2.1 |
Effects of light during incubationChapter 3 and 6 describe how lighting schedules during incubation affect leg health of broiler chickens at slaughter age (Table 1). In Chapter 3, broiler eggs were incubated under continuous cool white LED light (24L); 12L:12D of cool white LED light; or con-tinuous darkness from set until hatch of the eggs. In Chapter 6, a similar setup was used, but a circadian lighting schedule of 16 hours of light, followed by 8 hours of darkness (16L:8D) was applied instead of 12L:12D. It was found that 12L:12D resulted in a 7.1%
lower incidence of tibial dyschondroplasia compared to 24L, with 24D intermediate.
When leg pathologies were scored as 1 = absent to 4 = severe, it was found that 16L:8D and 24D resulted in a lower average score for epiphyseal plate abnormalities, and 16L:8D resulted in a lower average score for BCO than 24D, with 24L intermediate. 16L:8D furthermore tended to have a lower average score for tibial dyschondroplasia than 24D, with 24L intermediate. Numerically, 16L:8D also resulted in lowest incidence of rotated tibia and valgus/varus deformities, and the highest percentage of chickens without any leg problems.
When chickens were scored as having 1, 2, 3, or ≥ 4 leg bone pathologies (in which each pathology was counted per leg; for example, a chicken with tibial dyschondroplasia in both legs was scored as having 2 pathologies), 24L was shown to result in the highest number of chickens with 3 or ≥ 4 leg bone pathologies. This shows that incubation under 24L not only resulted in fewer chickens without leg bone pathologies, but also in a higher percentage of chickens that suffered from various types of leg problems, and in more than one leg, compared to 16L:8D and 24D.
The fact that incidence and severity of BCO, tibial dyschondroplasia, and epiphyseal plate abnormalities were affected on D35 post hatch by lighting schedules that were applied only during the incubation period suggests that differences in bone morphology or physiology had developed already during embryogenesis. To better understand how embryonic bone development may have resulted in differences in leg bone pathologies at slaughter age, the aetiology of BCO, tibial dyschondroplasia, and epiphyseal plate
Chapter 8
| 168
abnormalities is discussed in more detail.
Table 1. Overview of leg health variables (pathologies and gait scores) in broiler chickens incubated un-der continuous light (24L), 12 hours of light, followed by 12 hours of darkness (12L:12D; Chapter 3), 16 hours of light, followed by 8 hours of darkness (16L:8D; Chapter 6), or continuous darkness (24D) from set until hatch on D34 or D35 post hatch.
Leg problem variable
Pathologies (% incidence D35) 24L 12L:12D 24D P < 0.05
Tibial dyschondroplasia 8 1 2 Yes
24L 16L:8D 24D
BCO 3 1 6 Yes
Epiphyseal plate abnormalities 18 9 7 Yes
Epiphyseolysis 37 30 27
Rotated tibia 18 16 17
Tibial dyschondroplasia 13 7 15
Valgus/varus deformity 25 25 28
Incidence of pathologies within
a chicken (% of chickens)1 24L 16L:8D 24D P < 0.05
0 leg bone pathologies 23 29 24
1 leg bone pathology 9 17 13
2 leg bone pathologies 20 21 26
3 leg bone pathologies 20 9 15
≥4 leg bone pathologies 28 24 22
Gait scores 24L 16L:8D 24D P < 0.05
D21 1.5 1.4 1.5
D28 2.0 1.9 1.9
D34 2.9 2.8 2.8
1 Each pathology observed in 1 leg is considered 1 incidence; for example, tibial dyschondroplasia in both legs of 1 chicken counts as 2 leg bone pathologies.
Within a row, dark grey denotes the worst value in terms of leg health (highest incidence of the leg pa-thology or highest gait score), light grey denotes the intermediate value, and white denotes the best value in terms of leg health.
2.2 |
Development of leg pathologiesTibial dyschondroplasia, BCO, and epiphyseal plate abnormalities share a common origin in chondrocyte (cartilage cell) abnormalities at the epiphyseal plate. In tibial dyschondroplasia, hypertrophic chondrocytes fail to become vascularized and form a
General discussion
169 | surrounding calcified matrix. As a result, a plug of cartilage with necrotic and apoptotic chondrocytes is observed below the epiphyseal plate, possibly extending into the metap-hysis (Hargest et al., 1984). In BCO, damage to the poorly mineralized and vascularized columns of chondrocytes at the epiphyseal plate facilitates colonization by pathogenic bacteria, such as Staphylococcus aureus, Enterococcus cecorum, and Escherichia coli (Wideman and Prisby, 2013). Histologically, blood vessels of the epiphysis or epiphyseal plate are found to be partly or completely occluded by bacterial clumps, and the vessels are surrounded by cartilaginous matrix containing necrotic chondrocytes (McNamee and Smyth, 2000). The lesions observed in BCO may also extend into the metaphysis (McNamee et al., 2000). Epiphyseal plate abnormalities, as described here, comprise more general abnormalities, such as widening or an irregular shape of the epiphyseal plate, without the symptoms of tibial dyschondroplasia or BCO. Possibly, epiphyseal plate abnormalities as observed in this study are actually early stages of BCO or tibial dyschondroplasia, and all three may share a common aetiology in suboptimal early life cartilage conversion and vascularization at the epiphyseal plate.
Valgus/varus deformity and rotated tibia are abnormalities in the bone’s curvature, with valgus/varus showing angular deformity of the tibia and the hock joint (Duff and Thorp, 1985) and rotated tibia showing torsional deformity of the whole bone (Shim et al., 2012). Their aetiology is not well understood, but it can be speculated that suboptimal joint angles and bone conformity, weakness of tissue supporting the joint, and poor ossi-fication play a role (Bradshaw et al., 2002). Valgus/varus deformity and rotated tibia were not significantly affected by incubation lighting schedules. It seems that leg bone pa-thologies originating in abnormalities at the epiphyseal plate are more strongly affected by incubation lighting schedule than leg bone pathologies related to abnormal curving, although they are not completely independent of each other: there are indications that presence of tibial dyschondroplasia in the leg increases the chance that a chicken will develop valgus/varus deformities (Randall and Mills, 1981).
Leg abnormalities were determined macroscopically in the current thesis. Microscopic and histological examination of the lesions found in the BCO and tibial dyschondrop-lasia affected chickens may have provided more insight into the extent and nature of the abnormalities, and it would be suggested to perform these more detailed analyses in fu-ture studies on light during incubation and leg bone pathologies. Leg bone morphology, on the other hand, has been studied in more detail in the present thesis and could provi-de information about how leg bones of broiler chickens exposed to different incubation lighting schedules differ in their development, embryonically, at hatch, and post hatch.
These differences are described in the following paragraphs.
Chapter 8
| 170