Officials in New Zealand investigating Hepatitis A cases linked to berries have identified a connection with a past outbreak in Europe.
There are 12 hepatitis A infections from eating frozen berries in New Zealand. Eight have been linked by genetic sequencing, meaning they were likely exposed to the same source of the virus. Seven people have been hospitalized. The virus attacks the liver. The Ministry for Primary Industries (MPI) was informed by the Ministry of Health of three Hepatitis A cases in September.
Foodstuffs Own Brands has recalled various Pams brand frozen berry products because of a possible link to the hepatitis A cases. Products are being removed from New World, Pak’n Save and Four Square shops nationwide, and from Trents and Raeward Fresh stores in the South Island.
All batches and dates of Pams brand Mixed Berries 500-gram, Two Berry Mix 1-kilogram and 750-gram, Smoothie Berry Mix 500-gram, and raspberries 500-gram and 350-gram are involved.
THE HEPATITIS A VIRUS
Exposure to the 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). HAV vaccines were licensed in 1995 and 1999. These vaccines provide long-term protection against HAV infection.[6]
HAV 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, HAV does not develop into chronic hepatitis or cirrhosis, which are both potentially fatal conditions.[9] Nonetheless, infection with the HAV virus can lead to acute liver failure and death.[10]
Where does Hepatitis A Come From?
HAV 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 HAV.[15] In 1997, frozen strawberries were the source of a HAV 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?
HAV 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 HAV 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 seven to ten 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 six 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 HAV, 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 HAV 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, the incidence of fulminant hepatitis A 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 HAV 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, which 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
HAV 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 Western European countries.[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 HAV occur in the United States.[61] Historically, acute HAV 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 HAV 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, 25,000 new infections were estimated 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]
Hepatitis A outbreaks associated with fresh, frozen, and minimally processed produce, worldwide, from 1983 to 2016
| Year | # Cases | Implicated food | Location of cases | Source of implicated food | Suspected cause of contamination | Reference |
| 1983 | 24 | Raspberries (frozen) | Scotland | Scotland | Infected pickers or packers | Reid et al., 1987[68] |
| 1987 | 5 | Raspberries (frozen) | Scotland | Tayside, Scotland | Infected pickers | Ramsay and Upton, 1989[69] |
| 1988 | 202 | Iceberg lettuce | Kentucky | Unknown, suspected to be from Mexico | Believed to have occurred prior to distribution, since multiple restaurants involved | Rosenblum et al., 1990[70] |
| 1990 | 35 | Strawberries (frozen) | Montana, Georgia | California | Suspect an infected picker at farm | Sivapalasingam et al., 2004;[71]Niu et al., 1992[72] |
| 1996 | 30 | Salad ingredients | Finland | Imported salad ingredients | Unknown | Pebody et al., 1998[73] |
| 1997 | 256 | Strawberries (frozen) | Michigan, Maine, Wisconsin, Arizona, Louisiana, Tennessee | Grown in Mexico,processed and frozen at a single California facility a year before consumption | Inconclusive due to time between harvest and consumption, suspect barehanded contact with berries at harvesting, coupled with few latrines and handwashing facilities on site | Hutin et al., 1999[74] |
| 1998 | 43 | Green onions | Ohio | One of two Mexican farms or a farm in California | Believed to be contaminated before arrival at restaurant | Dentinger et al., 2001[75] |
| 2000 | 31 | Green onions or tomatoes | Kentucky, Florida | Green onions: California or MexicoTomatoes: Unknown | Unknown | Wheeler et al., 2005[76]; Datta et al., 2001[77]; Fiore, 2004[78] |
| 2002 | 81 | Blueberries | New Zealand | New Zealand, one orchard | Inadequate bathroom facilities in fields, workers had barehanded contact with product, polluted groundwater from nearby latrines a possibility | Calder et al., 2003[79] |
| 2003 | 601 | Green onions | Pennsylvania, Tennessee, Georgia, North Carolina | Mexico, two farms | Contaminated during or before packing at farm | CDC, 2003[80]; Wheeler et al., 2005[81] |
| 2009 | 562 | Tomatoes | Australia | Unknown; imported and domestic product involved | Product suspected to be imported due to concurrent outbreaks elsewhere at the time, source of contamination unknown | Donnan et al., 2012[82] |
| 2009 | 13 | Tomatoes | Netherlands | Unknown; imported product suspected | Identical strain to the 2009 Australian outbreak | Petrignani et al., 2010[83] |
| 2010 | 59 | Tomatoes | France | Likely Turkey, single batch of product | Unable to determine when and where contamination occurred. Virus was slightly different from one in the 2009 Australian and Dutch outbreaks. | Gallot et al., 2011[84] |
| 2012 | 9 | Pomegranate seeds (frozen) | Canada | Egypt | Suspect product contamination before export. Some history of travel to endemic areas among workers at Canadian processing facility, but less likely as only one product was associated with illness. | CDC 2013[85]; Swinkels et al., 2014[86] |
| 2013 | 103 | Strawberries (frozen)Other frozen berries may have been involved | Denmark, Finland, Norway, Sweden | Suspected Egypt and Morocco based on virus strain and import history | Unknown, some cases matched the strain of the larger 2013 European outbreak (see below) | Nordic Outbreak Investigation Team, 2013[87] |
| 2013 | 1589 | Berries (frozen) | Italy (90% of cases), Austria, Bulgaria, Denmark, England, Finland, France, Germany, Ireland, the Netherlands, Norway, Poland, Sweden | Multiple food items containing frozen mixed berries (cakes, smoothies); Bulgarian blackberries and Polish redcurrants were the most common ingredients in the implicated lots | Unknown, no single source found. Some cases also related to travel to Italy. | Severi et al., 2015[88]; EFSA 2014[89]; Chiapponi et al., 2014[90]; Rizzo et al., 2013[91]; Guzman-Herrador et al., 2014[92]; Fitzgerald et al., 2014[93] |
| 2013 | 165 | Pomegranate arils (frozen) | Arizona, California, Colorado, Hawaii, New Hampshire, New Jersey, New Mexico, Nevada, Utah, Wisconsin | Turkey | Unknown | Collier et al., 2014[94]; CDC 2013[95] |
| 2016 | 143 | Strawberries (frozen) | Arkansas, California, Maryland, New York, North Carolina, Oregon, Virginia, West Virginia, Wisconsin | Egypt | Unknown | CDC 2016[96] |
Estimates of the annual costs (direct and indirect) of HAV in the United States have ranged from $300 million to $488.8 million in 1997 dollars.[97] In one study conducted in Spokane, Washington, the combined direct and indirect costs for each case of HAV, from all sources, ranged from $2,892 to $3,837.[98] In a 2007 Ohio study, each case of HAV infection attributable to contaminated food was estimated to cost at least $10,000, including medical and other non-economic costs.[99] Nationwide, adults who become ill miss an average of 27 workdays per illness, and 11% to 22% of those infected are hospitalized.[100] All of these costs are entirely preventable, given the effectiveness of a vaccination in providing immunity from infection.[101]
[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] Reid, T., Robinson, H. (1987). Frozen raspberries and hepatitis A. Epidemiol Infect, 98: 109–112.
[69] Ramsay, C. N. and Upton, P. A. (1989). Hepatitis A and frozen raspberries. Lancet, 1: 43–44.
[70] Rosenblum, L. S., Mirkin, I. R., Allen, D. T., Safford, S., Hadler, S. C. (1990). A multifocal outbreak of hepatitis A traced to commercially distributed lettuce. American Journal of Public Health, 80(9): 1075-1079.
[71] Sivapalasingam, S., Friedman, C. R., Cohen, L., Taube, R. V. (2004). Fresh produce: a growing cause of outbreaks of foodborne illness in the United States, 1973 through 1997. J Food Prot, 67: 2342-2353.
[72] Niu, M. T., Polish, L. B., Robertson, B. H. (1992). Multistate outbreak of hepatitis A associated with frozen strawberries. J Infect Dis 166: 518-524.
[73] Pebody, R. G., Leino, T., Ruutu, P., Kinnunen, L., Davidkin, I., Nohynek, H., & Leinikki, P. (1998). Foodborne outbreaks of hepatitis A in a low endemic country: an emerging problem? Epidemiology and infection, 120(1): 55-59.
[74] Hutin, Y. J., Pool, V., Cramer, E. H., Nainan, O. V., Weth, J., Williams, I. T. et al. (1999). A multistate, foodborne outbreak of hepatitis A. New England Journal of Medicine, 340(8): 595-602.
[75] Dentinger, C. M., Bower, W. A., Nainan, O. V., Cotter, S. M., Myers, G., Dubusky, L. M., Fowler, S., Salehi, E. D. P., and Bell, B. P. (2001). An outbreak of hepatitis A associated with green onions. J Infect Dis, 183: 1273-1276.
[76] Wheeler, C., Vogt, T. M., Armstrong, G. L., Vaughan, G., Weltman, A., Nainan, O. V. et al. (2005). An outbreak of hepatitis A associated with green onions. New England Journal of Medicine, 353(9): 890-897.
[77] Datta, S. D., Traeger, M. S., & Nainan, O. V. (2001). Identification of a multi-state outbreak of hepatitis A associated with green onions using a novel molecular epidemiologic technique [abstract 896]. In Program and abstracts of the 39th Annual Meeting of the Infectious Diseases Society of America. Alexandra, VA: Infectious Diseases Society of America (Vol. 192).
[78] Fiore, A. E. (2004). Hepatitis A transmitted by food. Clinical Infectious Diseases, 38(5): 705-715.
[79] Calder, L. , Simmons, G., Thornley, G. (2003). An outbreak of hepatitis A associated with consumption of raw blueberries. Epidemiol Infect,131: 745-751
[80] Centers for Disease Control and Prevention (CDC). (2003). Hepatitis A outbreak associated with green onions at a restaurant–Monaca, Pennsylvania, 2003. MMWR, 52(47): 1155-1157. Available at https://www.cdc.gov/mmwr/preview/mmwrhtml/mm5247a5.htm
[81] Wheeler, C., Vogt, T. M., Armstrong, G. L., Vaughan, G., Weltman, A., Nainan, O. V. et al. (2005). An outbreak of hepatitis A associated with green onions. New England Journal of Medicine, 353(9): 890-897.
[82] Donnan, E. J., Fielding, J. E., Gregory, J. E., et al. (2012). A multistate outbreak of hepatitis A associated with semidried tomatoes in Australia, 2009. Clin Infect Dis, 54: 775–781.
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