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Commentary

The annual Surveillance for Acute Viral Hepatitis report provides a broad overview of the current epidemiology of acute viral hepatitis in the United States. Cases of acute viral hepatitis are voluntarily reported to CDC by state and territorial health departments via CDC’s National Notifiable Disease Surveillance System (NNDSS). Reports are received electronically via CDC’s National Electronic Telecommunications System for Surveillance (NETSS). These data are analyzed and summarized by CDC and have been published annually in the Morbidity and Mortality Weekly Report (MMWR) Surveillance Summaries series.

This report of the 2008 viral hepatitis data is a departure from the annual Surveillance Summary published by the Division of Viral Hepatitis (DVH) in previous years. First, in the current report, the data are not published in the annual surveillance summary format. Second, only a selection of the previously reported tables and figures are presented. These changes were made both to facilitate publication of the 2008 data and allow time for transition to a more comprehensive surveillance report that incorporates acute and chronic viral hepatitis. In this way, we hope to provide a more complete picture of viral hepatitis and the burden of the disease in the United States.

The 2008 Viral Hepatitis Surveillance Report is organized into 3 sections according to hepatitis type:

  1. Acute hepatitis A virus
  2. Acute hepatitis B virus
  3. Acute hepatitis C virus


Background

Viral hepatitis is caused by infection with any of at least five distinct viruses, of which the three most commonly identified in the United States are hepatitis A virus (HAV), hepatitis B virus (HBV) and hepatitis C virus (HCV). All three of these unrelated viruses can produce an acute illness characterized by nausea, malaise, abdominal pain, and jaundice. HBV and HCV also can produce a chronic infection that is associated with an increased risk for chronic liver disease and hepatocellular carcinoma.

This report describes the burden of acute disease attributed to infection with HAV, HBV, and HCV and describes acute disease trends over time. These data can be used to develop and evaluate prevention strategies and to identify persons in need of post-exposure prophylaxis. The data on acute illness presented in this report do not include the burden of disease caused by chronic infection with HBV or HCV, both of which remain a substantial public health problem.

Acute hepatitis A virus

HAV is transmitted through the fecal-oral route, spreading primarily through close personal contact. Asymptomatic infection is common among young children, and symptomatic cases in children younger than 6 years of age represent a limited proportion of infections that occur in this age group (1).

Effective vaccines to prevent hepatitis A virus infection have been available in the United States since 1995. In 1996, CDC’s Advisory Committee on Immunization Practices (ACIP) recommended administration of hepatitis A vaccine for persons at increased risk including international travelers, men who have sex with men (MSM), injection- and noninjection-drug users, and children living in communities with high rates of disease (2). ). In 1999, ACIP also recommended routine vaccination for children living in 11 states (i.e., Alaska, Arizona, California, Idaho, Nevada, New Mexico, Oklahoma, Oregon, South Dakota, Utah, and Washington) with average hepatitis A rates during 1987-1997 of ≥ 20 cases per 100,000 population and be considered for children in six states (i.e., Arkansas, Colorado, Missouri, Montana, Texas, and Wyoming) with rates of 10-20 cases per 100,000 population (3). In 2006, ACIP expanded these recommendations to include routine vaccination of children in all 50 states (4).

Acute hepatitis B virus

HBV is transmitted by percutaneous or mucosal exposure to the blood or body fluids of an infected person, most often through injection-drug use (IDU), sexual contact with an infected person, or contact from an infected mother to her infant during delivery. Transmission of HBV also can occur in settings involving nonsexual interpersonal contact for an extended period (e.g., among household contacts of a person with chronic HBV infection).

The risk of chronic HBV infection decreases as the age of HBV infection increases; approximately 5% of all acute HBV infections progress to chronic infection (1).Of infants who acquire HBV infection at birth from their mothers, as many as 90% become chronically infected. Among children between 1 and 5 years of age who become infected with HBV, 30% to 50% become chronically infected.

Effective vaccines to prevent hepatitis B virus infection have been available in the United States since 1981. In 1991, a comprehensive strategy was recommended for the elimination of HBV transmission in the United States (5,6). The four elements of this strategy are

  1. universal vaccination of infants beginning at birth
  2. prevention of perinatal HBV infection through routine screening of all pregnant women for HBV infection and the provision of immunoprophylaxis to infants born either to infected women or to women of unknown infection status
  3. routine vaccination of previously unvaccinated children and adolescents
  4. vaccination of adults at increased risk for infection (including health-care workers, dialysis patients, household contacts and sex partners of persons with chronic HBV infection, recipients of certain blood products, persons with a recent history of multiple sex partners or a sexually transmitted disease, MSM, and injection-drug users).

Acute hepatitis C virus

HCV is transmitted primarily through percutaneous exposure; however, transmission can occur through unapparent percutaneous or mucosal exposures (e.g., persons with evidence of high-risk sexual practices). With an estimated 3.2 million chronically infected persons nationwide, HCV infection is the most common bloodborne infection in the United States (7). There is no laboratory distinction between acute and chronic infection.

A vaccine against HCV infection does not exist. National recommendations for prevention and control of HCV infection (8), issued in 1998, emphasize primary prevention activities to reduce the risk for HCV transmission. These activities include screening and testing of blood donors, viral inactivation of plasma-derived products, risk-reduction counseling and screening of persons at risk for HCV infection, and routine practice of infection control in health-care settings.


Analyses Highlights

Acute hepatitis A virus

In 2008, a total of 2,585 acute, symptomatic cases of hepatitis A were reported nationwide. The overall incidence rate of 0.9 cases per 100,000 population was the lowest ever recorded (Table 1a, Slide 1a). The incidence rate ranged from 0.1 per 100,000 population in Montana to 3.6 per 100,000 population in Iowa (Table 2a). After asymptomatic infection and underreporting were taken into account, an estimated 22,000 new infections occurred in 2008.

  • Region: Historically, acute hepatitis A rates have varied geographically. Compared to other regions, higher rates were reported in the western region of the United States. Incidence in the West has declined substantially, most notably after issuance in 1999 of recommendations for routine childhood vaccination in states with consistently elevated rates of hepatitis A. Since 2002, rates in the West have been approximately equal to those in other regions of the United States (Slide 2a).
  • Age group: Incidence of acute, symptomatic hepatitis A varies by age; the highest rates were observed among children and young adults; the lowest rates were among persons aged ≥ 40 years. In 2008, rates were highest for persons aged 25-39 years (1.0 cases per 100,000 population); the lowest rates were among children < 5 years (0.3 cases per 100,000 population) (Slide 3a).
  • Sex: From 1996 through 2002, rates of acute, symptomatic hepatitis A have been higher among males than females, the difference in the sex-specific rates increased until nearly 2 male cases were observed for every female case. However, since 2006, overall rates have declined more among males than among females. In 2008, incidence among males was 0.9 cases per 100,000 population, compared with 0.8 cases per 100,000 population among females (Slide 4a).
  • Race/ethnicity: Acute, symptomatic hepatitis A rates vary by race; the highest rates occurred among American Indian/Alaska Natives (AI/ANs), and the lowest rates among Asian/Pacific Islanders (APIs). However, rates among AI/ANs, which were >60 cases per 100,000 population before 1996, have decreased dramatically; during 2003-2008, rates among AI/ANs were lower than or similar to other races. In 2008, the rate for AI/ANs was 0.6 cases per 100,000 population. Historically, acute, symptomatic hepatitis A rates also have differed by ethnicity; rates among Hispanics were consistently higher compared to non-Hispanics. In 2008, the rate for Hispanics was 1.0 cases per 100,000 population, the lowest rate ever recorded for this group Slide 5a).

Acute hepatitis B virus

In 2008, a total of 4,033 acute, symptomatic cases of hepatitis B were reported nationwide. The overall incidence rate of 1.3 cases per 100,000 population was the lowest ever recorded Table 1b, Slide 1b). The incidence rate ranged from 0.2 per 100,000 population in Montana to 4.6 per 100,000 population in West Virginia Table 2b). After asymptomatic infection and underreporting were taken into account, an estimated 38,000 new infections occurred in 2008.

  • Region: Acute, symptomatic hepatitis B rates vary geographically. Compared to the Northeast and Midwest, higher rates were reported in the western and southern regions of the United States. During 2000-2008, rates in the South have been higher than in other regions of the United States (Slide 2b)
  • Age group: These data indicates acute, symptomatic hepatitis B rates differ by age; the highest rates were observed among persons aged 15-44 years; the lowest rates were among persons aged < 15 years. In 2008, rates were highest for persons aged 25-44 years (2.6 cases per 100,000 population); the lowest rates were among children < 15 years (0.02 cases per 100,000 population) (Slide 3b).
  • Sex: Incidence of acute, symptomatic hepatitis B has been higher among males than females. During 1990-2008, the male-to-female ratio of rates remained stable (1.5-1.8). In 2008, the rate for males was approximately 1.8 times higher than for females. In 2008, incidence among males was 1.7cases per 100,000 population, compared with 1.0 cases per 100,000 population among females (Slide 4b).
  • Race/ethnicity: Historically, acute, symptomatic hepatitis B rates have differed by race; the highest rates occurred among non-Hispanic blacks and Asian/Pacific Islanders (APIs). In 2008, the rate of acute, symptomatic hepatitis B was highest for non-Hispanic blacks (2.2 cases per 100,000 population). The downward trend among APIs continued, and the rate for this population in 2008 (0.7 cases per 100,000 population) was similar to that for Hispanics (0.8 cases per 100,000 population) and non-Hispanic whites (0.9 cases per 100,000 population) (Slide 5b).

Acute hepatitis C virus

In 2008, a total of 878 acute, symptomatic cases of hepatitis C hepatitis were reported nationwide. The overall incidence rate remained stable at 0.3 cases per 100,000 population (Table 1c, Slide 1c). The incidence rate ranged from < 0.1 per 100,000 population in Arkansas, Iowa, and Mississippi to 1.6 per 100,000 population in Kansas (Table 2c). After asymptomatic infection and underreporting were taken into account, an estimated 18,000 new infections occurred in 2008.

  • Age group: Since 2003, acute, symptomatic hepatitis C hepatitis rates have plateaued within all age groups. In 2008, rates increased slightly among persons aged 15-24 years (0.4 cases per 100,000 population) and were highest for persons aged 25-39 years (0.5 cases per 100,000 population). Few cases were reported among persons aged < 15 years (Slide 2c).
  • Sex: Historically, rates of acute, symptomatic hepatitis C hepatitis have been higher among males than females. Since 2002, the male-to-female ratio of rates has declined. In 2008, incidence among males and females was 0.3 cases per 100,000 population, yielding a ratio of 1. (Slide 3c).
  • Race/ethnicity: In 2008, acute, symptomatic hepatitis C/ hepatitis rates were highest among American Indian/Alaskan Natives (0.5 cases per 100,000 population) and lowest among Asian/Pacific Islanders (0.04 cases per 100,000 population) compared to the other racial/ethnic groups (Slide 4c).


Technical Notes

Conditions for Which Surveillance is Conducted

National surveillance is conducted for acute hepatitis A, B, and C. Surveillance case definitions for viral hepatitis were developed in collaboration with epidemiologists at CDC and the Council of State and Territorial Epidemiologists (CSTE) (see Case Definitions for Acute Viral Hepatitis).

Data Sources

Cases of acute viral hepatitis are reported weekly by state and territorial health departments to CDC’s National Notifiable Diseases Surveillance System (NNDSS). In 1990, states began submitting electronically individual case reports without personal identifiers to CDC via the National Electronic Telecommunications System for Surveillance (NETSS). States’ participation in reporting nationally notifiable diseases, including acute viral hepatitis, is voluntary.

Case Definitions for Acute Viral Hepatitis

In 2008, cases were required to meet the clinical criteria for acute hepatitis and virus-specific laboratory criteria for diagnosis specified in the following CSTE-approved case definitions (case definitions available at http://www.cdc.gov/osels/ph_surveillance/nndss/casedef/case_definitions.htm#h).

Clinical Criteria

Acute hepatitis was defined as acute illness with 1) discrete onset of symptoms (e.g., nausea, anorexia, fever, malaise, or abdominal pain) and 2) jaundice or elevated serum alanine aminotransferase (ALT) levels. For acute hepatitis C, elevated ALT levels are defined as > 400 IU/L.

Laboratory Criteria

Because the clinical characteristics are the same for all types of acute viral hepatitis, laboratory testing is needed to identify the specific viral cause of illness. The laboratory criteria for confirming each type of acute viral hepatitis are as follows:

  • Acute hepatitis A
    • Immunoglobulin M (IgM) antibody to hepatitis A virus (anti-HAV) positive
  • Acute hepatitis B
    • IgM antibody to hepatitis B core antigen (anti-HBc) positive or hepatitis B surface antigen (HBsAg) positive, and
    • IgM anti-HAV negative (if performed)
  • Acute hepatitis C
    • IgM anti-HAV negative, and
    • IgM anti-HBc negative, and
    • One of the following:
      • Antibody to hepatitis C virus (anti-HCV) screening-test-positive with a signal to cut-off ratio predictive of a true positive for the particular assay as defined by CDC (signal to cut-off rations available at http:/www.cdc.gov/hepatitis/HCV/LabTesting.htm#section1)

        OR
      • Hepatitis C virus recombinant immunoblot assay (HCV RIBA) positive,

        OR
      • Nucleic acid test (NAT) for HCV RNA positive.

Case Classification

For this analysis, a confirmed case had to meet both the clinical case definition and laboratory criteria for diagnosis. For hepatitis A, a case also was considered confirmed that met the clinical case definition and was diagnosed in a person who had an epidemiologic link to a person who had laboratory-confirmed hepatitis A (i.e., household or sexual contact with an infected person during the 15–50 days before the onset of symptoms).

Analyses

Incidence Calculations

For this report, crude rates per 100,000 population were calculated using Bureau of the Census estimates of the U.S. resident population in 2008. The following U.S. geographic regions were used: Midwest, Northeast, South, and West. The Midwest is comprised of the following states: Illinois, Indiana, Iowa, Kansas, Michigan, Minnesota, Missouri, Nebraska, North Dakota, Ohio, South Dakota, and Wisconsin. The Northeast is comprised of the following states: Connecticut, Maine, Massachusetts, New Hampshire, New Jersey, New York, Pennsylvania, Rhode Island, and Vermont. The South is comprised of the following states: Alabama, Arkansas, Delaware, District of Columbia, Florida, Georgia, Kentucky, Louisiana, Maryland, Mississippi, North Carolina, Oklahoma, South Carolina, Tennessee, Texas, Virginia, and West Virginia. The West is comprised of the following states: Alaska, Arizona, California, Colorado, Hawaii, Idaho, Montana, Nevada, New Mexico, Oregon, Utah, Washington, and Wyoming.

Estimation Calculation

The estimation procedure for the number of new cases of acute hepatitis A, B, or C begins with the number of cases reported voluntarily to CDC via CDC’s NNDSS. The overall procedure makes 2 adjustments to the reported number of acute, symptomatic cases. One adjustment accounts for underreporting of cases to the passive surveillance system and the other adjustment accounts for anicteric infections assumed not to have been recognized or reported. The result of these adjustments yields the estimated number of new cases of acute hepatitis (9).


References

  1. CDC. Epidemiology and Prevention of Vaccine-Preventable Diseases. Atkinson W, Wolfe S, Hamborsky J, McIntyre L, eds. 11th ed. Washington DC: Public Health Foundation, 2009.
  2. CDC. Prevention of hepatitis A through active or passive immunization. MMWR 1996;45(No. RR-15).
  3. CDC. Prevention of hepatitis A through active or passive immunization. MMWR 1999;48(No. RR-12).
  4. CDC. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 2006;55(No. RR-7).
  5. CDC. A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States. Part 1: immunization of infants, children, and adolescents. MMWR 2005;54(No. RR-16).
  6. CDC. A comprehensive immunization strategy to eliminate transmission of hepatitis B virus infection in the United States—recommendations of the Advisory Committee on Immunization Practices (ACIP). Part 2: immunization of adults. MMWR 2006;55(No. RR-16).
  7. Armstrong GL, Wasley AM, Simard EP, McQuillan GM, Kuhnert WL, Alter MJ. The prevalence of hepatitis C virus infection in the United States, 1999 through 2002. Ann Intern Med 2006;144:705–14.
  8. CDC. Recommendations for prevention and control of hepatitis C virus (HCV) infection and HCV-related chronic disease. MMWR 1998;47(No. RR-19).
  9. CDC. Estimates of disease burden from viral hepatitis. Atlanta, GA: US Department of Health and Human Services, CDC; 2008. Available at http://www.cdc.gov/hepatitis/PDFs/disease_burden.pdf [PDF - 5 Pages].


Additional Resources

Epidemiology and Prevention of Vaccine-Preventable Diseases. The Pink Book: Course Textbook

Prevention of Hepatitis A Through Active or Passive Immunization: Recommendations of the Advisory Committee on Immunization Practices (ACIP): http://www.cdc.gov/mmwr/pdf/rr/rr5507.pdf [PDF - 30 pages]

A Comprehensive Immunization Strategy to Eliminate Transmission of Hepatitis B Virus Infection in the United States — Part I: Immunization of Infants, Children, and Adolescents: http://www.cdc.gov/mmwr/PDF/rr/rr5416.pdf [PDF - 39 pages]

A Comprehensive Immunization Strategy to Eliminate Transmission of Hepatitis B Virus Infection in the United States — Part II: Immunization of Adults: http://www.cdc.gov/mmwr/PDF/rr/rr5516.pdf [PDF - 40 pages]

Recommendations for Identification and Public Health Management of Persons with Chronic Hepatitis B Virus Infection: http://www.cdc.gov/mmwr/pdf/rr/rr5708.pdf [PDF - 28 pages]

Recommendations for Prevention and Control of Hepatitis C Virus (HCV) Infection and HCV-Related Chronic Disease: http://www.cdc.gov/mmwr/PDF/RR/RR4719.pdf [PDF - 54 pages]

2005 Guidelines For Viral Hepatitis Surveillance And Case Management: http://www.cdc.gov/hepatitis/Statistics/SurveillanceGuidelines.htm


 
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