Abstract

Multiple hypotheses into the age-based susceptibility of animals to Lawsonia intracellularis exist, including the decline of passively acquired antibodies. To determine whether the decline in passively acquired antibodies in horses is responsible for the age predilection of equine proliferative enteropathy (EPE). Additional objectives included examination of various risk factors for the development of EPE as well as the determination of naturally occurring attack rates for clinical and subclinical EPE. Prospective, multifarm field study. A total of 369 mare and foal pairs from 15 central Kentucky Thoroughbred farms were used in this study, which took place from January 2012 to February 2013. Serum samples were collected from mares and foals within 48 h of parturition, and then monthly from foals to February of their yearling year. Lawsonia intracellularis-specific antibodies were measured using an enzyme-linked immunosorbent assay. No effect of passively acquired antibodies on the occurrence of presumptive clinical or subclinical EPE was noted. In total, 5.3% and 6.3% of seropositive horses developed presumptive clinical or subclinical EPE, respectively. In multiple logistic regression models, colts were at a significantly greater risk than fillies of developing presumptive clinical EPE (odds ratio [OR] 5.468, 95% confidence interval [CI] 1.134-26.362, P = 0.034) or a combination of either presumptive clinical or subclinical EPE (OR 3.861, 95% CI 1.461-10.206, P = 0.006) while foals that were weaned in September or beyond were at a lower risk of developing presumptive EPE (OR = 0.281, 95% CI 0.0807-0.981, P = 0.05). This is the first study to show that passively acquired antibodies to L. intracellularis do not have an effect on the occurrence of clinical or subclinical EPE. A number of novel findings, including identification of the disease rate among naturally exposed horses, warrant additional work as they may help to identify potential risk factors for L. intracellularis exposure and/or the reservoir host(s) of the bacterium.

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