Abstract
Minimizing the clinical signs of Enterococcus cecorum infections causing enterococcal spondylitis in broiler herds is successful when initiated as metaphylaxis in the first week of life. Mechanistically, either the Enterococcus species present at that time are reduced by antibiotic treatment or antibiotic treatment might induce changes in intestinal microbiota composition with an indirect and subsequent influence. The aim of the present study was to examine the cecal microbiota of chickens after administering lincospectin or different additives to evaluate whether these additives have lincospectin-like effects on microbiota. Therefore, 157,400 broiler chickens were reared in four chicken houses (~40,000 birds each) on a broiler farm with history of enterococcal spondylitis. Each flock was treated either with lincospectin or water soluble esterified butyrins, Bacillus (B.) licheniformis or palm oil was added via drinking water during the first days of life. Ten birds per house were dissected at days 11, 20 and 33 of life and cecal microbiota were analyzed (16S rRNA gene sequencing). Lincospectin treatment elicited significant changes in the cecal microbiota composition until slaughter age. Among the tested additives, effects of B. licheniformis on cecal microbiota composition were most similar to those seen after the treatment with lincospectin at day 11.
Highlights
Enterococcus (E.) cecorum infections with a clinical course have been increasingly reported in different countries worldwide [1,2,3], forming an important emerging disease in modern broiler chickens associated with arthritis and osteomyelitis and leading to high mortality rates [1,2,4]
It is suggested that intestinal colonization, bacteremia and osteochondrosis dissecans of the free thoracic vertebra in early life are crucial for the pathogenesis of enterococcal spondylitis [6]
Chickens that had received B. licheniformis showed the highest similarity with lincospectintreated chickens at day 11, followed by chickens treated with esterified butyrins
Summary
Enterococcus (E.) cecorum infections with a clinical course have been increasingly reported in different countries worldwide [1,2,3], forming an important emerging disease in modern broiler chickens associated with arthritis and osteomyelitis and leading to high mortality rates [1,2,4]. E. cecorum with pathogenic genotypes were identified in the intestines of naturally infected birds as early as week one, in contrast to commensal E. cecorum strains that did not appear until week three [6] This ability to colonize the gut early in life may provide pathogenic E. cecorum strains with a competitive advantage and potentiate dissemination throughout a flock [6]. It is suggested that intestinal colonization, bacteremia and osteochondrosis dissecans of the free thoracic vertebra in early life are crucial for the pathogenesis of enterococcal spondylitis [6]. Infections with other intestinal pathogens decrease bacteremia and spinal lesions caused by pathogenic E. cecorum [11] These observations indicate interactions of Enterococcus spp. with other intestinal bacteria. Even if it is suggested that disruption of the intestinal structure could potentiate E. cecorum bacteremia, it was not observed that clinical intestinal diseases necessarily cause E. cecorum bacteremia [6]
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