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The first accounts of hepatitis, also referred to as epidemic jaundice, can be traced back to Hippocrates. Outbreaks of the disease were recorded in the 17th and 18th centuries, and were mostly associated with military campaigns (Wasley, Gallagher and Grytdal 3). The first epidemiological differentiation between Hepatitis A and B was in the 1940’s. Serological tests to differentiate between hepatitis B and A were developed in the 1970’s and consequently led to the identification of the causative agents (Marler). Maintenance of hygiene and passive protection was the primary preventive measure prior to the development of vaccines. Hepatitis vaccines were developed and consequently licensed in 1995 (Marler). The vaccines provide long-term protection against the causative agent, that is, the Hepatitis A virus (Wasley, Gallagher and Grytdal 4).
Hepatitis A is categorized as a picornavirus. It is a non-enveloped RNA stable virus which has the capability of surviving in the environment for several months. “The virus is stable at moderate temperatures and low pH, but can be deactivated by chemicals, such as chlorine and formalin. In addition, temperatures above 85°C can deactivate the virus” (FitzSimons, Hendrickx and Van Damme 584). Human beings are the only hosts for the virus, although primates have been successfully infected with the virus experientially (Hepatitis A 8). HAV replicates in the liver cells causing inflammation due to the destruction of hepatocytes by natural killer cells and cytotoxic cytokines. The inflammatory process is a consequence of an immune reaction (FitzSimons, Hendrickx and Van Damme 585).
The course of the disease after infection depends on age. Children can develop unapparent hepatitis A and portray no signs or symptoms. Serological or biochemical tests are the only methods to diagnose asymptomatic hepatitis A, other patients develop icteric hepatitis and show symptoms ranging from mild acute to severe chronic; the patients can either recover fully or die as a result of fulminant hepatitis (Marler). The incubation phase is the first stage and lasts from 10 to 50 days. At this stage, the patient is asymptomatic. In the second stage, known as the preicteric phase, the patient shows signs of nausea, vomiting, fatigue, loss of appetite and abdominal pain and mostly lasts from several days to weeks (Wasley, Gallagher and Grytdal 12). The third phase is the Icteric phase; at this stage the patient has massive liver necrosis and has severe abdominal pain, jaundice and hepatic encephalopathy that may result in seizures and consequently coma. Mortality is high at this stage. The last phase is the convalescent period; at this phase, the patient recovers from the disease or it may relapse in 3-20% of all patients. Patients who fully recover develop lifetime immunity. Conclusively, the symptoms of the illness include nausea, dark urine, loss of appetite, abdominal pain, fatigue, jaundice and fever (FitzSimons, Hendrickx and Van Damme 586).
Diagnosis is primarily through assessment of liver function biochemically. The method is favored as acute hepatitis manifests itself in a similar manner as other hepatitis viruses. As such, it cannot be differentiated from other forms of the disease. The disease is diagnosed by demonstrating the existence of Anti-HAV antibody. The presence of the antibody can be detected 5-10 days prior to the onset of illness. There is no treatment of therapy for the disease. Treatment is supportive in nature while symptomatic treatment focuses on patients with high risk of developing fulminant hepatitis A. Infection can be prevented through vaccination. Persons handling the patient should be vaccinated to avoid contracting the disease (FitzSimons, Hendrickx and Van Damme 588).
Works Cited
FitzSimons, David, Greet Hendrickx and Pierre Van Damme. “Hepatitis A and E: Update on Prevention and Epidemiology.” Vaccine 28.3 (2010): 583-588. Print.
Hepatitis A. PFD file. 2014. Web.
Marler, Billy. ” Publisher’s Platform: All About Hepatitis A”. Food Safety News. 2012. Web.
Wasley, Annemarie, Kathleen M Gallagher and Scott Grytdal. “Surveillance for Acute Viral Hepatitis, United States.” 2006.Web.
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