Hepatitis A epidemiology and demographics

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]

Overview

Prevalence

Incidence

Age

Gender

Race

Developed Countries

Developing Countries

Epidemiology and Demographics

Geographic Distribution

Areas with high levels of infection

In developing countries with very poor sanitary conditions and hygienic practices, most children (90%) have been infected with the hepatitis A virus before the age of 10. Those infected in childhood do not experience any noticeable symptoms. Epidemics are uncommon because older children and adults are generally immune. Symptomatic disease rates in these areas are low and outbreaks are rare.[1]

Areas with intermediate levels of infection

In developing countries, countries with transitional economies and regions where sanitary conditions are variable, children often escape infection in early childhood. Ironically, these improved economic and sanitary conditions may lead to a higher susceptibility in older age groups and higher disease rates, as infections occur in adolescents and adults, and large outbreaks can occur.[1]

Areas with low levels of infection

In developed countries with good sanitary and hygienic conditions, infection rates are low. Disease may occur among adolescents and adults in high-risk groups, such as injecting-drug users, men who have sex with men, people traveling to areas of high endemicity, and in isolated populations such as closed religious communities.[1]

Prevaccine Era

Hepatitis A epidemiology in the United States has fundamentally changed with licensure of hepatitis A vaccine and implementation of national ACIP recommendations for its use. Before vaccine licensure during 1995-1996, hepatitis A incidence was primarily cyclic, with peaks occurring every 10-15 years. In the United States, during 1980-1995, approximately 22,000-36,000 hepatitis A cases were reported annually to CDC (rate: 9.0-14.5 cases per 100,000 population), but incidence models indicate that the number of infections was substantially higher.[2][3] One such analysis estimated an average of 271,000 infections per year during 1980-1999, representing 10.4 times the reported number of cases.[2] Each year in the United States, an estimated 100 persons died as a result of acute liver failure attributed to hepatitis A.

The costs associated with hepatitis A are substantial. Surveillance data indicate that 11%-22% of persons with hepatitis A are hospitalized.[4] The average duration of work loss for adults who become ill has been estimated at 15.5 days for nonhospitalized patients and 33.2 days for hospitalized patients.[5] Estimates of the annual direct and indirect costs of hepatitis A in the United States have ranged from $300 million to $488.8 million in 1997 dollars.[6][5] A recent Markov model analysis estimated economic costs of $133.5 million during the lifetime of a single age cohort of children born in 2005, in the absence of vaccination.

Variation by Age, Race/Ethnicity, and Region

During the prevaccine era, the reported incidence of hepatitis A was highest among children aged 5-14 years, with approximately one third of reported cases involving children aged <15 years.[7] Because young children frequently have unrecognized or asymptomatic infection, a relatively smaller proportion of infections among children than adults are detected by routine disease surveillance. Incidence models indicate that during 1980-1999, the majority of HAV infections occurred among children aged <10 years, and the highest incidence was among those aged 0-4 years.[2] Before the use of hepatitis A vaccine, rates among American Indians and Alaska Natives were more than five times higher than rates in other racial/ethnic populations, and rates among Hispanics were approximately three times higher than rates among non-Hispanics.[8][9][10][11]

Since the 1960s, the highest hepatitis A rates and the majority of cases occurred in a limited number of states and counties concentrated in the western and southwestern United States.[12] Despite year-to-year fluctuations, rates in these areas consistently remained above the national average. In 11 states (Alaska, Arizona, California, Idaho, Nevada, New Mexico, Oklahoma, Oregon, South Dakota, Utah, and Washington) with consistently elevated rates, representing 22% of the U.S. population, average annual hepatitis A incidence was >20 cases per 100,000 during 1987-1997 (twice the national average of approximately 10 cases per 100,000 population); cases among residents of these states accounted for an average of 50% of reported cases.[13] An additional 18% of cases occurred among residents of six states (Arkansas, Colorado, Missouri, Montana, Texas, and Wyoming) with average annual rates above (but less than twice) the national average during this time.

Approximately 31% of the U.S. population had serologic evidence of previous HAV infection, when measured in the Third National Health and Nutrition Examination Survey (NHANES-III) conducted during 1988-1994 (50). Anti-HAV prevalence varied directly with age: among persons aged 6-11 years, prevalence was 9%; 20--29 years, 19%; 40--49 years, 33%; and >70 years, 75%. Age-adjusted anti-HAV prevalence was considerably higher among Mexican-American (70%) compared with black (39%) and white (23%) participants, and among foreign-born (69%) compared with U.S.-born (25%) participants.

Sources of Infection

In the prevaccine era, the majority of U.S. cases of hepatitis A resulted from person-to-person transmission of HAV during communitywide outbreaks.[14][15] The most frequently reported source of infection (in 12%-26% of cases) was household or sexual contact with a person with hepatitis A.[16] Cyclic outbreaks occurred among users of injection and noninjection drugs and among men who have sex with men (MSM),[17][18][19][20][21] and up to 15% of nationally reported cases occurred among persons reporting one or more of these behaviors. Other potential sources of infection (e.g., international travel and recognized foodborne outbreaks) were reported among 3%--6% of cases.[16] For approximately 50% of persons with hepatitis A, no source was identified for their infection.

Communitywide Epidemics

During communitywide epidemics, infection was transmitted from person to person in households and extended family settings. These epidemics typically spread throughout the community, and no single risk factor or risk group could be identified that accounted for the majority of cases.[14] Once initiated, epidemics often persisted for 1--2 years and proved difficult to control.[22][23] Because children often have unrecognized or asymptomatic infection, they played a key role in sustaining HAV transmission during these epidemics.

Vaccine Era

With the licensure of inactivated hepatitis A vaccines by the Food and Drug Administration (FDA) during 1995-1996, hepatitis A became a disease that was not only common but also vaccine-preventable. Since 1996, and particularly since ACIP's 1999 recommendations for routine vaccination of children living in areas with consistently elevated hepatitis A rates, national hepatitis A rates have declined sharply.[12] The 1999 recommendations called for routine vaccination of children living in states and communities in which the average hepatitis A rate during a baseline period of 1987-1997 was >20 cases per 100,000 population, approximately twice the national average, and for consideration of hepatitis A vaccination of children in those states and communities in which the average rate during the baseline period was at least the national average.[24]

In 2004, a total of 5,683 cases (rate: 1.9 cases per 100,000 population) were reported, representing an estimated 24,000 acute clinical cases when underreporting is taken into account. This rate was the lowest ever recorded and was 79% lower than the previously recorded low in 1992.[25] This decline is reflected in other fundamental shifts in hepatitis A epidemiology.

Variation by Age, Race/Ethnicity, and Region

Beginning in the late 1990s, national age-specific rates declined more rapidly among children than adults; as a result, in recent years, rates have been similar among all age groups.[12] Historic differences in rates among racial/ethnic populations also have narrowed in the vaccine era. For example, recent rates among American Indians and Alaska Natives represent a 99% decline compared with the prevaccine era and are now approximately the same or lower than those of other racial/ethnic populations.[11] Rates among Hispanics also declined 87% during this period, from 20.6 cases per 100,000 population during 1990-1997 to 2.7 per 100,000 in 2004, but remain higher than those for non-Hispanics.[12][26] Elimination of historic geographic differences in incidence rates has also occurred, and since 2001, rates in states where vaccination was recommended have been approximately equal to the rest of the United States.[27] In recent years, counties with higher rates have varied from year to year and have been distributed throughout the country.[12]

Incidence declined sharply in states with historically consistently elevated rates included in the 1999 ACIP recommendations for routine vaccination of children. As a result, the majority of hepatitis A cases during recent years have been reported from states with historically low rates in which hepatitis A vaccination of children has not been widely implemented.[12] In addition, the narrowing or elimination of national differences in age, race/ethnicity, and state-specific rates can be attributed largely to changes that occurred in the states in which routine hepatitis A vaccination of children was recommended and implemented. In 2004, for example, approximately two thirds of the nearly 6,000 cases were reported from states without childhood vaccination recommendations.[28] The 2004 rate among all Hispanics in these states remained four times higher than among non-Hispanics and was seven times higher among Hispanic compared with non-Hispanic children. The highest rate in any demographic subgroup occurred among Hispanic children in states for which routine hepatitis A vaccination of children is not recommended.[29]

Sources of Infection

In recent years, sexual or household contact with a person with hepatitis A has been reported in a smaller proportion of cases but continued to account for 13% of cases during 2002-2004 (5). The proportion of persons with hepatitis A reporting exposure to child care centers also has declined to approximately 9%.[30] The number of international travel-associated cases has remained approximately the same, but as overall incidence has declined, the proportion of cases attributable to this exposure has increased, accounting for an average of 13% of cases during 2002-2004.[31] During this time, >25% of cases among children aged <15 years could be attributed to international travel. Approximately 75% of all travel-related cases were associated with travel to Mexico or to Central or South America.[32] Outbreaks among MSM and users of illicit drugs also continue to occur.[33][21]

References

  1. 1.0 1.1 1.2 Hepatitis A. World Health Organization. Fact sheet N 328, updated June 2014. Accessed 07/28/2014.[1]
  2. 2.0 2.1 2.2 Armstrong GL, Bell BP (2002). "Hepatitis A virus infections in the United States: model-based estimates and implications for childhood immunization". Pediatrics. 109 (5): 839–45. PMID 11986444. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  3. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  4. CDC. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1999;48(No. RR-12):1-37
  5. 5.0 5.1 Berge JJ, Drennan DP, Jacobs RJ, Jakins A, Meyerhoff AS, Stubblefield W, Weinberg M (2000). "The cost of hepatitis A infections in American adolescents and adults in 1997". Hepatology (Baltimore, Md.). 31 (2): 469–73. doi:10.1002/hep.510310229. PMID 10655272. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  6. CDC. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1999;48(No. RR-12):1-37
  7. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  8. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  9. Shaw FE, Shapiro CN, Welty TK, Dill W, Reddington J, Hadler SC (1990). "Hepatitis transmission among the Sioux Indians of South Dakota". American Journal of Public Health. 80 (9): 1091–4. PMC 1404852. PMID 2166446. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  10. Bulkow LR, Wainwright RB, McMahon BJ, Middaugh JP, Jenkerson SA, Margolis HS (1993). "Secular trends in hepatitis A virus infection among Alaska Natives". The Journal of Infectious Diseases. 168 (4): 1017–20. PMID 8376812. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  11. 11.0 11.1 Bialek SR, Thoroughman DA, Hu D, Simard EP, Chattin J, Cheek J, Bell BP (2004). "Hepatitis A incidence and hepatitis a vaccination among American Indians and Alaska Natives, 1990-2001". American Journal of Public Health. 94 (6): 996–1001. PMC 1448379. PMID 15249305. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  12. 12.0 12.1 12.2 12.3 12.4 12.5 Wasley A, Samandari T, Bell BP (2005). "Incidence of hepatitis A in the United States in the era of vaccination". JAMA : the Journal of the American Medical Association. 294 (2): 194–201. doi:10.1001/jama.294.2.194. PMID 16014593. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  13. CDC. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1999;48(No. RR-12):1-37
  14. 14.0 14.1 Bell BP, Shapiro CN, Alter MJ, Moyer LA, Judson FN, Mottram K, Fleenor M, Ryder PL, Margolis HS (1998). "The diverse patterns of hepatitis A epidemiology in the United States-implications for vaccination strategies". The Journal of Infectious Diseases. 178 (6): 1579–84. PMID 9815207. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  15. CDC. Communitywide outbreaks of hepatitis A. Hepatitis surveillance. Report no. 51. Atlanta, GA: US Department of Health and Human Services, CDC; 1987:6-8.
  16. 16.0 16.1 Shapiro CN, Coleman PJ, McQuillan GM, Alter MJ, Margolis HS (1992). "Epidemiology of hepatitis A: seroepidemiology and risk groups in the USA". Vaccine. 10 Suppl 1: S59–62. PMID 1476001. |access-date= requires |url= (help)
  17. Cotter SM, Sansom S, Long T, Koch E, Kellerman S, Smith F, Averhoff F, Bell BP (2003). "Outbreak of hepatitis A among men who have sex with men: implications for hepatitis A vaccination strategies". The Journal of Infectious Diseases. 187 (8): 1235–40. doi:10.1086/374057. PMID 12696002. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  18. Harkess J, Gildon B, Istre GR (1989). "Outbreaks of hepatitis A among illicit drug users, Oklahoma, 1984-87". American Journal of Public Health. 79 (4): 463–6. PMC 1349976. PMID 2929804. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  19. Schade CP, Komorwska D (1988). "Continuing outbreak of hepatitis A linked with intravenous drug abuse in Multnomah County". Public Health Reports (Washington, D.C. : 1974). 103 (5): 452–9. PMC 1478131. PMID 3140269. |access-date= requires |url= (help)
  20. Hutin YJ, Bell BP, Marshall KL, Schaben CP, Dart M, Quinlisk MP, Shapiro CN (1999). "Identifying target groups for a potential vaccination program during a hepatitis A communitywide outbreak". American Journal of Public Health. 89 (6): 918–21. PMC 1508638. PMID 10358687. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  21. 21.0 21.1 Vong S, Fiore AE, Haight DO, Li J, Borgsmiller N, Kuhnert W, Pinero F, Boaz K, Badsgard T, Mancini C, Nainan OV, Wiersma S, Bell BP (2005). "Vaccination in the county jail as a strategy to reach high risk adults during a community-based hepatitis A outbreak among methamphetamine drug users". Vaccine. 23 (8): 1021–8. doi:10.1016/j.vaccine.2004.07.038. PMID 15620475. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  22. Shaw FE, Sudman JH, Smith SM, Williams DL, Kapell LA, Hadler SC, Halpin TJ, Maynard JE (1986). "A Community-wide epidemic of hepatitis A in Ohio". American Journal of Epidemiology. 123 (6): 1057–65. PMID 3706276. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  23. Craig AS, Sockwell DC, Schaffner W, Moore WL, Skinner JT, Williams IT, Shaw FE, Shapiro CN, Bell BP (1998). "Use of hepatitis A vaccine in a community-wide outbreak of hepatitis A". Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 27 (3): 531–5. PMID 9770153. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  24. CDC. Prevention of hepatitis A through active or passive immunization: recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR 1999;48(No. RR-12):1-37.
  25. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  26. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  27. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  28. Wasley A, Finelli L, Bell B. Hepatitis A among U.S. children in era of vaccination. [Abstract no. 1025]. 43rd Annual Meeting of the Infectious Diseases Society of America, October 6-9, 2005, San Francisco, California. Alexandria, VA: Infectious Diseases Society of America; 2005.
  29. Wasley A, Finelli L, Bell B. Hepatitis A among U.S. children in era of vaccination. [Abstract no. 1025]. 43rd Annual Meeting of the Infectious Diseases Society of America, October 6-9, 2005, San Francisco, California. Alexandria, VA: Infectious Diseases Society of America; 2005.
  30. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  31. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  32. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  33. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006

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