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

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Chapter | 28 Avian Clinical Biochemistry
group ranged between 184 and 465 μ g/dl. In a group of normal
cockatiels, the mean serum zinc concentration was 163 μg/dl.
It has been stated that in general blood zinc concentrations
1000 μg/dl (150μ mol/L) are considered diagnostic
and 200 μ g/dl ( 30 μ mol/L) suggest zinc poisoning in
psittacine birds ( Labonde, 1995 ).
C . Organophosphate and Carbamate
Organophosphates (OPs) and carbamates (CBMs) are
the most common causes of avian insecticide poisoning.
Poisoning occurs through inhalation or ingestion. The
mechanism of OP and CBM poisoning is acetylcholinesterase
(AChE) inhibition. The LD-50 of this group of poisons
is 10 to 20 times higher in birds than in mammals. Binding
of CBM to AChE is reversible as opposed to OP. Clinical
signs include acute anorexia, crop stasis, ptyalism, ataxia,
wing twitching, star gazing, weakness, diarrhea, prolapsed
nictitans, and muscular tremors or stiffness. Dyspnea and
bradycardia may be observed as the toxicity progresses.
In severe cases, the birds may be recumbent with varying
degrees of paralysis or seizures. An organophosphorus
ester-induced delayed neuropathy has been reported in
mammals and birds. The onset occurs 1 to 3 weeks after
exposure and is not associated with plasma cholinesterase
(ChE) inhibition. With aging of some OP compounds, a
metabolite can affect peripheral axons and myelin sheaths,
resulting in sensory and motor neuropathy. Associated
clinical signs include weakness, ataxia, and decreased proprioception
in the limbs progressing to paralysis ( LaBonde,
1992, 1995 ; Lumeij et al ., 1993b ; Porter, 1993 ).
Diagnosis of OP or CBM poisoning can be established
by AChE activity in blood, plasma, or serum. There are a
number of different test procedures, of which the results
are not interchangeable. Besides AChE, another compound
called pseudocholinesterase or butyrylcholinesterase
(BChE, EC 3.1.1.8.) is found in sera. Although its
physiological role has not been well defined, it is a useful
indicator of exposure to OP and CBM compounds ( Ludke
et al ., 1975 ; Sherman et al ., 1964 ).
Because plasma BChE activity increases with age
in nestling passerines, this might partially account for
decreasing sensitivity in older birds to OP and CBM poisoning.
Plasma BChE usually is inhibited more rapidly and
to a larger degree than brain AChE and may be scavenging
the active oxon forms of OP compounds that otherwise
might inhibit brain AChE activity. Because of the lack of
OP hydrolyzing enzymes in the plasma of many bird species
or the low affinity of this class of enzymes for OP
compounds in birds, the role of BChE in protecting individuals
becomes important ( Gard and Hooper, 1993 ).
It is important that results of ChE, AChE, or BChE
determinations are compared with results of samples from
nonexposed animals of the same species and age. Agedependent
changes in plasma ChE activities have been
reported for many avian species. Furthermore, development
patterns of plasma ChE differ between altricial and
precocial species. In contrast to plasma BChE activities
in nestlings of altricial species, plasma AChE and BChE
activity decreased significantly with age in precocial species
( Bennet and Bennet, 1991 ; Gard and Hooper, 1993 ).
Samples from cases of suspected CBM toxicity may
show normal ChE activities because of rapid regeneration,
and therefore these samples should be run as soon as possible
to be accurate. Because CBMs are reversible ChE
inhibitors in contrast to OP compounds, ChE inhibition
followed by thermal reactivation has been employed to
discriminate between these poisonings ( Hunt and Hooper
1993 ; Hunt et al ., 1993, 1995 ; Stansley, 1993 ).
Roy et al. (2005) , after studying 729 European raptors
of 20 species, reported age- and sex-related differences in
ChE activities and found a negative correlation between
ChE activity and body mass. They reported baseline values
for these raptor species to evaluate the effect of anticholinesterase
insecticides in the field.
XII . BLOOD COAGULATION
A . Introduction
Hemostatic disorders in birds have received less attention
than those in mammals, but they can be considered clinically
relevant. Although the knowledge of avian bleeding disorders
lags behind that of mammals, it was already in 1929
in chickens that the role of vitamin K in blood coagulation
was discovered in ( Dam, 1935 ). Currently avian hemostasis
research is still in its infancy, and the pathophysiology
of many clinically intriguing bleeding disorders, such as
the conure bleeding syndrome, awaits further clarification.
Although blood coagulation in birds was addressed extensively
in textbooks of avian physiology more than 30 years
ago (e.g., Sturkie and Grimminger, 1976 ), inclusion of separate
chapters on avian coagulation in clinical textbooks
was only initiated at the beginning of this century ( Espada,
2000 ; Powers, 2000 ). A brief synopsis of avian coagulation
will be presented here, followed by diagnostic tests and a
brief description of some known coagulation disorders.
B . Normal Hemostasis in Birds
When the vascular integrity in birds is disrupted, there are
several mechanisms that prevent blood loss from the circulation,
which are similar to those in mammals. In response to
small vascular defects, thrombocytes aggregate to form a vascular
plug. In larger defects, vasoconstriction reduces blood
flow to the area and the blood starts to clot. Briefly, coagulation
is a cascade of proteolytic reactions initiated through an
extrinsic or intrinsic pathway and ending in a common pathway
of which the end product is a solid fibrin plug.