Skip to main content
ARS Home » Research » Publications at this Location » Publication #95875
Title: LYMPHOGLANDULAR COMPLEXES OF THE COLON ARE INVADED BY CAMPYLOBACTER JEJUNI IN A SWINE ANIMAL MODEL

Author
item MANSFIELD, L - MICHIGAN STATE UNIV
item GAUTHIER, D - MICHIGAN STATE UNIV
item ABNER, S - MICHIGAN STATE UNIV
item JONES, K - MICHIGAN STATE UNIV
item Urban, Joseph

Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/22/1998
Publication Date: N/A
Citation: N/A

Interpretive Summary: Campylobacter jejuni is a bacteria that is the leading cause of diarrhea in humans. It is a widely distributed microorganism that is often carried in or on edible tissues especially from poultry and swine. One method for controlling the contamination of tissues is to manage the problem while the animal is living. However, it is difficult to experimentally infect healthy animals. This indicates that the normal immune system is protective, but is somehow weakened when Campylobacter invades the tissue. Studies were conducted to prove that pigs become susceptible to Campylobacter infection when they are exposed to a common gastrointestinal worm know as the whipworm or Trichuris suis. It was clearly shown that in pigs that were raised germ-free from birth a combined infection with Trichuris and Campylobacter gave diarrhea and disease, while Trichuris alone and Campylobacter alone expressed little or no disease. This demonstrates the synergy between these two infections and will help swine producers to raise pigs that are healthier and less susceptible to bacterial infection when they control worm infections or other conditions that perturb the intestinal immune system of growing pigs.

Technical Abstract: Twenty germ-free pigs were derived by Cesarean section and placed in germ-free incubators to examine whether Trichuris suis could facilitate invasion of Campylobacter jejuni. Pigs that were given a combination of T. suis and C. jejuni had more frequent and more severe signs of diarrhea, and there was bacterial invasion of the colonic epithelium and epithelium of lymphoglandular complexes (LGC) in the distal colon. Pigs given C. jejuni either alone or T. suis had transient fever, depression and diarrhea post-infection which resolved in 3 days. However, severe pathology was present only in the colon of pigs that had both T. suis and C. jejuni. Pigs with T. suis alone had no disease or pathology. Uninfected pigs, and either those infected with C. jejuni or T. suis alone were free of bacterial invasion when judged by histopathology, immunohistochemistry and electron microscopy. The cell types in the LGCs were analyzed for lymphocyte cell surface markers using specific monoclonal antibodies (mAb). Small numbers of CD8+ and CD4+ T cells were found in the LGC follicle in all groups. All groups also had IgM+ B cells within germinal centers (GC) of LGC; IgA+ B cells were seen in high numbers in the lamina propria and in the GC of groups receiving C. jejuni. Macrophages were also stained with a mAb specific for C. jejuni indicating invasion. We conclude that T. suis facilitates C. jejuni invasion of the colon.