AI, also known as avian flu/bird flu/fowl plague/fowl pest/chicken ebola, was relatively uncommon until 1997, but during the past 15 years its incidence has increased steadily. Between 1959 and 1998 AI outbreak affected 23 million birds, whereas it reached >200 million from 1999 through 2005. It is the most fearful viral disease of birds, particularly affecting domesticated birds with very high flock mortality (up to 100 %). Since the late 1990s, AI outbreaks pose great public health problems, especially through devastating consequences for the poultry industry, creating negative awareness among the public and the risk of generating a pandemic virus against mankind through an avian–human link.

AI, caused by the genus Influenzavirus A, consists of 18 HA and 11 NA subtypes, present mainly in wild waterfowl, shorebirds and gulls, and some constrained subset found in birds, human beings and other mammals (Wainwrighta et al. 2012; Brown et al. 2013; Wibawa et al. 2014; Wille et al. 2014). The H17N10 and H18N11 has been isolated only from bats (Tong et al. 2012, 2013). The H5 and H7 are responsible for generalized disease while the remaining subtypes are associated with localised form of the disease. Although AI is primarily a disease of domesticated poultry such as chickens, turkeys and pheasants, subclinical infections do occur in a wide range of feral migratory birds. Fowl act as the natural asymptomatic carriers of AI virus whereas major reservoirs for the virus are ducks, geese as well as migratory birds that play an important role in the disease transmission to domestic birds mainly through respiratory secretions and droppings (Swayne and Halvorson 2003; Arzey 2004; Campitelli et al. 2004; Musa et al. 2009; Stallknecht and Brown 2013). The high moisture and low temperature conditions favour its survival in poultry manure for more than 100 days. It has been reported that one million susceptible birds may become infected with 1 g faeces of the infected bird (Swayne and Halvorson 2003).

The disease is highly contagious and can spread to vast geographical areas very fast if strict biosecurity, prevention and control measures, etc., are not properly followed. From the infected birds, the viruses get excreted through their respiratory tract, conjunctiva and faeces and spread through direct contact as well as indirectly by means of aerosols, virus contaminated soil, feed, water, faeces, equipments, fomites, etc. (Alexander 2001; FAO 2004; de Jong et al. 2005; WHO 2006; Vong et al. 2008, 2009; Kandun et al. 2009). Another possible means of transmission is from the blood or body fluids of infected birds via slaughterhouse and other food processing practices (Greiner et al. 2007), consumption of uncooked poultry products, improper waste disposal practices, etc. (Beigel et al. 2005; de Jong et al. 2005; Apisarnthanarak et al. 2005; Gambotto et al. 2008; Coburn et al. 2009).

Subclinical infection has been recorded in South-East Asia in geese and ducks due to involvement of H5N1 virus. In Hong Kong, in May, 2001, increase in mortality has been recorded severely in chicken due to which a decision was made immediately to cull over a million birds within a single month, which resulted in no further report of poultry cases (Guan et al. 2002). Usually, in the winter months outbreaks have been recorded in poultry in Hong Kong due to poultry meat import in order to meet the requirements of lunar New Year activities (Smith et al. 2006). Although HPAI outbreak in wild birds is rare, there is discovery of highly pathogenic H5N1 cases in wild birds through surveillance. In free flying wild waterfowl, high mortality rates have been observed having consistent genetic marker with prior adaptation in land-based poultry birds (Ellis et al. 2004; Lui et al. 2005). Results based on laboratory diagnosis have revealed many genotypes of H5N1 that are in circulation in Hong Kong among wild birds. In southern China during 1999–2002, surveillance of AI in water fowl yielded several H5N1 isolates from ducks that were apparently healthy (Chen et al. 2004; Cowling et al. 2013). Shedding of virus has been recorded from trachea and cloaca in ducks causing death in inoculated chickens (Hulse-Post et al. 2005).

The movement of infected birds is responsible for the outbreak of low pathogenic avian influenza (LPAI) in commercial poultry. Along with this, some other factors like dirty or improperly cleaned crates and contaminated vehicles from the live bird market system (LBMS) to the poultry farms also play important roles in the spread of the virus. In North America, surveillance studies have shown that there is repeated recovery of influenza A viruses in waterfowl and shorebirds but the recovery of virus is influenced by geography and season, age and species of birds. In certain parts of the United States the LBMS has been considered as a reservoir made by man for influenza viruses in addition to the natural reservoirs of the virus (Senne et al. 2006; Stallknecht and Brown 2007). The role of live bird markets (LBM) in the epidemiology of AI was revealed in the 1997 Hong Kong epidemic (Sims et al. 2003; Kung et al. 2007). Since then several researchers have reported that H5N1 viruses circulated among geese, ducks and chickens in LBMs in affected Asian countries since 2003 (Nguyen et al. 2005; Webster et al. 2006; Jadhao et al. 2009; Liao et al. 2009; Van Kerkhove et al. 2009; Indriani et al. 2010; Wan et al. 2011; Sarkar et al. 2012). Additionally, many festivals associated with raising (either commercially or domestically) (Vong et al. 2009), selling and transporting the poultry birds also plays a role in spreading of the virus in Africa (Musa et al. 2009) and Thailand (Ortiz et al. 2007; Hinjoy et al. 2008; Tiensin et al. 2009; Santhia et al. 2009). Interspecies transmission among chickens, turkeys and wild birds, particularly ducks, may play an important role to introduce avian influenza viruses in susceptible flocks (Nagarajan et al. 2012). Influenza in turkeys is more common in countries where birds are kept in an environment to which wild birds have easy access.

Due to restriction on control and export due to notifiable viral infections, the ostrich industry in South Africa was found to be badly affected. A syndrome of green urine was first observed by the farmers in the early and mid-1980s. Local migratory water birds play an important role in spread of AI as revealed by surveys due to the involvement of free-range type of production systems. Wet and colder months are more favourable for survival as well as detection of virus. The severity of the disease is governed by management and population density, immune status as well as age (Hanson 2002; Olivier 2006).

Aquatic birds are considered the prime source of influenza viruses and this perpetuation in aquatic avian species along with its ecological features has been studied by the phylogenetic analysis of RNA segments coding for the spike proteins (HA, NA and M2) and the internal proteins (PB2, PB1, PA, NP, M and NS) of influenza A virus isolated from different host range and geographical regions. The study revealed the following facts regarding the influenza A virus subtypes:

Swine influenza is one among the primary porcine respiratory diseases (Brown 2000; Heinen 2003; Dhama et al. 2012) inflicting high morbidity but with low case fatality rate (Vincent et al. 2009). Since pig is susceptible to both human and avian influenza viruses, it can be an important host in disease ecology. The primary strains of influenza A viruses causing the disease include H1N1, H1N2 and H3N2 (Brown et al. 2012). Swine influenza was first reported in 1918 from US, Hungary and China along with a human pandemic influenza causing a worldwide mortality of 20 million (Chun 1919; Koen 1919; Beveridge 1977; Brown 2000) and later the presence of a common ancestor for porcine and human influenza virus A has been proven (Gorman et al. 1991; Kanegae et al. 1994; Reid et al. 1999). The most prevalent subtypes of Influenza A viruses infecting pigs are H1N1 (including classical swine H1N1 and avian-like H1N1) and H3N2 (human- and avian-like H3N2). It is endemic in swine populations worldwide and the increasing incidences are based on factors like antigenic shift, cold weather (more outbreaks in the colder months due to low humidity and poor sunlight) (Easterday 1980), lack of proper husbandry practices and other secondary infections. The disease can remain enzootic in farms particularly by young pigs and get transmitted mainly by aerosols, fomites as well as carriers like waterfowl and humans (Easterday and Van Reeth 1999). Over 80,000 influenza gene sequences have been published by the Influenza Genome Sequencing Project and other contributors from the isolates of numerous species around the world, leading to advances in molecular influenza epidemiology (Nelson and Holmes 2007). These studies have demonstrated a high frequency of genetic reassortment in A/H3N2 viruses, especially among the genetically distinct cocirculating dominant and subdominant lineages of previous seasons, resulting in new antigenic variants (Holmes et al. 2005; Nelson et al. 2006; Vasoo et al. 2009; Lee et al. 2011). In North America, Europe and Asia two genes have been recognized in the H1N1 subtype of swine influenza along with influenza virus genes of avian and human origin. This is regarded as a quadruple reassortant virus acquiring the capacity of man-to-man transmission. In recent years H1N1 swine flu virus (H1N1 triple human/avian/swine reassortant virus) have caused human pandemic (Dhama et al. 2012). The H3N2 virus currently has shown a novel reassortment from swine with confirmed cases in human affecting children mostly in United States (Skowronski et al. 2012). In the context of the concept of ‘original antigenic sin’ it has been postulated that if there is an exposure of a child to an influenza virus for the first time there is development of strongest immunity in the later generations to come. As a result of this, there may be development of natural immunity to the A/H1N1 pdm pandemic virus that is circulating at the moment (Chowell et al. 2011; Rifkin and Schaal 2012).

The most destructive outbreak of equine influenza is ‘The Great Epizootic of 1872’ occurred in North America, leading to a major economic panic in US for 6 years. Thereafter, epidemics of equine influenza occurred in Europe and North America during 1956 (H7N7), 1963 (H3N8), 1969, 1979, 1989 and 2007 (significantly affected the horse racing industry in Australia). The virus mainly spreads through inhalation of infected droplets and nasal discharge (Radostits et al. 2006) as well as through contaminated transport vehicles and other equipments. Infected horses excrete the virus in their exhaled air before they show any signs up to 8 days after initial infection, but recovered horses do not become carriers (Timoney 1996; Morley et al. 2000). There are evidences for natural case of mixed infection, suggesting that the virus infects other species and the donor equine host may possess the genetic diversity required for the virus adaptation to new host species. The unpredictable nature of the equine influenza virus H3N8 has been reported (Daly et al. 2011). Equine influenza virus can infect the human beings but the symptoms are very mild and mostly remain subclinical but may represent a potential biohazard to laboratory personnel (Alexander and Brown 2000). After a gap of nearly 20 years, equine influenza virus outbreak by H3N8 subtype was reported from India in 2008 from different regions. Molecular analysis revealed that its haemagglutinin gene was closely related to Clade 2 of the Florida sublineage in American lineage (Virmani et al. 2010).

Pets like dogs and cats have been domesticated by humans since at least 3,500 years and there is always a positive trend for keeping them as pets (Kumar et al. 2012a,b; Singh et al. 2013). Along with the advantages and benefits particularly as pets, dogs and cats may also serve as source of zoonotic diseases and the epidemiology of influenza infections in dogs and cats have been attaining considerable attention during the last decade (Verma et al. 2008). Canine and feline influenza is an infectious disease of the upper respiratory tract of dogs and cats, respectively, caused by influenza A virus (H3N8) (Rahman 2012). Canine influenza virus (CIV) is a recently identified, extremely contagious respiratory pathogen of dogs, inflicting high morbidity, low mortality and a case fatality rate of 5–8 % in greyhound dogs and less than 1 % in the general pet population (de Morais and Helio 2006).

The first report of the disease under natural condition was in greyhound dogs of Florida in 2004, after conducting dog racing on horse racing track (Dubovi and Njaa 2008). Now it is proved that canine influenza originated from equine influenza virus and jumped species in 1990. Since then, H3N8 was also responsible for a major dog flu outbreak in all breeds of dogs (Tremayne 2006) including pet dogs. At present the US is considered an endemic area for the presence of canine influenza virus (Yin 2007). Additional subtypes of influenza virus reported to be infecting dogs include H3N2 (avian-origin) from South Korea (Song et al. 2009; Lin et al. 2012) and southern China in 2007 (Li et al. 2010) and Brazil in 2012 (Mancini et al. 2012), HPAI H5N1 from south to east Asia in 2006 and the new North American H1N1 from New York in 2009. So far there is no report of its transmission to humans and other animals (Crawford et al. 2006). Heterogeneity of these viruses in their natural reservoirs and recent evidence on the establishment of natural clinical infections in carnivores necessitates that this infection should also be considered in canines and felines with lower respiratory diseases. Also, the possible epidemiological role of canine and feline species in interspecies transmission needs to be explored (Harder and Vahlenkamp 2010). Equine Influenza virus H3N8 was found to be transmitted from horses to dogs coming in close proximity to infected horses in Australia in 2007 (Kirkland et al. 2010; Crispe et al. 2011). However, dogs experimentally infected with canine influenza A H3N8 virus were unable to transmit infection to horses cohoused with these infected dogs (Yamanaka et al. 2012). The annual prevalence of influenza in dogs due to H3N8 in USA increased from 44 % in 2005 to 62 % in the year 2007, before decreasing to 38 and 15 %, in 2008 and 2009, respectively (Anderson et al. 2013). A seroprevalence for canine influenza virus H3N8 of 1.9 % in flyball dogs (Wiley et al. 2013), and 0 % in racing sled dog (Pecoraro et al. 2012) was reported.

In humans, influenza (flu) occurs either as an epidemic or as a pandemic (Nicholson 1998) and the infection is mainly from influenza viruses subtypes A, B or C that can be differentiated by serological tests using conserved viral nucleoprotein or matrix protein (Beard 1970). Recent human influenza outbreaks were inflicted by the antigenic variants of influenza A viruses (H1N1, H3N2 or their reassortant H1N2) and influenza B viruses. Genomic analysis of H1N1 subtype that occurred in Mexico in 2009 revealed its close relation with the common swine influenza A reassortant viruses found in Asia, North America and Europe (Trifonov et al. 2009). The clinical illness of human influenza include that for usual flu, viz. cough, sore throat, fever and in fatal cases leading to breathing problems as well as pneumonia. Immune status of the victim plays a major role in determining the severity of the infection and previous exposure of the virus renders partial immunity to the host. That is why there are severe clinical signs as well as higher death rate in young ones and emergence of new influenza A virus subtypes results in pandemic form of influenza. In those infants whose maternal antibodies have declined, exposure to an influenza agent may lead to an attack rate of 30–50 % (Noble 1982; Glezen et al. 1977).

Transmission of human influenza is mainly through aerosols (Tellier 2006) affecting all ages especially pregnant women (Steinhoff and MacDonald 2012) and those below 30 years (Wilde 2010). The incubation period for influenza A and B viruses is 3 and 4 days, respectively. The incidence of influenza is more during winter in temperate countries (Wilde 2010), whereas it is more common during winters and rainy seasons in tropical and subtropical countries.

Bird Flu in Humans Bird flu is an infectious disease affecting birds and was first observed in Italy in 1878. Although the bird flu influenza virus A usually does not affect humans but there are reports proving the infection of bird flu virus in human (Morens et al. 2009; Zimmer and Bruke 2009). Severe life-threatening complications are characteristics of bird flu in humans (Malik Peiris 2009; Riquelme et al. 2009). Juveniles and migrants play an important role in the seasonal epizootics of avian influenza virus (Dijk et al. 2014).