7

Hepatitis A Vaccine

INTRODUCTION

Hepatitis A virus (HAV) is a 27-nm spherical RNA virus that replicates in the liver of the infected individual (Fiore et al., 2008). HAV incubates for an average of 28 days, but this period can range from 15 to 50 days (CDC, 2006; Fiore et al., 2008). Prior to the onset of typical hepatitis symptoms such as darkening urine, pale stools, and jaundice, individuals may experience less specific symptoms including abdominal pain, anorexia, fatigue, fever, malaise, myalgia, nausea, or vomiting (Lemon, 1985; Tong et al., 1995). The illness lasts several weeks before the virus is eliminated from the body; recovery is virtually 100 percent (Fiore et al., 2008; Tong et al., 1995).

The severity of illness with HAV infection is directly correlated to the age of the individual at the time of infection. Fifty to 90 percent of infections in persons less than 5 years of age are asymptomatic, while 70–95 percent of adults experience some symptoms (Fiore et al., 2008). Although 11–22 percent of cases require hospitalization (CDC, 2006), serious or permanent complications from HAV infection are rare (Fiore et al., 2008). Atypical manifestations, which may occur in 7–11 percent of patients, include relapse, a prolonged cholestatic phase that occurs with itching and jaundice, and rash (Fiore et al., 2008; Tong et al., 1995). Itching and arthralgia are not uncommon during the prodromal phase before jaundice appears (Tong et al., 1995). A very rare occurrence is type I autoimmune chronic hepatitis (Tong et al., 1995). It is not known whether this is caused by hepatitis A infection, or whether the infection triggers a condition al-



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7 Hepatitis A Vaccine INTRODUCTION Hepatitis A virus (HAV) is a 27-nm spherical RNA virus that replicates in the liver of the infected individual (Fiore et al., 2008). HAV incubates for an average of 28 days, but this period can range from 15 to 50 days (CDC, 2006; Fiore et al., 2008). Prior to the onset of typical hepatitis symptoms such as darkening urine, pale stools, and jaundice, individuals may experience less specific symptoms including abdominal pain, anorexia, fatigue, fever, malaise, myalgia, nausea, or vomiting (Lemon, 1985; Tong et al., 1995). The illness lasts several weeks before the virus is eliminated from the body; recovery is virtually 100 percent (Fiore et al., 2008; Tong et al., 1995). The severity of illness with HAV infection is directly correlated to the age of the individual at the time of infection. Fifty to 90 percent of infec- tions in persons less than 5 years of age are asymptomatic, while 70–95 percent of adults experience some symptoms (Fiore et al., 2008). Although 11–22 percent of cases require hospitalization (CDC, 2006), serious or permanent complications from HAV infection are rare (Fiore et al., 2008). Atypical manifestations, which may occur in 7–11 percent of patients, include relapse, a prolonged cholestatic phase that occurs with itching and jaundice, and rash (Fiore et al., 2008; Tong et al., 1995). Itching and arthralgia are not uncommon during the prodromal phase before jaundice appears (Tong et al., 1995). A very rare occurrence is type I autoimmune chronic hepatitis (Tong et al., 1995). It is not known whether this is caused by hepatitis A infection, or whether the infection triggers a condition al- 421

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422 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY ready present (Tong et al., 1995). This condition resolves with prednisone treatment (Tong et al., 1995). Very rarely fulminant hepatitis associated with coma and occasionally death may occur (Wasley et al., 2010). In most cases of hepatitis A infection, all symptoms and the infection resolve completely (Gordon et al., 1984; Tong et al., 1995). The fecal-oral route is the most common mode of transmission for hepatitis A. An individual with HAV is most infectious, with highest stool HAV concentrations, during the 2 weeks prior to appearance of jaundice (Fiore et al., 2008). Transmission from a person with active infection may occur through food preparation, household contact, and sexual contact (Fiore et al., 2008). Because children with HAV are frequently asymptom- atic, they may serve as reservoirs of disease in households and close-contact environments such as day care (Smith et al., 1997; Staes et al., 2000). HAV has been transmitted through blood transfusion; however, screening has greatly reduced this risk (Soucie et al., 1998). Finally, HAV is resistant to most organic solvents, detergents, and heat, and can survive in the environ- ment (Fiore et al., 2008; Murphy et al., 1993; Peterson et al., 1983). As a result, HAV can be transmitted by food and water contamination, as well as through contact with infected soil and marine sediment (Fiore et al., 2008). Food and waterborne hepatitis is generally associated with contamination by HAV-infected workers, sewage contamination, and inadequate water treatment (Bergeisen et al., 1985; Bloch et al., 1990; Dalton et al., 1996; De Serres et al., 1999; Fiore, 2004). From 1980 through 1995, reports of hepatitis A to the Centers for Disease Control and Prevention (CDC) numbered between 22 and 36 thou- sand cases per year (CDC, 2006). Approximately 33 percent of reported cases were in children less than 15 years old (CDC, 2008), and outbreaks of hepatitis A were reported among injection and noninjection drug users and men who have sex with men (Cotter et al., 2003; Harkess et al., 1989; Hutin et al., 1999; Schade and Komorwska, 1988). Prior to the development and licensure of a vaccine, immune globulin, a sterile solution of antibodies collected and purified from a large group of donors, was used to prevent hepatitis A in those likely to be exposed or recently exposed to the virus (Fiore et al., 2008). In 1995–1996, in- activated vaccines for hepatitis A became available, and since 1999 the CDC has reported a significant decrease in HAV infection in the United States—markedly a 76 percent decrease in 2003 when compared to 1990– 1997 (Wasley et al., 2005). Currently, three inactivated vaccines—Havrix (GlaxoSmithKline Biologicals), VAQTA (Merck & Co., Inc.), and Twinrix (GlaxoSmithKline)—are available in the United States. In these vaccines, the virus is grown in MRC-5 cell cultures and harvested by cell lysis (Fiore et al., 2008). From there, the virus is inactivated and purified through vari- ous methods before being packaged with (Havrix and Twinrix) or without (VAQTA) a preservative (Fiore et al., 2008).

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423 HEPATITIS A VACCINE Havrix and VAQTA are single-antigen vaccines and are available in two formulations for individuals between 12 months and 18 years of age, and those who are 18 years of age and older (Fiore et al., 2008). The child for- mulations of both vaccines are prepared with half the concentration of the adult dose (Fiore et al., 2008). Havrix and VAQTA are given on a two-dose schedule at least 6 months apart (Fiore et al., 2008). Twinrix is approved for adults and contains antigens for HAV and hepatitis B virus (HBV). Twinrix is given on the same schedule commonly used for single-antigen HBV vac- cine and includes three doses of the vaccine given at 0, 1, and 6 months after the initial inoculation (CDC, 2006). By 2009 46.6 percent of children aged 19 to 35 months were vaccinated against HAV (CDC, 2010). ACUTE DISSEMINATED ENCEPHALOMYELITIS Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of acute disseminated encephalomyelitis (ADEM) after the administration of hepatitis A vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and ADEM. Mechanistic Evidence The committee identified two publications reporting the development of ADEM after administration of hepatitis A vaccine. The publications did not provide evidence beyond temporality, one too short based on the pos- sible mechanisms involved (Huber et al., 1999; Rogalewski et al., 2007). Rogalewski et al. (2007) reported the concomitant administration of vac- cines, making it difficult to determine which, if any, vaccine could have been the precipitating event. In addition, the patient described in Huber et al. (1999) had a concomitant Campylobacter jejuni infection. The publications did not contribute to the weight of mechanistic evidence. Weight of Mechanistic Evidence While rare, hepatitis A infection has been associated with the develop- ment of ADEM (Yiu and Kornberg, 2010). The committee considers the effects of natural infection one type of mechanistic evidence. The symptoms described in the publications referenced above are con- sistent with those leading to a diagnosis of ADEM. Autoantibodies, T cells,

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424 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY and molecular mimicry may contribute to the symptoms of ADEM; how- ever, the publications did not provide evidence linking these mechanisms to hepatitis A vaccine. The committee assesses the mechanistic evidence regarding an as- sociation between hepatitis A vaccine and ADEM as weak based on knowledge about the natural infection. Causality Conclusion Conclusion 7.1: The evidence is inadequate to accept or reject a causal relationship between hepatitis A vaccine and ADEM. TRANSVERSE MYELITIS Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of transverse myelitis after the administration of hepatitis A vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and transverse myelitis. Mechanistic Evidence The committee did not identify literature reporting clinical, diagnostic, or experimental evidence of transverse myelitis after the administration of hepatitis A vaccine. Weight of Mechanistic Evidence While rare, hepatitis A infection has been associated with the develop- ment of transverse myelitis (Wasley et al., 2010). The committee considers the effects of natural infection one type of mechanistic evidence. Autoantibodies, T cells, and molecular mimicry may contribute to the symptoms of transverse myelitis; however, the committee did not identify literature reporting evidence of these mechanisms after administration of hepatitis A vaccine. The committee assesses the mechanistic evidence regarding an as- sociation between hepatitis A vaccine and transverse myelitis as weak based on knowledge about the natural infection.

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425 HEPATITIS A VACCINE Causality Conclusion Conclusion 7.2: The evidence is inadequate to accept or reject a causal relationship between hepatitis A vaccine and transverse myelitis. MULTIPLE SCLEROSIS Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of multiple sclerosis (MS) after the administration of hepatitis A vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and MS. Mechanistic Evidence The committee identified one publication reporting symptoms of MS after administration of hepatitis A vaccine. Rogalewski et al. (2007) did not provide evidence beyond a temporal relationship between vaccination against hepatitis B, diphtheria and tetanus toxoids, poliovirus, and hepatitis A and development of symptoms. The concomitant administration of vac- cines make it difficult to determine which vaccine, if any, could have been the precipitating event. The publication did not contribute to the weight of mechanistic evidence. Weight of Mechanistic Evidence The symptoms described above are consistent with those leading to a diagnosis of MS. Autoantibodies, T cells, and molecular mimicry may con- tribute to the symptoms of MS; however, the publication did not provide evidence linking these mechanisms to hepatitis A vaccine. The committee assesses the mechanistic evidence regarding an as- sociation between hepatitis A vaccines and MS as lacking. Causality Conclusion Conclusion 7.3: The evidence is inadequate to accept or reject a causal relationship between hepatitis A vaccine and MS.

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426 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY GUILLAIN-BARRÉ SYNDROME Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of Guillain-Barré syndrome (GBS) after the administration of hepatitis A vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and GBS. Mechanistic Evidence The committee identified four publications reporting the development of GBS after the administration of hepatitis A vaccine. The publications did not provide evidence beyond temporality, some too short based on the possible mechanisms involved (Blumenthal et al., 2004; Huber et al., 1999; Pritchard et al., 2002; Uriondo San Juan et al., 2004). One publication also reported the concomitant administration of vaccines, making it difficult to determine which, if any, vaccine could have been the precipitating event (Uriondo San Juan et al., 2004). In addition, the patient described in Hu- ber et al. (1999) had a concomitant Campylobacter jejuni infection. These publications did not contribute to the weight of mechanistic evidence. Weight of Mechanistic Evidence While rare, hepatitis A infection has been associated with the develop- ment of GBS (Wasley et al., 2010). The committee considers the effects of natural infection one type of mechanistic evidence. The symptoms described in the publications referenced above are con- sistent with those leading to a diagnosis of GBS. Autoantibodies, comple- ment activation, immune complexes, T cells, and molecular mimicry may contribute to the symptoms of GBS; however, the publications did not provide evidence linking these mechanisms to hepatitis A vaccine. The committee assesses the mechanistic evidence regarding an as- sociation between hepatitis A vaccine and GBS as weak based on knowledge about the natural infection. Causality Conclusion Conclusion 7.4: The evidence is inadequate to accept or reject a causal relationship between hepatitis A vaccine and GBS.

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427 HEPATITIS A VACCINE CHRONIC INFLAMMATORY DISSEMINATED POLYNEUROPATHY Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of chronic inflammatory disseminated polyneuropathy (CIDP) after the administration of hepatitis A vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and CIDP. Mechanistic Evidence The committee did not identify literature reporting clinical, diagnostic, or experimental evidence of CIDP after the administration of hepatitis A vaccine. Weight of Mechanistic Evidence Autoantibodies, T cells, and molecular mimicry may contribute to the symptoms of CIDP; however, the committee did not identify literature reporting evidence of these mechanisms after administration of hepatitis A vaccine. The committee assesses the mechanistic evidence regarding an as- sociation between hepatitis A vaccine and CIDP as lacking. Causality Conclusion Conclusion 7.5: The evidence is inadequate to accept or reject a causal relationship between hepatitis A vaccine and CIDP. BELL’S PALSY Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of Bell’s palsy after the administration of hepatitis A vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and Bell’s palsy.

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428 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY Mechanistic Evidence The committee did not identify literature reporting clinical, diagnostic, or experimental evidence of Bell’s palsy after the administration of hepatitis A vaccine. Weight of Mechanistic Evidence The committee assesses the mechanistic evidence regarding an as- sociation between hepatitis A vaccine and Bell’s palsy as lacking. Causality Conclusion Conclusion 7.6: The evidence is inadequate to accept or reject a causal relationship between hepatitis A vaccine and Bell’s palsy. ANAPHYLAXIS Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of anaphylaxis after the administration of hepatitis A vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and anaphylaxis. Mechanistic Evidence The committee identified two publications identifying the development of anaphylaxis posthepatitis A vaccination (Bohlke et al., 2003; Peng and Jick, 2004). Bohlke et al. (2003) used records from participants in the Vaccine Safety Datalink to study the development of anaphylaxis postvac- cination. The authors did not observe a single case of anaphylaxis postvac- cination out of 23,185 doses of hepatitis A vaccine administered. Peng and Jick (2004) used computer records from general practitioners in the United Kingdom to study the incidence, cause, and severity of anaphylaxis. The authors reviewed 120 cases, out of 897, in detail. One report of anaphylaxis developing after vaccination against hepatitis A was identified.

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429 HEPATITIS A VACCINE Weight of Mechanistic Evidence The publications described above did not present evidence sufficient for the committee to conclude the vaccine may be a contributing cause of anaphylaxis after the administration of hepatitis A vaccine. A temporal relationship was established between the administration of a hepatitis A vaccine and the development of anaphylaxis in one case; however, clinical details were not presented. Also, while it was presumed the patient had experienced an IgE-mediated reaction, no data were reported to establish the mechanism of action. The committee assesses the mechanistic evidence regarding an asso- ciation between hepatitis A vaccine and anaphylaxis as weak based on one case presenting temporality consistent with anaphylaxis. Causality Conclusion Conclusion 7.7: The evidence is inadequate to accept or reject a causal relationship between hepatitis A vaccine and anaphylaxis. AUTOIMMUNE HEPATITIS Epidemiologic Evidence No studies were identified in the literature for the committee to evalu- ate the risk of autoimmune hepatitis after the administration of hepatitis A vaccine. Weight of Epidemiologic Evidence The epidemiologic evidence is insufficient or absent to assess an association between hepatitis A vaccine and autoimmune hepatitis. Mechanistic Evidence The committee identified two publications reporting the development of autoimmune hepatitis after the administration of hepatitis A vaccine. The publications did not provide evidence beyond temporality, one too short based on the possible mechanisms involved (Berry and Smith-Laing, 2007; Veerappan et al., 2005). One publication reported the concomitant administration of vaccines making it difficult to determine which, if any, vaccine could have been the precipitating event (Veerappan et al., 2005). In addition, the patient described by Berry and Smith-Laing (2007) presented

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430 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY with acute hepatitis 5 months before vaccination. The publications did not contribute to the weight of mechanistic evidence. Weight of Mechanistic Evidence Active autoimmune hepatitis is a recognized complication of infection with hepatitis A (Wasley et al., 2010). The committee considers the effects of natural infection one type of mechanistic evidence. The symptoms described in the publications referenced above are con- sistent with those leading to a diagnosis of autoimmune hepatitis. Autoanti- bodies, T cells, and complement activation may contribute to the symptoms of autoimmune hepatitis; however, the publications did not provide evi- dence linking these mechanisms to hepatitis A vaccine. The committee assesses the mechanistic evidence regarding an as- sociation between hepatitis A vaccine and autoimmune hepatitis as weak based on knowledge about the natural infection. Causality Conclusion Conclusion 7.8: The evidence is inadequate to accept or reject a causal relationship between hepatitis A vaccine and autoimmune hepatitis. CONCLUDING SECTION Table 7-1 provides a summary of the epidemiologic assessments, mech- anistic assessments, and causality conclusions for hepatitis A vaccine.

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TABLE 7-1 Summary of Epidemiologic Assessments, Mechanistic Assessments, and Causality Conclusions for Hepatitis A Vaccine Studies Cases Contributing to Contributing to Epidemiologic the Epidemiologic Mechanistic the Mechanistic Causality Vaccine Adverse Event Assessment Assessment Assessment Assessment Conclusion Hepatitis A Acute Disseminated Encephalomyelitis Insufficient None Weak None Inadequate Hepatitis A Transverse Myelitis Insufficient None Weak None Inadequate Hepatitis A Multiple Sclerosis Insufficient None Lacking None Inadequate Hepatitis A Guillain-Barré Syndrome Insufficient None Weak None Inadequate Hepatitis A Chronic Inflammatory Disseminated Insufficient None Lacking None Inadequate Polyneuropathy Hepatitis A Bell’s Palsy Insufficient None Lacking None Inadequate Hepatitis A Anaphylaxis Insufficient None Weak 1 Inadequate Hepatitis A Autoimmune Hepatitis Insufficient None Weak None Inadequate 431

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432 ADVERSE EFFECTS OF VACCINES: EVIDENCE AND CAUSALITY REFERENCES Bergeisen, G. H., M. W. Hinds, and J. W. Skaggs. 1985. A waterborn outbreak of hepatitis A in Meade County, Kentucky. American Journal of Public Health 75(2):161-168. Berry, P. A., and G. Smith-Laing. 2007. Hepatitis A vaccine associated with autoimmune hepatitis. World Journal of Gastroenterology 13(15):2238-2239. Bloch, A. B., S. L. Stramer, J. D. Smith, H. S. Margolis, H. A. Fields, T. W. McKinley, C. P. Gerba, J. E. Maynard, and R. K. Sikes. 1990. Recovery of hepatitis A virus from a water supply responsible for a common source outbreak of hepatitis A. American Journal of Public Health 80(4):428-430. Blumenthal, D., D. Prais, E. Bron-Harlev, and J. Amir. 2004. Possible association of Guillain- Barré syndrome and hepatitis A vaccination. Pediatric Infectious Disease Journal 23(6): 586-588. Bohlke, K., R. L. Davis, S. M. Marcy, M. M. Braun, F. DeStefano, S. B. Black, J. P. Mullooly, and R. S. Thompson. 2003. Risk of anaphylaxis after vaccination of children and ado- lescents. Pediatrics 112(4):815-820. CDC (Centers for Disease Control and Prevention). 2006. Prevention of hepatitis A through active or passive immunization—recommendations of the Advisory Committee on Im- munization Practices (ACIP). Morbidity & Mortality Weekly Report 55(RR7, Suppl. S):1-12, 13-23. CDC. 2008. Surveillance for acute viral hepatitis—United States, 2006. Morbidity & Mortality Weekly Report 57(SS2, Suppl. S):1-24. CDC. 2010. National, state, and local area vaccination coverage among children aged 19-35 months—United States, 2009. Morbidity & Mortality Weekly Report 59(36):1171-1177. Cotter, S. M., S. Sansom, T. Long, E. Koch, S. Kellerman, F. Smith, F. Averhoff, and B. P. Bell. 2003. Outbreak of hepatitis A among men who have sex with men: Implications for hepatitis A vaccination strategies. Journal of Infectious Diseases 187(8):1235-1240. Dalton, C. B., A. Haddix, R. E. Hoffman, and E. E. Mast. 1996. The cost of a food-borne out- break of hepatitis A in Denver, Colo. Archives of Internal Medicine 156(9):1013-1016. De Serres, G., T. L. Cromeans, B. Levesque, N. Brassard, C. Barthe, M. Dionne, H. Prud’homme, D. Paradis, C. N. Shapiro, O. V. Nainan, and H. S. Margolis. 1999. Molecular confirma- tion of hepatitis A virus from well water: Epidemiology and public health implications. Journal of Infectious Diseases 179(1):37-43. Fiore, A. E. 2004. Hepatitis A transmitted by food. Clinical Infectious Diseases 38(5):705-715. Fiore, A. E., S. M. Feinstone, and B. P. Bell. 2008. Chapter 12. Hepatitis A vaccines. In Vaccines, edited by S. A. Plotkin, W. A. Orenstein, and P. A. Offit. Philadelphia, PA: Saunders/Elsevier. Pp. 177-203. Gordon, S. C., K. R. Reddy, L. Schiff, and E. R. Schiff. 1984. Prolonged intrahepatic cholesta- sis secondary to acute hepatitis A. Annals of Internal Medicine 101(5):635-637. Harkess, J., B. Gildon, and G. R. Istre. 1989. Outbreaks of hepatitis A among illicit drug-users, Oklahoma, 1984-87. American Journal of Public Health 79(4):463-466. Huber, S., L. Kappos, P. Fuhr, S. Wetzel, and A. J. Steck. 1999. Combined acute disseminated encephalomyelitis and acute motor axonal neuropathy after vaccination for hepatitis A and infection with Campylobacter jejuni. Journal of Neurology 246(12):1204-1206. Hutin, Y. J. F., B. P. Bell, K. L. E. Marshall, C. P. Schaben, M. Dart, M. P. Quinlisk, and C. N. Shapiro. 1999. Identifying target groups for a potential vaccination program during a hepatitis A communitywide outbreak. American Journal of Public Health 89(6):918-921. Lemon, S. M. 1985. Type-A viral-hepatitis—new developments in an old disease. New England Journal of Medicine 313(17):1059-1067. Murphy, P., T. Nowak, S. M. Lemon, and J. Hilfenhaus. 1993. Inactivation of hepatitis A virus by heat-treatment in aqueous-solution. Journal of Medical Virology 41(1):61-64.

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433 HEPATITIS A VACCINE Peng, M. M., and H. Jick. 2004. A population-based study of the incidence, cause, and severity of anaphylaxis in the United Kingdom. Archives of Internal Medicine 164(3):317-319. Peterson, D. A., T. R. Hurley, J. C. Hoff, and L. G. Wolfe. 1983. Effect of chlorine treat- ment on infectivity of hepatitis A virus. Applied and Environmental Microbiology 45(1):223-227. Pritchard, J., R. Mukherjee, and R. A. C. Hughes. 2002. Risk of relapse of Guillain-Barré syndrome or chronic inflammatory demyelinating polyradiculoneuropathy following im- munisation. Journal of Neurology, Neurosurgery, and Psychiatry 73(3):348-349. Rogalewski, A., J. Kraus, M. Hasselblatt, C. Kraemer, and W. R. Schabitz. 2007. Improve- ment of advanced postvaccinal demyelinating encephalitis due to plasmapheresis. Neuro- psychiatric Disease and Treatment 3(6):987-991. Schade, C. P., and D. Komorwska. 1988. Continuing outbreak of hepatitis A linked with intravenous drug-abuse in Multnomah County. Public Health Reports 103(5):452-459. Smith, P. F., J. C. Grabau, A. Werzberger, R. A. Gunn, H. R. Rolka, S. F. Kondracki, R. J. Gallo, and D. L. Morse. 1997. The role of young children in a community-wide outbreak of hepatitis A. Epidemiology and Infection 118(3):243-252. Soucie, J. M., B. H. Robertson, B. P. Bell, K. A. McCaustland, and B. L. Evatt. 1998. Hepa- titis A virus infections associated with clotting factor concentrate in the United States. Transfusion 38(6):573-579. Staes, C. J., T. L. Schlenker, I. Risk, K. G. Cannon, H. Harris, A. T. Pavia, C. N. Shapiro, and B. P. Bell. 2000. Sources of infection among persons with acute hepatitis A and no iden- tified risk factors during a sustained community-wide outbreak. Pediatrics 106(4):e54. Tong, M. J., N. S. El-Farra, and M. I. Grew. 1995. Clinical manifestations of hepatitis A: Recent experience in a community teaching hospital. Journal of Infectious Diseases 171(Suppl. 1):S15-S18. Uriondo San Juan, B., D. Naval Valle, and F. Moreno Izco. 2004. Guillain-Barré syndrome after immunisation with hepatitis A and typhoid vaccines [in Spanish]. Atencion Primaria 34(7):379. Veerappan, G. R., B. P. Mulhall, and K. C. Holtzmuller. 2005. Vaccination-induced auto- immune hepatitis. Digestive Diseases and Sciences 50(1):212-213. Wasley, A., S. M. Feinstone, and B. P. Bell. 2010. Hepatitis A virus. In Mandell, Douglas, and Bennett’s principles and practice of infectious diseases. 7th ed. 2 vols. Vol. 2, edited by G. L. Mandell, J. E. Bennett, and R. Dolin. Philadelphia, PA: Churchill Livingstone Elsevier. Pp. 2367-2387. Wasley, A., T. Samandari, and B. P. Bell. 2005. Incidence of hepatitis A in the United States in the era of vaccination. Journal of the American Medical Association 294(2):194-201. Yiu, E. M., and A. J. Kornberg. 2010. Acute disseminated encephalomyelitis: Determinants and manifestations. In Inflammatory diseases of the central nervous system, edited by T. Kilpatrick, R. M. Ransohoff, and S. Wesselingh. New York: Cambridge University Press.

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