Reducing the incidence of bacterial chondronecrosis with osteomyelitis in broilers

 

Bacterial chondronecrosis with osteomyelitis (BCO) is a leading cause of lameness in commercial broilers produced in North America ^{(1, 2, 9)}. The lesions most often occur in the proximal femora and tibiae and are associated with osteochondrotic microfractures and clefts in rapidly growing broilers. Bacteria distributed hematogenously exit the bloodstream and colonize the structurally compromised regions of the bone. As the bacteria proliferate and an immunologic response occurs, the result is necrosis and caseous exudate ^{(4, 8, 9)}. Multiple bacteria of various species have been isolated from BCO lesions. Most predominantly, Staphylococcus spp., Escherichia coli, and Enterococcus spp. have been identified. ^{(4, 9)}

 

The portal of entry by pathogenic bacteria into the systemic circulation is considered to be through compromised tight junctions of the intestine. Stress and the composition of the intestinal microbiome appear to influence the integrity of the intestinal mucosa ^{(6, 7)} of bacterial translocation across the intestinal mucosa has been experimentally reproduced at a high incidence in male broilers reared on wire flooring. The wire flooring enhances the torque and shear stress on the growth plates of the proximal femora and tibiae. A diverse population of bacteria has been identified in association with this syndrome.

 

The hypothesis is that bacteria enter the blood stream by translocating from the intestinal tract. The hematogenous circulation of these bacteria infect micro-fractures and clefts in the growth plate region of rapidly growing bones. In this study, BacPackTM 2X was fed prophylactically, starting at one day-of-age to reduce intestinal bacterial translocation. This treatment was compared to hatch-mates that received a control diet and were reared in the same environmental and management conditions.

 

BacPack 2X is a proprietary blend of Calsporin® (Bacillus subtilis C-3102) and yeast cell wall product IMW50TM, which is incorporated into rations prior to feed pelleting. BacPack 2X is resistant to pelleting temperatures up to 90°C. Male broilers reared on wire flooring resulted in a significant (P ≤ 0.05) increase in the incidence of BCO compared to hatch-mates reared on wood shavings. The prophylactic feeding of BacPack 2X resulted in a significant (P ≤ 0.05) reduction in the incidence of BCO in broilers reared on wire flooring at 56 d of age compared to broilers receiving a control feed. The feeding of BacPack 2X also significantly (P ≤ 0.05) delayed the age of onset of BCO compared with broilers fed the control feed. Clinically healthy broilers that had been reared on wire flooring for 56 d had higher body weights when they had been fed the diet containing BacPack 2X. The results of this study indicate that the prophylactic feeding of BacPack 2X provides a mechanism toward the reduction of BCO-related lameness in broilers.

 

 

Environmental chambers were constructed and managed as previously reported ⁽⁹⁾. Feed (crumbles through wk three and pellets thereafter) and water were provided ad libitum. Corn and soybean meal-based broiler starter feed formulated to meet minimum National Research Council (1994) standards for all ingredients was provided as the control feed in chambers 1, 3, 5, and 7. The feed containing BacPack 2X was provided in chambers 2, 4, 6, and 8, and consisted of control feed mixed prior to pelleting with 1 lb/ton of Quality Technology International Incorporated's BacPack 2X, which contains the MOS beta-glucan yeast cell wall prebiotic IMW50 plus the Calsporin Bacillus subtilis C-3102 probiotic. Feed specifications were determined by QTI’s technical staff, and the feed was manufactured by the University of Arkansas Poultry Research Feed Mill.

Cobb 500 male chicks were obtained unvaccinated from a commercial hatchery and initially were placed at 61/pen. They were culled to 50/pen on d 14, yielding a density of 1 ft2/chick. Beginning on d 15, all birds were observed daily to detect the onset of lameness. Affected broilers had difficulty standing, exhibited an obvious limping gait while dipping one or both wing tips and, if not removed, became completely immobilized within 48 h. Birds were humanely euthanized as soon as the onset of lameness was noticed, and were necropsied within 20 min post-mortem. Birds found dead were necropsied to ascertain the cause of death and assess leg lesions. All birds that died or developed clinical lameness were recorded by date and pen number, and then they were necropsied and assigned to one of the following categories):

At the end of the experiment on d 56, representative survivors that appeared to be clinically healthy were euthanized, weighed and necropsied to assess sub-clinical lesion incidences (n = 20 each for the litter flooring chambers; 10 each for the wire flooring chambers).

 

 

The statistical application was performed as previously reported. ⁽⁹⁾

 

 

Between d 15 and 56, lameness due to KB, TW, TD, and LAME-UNK were minimal, and these non-BCO causes of lameness did not differ between diet treatments. Lameness overwhelmingly was attributable to BCO lesions of the proximal femora and tibiae. Incidences of BCO lameness and total lameness were significantly lower (P = 0.003) in broilers fed the BacPack 2X than in those fed the Control diet.

 

Regarding the time course of lameness progression, broilers fed the Control diet had higher incidences of BCO on d 36 (P = 0.036) through 43, and on d 46 through 56 (P = 0.001) when compared contemporaneously with broilers fed the BacPack 2X diet. The diet treatment groups did not differ (ns, P = 0.090) on d 44 and 45. The onset of BCO occurred earlier in broilers fed the Control diet, and the overwhelming majority of BCO lameness developing during the 7th and 8th wk in both of the diet treatment groups. Variation in total BCO incidences among the individual environmental chambers were observed. The lowest incidence among the wire flooring chambers receiving the control diet (36%, CW chamber 3) numerically exceeded the highest incidence for the wire flooring chambers receiving the BacPack 2X diet (32%, BW chamber 4). We consider this range of variability to be typical based on five years of prior experience with the wire flooring model.

 

Within each flooring category, broilers fed the Control and BacPack diets differed minimally, with the exception that survivors on litter flooring had higher incidences of normal proximal femora and lower incidences of FHT when they had been reared on the Control diet. Independent of diet treatment, broilers that survived eight weeks on wire flooring had significantly higher incidences of proximal tibial BCO lesions (THN+THNs+THNc) than the survivors reared on litter. Regarding, body weights of the clinically healthy survivors, broilers reared on litter and fed the Control diet were the heaviest. Broilers reared on wire and fed the Control diet were the lightest. Clinically healthy survivors that had been reared on wire flooring for 56 d had higher body weights when they had been fed the BacPack 2X diet instead of the control diet (4.03+0.05 vs. 3.81+0.07, respectively; P = 0.012). Pooling these data by diet treatment regardless of floor type eliminated all differences in eight wk body weights (3.99+0.06 for Control vs. 4.02+0.04 for BacPack 2X; P = 0.645).

 

 

The wire flooring model successfully triggered significant incidences of BCO lameness in Cobb 500 male broilers. In the present and previous studies most of the lameness triggered by wire flooring developed between six and eight wk of age, as has been reported for field outbreaks of BCO ^{(2, 3, 9)}. In this regard it is noteworthy that when chick quality is an issue, then osteomyelitis and typical BCO lesions can occur during the first few days post-hatch. Our standard protocol incorporates heavy culling on d 14, which is intended to minimize the appearance of clinical BCO prior to d 40. Accordingly, it is important to note that BCO lameness began to accumulate during the 4th and 5th wk for broilers fed the Control diet, but not until the 6th wk for broilers fed the BacPack diet.

 

BacPack 2X in the diet clearly delayed the onset of BCO lameness, and BacPack 2X also significantly reduced the eight wk incidence of BCO when compared with the Control diet. Virtually all of the BCO lameness occurred in broilers reared on wire flooring, and within the wire flooring category the eight wk survivors that had been fed BacPack 2X were significantly heavier than the survivors that had been fed the Control diet. The efficacy of BacPack 2X clearly cannot be attributed to restricting the growth of broilers reared on wire flooring. Also for broilers reared on wire flooring the BCO lesion incidences did not differ between diet treatments, either for the birds that developed BCO lameness or for the survivors at eight wk of age. Accordingly, although the specific biological mechanism remains to be determined, adding BacPack 2X to the diet did enable significantly more birds to survive eight wk on wire flooring, and those BacPack 2X survivors were heavier than survivors fed the Control diet.

 

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