Using a dynamic model we study the adaptive immune response to a sequence of two infections. We incorporate lymphocyte diversity by modeling populations as continuous distributions in a multi-dimensional space. As expected, memory cells generated by the primary infection invoke a rapid response when the secondary infection is identical (homologous). When the secondary infection is different (heterologous), the memory cells have a positive effect or no effect at all depending on the similarity of the infections. This model displays 'original antigenic sin' where the average effector affinity for the heterologous infection is lower than it would be for a naive response, but in cases with original antigenic sin we see a reduction in pathogen density. We model pathology resulting from the immune system itself (immunopathology) but find that in cases of original antigenic sin, immunopathology is still reduced. Average effector affinity is not an accurate measure of the quality of an immune response. The effectivity, which is the total pathogen killing rate, provides a direct measure of quality. This quantity takes both affinity and magnitude into account.