Paul has an A+ blood type but showed a weak reaction to anti-B, indicating an acquired B antigen. This phenomenon can occur due to bacterial enzymes modifying the A antigen into a similar B antigen structure. It is most commonly caused by E. coli, Clostridium tertium, and Proteus vulgaris. To confirm, additional anti-B reagents and secretor testing would be used, and the reactions may convert back to normal once the bacterial infection is resolved.
Paul has an A+ blood type but showed a weak reaction to anti-B, indicating an acquired B antigen. This phenomenon can occur due to bacterial enzymes modifying the A antigen into a similar B antigen structure. It is most commonly caused by E. coli, Clostridium tertium, and Proteus vulgaris. To confirm, additional anti-B reagents and secretor testing would be used, and the reactions may convert back to normal once the bacterial infection is resolved.
Paul has an A+ blood type but showed a weak reaction to anti-B, indicating an acquired B antigen. This phenomenon can occur due to bacterial enzymes modifying the A antigen into a similar B antigen structure. It is most commonly caused by E. coli, Clostridium tertium, and Proteus vulgaris. To confirm, additional anti-B reagents and secretor testing would be used, and the reactions may convert back to normal once the bacterial infection is resolved.
Forward typing – AB + reverse typing – A group. His ABO type is A + 2. What is the discrepant result in the ABO grouping? Weak reaction in Anti-B (1+) 3. Explain the phenomenon that caused this pattern, and briefly describe two processes by which this can occur. caused by the action of bacterial enzymes (deacetylase) which modi<es A sugar (N-acetyl-D- galactosamine) into D-galactosamine which is similar to the B sugar (D-galactose). This acquiredB antigen thus cross-reacts with Anti-B causing discrepancy in the forward typing. This phenomenon occurs mainly in the colon cancer, gram negative sepsis and other diseases of digestive tract. It can occur in vitro or in vivo. In vivo is a transient condition which occurs on red cells having A antigen. In vitro occurs by coating of A or O red cells with lipopolysaccharides from bacteria like E. coli and P. vulgaris 4. What bacteria are most commonly involved? E. coli, Clostridium tertium and Proteus vulgaris 5. What steps would you take to confirm your suspicions? 1-Use of different clone of anti-B preferably monoclonal reagent. Do not use ES4 clone. 2- Secretor studies (only works on actual secretor). Saliva of a person with acquired B does not have B antigen 3-Autoincubation – reaction of patient’s own anti-B with acquired B red cells show no agglutination 4- Acidifying Anti-B – when red cells are treated with acetic anhydride, there is no agglutination when tested with anti-B 6. Is the result of the antibody screen useful? Why or why not? As this is a discrepancy of forward typing (antigens in red cells), not the reverse typing, the negative antibody screen does help to rule out the presence of any auto/alloantibodies in this patient. 7. Define a secretor? Secretor is an individual who possess Se gene and secrete ABH-soluble antigen 8. What percent of the population are secretors? 78%-80% US population 9. Assuming he is SeSe, what ABO antigens will be present in Paul’s secretions? A AND H antigen 10. Will Paul’s ABO reactions convert back to normal? If so, when? Yes, the ABO reactions will convert back to normal once the causative microbial organism is eliminated from the patient’s body/infection is resolved