Delta-hepatitis – an infection caused by the hepatitis D virus, characterized by symptoms of acute liver damage and intoxication, in most cases proceeding heavier than other viral hepatitis. An essential condition for the manifestation of the negative effect of the hepatitis D virus is the presence of the hepatitis B virus multiplying. The delta infection exists in two forms: acute infection with simultaneous infection with hepatitis B virus and delta virus-coinfection and acute infection with infection of BDD carriers of the hepatitis B surface antigen – superinfection.
Delta-hepatitis, as well as hepatitis B, has almost universal, but uneven distribution. The frequency of coinfection cases varies in different countries from rare registration to 25-30% of the number of cases of acute HBsAg-positive hepatitis.
The frequency of detection of antibodies to delta antigen among carriers of hepatitis B virus and patients with chronic hepatitis serves as an indicator of the latitude of the spread of delta infection. It is estimated that about 5% of HBsAg carriers (approximately 15 million people) are infected with the delta virus. Regarding the level of spread of delta infection, regions, territories and countries can be conditionally assigned to one of four zones:
– a zone of high endemicity, with an incidence of anti-BHD over 20% in HBsAg carriers and more than 60% among patients with chronic hepatitis B (some countries in Africa:
Kenya, Central African Republic, Niger; Taiwan, as well as Venezuela; South Italy, Romania, Southern districts of Moldova);
– the zone of medium endemicity of anti-BHD – 10-19% in HBsAg carriers and from 30 to 60% among patients with chronic hepatitis B (some countries in Africa: Nigeria, Somalia, Uganda, Burundi, some areas of the USA – California, Russia – Yakutia, Tuva );
– low endemicity of 3 to 9% among carriers of HBsAg and from 10 to 30% among patients with chronic hepatitis B (Liberia, Ethiopia, South Africa, Lithuania, Estonia, Latvia, European Russia, USA);
– very low endemicity of up to 2% among HBsAg carriers and less than 10% among patients with chronic hepatitis B (Northern and Central European countries, China, Japan, Uruguay, Chile, Argentina, Southern Brazil, Australia).
The level of endemicity of delta infection is associated with the prevalence of hepatitis B in this area, however, this relationship is not absolute. So, despite the high intensity of the circulation of the hepatitis B virus among the Alaskan Eskimos, the delta infection there is recorded at a low level.
Infection with hepatitis D occurs only when the virus enters the blood directly, which then enters the liver with the bloodstream. It is suggested that the liver is the only organ where the hepatitis D virus multiplies. The mechanism of hepatocyte damage in hepatitis D is not fully understood. At the same time, it is considered that the direct destroying effect of the virus on the cell occupies a leading role in this process.
Hepatitis D has no specific signs and is characterized by common manifestations of inflammation. In this case, changes in hepatocytes are more pronounced in the absence of a clearly expressed inflammatory reaction. In coinfection, changes are observed that are characteristic of acute hepatitis B. In cases of acute superinfection, there are signs of acute inflammation and a chronic process caused by a previous infection of hepatitis B.
Infection with delta virus (both with coinfection and superinfection) leads to the development of an acute disease. At the initial stage of the study of delta-hepatitis, the relationship between the presence of delta-infection and the severity of the disease was emphasized. However, studies conducted in delta-hepatitis-endemic regions have demonstrated that delta-hepatitis can be associated with a wide range of clinical manifestations of the disease from asymptomatic carriage to extremely severe hepatitis and cirrhosis of the liver. Analysis of histological data of liver biopsy of patients with chronic delta-hepatitis in Italy revealed two types of course of the disease. At the first, approximately 10% of patients registered non-progressive hepatitis. In the second case, chronic hepatitis of high activity or active cirrhosis of the liver was noted in 90% of cases.
The duration of the incubation period varies from 3 to 7 weeks. The pre-egg phase of the disease has clinical symptoms similar to hepatitis B: increased fatigue, lethargy, loss of appetite, nausea, in some patients, fever, joint pain. With superinfection, the pre-jaundice period is shorter than with coinfection and hepatitis B and is usually only 4-5 days.
The beginning of the icteric period coincides with the appearance of yellowing of the skin and sclera, dark urine and light stools, an increase in the symptoms of intoxication, pain in the right hypochondrium. When superinfection for 3-5 days, a fever is recorded. The liver and spleen are enlarged.