Campylobacter Clearance in Chickens: Role of the Immune System

March 29, 2017
JoAnna Pendergrass, DVM

Dr. Pendergrass received her DVM degree from the Virginia-Maryland College of Veterinary Medicine. Following veterinary school, she completed a postdoctoral fellowship at Emory Universitys Yerkes National Primate Research Center. Dr. Pendergrass is the founder and owner ofJPen Communications, a medical communications company.

Antibodies in commercial broiler chickens have a limited effect on C. jejuni clearance from the intestine, particularly the ceca—indicating minimal impact on the risk for foodborne zoonotic transmission from these birds.

Within the lifetime of commercial broiler chickens, antibodies have a limited effect on Campylobacter jejuni clearance from the intestines, according to a study recently published in Nature Scientific Reports. This limited effect, wrote the authors, “is likely to have little impact on the risk of foodborne zoonotic transmission from [chickens].”

C. jejuni, whose main source is contaminated poultry, is the leading cause of bacterial food poisoning in humans. In chickens, it colonizes the intestinal tract, most heavily in the ceca. Even though C. jejuni can cause initial inflammation in chickens, the relationship between C. jejuni and chickens is considered commensal.

Control of C. jejuni infection in chickens has proven to be challenging, given the difficulties in developing a fully protective and cost-effective vaccine against this bacterium. In addition, very little is known about functional immunity in chickens and C. jejuni infection immunobiology.

For this study, the authors evaluated the effect of B-lymphocyte depletion on C. jejuni clearance from broiler chicken intestinal tracts. One-day-old Campylobacter-free chickens were divided into two treatment groups: bursectomized and control. Bursectomies were performed chemically with intramuscular cyclophosphamide injections to deplete B lymphocytes.

All chickens were infected with C. jejuni at 21 days of age, then sacrificed at 14, 28, and 63 days after infection. At necropsy, the authors collected ileal, jejunal, and cecal samples to assess C. jejuni colonization. Weekly cloacal swabs were taken for 9 weeks post infection to assess C. jejuni clearance.

Levels of anti—C. jejuni immunoglobulin (Ig) Y were measured, as were B- and T-cell percentages.

Cell Populations

Chemical bursectomy depleted the B lymphocyte population by over 90% but had no effect on T cell population. Bursectomy also decreased the bursa’s size, meaning B cells were not replaced following cell death.

Colonization

Overall, C. jejuni colonization levels were 19-fold higher in the bursectomized group than in the control group. Although these levels decreased over time in both groups, they remained higher in the bursectomized group, regardless of gut region.

Cecal C. jejuni counts were elevated at all post-infection time points in both treatment groups. Ileal and jejunal C. jejuni counts dropped markedly from day 14 to day 63 post infection, but only in the control group.

At 14 and 28 days post infection, serum anti—C. jejuni IgY levels were significantly higher in the control group than in the bursectomized group. Given the reduced ileal and jejunal C. jejuni counts in the control group at day 28, the authors suggested that antibodies could play a role in C. jejuni clearance from the small intestine.

Using structural equation modeling, the authors observed several correlations:

  • Bursectomy was negatively correlated with serum IgY levels.
  • Serum IgY levels were negatively correlated with cecal C. jejuni counts.
  • Cecal C. jejuni counts were positively correlated with ileal and jejunal C. jejuni counts.

Modeling results suggested that C. jejuni infection migrates against peristalsis from the cecum to the small intestine. Such movement warrants further investigation, the authors noted.

Clearance

C. jejuni shedding decreased in control birds, most markedly at 7 to 9 weeks post infection; this finding was important, given the 6-week lifetime of commercial broiler chickens. C. jejuni shedding remained high each week in bursectomized birds.

Taken together, this study’s findings indicate the limited functional immune response to C. jejuni infection in chickens. They also highlight the continued challenge to develop a vaccine that will fully protect chickens from C. jejuni infection before slaughter age.

Dr. JoAnna Pendergrass received her Doctor of Veterinary Medicine degree from the Virginia-Maryland College of Veterinary Medicine. Following veterinary school, she completed a postdoctoral fellowship at Emory University’s Yerkes National Primate Research Center. Dr. Pendergrass is the founder and owner of JPen Communications, a medical communications company.