PATHOGENESIS
Equine infectious anemia’s mechanism of injury involves inflammation of the monocyte-macrophage and lymphoid systems (spleen and lymph nodes mainly) which results in chronic-active splenitis and lymphadenitis (Equine Infectious Anemia 2012). The efficiency of virus replication depends upon the maturation of blood monocytes into tissue macrophages (Raabe et al. 1998).
The pathogenesis begins with a horse that has a penetrating skin wound, either from a fly/mosquito bite or a needle. The virus contaminates the wound and therefore the blood vascular system. Once in the blood the virus targets monocytes; however because they are not fully differentiated macrophages, the virus is unable to replicate completely. The monocytes therefore spread the virus by leukocyte trafficking, meaning the monocytes spread throughout the circulatory system to all organs where they are then able to migrate through blood vessel walls to gain entrance into the organ tissue. Here the monocytes differentiate into macrophages which enables virus replication within. Virus can then infect other macrophages and lymphocytes, especially in lymphoid tissue like the spleen and lymph nodes. Pro-inflammatory chemokines and cytokines are produced by the macrophages in order to attract more macrophages and lymphocytes into the tissue. The accumulation of cells in the tissues causes splenomegaly and lymphadenomegaly (the enlargement of the spleen and lymph vessels) (EIA 2012).
The anemia of EIA occurs because of phagocytosis and complement mediated lysis of red blood cells (RBCs) that have had alteration of their membranes. A number of cell types lining the vasculature in the spleen and lymph nodes act as a pool for virus and release it into the bloodstream. Virus that is not within cells, but is instead free in the circulatory system, adsorbs onto the surface of RBCs, thus acting as haptens. Cells of the monocyte-macrophage system see these haptens as foreign and phagocytose them. The hapten is then presented to lymphocytes which results in a humoral immune response and antibody secretion against the hapten as well as other antigens on the RBCs membrane. This process is known as a type II hypersensitivity response, where antibody targets and lyses the body’s own RBCs, thus resulting in anemia (EIA 2012).
The pathogenesis begins with a horse that has a penetrating skin wound, either from a fly/mosquito bite or a needle. The virus contaminates the wound and therefore the blood vascular system. Once in the blood the virus targets monocytes; however because they are not fully differentiated macrophages, the virus is unable to replicate completely. The monocytes therefore spread the virus by leukocyte trafficking, meaning the monocytes spread throughout the circulatory system to all organs where they are then able to migrate through blood vessel walls to gain entrance into the organ tissue. Here the monocytes differentiate into macrophages which enables virus replication within. Virus can then infect other macrophages and lymphocytes, especially in lymphoid tissue like the spleen and lymph nodes. Pro-inflammatory chemokines and cytokines are produced by the macrophages in order to attract more macrophages and lymphocytes into the tissue. The accumulation of cells in the tissues causes splenomegaly and lymphadenomegaly (the enlargement of the spleen and lymph vessels) (EIA 2012).
The anemia of EIA occurs because of phagocytosis and complement mediated lysis of red blood cells (RBCs) that have had alteration of their membranes. A number of cell types lining the vasculature in the spleen and lymph nodes act as a pool for virus and release it into the bloodstream. Virus that is not within cells, but is instead free in the circulatory system, adsorbs onto the surface of RBCs, thus acting as haptens. Cells of the monocyte-macrophage system see these haptens as foreign and phagocytose them. The hapten is then presented to lymphocytes which results in a humoral immune response and antibody secretion against the hapten as well as other antigens on the RBCs membrane. This process is known as a type II hypersensitivity response, where antibody targets and lyses the body’s own RBCs, thus resulting in anemia (EIA 2012).