before 1984, used to screen blood for Hepatitis B and syphilis
Adding donor interviews and doing volunteer only donations, plus better testing methods, have greatly reduced the risks of acquiring infections from blood transfusions
a large percentage of transfusion transmitted complications have a viral etiology
viruses are intracellular organisms, which use the host to reproduce
the transmission of viruses can be associated with cellular components or plasma
any blood product made from pooled plasma is more likely to transmit viruses
the hepatitis viruses attack the liver
there are 6 classes of primary hepatitis viruses (A-G), but the ones we are concerned with are A, B, C
secondary hepatitis viruses involve the liver secondary to another infection (EBV, CMV, etc)
all hepatitis viruses can be transmitted through blood products
only products that are specially treated to deactivate virus can viruses not transmit (e.g. plasma protein fraction)
the risk of hepatitis viral transmission via blood products is greatly reduced: HCV transmission is 1 in 1.1 million units; HBV is about 1 in 1.2 million units
the first hepatitis A epidemic was in the 17th century; it was discovered that it is shed through the stool
hepatitis A is a small, RNA, simple, nonenveloped virus with a nucleocapsid
40-45% of adults have evidence of prior exposure to hepatitis A, usually follows fecal-oral route
hepatitis A is transmitted via contaminated food and water; or person-to-person, especially when poor hygein is involved (day-care centers are prone to outbreaks)
risks of hep A: living in areas with poor sanitation, travel to endemic areas, people in prison, IV drug use
hepatitis A is rarely spread via transfusion because no chronic carrier state occurs
for hepatitis A transmission via blood products, donor would have to be in the 2-6 week incubation phase
many adults who would receive transfusion from donor with hepatitis A would have resistance due to prior exposure
there isn't a higher transmission rate of hepatitis A in patients who have had multiple transfusions
incubation for HAV is 14-45 days
viral replication of Hep A occurs in the liver, the virus is then excreted through the biliary system into the feces
in Hep A, see brief viremia (can be transmitted in transfusions in this stage of the disease)
symptoms of Hep A: nausea, vomiting, loss of appetite, malaise, diarrhea; jaundice is often present
we can use hepatitis A markers to ID current or past infections
if HAV is suspected, test for IgM antibodies to the virus
If there is no IgM, but you find IgG, indicates old infection
routine antibody screenings for HAV is not done
donor interview questions are designed to pick up symptoms that may indicate HAV infection
if HAV is discovered after the fact, can give recipient serum immune globulin which will decrease symptoms
Travelers to endemic places should get a HAV vaccination
HAV is seen mostly in unvaccinated, young children in resource-limited countries
hepatitis B was found as an antigen in Australian aborigines. It was called the Australian antigen (Au), now it is known as Hepatitis B surface antigen (HBsAg)
•HBV can also be found in Peking ducks, woodchucks, and some ground squirrels
HBV is a double-stranded DNA virus
HBV's inner core contains a partially double-stranded DNA surrounded by a surface coat composed of lipid and protein
also in core of HBV, along with the DNA is an enzyme -- DNA polymerase