In a field study designed to improve the knowledge of the immunopathogenic mechanisms of paratuberculosis, cohorts of vaccinated and unvaccinated animals from cattle herds with and without clinical history of paratuberculosis were followed up for 18 months with samplings every 6 months. Determinations of humoral immunity and specific and non-specific cellular immunity in response to a PPA-3, avian PPD and PBS were carried out. In addition, a blood PCR technique was used to detect bacteraemia. Animals were classified into four stages or immunopathological forms based on the results of immunity and bacteraemia: animals showing basal levels of cellular and humoral immunity and, therefore, considered as uninfected defined an Apathogenic/Non-bacteraemic Form. Animals showing a moderately intense but apparently efficient non-specific innate immune response and both specific cellular and humoral adaptive immune responses at moderate values, apparently tolerated the presence of Mycobacterium avium subsp. paratuberculosis(Map), were classified as in an Apathogenic/Bacteraemic Form. These could correspond with the focal lesional forms with little presence of acid alcohol resistant bacilli that do not alter the histological structure of the intestine or lymph nodes as described by Gonzalez et al. (2005). A Pathogenic/Non-Bacteraemic Form was defined for animals with an intense and uncontrolled innate immune response, which would likely be responsible for the tissue damage, and an equally increased specific cellular response that could be containing the diffusion of Map, and which would be translated into negative bacteraemia. This form could be assimilated to the previously defined as diffuse limphocytic paucibacillar lesional forms. The Pathogenic/Bacteraemic Form would represent an intense innate immune response that would be producing tissue damage. The specific cellular response was higher than that of apathogenic forms, but lower than those of the non-bacteraemic group. This suggests an inability to control the spread of the infection that would allow the circulation of mycobacteria. These, in turn, could act as an stimulus for humoral immunity which causes this group to have high levels of antibodies. The diffuse multibacillary lesional forms according to Gonzalez et al. (2005) would be consistent with this form. In conclusion, the model presented here, although very broad and panoramic and with few specific details, points out the relevance of innate immune responses that probably are common to other slow infections caused by low virulence pathogens.