Hepatitis A epidemiology and demographics

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [3]

Overview

The incidence of hepatitis A varies among eras, countries and even cities within the same country. In recent years it has been noted a shift in prevalence, what was once a disease more prevalent in children, is today predominant in adults. In the United States, the incidence of hepatitis A in 2011 was 0.4 cases per 100,000 population. In recent years, the rates of hepatitis A have been similar among all age groups. After the introduction of the HAV vaccine, historic differences in rates of hepatitis A among racial/ethnic populations have also narrowed. In developed countries, elimination of historic geographic differences in incidence rates has also occurred. In developing countries with very poor sanitary conditions and hygienic practices, most children (90%) are infected with the hepatitis A virus before the age of 10.

Incidence

Prevaccine Era

  • 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.[1][2]

Postvaccine Era

  • There were 1,398 reported cases of acute HAV in 2011, representing an estimated 2,700 (1,650- 4,370) actual acute cases.[3]
  • The number of acute hepatitis A cases reported in the United States declined by approximately 53%, from 2,979 in 2007 to 1,398 in 2011.[3]
  • Of the 50 states that reported hepatitis A cases in 2011, 24 states had rates below the national rate.[3]
  • The rate of acute hepatitis A in the United States declined from 1.0 case per 100,000 population in 2007 to 0.4 cases per 100,000 population in 2011.[3]
  • In 2011, the case rate ranged from no cases in New Hampshire and North Dakota to 1.2 cases per 100,000 population in Arizona.[3]

Improvement in Sanitation

  • The resistance of the virus allows it to survive in urban sewage. Accordingly, outbreaks of the disease occur in overcrowded areas where there is poor sanitation. Improvements made throughout the years have decreased the incidence of the infection in new infants, which has led to an increasing number of adults with hepatitis A.

Age

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.[4]
  • 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.[1]

Postvaccine Era

  • In recent years, rates of hepatitis A have been similar among all age groups.[5]

Race

Prevaccine Era

  • Hepatitis A 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.[6][7][8][9]

Postvaccine Era

  • The historic differences in the rates of hepatitis A among racial/ethnic populations have narrowed in the vaccine era.
  • 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.[9]
  • 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.[5][10]

Developed Countries

Prevaccine Era

  • 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.[5]
  • 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.[11]
  • 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.
  • The majority of U.S. cases of hepatitis A resulted from person-to-person transmission of HAV during communitywide outbreaks.[12][13]
  • The most frequently reported source of infection (in 12%-26% of cases) was household or sexual contact with a person with hepatitis A.[14]
  • For approximately 50% of persons with hepatitis A, no source was identified for their infection.

Postvaccine Era

  • There has been an elimination of the historic geographic differences in the incidence rates of hepatitis A in the United States. Since 2001, rates of hepatitis A in states where vaccination was recommended, have been approximately equal to the rest of the United States.[15] In recent years, counties with higher rates have varied from year to year and have been distributed throughout the country.[5]
  • 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.[16]

Developing Countries

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.

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.[16]

References

  1. 1.0 1.1 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. 
  2. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  3. 3.0 3.1 3.2 3.3 3.4 "Hepatitis A Epidemics". 
  4. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  5. 5.0 5.1 5.2 5.3 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. PMID 16014593. doi:10.1001/jama.294.2.194. Retrieved 2012-02-28. 
  6. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  7. 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 1404852Freely accessible. PMID 2166446. 
  8. 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. 
  9. 9.0 9.1 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 1448379Freely accessible. PMID 15249305. 
  10. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  11. 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
  12. 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. 
  13. CDC. Communitywide outbreaks of hepatitis A. Hepatitis surveillance. Report no. 51. Atlanta, GA: US Department of Health and Human Services, CDC; 1987:6-8.
  14. 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. 
  15. CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  16. 16.0 16.1 16.2 Hepatitis A. World Health Organization. Fact sheet N 328, updated June 2014. Accessed 07/28/2014.[1]

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