Page 759 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

720 SECTION | X Avian and Aquatic Toxicology

VetBooks.ir sodium in the feed and/or water deprivation as in com- derivative and tiamulin. This antibiotic interferes with the
metabolic degradation of monensin in the liver, causing
mercial poultry, or ingestion of saline waters or precipita-
accumulation at toxic concentrations.
tion of salt on feathers in waterfowls (Gordus et al.,
2002). The most common form of sodium associated with Excessive monensin exposure was reported in a 42-
intoxication is sodium chloride. High dietary sodium can week broiler flock due to feed mixing error. There was
be well tolerated if access to water is not restricted. high mortality and affected birds exhibited feed refusal,
A number of factors influence the toxicity of the decreased water consumption, diarrhea and severe paraly-
sodium ion, including bird age, bird species, dietary fac- sis that ranged from abnormal gait to complete inability
tors, water quality, and accessibility. Young birds are to move (Zavala et al., 2011). Another case report of
more sensitive to sodium ion toxicity, most likely due to monensin intoxication on a commercial ostrich farm in
a less-developed renal function. Turkeys are more suscep- northern Greece described similar clinical signs along
tible to intoxication than are chickens (Berger, 1993). In with elevated concentrations of serum aspartate amino-
addition, birds have less ability to excrete salts in excess transferase, creatine kinase, and lactate dehydrogenase
of water, so their ability to reduce high-plasma osmolality (Dedoussi et al., 2007). In layers, there will be a loss of
is limited. In general, the addition of 1% salt (as sodium egg production, hatchability, infertile eggs, early embry-
chloride) to poultry rations is safe, even for very young onic death, and weak ataxic chicks (Perelman and Smith,
birds. A level of 0.25% salt in drinking water is consid- 1993). Reported cases of salinomycin intoxication in birds
ered to be safe (Berger, 1993). were associated with high mortality, signs of dyspnea,
At high sodium intakes, birds develop acute, severe drowsiness, sternal recumbency with legs extended poste-
diarrhea and dehydration, dyspnea, weight loss, and die. riorly, inability to stand, stiffness, and weakness
Ascites, edema, fluid in the lungs, hydropericardium, car- (Andreasen and Schleifer, 1995). Gross postmortem find-
diac hypertrophy (right-sided in chickens and bilateral in ings may be absent or limited to hydropericardium, pale
poults), and dilatory cardiomyopathy (poults) are found myocardium, hepatic congestion and enteritis. However,
on postmortem examination. Most microscopic lesions significant findings occur histologically and, include
are secondary to cardiac failure, although bilaterally sym- extensive fragmentation and necrosis of skeletal and
metrical areas of cerebral necrosis, vascular congestion, myocardial muscle fibers (Dedoussi et al., 2007; Zavala
and edema were noted in intoxicated tom turkeys et al., 2011).
(Wages et al., 1995). Significant gross and microscopic Though avoidance of feed mixing errors and off-label
lesions in ruddy ducks intoxicated by sodium include use is the mainstay of prevention, results from few
conjunctivitis, lens opacity, cataract formation, vascular in vitro studies have been promising and show the
congestion in multiple organs, especially in the menin- protective effect of the herbal flavonolignan compound
ges; and myocardial and skeletal muscle degeneration silybin from Silybum marinum against the toxicity of sali-
(Gordus et al., 2002). nomycin, lasalocid, monensin and narasin in chicken hep-
Sodium concentrations in both the feed and the water atoma cell lines (Cybulski et al., 2015; Radko
need to be considered in assessing sodium exposure. A et al., 2013).
diagnosis of sodium ion intoxication relies on detection of
high dietary and/or water, serum, and/or brain sodium Pesticides
concentrations in conjunction with other historical, clini-
cal, and postmortem findings. Serum sodium concentra- A tabulation of the toxicity of a number of pesticides for
tions greater than 150 mEq/L are elevated, and brain birds is provided in Table 53.2.
sodium concentrations greater than 2000 ppm wet weight
are highly suggestive of intoxication (Puls, 1994).
Insecticides
Organochlorine Insecticides
Ionophores Historically, OCs were widely used from the 1940s to the
Monensin, lasalocid, salinomycin, narasin, maduramicin, 1970s in agriculture and forestry and for mosquito con-
and semduramicin are some of the ionophore antibiotics trol. The most widely used organochlorines included the
used in poultry. Accidental or intentional off-label use has dichlorodiphenylethanes (DDT, methoxychlor, and dico-
resulted in adverse reactions in adult poultry (laying fol), cyclodienes (aldrin, dieldrin, heptachlor, chlordane,
hens), ostriches, and ornamental or game birds. In addi- and endosulfan), and hexachlorocyclohexanes (lindane
tion, interactions with other drugs used in target and non- and benzene hexachloride). Although some of these insec-
target species can occur. Various antibiotics have been ticides are no longer used in the United States, Canada,
reported to potentiate ionophore toxicity. The most fre- and Europe, they continue to be used in developing coun-
quently reported drug interaction is with the pleuromotilin tries. These compounds are highly lipophilic and, in