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==Epidemiology and Demographics==
==Prevaccine Era==
Person-to-person transmission through the fecal-oral route is the primary means of HAV transmission in the United States. Transmission occurs most frequently among close contacts, especially in households and extended family settings. Because the majority of children have asymptomatic or unrecognized infections, they play a key role in HAV transmission and serve as a source of infection for others. In one study of adults without an identified source, 52% of their households included a child aged <6 years, and the presence of a young child was associated with HAV transmission in the household. In studies in which serologic testing of the household contacts of adults without an identified source of infection was performed, 25%-40% of contacts aged <6 years had serologic evidence of acute HAV infection (IgM anti-HAV).  
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<ref name="pmid11986444">{{cite journal |author=Armstrong GL, Bell BP |title=Hepatitis A virus infections in the United States: model-based estimates and implications for childhood immunization |journal=[[Pediatrics]] |volume=109 |issue=5 |pages=839–45 |year=2002 |month=May |pmid=11986444 |doi= |url=http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=11986444 |accessdate=2012-02-28}}</ref><ref>CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006</ref>. One such analysis estimated an average of 271,000 infections per year during 1980-1999, representing 10.4 times the reported number of cases<ref name="pmid11986444">{{cite journal |author=Armstrong GL, Bell BP |title=Hepatitis A virus infections in the United States: model-based estimates and implications for childhood immunization |journal=[[Pediatrics]] |volume=109 |issue=5 |pages=839–45 |year=2002 |month=May |pmid=11986444 |doi= |url=http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=11986444 |accessdate=2012-02-28}}</ref>. Each year in the United States, an estimated 100 persons died as a result of acute liver failure attributed to hepatitis A.


Common-source outbreaks and sporadic cases also can occur from exposure to fecally contaminated food or water. Uncooked foods have been recognized frequently as a source of outbreaks. Cooked foods also can transmit HAV if cooking is inadequate to kill the virus or if food is contaminated after cooking, as occurs commonly in outbreaks associated with infected food handlers. Waterborne outbreaks of hepatitis A are infrequent in developed countries with well-maintained sanitation and water supplies. The majority of waterborne outbreaks are associated with sewage-contaminated or inadequately treated water. Outbreaks in the context of floods or other natural disasters (e.g., hurricanes) have not been reported in the United States.  
The costs associated with hepatitis A are substantial. Surveillance data indicate that 11%-22% of persons with hepatitis A are hospitalized<ref>[http://www.cdc.gov/mmwr/preview/mmwrhtml/rr4812a1.htm 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]</ref>. 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<ref name="pmid10655272">{{cite journal |author=Berge JJ, Drennan DP, Jacobs RJ, Jakins A, Meyerhoff AS, Stubblefield W, Weinberg M |title=The cost of hepatitis A infections in American adolescents and adults in 1997 |journal=[[Hepatology (Baltimore, Md.)]] |volume=31 |issue=2 |pages=469–73 |year=2000 |month=February |pmid=10655272 |doi=10.1002/hep.510310229 |url=http://dx.doi.org/10.1002/hep.510310229 |accessdate=2012-02-28}}</ref>. 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<ref>[http://www.cdc.gov/mmwr/preview/mmwrhtml/rr4812a1.htm 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]</ref><ref name="pmid10655272">{{cite journal |author=Berge JJ, Drennan DP, Jacobs RJ, Jakins A, Meyerhoff AS, Stubblefield W, Weinberg M |title=The cost of hepatitis A infections in American adolescents and adults in 1997 |journal=[[Hepatology (Baltimore, Md.)]] |volume=31 |issue=2 |pages=469–73 |year=2000 |month=February |pmid=10655272 |doi=10.1002/hep.510310229 |url=http://dx.doi.org/10.1002/hep.510310229 |accessdate=2012-02-28}}</ref>. 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.


Depending on conditions, HAV can be stable in the environment for months. Heating foods at temperatures >185°F (>85°C) for 1 minute or disinfecting surfaces with a 1:100 dilution of sodium hypochlorite (i.e., household bleach) in tap water is necessary to inactivate HAV.  
===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<ref>CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006</ref>. 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<ref name="pmid11986444">{{cite journal |author=Armstrong GL, Bell BP |title=Hepatitis A virus infections in the United States: model-based estimates and implications for childhood immunization |journal=[[Pediatrics]] |volume=109 |issue=5 |pages=839–45 |year=2002 |month=May |pmid=11986444 |doi= |url=http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=11986444 |accessdate=2012-02-28}}</ref>. 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<ref>CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006</ref><ref name="pmid2166446">{{cite journal |author=Shaw FE, Shapiro CN, Welty TK, Dill W, Reddington J, Hadler SC |title=Hepatitis transmission among the Sioux Indians of South Dakota |journal=[[American Journal of Public Health]] |volume=80 |issue=9 |pages=1091–4 |year=1990 |month=September |pmid=2166446 |pmc=1404852 |doi= |url= |accessdate=2012-02-28}}</ref><ref name="pmid8376812">{{cite journal |author=Bulkow LR, Wainwright RB, McMahon BJ, Middaugh JP, Jenkerson SA, Margolis HS |title=Secular trends in hepatitis A virus infection among Alaska Natives |journal=[[The Journal of Infectious Diseases]] |volume=168 |issue=4 |pages=1017–20 |year=1993 |month=October |pmid=8376812 |doi= |url=http://www.jid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=8376812 |accessdate=2012-02-28}}</ref><ref name="pmid15249305">{{cite journal |author=Bialek SR, Thoroughman DA, Hu D, Simard EP, Chattin J, Cheek J, Bell BP |title=Hepatitis A incidence and hepatitis a vaccination among American Indians and Alaska Natives, 1990-2001 |journal=[[American Journal of Public Health]] |volume=94 |issue=6 |pages=996–1001 |year=2004 |month=June |pmid=15249305 |pmc=1448379 |doi= |url= |accessdate=2012-02-28}}</ref>.


On rare occasions, HAV infection has been transmitted by transfusion of blood or blood products collected from donors during the viremic phase of their infection. Since 2002, nucleic acid amplification tests such as polymerase chain reaction (PCR) have been applied to the screening of source plasma used for the manufacture of plasma-derived products.  
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<ref name="pmid16014593">{{cite journal |author=Wasley A, Samandari T, Bell BP |title=Incidence of hepatitis A in the United States in the era of vaccination |journal=[[JAMA : the Journal of the American Medical Association]] |volume=294 |issue=2 |pages=194–201 |year=2005 |month=July |pmid=16014593 |doi=10.1001/jama.294.2.194 |url=http://jama.ama-assn.org/cgi/pmidlookup?view=long&pmid=16014593 |accessdate=2012-02-28}}</ref>. 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<ref>[http://www.cdc.gov/mmwr/preview/mmwrhtml/rr4812a1.htm 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]</ref>. 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.


In experimentally infected nonhuman primates, HAV has been detected in saliva during the incubation period. However, transmission by saliva has not been demonstrated.  
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.


===Demographics===
===Sources of Infection===
Over the past several decades, the highest rates of hepatitis A have occurred in a limited number of states and counties in the United States<ref>CDC. Hepatitis surveillance report no. 56. Altanta, GA: U.S. Department of Health and Human Services, Public Health Service, CDC. 1996.</ref>, with rates being substantially higher in the western United States than in other U.S. regions. Although yearly rates in states with the highest disease rates can fluctuate, they consistently remain above the U.S. national average (Figure 4). During 1987-1997, an average of 50% of reported hepatitis A cases each year was from states with average disease rates greater than twice the national average of approximately 10 cases per 100,000, yet the total population of these states represented approximately 22% of the U.S. population. An additional 18% of cases were from states with average annual disease rates above the national average during this time but less than twice the national average.
In the prevaccine era, the majority of U.S. cases of hepatitis A resulted from person-to-person transmission of HAV during communitywide outbreaks<ref name="pmid9815207">{{cite journal |author=Bell BP, Shapiro CN, Alter MJ, Moyer LA, Judson FN, Mottram K, Fleenor M, Ryder PL, Margolis HS |title=The diverse patterns of hepatitis A epidemiology in the United States-implications for vaccination strategies |journal=[[The Journal of Infectious Diseases]] |volume=178 |issue=6 |pages=1579–84 |year=1998 |month=December |pmid=9815207 |doi= |url=http://www.jid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=9815207 |accessdate=2012-02-28}}</ref><ref>CDC. Communitywide outbreaks of hepatitis A. Hepatitis surveillance. Report no. 51. Atlanta, GA: US Department of Health and Human Services, CDC; 1987:6-8.</ref>. The most frequently reported source of infection (in 12%-26% of cases) was household or sexual contact with a person with hepatitis A<ref name="pmid1476001">{{cite journal |author=Shapiro CN, Coleman PJ, McQuillan GM, Alter MJ, Margolis HS |title=Epidemiology of hepatitis A: seroepidemiology and risk groups in the USA |journal=[[Vaccine]] |volume=10 Suppl 1 |issue= |pages=S59–62 |year=1992 |pmid=1476001 |doi= |url= |accessdate=2012-02-28}}</ref>. Cyclic outbreaks occurred among users of injection and noninjection drugs and among men who have sex with men (MSM)<ref name="pmid12696002">{{cite journal |author=Cotter SM, Sansom S, Long T, Koch E, Kellerman S, Smith F, Averhoff F, Bell BP |title=Outbreak of hepatitis A among men who have sex with men: implications for hepatitis A vaccination strategies |journal=[[The Journal of Infectious Diseases]] |volume=187 |issue=8 |pages=1235–40 |year=2003 |month=April |pmid=12696002 |doi=10.1086/374057 |url=http://www.jid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=12696002 |accessdate=2012-02-28}}</ref><ref name="pmid2929804">{{cite journal |author=Harkess J, Gildon B, Istre GR |title=Outbreaks of hepatitis A among illicit drug users, Oklahoma, 1984-87 |journal=[[American Journal of Public Health]] |volume=79 |issue=4 |pages=463–6 |year=1989 |month=April |pmid=2929804 |pmc=1349976 |doi= |url= |accessdate=2012-02-28}}</ref><ref name="pmid3140269">{{cite journal |author=Schade CP, Komorwska D |title=Continuing outbreak of hepatitis A linked with intravenous drug abuse in Multnomah County |journal=[[Public Health Reports (Washington, D.C. : 1974)]] |volume=103 |issue=5 |pages=452–9 |year=1988 |pmid=3140269 |pmc=1478131 |doi= |url= |accessdate=2012-02-28}}</ref><ref name="pmid10358687">{{cite journal |author=Hutin YJ, Bell BP, Marshall KL, Schaben CP, Dart M, Quinlisk MP, Shapiro CN |title=Identifying target groups for a potential vaccination program during a hepatitis A communitywide outbreak |journal=[[American Journal of Public Health]] |volume=89 |issue=6 |pages=918–21 |year=1999 |month=June |pmid=10358687 |pmc=1508638 |doi= |url= |accessdate=2012-02-28}}</ref><ref name="pmid15620475">{{cite journal |author=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 |title=Vaccination in the county jail as a strategy to reach high risk adults during a community-based hepatitis A outbreak among methamphetamine drug users |journal=[[Vaccine]] |volume=23 |issue=8 |pages=1021–8 |year=2005 |month=January |pmid=15620475 |doi=10.1016/j.vaccine.2004.07.038 |url=http://linkinghub.elsevier.com/retrieve/pii/S0264-410X(04)00622-X |accessdate=2012-02-28}}</ref>, 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<ref name="pmid1476001">{{cite journal |author=Shapiro CN, Coleman PJ, McQuillan GM, Alter MJ, Margolis HS |title=Epidemiology of hepatitis A: seroepidemiology and risk groups in the USA |journal=[[Vaccine]] |volume=10 Suppl 1 |issue= |pages=S59–62 |year=1992 |pmid=1476001 |doi= |url= |accessdate=2012-02-28}}</ref>. For approximately 50% of persons with hepatitis A, no source was identified for their infection.


In the U.S. population, the overall age-adjusted prevalence of HBV infection (including persons with chronic infection and those with previous infection) was 4.9% in the third National Health and Nutrition Examination Survey (NHANES III, 1988--1994). Foreign-born persons (particularly Asian/Pacific Islanders) who have emigrated from countries in which HBV is endemic contribute disproportionately to the burden of chronic HBV infection in the United States. The prevalence of chronic HBV infection among foreign-born persons immigrating to the United States from Central and Southeast Asia, the Middle East, and Africa varies (range: 5%--15%) and reflects the patterns of HBV infection in the countries and regions of origin for these persons. During 1994--2003, approximately 40,000 immigrants with chronic HBV infection were admitted annually to the United States for permanent residence (78; CDC, unpublished data, 2005).
===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<ref name="pmid9815207">{{cite journal |author=Bell BP, Shapiro CN, Alter MJ, Moyer LA, Judson FN, Mottram K, Fleenor M, Ryder PL, Margolis HS |title=The diverse patterns of hepatitis A epidemiology in the United States-implications for vaccination strategies |journal=[[The Journal of Infectious Diseases]] |volume=178 |issue=6 |pages=1579–84 |year=1998 |month=December |pmid=9815207 |doi= |url=http://www.jid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=9815207 |accessdate=2012-02-28}}</ref>. Once initiated, epidemics often persisted for 1--2 years and proved difficult to control<ref name="pmid3706276">{{cite journal |author=Shaw FE, Sudman JH, Smith SM, Williams DL, Kapell LA, Hadler SC, Halpin TJ, Maynard JE |title=A Community-wide epidemic of hepatitis A in Ohio |journal=[[American Journal of Epidemiology]] |volume=123 |issue=6 |pages=1057–65 |year=1986 |month=June |pmid=3706276 |doi= |url= |accessdate=2012-02-28}}</ref><ref name="pmid9770153">{{cite journal |author=Craig AS, Sockwell DC, Schaffner W, Moore WL, Skinner JT, Williams IT, Shaw FE, Shapiro CN, Bell BP |title=Use of hepatitis A vaccine in a community-wide outbreak of hepatitis A |journal=[[Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America]] |volume=27 |issue=3 |pages=531–5 |year=1998 |month=September |pmid=9770153 |doi= |url=http://www.cid.oxfordjournals.org/cgi/pmidlookup?view=long&pmid=9770153 |accessdate=2012-02-28}}</ref>. Because children often have unrecognized or asymptomatic infection, they played a key role in sustaining HAV transmission during these epidemics.
During 1990-2004, overall incidence of reported acute hepatitis B declined 75%, from 8.5 to 2.1 per 100,000 population. The most dramatic declines occurred in the cohort of children to whom recommendations for routine infant and adolescent vaccination have applied. Incidence among children aged <12 years and adolescents aged 12--19 years declined 94%, from 1.1 to 0.36 and 6.1 to 2.8 per 100,000 population, respectively (Figure 2). Since implementation of routine childhood immunization, an estimated 6,800 perinatal infections and an additional 18,700 infections during the first 10 years of life have been prevented annually in the United States.
 
Although infections in infants and children aged <10 years represented <10% of all HBV infections before implementation of childhood immunization programs, childhood infections resulted in an estimated 30%-40% of the chronic HBV infections among persons who acquired their infections in the United States. In two population-based studies conducted among Asian/Pacific Islander children who were born in the United States before perinatal hepatitis B prevention programs were widely implemented, 61%-66% of the chronic HBV infections occurred in children born to HBsAg-negative mothers. A substantial proportion of these chronic infections would not have been prevented by a selective program of identification and immunization of only infants born to HBsAg-positive mothers.
 
In addition to declines in incidence among all age groups, racial disparities in hepatitis B incidence among children have been substantially reduced. The reduction of the disparity between Asian/Pacific Islander and other children is consistent with recent observations noting a decline in seroprevalence of HBV infection after successful implementation of routine hepatitis B vaccination among Asians who have recently immigrated to the United States. However, as hepatitis B incidence has declined among U.S.-born children, unvaccinated foreign-born children account for a high proportion of infections. During 2001--2002, of 19 children born after 1991 in whom acute hepatitis B had been verified, eight (42%) were foreign born.
 
===Age===
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 (Figure 1)<ref>CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. In press, 2006.</ref>. 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<ref name="pmid11986444">{{cite journal |author=Armstrong GL, Bell BP |title=Hepatitis A virus infections in the United States: model-based estimates and implications for childhood immunization |journal=[[Pediatrics]] |volume=109 |issue=5 |pages=839–45 |year=2002 |month=May |pmid=11986444 |doi= |url=http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=11986444 |accessdate=2012-02-28}}</ref>.
 
About a third of the U.S. population has serologic evidence of prior HAV infection, according to data from the Third National Health and Nutrition Examination Survey (NHANES-III) conducted during 1988-1994 (CDC, unpublished data, 1998). Anti-HAV prevalence varies directly with age: among persons 6-11 years of age, the prevalence is 9%; 20-29 years of age, 19%; 40-49 years of age, 33%; and greater than 70 years of age, 75%.
 
===Ethnicity===
Hepatitis A incidence varies by race/ethnicity, with highest rates among American Indians/Alaskan Natives and lowest rates among Asians; rates among Hispanics are higher than among non-Hispanics (Figure 2). Racial/ethnic differences in rates most likely reflect differences in the risk for infection related to factors such as differences in socioeconomic levels and resultant living conditions (e.g., crowding) and more frequent contact with persons from countries where hepatitis A is endemic (e.g., Mexico and Central America). Age-adjusted anti-HAV prevalence is highest among Mexican-Americans (70%), compared with non-Hispanic blacks (39%) and non-Hispanic whites (23%). Anti-HAV prevalence is inversely related to income and household size.


==References==
==References==
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S. [2]

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.

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[21][22]. Because children often have unrecognized or asymptomatic infection, they played a key role in sustaining HAV transmission during these epidemics.

References

  1. ↑ 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)
  2. ↑ CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  3. ↑ 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. ↑ 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)
  5. ↑ 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
  6. ↑ CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  7. ↑ CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006
  8. ↑ 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)
  9. ↑ 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)
  10. ↑ 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. ↑ 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)
  12. ↑ 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. ↑ 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)
  14. ↑ 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. ↑ 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)
  16. ↑ 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)
  17. ↑ 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)
  18. ↑ 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)
  19. ↑ 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)
  20. ↑ 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)
  21. ↑ 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)
  22. ↑ 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)

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