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Clinical Biochemistry of Domestic Animals (Sixth Edition) - UMK ...

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VIII. Calcium and Phosphorus: Metabolic Bone Disease<br />

859<br />

cause <strong>of</strong> elevated activities <strong>of</strong> plasma enzymes from muscle<br />

origin ( Fig. 28-16 ). When physiological or iatrogenic causes<br />

<strong>of</strong> hyperCKemia can be ruled out, primary neuromuscular<br />

disease should be considered.<br />

In birds, several causes <strong>of</strong> degenerative myopathy have<br />

been reported. In poultry, furazolidone and ionophore coccidiostats<br />

are well-known causes <strong>of</strong> myocyte degeneration<br />

( Julian, 1991 ). Ingestion <strong>of</strong> the beans <strong>of</strong> c<strong>of</strong>fee senna ( Cassia<br />

spp.) has been suggested as a possible cause <strong>of</strong> acute myocyte<br />

degeneration in birds ( Rae, 1992 ). Two important causes<br />

<strong>of</strong> degenerative myopathy in birds are exertional rhabdomyolysis<br />

(capture myopathy) and nutritional myopathy.<br />

One <strong>of</strong> the signs <strong>of</strong> a deficiency <strong>of</strong> selenium or vitamin E<br />

in birds is muscular degeneration. Some authors believe that<br />

exertional rhabdomyolysis is an acute manifestation <strong>of</strong> nutritional<br />

myopathy although it has been recorded in species<br />

with apparently normal vitamin E levels ( Spraker, 1980 ).<br />

Capture myopathy has been reported in flamingos<br />

( Fowler, 1978a, 1978b ; Young, 1967 ), cranes ( Brannian<br />

et al ., 1987 ; Carpenter et al ., 1991 ; Windingstad, 1983),<br />

Canada geese (Chalmers and Barrett, 1982), turkeys<br />

( Spraker et al ., 1987 ), and ratites ( Dolensek and Bruning,<br />

1978 ; Phalen et al ., 1990 ; Rae, 1992 ).<br />

Nutritional related myopathies have been reported<br />

in piscivorous birds after feeding an unsupplemented<br />

diet <strong>of</strong> previously frozen fish, primarily smelt ( Campbell<br />

and Montali, 1980 ; Carpenter et al ., 1979 ; Nichols and<br />

Montali, 1987 ; Nichols et al ., 1986 ). Vitamin E deficiency<br />

has also been associated with muscle lesions in raptors<br />

( Calle et al ., 1989 ; Dierenfeld et al ., 1989 ). Rae (1992)<br />

reported that a large percentage <strong>of</strong> young ratites submitted<br />

for necropsy exhibited evidence <strong>of</strong> degenerative myopathy<br />

and considered nutritional deficiency <strong>of</strong> vitamin E and possibly<br />

selenium as the most probable cause.<br />

The muscle lesions produced by the various causes cannot<br />

be distinguished from each other and the clinical history<br />

is important to establish a diagnosis ( Rae, 1992 ). The use <strong>of</strong><br />

serum or plasma vitamin E concentrations has been advocated<br />

to enable a clinical diagnosis <strong>of</strong> nutritional myopathy in birds<br />

(Rae, 1992 ). Mean ( SE) plasma concentrations <strong>of</strong> vitamin E<br />

(quantified as α -tocopherol) established in 274 captive cranes<br />

were 6.57 0.82 μ g/ml. Cranes species that evolved in temperate<br />

habitats had higher circulating levels <strong>of</strong> α-tocopherol<br />

than tropical or subtropical species: for example, Black<br />

crowned crane ( Balearica pavonina ) (n 10) 2.77 0.23 μg/<br />

ml and Siberian crane ( Grus leucogeranus ) (n 51)<br />

9.41 0.64 μ g/ml ( Dierenfeld et al ., 1993 ). In peregrine falcons<br />

( Falco peregrinus ), circulating α-tocopherol concentrations<br />

10 μ g/ml were considered a reflection <strong>of</strong> a marginal<br />

vitamin E status, whereas plasma concentrations 5 μg/ml<br />

were considered deficient ( Dierenfeld et al ., 1989 ). Only limited<br />

data are available on normal plasma concentrations <strong>of</strong> α -<br />

tocopherol in ratites. In apparently healthy rheas, circulating<br />

α -tocopherol concentrations ranged between 9.0 and 14.5 μg/<br />

ml, whereas two rheas with muscular problems exhibited<br />

mean plasma concentrations <strong>of</strong> 1.34 μ g/ml ( Dierenfeld, 1989 ).<br />

For the diagnosis <strong>of</strong> cardiac diseases in birds plasma<br />

chemistry has also been used. Enzymes that have been used<br />

include AST, LDH, and CPK. CPK activity in plasma from<br />

cardiac muscle origin (CPK-MB isoenzyme) was significantly<br />

higher in ducklings with furazolidone-induced cardiotoxicosis<br />

when compared to controls ( Webb et al ., 1991 ).<br />

Cardiac troponin T (c TnT), a cardiac specific protein<br />

that forms part <strong>of</strong> the contractile apparatus <strong>of</strong> striated<br />

muscle, is a specific and sensitive serological indicator<br />

<strong>of</strong> acute myocardial infarction in human patients. Elevated<br />

serum c TnT concentrations have also been used as a<br />

marker for early myocardial damage in broiler chicks<br />

( Maxwell et al ., 1995 ). Whether plasma or serum is used<br />

seems not to be critical, according to Dominici et al .<br />

(2004) . In Siamese fighting fowl, sex-specific differences<br />

have been demonstrated in plasma c TnT concentrations<br />

( Sribhen et al ., 2006 ).<br />

VIII . CALCIUM AND PHOSPHORUS:<br />

METABOLIC BONE DISEASE<br />

A . Relation between Calcium and Protein in<br />

Avian Plasma<br />

Between 50% and 80% <strong>of</strong> plasma calcium is biologically<br />

inactive and consists <strong>of</strong> protein-bound calcium and<br />

complexed calcium. Total calcium (tCa) concentration is<br />

influenced by plasma protein concentrations. Ionized calcium<br />

(iCa) is important with regard to deposition <strong>of</strong> calcium<br />

salts and excitability <strong>of</strong> nervous tissues. In most laboratories,<br />

for technical reasons, only tCa is measured. Hence,<br />

when tCa is measured it is also important to measure plasma<br />

protein concentrations and to make allowances for any deviations<br />

from the normal in the latter. A significant linear correlation<br />

was found between tCa and Alb in the plasma <strong>of</strong><br />

70 healthy African grey parrots (r 0.37; p 0.05), and<br />

a correction formula was derived on the basis <strong>of</strong> the concentration<br />

<strong>of</strong> Alb: Adjusted tCa (mmol/L) measured tCa<br />

(mmol/L) 0.015 Alb (g/L) 0.4. Approximately 14% <strong>of</strong><br />

the variability <strong>of</strong> tCa was attributable to the change in the<br />

concentration <strong>of</strong> plasma Alb (R 2 0.137) (Lumeij, 1990 ).<br />

A significant correlation was also found between tCa and<br />

TP in 124 plasma samples <strong>of</strong> peregrine falcons (r 0.65;<br />

p 0.01). About 42% <strong>of</strong> the variability in tCa was attributable<br />

to the change in the plasma TP (R 2 0.417). The<br />

correlation between tCa and Alb was significant (r 0.33;<br />

p 0.01), but it was significantly smaller than the correlation<br />

between tCa and TP ( p 0.01). Only 11% <strong>of</strong> the<br />

tCa was attributable to difference in concentration <strong>of</strong> Alb<br />

(R 2 0.108). An adjustment formula for tCa concentration<br />

in the peregrine falcon was derived on the basis <strong>of</strong> TP:<br />

Adj.tCa (mmol/L) measured tCa (mmol/L) 0.02 TP<br />

(g/L) 0.67 (Fig. 28-18 ; Lumeij et al ., 1993a ).<br />

In ostriches a significant correlation was found between<br />

tCa and TP (R 2 0.55; p 0.001). The adjustment

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