| Features |
I: Silent infection |
II: Inapparent carrier |
III: Clinical disease |
IV: Advanced clinical disease |
| Replication of MAP |
Slow proliferation in jejunal and ileal mucosa and spread to regional lymph nodes |
Continued replication in infected tissues |
Infection becoming disseminated. MAP present in extra intestinal sites |
Widespread proliferation and replication of MAP |
| Shedding |
Intermittent shedding of the organism atlow levels in feces |
Most animals shed the organism in feces and possibly in milk |
Shed increasing numbers of MAP in feces and milk |
Shedding large numbers of MAP in feces and milk - >1000 cfu/g feces=super shedders |
| CMI response |
Th1 CMI responses initiated to control infection |
Increasing CMI response. Gradual switch from Th1 to Th2 |
May be detectable |
Possibly energy |
| Humoral immune response |
none |
Increasing antibody response IgG2,IgG1 |
Predominantly strong antibody response |
Predominantly strong antibody response |
| Clinical signs |
None |
None |
Gradual weight loss and diarrhea |
Emaciation, profuse diarrhea, bottle jaw, cachexia |
| Histopathological changes |
None detected |
Detectable granulomas if multiple tissues examined |
Abundance of lymphocytes, epithelioid macrophages and giant cells in infected tissues, blunted villi |
Abundance of lymphocytes, epithelioid macrophages |
