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ScienceDirect www.sciencedirect.com Médecine et maladies infectieuses 45 (2015) 301–302
Case report
Hepatitis E in French Polynesia Hépatite virale E en Polynésie fran¸caise A. Le Guern a , S. Eftekhari-Hassanlouie a , S. Lastere b , E. Beaugendre c , E. Oehler a,∗ a
Department of internal medicine, French Polynesia hospital center, 98716 Pirae, Tahiti, French Polynesia b Clinical laboratory, French Polynesia hospital center, 98716 Pirae, Tahiti, French Polynesia c Department of gastroenterology, French Polynesia hospital center, 98716 Pirae, Tahiti, French Polynesia Received 26 February 2015; received in revised form 29 April 2015; accepted 18 May 2015 Available online 15 June 2015
Keywords: Viral hepatitis E; French Polynesia Mots clés : Hépatite virale E ; Polynésie franc¸aise
1. Introduction The hepatitis E virus (HEV) is the main cause of enterically transmitted viral hepatitis worldwide, for both sporadic cases and epidemics in developing countries. HEV was suspected to be present in French Polynesia; this had not been proved so far. We present the first case of acute autochthonous hepatitis E observed in French Polynesia. 2. Observation A 45-year-old male patient with no prior medical history was admitted to the French Polynesia Hospital center in the department of internal medicine for a 4-day history of flu-like illness associated with abdominal pain. He complained of asthenia, spasmodic abdominal pain, and nausea. The physical examination revealed fever and icterus, with an unremarkable abdominal examination. He did not report any alcohol or drug consumption, or blood transfusion. He had never traveled outside French Polynesia and was not vaccinated against hepatitis B. The laboratory findings revealed a marked hepatic cytolysis with hypertransaminasemia predominant on alanine aminotransferase (ALAT, 45-fold increase), aspartate aminotransferase (ASAT, 30-fold increase), and a cholestatic syndrome with gamma-glutamyl transferase (GGT, 20-fold increase) with an increase in conjugated bilirubin (37 mg/L, N < 3). The abdominal ultrasound ∗
Corresponding author. E-mail address: [email protected] (E. Oehler).
http://dx.doi.org/10.1016/j.medmal.2015.05.005 0399-077X/© 2015 Elsevier Masson SAS. All rights reserved.
was normal. The tests for serologic markers of acute hepatitis A (IgM), hepatitis B (HBs antigen, anti-HBc IgM and IgG, and anti-HBs antibodies), and hepatitis C (anti-HCV) were negative, as well as for leptospirosis (plasmatic polymerase chain reaction [PCR]), and dengue (PCR and serological tests [IgM and IgG]). The serological tests for cytomegalovirus, EpsteinBarr virus, and herpes zoster virus proved previous infections (positive IgG and negative IgM). Wilson’s disease, hemochromatosis, alpha 1-antitrypsin deficiency, and liver autoimmune diseases were ruled out by negativity of appropriate biological tests. HEV specific IgM were detected in serum samples collected 7 days after the beginning of symptoms, and there was an increase in the IgM levels on day 10 (WANTAI HEV-IgM Rapid Test [Eurobio, France]). The plasmatic HEV RNA was amplified by RT-PCR and the genotypic analysis of the amplified fragment of nucleotides yielded a genotype 3f HEV. The patient’s global condition improved within a month, with normalization of biochemical liver tests, except for GGT that were still increased by 4-fold. A retrospective anamnesis on his habits (recent travel, leisure, occupation, and diet) did not reveal any evident risk factors for HEV infection. 3. Discussion HEV is a single-strand positive-sense RNA non-enveloped virus, currently classified as a Hepeviridae. Human-infecting HEV was classified in 4 major genotypes. HEV1 and 2 have been isolated worldwide, causing human epidemic outbreaks transmitted via the fecal-oral route in developing countries (Asia,
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A. Le Guern et al. / Médecine et maladies infectieuses 45 (2015) 301–302
South America, Africa, and Mexico) [1,2]. Genotypes 3 and 4 have been described in several animal reservoirs, particularly domestic and wild pigs, in both developing and industrialized countries [3]; they have been isolated from sporadic cases of acute human HEV infection due to zoonotic and/or foodborne transmission. Genotype 4 has been reported in East Asia and Central Europe [4]. Genotype 3 is distributed worldwide, including in other South-Pacific islands since it was first described in swine, in New Caledonia [5]. It was suspected to be present in French Polynesia also, since HEV IgG were sometimes but rarely identified in blood samples of patients presenting with hepatic cytolysis. Drinking water contaminated by feces, consumption of fruit/vegetables washed with contaminated water, and consumption of raw/undercooked meat of HEV-infected domestic (pigs, rabbits) or wild (deers, boars) animals are the main causes of infection in regions with poor sanitation practices. Shellfish consumption has also been suggested as a potential source of HEV infection, since several HEV strains were detected in mussels sold in various European countries [6,7]. Giant clams, which are consumed in French Polynesia, might have been the source of contamination for our patient since no other risk factor was identified. Direct contacts with infected animals have also been reported, in cases concerning farmers, veterinarians, and farmhands [8]. HEV causes a specific acute hepatitis that is indistinguishable from other acute viral hepatitis presentations. Acute hepatitis is usually a self-limiting illness lasting less than 6 to 7 weeks, with jaundice lasting for 2 to 4 weeks, asthenia, fever, nausea/vomiting, and joint and abdominal pain [9]. Chronic cases of hepatitis have also been reported recently, but only with genotype 3 HEV. 4. Conclusion HEV was suspected to be present in French Polynesia, since HEV IgG were sometimes and rarely found in the blood samples of patients presenting with hepatic cytolysis but negative for other viral infections; nevertheless its presence had never been proved until recently. Our first case of autochthonous acute hepatitis E confirms this hypothesis and should prompt us to study the incidence of HEV in French Polynesia, in human and in animal reservoirs.
Contribution of authors A.L.G., S.L., and E.O. participated in writing the article. A.L.G., S.E.-H., E.B., and E.O. managed the patient. S.L. helped with the virological management. All the authors proofread and approved the article. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article. Acknowledgment The authors would like to thank Dr. Florence Abravanel for the genotyping performed at the Toulouse Hepatitis E National Reference Center. References [1] Pérez-Gracia MT, Mateos Lindemann ML, Montalvo Villalba MC. Hepatitis E: current status. Rev Med Virol 2013;23(6):384–98. [2] Khuroo MS. Discovery of hepatitis E: the epidemic non-A, non-B hepatitis 30 years down the memory lane. Virus Res 2011;161(1):3–14. [3] Okamoto H. Genetic variability and evolution of hepatitis E virus. Virus Res 2007;127(2):216–28. [4] Mirazo S, Ramos N, Mainardi V, Gerona S, Arbiza J. Transmission, diagnosis, and management of hepatitis E: an update. Hepat Med 2014;3(6): 45–59. [5] Kaba M, Davoust B, Cabre O, Colson P. Hepatitis E virus genotype 3f in pigs in New Caledonia. Aust Vet J 2011;89(12):496–9. [6] Crossan C, Baker PJ, Craft J, Takeuchi Y, Dalton HR, Scobie L. Hepatitis E virus genotype 3 in shellfish, United Kingdom. Emerg Infect Dis 2012;18(12):2085–7. [7] Diez-Valcarce M, Kokkinos P, Söderberg K, Bouwknegt M, Willems K, de Roda-Husman AM, et al. Occurrence of human enteric viruses in commercial mussels at retail level in three European countries. Food Environ Virol 2012;4(2):73–80. [8] Renou C, Cadranel JF, Bourlière M, Halfon P, Ouzan D, Rifflet H, et al. Possible zoonotic transmission of hepatitis E from pet pig to its owner. Emerg Infect Dis 2007;13(7):1094–6. [9] Aggarwal R. Hepatitis E: clinical presentation in disease-endemic areas and diagnosis. Semin Liver Dis 2013;33(1):30–40.
ScienceDirect www.sciencedirect.com Médecine et maladies infectieuses 45 (2015) 301–302
Case report
Hepatitis E in French Polynesia Hépatite virale E en Polynésie fran¸caise A. Le Guern a , S. Eftekhari-Hassanlouie a , S. Lastere b , E. Beaugendre c , E. Oehler a,∗ a
Department of internal medicine, French Polynesia hospital center, 98716 Pirae, Tahiti, French Polynesia b Clinical laboratory, French Polynesia hospital center, 98716 Pirae, Tahiti, French Polynesia c Department of gastroenterology, French Polynesia hospital center, 98716 Pirae, Tahiti, French Polynesia Received 26 February 2015; received in revised form 29 April 2015; accepted 18 May 2015 Available online 15 June 2015
Keywords: Viral hepatitis E; French Polynesia Mots clés : Hépatite virale E ; Polynésie franc¸aise
1. Introduction The hepatitis E virus (HEV) is the main cause of enterically transmitted viral hepatitis worldwide, for both sporadic cases and epidemics in developing countries. HEV was suspected to be present in French Polynesia; this had not been proved so far. We present the first case of acute autochthonous hepatitis E observed in French Polynesia. 2. Observation A 45-year-old male patient with no prior medical history was admitted to the French Polynesia Hospital center in the department of internal medicine for a 4-day history of flu-like illness associated with abdominal pain. He complained of asthenia, spasmodic abdominal pain, and nausea. The physical examination revealed fever and icterus, with an unremarkable abdominal examination. He did not report any alcohol or drug consumption, or blood transfusion. He had never traveled outside French Polynesia and was not vaccinated against hepatitis B. The laboratory findings revealed a marked hepatic cytolysis with hypertransaminasemia predominant on alanine aminotransferase (ALAT, 45-fold increase), aspartate aminotransferase (ASAT, 30-fold increase), and a cholestatic syndrome with gamma-glutamyl transferase (GGT, 20-fold increase) with an increase in conjugated bilirubin (37 mg/L, N < 3). The abdominal ultrasound ∗
Corresponding author. E-mail address: [email protected] (E. Oehler).
http://dx.doi.org/10.1016/j.medmal.2015.05.005 0399-077X/© 2015 Elsevier Masson SAS. All rights reserved.
was normal. The tests for serologic markers of acute hepatitis A (IgM), hepatitis B (HBs antigen, anti-HBc IgM and IgG, and anti-HBs antibodies), and hepatitis C (anti-HCV) were negative, as well as for leptospirosis (plasmatic polymerase chain reaction [PCR]), and dengue (PCR and serological tests [IgM and IgG]). The serological tests for cytomegalovirus, EpsteinBarr virus, and herpes zoster virus proved previous infections (positive IgG and negative IgM). Wilson’s disease, hemochromatosis, alpha 1-antitrypsin deficiency, and liver autoimmune diseases were ruled out by negativity of appropriate biological tests. HEV specific IgM were detected in serum samples collected 7 days after the beginning of symptoms, and there was an increase in the IgM levels on day 10 (WANTAI HEV-IgM Rapid Test [Eurobio, France]). The plasmatic HEV RNA was amplified by RT-PCR and the genotypic analysis of the amplified fragment of nucleotides yielded a genotype 3f HEV. The patient’s global condition improved within a month, with normalization of biochemical liver tests, except for GGT that were still increased by 4-fold. A retrospective anamnesis on his habits (recent travel, leisure, occupation, and diet) did not reveal any evident risk factors for HEV infection. 3. Discussion HEV is a single-strand positive-sense RNA non-enveloped virus, currently classified as a Hepeviridae. Human-infecting HEV was classified in 4 major genotypes. HEV1 and 2 have been isolated worldwide, causing human epidemic outbreaks transmitted via the fecal-oral route in developing countries (Asia,
302
A. Le Guern et al. / Médecine et maladies infectieuses 45 (2015) 301–302
South America, Africa, and Mexico) [1,2]. Genotypes 3 and 4 have been described in several animal reservoirs, particularly domestic and wild pigs, in both developing and industrialized countries [3]; they have been isolated from sporadic cases of acute human HEV infection due to zoonotic and/or foodborne transmission. Genotype 4 has been reported in East Asia and Central Europe [4]. Genotype 3 is distributed worldwide, including in other South-Pacific islands since it was first described in swine, in New Caledonia [5]. It was suspected to be present in French Polynesia also, since HEV IgG were sometimes but rarely identified in blood samples of patients presenting with hepatic cytolysis. Drinking water contaminated by feces, consumption of fruit/vegetables washed with contaminated water, and consumption of raw/undercooked meat of HEV-infected domestic (pigs, rabbits) or wild (deers, boars) animals are the main causes of infection in regions with poor sanitation practices. Shellfish consumption has also been suggested as a potential source of HEV infection, since several HEV strains were detected in mussels sold in various European countries [6,7]. Giant clams, which are consumed in French Polynesia, might have been the source of contamination for our patient since no other risk factor was identified. Direct contacts with infected animals have also been reported, in cases concerning farmers, veterinarians, and farmhands [8]. HEV causes a specific acute hepatitis that is indistinguishable from other acute viral hepatitis presentations. Acute hepatitis is usually a self-limiting illness lasting less than 6 to 7 weeks, with jaundice lasting for 2 to 4 weeks, asthenia, fever, nausea/vomiting, and joint and abdominal pain [9]. Chronic cases of hepatitis have also been reported recently, but only with genotype 3 HEV. 4. Conclusion HEV was suspected to be present in French Polynesia, since HEV IgG were sometimes and rarely found in the blood samples of patients presenting with hepatic cytolysis but negative for other viral infections; nevertheless its presence had never been proved until recently. Our first case of autochthonous acute hepatitis E confirms this hypothesis and should prompt us to study the incidence of HEV in French Polynesia, in human and in animal reservoirs.
Contribution of authors A.L.G., S.L., and E.O. participated in writing the article. A.L.G., S.E.-H., E.B., and E.O. managed the patient. S.L. helped with the virological management. All the authors proofread and approved the article. Disclosure of interest The authors declare that they have no conflicts of interest concerning this article. Acknowledgment The authors would like to thank Dr. Florence Abravanel for the genotyping performed at the Toulouse Hepatitis E National Reference Center. References [1] Pérez-Gracia MT, Mateos Lindemann ML, Montalvo Villalba MC. Hepatitis E: current status. Rev Med Virol 2013;23(6):384–98. [2] Khuroo MS. Discovery of hepatitis E: the epidemic non-A, non-B hepatitis 30 years down the memory lane. Virus Res 2011;161(1):3–14. [3] Okamoto H. Genetic variability and evolution of hepatitis E virus. Virus Res 2007;127(2):216–28. [4] Mirazo S, Ramos N, Mainardi V, Gerona S, Arbiza J. Transmission, diagnosis, and management of hepatitis E: an update. Hepat Med 2014;3(6): 45–59. [5] Kaba M, Davoust B, Cabre O, Colson P. Hepatitis E virus genotype 3f in pigs in New Caledonia. Aust Vet J 2011;89(12):496–9. [6] Crossan C, Baker PJ, Craft J, Takeuchi Y, Dalton HR, Scobie L. Hepatitis E virus genotype 3 in shellfish, United Kingdom. Emerg Infect Dis 2012;18(12):2085–7. [7] Diez-Valcarce M, Kokkinos P, Söderberg K, Bouwknegt M, Willems K, de Roda-Husman AM, et al. Occurrence of human enteric viruses in commercial mussels at retail level in three European countries. Food Environ Virol 2012;4(2):73–80. [8] Renou C, Cadranel JF, Bourlière M, Halfon P, Ouzan D, Rifflet H, et al. Possible zoonotic transmission of hepatitis E from pet pig to its owner. Emerg Infect Dis 2007;13(7):1094–6. [9] Aggarwal R. Hepatitis E: clinical presentation in disease-endemic areas and diagnosis. Semin Liver Dis 2013;33(1):30–40.
