Influenza (Swine Influenza; Swine Flu)
Swine influenza is a rapidly spreading viral disease characterized by sudden onset of fever, occulonasal discharge, prostration and weakness, followed by paroxysmal coughing over a relatively short course of 5-7 days, and relatively low mortality in uncomplicated outbreaks.
In the United States, swine influenza (SIV) is common and widespread. Serologic surveys show that nearly all of the herds in the Midwest have antibodies to SIV.
Swine influenza occurs in swine of all ages. Outbreaks once were seen mainly in the fall and winter in finishing animals but now occur throughout the year and can be seen in younger, nursery age pigs. The disease is present in most major swine-raising countries.
Swine influenza subtype H1N1 first appeared in western Illinois in 1918 during an influenza pandemic that killed an estimated 20 million people worldwide.
Increased interest in zoonoses and public health has included an intense interest in all influenza viruses. There now is clear evidence of interspecies transmission of influenza viruses among swine, chickens, ducks, turkeys, many wild birds and people. When concurrent infection of poultry or swine with 2 or more strains of virus occurs, there is potential for reassortment of segments of genetic material with development of new strains resulting (genetic “shift”).
In the United States, SIV is caused by type A influenza viruses (family Orthomyxoviridae). Swine influenza viruses have glycoprotein “spikes” on their surface that act as major surface antigens. There are 16 hemagglutinin (H) and 9 neuraminidase (N) surface glycoproteins that are numbered to help identify virus strains. The surface antigens of influenza viruses can change because of antigenic drift, reassortment of genes during concurrent infections with different strains of virus (antigenic shift), or cross species transmission.
The classic subtype in swine, H1N1, has been the predominant subtype in swine in the US since 1918 but H3N2 and H1N2 emerged during the 1990s and have persisted as significant causes of disease in US commercial swine. These H3N2 and H1N2 isolates vary in their origin and “triple reassortment” variants that are comprised of swine, human, and avian viral genes have been identified. In Europe, subtypes H3N2, H1N1 and a second H1N1 of avian origin cause most outbreaks.
Most SIV viruses grow readily in 9-12 day old chick embryos or cell cultures and will hemagglutinate certain kinds of erythrocytes. In the laboratory this is a useful characteristic in identifying viruses through hemagglutination and hemagglutination inhibition serological tests.
Swine influenza virus probably does not survive more than two weeks outside the host and can be inactivated by many disinfectants.
Acute outbreaks are a result of rapid transmission of SIV through a susceptible population, probably by nasal secretions and short-distance aerosols of infected animals; a persistent or asymptomatic carrier status does not appear to occur. Cases of human-to-pig and pig-to-human transmission have been documented to occur. The presence of antibody (maternal or active) will mitigate the severity of disease and influence the rapidity of spread through a population. Thus, swine influenza often is endemic in populations that use continuous pig flows. The importance of aerosol transmission farm-to-farm is difficult to quantify but likely occurs only over short distances.
Swine simultaneously infected with different SIV subtypes (including viruses derived from turkeys, chickens, ducks, certain waterfowl and people) may recombine to produce novel subtypes that, on rare occasion, are maintained in swine populations or transmit to other species. This “mixing vessel” effect is relatively rare and most likely to occur where there are many small farms with poultry and pigs in close association (Asia). Spread of SIV from swine to people has been documented several times but is unusual; a few deaths have been reported. Lungworms and their ova were at one time thought to be involved in the transmission of SIV but this notion has been convincingly disproven.
The SIV gains access by the nasopharyngeal route and enters respiratory epithelium where it causes inflammation with widespread degeneration and necrosis of cells lining bronchi and bronchioles. Also, virus can be demonstrated in interalveolar septa, sometimes in turbinate epithelium, and mediastinal lymph nodes. In the lung, alveolar type 2 pneumocytes are affected and produce less surfactant. This impairs phagocytosis of secondary microorganisms by alveolar macrophages. Inflammatory exudate in smaller airways sometimes blocks them, leading to atelectasis, emphysema and bronchointerstitial pneumonia. In most cases epithelial damage is repaired and the lesions resolve in five to seven days. The severity of the effect of infection is mitigated by the quantity of homologous circulating antibody (maternal or active). Most of the mortality associated with SIV is the result of secondary bacterial infections or concurrent infections with other primary agents of pneumonia.
In a typical outbreak, there is a sudden onset of a marked respiratory illness affecting most pigs in the herd. Signs include prostration, weakness, fevers (104° to 106° F), paroxysmal coughing, anorexia, and conjunctivitis with occulonasal discharge. Recovery begins about the sixth day and the herd is largely recovered in one to two weeks. Morbidity is high and mortality is low or absent in most uncomplicated outbreaks. Uncomplicated SIV usually causes little death loss but losses of weight and body condition, as well as cost of medication, can be significant. Concurrent infections with other respiratory diseases can increase mortality and culls. SIV may have a less abrupt and more prolonged clinical course when there is individual variation in immunity in the population. This endemic form of the disease course is not uncommon in the nursery and early grower period and can prove challenging to diagnose and control.
Reproductive problems occasionally associated with SIV likely are incidental to the acute illness. Infection during pregnancy may result in abortion due to acute illness in sows and sometimes small, weak litters. Transplacental infection is rare.
The gross lesions include lobular distribution of congestion, firmness, atelectasis, emphysema and perhaps pneumonia. Gross lesions often are restricted to the apical and cardiac lobes but may affect entire lungs. Areas of atelectasis are irregular, darkened and firm. Lesions often appear as distinct, scattered lobules. Airways may contain blood-tinged exude. Regional lymph nodes are moderately enlarged. Microscopic lesions include degeneration and necrosis of portions of airway epithelium and obstruction of airways with exudate. There may be bronchointerstitial pneumonia. Marked edema and congestion of the entire lung may be present in severe cases. Necrotizing bronchiolitis is highly suggestive of SIV.
A history of sudden onset of a severe respiratory illness in many animals, along with typical signs and lesions, often is adequate for a field diagnosis. It is useful to confirm the diagnosis since the disease may reappear and go unrecognized in a less typical, subacute form.
Confirmation of diagnosis can be made in several ways but detection of antigen or virus is most successful from acutely affected (febrile) pigs. The virus can be identified by fluorescent antibody technique on fresh lung sections or by immunohistochemistry techniques on formalin-fixed lung sections (successful only in acutely affected, euthanized pigs). The virus can be isolated from nasal swabs or lung tissue in chick embryos. A polymerase chain reaction (PCR) can be used to detect virus in nasal swabs or lungs. There are commercially available influenza A antigen detection kits (enzyme immunoassays) that can be used to detect SIV on nasal swabs. In some cases, paired serum samples taken early and late in an outbreak can be used to demonstrate a rising serotype-specific antibody titer to SIV. Serologic testing is complicated by the fact several subtypes of SIV can be present in a group of pigs and that most serologic tests do not sufficiently cross-react to detect antibodies of all SIV subtypes.
Because there are multiple subtypes of SIV in swine populations, mere detection of SIV is not sufficient to implement specific control strategies. The offending SIV can be subtyped by some laboratories by PCR, genetic sequencing, or serologic methods.
It is quite common to have other viral, bacterial, mycoplasmal and parasitic diseases in association with SIV, especially in outbreaks with considerable mortality.
Reproductive failure is due to the affects of acute disease in sows. The virus cannot be detected in aborted fetuses but can be detected in acutely affected sows. Serology is not a reliable method of diagnosis of reproductive failure since most sow herds will be serologically positive from previous exposure to the agent.
There are no specific therapeutics for SIV. Often, antimicrobials are used to control or prevent secondary bacterial infections. Aspirin or other anti-inflammatory agents may offer relief to severely affected pigs. Treatment should emphasize providing a comfortable environment and ready access to fresh feed and water.
Prevention has depended largely on maintaining a closed herd to avoid introducing infected pigs. Inactivated vaccines are widely used in Europe and the United States. Several types of commercial vaccines are available and autogenous products are commonly used. Directions provided with the vaccine should be closely followed. Cross-protection between subtypes should not be expected in most situations.
Control of SIV in recently-weaned pigs in modern systematic production units usually requires stabilization of the breeding herd by acclimatization or vaccination. Vaccination prior to farrowing to stimulate colostral protection for the young piglets is sometimes practiced. New additions to the breeding herd should be vaccinated during their isolation period.
Successful control of SIV in the grow/finish phase of SIV-positive herds can be daunting. Nursery pigs can be vaccinated prior to moving them to the finisher. Maternal antibody interference with vaccination is a major concern in timing of vaccination since antibody levels are highly variable in populations and even low detectable antibody may interfere with immune response. There is little cross-protection between subtypes, making vaccine selection challenging. Often, the offending virus must be subtyped to aid in selection of the correct antigen.
On infected premises, the all in/all out system with cleaning and disinfection of facilities between farrowings helps prevent virus carryover as does vaccination of the breeding herd to “stabilize” the infection to prevent virus transmission to offspring. Depopulation of a continuous-flow nursery or finisher may be necessary to stop virus circulation.