Polyagglutination Flashcards
polyagglutination
red blood cells that agglutinate in the presence of virtually all adult serum
polyagglutination cause
altered red blood cells exposing an antigen that is normally hidden from the immune system
classifications of polyagglutination
microbial and non-microbial
microbial polyagglutination examples
T, Th, Tk, Tx, acquired B, VA
non-microbial polyagglutination examples
Tn, Cad, HEMPAS, hemoglobin M
microbial polyagglutation cause
bacterial enzymes removing carbohydrates normally present on red cells and exposing new antigens
non-microbial polyagglutination cause
abnormal synthesis of red blood cell membrane structures
T polyagglutination/T activation
neuraminidase action cleaves N-acetylneuraminic acid residues terminally from RBC membrane glycolipids and glycoproteins, causing subterminal T receptor to be exposed. Binds with IgM anti-T
Th polyagglutination
incomplete or intermediate form of T activation; weakened expression or early form of T polyagglutination
bacteria involved in Th polyagglutination
Bacteroides, Clostridia, E. coli, Proteus
bacteria involved in T polyagglutination
Clostridium perfringens, pneumococci, Vibrio cholerae, flu virus
Tk polyagglutination
microbial beta-galactosidases cleave a galactose residue from para-globoside, exposing N-acetylglucosamine
polyagglutination associated with kids with pneumococcal infections
Tk
bacteria involved in Tk polyagglutination
Bacteroides fragilis, Aspergillus niger, Candida albicans, Serratia
polyagglutination that results in altered expression of ABH, Ii, Lewis, P1 antigens
Tk
Tx polyagglutination
caused by unidentified bacteria, seen in kids with pneumococcal infections, mechanism not fully understood
polyagglutination in which H antigens are depressed significantly
VA
Tn polyagglutination
caused by somatic mutation in faulty hematopoietic stem cell clone
polyagglutination associated with myelodysplastic syndromes and acute leukemia
Tn
polyagglutination with mixed field agglutination
Tn
polyagglutination that results in incomplete structure on MN antigen
Tn
inherited permanent polyagglutination forms
HEMPAS, Cad, NOR, hemoglobin M-Hyde Park
HEMPAS
hereditary erythroblastic multinuclearity with positive acidified serum
polyagglutination with increased amounts of I and i antigens, decreased H antigen
HEMPAS
polyagglutination with increased susceptibility for complement lysis
HEMPAS
positive acidified serum test confirms presence of ___ polyagglutination
HEMPAS
polyagglutination that has considerable resistance to Plasmodium falciparum invasion
Cad
polyagglutination agglutinated by anti-Sda
Cad
polyagglutination with positive reaction to Dolichos biflorus lectin
Cad
polyagglutination associated with P blood group system
NOR
inherited form of polyagglutination that has been identified in South African families
hemoglobin M-Hyde Park
cause of Hemoglobin M-Hyde Park polyagglutination
reduction in sialylation of O-linked oligosaccharide chains on membrane components of M-Hyde Park; heterogeneity of the molecular size of SGP’s
why is polyagglutination no longer seem in routing blood banking?
monoclonal antisera replaced human ABO forward typing reagents and antiglobulin reagents; lack naturally occurring polyagglutinins that are found in human adult serum
transfusion protocols for T-activated polyagglutination patients
washed or plasma reduced red cells and platelets, low anti-T titer plasma
enzyme treatment of polyagglutinable cells
Tk, Cad, NOR enhanced
Th, Tn destroyed
T, VA, HEMPAS not affected
polyagglutination should be suspected if:
agglutination with group AB adult sera
no agglutination with cord sera
no agglutination with patient’s own serum
negative direct Coombs
