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H1N1 Influenza (Swine Flu)

  • Author: Michael Stuart Bronze, MD; Chief Editor: Russell W Steele, MD  more...
 
Updated: Feb 22, 2016
 

Practice Essentials

Swine flu is a highly contagious respiratory disease in pigs caused by one of several swine influenza A viruses (see the image below). Transmission of swine influenza viruses to humans is uncommon. However, the swine influenza virus can be transmitted to humans via contact with infected pigs or environments contaminated with swine influenza viruses.

Swine influenza virus. Colorized transmission elec Swine influenza virus. Colorized transmission electron micrograph (37,800X) of the A/New Jersey/76 (Hsw1N1) virus under plate magnification. Image taken during the virus' first developmental passage through a chicken egg. Courtesy of the CDC/Dr. E. Palmer; R.E. Bates.

Signs and symptoms

Manifestations of H1N1 influenza are similar to those of seasonal influenza. Patients present with symptoms of acute respiratory illness, including at least 2 of the following:

  • Fever
  • Cough
  • Sore throat
  • Body aches
  • Headache
  • Chills and fatigue
  • Diarrhea and vomiting (possible)

In children, signs of severe disease include apnea, tachypnea, dyspnea, cyanosis, dehydration, altered mental status, and extreme irritability.[1]

See Clinical Presentation for more detail.

Diagnosis

The CDC criteria for suspected H1N1 influenza are as follows[2] :

  • Onset of acute febrile respiratory illness within 7 days of close contact with a person who has a confirmed case of H1N1 influenza A virus infection, or
  • Onset of acute febrile respiratory illness within 7 days of travel to a community (within the United States or internationally) where one or more H1N1 influenza A cases have been confirmed, or
  • Acute febrile respiratory illness in a person who resides in a community where at least one H1N1 influenza case has been confirmed.

See Workup for more detail.

Management

Treatment is largely supportive and consists of bedrest, increased fluid consumption, cough suppressants, and antipyretics and analgesics (eg, acetaminophen, nonsteroidal anti-inflammatory drugs) for fever and myalgias. Severe cases may require intravenous hydration and other supportive measures. Antiviral agents may also be considered for treatment or prophylaxis.

See Treatment and Medication for more detail.

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Background

Swine influenza is a highly contagious respiratory disease in pigs caused by one of several swine influenza A viruses. In addition, influenza C viruses may also cause illness in swine. Current strategies to control swine influenza virus (SIV) in animals typically include one of several commercially available bivalent swine influenza virus vaccines.

Transmission of swine influenza viruses to humans is uncommon. However, the swine influenza virus can be transmitted to humans via contact with infected pigs or environments contaminated with swine influenza viruses. Once a human becomes infected, he or she can then spread the virus to other humans, presumably in the same way as seasonal influenza is spread (ie, via coughing or sneezing).

History

The ability to trace outbreaks of swine flu in humans dates back to investigation of the 1918 Spanish influenza pandemic, which infected one third of the world’s population (an estimated 500 million people) and caused approximately 50 million deaths. In 1918, the cause of human influenza and its links to avian and swine influenza was not understood. The answers did not begin to emerge until the 1930s, when related influenza viruses (now known as H1N1 viruses) were isolated from pigs and then humans.[3]

In humans, the severity of swine influenza can vary from mild to severe. From 2005 until January 2009, 12 human cases of swine flu were reported in the United States. None were fatal. In 1988, however, a previously healthy 32-year-old pregnant woman in Wisconsin died of pneumonia as a complication of swine influenza.

A 1976 outbreak of swine influenza in Fort Dix, New Jersey, involved more than 200 cases, some of them severe, and one death.[4] The first discovered case involved a soldier at Fort Dix who complained of feeling weak and tired. He died the next day.

The fear of an influenza pandemic in 1976 led to a national campaign in the United States designed to immunize nearly the entire population. In October, 1976, approximately 40 million people received the A/NewJersey/1976/H1N1 vaccine (ie, swine flu vaccine) before the immunization initiative was halted because of the strong association between the vaccine and Guillain-Barré syndrome (GBS).[5, 6] About 500 cases of GBS were reported, with 25 deaths due to associated pulmonary complications.[7]

A recent investigation sought to determine the link between GBS and the 1976 swine flu vaccine, since subsequent influenza vaccines did not have this strong association. Nachamkin et al found that inoculation of the 1976 swine flu vaccine, as well as the 1991-1992 and 2004-2005 influenza vaccines, into mice prompted production of antibodies to antiganglioside (anti-GM1), which are associated with the development of GBS. They proposed that further research regarding influenza vaccine components is warranted to determine how these components elicit antiganglioside effects.[8] See the images below.

This preliminary negative stained transmission ele This preliminary negative stained transmission electron micrograph depicts some of the ultrastructural morphology of the A/CA/4/09 swine flu virus. Courtesy of CDC/ C. S. Goldsmith and A. Balish.
This preliminary negative stained transmission ele This preliminary negative stained transmission electron micrograph depicts some of the ultrastructural morphology of the A/CA/4/09 swine flu virus. Courtesy of CDC/ C. S. Goldsmith and A. Balish.

Current H1N1 influenza (formerly called swine influenza) outbreak

Human cases of influenza A (H1N1) have been reported worldwide. In 2009, cases of influenzalike illness were first reported in Mexico on March 18; the outbreak was subsequently confirmed as H1N1 influenza A.[9] Investigation is continuing to clarify the spread and severity of H1N1 influenza (swine flu) in Mexico. Suspected clinical cases had been reported in 19 of the country's 32 states. Although only 97 of the Mexican cases had been laboratory-confirmed as Influenza A/H1N1[10] (12 of them genetically identical to Influenza A/H1N1 viruses from California[9] ). As of May 5th, 2009, nearly 600 H1N1 influenza cases had been confirmed in Mexico, including 25 deaths.[11]

On April 17, 2009, the CDC determined that two cases of febrile respiratory illness in children who resided in adjacent counties in southern California were caused by infection with a swine influenza A (H1N1) virus.[12] By April 26, 2009, the US Department of Health and Human Services declared a national public health emergency involving H1N1 influenza A, citing its significant potential to affect national security.[13] By June 25, 2009, 27,717 lab-defined cases of H1N1 influenza had been confirmed in the United States.[10, 14, 15, 16]

Estimates in the United States for the first 6 months of the pandemic report approximately 22 million people in the United States became ill from the H1N1 influenza, nearly 100,000 were hospitalized, and about 3900 have died. Deaths include an estimated 540 children younger than 18 years, 2900 adults aged 18-64 years, and about 440 elderly individuals. These estimates are from the CDC's Emerging Infection Program, rather than using only laboratory-confirmed cases.[17]

For an updated tally and case counts in specific states, see the CDC's H1N1 Flu (Swine Flu) Web page.

On June 11, 2009, WHO raised the pandemic alert level to phase 6 (indicating a global pandemic) because of widespread infection beyond North America to Australia, the United Kingdom, Argentina, Chile, Spain, and Japan.[10] As of September 1, 2009, the World Health Organization (WHO) reported that H1N1 influenza had been confirmed in over 200,000 people in more than 100 countries and that they are aware of at least 2185 confirmed deaths. For an updated tally of affected countries and counts, see WHO's Influenza A (H1N1) Web page.

On October 24, 2009, President Obama declared the 2009 H1N1 influenza pandemic a national emergency, explaining that "...the rapid increase in illness across the Nation may overburden health care resources and that the temporary waiver of certain standard Federal requirements may be warranted in order to enable U.S. health care facilities to implement emergency operations plans, the in the United States 2009 H1N1 influenza pandemic constitutes a national emergency." This declaration makes way for waiving certain requirements of the Medicare, Medicaid, and State Children's Health Insurance programs and of the Health Insurance Portability and Accountability Act Privacy Rule throughout the duration of the public health emergency.[18]

Government and public health officials are monitoring this situation worldwide to assess the threat from H1N1 influenza and to provide guidance to health care professionals and the public. Because the situation is changing rapidly, it is important to check regularly for changes in recommendations as new information becomes available. Online resources for daily guidance include the Centers for Disease Control and Prevention (CDC), World Health Organization (WHO), and Medscape's H1N1 Influenza A (Swine Flu) Alert Center.

Domínguez-Cherit et al (2009) conducted an observational study of consecutive critically ill patients in Mexican hospitals that treated most patients with confirmed, probable, or suspected H1N1 influenza during the 2009 epidemic. Critical illness occurred in 58 (6.5%) of 899 patients. Median age of critically ill patients was 44 years (range, 10-83 y). All presented with fever, and all but one with respiratory symptoms. Few patients had comorbid respiratory disorders, but 36% were obese. All patients but 2 received mechanical ventilation for severe acute respiratory distress syndrome and refractory hypoxemia. By 60 days, 24 patients had died (41.4%; 95% confidence interval, 28.9%-55%). Patients who died had greater initial severity of illness, worse hypoxemia, higher creatine kinase and creatinine levels, and ongoing organ dysfunction. Treatment with neuraminidase inhibitors was associated with improved survival (odds ratio, 8.5; 95% confidence interval, 1.2-2.8).[19]

See Medscape's H1N1 influenza algorithm adaptation for guidance in managing suspected cases.

A WHO report on the 2009 influenza pandemic indicated that nearly all countries reported cases of H1N1 virus infection, with more than 17,000 deaths worldwide. In the United States, the number of clinical illnesses was estimated at 59 million, 265,000 hospitalizations, and 12,000 deaths.[20] . H1N1 strains are still prevalent in India, whose Health Ministry has reported over 2500 deaths to date.

In the second half of 2011, a novel swine influenza virus emerged. Twelve cases from 5 states were reported by the CDC in January 2012. The new strain, dubbed A (H3N2)v, includes a gene from the human pandemic strain and affects mostly children. In 3 of the 5 states where the virus emerged (Pennsylvania, Maine, and Indiana), the virus was a result of pig-to-human transmission.[21] According to the Department of Health and Human Services (HHS), a precautionary vaccine against this variant is in development and will likely be ready for clinical trials in the spring of 2012.

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Epidemiology

Mortality/Morbidity

H1N1 influenza (swine flu) tends to cause high morbidity but low mortality rates (1%-4%).

Age

Belongia et al provide an excellent epidemiologic comparison of the clinical characteristics of the 2009 influenza A H1N1 versus other seasonal influenza A strains.[22] In their study, the clinical manifestations and risk for hospitalization were similar between the 2009 H1N1 strain and other seasonal influenza A strains. However, children were disproportionately affected by the 2009 H1N1 strain but not necessarily by severity of illness.

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Contributor Information and Disclosures
Author

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Russell W Steele, MD Clinical Professor, Tulane University School of Medicine; Staff Physician, Ochsner Clinic Foundation

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, Southern Medical Association

Disclosure: Nothing to disclose.

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This preliminary negative stained transmission electron micrograph depicts some of the ultrastructural morphology of the A/CA/4/09 swine flu virus. Courtesy of CDC/ C. S. Goldsmith and A. Balish.
Swine influenza virus. Colorized transmission electron micrograph (37,800X) of the A/New Jersey/76 (Hsw1N1) virus under plate magnification. Image taken during the virus' first developmental passage through a chicken egg. Courtesy of the CDC/Dr. E. Palmer; R.E. Bates.
Phase 6 criteria: In addition to the criteria defined in Phase 5, the same virus has caused sustained community-level outbreaks in at least one other country in another WHO region. Courtesy of the WHO.
Negative stained transmission electron micrograph of recreated 1918 influenza virions. Courtesy of CDC/ Dr. Terrence Tumpey.
This preliminary negative stained transmission electron micrograph depicts some of the ultrastructural morphology of the A/CA/4/09 swine flu virus. Courtesy of CDC/ C. S. Goldsmith and A. Balish.
 
 
 
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