A paradoxical observation has been the strong association of certain microbial organisms with autoimmune diseases. For example, Klebsiella pneumoniae and coxsackievirus B have been strongly correlated with ankylosing spondylitis and diabetes mellitus type 1 , respectively. This has been explained by the tendency of the infecting organism to produce super-antigens that are capable of polyclonal activation of B-lymphocytes , and production of large amounts of antibodies of varying specificities, some of which may be self-reactive (see below).
In general, AIHA in children has a good prognosis and is self-limiting. However, if it presents within the first two years of life or in the teenage years, the disease often follows a more chronic course , requiring long-term immunosuppression , with serious developmental consequences. The aim of therapy may sometimes be to lower the use of steroids in the control of the disease. In this case, splenectomy may be considered, as well as other immunosuppressive drugs. Infection is a serious concern in patients on long-term immunosuppressant therapy, especially in very young children (less than two years). 
When you look at a blood smear from a patient with cold AIHA, you’ll see big red cell agglutinates (but only if you have smart lab techs who cool the blood down first before making the smear, so you can see the agglutinates! Most lab techs are very smart.) You might see some spherocytes here and there too (because there is a little bit of macrophage nibbling going on) but they are way less numerous than they are in warm AIHA. To prove that your patient’s anemia is, in fact, an autoimmune hemolytic anemia, you need to do a DAT. The DAT will be positive in cold AIHA because the DAT looks for both IgG and complement bound to the patient’s red cells. Good thing they include the complement in the test (if they just included IgG, then cold AIHA cases would have a negative DAT).