(2) Frequency:

Approximately 1 per 38,500 U transfused

with low prevalence of septic reactions (1 in

250,000) for RBCs.

Approximately 1 per 5,000 U transfused with

septic reactions in 1 in 116,000 for platelets,

when pretransfusion bacterial screening (i.e.,

BacT/ALERT system) is employed. Lower bacterial contamination rates and septic reactions

exist for apheresis platelets compared to WBderived platelets (53).

(3) Organisms:

Common RBC contaminants include

Yersinia enterocolitica, Serratia

Spp., and Pseudomonas spp., Enterobacter

spp., Campylobacter spp., and Escherichia coli.

All have the potential to cause endotoxinmediated shock in recipients.

Common platelet contaminants include

Staphylococcus aureus,

Staphylococcus epidermidis, Bacillus spp.

diphtheroid bacilli and Streptococci. Most fatal

cases of bacterial contaminated platelets involve

gram-negative organisms.

(4) Treponema pallidum: No new transfusiontransmitted cases reported in >30 years (48).

c. Protozoa

(1) Malaria: Rare in the United States but reported

even in nonendemic areas (45)

(2) Babesiosis

(3) Chagas disease (Trypanosoma cruzi)

d. Prions: Creutzfeldt—Jakob

(1) Few proven cases of transfusion-transmitted

new-variant Creutzfeldt–Jakob disease at present. Those described have been in the United

Kingdom (54).

(2) Most blood collection centers attempt to minimize the risk by excluding donors considered to

be at higher risk for possibly harboring the infection, by family and travel history and specific

medical history (47).

2. Hemolytic reactions

a. Acute hemolytic immunologic reactions: Rare,

because of absence in infant of naturally occurring

anti-A or anti-B antibodies, and infrequent posttransfusion red cell alloimmunization despite multiple

transfusions.

b. T-activation: A form of immune-mediated hemolysis

associated with the transfusion of adult blood containing naturally occurring anti-T antibodies, into

neonates with exposure of a normally masked

Thomsen–Friedenreich (T) cryptantigen on their

RBC surface. T-activation can present with evidence

of intravascular hemolysis following transfusion of

blood products, or unexplained failure to achieve

the expected posttransfusion hemoglobin increment

(24,30).