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In: A Guide
to Plant Poisoning of Animals in North America, Knight A.P. and Walter R.G. (Eds.) Plants Affecting the Blood (Last Updated:
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Table of Contents Plants - Allium
spp. (Habitat, Description, Principal Toxins, Clinical Signs,
Treatment) Glucosinolate
Poisoning (Clinical Signs, Treatment, Preventive Measures) Plants - Acer
Rubrum (Habitat, Description, Principal Toxins, Clinical Signs,
Treatment) Plants - Melilotus
Officinalis, Bracken
Fern, Brake Fern, Eagle Fern Clinical
Signs of Bracken Fern Poisoning in Cattle and Sheep Bracken
Fern Poisoning in Sheep |
A variety of plants contain compounds that damage red blood cell (RBCs)
metabolism and cell membrane integrity causing them to be removed from the
circulation by the spleen. As a result, the excess hemoglobin from the
damaged RBCs is filtered by the kidneys causing hemoglobinuria. If present in
large quantity, the hemoglobin causes the urine to become red or dark brown
in color. Plants that contain toxic compounds capable of affecting the RBCs
include onions (Allium spp.); common crop plants such as kale, rape,
turnips (Brassica spp.); and red maple (Acer rubrum). Red
colored urine may also be encountered with hairy vetch (Vicia villosa)
poisoning. In cattle, plants such as bracken fern (Pteridium aquilinum),
and sweet clover (Melilotus officinalis) inhibit normal blood clotting
with resulting hemorrhage into the urinary system (hematuria). Bracken fern
is also capable of inducing the formation of urinary bladder tumors in cattle
which may cause red-colored urine.
Onion Poisoning
Allium spp.
A. cepa - Domesticated
onion
A. canadensis - Wild
onion
A. validum - Wild
onion Liliaceae (Lily family)
Habitat
Wild onions are usually found in moist meadows, open hillsides, and in sandy
bottomlands throughout North America.
Habitat of Allium spp. - Wild onion Liliaceae (Lily
family). - To view click on
figure -
Description
Onions are herbaceous plants with bulbs and narrowly linear leaves that smell
of "onion" The leaves are sheathing, usually basal, and hollow. The
stem is simple and erect with a terminal umbel subtended by two or three
membranous bracts. The six- parted flowers may be white, purple, pink, or
green and are borne on slender pedicels (Fig.5-1). All parts
of the plant smell of onion if crushed.
Figure 5-1. Wild onion (Allium) spp. - To
view click on figure -
Principal Toxin
An alkaloid, N-propyl disulphide, present in both cultivated and wild onions,
chives, and garlic, affects the enzyme, glucose-6-phosphate dehydrogenase in
RBCs thereby interfering with the hexose monophosphate pathway [1,2].
Oxidation of hemoglobin results because there is insufficient phosphate
dehydrogenase or glutathione to protect the RBCs from oxidative injury [1]. The
oxidized hemoglobin precipitates in the RBCs to form Heinz bodies. The cells
containing Heinz bodies are removed by the spleen with the resulting anemia
being proportional to the number of Heinz bodies formed and the rate at which
the spleen removes the damaged cells. Cattle are the most susceptible to
onion poisoning; horses and dogs are intermediate; and sheep and goats are
the most resistant [3-8]. Pregnant
ewes are able to eat a diet consisting of 90 to 100 percent cull onions
without developing a severe anemia as would cattle on a ration with more than
25 percent dry matter of onions. The sheep's adaptation to onions appears to
be related to the ability of the animal's rumen microflora to rapidly change
to a population of organisms capable of reducing the sulfide in the onions [9]. Sheep
are therefore able to metabolize the sulfide in the rumen more effectively
than can cattle, thus preventing a progressive Heinz body anemia from
developing.
Dog breeds such as Akitas and Shibas with high erythrocyte levels of
reduced glutathione and potassium are especially susceptible to the hemolytic
effects of oxidants such as N-propyl disulfide [10]. Dogs
may also be poisoned after eating quantities of onion even after the plants
are cooked [11].
The severity of Heinz body anemia that develops will vary with the
quantity and the rate at which onions are consumed and the species of animal.
Diets containing more than 25 percent dry matter of onion have the potential
to cause clinical signs of anemia. Calves 6 to 12 months old consuming 8 to
15 kg/day of onions for 5 days develop characteristic Heinz body anemia [12]. The
formation of Heinz bodies in sufficient numbers to cause anemia and
hemoglobinuria may occur within 1 to 3 weeks of eating onions. Small numbers
of Heinz bodies will be formed in cattle even though the amount of onion
consumed may be less than that necessary to induce anemia.
Clinical Signs
Most onion poisoning is associated with the feeding of cull domestic onions
to animals. It is rare to encounter poisoning from wild onions. The first
noticeable sign of onion poisoning is often the presence of dark red-brown
urine (hemoglobinuria). Affected animals have pale mucous membranes and a
fast, weak pulse; they may stagger and collapse as a result of anemia. There
is frequently a distinct odor of onion on the breath, feces, urine, and milk
of poisoned animals. In severely anemic animals, additional stress and heavy
parasite infestations may be sufficient to cause death of the animal.
Lactating animals eating onions may have an onion flavor to their milk making
it undesirable for human consumption. The onion flavor disappears from the
milk after the lactating animal has been off of onions for 24 hours.
Treatment
Animals that are anemic from onion poisoning should not be stressed, and
onion feeding should be discontinued. Whole blood transfusions may be
necessary in severely anemic animals. Sheep being fed onions rarely require
any treatment even though they are anemic because they adapt to an onion diet
and do not develop a progressive Heinz body anemia that is fatal [9].
Cull onions can be a valuable food source for livestock in onion-growing
areas. Up to 25 percent dry matter of onions and can be successfully fed to
cattle in a balanced ration [12]. The
onions should be chopped and well mixed in cattle rations to avoid choking
the animals. Sheep are able to eat far higher quantities of onion than cattle
without detriment, although weight gains in feeder lambs on diets containing
more than 50 percent dry matter of onions tend to be reduced [9]. Because
cull onions consist of about 90 percent water, the total caloric intake necessary
for growth will be limited due to the limited capacity of the rumen. Growth
rates and milk production in cows may therefore be reduced if onions comprise
the bulk of an animal's diet.
Brassica Poisoning
Members of the Brassicaceae (Cruciferae), especially those grown as
crop plants (turnips, kale, rape, cabbage, cauliflower, broccoli, and
brussels sprouts) contain a variety of toxic compounds that have different
effects on animals that eat them [13-18].
Glucosinolates and sulfur-containing amino acids in these plants cause signs
of poisoning ranging from goiter, hypothyroidism, blindness, diarrhea,
red-colored urine, and pulmonary emphysema. These compounds are found in greatest
quantity in the young green plant and in the seeds. However, signs of
poisoning produced depends on the glucosinolate unique to the particular
brasicca or mustard. Hemolytic anemia occurs in cattle due to the presence of
the compound S-methy-L-cystein sulfoxide (SMCO), a sulfur-containing amino
acid unique to the family Brassicaceae [19] is
converted in the rumen to dimethyl disulphide that oxidizes hemoglobin in a
similar manner to N-propyl disulphide, a closely allied compound found in
onions. The denatured hemoglobin is detectable as Heinz bodies in the RBCs
that are removed from circulation by the spleen's reticuloendothelial system.
Hemolysis of the cells also occurs as a result of oxidative damage to the
cell membranes that result in the hemoglobinuria seen in affected animals.
The severity of poisoning is greatest in cattle that are fed kale (B.
oleracea), rape (B. napus), and turnips (B. campestris)
grown as forage crops; sheep appear to be less susceptible [19].
Cattle grazing various brassicas including turnips, rape, and canola may
experience up to a 10 percent death loss as a result of bloat and acute
pulmonary emphysema [18]. Green
turnip tops are a rich source of tryptophan that is converted in the rumen to
3-methylin- dole (a 3-substituted furan). The bioactivated furans bind with
the protein of type I cells of the lung airways, causing acute pulmonary
emphysema and edema. If the animal survives the acute stage, rapid
proliferation of cells in the lungs (type II alveolar cells) decrease normal
air exchange and cause death from an interstitial or proliferative pneumonia.
Other plants that contain similar 3-substituted furans capable of causing
acute pulmonary emphysema and edema in cattle include perilla mint (Perilla
frutescen) (Fig.5-2),
and sweet potato (Ipomoea batata).
Figure 5-2. Perilla, or purple mint (Perilla frutescens). - To view click on figure -
The toxicity of the turnip tops is markedly
reduced after they have been frozen. The turnips themselves are relatively
low in tryptopohan and are more likely the cause of thiamine deficiency
induced polioencepahalomalacia a disease characterized by blindness,
depression, and death [18]. Cattle
may concurrently develop hemolytic anemia that can be overlooked in the
presence of the other accompanying diseases. Nitrate poisoning may also
result from feeding turnips and other brassicas.
Glucosinolate Poisoning
Brassica spp. contain various glucosinolates that can cause
goiter and hypothyroidism, poor growth rates, and reproductive failure [20].
Glucosinolates are the precursors of active metabolites such as
isothiocyanates and nitriles, irritants that can cause colic and diarrhea [21]. Glucosinolate
levels are highest in seeds of brassicas, especially of the mustards, and it
is for this reason that caution should be exercised when feeding rape seed
meal to animals [20].
Decreased feed consumption, poor growth rates, and decreased milk production
have been credited to the feeding of high levels of rape seed [22]. Acute
fatal poisoning of cattle characterized by severe edema of the forestomachs
and abomasum has been reported following consumption of large quantities of
discarded mustard seed [23,24]. The
irritant effects of the isothiocyanates presumably causes vascular damage and
edema of the stomachs [23,24].
Clinical Signs
If cattle are given sudden access to turnip fields after being on relatively
dry, high roughage diets, they may develop nonfrothy bloat and acute
respiratory distress as a result of pulmonary emphysema and edema [18].
Panting, open-mouthed breathing, coughing, and frothing at the mouth are
typical of acute pulmonary emphysema. Mortality is usually high in animals
with the acute respiratory involvement. Blindness and marked depression due
to polioencephalomalacia may develop in some cattle after about a week of
eating turnips. As with onion poisoning, cattle consuming brassicas develop
hemoglobinuria, hematuria, and jaundice depending on the quantity of brassica
consumed [1].
Cattle become progressively weaker and may eventually die from severe anemia
unless they are removed from the source of the plants. Death of anemic
animals can be accelerated by stress and by concurrent parasitic diseases
that may worsen the anemia. Lactating cows fed Brassica spp. may also
have off- flavored milk due to the presence of glucosinolates.
Tansy mustard (Descurainia pinnata), a member of the Brassica
family and a common weed throughout North America, is sporadically associated
with a syndrome in cattle characterized by photosensitization involving the
nonpigmented skin around the face, neck, and udder (see Chapter 4) [26].
Feeding trials with tansy mustard, however, have been unsuccessful in
creating the disease, suggesting other factors are involved [26]. Symptoms
of poisoning appear to coincide with years in which timely rainfall results
in lush growth of tansy mustard. Blindness, protrusion of the tongue, and
difficulty in eating suggestive of polioencepalomalacia have also been
associated with cattle forced to eat nothing but tansy mustard.
Treatment
When possible the affected cattle should be removed from the source of the
brassica and provided a good-quality roughage diet. Severely anemic animals
should be carefully handled to avoid stress. Blood transfusions may be
lifesaving in animals that are severely anemic. For similar reasons, animals
with pulmonary emphysema should be handled very carefully. Large doses of
corticosteroids and diuretics, and oxygen therapy, if available and
practical, may help reduce the acute lung edema and emphysema in the early
stages of poisoning.
Cattle showing signs of blindness should be injected with large doses of thiamin (10 mg/kg body weight intravenously
every 3 to 4 hours for 2 to 3 days). Corticosteroids may be beneficial in
reducing brain edema. Rehydrating severely affected animals with large
volumes of oral fluids and providing a good-quality grass/alfalfa hay is beneficial
in treating animals with brassica poisoning.
Preventive Measures
In situations where brassicas and mustards are intended for cattle forage,
problems with bloat and pulmonary emphysema can be reduced by gradually
introducing the animals to the new food source. Waiting until after a hard
freeze will markedly reduce the risk of acute pulmonary emphysema. To reduce
the rapid consumption of the turnip tops, cattle should be fed a good-quality
roughage beforehand so as to limit turnip intake. Feeding a few pounds of
grain per head per day, along with roughages such as corn stalks prior to the
turnips works well in some circumstances. The use of antibiotics such as
monensin and lasalocid are also effective in reducing the conversion of
tryptophan to 3-methylindole, the instigator of pulmonary emphysema.
Additionally the antibiotics reduce rumen lactic acidosis and subsequent
thiamin deficiency. Monensin can be administered as part of the grain or as a
component of a liquid mineral/protein supplement [18].
Red Maple Poisoning
Acer rubrum
Aceraceae - (Maple family)
Habitat
Red maple trees are common throughout most of eastern North America and south
to Florida and Texas. They adapt to moist or dry areas and are often planted
as ornamental trees for their striking fall colors.
Habitat of Red Maple. Acer rubrum Aceraceae - Maple family. - To view click on figure -
Description
These large trees attain heights of 100 feet (30 meters) at maturity (Fig. 5-3A). Leaves
have three to five lobes and are simple, opposite with red petiole, shiny
green topside and white/gray underside (Fig. 5-3B). Leaves
turn bright red in the fall. Dense clusters of red flowers appear before
leaves, the male and female flowers being on separate trees. Fruits are red
in color and have two wings 0.75 to 1 inch (2 to 2.5 cm) long.
Figure 5-3A. Red maple tree (Acer rubrum). - To
view click on figure -
Figure 5-3B. Red maple leaves (A. rubrum). - To
view click on figure -
Principal Toxin
An unidentified toxin with oxidant properties is present in the wilted or
dried leaves of red maples [27-30].
Only the red maple (A. rubrum) and possibly closely related hybrids
are known to be toxic. Horses, ponies, and zebras appear to be the only
animals affected by the toxin in red maples [27,28,31]. The
toxin causes oxidant damage to hemoglobin resulting in the precipitation of
the oxidized hemoglobin as Heinz bodies in the RBCs. Damage apparently also
occurs to the RBC membranes, which results in hemolytic anemia [28].
Poisoning is especially likely in the fall or after a storm when leaves of
fallen branches become accessible to horses [32]. The
fresh green leaves apparently are not toxic, but once dried they may remain
toxic for up to 30 days. The bark from red maple trees is also toxic. Fatal
poisoning of ponies fed 3.0 kg of dried red maple leaves occurred in 1 to 5
days [32].
As little as 1.5 kg of dried red maple leaves will induce formation of Heinz
bodies and anemia [32].
Clinical Signs
After they eat relatively small amounts of dried red maple leaves, horses
exhibit clinical signs within 1 to 2 days. Poisoning is characterized by an
acute hemolytic anemia that causes weakness, increased respiratory and heart
rates, cyanosis, icterus, and a red-brown coloration of the urine [27-30].
Pregnant mares may abort without showing signs of hemolytic anemia [32]. Blood
changes include a marked reduction in the hematocrit, methemoglobinemia,
Heinz bodies in the erythrocytes, and depletion of erythrocyte glutathione,
the product essential to maintain hemoglobin in its reduced state [28,30]. Serum
aspartate aminotransferase, sorbitol dehydrogenase, protein, and bilirubin
blood levels are usually elevated [28-30].
A diagnosis of red maple poisoning can generally made when horses develop
an acute hemolytic anemia, with Heinz body formation, and evidence indicates
that they have had access to and have eaten wilted or dried red maple leaves.
The prognosis is always guarded to poor for horses with red maple poisoning
because of the rapid development of intravascular hemolysis, coagulopathy,
precipitation of hemoglobin in the kidneys, and vascular thrombosis [32,34].
Postmortem examination of horses fatally poisoned by red maple leaves reveals
pale organ color due to the anemia, hemorrhages on serosal surfaces, and
splenic enlargement [32]. In
acutely poisoned horses, there may be dark brown blood and brownish
discoloration of tissues due to the severe methemoglobinemia [32]. In the
acute case, there is often evidence of liver lipidosis and necrosis [31,32].
Treatment
Affected horses should be denied further access to red maple leaves and blood
transfusions given as necessary. Administration of intravenous fluids is of
benefit in preventing dehydration and maintaining kidney function [30].
Concurrent use of large doses of vitamin C (ascorbic acid) are also of
benefit [35].
Methylene blue advocated for the treatment of erythrocyte oxidant damage
should be used with caution in horses. Methylene blue is contraindicated if Heinz
bodies are already formed because it induces Heinz body formation. The dosage
of methylene blue should not exceed 8 mg/kg
body weight and should be administered slowly intravenously as a 1 percent
solution.
Prevention of red maple poisoning is best accomplished by maintaining a
good feeding program for horses and removing red maple leaves and fallen
branches from horse pens. It is inadvisable to plant red maple trees in or
closely surrounding horse enclosures.
Yellow Sweet Clover
Melilotus
officinalis
M. alba (White sweet clover) - Fabaceae
(Legume family)
Habitat
Yellow sweet clover is commonly grown in the northwestern United States and
western Canada as a forage for livestock. It has, however, become established
as a drought-tolerant weed and grows wild over much of the continent
especially along roadsides and waste areas.
Habitat of Yellow Sweet Clover. Melilotus officinalis - Fabaceae
(Legume family). - To view click on
figure -
Description
As biennials, both species grow to 5 feet (1.5 meters) in height and have
compound leaves with three leaflets that have serrated edges, with the
terminal leaflet on a stalk. The pea-like yellow flowers are produced in
axillary racemes up to 5 inches (12 to 13 cm) in length (Fig. 5-4A). White
sweet clover is very similar except for its white flowers (Fig. 5-4B). Smooth
yellow seeds are produced in pods 0.2 to 0.3 cm (2 to 3 mm) long.
Figure 5-4A. Yellow sweet clover (Melilotus officinalis). - To view click on figure -
Figure 5-4B. White sweet clover (Melilotus alba). - To view click on figure -
Principal Toxin
Yellow sweet clover in itself is not poisonous. If, however, it becomes
moldy, a variety of different fungi including Penicillium and Aspergillus,
and Mucor spp. growing on sweet clover are capable of converting
coumarin in the plant to dicoumarol (dicoumarin or dihydroxycoumarin), a
potent anticoagulant [36,37].
Other plants containing coumarin and melilotin include sweet vernal grass (Anthoxanthum
odoratum), Lespedeza stipulacea and other species of melilotus
(melilot). It is the coumarin in grass that is responsible for the smell of
freshly cut hay [37,38].
Sweet clover poisoning is clinically identical to warfarin poisoning, a
common rodenticide. Moldy sweet clover poisoning is most commonly encountered
in cattle, but occasionally horses and other livestock are susceptible to the
effects of dicoumarol [39-44].
Sheep appear quite resistant to the toxic effects of dicoumarol [41,42,44,45].
Signs of poisoning may not appear for up to 3 weeks after feeding moldy sweet
clover hay and depend on the quantity of dicoumarol consumed. Poisoning is
likely to occur when dicoumarol levels exceed 10 mg/kg of hay [45]. Hay containing
dicoumarol levels of 10 to 20 mg/kg of feed can be fed for 100 days before
poisoning develops. Feeds containing 60 to 70 mg/kg of feed can cause
poisoning in as little as 21 days [45].
Dicoumarol has strong anticoagulant properties that interferes with the
production of vitamin K and therefore affects vitamin K- dependent
coagulation factors VII, IX, and X and prothrombin. The rate of depletion of
these factors is directly related to the duration and amount of dicoumarol
ingested, usually over a period of several weeks. Affected animals, unable to
synthesize these factors, fail to stabilize fibrin necessary for normal
clotting of blood with resulting internal and external hemorrhaging. Calves
are usually more severely affected than adult cattle, and dicoumarol can
cross the placenta to affect the newborn calf [46].
Sweet clover, being a legume, can also cause acute rumen bloat in cattle,
especially if it is lush and leafy, and cattle are not accustomed to it. Like
alfalfa, sweet clover produces a frothy bloat that can cause high mortality
unless treated early.
Clinical Signs
Early signs of sweet clover poisoning are not easily recognized because
affected animals may only appear weak and depressed. The sudden appearance of
subcutaneous swellings, bleeding from the nose, and melena are common in
sweet clover poisoning. Subcutaneous hematomas, especially ventrally and over
areas that are easily traumatized, frequently develop. These fluctuant
swellings are painless and are not hot to the touch, thus differentiating
them from abscesses. Hematomas in the mesentery with resulting colic may also
develop [38].
Hemarthrosis is often seen in the carpal and hock joints. Lameness due to
massive intramuscular hemorrhage can be the primary presenting sign, and a
swollen leg can resemble blackleg, a severe myositis caused by Clostridium
chauvoei [37].
Hemorrhaging may be observed in the anterior chamber of the eye, and
hemorrhages may be seen in the mucous membranes. Vaginal hemorrhaging may be
a presenting sign in dairy cattle with sweet clover poisoning [43]. Fatal
hemorrhaging in cows at calving is a common occurrence [41].
Abdominocentesis often reveals intra-abdominal hemorrhage. The hemorrhagic
syndrome of sweet clover poisoning has been likened to hemorrhagic septicemia
due to Pasteurella hemolytica infections without the signs of
inflammation [47].
Signs of anemia including pale mucous membranes and a rapid weak pulse are a
consistent finding in sweet clover poisoning. Affected animals are afebrile
and maintain a good appetite. Mortality is usually high.
Sweet clover poisoning should be suspected when hemorrhaging is excessive
after surgical procedures such as castration and dehorning. Before any
surgical procedures are performed, it is important to ensure that animals
have not been fed sweet clover in the last month. Prothrombin times should be
determined if animals have been eating sweet clover and surgery is
contemplated. Prothrombin times above 40 seconds suggest decreased clotting
ability. Blood prothrombin, activated partial thromboplastin times, and
clotting times are markedly increased from their normal values of 9 to 12
seconds, 30 to 45 seconds, and 3 to 15 minutes, respectively.
Improperly cured or spoiled sweet clover hay and haylage is not always
toxic, but should only be used for animal feed after it has been tested for
the presence of dicoumarol. In one survey of 272 cured sweet clover hay
samples, over one-third contained more than 10 mg/kg of dicoumarol (range, 0
to 164.7 mg/kg) [48]. The
concentration of dicoumarol tends to be higher in large round bales where the
hay is more likely to have a higher moisture content [38].
Dicoumarol-containing sweet clover may be fed to livestock as long as it does
not constitute more than 25 percent of the animals' total diet, although
feeding any moldy feed is not recommended. Sweet clover hay containing less
than 20 μg/g is safe to feed to cattle. Concentrations of dicoumarol
exceeding 50 μg/g are toxic and will severely affect an animal's blood
clotting ability after 3 weeks of feeding the affected hay [52]. To
prevent the risk of moldy sweet clover poisoning, sweet clover hay or haylage
should not be fed for at least 3 weeks before parturition or elective surgery
such as castration, dehorning or tail docking. There are select varieties of
sweet clover that contain very low levels of coumarin and, therefore, hay
from these varieties is safe, even if moldy [49].
Properly cured sweet clover silage is low in dicoumarol because
dicoumarol-producing fungi require oxygen.
Treatment
Affected animals should be treated with whole blood transfusions as necessary
at the rate of 10 mL/kg body weight. Ideally, 1 mg/lb body wt of vitamin K1
should be injected to restore prothrombin time to normal within 24 hours [50,51].
However, the cost may be prohibitive and vitamin K3 (menadione sodium bisulfite) although less effective is often
administered [5].
Beneficial results can be obtained if treatment with large doses of vitamin K3 is continued for 4 to 6 days [40,50].
Supplementing the ration with vitamin K3
where dicoumarol is present is not effective in preventing poisoning [52]. If
vitamin K3 is given parenterally, the
dosage should be 1 mg/kg body weight and should not exceed 2 mg/kg body
weight. Greater than 2 mg/kg of vitamin K3
administered parenterally greatly increases the risk of vitamin K renal
toxicosis, especially in horses [50].
Bracken
Fern, Brake Fern, Eagle Fern
Pteridium aquilinum -
Polypodiacae (Fern family)
Habitat
Bracken fern is found throughout the United States and has been associated
with poisoning in cattle, sheep, pigs, horses, and humans [53,54]. In
North America bracken fern is commonly found in the eastern, intermountain
and western states, from Canada to Mexico. Its growth in the midwestern
states is sparse. Bracken fern prefers to grow in moist open woodlands with
sandy soils, often forming dense stands following clear-cutting or burning of
forests. It will grow in relatively dry soils, and because of its prolific
root system spreads rapidly to form dense monocultures to the exclusion of
any other plants.
Habitat of Bracken Fern, Brake Fern, Eagle Fern. Pteridium aquilinum - Polypodiacae
(Fern family). - To view click on
figure -
Bracken fern is also found in many parts of the
world with the majority of animal poisoning reported in England and Europe [53,54].
Description
Bracken fern is a perennial fern with a black, horizontal branching root
system often extending for several meters. Leaves arise directly from the
rhizome, are broadly triangular, up to 6.5 feet (2 meters) in height,
bipinnately compound, and heavily haired on the underside (Fig. 5-5A). The
characteristic brown reproductive spores are produced under the rolled edge
of the leaflets in late summer Fig. 5-5B.
Figure 5-5A. Bracken fern (Pteridium aquilinum). - To
view click on figure -
Figure 5-5B. Spores lining the underside of bracken fern leaflets. - To view click on figure -
Bracken
Fern Poisoning
Bracken fern has been associated with a variety of syndromes in animals, the
best recognized of which include:
- Thiamin
deficiency
- Retinal
degeneration and blindness
- Hemorrhaging
and bone marrow destruction (thrombocytopenia)
- Urinary
bladder cancer (enzootic hematuria)
- Digestive
tract cancers
In the interest of continuity, all the syndromes of bracken fern poisoning
will be discussed in this chapter and only mentioned in subsequent chapters
on plants causing digestive and urinary system diseases.
Principal Toxins
Bracken fern contains an enzyme thiaminase, which splits the essential
vitamin thiamin (B1) into its two
inactive components pyrimidine and thiazole [55].
Thiamin is essential in energy metabolism, especially in the conversion of
pyruvate to acetyl-coenzyme A, and the oxidation of α-ketoglutarate to
succinylcoenzyme A in the citric acid cycle [55]. Horses
and pigs are most susceptible to the effects of thiaminase. Ruminants are
rarely affected because they produce ample thiamin in the rumen [56-59].
Horses have to consume a diet containing 3 to 5 percent bracken fern for at
least 30 days before clinical signs appear [60]. Sheep
can be experimentally poisoned if they are fed large quantities of bracken
fern for prolonged periods [61].
Affected animals develop a thiamin deficiency that is characterized by
central nervous system depression and polioencephalomalacia. A similar
thiaminase enzyme is also found in other plants including horsetail (Equisetum
arvense), the Australian nardoo fern (Marsilea drummondii), and
the
rock fern (Cheilanthes sieberi) [62,63].
Bracken fern and rock ferns (Cheilanthes spp.) also contain
ptaquiloside, a norsesquiterpene glycoside that has carcinogenic and bone
marrow depressant activity [64-69]. All
species of bracken fern should probably be considered toxic because at least P.
aquilinum, P. esculentum, and P. revolutum are known to be
toxic [70-72].
The root rhizome is the most toxic part of the plant; the leaves are
poisonous whether green or dried. The concentration of ptaquiloside varies in
bracken fern depending on its geographic distribution. In one survey of 77
samples from plants collected worldwide, 43 percent had ptaquiloside
concentrations of over 1000 μg/g bracken [73]. Some
bracken fern samples from Australia have had as high as 12,000 μg
ptaquiloside/g of plant [73].
Ptaquiloside is transferred through the milk of animals eating bracken fern
and consequently has the potential of affecting the suckling young [73]. In
addition to ptaquiloside, bracken fern also contains various pterosides, the
toxicity of which have not been determined [55,75].
Cattle appear to be the most susceptible to the effects of ptaquiloside;
sheep are minimally affected, and horses are resistant [75]. The
newly emerging fiddleheads and fronds of bracken fern are five times as toxic
as the mature fronds and are quite palatable to cattle if other forage is
scarce. In general, cattle have to eat their weight in bracken fern over
several months to develop disease. If large quantities of fern are eaten in a
short period, cattle develop an acute, usually fatal, hemorrhagic disease due
to severe bone marrow destruction probably induced by ptaquiloside [76].
Long-term consumption of bracken fern leads to the development of tumors in
the urinary bladder (enzootic hematuria or red water disease) [72] and
possibly other parts of the digestive tract [77-79]. The
susceptibility of cattle to the carcinogenic effects of ptaquiloside is
possibly due to the fact they generally have alkaline urine. Under alkaline
conditions, ptaquiloside is converted to the active carcinogen dienone that
alkylates DNA leading to tumor formation [75].
In cattle evidence suggests that bracken fern may predispose papilloma
(wart) type 4 virus to produce malignant tumors in the mouth, esophagus, and
rumen. The compound quercetin found in bracken fern acts as a cocarcinogen
with the papilloma virus to produce the tumor [79-83]. A
variety of different tumors in people have been associated with carcinogens
in bracken fern [84-86].
Clinical Signs of Bracken Fern Poisoning in
Cattle and Sheep
Bracken fern poisoning in cattle and sheep may present in various forms
depending on the quantity and duration of consumption of the plant [53,83,87,88]. In
acute poisoning, cattle develop severe bone marrow depression that decreases
blood platelets (thrombocytopenia) and produces anemia and leukopenia. The
clinical signs that appear after animals have eaten the plant 1 to 2 months
include depression and hemorrhages on the mucous membranes of the nose and
mouth. Hemorrhaging may occur from the nose, mouth, and vagina. The anterior
chamber of the eyes may fill with blood (hyphema). Hemorrhagic diarrhea,
melena, and red urine (hematuria) are indicative of hemorrhaging into the
digestive and urinary tracts [87]. Anemia
results both from blood loss and bone marrow depression. Affected animals may
have a high temperature due to secondary bacterial infection resulting from
the severely depleted bone marrow and decreased circulating neutrophils.
Mortality is very high in animals whose leukocyte count is below 2000/μL
and platelet count less than 50,000/μL.
Enzootic Hematuria of Cattle
Enzootic hematuria (red water disease) occurs worldwide in cattle wherever
bracken fern is grazed [72,87].
Ptaquiloside is the primary carcinogen in bracken fern, and has been shown
experimentally to produce cancer of the urinary bladder if cattle consume
bracken fern for extended periods [64,71,74,80,88-91].
Small polyp-like tumors develop in the bladder and form bleeding tumor masses
(hemangiomas) that result in the formation of red urine (hematuria).
Cattle with enzootic hematuria are often first noticed when voiding
red-colored urine, which over time leads to severe blood loss and anemia.
There is no effective treatment for the bladder tumors, and usually the
animal will die from severe anemia or local tumor invasion of the tissue
around the bladder. A variety of tumor types including hemangiomas,
hemangiosarcomas, papillomas, fibromas, adenomas, and transitional cell
carcinomas have been associated with bracken fern carcinogenicity [72,92,93].
Treatment
Early treatment with blood transfusions and bone marrow stimulants may be
beneficial [87].
Batyl alcohol has been used as a bone marrow stimulant in cattle, but it is
not consistently effective when thrombocytes and leukocytes are severely
depleted [88].
Cattle have also been treated effectively before severe bone marrow depletion
has occurred by administering protamine sulfate and blood intravenously [89].
Protamine sulfate is a heparin antagonist and therefore will counteract the
increase in heparin that may occur in bracken fern poisoning. Broad-spectrum
antibiotics are indicated to help protect the animal against secondary
bacterial infections that may develop as a result of bone marrow depletion.
Diagnosis of bracken fern poisoning should be based on the history of the
fern being eaten for an extended period of time, a hemorrhagic syndrome
caused by bone marrow depletion resulting in thrombocytopenia, and
leukopenia. At postmortem examination, there is usually diffuse hemorrhaging
involving multiple organs.
Bracken Fern Poisoning in Sheep
"Bright blindness" of sheep is a syndrome of retinal degeneration
and blindness associated with grazing of bracken fern in England [94,95]. The
disease has been produced experimentally in sheep by feeding them a diet of
50 percent bracken fern for a period of 63 weeks [75]. The
blind sheep have a dilated pupil that reflects light from the depigmented
retina giving the syndrome its name. The exact cause of the retinal
depigmentation is not known, and blindness is permanent.
Bracken Fern Poisoning in Horses
Bracken fern poisoning in horses is uncommon. When encountered it is
characterized by a nervous system disease resulting from depletion of
thiamin, a vitamin essential for normal energy metabolism [53,94]. Affected
horses refuse to eat and consequently lose weight. Depression, muscle
tremors, uncoordinated gait, especially of the hind legs and paralysis are
typical of bracken fern poisoning. Horses may show colic, constipation,
hemoglobinuria, severe anemia, elevated temperature, and rapid heart rate [96].
Diagnosis of bracken fern poisoning should be based on evidence that
horses have eaten the fern, the clinical signs, and the animal's response to
thiamin therapy. Elevated serum pyruvic acid levels (normal 2 to 3
μg/dL) and decreased thiamin levels (normal 8 to 10 μg/dL) are
helpful in confirming the diagnosis. Bracken fern poisoning in horses should
be differentiated from viral encephalitis and hepatic encephalopathy, which
have similar clinical signs.
Treatment
Horses with thiamin deficiency should be treated with intravenous thiamin, 5 mg/kg body weight. This dose
should be repeated intramuscularly for several days. Horses should be
provided with a balanced diet that is free of bracken fern.
Bracken Fern Poisoning in People
The young bracken fern shoots (fiddleheads) have for years been considered a
delicacy in many Asian countries. A strong correlation appears to exist
between the chronic consumption of bracken fern shoots and the high incidence
of stomach cancer, especially in Japan [84,85].
Cooking and treating bracken fern by boiling in an alkaline solution reduces
but does not eliminate the carcinogenic properties of bracken fern [86].
Because good evidence also indicates that bracken fern causes tumors in the
esophagus, stomach, and intestine of animals, it is recommended that people
do not eat bracken fern under any circumstances.