It is important to point out that while A and B molecules were originally found on human red blood cells, it was later established that bacteria also express identical molecules on their cell surface [12, 16,17,18,19,20,21,22,23]. The presence of such shared antigens helps to explain why persons with blood type A have antibodies in their circulation specific for type B (and vice versa) and are thus not suitable matches for blood transfusion [14]. Because AB antigens are shared among humans and bacteria, one cannot be certain if typing results are authentic when dealing with aged or contaminated samples using these methods. A sample could test positive for AB without any red blood cells even being present. Thus, when one considers that a common denominator among such objects is the presence of bacteria, probability statistics such as ≥ 3.2 million to 1 become much less impressive and scientifically shift to a different result. It should also be emphasized that for even the most studied of these artifacts, the Shroud of Turin, the Sudarium, and the Tunic, such typing studies have never been published in a peer-reviewed scientific journal, which is the normal pathway for such findings. Relatedly, assertions of geometric congruence between certain bloodstains on the Shroud and the Sudarium have been relatively self-contained [2]; it is unfortunate that such studies have not been forensically evaluated by an extensive group of blood pattern experts.

Regarding the Shroud, the primary scientist on the Shroud of Turin Research Project (STURP) team who characterized the general chemical properties of the blood in 1978, Dr. Alan Adler, seriously questioned the AB findings because of the very issue that carbohydrates were shared between bacteria and other organisms [24]. In subsequent microscopic examinations conducted years later, Dr. Garza Valdes, a microbiologist, reported that Shroud blood fibers were heavily contaminated with bacteria and fungi [25]. Microbial contamination has also been found in various instances involving modern Eucharistic miracles, as well [8, 15], and has been suggested to be the primary cause for many of these appearances [26, 27]. In the case of the Shroud, adjacent white fibers (without blood) were found to be negative for AB; however, the argument can be made that contamination would primarily be localized within the bloodstains, which is the most abundant food source [28]. In analysis of the Sudarium, some B antigen reactivity in non-bloodstained areas was observed, together with strong B antigen and weak A antigen positivity of bloodstains [2]. In certain cases, bacteria may convert some type A structures to B antigens through deacetylation, known as acquired B type [29, 30]; however, with aged and/or contaminated samples it is difficult to have confidence in the true nature of AB antigens that are defined using serological methods. In any of the above cases, the types of serological (antibody) tests that were performed would not distinguish the true source of AB molecules as they recognize identical structures in both bacteria and humans.

In many of the Eucharistic miracle reports, the evidence of specificity controls in antibody binding was noticeably unmentioned [6,7,8,9, 31], raising additional questions about the validity of the results. In his book on the scientific examination of Eucharistic miracles, Serafini states that “the overall risk of an incorrect blood group determination for these analyzed blood samples [of miracle events] is becoming increasingly small” as methods have improved and have been carried out in various laboratories [8]. This is an oversimplification of the fact that even though techniques may slightly vary, the molecular principles of antigen recognition by antibodies remain unchanged. As none of the above articles in question is sterile (quite the converse), it is reasonable to propose that shared AB antigens from bacteria could readily explain the observed shared blood type. Even with the use of more modern serological techniques (monoclonal antibodies, fluorescent labeling, etc.), the likely contribution of AB antigens from microorganisms cannot be excluded.