Swine Flu Basics

After years of bird flu talk, many people were surprised to learn that the first pandemic of the 21st century was caused by a “swine flu.” The term itself stirred fears in the early days of the outbreak and led to overreactions such as the killing of all swine in Egypt CDC and WHO officials quickly changed the name to ‘novel influenza A (H1N1)’ or ‘2009 H1N1 A’ to take the swine out of swine flu, providing an example of how the public health story can differ from the scientific story—since most of the genes in this pandemic strain essentially are of swine origin.

This section offers a quick overview of swine influenza, from the seasonal flu version in pigs to occasional infections in humans to the new pandemic strain.

On this page...
  Swine as the “mixing vessel” »
  Swine Influenza in humans »
  The 2009 H1N1 influenza virus »
  The 2009 H1N1 pandemic »
  Clinical symptoms »
  Detection »
  Treatment  »
  Vaccines »

Swine as the “mixing vessel”

Swine influenza is a respiratory disease caused by type A influenza that regularly infects pig herds. The disease causes high levels of illness and low death rates among pigs. Most of the outbreaks occur during the late fall and winter, similar to influenza outbreaks among humans.

Swine influenza viruses change (mutate) constantly. Pigs can be infected by both avian and human influenza viruses. Therefore, swine can serve as the “mixing vessel” for new influenza types when they are infected with two or more influenza viruses.

Over the years, different variations of swine influenza viruses have emerged. Currently, four types of influenza A have been isolated in pigs: H1N1, H1N2, H3N2, and H3N1.

Swine Influenza in humans

Publications noted 37 cases of humans with swine-origin influenza between 1958 and 2005. Most of the cases occurred in the United States (19), but a few cases occurred in Canada, Hong Kong, and four European countries. Sixty one percent (22) of the infected reported recent exposure to swine.1

Between December 2005 and February 2009, the Centers for Disease Control and Prevention (CDC) had reports of 11 sporadic cases of infection with triple reassortant swine influenza A H1 viruses. Ten cases were caused by triple reassortant H1N1 viruses and one by triple reassortant H1N2. Nine patients had some contact or association with pigs (direct exposure or being around pigs). All patients survived illness, but four were hospitalized, and two required mechanical ventilation.2

The 2009 H1N1 influenza virus

The new influenza virus 2009 H1N1 causing the current human pandemic arose from a reassortment event between a triple reassortant influenza virus containing human, swine and avian influenza genes and an Eurasian swine influenza virus.3 This novel H1N1 influenza virus spreads via human-to-human transmission rather than swine-to-human, and many people have no natural immunity.

As any influenza virus, the new 2009 H1N1 strain has eight genes:

PA, PB2 are swine genes that originated in birds (a triple reassortant strain)
PB1 is a swine gene that passed from birds to humans then swine (a triple reassortant)
HA, NP, NS are swine genes that originated in birds (classical swine virus/triple reassortant).
NA, M are Eurasian swine genes that originated in birds (Eurasian swine influenza virus)4 5

2009 H1N1 was identified among swine in Canada (May 2009), Argentina (June 2009), and Australia (July 2009). The Canadian swine outbreak was thought to have arisen from a farm worker returning from Mexico. In Argentina, about 30 percent of a swine herd experienced symptoms, but none of the animals died from a swine influenza outbreak. Two workers had influenza-like illnesses but they were not confirmed as H1N1.

In August 2009, the novel H1N1 strain was isolated from domestic turkeys in Chile. The birds were allowed to recover before going to market rather than being culled. It is possible that other poultry flocks could be infected.

Monitoring the spread of the new pandemic strain in animals is important because it may lead to the emergence of a reassorted strain more lethal to humans than the current 2009 H1N1 strain.

The 2009 H1N1 pandemic

The first cases of novel 2009 H1N1 influenza occurred in mid-March 2009 in Mexico. Additional cases of this novel virus were soon noted in Mexico and then in other countries worldwide. The virus likely spread rapidly via air travel from its source in Mexico to other areas of the world.

WHO and CDC officials recorded numbers of human cases for only the first few months. On Jun 11, 2009, WHO declared a pandemic. You can find the most recent case numbers and updates for the United States on the CDC Web site and access global numbers through the WHO influenza surveillance network.

Clinical symptoms

The 2009 H1N1 virus is most likely transmitted in the same manner as seasonal influenza: by the coughing or sneezing of infected people. People may also contract the disease by touching an object that has influenza viruses on it (such as a door handle) and then touching their mouth or noses. People cannot get the disease from eating pork.

Clinical symptoms of people infected with 2009 H1N1 are expected to be similar to those of seasonal human influenza. The most commonly reported symptoms thus far have been:

Sore throat
Runny or stuffy nose
Body aches
Diarrhea and vomiting have been reported in about 25% of patients.


The H1N1 swine-origin influenza virus is antigenically very different from human H1N1 viruses.

The 2009 H1N1 virus can be detected in clinical samples (nose and throat swab or aspirates) using molecular detection techniques (reverse transcription-polymerase chain reaction, or RT-PCR).

Other diagnostic tests such as rapid tests or immunofluorescence can distinguish between influenza A and B, but are not specific for the 2009 H1N1. Culture techniques can isolate H1N1 virus, but culture is not rapid, and a negative test does not exclude infection with the 2009 H1N1 virus.


There are two classes of antiviral drugs for influenza: inhibitors of neuraminidase such as oseltamivir and zanamivir; and adamantanes, such as amantadine and rimantadine. Tests on viruses obtained from patients in Mexico and the United States have indicated that the new H1N1 viruses are sensitive to neuraminidase inhibitors, but they are resistant to the other class, the adamantanes.

Zanamivir (brand name: Relenza) or oseltamivir (Tamiflu) should be given within 48 hours of illness or exposure to ill persons.

The CDC has released detailed guidelines for use of antiviral agents to treat 2009 H1N1 infections either pre- or post-exposure.6

Antiviral treatment is recommended for:

Household contacts at high risk of complications for influenza (e.g., those with chronic medical conditions, those older than age 65, children younger than age 5) of a confirmed or probable case.
Healthcare workers or public health workers not using protective equipment during close contact with an ill, confirmed, probable, or suspected case of novel H1N1 during the infectious period.

Additional treatment guidelines for others are detailed on the CDC site. The CDC has also issued multiple guidelines on mitigating spread of influenza.


Vaccines are available to protect swine from regular swine influenza caused by an H1N1 strain, but these vaccines are not designed for the 2009 H1N1.

As for humans, the 2009/2010 seasonal influenza vaccine provides partial protection against swine H3N2, but not the novel H1N1.

Based on patient cases of the 2009 H1N1, statistics suggest that people born before 1957 may have some residual immunity from past exposure to previous pandemics.

A new vaccine for 2009 H1N1 is available since October 2009. The Advisory Committee on Immunization Practices (ACIP) released guidelines on use of the vaccine. The ACIP recommended that those initially given the vaccine should be:

Pregnant women
Parents, siblings or daycare providers of infants younger than age 6 months
Healthcare and emergency medical services personnel
Persons between age 6 months and 24 years
Persons between age 25 and 64 years who have medical conditions that place them at higher risk for influenza-related complications.7


  1. Kendall P. Myers, Christopher W. Olsen, Gregory C. Gray, “Cases of swine influenza in humans: a review of the literature,” Clinical Infectious Diseases 44 (April 15, 2007): 1084-1088.

  2. Vivek Shinde, Carolyn B. Bridges, Timothy M. Uyeki, et al., “Triple-Reassortant Swine Influenza A (H1) in Humans in the United States, 2005–2009,” New England Journal of Medicine 360 (June 18, 2009): 2616-2665.

  3. Rebecca J. Garten, C. Todd Davis, Colin A. Russell, et al., “Antigenic and Genetic Characteristics of Swine-Origin 2009 A(H1N1) Influenza Viruses Circulating in Humans,” Science 325 (July 10, 2009): 197-201.

  4. Jon Cohen, New Details on Virus's Promiscuous Past, Science 324 (May 29, 2009): 1127.

  5. Garten, et. al., op. cit.

  6. Centers for Disease Control and Prevention, Updated interim guidelines for the use of antiviral medications in the treatment and prevention of influenza for the 2009-2010 season, Sept. 22, 2009.

  7. National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention, “Use of influenza A (H1N1) 2009 monovalent vaccine: Recommendatons of the advisory committee practices (ACIP),” Morbidity and Mortality Weekly Report 58 (Aug. 21, 2009): 1-8.

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