Case Reports in Infectious Diseases

Case Reports in Infectious Diseases / 2019 / Article

Case Report | Open Access

Volume 2019 |Article ID 9782892 |

I. Ranathunga, L. S. Kannangara, K. A. S Bandara, S. B. Gunatilake, "A Rare Presentation of Coinfection: Dengue Virus and Hepatitis A Virus", Case Reports in Infectious Diseases, vol. 2019, Article ID 9782892, 2 pages, 2019.

A Rare Presentation of Coinfection: Dengue Virus and Hepatitis A Virus

Academic Editor: Gloria Taliani
Received29 Apr 2019
Accepted25 Jun 2019
Published18 Aug 2019


Dengue fever caused by dengue virus is a common tropical infection transmitted by the mosquitos Aedes aegypti and Aedes albopictus. Four strains of the genus flavivirus is responsible for the epidemics of varying severity. Hepatitis A caused by hepatitis A virus is spread by faecal-oral route. The culprit virus is a hepatovirus. Coinfection with dengue virus and hepatitis A virus is rare and is a diagnostic as well as management challenge to the medical professional. We report a patient who presented to us with dengue virus and hepatitis A virus coinfection.

1. Introduction

Dengue fever (DF) is a common arthropod-borne tropical infection. It is caused by four serotypes of the genus flavivirus [1]. The incidence is high with up to 50 million infections occurring annually with only 5,00,000 developing dengue haemorrhagic fever (DHF) [1]. Hepatitis A caused by hepatitis A virus is transmitted by faecal-oral route, and annually 1.4 million new cases occur [1]. Coinfection with dengue virus and hepatitis A virus is rare entity and is a diagnostic as well as a management challenge to the medical professional. Coinfection with other infections such as leptospira, malaria, hepatitis E, and typhoid fever has also been documented [2].

2. Case Report

A 34-year-old previously healthy male presented with high grade fever associated with constitutional symptoms of five days’ duration. He was complaining of right hypochondrium pain and tea-coloured urine for two days associated with yellowish discolouration of the eyes. He had severe loss of appetite to food and water, but his bowel habits had been normal throughout the illness. On admission, he was afebrile with normal vital signs but was deeply icteric. His abdominal examination revealed a tender, mild hepatomegaly while his cardiovascular, respiratory, and nervous system examination was normal.

His full blood count revealed a white cell count of 3 × 103μL with a platelet count of 116 × 103μL. His aspartate aminotransferase (AST) and alanine aminotransferase (ALT) were 5162 U/L and 3964 U/L, respectively. Initial total bilirubin was found to be 61.7 μmol/L with an increased direct fraction. His prothrombin time/international normalized ratio (PT/INR) and serum protein were normal throughout the illness. His dengue IgM antibody done by chromatographic immunoassay was positive on the 6th day of the illness. Hepatitis A IgM antibody done by the ELISA technique was positive on day 6 of the illness, while hepatitis A IgG antibody was negative. Other investigations done during the hospital stay are summarized in Table 1.


White cell count (×103)33.774.864.414.13
Haematocrit (%)4848.645.643.141.5
Platelet count (×103)116108141152131
AST (U/L)51622686635
ALT (U/L)39642510250
Total bilirubin (μmol/L)61.758.555.571.425
Direct bilirubin (μmol/L)49.145.848.860.718

During the course of the illness, the patient was closely monitored for features of development of liver failure while continuing with the precritical monitoring of the dengue fever. The patient’s hospital stay was uneventful, and he did not develop features of acute liver failure or features of plasma leakage as in DHF. He was discharged on day 10 of the illness. On follow-up, his AST, ALT, and bilirubin have become normal.

3. Discussion

DF is caused by dengue virus and transmitted by vector Aedes mosquito. Hepatitis A infection is caused by hepatitis A virus and transmitted via faecal-oral route. Although both infections are common in the population occurring as isolated infections, coinfection is rare.

Coinfection of dengue virus with other infections has been documented in the past [2]. DF per se is associated with hepatic involvement which ranges from minor alterations in the aminotransferase levels to acute hepatitis [3]. DHF is associated with a greater incidence of hepatitis and fulminant hepatitis than simple dengue fever [3]. The pathogenesis of liver involvement in DF is still poorly understood. Direct viral invasion of the liver cells or products of host immune response acting on liver cells is thought to contribute to the liver cell injury [3]. The elevation of transaminases is mild to moderate in most cases of DF, and the level of AST is greater than that of ALT [3]. The levels decrease to normal levels usually within six weeks of resolution of infection [4]. However, jaundice is an uncommon finding in DF [4].

Liver biopsies performed on hepatitis A patients have revealed hepatocellular necrosis with ballooning, eosinophilic degeneration, and infiltration of mononuclear cells, accounting for the liver injury due to direct viral invasion and cellular immune response [5]. Serum AST/ALT levels both rise rapidly during the prodromal period, reach peak levels, and then decrease by approximately 75% per week. Serum bilirubin concentrations reach peak levels later and decline less rapidly than serum aminotransferases. Complete clinical recovery with restoration of normal serum bilirubin and aminotransferase values is usually achieved by 6 months [6].

Differentiating between the two infections and determining the possibility of coinfection are important in the management of an acutely ill patient with hepatitis. A patient presenting with haemoconcentration, thrombocytopenia, and plasma leakage in the presence of features of hepatitis should alert the clinician about the possibility of DF, while on the contrary, elevated bilirubin levels and deranged coagulation profile should lead towards the possibility of viral hepatitis as they are usually unchanged in DF [4].

Conflicts of Interest

The authors declare that they have no conflicts of interest.


  1. World Health Organization, Health Topics, World Health Organization, Geneva, Switzerland, 2017,
  2. S. A. Zaki and V. Lad, “Concurrent infection of dengue fever and hepatitis A infection: a case report,” Indian Journal of Critical Care Medicine, vol. 15, no. 4, pp. 238–240, 2011. View at: Publisher Site | Google Scholar
  3. S. L. Seneviratne, G. N. Malavige, and H. J. de Silva, “Pathogenesis of liver involvement during dengue viral infections,” Transactions of the Royal Society of Tropical Medicine and Hygiene, vol. 100, no. 7, pp. 608–614, 2006. View at: Publisher Site | Google Scholar
  4. S. A. M. Kularatne, I. B. Gawarammana, and P. R. V. Kumarasiri, “Epidemiology, clinical features, laboratory investigations and early diagnosis of dengue fever in adults: a descriptive study in Sri Lanka,” The Southeast Asian Journal of Tropical Medicine and Public Health, vol. 36, no. 3, pp. 686–692, 2005. View at: Google Scholar
  5. J. A. Cuthbert, “Hepatitis A: old and new,” Clinical Microbiology Reviews, vol. 14, no. 1, pp. 38–58, 2001. View at: Publisher Site | Google Scholar
  6. R. S. Koff, “Clinical manifestations and diagnosis of hepatitis A virus infection,” Vaccine, vol. 10, no. 1, pp. S15–S17, 1992. View at: Publisher Site | Google Scholar

Copyright © 2019 I. Ranathunga et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Related articles

No related content is available yet for this article.
 PDF Download Citation Citation
 Download other formatsMore
 Order printed copiesOrder

Related articles

No related content is available yet for this article.

Article of the Year Award: Outstanding research contributions of 2020, as selected by our Chief Editors. Read the winning articles.