Plant Poisonings Causing Acute Respiratory Signs
Perilla frutescens (perilla mint) and moldy sweet potatoes might be expected to produce severe pulmonary edema, emphysema, and adenomatosis in goats, as in other ruminants (Linnabary et al.
1978; Belknap 2002). There is no specific therapy, and exertion by affected animals may precipitate death. Dyspnea may be a prominent sign associated with cardiotoxic effects of avocado (Persea) (Sani et al. 1991) or other plants discussed in Chapter 8. Acacia nilotica subsp. kraussiana causes methemoglobinemia, hemolysis, anoxia, and dyspnea that may be severe enough to cause abortion or death (Terblance et al. 1967).Even though cyanide and nitrate toxicoses are conditions that interfere with cellular respiration rather than affecting the respiratory tract per se, the severe dyspnea associated with these poisonings suggests respiratory tract disease.
Cyanide Poisoning
Hydrocyanic acid (HCN), or prussic acid, is present as a glycoside in certain plants. Hydrolysis in the course of wilting, frosting, or digestion within the rumen releases free HCN. A plant enzyme, glycosidase, hydrolyzes the terminal glucose on a cyanogenic glycoside such as amygdalin, producing the aglycone compound hydroxynitrile. Another enzyme catalyzes a further breakdown into HCN and benzaldehyde (Conn 1978). The cyanide is absorbed directly from the rumen.
Etiology and Epidemiology
A variety of plants are potentially cyanogenic; the level of HCN can be affected by genetic selection. Immature or rapidly growing plants, and plants heavily fertilized with nitrogen, tend to have higher concentrations of cyanogenic glycosides. Damage to the plants by drought, wilting, frosting, or chewing increases toxicity because glycoside and enzyme combine more rapidly. Other ingesta in the rumen may react with cyanide and prevent absorption.
There are few reports of cyanide poisoning in goats (Webber et al.
1985; Shaw 1986; van der Westhuysen et al. 1988; Gough 1995; Tegzes et al. 2003; Radi et al. 2004), but toxicity levels should be comparable with those reported in other ruminants. The goat's propensity for browsing and for escaping from enclosures increases the potential hazard of cyanogenic shrubs and trees. A list of some potentially toxic plants follows.• Cynodon spp. (quick grass, star grass)
• Eucalyptus cladocalyx (sugar gum)
• Heteromeles arbutifolia (toyon, California holly)
• Linum (flax)
• Lotus corniculatus (birdsfoot trefoil)
• Manihot esculenta (cassava)
• Phaseolus lunatus (lima bean - tropical varieties)
• Prunus spp. (cherries, apricots, peaches)
• Pyrus malus (apple)
• Sambucus canadensis (elderberry)
• Sorghum spp. (Sudan grass, Johnson grass)
• Suckleya suckleyana (poison suckleya)
• Triglochin maritima (arrow grass)
• Trifolium repens (white clover)
• Zea mays (corn)
Pathogenesis and Clinical Signs
The cyanide ion binds to the ferric ion in cytochrome oxidase, yielding a stable complex that cannot transport electrons in the process whereby O2 is used in metabolic respiration. Oxygen bound to hemoglobin in the blood is not available within cells; cellular asphyxiation occurs. The oxygen-laden blood is bright red, but the animal rapidly becomes severely dyspneic. Cerebral anoxia leads to the clinical signs; initial excitement and muscle tremors are followed by gasping and convulsions. Pupils are dilated. Signs are generally peracute, with death occurring within 15 minutes to a few hours after plant consumption.
Diagnosis
Venous blood is bright red in peracute cases, but cyanosis of mucous membranes supervenes if death is delayed. There may be an odor of “bitter almond” because of benzaldehyde in the rumen contents. Feed, blood, rumen contents, liver, or muscle tissue may be analyzed. Quick freezing or immersing in 1-3% mercuric chloride prevents additional release and loss of HCN from the sample.
Levels in plants of 200mg∕kg HCN or more are considered potentially toxic, and with cyanide toxic usually means lethal. A field test using picrate paper has been described (Kingsbury 1964; Radostits et al. 2007), but this detects cyanide at less than the toxic level. A more recently developed test strip uses Cyantesmo paper and is semi-quantifiable (Rella et al. 2004). Other causes of sudden death (see Chapter 16) must be considered.Treatment
Because death occurs so rapidly (often in two to three minutes), treatment is rarely possible. However, prompt IV injection of sodium nitrite (22 mg/kg) converts some hemoglobin to methemoglobin, which preferentially picks up CN ions from the cytochrome oxidase enzymes. Simultaneous sodium thiosulfate (67 mg/kg) converts cyanide to stable, less toxic thiocyanate. More recently, an increased IV dosage of sodium thiosulfate (660 mg/kg) has been proposed (Burrows and Way 1979). Oral or intrarumi- nal sodium thiosulfate (perhaps 6 g to a large goat) at hourly intervals is recommended to fix free HCN in the rumen of affected or exposed animals.
Nitrate Poisoning
Ruminant digestion converts ingested nitrates to nitrites, and then reduces the nitrites to ammonia. Nitrite is considered to be 10 times more toxic than nitrate (Kingsbury 1964; El Bahri et al. 1997).
Etiology and Epidemiology
Atmospheric nitrogen is converted to nitrate (NO3-) by nitrogen-fixing bacteria, including those associated with the roots of certain plants such as legumes. The plants can then reduce nitrates to nitrites, and eventually convert the nitrogen into plant protein. Animal wastes (urea and ammonia) can also enter into the nitrogen cycle.
Animals most often consume excess nitrates by eating plants containing increased nitrate concentrations. Water contaminated with animal wastes or runoff from fertilized fields and direct consumption of fertilizers (Issi et al. 2009) are other possible sources.
Sources of nitrate are cumulative. Some plants that may accumulate toxic levels of nitrates are listed below.• Amaranthus (pigweed) (Arguroudis et al. 1985)
• Avena sativa (oats)
• Beta vulgaris (beet)
• Brassica spp.
• Chenopodium spp. (lambsquarters, goosefoot)
• Medicago sativa (alfalfa)
• Sorghum spp. (Sudan grass, Johnson grass)
• Zea mays (corn)
Heavily fertilized soils make more nitrates available for plant uptake. Uptake is also favored by a.cid and moist soils, soils deficient in certain minerals (molybdenum, phosphorus, or sulfur), and low temperatures. Rapidly growing plants after drought or hormonal herbicide application accumulate increased nitrates. Finally, decreased light results in accumulation of nitrates within plants, because nitrate reductase enzyme requires light for normal activity. Nitrates accumulate in vegetative tis - sue rather than fruits or grains, and nitrate levels in the whole plant decrease rapidly after flowering and setting of fruit. Corn, for instance, is not dangerous after tas - seling out.
Pathogenesis and Clinical Signs
Nitrate toxicosis is caused by nitrite formation within the rumen or, occasionally, in ensiled forages. Starved animals are at greatest risk because they are less selective grazers. Also, active rumen microorganisms supplied with rapidly digestible carbohydrates (the well-fed animal) can convert nitrates to microbial protein and thereby escape toxicosis.
Nitrite is absorbed from the rumen. The nitrite causes oxidation of ferrous hemoglobin to ferric hemoglobin (methemoglobin) that cannot transport oxygen. The blood turns a dark, chocolate brown color. In addition to cyanosis, clinical signs include weakness, trembling, severe dyspnea, and frothing at the mouth.
Clinical signs are visible when 30-40% of the hemoglobin is converted to methemoglobin. Death occurs at 80-90% conversion, although this is influenced by stress and exertion. Death usually occurs within 12-24 hours after ingestion.
Plants containing more than 1% nitrates (as KNO3) on a dry weight basis and water with more than 1500 parts per million (ppm) nitrates may cause acute toxicosis (Osweiler et al. 1985). In one report, cabbages containing 6.6% nitrate on a dry matter basis caused a 78% hemoglobin fraction and death of goats (Nguta 2019). Toxicity to goats caused by low-level nitrate exposure has not been described (Mondal et al. 1999).
Diagnosis
Unless there is a history of direct nitrate consumption (e.g., with fertilizer), diagnosis usually requires laboratory confirmation. Dark brown blood and cyanotic membranes indicate the need for methemoglobin determination. Use of a phosphate buffer as a preservative is recommended if testing of heparinized blood will be delayed longer than a few hours (Osweiler et al. 1985). Nitrate levels may be determined in feed, water, rumen contents, or body fluids (including aqueous humor after death). Water-quality test strips and urinalysis strips may be of value in the field. Diphenylamine in sulfuric acid has also been used as a spot test for nitrate in plant specimens and tissue fluids (Kellerman et al. 2005). Nitrite is converted to nitrate very rapidly after death and is often undetectable in field specimens (Boermans 1990). Samples should be preserved by freezing.
Treatment
If nitrate toxicosis is likely and respiratory signs are present, the clinician should not delay therapy while awaiting laboratory confirmation. Affected animals are treated intravenously with 4-15 mg/kg of methylene blue as a 1% solution in distilled water (Burrows 1984; Mondal and Pandey 2000); this is repeated if necessary. The methylene blue is reduced in blood and body tissues to leukomethylene blue, which in turn rapidly reduces methemoglobin to hemoglobin. When methylene blue is given IV to goats, it passes readily into the milk (Ziv and Heavner 1984). In countries where methylene blue is not available as a commercial antidote, an extralabel fish tank treatment product might be used, but meat and milk withdrawals will be long (Haskell et al. 2005). Another injectable dye, tolonium chloride, has also been used successfully to treat goats with experimental nitrate toxicosis (Mondal and Pandey 2000).
Ruminal lavage with cold water or administration of oral antibiotics or a laxative may decrease additional ruminal reduction of nitrate to nitrite.