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Human and murine erythrocytes (RBC) were invaded by Yersinia pestis in vivo and in vitro during a short period and were probably used as an essential source of iron and porphyrin for survival, effective gross multiplication and rapid spread of these bacteria in the bloodstream of mammals. Both iron and porphyrin were extracted by Y. pestis from the RBC through oxidase-catalase activity which produced oxidation of the RBC glucose with generation of H2O2 in large concentration leading to oxidative transformation of haemoglobin into haemin. Furthermore, some mainly chromosomally encoded effector proteins were implicated in this process because all were synthesised by Y. pestis grown in media simulating the intracellular conditions of mammalian RBC. Damaged RBC lost the ability to transport O2 in the mammalian organism. As a result, significant oxygen deficiency developed in host tissues providing specific clinical disease features of plague which are similar to characteristic symptoms of poisoning with haemotoxic substances when the transformation of the haemoglobin Fe2+ to Fe3+ occurs.