Inapparent to rapidly fatal disease is evident in case of domestic fowl. Particularly in young birds, there is quick strike by the lethal strain of the avian influenza virus resulting in sudden death without manifestation of clinical signs. The disease syndrome in birds ranges from asymptomatic/subclinical to mild upper respiratory tract illness and egg production losses to a highly fatal systemic disease causing severe epidemics due to the highly contagious nature of the virus. Morbidity and mortality both remain very high in fatal disease episodes. Incubation period of the virus is a few hours to 3 days. The majority of the avian influenza viruses also cause local infection in the respiratory tract or in the gut, which frequently remains asymptomatic (WHO 2011). By contrast, other avian strains are highly pathogenic (H5, H7) causing fowl plague, a systemic infection that is often fatal. The birds may die without showing any signs in peracute cases. In acute cases there is dullness, cyanosis of comb and wattle, oedema of face, cessation of egg production, respiratory signs, diarrhoea and sometimes nervous disorders such as convulsion, blindness or paralysis. The mortality may be as low as 0 %, or as high as 80–100 % (WHO 2011) depending on the virulence of the strain.

Typical flu-like symptoms are characteristics of swine influenza. Affected animals develop fever, nasal and ocular discharge, sneezing, rapid and laboured breathing and severe spasms of coughing (Van Reeth 2007; OIE 2008; Simon-Grife et al. 2012). Secondary bacterial or viral infections are the complications. Severe, potentially fatal bronchopneumonia is occasionally seen (Fenner et al. 1987). Lethargy and anorexia also prevail. Sudden onset and rapid spread of these signs for 7 days are common which often are followed by quick recovery (Easterday and Van Reeth 1999; Kothalawala et al. 2006). In some cases, swine influenza may be associated with reproductive disorders including abortion. If the virus is introduced for the first time into susceptible herds, acute infections occur and may result in severe outbreaks. In swine populations, influenza epidemic or endemic are common. Within a herd, the virus can circulate for an extended period provided there is presence of susceptible pigs. Poor growth rate as well as loss in weight are also evident. These are the major causes of threat to the economical stability for those farmers who rear pigs (Kothalawala et al. 2006). The virus quickly moves through the swine population epidemically with rapid recovery if there are no secondary bacterial infections. All pigs may not demonstrate classical signs which are obvious in endemic form. Morbidity reaching 100 % is common with SIV infections and mortality rates usually found to be low. However, clinical manifestations may be exacerbated by secondary bacterial infections, and after 2–6 days infected pigs might recover if the condition has not been complicated. Typically, the outbreaks occur during the fall as well as early winter. These are frequently observed in finishing age pigs kept in nursery (Kothalawala et al. 2006; Lynch and Walsh 2007; Vincent et al. 2008).

On examination of gross lesions during post mortem examination, a clear-cut demarcation is noticed between normal as well as affected tissues of the lungs (Easterday and Van Reeth 1999; Kothalawala et al. 2006). There may be interlobular oedema along with involvement of various areas which are often purple as well as firm. Fibrinous exudates that are tinged with blood may fill the airways along with appreciable enlargement and oedema of mediastinal and mesenteric lymph nodes along with bronchial and cervical lymph nodes. There may be hyperemia of the mucosa of the larynx and pharynx along with a covering of tenacious mucus. Interstitial pneumonia along with fibrinous pruritis may be observed in severe cases of swine influenza. Congestion in the parenchyma of lungs in a widespread fashion; thickening of septa of the alveoli; degenerative changes in the small bronchi epithelium along with their necrosis; atelectasis as well as focal emphysema are among the microscopic lesions. Along with this, cellular infiltration in the peribronchial as well as perivascular space is also observed (Dhama et al. 2005b; Kothalawala et al. 2006). Pigs infected with H1N1 were observed to have more lesions in the lungs than pigs infected with H3N2 (Sreta et al. 2009). A human-like H1N2 influenza virus has recently been isolated from captive wild boars in Brazil (Biondo et al. 2014).

Equine influenza commonly occurs in horses and worldwide is responsible for notifiable morbidity. Equine influenza outbreaks are characterised by sudden onset and rapid spread. Clinical signs most commonly encountered are high fever, dry, harsh and non-productive cough, serous nasal discharge that becomes yellow with secondary bacterial infection, depression, loss of appetite, weakness, watery eyes; swollen lymph nodes, submandibular lymphadenopathy, oedema with stiffness of legs, laboured breathing, generalised weakness; pneumonia in young foals and donkeys, encephalitis in horses may also occur but rarely. Tracheobronchitis is a common complication in most young horses. This along with deep and dry hacking cough worsens the condition (Gerber 1970; Radostits et al. 2003; Daly et al. 2006). The incubation period of the disease is generally about 1–5 days. A high morbidity (80–100 %) is commonly seen in affected equine population. Strangles, purpura haemorrhagica, chronic bronchiolitis and alveolar pulmonary emphysema and asthmatic conditions were notifiable in certain horses affected with secondary form of the disease. In mild cases horses usually recover within a few weeks. In the absence of complete rest, full recovery in severely ill horses is achieved within a few months. Adult horses which are healthy, however, recover within 10 days in case of uncomplicated cases but there may be persistent coughing (Newton and Mumford 2005; Cullinane et al. 2006; Landolt et al. 2007, www.​agric.​wa.​gov.​au).

The horses may develop fever (~103–106 °F) that may last for 2–3 days. Explosive outbreaks due to equine influenza have been recorded that are characterised by persistence of cough along with discharge from the nostrils; depression as well as anorexia in population of horses that remains unvaccinated. There is interestingly no carrier state of the disease for a long time but in recently infected horses either mild or sub-clinical disease is observed if status of vaccination remains unnoticed. Unless there is stress or sickness in the horses for some reason, morbidity remains high, while there is less mortality in young foal observed occasionally. There may be secondary involvements, viz. strangles and purpura haemorrhagica, chronic bronchiolitis as well as pulmonary emphysema in the alveoli. With relatively mild cases of equine influenza, horses usually recover in 1 or 2 weeks, but those that are severely ill and deprived of rest may require weeks to months for complete recovery. On rare occasions pneumonia is observed in young foals in addition to encephalitis-like neurological symptoms in adult horses (Livesay et al. 1993; Daly et al. 2006; Webby et al. 2007).

In certain instances gentle clinical signs are prominent. Affected horses show fever and loss of appetite; coughing and nasal discharge at varying degrees. Usually, healthy adult horses convalesce from uncomplicated equine influenza within 10 days but coughing may remain for longer periods. It needs several weeks for the Performance horses to recover fully. Secondary bacterial infections such as pneumonia are common for horses that are particularly elder, sick and young ones, which are worked during the course of the infection, and ultimately it may result in death. Abortion in pregnant mares and testicular degeneration in stallions are also common features of the diseases (Yurisich 2008). Thus, equine influenza is also one of the causes of reduced male fertility.

The ciliated epithelial cells of the upper as well as lower respiratory tracts are usually infected and damaged by the virus. This leads to reduced ability to cleanse bacteria as well as foreign substances. A protein called Neu5Gc2-3Gal when present in abundance in the horse trachea in the epithelial cells is recognised as critical for equine influenza virus replication in horses. General mechanism of cell death in trachea of infected horse is apoptosis. The cytotoxicity mediated by the virus is dependent on activation of caspase and its cellular targets’ cleavage (Hinshaw et al. 1994; Suzuki 2000; Lin et al. 2002; Radostits et al. 2003).

Nevertheless, it is to be noted that equine influenza is similar to an array of other viral respiratory infections, viz. equine herpesvirus, equine rhinovirus and equine adenovirus infections. These viruses mostly produce mild signs including runny nose along with coughing.

Influenza Type A (H3N8) was first identified in Florida in 2004 among dogs. It is the most well characterised subtype of canine influenza and can cause two clinical syndromes: mild form or subclinical and clinical or severe form. Two to five days after exposure, clinical signs in infected dogs lead to virus shedding for 7–10 days. Twenty percent of infected dogs may be asymptomatic carriers. The mild form occurs in almost 80 % of cases and the clinical signs include cough lasting for 10–21 days with greenish purulent nasal discharge with mild fever. Moist cough is evident along with discharges from the nostril. Symptoms may last for around 1 month. In most instances the mild form of the disease is self-limiting. In severe cases, high fever (104–106 °F) and pneumonia may also occur, which is due to secondary bacterial infection. These symptoms appear very quickly. The symptoms last for 10–30 days and disappear afterwards. In severe cases, the CFR may reach up to 50 % (Yin 2007) if not treated. Almost all dogs are vulnerable to infection due to new pathogen like H3N8. Eighty percent of exposed dogs may get affected clinically. Initially the case fatality rate is high. This leads to a case fatality rate of approximately 36 %. Dogs may be affected by other influenza viruses too. Severe lower respiratory tract disease along with high mortality rate is prominent in disease induced by subtype H3N2. Whole virus adaptation from an avian virus into a naïve population leads to different pathogenicity. Similar kinds of viral infections are also observed because of infection caused by H3 and H5 viruses both in dogs as well as cats (Harder and Vahlenkamp 2010). In Thailand, ingestion of chicken tissue infected with HPAI H5N1 has led to severe respiratory disease as well as fatal infection in a dog. In New York during 2009 H1N1 infection was also reported (Dubovi and Njaa 2008). Aerosols are the main source for easy transmission of the H3N2 influenza virus of canine. Elevated gene expression in relation to inflammation as well as apoptosis may result in severe pneumonia. There may be severe pneumonia in the left cranial, middle as well as caudal lobes of lungs that are infected. Along with this, there may be oedema and haemorrhages. Numerous inflammatory cells may get infiltrated if there is interstitial pneumonia. Lung tissue may show accumulation of anti-influenza A nucleoprotein antibody which are predominantly in the pneumocytes as well as some macrophages of the alveoli (Kang et al. 2013).