Page 1012 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

944 SECTION | XIV Poisonous Plants

VetBooks.ir becomes chocolate brown in color. In sheep, the half-life when drawn into a syringe or spread on a white cloth.
However, this color change may not be as apparent with
of methemoglobinemia is approximately 1.5 h (Schneider
necropsy of animals that have been dead several hours.
and Yeary, 1975). Clinical signs such as exercise intoler-
ance appear at 30% 40% methemoglobinemia, with Three cows fed Chenopodium album hay died 30 min
death from hypoxia likely when concentrations exceed after showing ataxia, bluish-brown mucous membranes,
80% (Burrows, 1980). In nonfatal cases, a red blood cell rapid and difficult breathing, increased heart rates, tre-
intrinsic NADH-dependent diaphorase or reductase sys- mors, and coma. Brown-colored and badly coagulated
tem gradually reduces methemoglobin to hemoglobin, blood was the prominent necropsy finding. Slight pulmo-
which then is able to accept molecular oxygen and carry nary edema was prominent, and all visceral organs were
it to the tissues. hyperemic. The hay contained 1.1% nitrate and 33 ppm
nitrite (Ozmen et al., 2003). Nitrate nitrite poisoning
killed four adult alpacas and induced the abortion of a
TOXICITY
full-term fetus after access to oat hay (Avena sativa) con-
Total dietary intake of nitrate should be considered in the taining 1.95% nitrate on a dry matter basis (McKenzie
evaluation of toxic risk. Nitrate in drinking water adds to et al., 2004a). Necropsy findings were cyanosis, dark-
dietary intake. Nitrate concentrations in water in excess of colored blood, and pulmonary congestion and edema.
1000 ppm may cause nitrate poisoning in livestock. In cattle, abortions may occur in the herd 2 10 days
Nitrate level ,100 ppm in drinking water is considered after acute nitrate toxicosis. Less oxygen is available to
safe (Puls, 1994). Water source nitrate can be more toxic the fetus because of decreased vascular perfusion
than forage source, as forage nitrate must first leach from (decreased arterial pressure) and methemoglobinemia in
the plant material, allowing for more gradual increases the cow, and nitrite induces methemoglobinemia in fetal
that rumen microbes could more efficiently handle. This blood (Bruning-Fann and Kaneene, 1993). Bovine abor-
was found when nitrate salt was compared to nitrate in tion has been reported to occur with forages containing
forage, with the toxic dose of the salt form in cattle being 0.61% 1% nitrate (van’t Klooster et al., 1990).
half that of the forage nitrate (Crawford et al., 1966).
The nitrate content of plant material that is generally DIAGNOSTIC TESTING
accepted as safe for all classes of livestock is less than
0.5% on a dry weight basis. Nitrate content greater than Differential diagnoses to consider include acute toxicoses
1.0% on a dry weight basis is most likely to cause lethal caused by insecticides, carbohydrate overload, hypomag-
nitrate poisoning in ruminants, with cattle appearing to be nesemia in cattle, cyanide, blue-green algae, urea (ammo-
the most susceptible, due to feeding behavior. It is recom- nia), and potent oxidizing agents such as sodium chlorate
mended that pregnant animals not be fed forage or hay herbicide and aniline dyes. Lesions are not diagnostic.
with a nitrate content greater than 0.5% on a dry weight Blood and tissues may appear brown at time of death, but
basis, but due to known potential error in testing, some this becomes less obvious as autolysis proceeds. Dark
recommendations are to not feed pregnant animals greater blood may also suggest septicemia. Agonal hemorrhages
than 0.2% nitrate forage on a dry weight basis. The rate in the epicardium or mild pulmonary congestion/edema
of conversion of nitrate to nitrite and then to ammonia is may be present.
a limiting factor in safe utilization of nitrates by rumi- Ocular fluid is an excellent postmortem sample for
nants. Hungry animals are at greater risk, and intake of nitrate analysis and is stable at room temperatures for
dry matter from hay may be faster than from grazing. 24 h and for a week when refrigerated (Boermans, 1990).
The rumen flora can safely utilize higher amounts of Because of continued microbial metabolism after death,
nitrate if sufficient dietary energy is present to promote rumen content analysis is not recommended for suspected
reductive activity. Feeding corn-based supplements to cat- nitrate poisoning cases. Plasma and serum are also
tle reduced nitrite accumulation (Burrows et al., 1987). In acceptable samples. Ocular fluid nitrate concentrations
this study, the feeding of 3.2 kg of corn protected against are 35% lower than serum (Boermans, 1990). The diphe-
nitrate poisoning by reducing intraruminal nitrite and nylamine blue test is widely used for testing fluids and
blood methemoglobin (P , .05). plant tissues (Burrows, 1980; Bhikane and Singh, 1990).
Clinical signs of nitrate nitrite toxicosis in cattle The diazotization test has also been used (Bhikane and
include weakness, cyanosis of mucous membranes, tre- Singh, 1991). Nitrate test strips and ion- specific electro-
mors, ataxia, collapse, tachypnea, dyspnea, abortions, and des are also being utilized.
death. Affected animals may remain standing but then Normal background ocular nitrate content is generally
collapse and die within minutes. Dead animals may be ,5.0 ppm. Nitrate concentrations in ocular fluid of
found in sternal recumbency or lying on their side. Blood 10 20 ppm are indicative of excessive nitrate exposure,
is generally dark and may have an obvious brown color and concentrations greater than 20 ppm are considered