effects of temperature and humidity on transmission. Although climate conditions undoubtedly play a direct role in several directly transmitted infections, they may play a more nuanced role in vector-borne disease systems in which they modulate vector population dynamics and subsequently disease transmission. For example, in the case of African sleeping sickness (Table 1), the rainy season is hypothesized to modify tsetse fly distribution, which results in changes in human–tsetse fly contact and subsequently African sleeping sickness incidence; in this case, we can classify the seasonal driver as (1) vector seasonality alone or as (2) seasonal climate influencing vector seasonality and vector seasonality having a downstream effect on seasonal exposure. Abiotic and biotic seasonal drivers are therefore interconnected and not mutually exclusive.
The lynx that we studied was a wild ~9-month-old male, born to a healthy 3-year-old dam. It belonged to the first two litters born in Extremadura (SW Spain) after Lynx pardinus was re-established in this region through the LIFE+ 10NAT/ES/ 000570 project. Using camera trapping, the estimated date of its birth was established to have been between March 8 and 12, 2015.
This lynx was captured, subjected to a routine sanitary evaluation protocol, radio-collared, vaccinated against Feline Leukemia Virus (PureVax FeLV, Merial, Barcelona; Spain) and relocated back into the wild on Nov. 18, 2015. A complete blood count and plasma protein tests showed normal levels. Plasma biochemistry results were within normal ranges, although plasma concentrations of glutamyl transpeptidase and creatine phosphokinase were slightly increased. PCR tests were negative for infection with Feline Leukemia Provirus (FeLV), Feline Immunodeficiency Virus (FIV) and Canine Distemper Virus (CDV) in the blood; Feline Calicivirus (FCV) and Feline Herpesvirus (FHV1) in oropharyngeal swabs; and Feline Coronavirus (FCoV) and Feline Parvovirus (FPV) in rectal swabs. The lynx was found to be antigen-ELISA (enzyme-linked immunosorbent assay) negative for FHV1, FCoV and CDV as well as negative for FCV and FPV by fluorescent antibody testing. These tests were performed as previously described [8, 30, 31]. Finally, a blocking ELISA test (CIVTEST SUIS ADV gE, Hipra, Gerona, Spain) was used to detect the presence of serum antibodies against PRV, obtaining negative results.
The lynx was found dead on Dec 1, 2015 on private land consisting of a mixture of dense scrub and open pasture in an area known as “Hornachos-Valle del Matachel” located southwest of Badajoz (Extremadura), Spain (Latitude: 38°27′10.98″ N, Longitude: 5°54′30″W).
Post-mortem examination was carried out at the Veterinary Teaching Hospital of Extremadura (Cáceres, Spain). Upon presentation for necropsy, the lynx weighed 3,060 g, and the carcass was preserved without putrefaction changes. An X-ray examination excluded general traumatisms or the presence of shotgun wounds. Gross lesions of the lynx were minimal. In agreement with our observations, AD in many cases does not develop significant macroscopic lesions in other carnivores such as dogs and cats [32, 33] and wolves. The skin of the ventral neck was denuded of hair and the radio-collar appeared torn (Fig. 1a). Intense pruritus can sometimes lead to these types of lesions due to scratching and self-mutilation as has been suggested in coyotes, dogs [26, 35] and cats. The stomach and small intestine contained a moderate amount of partially digested blood (Fig. 1b). The large intestinal contents consisted of varying amounts of dark red to black semi-formed fecal material. The meninges were congested (Fig. 1c). These lesions are similar to those reported in the Florida panther, coyotes and dogs.
Representative portions of sampled tissues were fixed in 10% neutral buffered formalin, routinely embedded in paraffin and hematoxylin and eosin (HE) stained. A histopathological analysis of the CNS showed diffuse nonsuppurative meningoencephalitis similar to that reported in domestic cats [32, 36] and other unnatural hosts such as dogs [11, 33, 35, 37], foxes and coyotes. Similar to that described for coyotes, the leptomeninges and subarachnoid space were infiltrated and expanded by slight perivascular accumulations of mononuclear cells (Fig. 2a). This meningoencephalitis was characterized by mononuclear cellular infiltrates around blood vessels (perivascular cuffs) and neuropil (Fig. 2b) composed mainly of lymphocytes, as well as multifocal to diffuse microgliosis, perineuronal glial satellitosis (Fig. 2c and d), neuronal necrosis and neuronophagia (Fig. 2d). Most neurons appeared unaffected; although within damaged brain regions, several neurons showed eosinophilic intranuclear inclusion bodies (Fig. 2e), even though eosinophilic intranuclear inclusions could be absent in the neurons of cats. Diffuse areas of demyelination and malacia were observed in sections of the cerebrum and cerebellum (Fig. 2b). These lesions have been previously described in raccoons. Gastrointestinal tract lesions observed in the lynx consisted of necrotizing gastritis and enteritis of the small intestine with foci of epithelial necrosis with minimal inflammatory reactions. These lesions have been reported in cats and dogs [36, 41] and in piglets.
PCR tests were negative for infection with FCoV (clot, spleen, mesenteric ganglia, small intestine and intestinal scraping samples), FCV (clot samples), CDV (brain tissue, clot, mesenteric ganglia and intestinal scraping samples), FPV (clot, mesenteric ganglia and intestinal scraping samples), FHV1 (clot, spleen, mesenteric ganglia, small intestine, intestinal scraping and brain tissue samples), FIV (clot and spleen samples), FeLV provirus (clot, mesenteric ganglia, intestinal scraping and brain tissue samples), Mycoplasma haemofelis, Candidatus mycoplasma haemominutum, Candidatus mycoplasma turicensis, Anaplasma phagocytophilum, Bartonella henselae, Chlamydophila felis, Cytauxzoon felis (clot samples) and Leptospira spp. (kidney samples). PCR tests were positive for infection with FeLV provirus (spleen and bone marrow samples) and Pasteurella spp. (lung samples) using PrimerDesign™ genesig Kit for Pasteurella multocida (Genesig, Chandler’s Ford, United Kingdom). Toxicological analyses were negative for pesticides and other organic compounds (chloralose, barbiturates, and metaldehyde), anticoagulant rodenticides and anticholinesterase pesticides. No intestinal parasites were detected in the lynx feces.
The polymer detection method (PDM) to detect porcine PRV was carried out on deparaffinized tissue sections using an UltraVision Quanto Detection System HRP DAB (Thermo Scientific, Fremont, USA, #TL-060-QHD) following manufacturer’s directions. Primary antiserum was gE PRV-specific monoclonal antibody (Ingenasa, Madrid; Spain #M.11.ADV.B2CF2). In order to determine the specificity of the immunohistochemical reaction, primary antibody was replaced with PBS or with non-immune mouse serum (1:100). The positive control consisted of a slide containing known positive tissue (CNS of naturally PRV infected pig). Negative control slides consisted of brain sections of a PRV-free lynx. The PRV antigen was detected in the tonsils (Fig. 2f) of the Lynx. PRV has been previously detected by immunohistochemistry in the tonsils of pigs and it was isolated from de tonsils of dogs and racoons. The replication of the virus in tonsils after its entrance via the oral route has been described in cats. Positive immunostaining was also observed in numerous gastric glandular epithelial cells (Fig. 2g), consistent with that previously described in dogs. The PRV antigen was found in the cytoplasm of neuronal (Fig. 2h) and non-neuronal cells (Fig. 2i) in inflamed brain areas. This localization has been described in dogs [11, 37]. Like other viruses belonging to the subfamily Alphaherpesvirinae, PRV first replicates in the epithelium of the mucous membranes, and then reaches the CNS via the nerve fibres that innervate the colonised tissues. Specific staining was not detected in the negative control samples (Fig. 3a). The positive control, showed positive immunoreaction against the gE PRV-specific monoclonal antibody (Fig. 3b).
To assess the presence of PRV in the CNS of the affected animal, a specific nested PCR reaction (Fig. 4) designed to amplify the viral glycoprotein B gene was performed, using two pairs of primers previously described. DNA from brain tissue was obtained using a commercial kit (QiAmp DNA Mini Kit®, Qiagen Ltd., Crawley, West Sussex, UK) following the manufacturer’s protocol. A total of 5 μl of the extracted DNA was used as a template for the nested PCR in a 25 μl reaction mixture containing 12.5 μl of PCR Master Mix (2x) (Green Taq, Thermo Fisher Scientific, Waltham, MA, USA) and 0.2 μM of each primer. DNA was amplified using the following amplification procedure: 1 cycle at 95 °C for 3 min, 30 cycles of denaturalization (94 °C, 45 s), annealing (62 °C, 1 min) and extension (72 °C, 1 min); and a final extension at 72 °C for 10 min. The second step of the nested PCR was performed using 0.5 μl of the first PCR product as template and following the amplification procedure previously described. PCR products were separated by 2% agarose gel electrophoresis and visualized by ethidium bromide staining under UV light.
The obtained 195 bp band was cut out of the gel, and DNA was extracted using an Ultra Clean™ GelSpin DNA Purification Kit (Mo Bio Laboratories, Inc., Carlsbad, California, 92010, USA). The 195 bp amplified product was sequenced in both directions using a BigDye Terminator v3.1 cycle sequencing kit according to the manufacturer’s instructions (Applied Biosystems). Nucleotide sequences were read on a 3730xl DNA Analyzer (Applied Biosystems). After trimming sequence primers, the 146 bp sequence was initially compared with GeneBank sequences using the Basic Local Alignment Search Tool (BLAST) (http://www.ncbi.nlm.nih.gov/blast/Blast.cgi) to verify the identity of the fragment. The BLAST analysis showed that the 146 bp sequence matched with the PRV genome. The obtained sequence and PRV available sequences were aligned by Clustal Omega. The alignment showed that the analyzed fragment presented 100% sequence identity with reference PRV strains such as Kaplan or Bartha. One substitution was found in strains such as NIA3 or Becker, while 2–4 substitutions were found when isolates with an Asian origin were aligned, like HUYD (DDBJ accession number KJ526432) or Rang (DDBJ accession number KP895102) isolates. An additional PCR was carried out to amplify glycoprotein D gene with primers and conditions previously described. Furthermore, in order to assess whether PRV infection was produced by a wild-type or a vaccine PRV strain, a TaqMan® base real-time PCR assay for the detection of gE gene was conducted as previously described using DNA extracted from CNS as template. Specific DNA from glycoprotein D and E encoding-genes was detected confirming the latter that this infection was produced by a wild-type PRV strain.
This article describes the first reported case of pseudorabies in Iberian lynxes, and it confirms that they are susceptible to PRV infection. Like other felids, PRV-infected lynxes develop lethal neurological disorders. In cats, PRV infection with brief two- to four-day incubation period, produces acute encephalitis and can cause 100% mortality in experimentally infected domestic cats [32, 51]. The cats suffer from anorexia, occasional severe itching with lesions caused by scratching and self mutilation and uncoordinated movements and paralysis [32, 51]. The outcome is invariably fatal and leads to death within 12–48 h of the first appearance of clinical signs. This peracute death does not allow time for a serologic response to occur. If Iberian lynxes succumb as rapidly as domestic cats, detection of the clinical phase can prove to be very difficult.
The main sources of infection for cats are uncooked pig or offal. Direct spread of virus from infected to noninfected carnivores likely does not occur. Wild boar are a well known reservoir for PRV and hence, may pose a risk to transmit the infection to wildlife carnivores species [25, 34]. Some authors have described recently, rates of 69.70% ELISA seropositivity and 11.30% of PRV lung infections in wild boar population throughout SW Spain [53, 54]. Wild boar are not the main component of the Iberian lynx diet; however, these animals do occasionally consume wild boar as prey and as carrion. Therefore, it is conceivable that some lynxes will be exposed to PRV from the ingestion of wild boar. Indirect transmission can also occur through viral excretion by pigs, without direct contact with the pigs themselves. The presence of wild boar infected with the PRV could have a negative impact on conservation of wild carnivores which consume wild boar such as lynxes.
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.
Porcine epidemic diarrhea (PED) is an important swine disease that causes a significant impact in most pig-producing countries. The causative agent, the PED virus (PEDV), belongs to the genus Alphacoronavirus, family Coronaviridae, and order Nidovirales. Although PEDV was first observed in Europe in the early 1970s, it has become an increasing problem worldwide, including in the Americas [3–5], Asia [6–11] and Europe [12, 13]. The devastating effect of PEDV infection is mainly due to the acute watery diarrhea and dehydration induced in infected pigs that not only leads to high (80–100%) mortality in neonatal piglets [3, 9] but also impairs the health and performance of the surviving pigs.
The impact of PEDV infection on the reproductive performance of gilts and sows depends on the period of pregnancy, during which females are exposed to the pathogen and the parity number. The farrow rate (FR) (-3.8%), percentage of stillborn piglets per litter (+1.8%), and percentage of mummified fetuses per litter (+1.1%) were significantly different during the 4-month period of the PEDV outbreak compared with the same period in the year before the outbreak. However, limited information on the productivity index of the gilts and sows that were exposed to the PEDV during the 1-year period of the PEDV outbreak is available. Mated female nonproductive days (NPDs) in the herd with the PEDV outbreaks have not been reported.
NPDs are the days that a mated sow or gilt is present in the herd and is neither gestating or lactating. The formula for calculating NPD is NPD = 365−[(litter/female/year) × (gestation days + lactation days)]. Several factors affect the NPDs: i) replacement gilt days, entry to first service, entry to culling and entry to death; ii) weaning-to-first service days (the number of days from weaning until a female is mated again); iii) first to repeat service interval (days to find re-cycling females after breeding); iv) weaning to removal period; and v) death loss and gestation days that do not result in farrowing. Therefore, NPDs represent key performance indicators of breeding herd performance.
The objectives of the present study were to investigate the effects between a 1-year period before and after PEDV outbreak on a sow’s reproductive traits on a commercial pig farm in Taiwan.
The probability of introduction of the j disease into the European Union through live animal's trade from the country i
(PIAji) is calculated as the proportion of animals that are annually transported to Europe coming from the country i multiplied by the probability of the country i being affected by the disease j
Swine influenza is a highly contagious acute respiratory viral disease of pigs, caused by H1N1, H1N2 and H3N2 subtypes of Influenza A virus (IAV). The disease is responsible for significant economic loss to the swine industry. Pigs also play a critical role in the emergence of new strains of influenza viruses by acting as a “mixing vessel”. Current swine flu vaccines are strain specific and they have been failed to induce cross-protection against genetically variant flu viruses. Moreover, intramuscularly delivered flu vaccine induces poor mucosal IgA antibody and T cell responses.
The highly conserved influenza viral proteins across IAV subtypes are matrix (M1 and M2), nucleocapsid (NP) and stalk domain of hemagglutinin (HA). Promising new generation flu vaccine platforms include use of highly conserved peptides in a vaccine formulation; because, recent developments in biotechnology tools have made the large scale production of antigenic peptides highly feasible at low cost. Attempts were made to develop IAV peptide vaccine by coexpressing conserved peptides of M protein 2 ectodomain (M2e) with Hepatitis B capsid protein, and also using cocktail of conserved T and B cells peptides. But due to lack of identified effective vaccine delivery and potent adjuvant system, peptides based vaccine candidates have been unsuccessful to induce robust response in pigs. Moreover, in intramuscularly vaccinated animals mucosal immune system is weakly activated. Recently, chimeric construct that express M2e on the surface loop of norovirus P particle (M2e-PP) was shown to produce high levels of antibody response and protect mice from a lethal challenge. In pigs, M2e-PP also induced specific immune response, but failed to provide protection from disease (unpublished data).
Potent vaccine delivery and adjuvant systems are essential to enhance immunogenicity of peptides vaccine. One of the endeavors of 21st century is delivery of vaccines and drugs through biocompatible and biodegradable polymer based nano or microparticles. PLGA (poly lactic-co-glycolic acid) is a nontoxic, FDA and European Medicines Agency approved polymer, and widely used as a vehicle for drug and vaccine delivery. The properties of PLGA made it ideal to entrap even soluble vaccine Ags in nanoparticles (NP) (200–600 nm) to elicit strong immune response. PLGA-NP entrapped peptide Ags are being protected from enzymatic or ionic degradation in vivo until they are uptaken by antigen presenting cells (APCs). Particulate antigens are readily taken up by mucosal M cells and APCs in the nasal-associated lymphoid tissues in intranasally vaccinated animals, which enhances antigen specific IFNγ secreting T cell response and production of high-affinity neutralizing antibodies in pigs. Benefits of PLGA based intranasal vaccine delivery system with the inactivated porcine reproductive and respiratory syndrome virus (PRRSV) in pigs and Hepatitis B Ags in rodents has been demonstrated [14–17].
In this study, a cocktail of conserved two each of T and B cell peptides of human H1N1 IAV and M2e-PP of SwIV H1N1 were entrapped in PLGA-NPs and characterized their vaccine properties in vitro. Further, efficacy of the candidate vaccine was evaluated against a virulent heterologous zoonotic SwIV H1N1 challenge in intranasally vaccinated pigs, coadministered with or without an adjuvant M. vaccae WCL. Our results indicated induction of peptide specific T cell response, reduction in the lung viral load and clinical flu symptoms, but the specific antibody response was not boosted both in the pre- and post-challenged NP based H1N1 peptides vaccinated pigs.
Communicable disease is one of the leading causes of death worldwide. Lower respiratory infections were responsible for 3.0 million deaths in 2016 according to the World Health Organization (WHO), and diarrheal infections contributed to another 1.4 million deaths in the same year. Viral diseases contribute to these categories; influenza, coronavirus, and adenovirus are all considered lower respiratory infections, and viruses such as rotavirus can cause diarrheal disease. Viral disease outbreaks occur often, with WHO reporting outbreaks of influenza, coronavirus, hepatitis E, yellow fever, Ebola virus, Zika virus, poliovirus, dengue fever, and chikungunya in 2017 alone, located in countries all over the world such as Brazil, Chad, China, France, Italy, Saudi Arabia, and Sri Lanka. Moreover, environmental factors such as water, soil, and zoonotic vectors such as mosquitos and animals have been cited as important contributing factors to viral outbreaks.
WHO gathers surveillance statistics for specific viruses and estimates between 290,000 to 650,000 annual deaths from influenza, greater than previous estimates. Data from February 2018 indicated that the disease burden of influenza was highest in north and east Africa, South America, and Europe. Data from the WHO Mortality Database shows over 100,000 deaths from viral hepatitis since 2012 throughout the world. Outbreaks of gastrointestinal disease are also common around the world. Rotavirus, for example, is associated with high rates of pediatric mortality; rotavirus infection was found to be responsible for approximately 453,000 pediatric deaths in 2008 worldwide, accounting for 5% of all deaths in children younger than five years. Viral disease also disproportionately impacts poorer communities around the world. The aforementioned rotavirus study determined that over half of the pediatric rotavirus deaths worldwide occurred in just five developing nations (Democratic Republic of the Congo, Ethiopia, India, Nigeria, and Pakistan). Academic studies assessing global disease burden also report substantial burden due to viral disease. One study investigating global foodborne disease burden reported approximately 684 million disease cases and 212,000 deaths due to norovirus globally for the year 2010, the largest for any pathogen studied. The same study found hepatitis A virus responsible for approximately 47 million illnesses and 94,000 deaths in 2010.
Beyond diseases arising from direct infection, there are other secondary diseases associated with viruses, such as cervical cancer, which is strongly associated with papillomavirus. Other viruses have also been linked to increased incidences of heart disease and kidney disease, particularly in immunocompromised patients. Additionally, it is thought that the true impact of viral disease is underestimated. Many disease outbreaks are reported to be caused by agents of unknown etiology, and some of these outbreaks are suspected to be viral in origin. A One-Health approach could assist in discovering the origin of these disease outbreaks.
In the United States, the Centers for Disease Control (CDC) publish surveillance statistics regarding the rate and occurrence of disease for a number of human viruses, including influenza, adenovirus, hepatitis A virus, rotavirus, and West Nile virus. Annual summaries of these surveillance statistics are published in various forms from the CDC. The Summary of Notifiable Diseases (SoND) is an annual report containing information on those diseases for which “regular, frequent, and timely information regarding individual cases is considered necessary for the prevention and control of the disease or condition”, a list of which is updated regularly by the CDC. Viruses reported in the SoND include hepatitis A virus, West Nile virus, and Dengue virus. The CDC also maintains the National Outbreak Reporting System (NORS), which includes information on the number of disease cases and outbreaks for a number of infectious agents, including norovirus, rotavirus, and sapovirus. Influenza statistics are reported most frequently by the CDC via published FluView Weekly Influenza Surveillance Reports, documenting the number of cases of influenza and influenza-like illnesses in the United States. Each of these sources includes both monthly and geographic data regarding disease cases. This allows for the analysis of viral disease trends on both a temporal and spatial basis, many of which are unique from one virus to another [,,,,,,].
Porcine respiratory disease complex (PRDC) is one of the major problems to the swine industry worldwide and arguably the most important swine health concern for the swine producers today. During the past 30 years, swine production has been intensified with larger herd sizes and confinement rearing, contributing to the increased incidence and complexity of the respiratory diseases. Porcine respiratory disease complex often occurs in pigs around 6 to 20 weeks of age, especially in large pig farms with continuous production system. It is characterized clinically by slow growth, decreased feed efficiency, anorexia, lethargy, fever, cough, and difficult breathing. A multifactorial complex of swine respiratory pathogens has been reported to play a role or roles in PRDC, including bacteria and viruses, which are complicated by management and environmental factors. However, the pathogens involved vary significantly among farms and production sites. The viral agents that have been isolated from PRDC are porcine reproductive and respiratory syndrome virus (PRRSV), porcine circovirus type 2 (PCV2), swine influenza virus (SIV), pseudorabies virus (PRV), porcine respiratory coronavirus (PRCV), and recently Torque Teno viruses (TTV). The bacterial pathogens involved in PRDC include Mycoplasma hyopneumoniae, Pasteurella multocida, Actinobacillus pleuropneumonia, Streptococcus suis, Haemophilus parasuis, and Salmonella enterica serotype Chloeraesuis[1,3,7]. Procine circovirus type 2, PRRSV, P. multocida, and M. hyopneumoniae are the most important PRDC-inducing viral and bacterial pathogens, respectively, in Taiwanese swine industry.
Porcine circovirus type 2 and PRRSV have been suggested to be two of the important etiological factors for PRDC, and pigs with dual infections of PCV2 and PRRSV, however, consistently have more severe clinical symptoms and interstitial pneumonia. Swine alveolar macrophages (AMs) co-inoculated with PCV2 and PRRSV have been shown to have significantly higher expression levels of Fas ligand and Fas than those inoculated with PRRSV alone. In addition, co-infection of PCV2 and PRRSV in piglets synergistically has been found to suppress the mRNA expression profiles of T helper (Th) 1- and Th2-type cytokines in the peripheral blood mononuclear cells (PBMCs). Furthermore, dual infection of PCV2 and PRRSV in pigs with a PCV2 mutant that has the mutation at the interferon-stimulated response element (ISRE)-like element could exacerbate the pathological lesions and increase the PCV2 viral DNA load in the tissues. These findings indicate that the interactions of PCV2 and PRRSV are critical to the pathogenesis of PRDC.
Pulmonary alveolar and/or intravascular macrophages are known as the major target cells for both PCV2 and PRRSV in the lungs. We have previously used in vitro approaches to study the effect of infection with PCV2 alone or PRRSV alone on the functional changes of swine AMs; it was found that either PCV2 alone or PRRSV alone could cause significant reduction in the microbicidal capability and induce changes in expression levels of cytokine and chemokine, which may explain partially the pathologic changes in the infected pig lungs. In a co-infection study with PCV2 and PRRSV, instead of observing an enhanced effect, PCV2 reduced PRRSV replication and PRRSV-associated cytopathy by inducing IFN-α production in swine AMs. Such findings, however, do not reflect and explain the enhanced clinical disease observed in PRRSV and PCV2 dually infected cases in the field. Therefore, the effects of dual PCV2 and PRRSV infection on the functions of swine AMs need further elucidated.
In a pig farm infected with PCV2 and PRRSV, it is conceivable that individual pigs may be attacked by both viruses in different sequence or order. The objective of the present study was to determine if different infection orders of PCV2 and PRRSV would result in different consequences in the functions of swine AMs by the in vitro inoculation of swine AMs with PCV2 and/or PRRSV.
Pandemic influenza A (H1N1) 2009 virus was first recorded in Norwegian pig herds in October 2009. Before that, documentation on freedom from several specific viral diseases in the pig population was provided by the surveillance and control program, where swine influenza (subtypes H1N1 and H3N2) has been included since 1997. All the nucleus and multiplying herds are included in this program.
The Norwegian pig population is also documented free from porcine reproductive and respiratory syndrome virus, Aujeszky's disease, porcine respiratory corona virus, and transmissible gastroenteritis. In 2009 the pig population in Norway was declared free from enzootic pneumonia (Mycoplasma hyopneumoniae). Porcine circovirus type 2 is, however, presumed to be present in all Norwegian swine herds, including nucleus and multiplier herds.
In contrast to Norway, the pig populations in most other countries are endemically infected with different swine adapted subtypes of influenza A virus [4–6]. Typical clinical signs associated with influenza infection are characterized by an acute onset of fever of short duration, inappetence, lethargy, coughing, dyspnea, and nasal discharge. Morbidity within infected herds is high (approaching 100%), but mortality is typically low (less than 1%). In recent experimental studies with pandemic influenza (H1N1) 2009 virus, a similar clinical picture has been described [8, 9]. Influenza viruses can also act synergistically with other viral and bacterial pathogens to cause porcine respiratory disease complex [10–12]. The course and severity of an influenza virus infection in pigs are influenced by co-infecting agents, the pig's age, overall health and immune status, and potentially the strain of influenza virus involved. It has been suggested that influenza infections may lead to reduced reproductive performance in affected animals. However, there is insufficient data to conclude that influenza viruses have a specific and direct relationship to the occurrence of reproductive problems in pigs.
The favorable health situation provided a unique opportunity to study the clinical impact of infection with pandemic influenza (H1N1) 2009 virus, and this paper describes the results of a case-control study performed on a naïve Norwegian pig subpopulation consisting of all nucleus and multiplier herds.
Porcine epidemic diarrhea (PED) emerged for the first time in Europe during the 1970s. The virus responsible for this disease is an alphacoronavirus known as porcine epidemic diarrhea virus (PEDV). The PEDV has a single-stranded, positive-sense RNA genome. An infection with PEDV in pigs leads to severe liquid diarrhea, vomiting and dehydration. In suckling piglets population, PEDV causes high mortality. In older animals, morbidity may approach 100%, but mortality remains low between 1 and 3%. Economic losses due to this virus are significant [2, 4–7]. Currently, PEDV is present on the Asian, American and European continents. In 2013, 40 years after the first cases of PED in Europe, the disease emerged in the United States (US), in the Midwestern state of Iowa, and ultimately affected the swine population of the entire country; until this date, the US had been free from PED. The virus spread rapidly causing a major impact on pig production including mortality of 10% of the total US swine production or approximately 7 million piglets in less than 1 year. Two genetically strains of PEDV have been identified in the USA, namely, the “non-InDel” strain, close to the aforementioned Asian strains, and the “InDel” strain, showing insertion-deletion in the S1 part of the S gene. Currently, PEDV is endemic in the US with periodic waves of infection occurring mostly during winter. The virus also spread to others countries in North and South America, such as Canada and Mexico [2, 10, 11]. In Europe, PED cases associated with the InDel strains have been detected since 2014 [10, 12–14].
Different PEDV transmission routes have been identified. The major mode of transmission is the fecal–oral route through direct or indirect contact with infected pigs or contaminated feces [2, 15]. Transmission of PEDV also occurs through contact with contaminated equipment, contaminated vehicles used for animal transport, or farm employees [2, 16, 17]. Experimental studies have shown that airborne samples containing PEDV can be infectious for pigs so PEDV could be spread through aerosols. In addition, PEDV has been transmitted vertically through contaminated milk from the sow to its piglets. PEDV transmission through semen has also been a concern due to a viremia that occurs during the acute phase of infection during which the virus may be recovered in blood and sexual organs. Contamination of semen by PEDV during processing may also occur. A recent study demonstrated PEDV nucleic acid detection in infected boars’ semen; however, the authors were not able to rule out external contamination by fecal material during collection and/or preparation of the semen. The PEDV genome has also been detected in the semen of healthy boars from three different farms in China. The quantity of detected PEDV genome ranged from 101.46 to 103.65 genome copies/mL of semen. It is known that some viruses such as porcine reproductive and respiratory syndrome virus (PRRSV), porcine parvovirus (PPV), African swine fever virus (ASFV), classical swine fever virus (CSFV), foot and mouth disease virus (FMDV), Japanese B encephalitis virus (JBEV) and porcine circovirus type 2 (PCV2) are shed in semen. However, PEDV detection in and transmission via semen has not been previously studied in experimentally infected boars. Contamination of semen by different porcine viruses via contaminated feces or aerosols could be possible. In France, non-InDel strains of PED are classified in the first category of regulated animal health hazards (Order Number: AGRG1410808A). In order to maintain the PEDV free status for non-InDel strains in France and in Europe, importing boars and boar semen from countries where non-InDel strains are endemic is strictly controlled. Therefore, it is important to know if PEDV can be shed in semen from infected boars in order to determine appropriate biosecurity measures necessary to prevent transmission of the virus. The objective of this study was to determine if PEDV can be shed in semen from specific pathogen-free (SPF) boars infected by a US non-InDel strain of PEDV.
Aujeszky’s disease (AD) is a viral disease of suids caused by Suid Herpesvirus 1 (SHV1), also referred to as Aujeszky’s disease virus (ADV). The virus belongs to the genus Varicellovirus, subfamily Alphaherpesvirinae, family Herpesviridae. It has a double-stranded DNA genome composed of 143461 nucleotides with more than 70 open reading frames homologues to related Alphaherpesviruses. Based on restriction fragment length polymorphism (RFLP) analysis patterns, ADV can be divided into four major genotypes. But according to partial gC (ul44) coding region, it is possible to divide ADV into five genotypes that appear to be unspecific to countries or continents.
AD is also named pseudorabies (PR) and the virus Pseudorabies Virus (PRV), because carnivores and pigs may display neurological signs which can be similar to rabies.
Wild boar (Sus scrofa) are the natural host, but a wide range of species can be infected with SHV1. Wild boars are known as reservoirs for many important infectious diseases in domestic animals, such as classical swine fever, brucellosis and trichinellosis. Also, they can play a role of reservoirs for zoonotic diseases such as hepatitis E, tuberculosis, leptospirosis and trichinellosis. Worldwide distribution, great potential of adaptation, fast reproductive rate and complex social behaviour make wild boar almost ideal reservoir species.
However, some diseases, like AD can sporadically occur in free living wild boars under natural conditions. Occurrence of these diseases is facilitated by social stress, age related change from passive to active immunity, individual susceptibility to ADV infection and environmental conditions.
AD has worldwide distribution. The economic impact of AD is significant, consequently many developed countries (Belgium, Czech Republic, Denmark, Germany, Ireland, Cyprus, Luxembourg, Netherlands, Austria, Slovenia, Slovakia, Finland, Sweden, UK) have eradicated, or are in the process of eradication of the infection from domestic pigs1. AD may also be controlled nationally by a vaccination programme. In Serbia, there is neither an AD eradication nor national vaccination programme of domestic pigs. Vaccination is conducted on individual voluntary basis only. Only in commercial farms, pigs are regularly vaccinated to reduce potential losses due to AD and therefore AD has rarely been reported in swine.
In Serbia, intensive pig production is located in the north part of the country, in the Autonomous Province of Vojvodina. In this area AD has moderate impact on intensive pig production, with the 32.8 % ADV seroprevalence in unvaccinated breeding pigs. Pusic et al. demonstrated that the swine population in Vojvodina region, the most developed region in Serbia with the biosecurity measures most applied, was enzootically infected with ADV and that vaccination was only performed on large commercial farms. Those farms were usually surrounded by small backyard holdings with occasionally vaccinated animals, which presented a potential source of infection. Due to vaccination with attenuated vaccine of Bartha strain, which is not a marker vaccine, seroprevalence attributed to the natural infection is difficult to estimate. The sampling has been done in this region where the virus can be transferred from wild to domestic pigs since it is separated from Vojvodina only by the river Danube.
Clinical AD in wild boar has rarely been seen, although Gortazar et al. described an outbreak in wild boar in Spain. It has been demonstrated that the virus could be successfully isolated from latently infected wild boars. Serosurveillance studies have demonstrated that the prevalence of AD could be high within the European wild boar population, indicating a potentially significant wildlife reservoir of ADV. Seroprevalence ranges from 0 % in the Netherlands and Sweden [14, 15] to more than 50 % in Croatia and central Italy and 100 % in Spain, on local level. As documented in Germany, continuous parallel increase of both AD seroprevalence and wild boar population density implies the correlation of these two parameters.
Within the Classical Swine Fever (CSF) monitoring programme in Serbia, 20 % of wild boars tested annually for CSF were also tested for ADV antibodies. The Monitoring is issued annually by The Ministry of Agriculture and Environmental protection and prescribes the number of samples to be collected for each district. Hunting season in Serbia lasts from April 15th to February 28th for boars and young wild boars up to 60 kg and from July 1st to December 31st for sows, although hunting is the most intensive from November to February. Specified percent of wild boars were subjected to AD serology tests, either VNT or ELISA. ADV seroprevalence in different regions varies with the highest percentage found in the east - 83 % as average for the last three years (unpublished data).
Until 2011, vaccination of wild boar against classical swine fever has been performed in hunting grounds in Serbia. Wild boars have been trapped, vaccinated, ear tagged and released back in the nature. Classical swine fever vaccine used for wild boar vaccination was produced by local company and composed of CSF C strain and attenuated ADV Bartha strain viruses. Therefore, unintentionally, some wild boars had been vaccinated against AD. The wild boar population in Serbia is estimated at around 20000 animals, with density of 0.2 - 1.38 animals/km2.
Natural transmission of Suid Herpesvirus 1 requires close contact between animals such as during coitus, licking, or nuzzling. Although, in high density commercial farms, sneezing and short distance droplet spreads are major routes of transmission.
The clinical presentation of ADV infection depends on the virulence and initial dose of virus; and also the age, immunological and reproductive status of the host. Within wild boar, Gortazar et al. reported that young animals were mostly affected, between four and eight months of age, with 14 % mortality. Although there is no evidence of any different susceptibility and disease course between wild and domestic pigs, it has been shown that strains from free-living wild boars differed genetically from those isolated from domestic pigs, but that both might have had a common origin [1, 22].
An important mechanism of ADV persistence, characteristic of all Alphaherpesviruses, is lifelong latency within the peripheral nervous system.
Diagnosis of Aujeszky’s disease can be achieved using various tests including viral isolation, molecular biology (PCR) and serology.
Since clinical symptoms of Aujeszky’s disease are not specific, it is important to establish a link between clinical signs and presence of ADV active infection in wild boars. The aim of this study was to investigate the possibility of active infection within wild boar showing signs of ADV and also to examine relationship between isolates from domestic pigs and wild boar. Having in mind that virus has not been previously isolated from wild boars in Serbia, we report the first isolation of Suid Herpesvirus 1 from this species in Serbia.
Over the past decade, outbreaks of new or reemergent viruses such as severe acute respiratory syndrome (SARS) virus, Middle East respiratory syndrome (MERS) virus, and Zika have claimed thousands of lives and cost governments and healthcare systems billions of dollars. Whether these outbreaks were caused by increased international travel, mutating viruses, or climate change, it is clear that our generation and future generations must find ways to recognize and contain outbreaks of new viruses quickly.
The ultimate goal should be the prediction of emergent diseases before they strike the human population. This is a lofty goal that will require dramatic advances in pathology, genetics, and ecology, along with major advances in computational science and public health practice. A complementary and achievable near-term strategy is surveillance of human populations for early signs of infectious outbreaks. While still a formidable task, we can build on comprehensive surveillance systems already in place in the United States and much of the world [3–7].
The simplest univariate detection algorithms track a time-series of a single value, such as emergency department visits or thermometer sales, and look for significant deviations from a baseline level of expected activity. Multivariate systems combine several indicators into a single compound indicator in seeking to increase performance. However, these systems suffer from two problems. First, if an outbreak of a new disease occurs during a larger outbreak of a known disease, it might not be noticed. For instance, imagine if a new disease causes fever. People with this disease might purchase thermometers. However, if an outbreak of this new disease occurs during a large outbreak of influenza the increased thermometer sales due to the new disease would be overshadowed by the number of thermometer sales due to influenza. Second, they assume that the future will be like the past, and that outbreaks of influenza and other known diseases occur at the same time each year. For instance, suppose that the system expects increased thermometer sales during the month of January because that is when outbreaks of influenza typically occur but, in fact, there is no January outbreak of influenza in the current year. Then, an increase in thermometer sales in January due to an outbreak of a new disease might well be attributed to the expected outbreak of influenza and dismissed.
The WSARE (What’s Strange About Recent Events) system addresses these issues by representing the joint distribution of patient data with a Bayesian network that includes several environmental attributes to represent influenza activity, season, weather, etc. and several response attributes to represent patient attributes such as age, gender, location, and reported symptom (which is similar to a patient’s chief complaint and takes a value from none, respiratory problems, nausea, or rash). The network is conditioned on the current values of the enviromental attributes to create a conditional joint distribution of response variables for the current day. Thus, the conditional joint distribution represents what would be expected for the current day if there are no outbreaks of new diseases. Thus, WSARE does not take a strictly technical approach to predicting cyclic patterns, but rather incorporates current conditions. The WSARE system then searches for rules that describe significant differences between the actual current data and the conditional joint distribution. For instance, if there are many patients with fever in the current data, but the conditional joint distribution predicted few patients with fever, WSARE would report this. The WSARE system has two important shortcomings, however. First, as with time-series methods, if an outbreak of a new disease occurs during a large outbreak of influenza it might not be noticed. Second, it can be misled by outbreaks of other known diseases such as RSV, parainfluenza, hMPV, etc. For instance, if the environmental attribute influenza activity is low, but there is an outbreak of RSV, the resulting surge of patients with respiratory ailments would cause a false alarm. (We note that these shortcomings could be corrected by adding additional enviromental attributes for each known disease and additional response attributes for a set of clinical findings sufficient to distinguish between different respiratory illnesses).
A patient’s chief complaint is a concise statement of the symptom or problem that caused the patient to seek medical care. Often stated in the patient’s own words, a chief complaint typically does not mention predefined syndromes or disease categories. Keyword-based systems can operate in real-time to identify anomalies or clusters of unusual findings from text. describes a semantic scan sytem that infers a set of topics (probability distributions over words) from the free-text of chief complaints. The system learns one set of topics using past data and a second set of topics from the most recent 3-hour moving window, assigns each patient case to its most likely topic, then looks for anomalous counts and clusters of topics. extends this approach to identify clusters also based on geography or social patterns.
A distinctive feature of an infectious outbreak is an initial period of exponential growth. describes a Bayesian system, based on moving windows of ILI records, to detect a period of exponential growth that can signal the start of an outbreak. That system uses Bayes’ factors to determine when it is likely that an outbreak has started.
This paper describes a Bayesian modeling approach called DUDE (Detection of Unmodeled Diseases from Evidence) that can recognize outbreaks of new forms of influenza-like illness (ILI) and create clinical characterizations of them. We demonstrate its operation on data from real-world outbreaks including an outbreak of Enterovirus EV-D68. DUDE avoids the shortcomings of previous sytems by building probabilistic models of normal (baseline) ILI activity using a large set of patient findings extracted from patient-care reports using natural language processing. (This approach to ILI detection and characterization was developed in). It then looks for statistically significant deviations from baseline normal activity. Thus, DUDE does not rely on just a small set of findings (as might be extracted from patients’ chief complaints). Also, it does not model temporal patterns and therefore does not assume that the present is like the past. Finally, by removing cases of known forms of ILI (such as influenza, RSV, etc.) from the input data, it can recognize new, emergent kinds of ILI.
A large number of virus genomes have been engineered to carry additional sequences for a variety of purposes. Viruses are often used as vectors for heterologous gene expression in cultured cells or the natural host. For example, the baculovirus expression system is widely used for expression work (Chambers et al. 2018), lentiviruses show great promise for gene therapy (Milone and O’Doherty 2018), and phage display allows for selection of desired epitopes (Wu et al. 2016). Marker genes have also been built into viruses to facilitate tracking infection spread (Dolja, McBride, and Carrington 1992). As viruses evolve rapidly, including the incorporation of genome-rearrangements, it is therefore unsurprising that the insertion of sequences into viral genomes often goes hand in hand with the rapid occurrence of deletions (Koonin, Dolja, and Morris 1993; Pijlman et al. 2001; Zwart et al. 2014). The inserted sequence, and sometimes parts of the viral genome, are then rapidly lost. This genomic instability can have economic ramifications, leading to decreases in heterologous protein expression (Kool et al. 1991; De Gooijer et al. 1992; Scholthof, Scholthof, and Jackson 1996). It can also introduce limitations and complications to working with marker genes (Dolja et al. 1993; Majer, Daròs, and Zwart 2013). Understanding the stability of inserted sequences therefore has value from an applied perspective, but it could also shed light on basic questions. First, how stable are natural virus genomes, and under what conditions do they become unstable? Second, since horizontal gene transfer (HGT) plays an important role in virus evolution, under what conditions are transferred sequences likely to be retained?
In this review, we consider the stability of inserted sequences and the dynamics of their removal from virus genomes from an evolutionary perspective. First, we provide an overview of empirical results which shed light on insert-sequence stability for viruses, based on the Baltimore classification. Second, we present some conceptual considerations pertaining to sequence stability, identifying important parameters for understanding and potentially predicting stability. We identify theory and experiments that point toward viable strategies for mitigating the rapid loss of inserted genes, and point out key questions that should be addressed in future research. We argue that virus genome organization has a large impact on the stability of inserted sequences, whilst stability is a complex trait that can depend on environmental conditions.
Influenza in pigs is a highly contagious viral disease of the respiratory tract. Influenza is currently endemic in most swine populations around the world, and the virus tends to spread easily in susceptible populations. Many factors contribute to the severity of the disease including age, viral strain, concurrent infections, and immune status of the animals.
With the detection of new influenza subtypes in the last decade (i.e. H1N1, H1N2 and H3N2 triple reassortant viruses) in pigs and the recent appearance of the 2009 pandemic H1N1, both human and animal health officials have paid greater attention to flu in pigs due to the role that pigs play in inter-species transmission. The control of influenza in pigs is often accomplished by the use of vaccines. Both inactivated licensed commercial vaccines and autogenous licensed inactivated vaccines are commonly used in pigs. Commercial vaccines confer protection against flu infection and disease presentation but often this protection is only partial. Commercial vaccines usually include one or more isolates representative of the strains in a region but they may not always confer protection against the isolate infecting a specific farm or population. On the other hand, autogenous vaccines may be prepared with the isolate or isolates recovered from a specific production system and restricted to use in only that system. These vaccines have gained popularity in the US in the past few years. Although vaccination can result in the reduction of clinical signs and virus shedding, limited information is available on the effect that vaccination has on population susceptibility, the spread of infection and how vaccination may prevent transmission to other species.
Transmission experiments and mathematical models have been used to quantify vaccine-induced reduction in the spread of Mycoplasma hyopneumoniae, pseudorabies virus, classical swine fever, Actinobacillus pleuropneumoniae, encephalomyocarditis virus (EMCV), foot and mouth disease (FMDV), porcine reproductive and respiratory syndrome virus (PRRSV), hepatitis E virus, and porcine circovirus type 2 (PCV-2) in pigs. In order to quantify transmission of a pathogen, a key parameter is the reproduction ratio (R) of the infection which is defined as the average number of secondary cases caused by an infectious individual in a population during its entire infectious period. When R is greater than 1, an infection can spread in a population but if R is less than 1, the infection will die out within a population. The estimation of R can provide important information about the potential for transmission of infection, the dynamics of infection at the population level, and the impact of disease control strategies.
The reproduction ratio has been assessed for influenza A virus in humans, birds, and horses, but R has not been reported for influenza virus A in pigs. In this study, a deterministic SIR model (Susceptible-Infected-Recovered/Removed) was used to compare transmission parameters between a non-vaccinated population and vaccinated populations of pigs following the introduction of a non-vaccinated, infected pig with a triple reassortant H1N1 influenza A virus. The introduction of infected pigs into populations is one of the primary modes of influenza virus transmission in field settings and this study mimics a similar scenario. Specifically we aimed at assessing the effect of vaccination on pig susceptibility to infection. Since different vaccines containing inactivated viruses that were either homologous or heterologous to the challenge virus were used in this study, an additional comparison could be made between vaccine types. Results from this study provide relevant information on the use of vaccination to control influenza transmission, and highlight the implications of partial protection may have in transmission dynamics and risk of infection.
Porcine circovirus 2 (PCV2), a single-stranded DNA virus of Circoviridae family, causes multi-systemic disease referred as porcine circovirus-associated disease (PCVAD). PCV2 is transmitted horizontally as well as vertically. Direct contact is the most efficient way of horizontal transmission of this virus. The clinical signs of PCV2 infection include poor weight gain, respiratory problems, dermatitis, enteritis, nephropathy and reproductive failures. Five genotypes of PCV2 (PCV2a to PCV2e) are identified and circulate with high prevalence in swine herds causing significant economic losses worldwide.
Porcine parvovirus (PPV) is the common cause of reproductive failure in swine herds. This single-stranded DNA virus of Parvoviridae family is transmitted through oral-nasal routes. Stillbirths, mummification, embryonic death, and infertility (SMEDI syndrome) are linked to PPV infection. Conventionally, PPV was considered genetically conserved but recent evidences suggest that several virulent strains have emerged due to its high mutation rate.
Aujeszky’s disease or pseudorabies in pigs is caused by Suid herpesvirus 1, a double stranded DNA virus belonging to Herpesviridae family. The causative agent is spread primarily through direct animal-to-animal (nose-to-nose or sexual) contact. Pseudorabies is characterized by nervous disorders, respiratory problems, weight loss, deaths in younger piglets and reproductive failures; and is one of the most devastating infectious diseases in pig industry [18, 19].
African Swine Fever (ASF) causes hemorrhagic infection with high morbidity and mortality. The etiologic agent, ASF virus (ASFV), is a double stranded DNA virus of Asfarviridae family. Virus transmission occurs through direct contact with infected animals, indirect contacts with fomites or through soft tick species of the genus Ornithodoros. Clinical disease may range from asymptomatic infection to death with no signs. Acute infections are characterized by high fever, anorexia, erythema, respiratory distress, reproductive failure in pregnant females and death. ASF is OIE notifiable disease. United States is free of ASFV, however, this virus is endemic in domestic and wild pig population in many parts of the world with possibility of transmission to the US and other nonendemic regions through animal trades. The economic losses are associated with production loss, trade limitations and tremendous expenditures in eradication programs.
Besides the RNA and DNA viruses described above, many other emerging and re-emerging viruses such as porcine hepatitis E virus, porcine endogenous retrovirus, porcine sapovirus, Japanese encephalitis virus, encephalomyocarditis virus and others cause variable degree of impact in swine health and economic losses in pig industry globally [2, 21, 22].