Passive immunization does not provide protection against experimental infection with Mycoplasma haemofelis

Sugiarto, Sarah; Spiri, Andrea M.; Riond, Barbara; Novacco, Marilisa; Oestmann, Angelina; de Miranda, Luisa H. Monteiro; Meli, Marina L.; Boretti, Felicitas S.; Hofmann-Lehmann, Regina; Willi, Barbara

The bilirubin concentrations were also higher in the passively immunized versus control cats at some time points during infection. RBC destruction leads to the formation of free hemoglobin, which is processed by the mononuclear phagocytic system. During this process, bilirubin is formed, released in the blood stream and further metabolized and excreted by the liver. During pronounced RBC destruction, the capacity of the liver to metabolize bilirubin is overwhelmed, and hyperbilirubinemia occurs. Hyperbilirubinemia was observed in three cats of group A, although mean bilirubin concentrations in both groups remained within the reference interval. Nevertheless, the higher RBC OF values and occasionally higher bilirubin concentrations could point towards a more pronounced RBC destruction in the passively immunized cats following subsequent Mhf challenge exposure. The passively immunized cats showed signs of a more pronounced immune response when compared to control cats. Cats of group A showed higher lymphocyte, monocyte and B lymphocyte counts and higher total protein and globulin concentrations than the control cats at several time points during the experiment. Furthermore, peak globulin concentrations coincided with peak anti-DnaK antibody levels in both groups. This result was also found in our recent study, where we documented polyclonal hypergammaglobulinemia during Mhf infection coinciding with high anti-DnaK antibodies [15] . We speculated that a large portion of the immune globulin pool was not hemoplasma-specific and was potentially due to a polyclonal B lymphocyte activation. The induction of autoreactive antibodies has recently been reported for the porcine hemoplasma Mycoplasma suis and is thought to be caused by the upregulation of B lymphocytes in response to changes to the RBC surface of the infected host [43] .