Multiple HBV transfusion transmissions from undetected occult infections: revising the minimal infectious dose.

OBJECTIVE: HBV infection by blood components is currently prevented in most developed countries by combining sensitive HBV surface antigen (HBsAg) assays, nucleic acid testing (NAT) and in a few of them antibodies against the HBV core antigen (anti-HBc) screening. HBV transmissions by blood components from three repeat donors tested negative for HBsAg and HBV DNA with a highly sensitive screening test (limit of detection (LOD): 3.4 IU/mL) were investigated. DESIGN: 30 of the 47 recipients of components produced from these three donors were examined. Transfusion transmission was confirmed by phylogenetic analysis of viral sequences obtained from recipients and donors following viral particle concentration. RESULTS: 9 of 31 (29%) recipients were infected: 7 infections were related to 200 mL of fresh frozen plasma and 2 infections to red blood cells containing 20 mL plasma. Transfusion transmission was confirmed by >99% identity of donor/recipient sequences in five cases, probable in three and possible in one. HBV active infection remained unsuspected for 24-57 months in three recipients. Five non-infected recipients carried anti-HBs when transfused. Six patients transfused with platelet concentrates treated with a pathogen reduction method were not infected. These data enabled to revise previous estimate of the minimal infectious dose from approximately 100 to 16 copies (or 3 IU) of HBV DNA. CONCLUSIONS: HBV transfusion transmission from occult HBV infection carrying extremely low viral loads is related to plasma volume transfused and possibly prevented by anti-HBs. HBV blood safety could be further improved by either anti-HBc screening, HBV DNA NAT with a LOD of 0.8 copies/mL (0.15 IU/mL) or pathogen reduction of blood components.

Severe human granulocytic anaplasmosis transmitted by blood transfusion.

A 36-year-old woman acquired severe human granulocytic anaplasmosis after blood transfusion following a cesarean section. Although intensive treatment with mechanical ventilation was needed, the patient had an excellent recovery. Disease caused by Anaplasma phagocytophilum infection was confirmed in 1 blood donor and in the transfusion recipient.

Anti-HBs positive occult hepatitis B virus carrier blood infectious in two transfusion recipients.

BACKGROUND/AIMS: Occult hepatitis B infection (OBI) in blood donations is not considered infectious when anti-HBs is present. METHODS: Four months after transfusion of eight blood components during coronary arterial bypass surgery, a 59-year-old patient developed acute hepatitis B. A second 71-year-old patient transfused with a red cell concentrate (RCC) from one of these donations had early HBV infection 7 months post-transfusion. Samples were tested for HBV serological markers and HBV DNA was quantified and sequenced. RESULTS: One implicated donation contained anti-HBc, anti-HBs (12 IU/L) and 180 IU/ml of HBV DNA. Previous and subsequent samples contained 3-10 times lower viral load and slightly variable anti-HBs. Two previous donations did not cause HBV infection. Recipients of the FFP and RCC from the index donation were both HBV infected and carried genotype D strains with sequences identical to the donor strain. CONCLUSIONS: Despite anti-HBs, an OBI carrier transmitted HBV to two immunocompetent transfusion recipients.

Hepatitis B surface antigen escape mutant in a first time blood donor potentially missed by a routine screening assay.

Mutant forms of hepatitis B surface antigen have developed from a matter of academic interest into a real threat due to the fact that they may remain undetected by certain commercial immunoassays. The risk is especially high when hepatitis B surface antigen is the only strategy to detect an asymptomatic HBV carrier in blood donor screening. Surface antigen escape mutants arise in individuals under medically or naturally induced selective immune pressure and certain mutations are known to be stable and horizontally transmittable. Currently, only one case report has been published from a blood donor carrying an escape mutant. We herewith present a further case of a blood donor with a mutation so far undescribed that alters the common 'a' determinant of HBsAg in such a way that several immunoassays fail to detect this hepatitis B virus infected patient. We conclude that it is absolutely necessary to use HBsAg assays with a high sensitivity for mutant forms in blood donor screening.