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

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Chapter | 28 Avian Clinical Biochemistry
In racing pigeons (n 24), plasma amylase and lipase
activities were determined with a Synchron CX chemistry
analyzer (Beckman Coulter, Mijdrecht, The Netherlands)
with reagents provided by the manufacturer. Lipase was
measured by a time enzymatic rate method. Briefly, 1–2
diglyceride substrate is hydrolyzed by pancreatic lipase to
2-monoglyceride and fatty acid. The change of absorbance
at 560 nm because of formation of the red quinone dimine
dye after four consecutive chemical reactions is directly
proportional to lipase activity. Amylase was measured by
the rate of formation of maltose from maltotetraose through
three coupled reactions. The change of absorbance at 340 nm
is directly proportional to amylase activity. Reference values
(inner limits of P 2.5 and P 97.5 with a probability of 90%) for
plasma amylase and lipase activities in pigeons were 382 to
556 IU/L and 0 to 5 IU/L, respectively ( Amann et al., 2006 ).
Chronic pancreatitis may results in fibrosis and decreased
production of pancreatic hormones. When insufficient pancreatic
enzymes are available in the duodenum, maldigestion
and passing of feces with excessive amylum and fat will
occur. Affected animals have voluminous, pale, or tan greasy
feces. Fat can be demonstrated by Sudan staining.
Fecal amylase and proteolytic activity were determined
in African grey parrots ( n 87) by Van der Horst and
Lumeij (unpublished observations), using radial enzyme
diffusion as reported by Westermarck and Sandholm
(1980) . Reference values (inner limits of P 2.5 to P 97.5 with a
probability of 90%) for fecal amylase were 6 to 18 mm and
for fecal trypsin 14 to 19 mm. In racing pigeons ( n 24),
these values were 13 to 16 mm and 11 to 14 mm, respectively
( Amann et al ., 2006 ). In a clinical case of exocrine
pancreatic insufficiency in a racing pigeon, which was histologically
confirmed at postmortem examination, values
for fecal amylase and proteolytic activity were 0 and 2 mm,
respectively, whereas plasma amylase and lipase activities
were within the reference limits ( Amann et al. , 2006 ) .
XI . TOXICOLOGY
A . Lead
Lead (Pb) poisoning is common in birds ( Dumonceaux and
Harrison, 1994 ; Lumeij 1985b ). A clinical diagnosis can be
made by demonstrating elevated Pb concentrations in whole
blood or by demonstrating secondary effects of Pb on various
enzymes involved in heme synthesis. Blood Pb concentrations
in clinically normal birds and in birds with signs of
Pb poisoning can be much higher than in mammals ( Lumeij,
1985b ). Blood Pb in birds without clinical signs and without
known exposure to Pb ranged between 2.5 and 180 μg/dl
(100μg/dl 4.8 μ mmol/L). Birds that had been exposed
to Pb but showed no clinical signs had Pb concentrations
ranging between 40 and 2000μ g/dl, whereas birds with
clinical signs had blood Pb concentrations ranging from
52 to 5840μ g/dl. Dieter (1979) proposed that a blood Pb
concentration of 20μ g/dl was physiologically detrimental in
canvasback ducks, Aythya valisaneria, because a significant
inhibition of δ -aminolevulinic acid dehydratase (ALA-D)
activity, was observed at these Pb concentrations. The U.S.
Fish and Wildlife Service (1986) accepted that blood Pb
concentrations 20 μ g/dl in 5% of hunter-killed or livetrapped
waterfowl indicate that some type of Pb has been
assimilated in tissues (U.S. Federal Register 29673, August
20, 1986). Draury et al . (1993) used the terms “detrimental ”
and “deleterious ” in association with blood Pb of 20μg/dl.
Although a blood Pb of 20 μ g/dl indicates increased exposure
to Pb these values are not considered harmful to animals.
The current clinical view is that blood Pb 50 μg/dl
( 2.4 μ mol/L) is generally not associated with clinical signs
and has a good prognosis, even without treatment. Lead
between 50 and 100μ g/dl is associated with mild clinical
signs and carries a good prognosis for recovery with treatment.
Clinical signs and prognosis worsen when blood Pb
exceeds 100μg/dl. When concentrations exceed 200μg/dl,
the prognosis is guarded to poor ( Degernes, 1995 ). When
clinical signs are present, blood Pb 35 μ g/dl suggests of
Pb toxicosis ( Klein and Galey, 1989 ). In psittacines, blood
Pb levels as low as 20 μ g/dl are considered suggestive for Pb
exposure ( Dumonceaux and Harrison, 1994 ).
Most of the Pb in whole blood is associated with the red
blood cells ( Buggiani and Rindi, 1980 ). The nuclear inclusions
which have been observed by electron microscopy
in nucleated erythrocytes of pigeons with high blood Pb
concentrations have led to the assumption that these could
serve as storage sites, just like the Pb inclusion bodies that
have been described in kidneys from Pb-poisoned rats. The
capacity of birds to survive high blood Pb concentrations
without overt toxicosis might be associated with these
erythrocytic inclusion bodies ( Barthalmus et al ., 1977 ).
Lead interferes with two enzymes in the hemoglobin
biosynthetic pathway: δ-aminolevulinic acid dehydratase
(ALA-D) and heme synthetase ( Fig. 28-19 ). In humans,
ALA-D inhibition occurs even at normal blood Pb levels
( McIntire et al ., 1973 ). When there is an increase in Pb,
ALA-D is uniformly low. A level 600 IU/dl excludes Pb
poisoning ( Beeson et al ., 1979 ). A significant negative correlation
exists between blood Pb and ALA-D in pigeons,
urban-dwelling humans, urban rats, and Pb dosed wildfowl,
as long as the blood Pb concentrations are moderately
elevated. If the blood Pb increases above a moderate
level blood, ALA-D activity fails to decrease further. This
has been observed in pigeons and humans ( Hutton, 1980 ).
The inhibition of ALA-D leads to accumulation of δ -aminolevulinic
acid (ALA) and excessive amounts of ALA are
excreted in the urine.
Because Pb inhibits heme synthetase, protoporphyrin IX
also accumulates in the erythrocytes. In human Pb poisoning,
free erythrocyte protoporphyrin (FEPP) is found in the range
of 300 to 3000 μg/dl (reference range 15 to 60 μ g/dl). If a
fresh wet film of blood of a patient is examined under UV