Hepatitis A epidemiology and demographics: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
m (Bot: Removing from Primary care)
 
(44 intermediate revisions by 8 users not shown)
Line 1: Line 1:
__NOTOC__
{{Hepatitis A}}
{{Hepatitis A}}
{{CMG}}
{{CMG}}; {{AE}} {{JS}}


==Epidemiology and Demographics==
==Overview==
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).  
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.


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.  
==Incidence==
===Prevaccine Era===
* Before [[vaccine]] licensure during 1995-1996, hepatitis A [[incidence]] was primarily cyclic, with peaks occurring every 10-15 years.


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.  
* 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>


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.  
===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.<ref name=CDC>{{cite web | title = Hepatitis A Epidemics | url = http://www.cdc.gov/hepatitis/Statistics/2011Surveillance/Commentary.htm#hepA }}</ref>


In experimentally infected nonhuman primates, HAV has been detected in saliva during the incubation period. However, transmission by saliva has not been demonstrated.  
* 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.<ref name=CDC>{{cite web | title = Hepatitis A Epidemics | url = http://www.cdc.gov/hepatitis/Statistics/2011Surveillance/Commentary.htm#hepA }}</ref>


===Demographics===
* Of the 50 states that reported [[hepatitis A]] cases in 2011, 24 states had rates below the national rate.<ref name=CDC>{{cite web | title = Hepatitis A Epidemics | url = http://www.cdc.gov/hepatitis/Statistics/2011Surveillance/Commentary.htm#hepA }}</ref>
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 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).  
* 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.<ref name=CDC>{{cite web | title = Hepatitis A Epidemics | url = http://www.cdc.gov/hepatitis/Statistics/2011Surveillance/Commentary.htm#hepA }}</ref>


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.  
* 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.<ref name=CDC>{{cite web | title = Hepatitis A Epidemics | url = http://www.cdc.gov/hepatitis/Statistics/2011Surveillance/Commentary.htm#hepA }}</ref>


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.  
===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]].


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==
===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>


===Age===
* 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>
The reported incidence of hepatitis A is highest among children 5-14 years of age, with approximately one-third of reported cases involving children less than 15 years of age<ref>CDC. Hepatitis surveillance report no. 56. Altanta, GA: U.S. Department of Health and Human Services, Public Health Service, CDC. 1996.</ref>. Many more children have unrecognized, asymptomatic infection and can be the source of infection for others.


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%.
===Postvaccine Era===
* In recent years, rates of hepatitis A have been similar among all age groups.<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>


===Ethnicity===
==Race==
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.
===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.<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>
 
===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.<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>
 
* 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.<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><ref>CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006</ref>
 
==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.<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.
 
* 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>
 
* 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.<ref>CDC. Hepatitis surveillance. Report no. 61. Atlanta, GA: US Department of Health and Human Services, CDC. 2006</ref> In recent years, counties with higher rates have varied from year to year and have been distributed throughout the country.<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>
 
* 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.<ref name=WHO1>Hepatitis A. World Health Organization. Fact sheet N 328, updated June 2014. Accessed 07/28/2014.[http://www.who.int/mediacentre/factsheets/fs328/en/]</ref>
 
==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]].
 
* [[Epidemics]] are uncommon because older children and adults are generally [[immune]]. [[Symptomatic]] disease rates in these areas are low and [[outbreaks]] are rare.<ref name=WHO1>Hepatitis A. World Health Organization. Fact sheet N 328, updated June 2014. Accessed 07/28/2014.[http://www.who.int/mediacentre/factsheets/fs328/en/]</ref>
 
===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.<ref name=WHO1>Hepatitis A. World Health Organization. Fact sheet N 328, updated June 2014. Accessed 07/28/2014.[http://www.who.int/mediacentre/factsheets/fs328/en/]</ref>


==References==
==References==
{{reflist|2}}
{{reflist|2}}
{{WH}}
{{WS}}


[[Category:Foodborne illnesses]]
[[Category:Foodborne illnesses]]
[[Category:hepatitis|A]]
[[Category:Hepatitis|A]]
[[Category:Picornaviruses]]
[[Category:Picornaviruses]]
[[Category:Viral diseases]]
[[Category:Viral diseases]]
[[Category:Mature chapter]]
[[Category:Disease]]
[[Category:Emergency mdicine]]
[[Category:Up-To-Date]]
[[Category:Infectious disease]]
[[Category:Hepatology]]
[[Category:Gastroenterology]]

Latest revision as of 22:04, 29 July 2020

Hepatitis Main Page

Hepatitis A

Home

Patient Information

Overview

Historical Perspective

Pathophysiology

Causes

Differentiating Hepatitis A from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

History and Symptoms

Physical Examination

Laboratory Findings

CT

Ultrasound

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Case Studies

Case #1

Hepatitis A epidemiology and demographics On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of Hepatitis A epidemiology and demographics

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on Hepatitis A epidemiology and demographics

CDC on Hepatitis A epidemiology and demographics

Hepatitis A epidemiology and demographics in the news

Blogs on Hepatitis A epidemiology and demographics

Directions to Hospitals Treating Hepatitis A

Risk calculators and risk factors for Hepatitis A epidemiology and demographics

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. Unknown parameter |month= ignored (help)
  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. doi:10.1001/jama.294.2.194. PMID 16014593. Retrieved 2012-02-28. Unknown parameter |month= ignored (help)
  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 1404852. PMID 2166446. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  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. Unknown parameter |month= ignored (help)
  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 1448379. PMID 15249305. Unknown parameter |month= ignored (help); |access-date= requires |url= (help)
  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. Unknown parameter |month= ignored (help)
  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. |access-date= requires |url= (help)
  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]

Template:WH Template:WS

Retrieved from "https://www.wikidoc.org/index.php?title=Hepatitis_A_epidemiology_and_demographics&oldid=1639105"