Abstract
Coccidial infections reduce fat-soluble vitamin status and bone mineralisation in broiler chickens. We hypothesised that broilers infected with Eimeria maxima would benefit from increased dietary supplementation with vitamin D (vitD) or with 25-hydroxycholecalciferol (25(OH)D3 or 25D3). Broilers were assigned to diets with low (L) or commercial (M) vitD levels (25 v. 100 μg/kg) supplemented as cholecalciferol (D3) or 25D3. At day 11 of age, birds were inoculated with water or 7000 E. maxima oocysts. Pen performance was calculated over the early (days 1-6), acute (days 7-10) and recovery periods (days 11-14) post-infection (pi). At the end of each period, six birds per treatment were dissected to assess long bone mineralisation, plasma levels of 25D3, Ca and P, and intestinal histomorphometry. Parasite replication and transcription of cytokines IL-10 and interferon-γ (IFN-γ) were assessed at day 6 pi using quantitative PCR. Performance, bone mineralisation and plasma 25D3 levels were significantly reduced during infection (P < 0·05). M diets or diets with 25D3 raised plasma 25D3, improved performance and mineralisation (P < 0·05). Offering L diets compromised feed efficiency pi, reduced femur breaking strength and plasma P levels at day 10 pi in infected birds (P < 0·05). Contrastingly, offering M diets or diets with 25D3 resulted in higher parasite loads (P < 0·001) and reduced jejunal villi length at day 10 pi (P < 0·01), with no effect on IL-10 or IFN-γ transcription. Diets with M levels or 25D3 improved performance and mineralisation, irrespective of infection, while M levels further improved feed efficiency and mineralisation in the presence of coccidiosis.
Highlights
Coccidiosis, caused by parasites of the genus Eimeria, is a widespread condition which adversely impacts broiler chicken farm profitability, by reducing growth rate and feed efficiency due to anorexia[1,2] and impaired nutrient absorption[1, 3, 4]
We investigated whether vitamin D (vitD) supply influences parasite replication and cytokine transcription in the jejunum, the primary site of Eimeria maxima colonisation and replication, at the peak of parasite replication (i.e. d6 pi[28]), and on intestinal histomorphometric features which are indicative of gastrointestinal tract (GIT) damage
The main effects of vitD level, vitD source and infection on performance variables over the periods pre- and post-infection are presented in Table 4.VitD level significantly interacted with infection for feed conversion ratio (FCR) (P < 0.05) over the overall period pi (d0 – 14 pi), being the highest in infected birds on LD diets (Figure 1)
Summary
Coccidiosis, caused by parasites of the genus Eimeria, is a widespread condition which adversely impacts broiler chicken farm profitability, by reducing growth rate and feed efficiency due to anorexia[1,2] and impaired nutrient absorption[1, 3, 4]. Malabsorptive coccidiosis, caused by infection with species such as Eimeria maxima and E. acervulina which affect the small intestine, is characterized by inflammation and intestinal epithelium damage, impaired absorption of fat, calcium (Ca) and phosphorus (P)(5,6), and long bone mineralisation[7,8,9]. Dietary vitamin D (vitD) supply plays a critical role in bone mineralisation of broilers[11]. It may be supplied in the form of cholecalciferol (D3) or as 25-hydroxycholecalciferol (25D3). In addition to its skeletal effects, 1,25D3 acts as an immune system modulator[14] having beneficial effects in the case of infectious and autoimmune diseases[15,16,17]
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