Hepatitis A historical perspective: Difference between revisions
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==Historical Perspective== | ==Historical Perspective== | ||
Hepatitis A virus was first identified in 1973. | Hepatitis A virus was first identified in 1973. It was classified as a separate disease from other heptitis during the second world war. However, it's true prevalence and route of transmission would only be recognized later. | ||
The incidence of hepatitis A varies among eras, countries and even cities within the same country. In recent years it has been noticed a shift in prevalence, what was once a disease more prevalent in children, is today predominant in adults. | |||
The measurement of anti-HAV antibodies is the best definition of the disease's true epidemology. | |||
The resistance of the virus allows it to survive in urban sewage. Accordingly, outbreaks of the disease occur in areas where there is poor sanitation and | |||
HAV is a very stable virus, frequently found in urban sewage. Infections occur early in life when sanitation is poor and living conditions crowded, but improvements in sanitation and hygiene have delayed infection, resulting in increasing numbers of adults susceptible to HAV. Transmission of HAV by blood is rare. High-risk persons include injection drug users, institutionalized persons and their caretakers, and those who travel from low-prevalence to high-prevalence countries | |||
===Prevaccine Era=== | ===Prevaccine Era=== | ||
Revision as of 11:46, 29 July 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Historical Perspective
Hepatitis A virus was first identified in 1973. It was classified as a separate disease from other heptitis during the second world war. However, it's true prevalence and route of transmission would only be recognized later.
The incidence of hepatitis A varies among eras, countries and even cities within the same country. In recent years it has been noticed a shift in prevalence, what was once a disease more prevalent in children, is today predominant in adults.
The measurement of anti-HAV antibodies is the best definition of the disease's true epidemology.
The resistance of the virus allows it to survive in urban sewage. Accordingly, outbreaks of the disease occur in areas where there is poor sanitation and
HAV is a very stable virus, frequently found in urban sewage. Infections occur early in life when sanitation is poor and living conditions crowded, but improvements in sanitation and hygiene have delayed infection, resulting in increasing numbers of adults susceptible to HAV. Transmission of HAV by blood is rare. High-risk persons include injection drug users, institutionalized persons and their caretakers, and those who travel from low-prevalence to high-prevalence countries
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.[1][2] One such analysis estimated an average of 271,000 infections per year during 1980-1999, representing 10.4 times the reported number of cases.[1] 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.[3] 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.[4] 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.[5][4] 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.[6] 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] 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.[7][8][9][10]
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.[11] 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.[12] 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.[13][14] The most frequently reported source of infection (in 12%-26% of cases) was household or sexual contact with a person with hepatitis A.[15] Cyclic outbreaks occurred among users of injection and noninjection drugs and among men who have sex with men (MSM),[16][17][18][19][20] 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.[15] For approximately 50% of persons with hepatitis A, no source was identified for their infection.
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.[11] 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.[21]
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.[22] This decline is reflected in other fundamental shifts in hepatitis A epidemiology.
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.[13] Once initiated, epidemics often persisted for 1--2 years and proved difficult to control.[23][24] Because children often have unrecognized or asymptomatic infection, they played a key role in sustaining HAV transmission during these epidemics.
References
- ↑ 1.0 1.1 1.2 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) - ↑ CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
- ↑ 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
- ↑ 4.0 4.1 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) - ↑ 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
- ↑ CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
- ↑ CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
- ↑ 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) - ↑ 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) - ↑ 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) - ↑ 11.0 11.1 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) - ↑ 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
- ↑ 13.0 13.1 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) - ↑ CDC. Communitywide outbreaks of hepatitis A. Hepatitis surveillance. Report no. 51. Atlanta, GA: US Department of Health and Human Services, CDC; 1987:6-8.
- ↑ 15.0 15.1 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) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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) - ↑ 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.
- ↑ CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
- ↑ 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) - ↑ 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)