Introduction
Rickets is a condition normally associated with limb weakness in broiler chickens and continues to be an important economic problem in the poultry industry (Wise, Reference WISE1975; Wise, Reference WISE1978; Bradshaw et al., Reference BRADSHAW, KIRKDEN and BROOM2002). The fact that rickets is encountered more often among meat type birds (broilers) and develops much faster in this type of birds suggests that it is caused by fast growth rate (Riddell, Reference RIDDELL1992). Rickets is usually observed from the second to the fourth week of age (Long et al., Reference LONG, LEE, ROWLAND and BRITTON1984a). The occurrence of rickets is normally related to disturbances in the levels of calcium (Ca), phosphorus (P) or vitamin D and inadequately balanced rations or mixed dietary ingredients (Wise, Reference WISE1975; Wise, Reference WISE1978; Itakura et al., Reference ITAKURA, TAKESHI, MIJAKURA and GOTO1979).
Defining rickets
Rickets is a metabolic disorder in young growing birds, characterised by thickening and poor mineralisation of the growth plates and the bone. The etiological factors include dietary Ca, P and vitamin D3 deficiency; disturbed Ca/P ratio, or impaired absorption of one of these elements (Riddell, Reference RIDDELL1992; Thorp, Reference THORP1992). Outbreaks can occur due to erroneous feed mixing (Riddell, Reference RIDDELL1992). In both forms (Ca-deficient and P-deficient) the correct calcification of the metaphyseal cartilage is disturbed.
In hypocalcaemic rickets, a thickening of the epiphyse plate may be observed, caused by the accumulation of proliferating chondrocytes (Jande and Dickson, Reference JANDE and DICKSON1980) accompanied by prolongation of perforating epiphyseal blood vessels (Lacey and Huffer, Reference LACEY and HUFFER1982). This expression is typical for most cases of field rickets and low levels of plasma calcium are incriminated as the common cause. In hypophosphataemic rickets, there is an accumulation of hypertrophic chondrocytes (Lacey and Huffer, Reference LACEY and HUFFER1982).
An important fact is that the Ca:P ratio is essential to the onset of rickets and that high dietary phosphorous levels have a similar effect as low Ca levels (Whitehead, Reference WHITEHEAD2002). However, if the concentration of vitamin D3 is also low, some proximal tibiotarsi exhibit moderate rickets-related changes. Vitamin D3 deficiency causes lesions similar to those observed in calcium deficit conditions (Cheville and Horst, Reference CHEVILLE and HORST1981).
Subclinical cases of rickets are common in broilers, probably caused by the dietary deficiency of calcium and phosphorus excess (Riddell and Pass, Reference RIDDELL and PASS1987). Research on enchondral ossification defects in commercial broiler flocks in Australia has revealed that 50% of the birds in three out of six flocks exhibited rickets lesions of the tibiotarsus at the age of two weeks. In the other flocks, the prevalence varied within 12–16%. Lesions were not severe enough to cause lameness (Vaiano et al., Reference VAIANO, AZUOLAS, PARKINSON and SCOTT1994). Clinically severe lesions are rare (Pattisson, 1992). Despite the amount of available knowledge about dietary requirements, rickets remains a significant problem in broiler production (Riddell, Reference RIDDELL1992).
Rickets and skeletal growth
Skeletal growth rate during the first two weeks significantly exceeds those of other periods of the bird's life. Calcium absorption at this time is low because the chicken is not yet capable of synthesising 1,25(ОН)2D3 in sufficient amounts (Vaiano et al., Reference VAIANO, AZUOLAS, PARKINSON and SCOTT1994), and these factors can be responsible for the occurrence of rickets lesions. In support of this theory, Elliot and Edwards (1994) found out that early feed restriction reduced the spread of rickets observed at the age of 16 days.
Outbreaks of rickets due to erroneous feed ingredient mixing have been observed. In broiler chickens, where the symptoms include homogenous prolongation of the growth plates, the causes usually include marginal dietary levels of Ca and P excess (Riddell, Reference RIDDELL1992). Marginal levels of Ca do not lead to rickets but cause dyschondroplasia. Riddell (Reference RIDDELL1992) reported that Mg excess caused lesions similar to rickets.
Based on the pathological lesions, two types of rickets were identified: hypocalcaemic; characterised by accumulation of proliferated chondrocytes (Jande and Dickson, Reference JANDE and DICKSON1980), and hypophosphatemic (phosphorus-deficient); characterised by accumulation of hypertrophic chondrocytes in the metaphyseal zone (Lacey and Huffer, Reference LACEY and HUFFER1982). Symptoms include the vertebral column being bent downwards and the sternum appearing crooked to one side (Leеson and Summers, 2001). These structural changes reduce the size of the thorax with consequent compression of thoracal organs.
Histopathological diagnosis could be harder to establish in field cases and it is possible that hypophosphatemic and hypocalcaemic rickets cannot be distinguished (Randall, 1991) as both forms are easily confused. Thorp (Reference THORP1994) had reported that cases of TD with nutritive etiology could be classified as forms of rickets with different histopathology just as the forms of hypocalcaemic and hypophosphatemic rickets. Although the gross pathology of rickets may be indistinguishable from dyschondroplasia, there are differences on the cellular level (Thorp et al., Reference THORP, WHITEHEAD and RENNIE1991).
Radiographical, macroscopical, and microscopical studies were performed to differentiate the lesions in the growth plate of the tibio-tarsus, induced experimentally in broiler chickens by feeding them diet with modified Ca, P, Mg, or vitamin D contents (Long et al., Reference LONG, LEE, ROWLAND and BRITTON1984a; Reference LONG, LEE, ROWLAND and BRITTON1984b; 1984 c). In recent large-scale field tests, the prevalence of clinical cases of rickets and their association with co-morbidity in broiler chickens was researched (Dinev, Reference DINEV2011). Both commonly established types of rickets were established; hypocalcaemic and hypophosphatemic, (Jande and Dickson, Reference JANDE and DICKSON1980; Lacey and Huffer, Reference LACEY and HUFFER1982; Long et al., Reference LONG, LEE, ROWLAND and BRITTON1984a; Reference LONG, LEE, ROWLAND and BRITTON1984b). The results of these studies showed that the lesions caused by Ca deficiency were very different from those caused by either P deficiency or Ca excess. Based on this it can be assumed that gross lesions in the proximal tibiotarsus can be used to distinguish Ca-deficient from P-deficient rickets in broiler chickens in field cases, as was shown under experimental conditions (Long et al., Reference LONG, LEE, ROWLAND and BRITTON1984a; Reference LONG, LEE, ROWLAND and BRITTON1984b; Reference LONG, LEE, ROWLAND and BRITTON1984c).
Lesions in the remaining parts of the skeleton of the pelvic limb (femur and tarso-metatarsus) were unreliable for differentiating the types of rickets due to the insufficient intensity of lesion occurrence in these bones (Dinev, Reference DINEV2011). This dependency could be related to a transient mineral deficiency or imbalance during the fast growth stage of long bones, especially the tibia, because the proximal tibia is the site of the fastest growing growth plate (Angel, Reference ANGEL2007). That aside, the lesions observed for the same form of rickets can vary in their extent of expression. Large-scale field studies have confirmed that the gross differentiation of Ca-deficient rickets from TD is difficult (Dinev, Reference DINEV2011). In these cases, the differences on the cellular level should be taken into account (Thorp et al., Reference THORP, WHITEHEAD and RENNIE1991).
Links with other diseases
Expressions of various pathological conditions due to different causes have been observed; femoral head necrosis (FHN), osteomyelitis, fractures, tibial dyschondroplasia (TD), vertebral column deformations with clinical signs indistinguishable from spondylolisthesis, chronic respiratory disease (CCRD), and ascites syndrome which were preceded by rickets at an earlier age in all flocks. This gives reason to believe that some persistent skeletal deformations due to past rickets exposure can be major prerequisites to the onset of various health problems during the finisher period, leading to various extents of morbidity in flocks (Dinev, Reference DINEV2011).
Regarding the observed FHN, ostemyelites, fractures, cellulites and CCRD, it is assumed that the original causes are previously occurring lameness and frequent lying down, which lead to overall weakening of the body's resistance. The above mentioned pathological conditions are believed to be mostly complications of secondary E. coli and M. gallisepticum infections. The characteristics of these conditions (morphological and microbiological) are described in a previous work (Dinev, Reference DINEV2009).
The observed TD lesions with preceding Ca-deficient rickets gave us reason to support the position of authors who believed that rickets lesions could play a role in the development of TD (Edwards, Reference EDWARDS1992; Thorp, Reference THORP1994). It is also assumed that TD can follow rickets as a result of the lowered hypertrophy of chondrocytes when birds try to adapt to the low-calcium diet (Long et al., Reference LONG, LEE, ROWLAND and BRITTON1984b). Supporting these assumptions are results from experimental studies, where a high-phosphorus diet had caused rickets in 2-week-old chickens and, later, TD at the age of 4 weeks (Long et al., Reference LONG, LEE, ROWLAND and BRITTON1984b; Riddell and Pass, Reference RIDDELL and PASS1987), along with data from a field study on the high prevalence of rickets in 2-week-old broilers, resulting in TD at the age of 3-4 weeks (Parkinson et al., Reference PARKINSON, VAIANO and AZUOLAS1992). Of course, it will be noted that not all authors support this view. Riddell (Reference RIDDELL1992) classified TD and rickets as different metabolic diseases.
Observed cases alternative to spondylolisthesis were associated with a possible effect on the vertebral column due to past Ca-deficiency rickets (Leеson and Summers, 2001). Clinically, the condition is indistinguishable from the described cases of spondylolisthesis (Pattison, Reference PATTISON1992: Riddell, Reference RIDDELL1992), yet this is clearly an issue of differences in etiology that the problem has been related to until now (Riddell and Howell, Reference RIDDELL and HOWELL1972; Riddell and Topp, Reference RIDDELL and TOPP1972; Riddell, Reference RIDDELL1973; Wice, 1973).
Rickets and respiration
A case of an ascites syndrome outbreak in broilers after the 29th day has been related to the anatomical morphophysiological peculiarities of the respiratory system of birds and consequences of persistent skeletal deformations of the thorax due to preceding rickets (Dinev, Reference DINEV2011). It is known that, due to the lack of diaphragm, respiratory movements are performed by compressing the thorax in birds. In cases of rickets, the thorax compression is slowed down due to poor rib strength (Julian, Reference JULIAN1989). It is logical to assume that the ascites observed in this case was due to a right ventricular failure in response to the higher respiratory demands, especially during the finisher period (Julian, Reference JULIAN1998). Without a doubt, the ascites etiology in this case is also strengthened by the permanent skeletal deformations of the thorax, leading to compression of the thoracal organs (Leеson and Summers, 2001).
Conclusions
In conclusion, the spread of rickets in subclinical or clinical form within the broiler flocks is a possible precursor to a number of pathological conditions related to morbidity in flocks such as FHN, TD, and ascites syndrome. The gross lesions in the proximal tarsus can be used for differentiation of clinical hypocalciaemic and hypophosphataemic rickets in broiler chickens. The cases of Ca-deficiency rickets and TD are hardly distinguished by macroscopy alone because the second condition could be an etiological consequence of the first (Edwards, Reference EDWARDS1992; Thorp, Reference THORP1994).
