Hepatitis A Information

Thanks to HepMag.com for a great summary of ongoing hepatitis A outbreaks going on in the US.

California

Public health officials first detected the hepatitis A outbreak in November 2016 and as of July 21, 2017, 251 cases and 5 deaths have been reported in San Diego. Those affected have largely been homeless individuals, which has made public health efforts more challenging to implement, particularly in reaching individuals with vaccinations and improving hygiene practices. Local officials and community organizations have been working to raise awareness of hepatitis A vaccination, distribute “Hepatitis A Prevention Kits” (containing sanitary supplies), and plans are underway to install hand-washing stations in areas frequented by homeless persons to help stop the spread. Since the outbreak began, the county has administered over 4,000 hepatitis A vaccinations, and more work is planned to expand those efforts. With this combined approach, San Diego is hoping to end the outbreak, the largest in California in nearly 20 years.

Colorado

Between January and early July 2017, 43 cases of hepatitis A were reported in Colorado, a significant increase from 2016 where 23 cases were reported for the full year. Half of these cases resulted in hospitalization and one person has died. Unlike many hepatitis A outbreaks, there is no apparent common link to a restaurant or food item. 74% of hepatitis A cases are men and at least half are men who have sex with men (MSM). Local public health agencies are working to battle the epidemic by targeting MSM with outreach and offering vaccination at a variety of sites.

Michigan

Between August 2016 and June 2017 in southeast Michigan, almost 200 people have been diagnosed with hepatitis A infection, 90% of those infected have required hospitalization, and 10 people have died. Public health officials believe the outbreak to be unrelated to water or food contamination, but rather person-to-person spread through use of illicit drugs, sexual contact, and close proximity. Nearly 50% of those infected report a history of substance use disorders and 20% are also infected with hepatitis C.

A comprehensive hepatitis A vaccination program established in Alaska in the 1990s, which became a requirement for school entry in 2001, has virtually wiped out the virus in the native peoples of Alaska, where it had been endemic.

Data from the program is being presented at this year’s World Indigenous Peoples’ Conference on Viral Hepatitis in Anchorage, Alaska, USA (8-9 August) by Stephanie Massay, Epidemiology Specialist with the Alaska Division of Public Health, Section of Epidemiology, Anchorage, AK, USA, and colleagues.

Hepatitis A is an acute (short-term but severe) infection of the liver caused by the hepatitis A virus. Fever, weakness, nausea, aches and pains, and jaundice can be among the symptoms experienced. The hepatitis A virus can survive in the environment on and in food. It is also relatively resistant to detergents but can be inactivated by high temperature (85°C or higher) and by chemicals such as chlorine. Although it occurs worldwide, HAV occurs more commonly in populations with poor sanitation, such as poor populations in developed countries (e.g. Indigenous populations) and also in developing countries more generally.

Alaska experienced epidemics of hepatitis A every 10-15 years during the 1950s to the 1990s, resulting in thousands of cases. Alaska Native (AN) people living in rural communities were disproportionately impacted.

Hepatitis A virus (HAV) vaccines were licensed in 1995 and recommended by the Advisory Committee on Immunization Practice (ACIP) for routine vaccination of US children in populations with high HAV infection rates. Alaska began universal vaccination for children aged 2-14 years in 1996? HAV vaccination became required for school entrance in 2001. In 1997, following ACIP recommendations, this was expanded to include all children age 2 – 18 years, and in 2006 this was further expanded to include children age 1 – 18 years.

The data showed that during 1972-1995, Alaska’s average annual incidence of hepatitis A was 60 per 100,000 population. Rates by race were substantially higher for AN people compared to non-AN people (244 vs 19 per 100,000 respectively, with AN people being 13 times more likely to be infected than non-AN people).

Compared to 1972-1995 (pre-vaccine), 2002-2007 (post­vaccine) statewide hepatitis A incidence fell by 98% (0.9 vs. 60 per 100,000); among AN peoples the incidence fell by 99.9% (0.3 vs. 243.8 per 100,000). During 2008-2016, 23 HAV cases were reported in Alaska? 5 among AN, 11 among non­AN, and 7 among people of unknown race/ethnicity.

The 2008-2016 statewide incidence of hepatitis A was 0.35 cases per 100,000 people? the incidence in children aged <14 years was 0.14 cases per 100,000 children. Of the 17 cases with documentation on travel, 15 (88%) had recent travel outside of Alaska. In 2015, National Immunization Survey data estimated that among children aged 19-35 months, HAV vaccine coverage was similar in Alaska (84%) and all US children (86%).

The authors conclude: “Dramatic declines in the incidence of hepatitis A occurred after HAV vaccine was recommended as a routine childhood vaccine and after it was required for school entry. Prior to routine vaccination, most the reported HAV cases were associated with outbreaks occurring within Alaska. Since 2008 however, 88% of reported hepatitis A cases have been imported, many of which were acquired during travel outside of the United States.”

THE HEPATITIS A VIRUS

Exposure to hepatitis A virus (“HAV”) can cause an acute infection of the liver that is typically mild and resolves on its own.[1] The symptoms and duration of illness vary a great deal, with many persons showing no symptoms at all.[2] Fever and jaundice are two of the symptoms most commonly associated with HAV infection.[3]

Throughout history, hepatitis infections have plagued humans. The “earliest accounts of contagious jaundice are found in ancient China.”[4] According to the CDC:

The first descriptions of hepatitis (epidemic jaundice) are generally attributed to Hippocrates. Outbreaks of jaundice, probably hepatitis A, were reported in the 17th and 18th centuries, particularly in association with military campaigns. Hepatitis A (formerly called infectious hepatitis) was first differentiated epidemiologically from hepatitis B, which has a long incubation period, in the 1940s. Development of serologic tests allowed definitive diagnosis of hepatitis B. In the 1970s, identification of the virus, and development of serologic tests helped differentiate hepatitis A from other types of non-B hepatitis.[5]

Until 2004, HAV was the most frequently reported type of hepatitis in the United States. In the pre-vaccine era, the primary methods used for preventing HAV infections were hygienic measures and passive protection with immune globulin (IG). Hepatitis A vaccines were licensed in 1995 and 1999. These vaccines provide long-term protection against HAV infection.[6

Hepatitis A is the only common vaccine-preventable foodborne disease in the United States.[7] This virus is one of five human hepatitis viruses that primarily infect the human liver and cause human illness.[8] Unlike hepatitis B and C, hepatitis A does not develop into chronic hepatitis or cirrhosis, which are both potentially fatal conditions.[9] Nonetheless, infection with the hepatitis A virus (HAV) can lead to acute liver failure and death.[1

Where does Hepatitis A Come From?

Hepatitis A is a communicable (or contagious) disease that often spreads from person to person.[11] Person-to-person transmission occurs via the “fecal-oral route,” while all other exposure is generally attributable to contaminated food or water.[12] Food-related outbreaks are usually associated with contamination of food during preparation by a HAV-infected food handler.[13] The food handler is generally not ill because the peak time of infectivity—that is, when the most virus is present in the stool of an infected individual—occurs two weeks before illness begins.[14]

Fresh produce contaminated during cultivation, harvesting, processing, and distribution has also been a source of hepatitis A.[15] In 1997, frozen strawberries were the source of a hepatitis A outbreak in five states.[16] Six years later, in 2003, fresh green onions were identified as the source of a HAV outbreak traced to consumption of food at a Pennsylvania restaurant.[17] Other fruits and vegetables, such as blueberries and lettuce, have also been associated with HAV outbreaks in the U.S. as well as in other developed countries.[18] HAV is relatively stable and can survive for several hours on fingertips and hands and up to two months on dry surfaces.[19] The virus can be inactivated by heating to 185°F (85°C) or higher for one minute, or disinfecting surfaces with a 1:100 dilution of household bleach in tap water.[20] HAV can still be spread from cooked food if it is contaminated after cooking.[21]

Although ingestion of contaminated food is a common means of spread for HAV, it may also be spread by household contact among families or roommates, sexual contact, or by direct inoculation from persons sharing illicit drugs.[22] Children are often asymptomatic, or have unrecognized infections, and can pass the virus through ordinary play, unknown to their parents, who may later become infected from contact with their children.[23]

What are the Symptoms of Hepatitis A?

Hepatitis A may cause no symptoms at all when it is contracted, especially in children.[24] Asymptomatic individuals will only know they were infected (and have become immune, given that you can only get hepatitis A once) by getting a blood test later in life.[25] Approximately 10 to 12 days after exposure, HAV is present in blood and is excreted via the biliary system into the feces.[26] Although the virus is present in the blood, its concentration is much higher in feces.[27] HAV excretion begins to decline at the onset of clinical illness, and decreases significantly by 7 to 10 days after onset of symptoms.[28] Most infected persons no longer excrete virus in the feces by the third week of illness. Children may excrete HAV longer than adults.[29]

Seventy percent of HAV infections in children younger than six years of age are asymptomatic; in older children and adults, infection tends to be symptomatic with more than 70% of those infected developing jaundice.[30] Symptoms typically begin about 28 days after contracting HAV, but can begin as early as 15 days or as late as 50 days after exposure.[31] The symptoms include muscle aches, headache, anorexia (loss of appetite), abdominal discomfort, fever, and malaise.[32]

After a few days of typical symptoms, jaundice (also termed “icterus”) sets in.[33] Jaundice is a yellowing of the skin, eyes, and mucous membranes that occurs because bile flows poorly through the liver and backs up into the blood.[34] The urine will also turn dark with bile and the stool light or clay-colored from lack of bile.[35] When jaundice sets in, initial symptoms such as fever and headache begin to subside.[36]

In general, symptoms usually last less than two months, although 10% to 15% of symptomatic persons have prolonged or relapsing disease for up to 6 months.[37] It is not unusual, however, for blood tests to remain abnormal for six months or more.[38] The jaundice so commonly associated with HAV can also linger for a prolonged period in some infected persons, sometimes as long as eight months or more.[39] Additionally, pruritus, or severe “itchiness” of the skin, can persist for several months after the onset of symptoms. These conditions are frequently accompanied by diarrhea, anorexia, and fatigue.[40]

Relapse is possible with hepatitis A, typically within three months of the initial onset of symptoms.[41] Although relapse is more common in children, it does occur with some regularity in adults.[42] The vast majority of persons who are infected with hepatitis A fully recover, and do not develop chronic hepatitis.[43] Persons do not carry HAV long-term as with hepatitis B and C.[44]

Fulminant Hepatitis A

Fulminant hepatitis A, or acute liver failure, is a rare but devastating complication of HAV infection.[45] As many as 50% of individuals with acute liver failure may die or require emergency liver transplantation.[46] Elderly patients and patients with chronic liver disease are at higher risk for fulminant hepatitis A.[47] In parallel with a declining incidence of acute HAV infection in the general population, however, the incidence of fulminant HAV appears to be decreasing.[48]

HAV infects the liver’s parenchymal cells (internal liver cells).[49] Once a cell has been penetrated by the viral particles, the hepatitis A releases its own toxins that cause, in essence, a hostile takeover of the host’s cellular system.[50] The cell then produces new viral components that are released into the bile capillaries or tubes that run between the liver’s parenchymal cells.[51] This process results in the death of liver cells, called hepatic necrosis.[52]

The fulminant form of hepatitis occurs when this necrotic process kills so many liver cells—upwards of three-quarters of the liver’s total cell count—that the liver can no longer perform its job.[53] Aside from the loss of liver function, fulminant hepatic failure can lead to encephalopathy and cerebral edema.[54] Encephalopathy is a brain disorder that causes central nervous system depression and abnormal neuromuscular function.[55] Cerebral edema is a swelling of the brain that can result in dangerous intracranial pressure.[56] Intracranial hypertensions leading to a brain stem death and sepsis with multiple organ failure are the leading causes of death in individuals with fulminant hepatic failure.[57]

Incidence of Hepatitis A Infection

Hepatitis A is much more common in countries with underdeveloped sanitation systems and, thus, is a risk in most of the world.[58] An increased transmission rate is seen in all countries other than the United States, Canada, Japan, Australia, New Zealand, and the countries of Western Europe.[59] Nevertheless, infections continue to occur in the United States, where approximately one-third of the population has been previously infected with HAV.[60]

Each year, approximately 30,000 to 50,000 cases of hepatitis A occur in the United States.[61] Historically, acute hepatitis A rates have varied cyclically, with nationwide increases every 10 to 15 years.[62] The national rate of HAV infections has declined steadily since the last peak in 1995.[63] Although the national incidence—1.0 case per 100,000 population—of hepatitis A was the lowest ever recorded in 2007, it is estimated that asymptomatic infections and underreporting kept the documented incidence-rate lower than it actually is. In fact, it is estimated that there were 25,000 new infections in 2007.[64]

In 2007, the CDC reported a total of 2,979 acute symptomatic cases of HAV.[65] Of these, information about food and water exposure was known for 1,047 cases, leading to an estimate that 6.5% of all infections were caused by exposure to contaminated water or food.[66] In 2,500 of the cases, no known risk factor was identified.[67]

Estimates of the annual costs (direct and indirect) of hepatitis A in the United States have ranged from $300 million to $488.8 million in 1997 dollars.[68] Nationwide, adults who become ill miss an average of 27 workdays per illness, and 11 to 22 percent of those infected are hospitalized.[69] All of these costs are entirely preventable given the effectiveness of a vaccination in providing immunity from infection.[70]

[1]           Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” in Mandell, Douglas, & Bennett’s PRINCIPLES AND PRACTICE OF INFECTIOUS DISEASES, Fifth Edition, Chap. 161, pp. 1920-40 (2000); Mayo Clinic Staff, “Hepatitis A,” (last updated Sept 1, 2011). Articles available online at http://www.mayoclinic.com/health/hepatitis-a/DS00397.

[2]           Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[3]           Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[4]           Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[5]           CDC, “Hepatitis A,” in EPIDEMIOLOGY AND PREVENTION OF VACCINE-PREVENTABLE DISEASES (also known as “The Pink Book”), Atkinson W, Wolfe S, Hambrosky J, McIntyre L, editors, 12th edition. Chapter available online at http://www.cdc.gov/vaccines/pubs/pinkbook/hepa.html.

[6]           Id.

[7]           Id.; See also Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” Clinical Infectious Diseases, Vol. 38, 705-715 (March 1, 2004). Full text online at http://www.cdc.gov/hepatitis/PDFs/fiore_ha_transmitted_by_food.pdf.

[8]           Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[9]           Id.

[10]          Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[11]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[12]          Id.; See also Jaykus Lee Ann, “Epidemiology and Detection as Options for Control of Viral and Parasitic Foodborne Disease,” Emerging Infectious Diseases, Vol. 3, No. 4, pp. 529-39 (October-December 1997). Full text of the article is available online at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2640072/pdf/9366607.pdf

[13]          Fiore, Anthony, supra note 7; CDC, “Hepatitis A,” supra note 5; See also CDC, “Surveillance for Acute Viral Hepatitis – United States, 2007, Morbidity and Mortality Weekly Report, Surveillance Summaries, Vol. 58, No. SS03 (May 22, 2009) at http://www.cdc.gov/mmwr/preview/mmwrhtml/ss5803a1.htm.

[14]          Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7.

[15]          Id.; See also, Wheeler, C, et al., “An Outbreak of Hepatitis A Associated with Green Onions,” New England Journal of Medicine, Vol. 353, 890-97 (2005). Full text of article available at http://www.nejm.org/doi/full/10.1056/NEJMoa050855.

[16]          Hutin YJF, et al., “A Multistate, Foodborne Outbreak of Hepatitis A,” New England Journal of Medicine, Vol. 340, pp. 595-602 (1999). Full text of article is online at http://nejm.org/doi/full/10.1056/NEJM199902253400802.

[17]          Wheeler, C, et al., “An Outbreak of Hepatitis A Associated with Green Onions,” supra note 15.

[18]          Butot S, et al., “Effects of Sanitation, Freezing and Frozen Storage on Enteric Viruses in Berries and Herbs,” Intentional Journal of Food Microbiology, Vol. 126, No. 4, pp. 233-246 (2003). Full text of article is available at http://www.prograd.uff.br/virologia/sites/default/files/bulot_et_al_2008_inactivation.pdf.; Calder, L, et al., An Outbreak of Hepatitis A Associated with Consumption of Raw Blueberries,” Epidemiology and Infection, Vol. 131, No. 1 745-51 (2003) at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2870016/pdf/12948375.pdf.

[19]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[20]          CDC, “Updated recommendations from Advisory Committee on Immunization Practices (ACIP) for use of hepatitis A vaccine in close contacts of newly arriving international adoptees,” Morbidity and Mortality Weekly Report, Vol. 58, No. 36,  (Sept. 18, 2006), http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5836a4.htm; Fiore, Anthony, et al., Advisory Committee on Immunization Practices (ACIP), Prevention of Hepatitis-A Through Active or Passive Immunization: Recommendations, Morbidity & Mortality Weekly Review, Vol. 55, Report 407, (May 29, 2006) at http://www.cdc.gov/mmwr/preview/mmwrhtml/rr5507a1.htm; Todd, Ewan C.D., et al., “Outbreaks Where Food Workers Have Been Implicated in the Spread of Foodborne Disease. Part 6. Transmission and Survival of Pathogens in the Food Processing and Preparation-environment,” Journal of Food Protection, Vol. 72, 202-19 (2009). Full text of the article is available online at http://courses.washington.edu/eh451/articles/Todd_2009_food%20processing.pdf.

[21]          Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7.

[22]          Id.; See also, Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[23]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Piazza, M, et al., “Safety and Immunogenicity of Hepatitis A Vaccine in Infants: A Candidate for Inclusion in Childhood Vaccination Program,” Vol. 17, pp. 585-588 (1999). Abstract at http://www.ncbi.nlm.nih.gov/pubmed/10075165; Schiff, E.R., “Atypical Manifestations of hepatitis-A,” Vaccine, Vol. 10, Suppl. 1, pp. 18-20 (1992). Abstract at http://www.ncbi.nlm.nih.gov/pubmed/1475999.

[24]          Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7

[25]          Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[26]          CDC, “Hepatitis A,” supra note 5; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1

[27]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1

[28]          Id.

[29]          Id.; See also Sagliocca, Luciano, et al., “Efficacy of Hepatitis A Vaccine in Prevention of Secondary Hepatitis A Infection: A Randomized Trial,” Lancet, Vol. 353, 1136-39 (1999). Abstract at http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(98)08139-2/abstract.

[30]          CDC, “Hepatitis A,” supra note 5.

[31]          Id.; See also Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7.

[32]          CDC, “Hepatitis A,” supra note 5; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[33]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[34]          Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[35]          CDC, “Hepatitis A,” supra note 5; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[36]          Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[37]          Fiore, Anthony, et al., Advisory Committee on Immunization Practices (ACIP), Prevention of Hepatitis-A Through Active or Passive Immunization: Recommendations,” supra note 20; Gilkson Miryam, et al., “Relapsing Hepatitis A. Review of 14 cases and literature survey,” Medicine, Vol. 71, No. 1, 14-23 (Jan. 1992). Abstract of article online at http://www.ncbi.nlm.nih.gov/pubmed/1312659.

[38]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[39]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[40]          CDC, “Hepatitis A,” supra note 5; Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[41]          Gilkson Miryam, et al., “Relapsing Hepatitis A. Review of 14 cases and literature survey,” supra note 37.

[42]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Gilkson Miryam, et al., “Relapsing Hepatitis A. Review of 14 cases and literature survey,” supra note 37.

[43]          Mayo Clinic Staff, “Hepatitis A,” supra note 1.

[44]          CDC Summary, “Disease Burden from Viral Hepatitis A, B and C in the United States, 2004-2009, at http://www.cdc.gov/hepatitis/pdfs/disease_burden.pdf; CDC, “Hepatitis A,” supra note 5.

[45]          Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” World Journal of Gastroenterology, Vol. 12, No. 46 pp. 7405-7412 (Dec. 14, 2006). Full article is available online at http://www.wjgnet.com/1007-9327/12/7405.pdf.

[46]          Taylor, Ryan, et al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” Hepatology, Vol. 44, 1589-1597. Full text http://deepblue.lib.umich.edu/bitstream/2027.42/55879/1/21349_ftp.pdf.

[47]          Id.; See also Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[48]          Taylor, Ryan, et. al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” supra note 46.

[49]          Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[50]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Schiff, E.R., “Atypical Manifestations of hepatitis-A,” supra note 23.

[51]          Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45.

[52]          Id.; See also Taylor, Ryan, et. al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” supra note 46.

[53]          Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45; Taylor, Ryan, et. al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” supra note 46.

[54]          Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45.

[55]          Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45; Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1.

[56]          Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45.

[57]          Detry, Oliver, et al., “Brain Edema and Intracranial Hypertension in Fulminant Hepatic Failure: Pathophysiology and Management,” supra note 45; Taylor, Ryan, et. al., “Fulminant Hepatitis A Virus Infection in the United States: Incidence, Prognosis, and Outcomes,” supra note 46.

[58]          Feinstone, Stephen and Gust, Ian, “Hepatitis A Virus,” supra note 1; Jaykus Lee Ann, “Epidemiology and Detection as Options for Control of Viral and Parasitic Foodborne Disease,” supra note 12.

[59]          CDC, “Update: Prevention of Hepatitis A after Exposure to Hepatitis A Virus and in International Travelers, Updated ACIP Recommendations,” Morbidity and Mortality Weekly Report, Vol. 56, No. 41, pp. 1080-84 (Oct. 19, 2007), online at http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5641a3.htm.

[60]          CDC, “Surveillance for Acute Viral Hepatitis – United States 2007,” supra note 13; Fiore, Anthony, Division of Viral Hepatitis, CDC, “Hepatitis A Transmitted by Food,” supra note 7.

[61]          CDC, Summary, “Disease Burden from Viral Hepatitis A, B, and C in the United States,” supra note 44; CDC, “Hepatitis A,” supra note 5.

[62]          Hutin YJF, et al., “A Multistate, Foodborne Outbreak of Hepatitis A,” supra note 16.

[63]          CDC, Summary, “Disease Burden from Viral Hepatitis A, B, and C in the United States,” supra note 44; CDC, “Surveillance for Acute Viral Hepatitis – United States 2007,” supra note 13.

[64]          CDC, “Surveillance for Acute Viral Hepatitis – United States 2007,” supra note 13; Schiff, E.R., “Atypical Manifestations of hepatitis-A,” supra note 23.

[65]          CDC, “Surveillance for Acute Viral Hepatitis – United States 2007,” supra note 13.

[66]          Id.

[67]          Id.

[68]          CDC, Summary, “Disease Burden from Viral Hepatitis A, B, and C in the United States,” supra note 44.

[69]          CDC, “Surveillance for Acute Viral Hepatitis – United States 2007,” supra note 13; CDC, “Hepatitis A,” supra note 5.

[70]          CDC, “Hepatitis A,” supra note 5; Fiore, Anthony, et al., Advisory Committee on Immunization Practices (ACIP), Prevention of Hepatitis-A Through Active or Passive Immunization: Recommendations,” supra note 20.

hepatitisa1Oakland County Jail officials are warning inmates incarcerated there earlier this month that they may have been exposed to hepatitis A.

A male prisoner in the jail tested positive for the virus, an infection of the liver which can lead to liver failure in people with a weak immune system. It’s caused by a virus expelled in feces and most often spread person to person by contaminated hands.

The sheriff’s office is advising anyone detained in the jail between May 8-23 to contact the county health division to determine potential exposure.

Bouchard said jail officials already have sanitized the areas where the inmate was housed and begun contacting anyone who might have come in contact with him.

Hepatitis A symptoms may appear from two to six weeks after exposure and include sudden abdominal pain, fever, fatigue, diarrhea, nausea, headache, dark urine, light-colored bowel movements and vomiting.

“Hepatitis A is contagious, but can be prevented with vaccination if given within 14 days of last exposure,” said Leigh-Anne Stafford, a county health officer.

Forty-two hepatitis A cases have been reported in the San Diego region since November 2016, more than four times the monthly average typically reported, the County Health and Human Services Agency announced today.

Thirty-six people were hospitalized and two died from the disease.  Twenty-three cases are men, and the cases range in age from 26 to 72 years, with an average age of 42 years.  Twenty-nine cases have a history of substance abuse, and 27 are homeless.  Five people became ill with hepatitis A after traveling outside the United States.  No common sources of infection have been identified, and investigations are still continuing.

“The County is working closely with the local health community to increase outreach to vulnerable populations to raise awareness and promote hepatitis A vaccination,” said Wilma Wooten, M.D., M.P.H., County public health officer.  “Those at risk are urged to talk to their health care providers and get vaccinated for hepatitis A.”

Hepatitis A is a vaccine-preventable disease. While the hepatitis A vaccine is recommended as part of the routine childhood vaccination schedule, most adults have not been vaccinated and may be susceptible to the hepatitis A virus.

Two doses of hepatitis A vaccine are recommended for:

  • All children (first dose of vaccine between 12 months and 23 months of age, and the second dose six to 18 months later)
  • Travelers to countries that have higher rates of hepatitis A (high-risk areas include parts of Africa and Asia, and moderate risk areas include Central and South America, Eastern Europe, and parts of Asia)
  • Men who have sex with men
  • Users of injection and non-injection illegal drugs
  • Homeless people who are living outdoors
  • Household or sexual contacts of hepatitis A patients
  • People with chronic liver diseases, such as cirrhosis, hepatitis B or hepatitis C
  • Family members or caregivers of a recent adoptee from countries where hepatitis A is common
  • People who are treated with clotting-factor concentrates

Symptoms of hepatitis A include jaundice (yellowing of the skin and eyes), fever, fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, and light-colored stools.  Symptoms usually appear over a number of days and last less than two months.  However, some people can be ill for as long as six months. Hepatitis A can sometimes cause liver failure and death.

At least 71 people in Europe have been sickened with Hepatitis A in an outbreak believed to be linked to frozen berries served in smoothies, according to the latest report from Eurosurveillance. That’s an increase of 15 cases since Food Safety News first reportedon the outbreak April 17.

There are at least 35 people sickened in Denmark, and another 36 sickened between Finland, Norway and Sweden. Swedish authorities say the country is experiencing ten times the normal number of Hepatitis A cases so far this year.

Most case patients reported consuming berries or smoothies around the time of exposure, but investigators have not identified a specific brand or berry origin.

This is the first foodborne Hepatitis A outbreak of nordic origin, Eurosurveillance said.

Due to Hepatitis A’s incubation range of 15 to 50 days, and the delay involved in reporting the disease, authorities expect more illnesses to surface in the coming weeks.

sushiThe Hawaii State Department of Health has ordered all Oahu and Kauai Genki Sushi Restaurants to close for business immediately.  The Department of Health has determined the Hepatitis A outbreak on Oahu is likely due to imported frozen scallops served raw at Genki Sushi Restaurants on Oahu and Kauai. The restaurants have been closed tonight to prevent any further illness and protect the public.

As of Wednesday, the Hawaii Department of Health (HDOH) has identified 33 new cases of Hepatitis A, bringing the total to 168.

All cases have been adults with 46 requiring hospitalization.

Findings of the investigation suggest that the source of the outbreak is focused on Oahu.

Eight individuals now live on the islands of Hawaii, Kauai, and Maui, and one visitor has returned to the mainland.

Onset of illness has ranged between June 12th to August 1st.

The Health Department is eying poke as one of dozens of possible culprits, but health officials stressed the investigation remains preliminary.

AP reports that the state Department of Health is investigating an outbreak of hepatitis A on Oahu.

The department said Friday there are at least 12 cases of hepatitis A infection in adults. Six of them have required hospitalization.

Onsets of the illnesses range from June 16 through June 27.

Health officials say the virus can be spread by eating contaminated food, drinking contaminated water, close personal contact or sex. Symptoms include fever, fatigue, appetite loss, abdominal discomfort and diarrhea.

Health Director Dr. Virginia Pressler says it’s a vaccine-preventable disease. She says that while it’s a routine childhood vaccination, many adults haven’t been vaccinated and remain susceptible.

The vaccine is readily available at local pharmacies.

4KWSlaRThe hepatitis A virus can trigger acute liver inflammation which generally has a mild course in small children but which can become dangerous in adults. The virus, which is found worldwide, has previously been considered to be a purely human pathogen, which at most is found in isolated cases in non-human primates. An international team of researchers under the direction of the University of Bonn has now discovered in a large-scale study with nearly 16,000 specimens from small mammals from various continents that the hepatitis A virus – like HIV or Ebola as well – is of likely animal origin. The results currently appear in the renowned journal Proceedings of the National Academy of Sciences of the United States of America (PNAS).

An infection with the hepatitis A virus can trigger acute inflammation of the liver, which generally does not cause any symptoms in children and resolves without major complications. “In tropical regions, nearly all young children are infected with the hepatitis A virus and from that time on, they are immune to this disease,” says Prof. Dr. Jan Felix Drexler from the Institute of Virology at the University of Bonn Medical Centre and the German Centre for Infection Research (DZIF). By contrast, if adults become infected with the hepatitis A virus, the symptoms can be more serious, and the disease can even have a fatal outcome. The virus has been found to date only in humans and a few non-human primates. Its origins were mysterious.

Virologists from the University of Bonn Hospital, together with their colleagues from several German and international research institutes worldwide, searched for viruses related to the hepatitis A virus. They investigated a total of 15,987 specimens from 209 different species of small mammals: from rodents to shrews and bats to hedgehogs. Viruses from these mammals are very similar to the human hepatitis A virus with regard to their genetic properties, protein structures, immune response and patterns of infection. “The seemingly purely human virus is thus most likely of animal origin,” says Drexler. “The study enables new perspectives for risk assessments of emerging viruses by investigating functional, ecologic and pathogenic patterns instead of phylogeny only”.

The scientists’ evolutionary investigations may even hint at distant ancestry of the hepatitis A virus in primordial insect viruses. “It is possible that insect viruses infected insect-eating small mammals millions of years ago and that these viruses then developed into the precursors of the hepatitis A virus,” says the virologist from the University of Bonn Medical Centre.

The researcher assumes that small mammals were important hosts for the preservation and evolution of the viruses. “Otherwise the hepatitis A virus would actually have gone extinct long ago in small human populations due to the lifelong immunity of the persons once infected with it,” Drexler reasons. “However, patients need not fear that they could contract a hepatitis A virus infection through bats or hedgehogs. It has likely been a very long time since humans first contracted the hepatitis A precursor virus from animals – moreover, such incidents are very rare,” says the virologist from the University of Bonn Medical Centre.