Here are some quotes from the late 1970's animal studies. They had consistently shown transmissibility and induction of chronic intestinal inflammation in animals inoculated with isolates from Crohn's patients and not in animals inoculated with isolates from Ulcerative Colitis or other GI diseases. Induced disease, although not 100% the same as human disease had a lot of its elements and similar incubation (slow growth) period. Here are some of the accounts:

1. The animals receiving Crohn's homogenates put on less weight than the controls; mucosal
ulceration, ileal thickening, and abscess formation were seen in 8 animals and granulomatous changes evolved in 9. No significant macroscopic abnormalities or granulomatous changes were present in
any of the 22 control inoculated rabbits. Successful first passage was achieved from 6 of 11 rabbits. The results of these experiments therefore confirm and extend those of our earlier reports and demonstrate that the transmissible agent or agents responsible must approximate to the size of a virus or be capable of being deformed to pass through a 0.2-mu filter.(Cave DR, Mitchell DN, Brooke BN. Gastroenterology 1975 Sep;69(3):618-24)

2. The epithelioid- and giant-cell granulomas evolved slowly over a period of many months following the inoculation of Crohn's tissue or passage homogenates and persisted thereafter. The transmissible
agent is inactivated when homogenate from Crohn's tissue is autoclaved, can be passaged
successfully into footpads or intravenously (Mitchell DN, Rees RJ. Ann N Y Acad Sci
1976;278:546-59)

3. White rabbits received inoculum of tissue homogenates from the terminal ileum of normal,
ulcerative colitic, and Crohn's disease patients. This inoculum was injected into the wall of the
ascending colon and the animals were examined after one year. Changes were noted consistently
only in those animals receiving the Crohn's disease inoculum. These changes consisted of thickened bowel wall with increased mucosal folds, thickened mesenteric fat with some creeping, irregular areas of thin colonic mucosa, and hyperplastic mesenteric lymph nodes. The terminal ileum distant from the inoculum site was smooth with atrophic changes only in the Crohn's inoculated group of animals. These animals also had discrete collections of macrophages in colon or sacculus, mucosal and submucosal edema, and chronic inflammation of the colon.(Simonowitz D, Block GE, Riddell
RH, Kraft SC, Kirsner JB. Surgery 1977 Aug;82(2):211-8)

4. The granulomas evolved slowly, predominantly between 9 and 27 months. The granuloma-inciting agent has been shown to be present in ileum, colon, and mesenteric lymph nodes of patients with
Crohn's disease and it withstands freezing to -70 degree C. The use of Crohn's tissues common to
this study and one in rabbits previously reported, suggests that the induction of granulomas by this agent is not strain- or species-specific, and is independent of the immune status of CBA mice.  (Cave DR, Mitchell DN, Brooke BN. Gastroenterology 1978 Oct;75(4):632-7)

5. The rabbit bowel was examined after 1 year, and lesions were noted in each of the rabbits
injected with Crohn's disease homogenate, irrespective of the type of tissue preparation. The
observed lesions were diffuse and occurred both at the injection site and in the terminal ileum. These changes were not noted in the control group. (Simonowitz D, Block GE, Riddell RH, Kraft SC, Kirsner JB. Am J Surg 1979 Sep;138(3):415-7)
 

The addition of an antibiotic (ampicillin) prevented the appearance of these Crohn’s-like changes in 12 out of 12 rabbits (Donnelly BJ, Delaney PV, Healy TM. Gut 1977 May;18(5):360-3), pointing to an infectious agent rather than a toxic chemical content in the isolate from Crohn's patient's intestines.