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تحميل الدليل التدريبي

أسئلة شائعة


 

Toxic plants in KSA

Introduction

 

Poisonous
Plants



Vegetation helps sustain life. We eat many plants, herbs and so forth in our daily diet. But, we must remember to be choosy. Some plants, trees or shrubs are potential killers of man. Some part of the ornamental plants or flowers in your yard may contain deadly poison. Many poisonous plants are so common and seemingly innocuous you do not suspect their toxic qualities. For example, who would expect that the beautiful oleander bush-grown indoors and outdoors all over the country-contains a deadly heart stimulant, similar to the drug digitalis? It is easy to be deceived by plants. .one part may be edible while another is poisonous.

Introduction to Poisonous Plants

Plants contain a large number of biologically active chemicals. Some of these have been found to be extremely useful for treating various human and animal diseases. However, some plant constituents produce adverse health effects following exposure. The onset of these adverse effects can be quite sudden or take some time to develop. Fortunately, there are relatively few plants that, when ingested, cause acute life-threatening illnesses.

The diversity of chemical substances in plants is quite amazing. In many instances, the role that a particular chemical plays in the normal ecology of the plant is unknown. In many cases, the presence of certain chemicals in plants is believed to confer some degree of protection from plant predators such as insects and ruminants.

There are a number of broad categories of toxicologically significant plant constituents. These include alkaloids (basic substances with nitrogen bound in a ring structure), amino acids, peptides and proteins, glycosides (chemical groups such as cyanide linked to sugars), acids (oxalic acid), terpenes (substances that contain the branched 5-carbon skeleton of isoprene), phenolics and tanlnins, and essential oils (various steam-volatile, primarily lipophilic plant metabolites stored in special plant organs and percieved by man through the stimulation of the sense of smell)

A number of factors can contribute to an animal being poisoned by plants. Fundamentally, there is the requirement that a sensitive species of animal ingest, or otherwise be exposed to, a toxic plant at an appropriate time. There are many examples of species differences with regard to sensitivity to the toxic effects of plants. In addition, it is possible for species to adapt to a potentially toxic plant if exposure is allowed to occur over a period of time. For example, ruminants adapted to oxalate-containing plants such as Halogeton glomeratus can tolerate concentrations that are lethal to non-adapted animals .

Ingestion of a potentially toxic plant is the number one route of poisoning in animals. It is important to emphasize that many, but certainly not all, toxic plants are not very palatable. Therefore, if given the choice, animals will avoid ingesting them even though they may be prevalent in the environment of the animal. In these situations, animals will often eat these plants only when other suitable feedstuffs are not available or when the animal is not able to selectively avoid the plants. The later situation may occur when toxic plants or plant parts such as seeds are inadvertently incorporated into hays, silages, or other foodstuffs

The timing of ingestion may be critical. The concentrations of toxic constituents in plants can vary from year to year, throughout the growing season of the plant, or as a result of environmental factors such as drought. As one example, the accumulation of potentially toxic concentrations of nitrate in forages most often occurs during periods of drought that prevent the normal growth of the plants (Pfister, 1984).

The diagnosis of plant poisonings can be difficult. Ingestion of many plants produce non-specific clinical signs that must be differentiated from other disease conditions. In addition, death due to toxic plant ingestion often does not result in characteristic post-mortem lesions. Relatively few tests are available to detect plant toxins in either ante-mortem or post-mortem samples. In many cases, the best way to support a diagnosis of plant poisoning is to confirm the presence of a toxic plant in the animal's environment (this will require positive identification of the suspect plant), to confirm that the plant has been ingested (noting that the candidate plants have been chewed and/or finding plant fragments in vomitus or gastrointestinal tract samples), and to correlate clinical findings, where possible, with those know to be associated with the suspect plant.

Unfortunately, there are few antidotal therapies for treating plant poisonings. The best approach for treating intoxicated animals often involves routine decontamination procedures such as induction of emesis (in appropriate species) and the administration of activated charcoal and a cathartic to hasten elimination of the plant from the gastrointestinal tract. In addition, symptomatic and supportive care need to be provided. Obviously, continued exposure to the suspect plant should be stopped. For a few plant poisonings, specific antidotes may be indicated; the treatment of cyanide or nitrate intoxicated animals are examples (see Prunus and Nitrate-Containing Plants for specific treatment protocols).

Information on poisonous plants can be found in a number of books. In addition, veterinary toxicologists at veterinary schools and/or veterinary diagnostic laboratories can provide information and identification services.

When submitted plants for identification it is important to collect specimens of the entire plant, including the roots. Wet newspaper should be wrapped around the roots of the specimen and the specimen placed in a plastic bag (it is acceptable to bend the plant along its stem so that it will fit in the plastic bag). The specimen should then be kept chilled until it arrives at the laboratory. Alternatively, plants can be dried and pressed, although this will take more time for processing.

 

Number of plants in KSU is 2240 and the toxic plants represent 10% of them.

 

 Plants are very important for man:

       a -   as they are  source of foods, and drugs

b - also the plants are very important as ornamental   and  shade plants in houses

c- Cattle keeping

Toxicity of plants is due to

1-       Presence of toxic chemicals as alkaloids, hormones and antibiotics

2-       Presence of some metals as molybdenum, cadmium and lead

3-       Mechanical toxicity due to presence of stiff hairs, spines….

4-       Sensitivity caused by the plants due to pollen grains eg. Prosopis spicigeraالمسكيت

Distribution of toxic material in plants

In the whole plant parts e.g. Datura stramnium or in pointed hair e.g. Urtica urans…………

Strength of toxicity

-         Highly toxic e.g. lantana camnara as its green fruit is very toxic and fatal

-         Slightly toxic e.g. Medicago sativa which causes flatulence due to saponin content

-         The toxicity of the plants different according to the stage of growth e.g. Lolium tomulertum is very toxic after flowering as toxic matters are concentrated in seeds

-         Type of soil also affect on  the toxicity e.g. Solanum nigrum is more toxic in damp soil than in dry soil

-         Some plants have toxic part und other safe one e.g. Corchorus olitorius  الملوخية leaves are edible after cooking while the seeds are toxic and Carissa grandiflora الكاريسا  leaves and stems are  toxic while the fruit are edible

Definition:

Toxic plants are the plants which cause when eaten by animal or man abnormal or illness symptoms which may be fatal

Some toxic plants

Citrullus colocynthisits   نبات الحنظل       its use in treatment of constipation may leads to irritation of mucous membrane of colon (hemorrhagic colitis)

Euphoria                                نبات الاعية

Hypericum نبات العرنة                           

Psidia arabica

Conyza incana

Cleame chrysantha

Catha edulis causes side effect on blood and causes anomalous structure in fetus

The is a relationship between toxicity of plants and the presence of calcium oxalate crystals

Toxicity of plants

By touch

-         Stiff and hard spine

-         Sensitivity and burning

By eating

-         Nausea

-          Spasm

-          disturbance in breathing, nervous system and blood circulation

Phytotoxinالسموم النباتية

Toxic materials secreted by the plants inside their living tissues.

Constituents of plants

a-    Inert constituents show no any physiological effect on the body

b-   Active constituents show physiological effect on the body, the phytotoxins belong to this class of constituents

 

Importance of phytotoxins to the plants

-         Protection against bacteria

-         Chemical defense against infection

Phytotoxins are divided into according to chemical structure:

☺▬ Alkaloids

-          Indole alkaloids  e.g. lysergic acid form ergot

-         Pyrrolizidine alkaloids e.g. retrorsine  which cause depressant, loss of appetite and give bad odour from the skin

-         Pyridine alkaloids e.g. coniine  from conium maculatum

-         Isoquinoline alkaloids

-         Quinolizidine alkaloids e.g. lupinine

-         Steroidal alkaloids  e.g. tomatidine and solanine

 

☺▬ Glycosides

a-   Steridal glycoside causes tachycardia , nausea, diarrhea  and visual disturbance as digitoxin

b-    Saponin glycosides cause blood heamolysis in RBC (systemic effect), and cause inflammation and irritation of GIT when taken orally as hederagenin

c-    Anthracene glycosides cause spasm  as oloin, sennasoides

☺▬ Nitrogenous compounds NO3 and NO2 which cause abortion

☺▬ Proteins act as enzymes cause protein lysis

☺▬ Bitter principle Santonin , artemisin

☺▬ Volatile oils

☺▬ Minerals selenium cause paralysis of limb, blue colour of skin, Cu النحاس, Pbالرصاص, Cdالكادميوم , Fالفلورين, Mn المنجنيز

☺▬ Phenolics

 

Examples for toxic plants in KSA

1- Foxglove
Digitalis
Digitalis purpurea
L.
 FAMILY: Scrophulariaceae

DESCRIPTION:
Biennial herb, erect to 4 ft tall. Leaves vary with species. Flowers tubular-bell shaped, spotted on inside, borne in pendant raceme, from plant stalk. Color varies from white, yellow, lavender, violet, to purple. Wild type - purple. Fruit is a small dry capsule containing many seeds.

DISTRIBUTION:
Common flowering garden plant. Common in open rich land

TOXIC PRINCIPLES :
Toxic principles are many cardiac or steroid glycosides, including digitoxin, digoxin, and gitoxin. Dry plants still toxic, flowers, seeds, leaves, and vase water toxic.

Primary mechanim is thought to be inhibition of the Na+ - K+- ATPase. Decreases intracellular K+ levels. Leads to high grade cardiac block, and increased vagal tone. Loss of pacemaker function.

TOXICITY:
In humans toxic reactions include gastric upset, nausea, diarrhea, abdominal pain, severe headache, pulse and cardiac rhythm abnormalities, mental irregularities, drowsiness, tremors, convulsions, and death.

In livestock symptoms are similar and include bloody stools, lack of appetite, and the urge to urinate. . Lethality due to cardiac arrhythmias

TOXIC PARTS:
The herbage, both fresh and dried, contains powerful, highly toxic compounds.

  TREATMENT
Emesis if recent exposure, in animals that can vomit. Atropine for bradycardia to prevent additional vagal stimulation during passage of endotracheal tube to establish respiration. Activated charcoal, saline cathartic, cholestyramine (for enterohepatic circulation). Administration of antidigitalis antibody fragments (Digibind). Monitor potassium levels hourly. Phenytoin to to improve AV conduction, increase heart rate, treat complete heart block. Avoid calcium containing solutions.

 

 

 

2- Moon-lily
Datura
Datura inoxia

FAMILY: Solanaceae

PARTS:
All parts are poisonous~ especially seeds and leaves. Lethal dosages for cattle may be 10-14 oz (0.06-0.09% of the animal's body weight). It is estimated that 4-5 g of leaf or seeds would be fatal to a child.

TOXICITY:
 Symptoms vary in time of appearance (a few minutes for decoctions to several hours for ingestion of seeds). They include intense thirst, visual disturbance, fushed skin, and central nervous system hyperirritability. Victims become delirious, incoherent, and perform insensible antics. Heart beat may be rapid with elevated temperature. Subjects may be prone to violence, hallucination, convulsions, coma, and death, Ingestion of small amounts produces symptoms; larger amounts, death.

Symptoms in livestock approximate those in humans Postmortem: gross and histological lesions are nonspecific.

TOXIC PRINCIPLES:
Solanaceous (tropane)  alkaloids including atropine, hyosayamine (isomeric with atropine), and hyoscine (scopolamine). Datura alkaloids concentration decreases during the day but increases at night.

TREATMENT:
 Gastric lavage, emesis ; treat symptoms saw they appear, supportive therapy. Artificial respiration and oxygen: Paraldehyde (2-10 cc)IM.

 

 

 

 

3- Black nightshade
Solanum
Solanum nigrum
L —; deadly nightshade; common nightshade; garden nightshade
FAMILY: Solanaceae

DESCRIPTION :
 Annual, thornless, essentially glabrous herb, .1 to 1 m tall. Leaves alternate, sinuately or coarsely toothed, 5 to 10 cm long, 2 to 5 cm wide. Flowers white, 6 to 8 mm broad. Fruit shiny, black when ripe, several seeded, 5 to 9 mm in diameter.  

DISTRIBUTION
Found throughout the south, in gardens croplands, and the edge of woodlands.

TOXICITY
A toxic glycoalkaloid and a steroidal alkaloid, solanine and solanidine, have been isolated from this group of plants. Toxicity of a given species varies with environment, portion of plant ingested or degree of maturity. Green berries are more toxic than red or black berries which are more toxic than leaves which are more toxic than stems or roots. The berries of both Carolina horse nettle and black nightshade are green when immature. However, horse nettle berries turn yellow when mature and nightshade berries become black.

All classes of livestock and humans have been poisoned. The acutely poisoned animal is characterized by irritation of the mouth and gastrointestinal lesions or nervous signs such as lethargy, drowsiness, salivation, dyspnea, weakness, paralysis, coma, death. Chronically poisoned animals may demonstrate unthriftiness, jaundiced mucous membranes, ascites and constipation.

TOXIC PARTS:
The berries and vegetation are poisonous. The toxicity is not lost in drying and may be toxic in hay.

TOXIC PRINCIPLES:
 Solanine, a saponic glycoalkaloid that breaks down into a sugar (solanose) and an alkamine (solanidine), is responsible for poisoning. The alkamines are steroidal. Concentration of solanine may increase 10 times with maturity.

TREATMENT: Gastric lavage, emesis ; treat symptoms saw they appear, supportive therapy. Paraldehyde (2-10 cc)IM.

 

 

4- Castor bean 
 Ricinus
Ricinus communis L 
FAMILY: Euphorbiaceae

DESCRIPTION 
Large, robust, annual (in the south) or perennial (in tropics and subtropics), woody herb, to 3 m tall. Leaves alternate, up to 40 cm long, simple, palmately 7 to 9 lobed, serrate with gland-tipped teeth. Flowers green, inconspicuous; staminate flowers near the base and pistillate flowers mostly near the top of a small panicle. Fruit a three-lobed capsule with a soft, spiny exterior, 1.5 to 2 cm long; seeds three per capsule, resembling a female tick, shiny, grayish-brown mottled with reddish-brown, 10 mm long and 6 to 7 mm wide.

DISTRIBUTION

Castor bean is native to the tropics of Africa but is plated in gardens throughout the U.S. for its large, striking appearance. Found throughout our area and in the south where winters are mild; cultivated and occasionally escaping and persisting in pinelands, waste places and roadsides.

TOXICITY 
Principle poisonous found in castor bean is a phytotoxin called ricin, also termed a toxalbumin. Ricin may comprise up to 3% of the seed weight. Another phytotoxin found in castor bean is ricinine, it is reported to be goitrogenic, but the significance of this compound is not clearly established. All parts of the plants re toxic, but the most toxic are the seeds. Horses are most susceptible to poisoning but all livestock. Seeds ingested at 0.2% of body weight have cased toxicosis in cattle and 0.01% of body weight was toxic to horses. Toxicity is seen most often in spring and summer.

TOXIC PARTS:
 Seeds, and to a lesser extent foliage, are toxic; 1-3 seeds may be fatal to a child, 2-4, to an adult.

TOXIC PRINCIPLES
The highly toxic glycoprotein ricin is responsible for poisoning. This phytotoxin, a composite of various amino acids, consists of a neutral alpha-chain capable of inhibiting protein synthesis and an acidic beta-chain, which functions as a carrier and moiety that binds the toxin to cell surface. Phytotoxins may act as antigens eliciting an antibody response.

TREATMENT
Intestinal detoxificaton and intestinal protectants, administered by stomach tube are indicated. If dehydrated, large amounts of intravenous fluids assist in recovery. Ascorbic acid increases survival. Support respiration.

5- Hedera helix L
FAMILY
: Araliaceae

DISTRIBUTION:
Hedera helix
is a cultivated plant grown indoors as a pot subject or outside, usually as a wall or ground cover.

DESCRIPTION:
English ivy is a trailing or climbing vine with a diversity of leaf shapes ranging from ovate, rotund to variously 3- to 5-lobed or angled, leaves: firm, evergreen; flowers: small, greenish, produced only when the branches reach a height of more than 15 feet; sepals: 5, very short; petals: 5, fleshy; stamens: 5; ovarv: 5-celled, 1 style; fruit: a round, 3- to 5-seeded berry.

TOXIC PARTS:
The black berries and leaves of English ivy are poisonous if consumed in quantlty.

TOXICITY:
 Hedera helix is a purgative that produces local irritation, excessive salivation, nausea, excitement, difficulty in breathing, severe diarrhea, thirst, and coma.

TOXIC PRINCIPLES:
The toxic substance is hederin, a glycoside of the steroidal saponin hederagenin.

TREATMENT: -
 Gastric lavage, emesis ; paraldehyde (2-10 cc) IM; Artificial respiration and oxygen

6- Narcissus pseudo-narcissus Lالنرجس
FAMILY: Amaryllidaceous

 TOXIC PARTS:

All parts specially leaves and bulbs

TOXICITY:

Nausea , vomiting, diarrhea, convulsion

TOXIC PRINCIPLES:

Alkaloids , narcissin

TREATMENT:

Gastric lavage, emesis

 

7- Ammi majus Lالخلة الشيطانى
FAMILY: Ambelliferae (Apiaceae)

 TOXIC PARTS:

All parts

TOXICITY:

It causes for horses blindness and blurred vision

TOXIC PRINCIPLES:

Ammoidin, xanthotoxin and pergaptin. The plant contains nitrite

 

TREATMENT:

Gastric lavage, emesis

8-Apium graveolin- L الكرفس
FAMILY: Apiaceae

 TOXIC PARTS:

Aerial parts

ِTOXICITY:

It causes abortion

TOXIC PRINCIPLES:

Flavonoidal glycsides ap, flarinoniin

TREATMENT:

Gastric lavage, emesis

9-Conium maculatum- L الشوكران
FAMILY:  (Umbellifera) Apiaceae

 TOXIC PARTS:

All parts specially seeds and fruits

ِTOXICITY:

It causes drowsiness, gradual loss of sensation and movement, paralysis of muscles of limbs and chest which leads to difficulty in respiration

6 gm can kill man, the dangerous comes from that the plant leaves like that of السبانخ و البقدونس and the fruits like lemon fruits

TOXIC PRINCIPLES:

Alkaloids coniine, cicutine and conicine

TREATMENT:

Gastric lavage, emesis

Conium
Conium maculatum L.
FAMILY: Umbelliferae (Apiaceae)

and oxygen;Anti-convulsents(e.g. parental short acting barbiturates). DISTRIBUTION:
It is found in disturbed or waste areas such as roadsides and the edges of cultivated fields. Poison hemlock was introduced into North America from Europe and is and can be found in all areas of the U.S. except for dessert areas. Poison hemlock can be found growing in the same kind of habitats as the water hemlock.

DESCRIPTION
Glabrous, branching, biennial herb, to 2 m tall with smooth, purple-spotted, hollow spotted stems arising from a thick taproot. Very similar to the much more poisonous Cicuta maculata and often confused with it. However, it usually has only one fleshy taproot; there are no pithy partitions in a hollow area at the juncture of the root; stem and upper stem leaves are divided. Also, the leaf veins of the poison hemlock run to the tip of the teeth: those of the water hemlock run to the notches between the teeth. flowering umbel: 4-6 cm wide (umbels are numerous); fruit: broadly ovoid, about 3 mm, laterally constricted; petals: white

 

Toxic PARTS:
 All parts of Conium maculatum are extremely poisonous. Some studies reveal toxicosis at 0.25% (green-weight basis) of a horse's weight; 0.5% for a cow's. In contrast, experimental feeding studies on a cow showed symptoms at 2% of the animal's weight and produced death at about 4%.

TOXICITY:
Gastrointestinal irritation, bloating, rapid but feeble pulse, nervousness, trembling, staggering, coldness of thee extremities. Animals will also display evidence of muscular incoordination and appear to have great abdominal pain. In animals that die, breathing ceases due to respiratory paralysis before cardiac arrest. Unlike water hemlock convulsions do not occur after eating poison hemlock.

Teratogenic effects due to ingesting poison hemlock that occur in calves and piglets include crooked legs, cleft plate and kinked tails. Arthrogrypotic skeletal malformations occur in calves when poison hemlock is ingested by pregnant cows between 40-70 days of gestation. Similar skeletal lesions occur in pigs between days 40-61 of gestation. Cleft plates can occur in piglets if pregnant swine ingest poison hemlock between days 30-45 of gestation.

TOXIC PRINCIPLES:
 Alkaloids Gamma-coniceine, coniine, N-methylconiine, conLydrine, lambbaconiceine, and pesudoconhydrine. Toxicity levels vary with the stage of growth (time of year), plant part, and the plant's geographic location. The Conium alkaloids are similar in structure and function to nicotine. Gamma-coniceine appears to be the major alkaloid in the vegetative stage. Flowers and immature fruit contain coniine and N-methylconiine. In mature fruit the alkaloid is Nmethylconiine. The root contains the least amount of toxins; mature seeds contain the greatest. It has been shown experimentally that the toxic principles in a plant vary even from hour to hour.

TREATMENT:
 Gastric lavage, emesis ;Saline catharic;Artificial respiration

10-Catharanthus roseus- L فنكا

FAMILY:  Apocyanaceae

 TOXIC PARTS:

All parts

ِTOXICITY:

Toxemiaتسمم الدم  

TOXIC PRINCIPLES:

Alkaloids vincistine, vinblastine

TREATMENT:

Gastric lavage, emesis

11- Thevitia peruvianaالدفلة الصفراء

FAMILY:  Apocyanaceae

 TOXIC PARTS:

All parts

ِTOXICITY:

Abortion and death  

TOXIC PRINCIPLES:

Thevetoxin, kokilphin, phytosterolin

TREATMENT:

Gastric lavage, emesis

12- Lolium temulentum L  
FAMILY: Gramineae (Poaceae)

DESCRIPTION:
 Darnel is an annual grass with stems: solitary or a few clumped together, 4-8 dm tall; blades: glabrous beneath, scabrous above, 3-9 mm wide; spike: 1-2 dm; spikelets: placed edgewise to the rachis, 5-8 flowered; glume: firm, straight, 5-7 nerved, equalling or surpassing the uppermost lemma, 12-22 mm; lemmas: obtuse, awned, or awnless.

TOXIC PARTS: 
The seeds and seed heads are considered poisonous.

TOXICITY:
 In humans, darnel poisoning is characterized by the sensation of intoxication, ataxia, giddiness, apathy, various abnormal sensations, mydriasis, nausea, vomiting, gastroenteritis, and diarrhea. It is rarely fatal.

  TOXIC PRINCIPLES:
 The alkaloids temuline and loliine possibly are responsible for toxicity of darnel. It also has been suggested that toxicity may be due to a parasitic fungus living within the seed head.

TREATMENT: 1- Contact physician and /or  poison control centre

…… Poisonous plant

Scientific Name
Aconitum spp.
Common Name
Aconite,

Characteristics

Family

Ranunculaceae

Plant Description

Perennial herbs with ascending or nearly trailing stems; leaves alternate, simple, palmately 3-9-lobed; flowers white or blue-purple, the upper part hood- or helmit-like.

Origin

USA, NC; garden hybrids and cultivars

Distribution

Mountains, Piedmont.

Where Found

Forest or natural area, moist woods and along creek banks; landscape, flower garden as herbaceous perennial.

Mode

Ingestion.

Poisonous Part

All parts.

Symptoms

Burning of lips and mouth, numbness of throat; intense vomiting and diarrhea, muscular weakness and spasms, weak pulse, paralysis of the respiratory system, convulsions; may be fatal.

 

Scientific Name
Arnica montana
Common Name
Leopard's-bane, mountain tobacco, mountain snuff, arnica root

Characteristics

Family

Asteraceae

Plant Description

Herbaceous perennial with few branches; basal leaves clustered, stem leaves opposite, simple; flowers in a head, all yellow.

Origin

Europe.

Where Found

Landscape, cultivated in rock gardens or borders of flower beds.

Mode

Dermatitis, ingestion.

Poisonous Part

Flowers, roots.

Symptoms

Skin irritation upon contact. After ingestion, heart palpitation, vomiting, drowsiness, shortness of breath, and coma in children.

Toxic Principle

Helenalin.

Severity

TOXIC ONLY IF LARGE QUANTITIES EATEN. SKIN IRRITATION MINOR, OR LASTING ONLY FOR A FEW MINUTES.

 

………..'

 

 

 

 

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Mustards
Brassica
Brassica
FAMILY: Cruciferae (Brassicaceae)

DISTRIBUTION:
 Some species of Brassica are cultivated plants; others are troublesome weeds of fields, waste places, gardens, and roadsides.

DESCRIPTION:
 Taxonomically the genus has been organized in several different fashions. Most members encountered in the Commonwealth bear saccate sepals, yellow petals, and have 4 rounded staminal glands at the base of the ovary. The fruit is terminated by a conspicuous beak, sometimes containing a basal seed.

TOXIC PARTS:
Seeds and plants with seed capsules are poisonous.

TOXICITY:
 The effects of Brassica poisoning vary depending upon the species of plant consumed Brassica Kaber(DC) L. (charlock; wild mustard) is known to cause gastroenteritis, pain, salivation, diarrhea, and upper digestive tract disturbances, including irritation of the mouth. These symptoms also are associated with B. hirta Moench. (white mustard) ingestion. Some cultivated mustards such as Brassica oleracea var acephala DC (common kale), B. o. var capitata L. (cabbage), and B. o. var. gemmifera Zenker, (Brussels sprouts), cause hemolytic anemia and hemoglobinuria in some livestock. Goitrogenic substances (LS-vinyl-2-thioaxazolidone) are known in kale, cabbage, and turnip (Brassica rapa L.),

TOXIC PRINCIPLES:
The substance responsible for toxicosis is sinigrin, which in the presence of the enzyme myrosinase, is converted to glucose, allyl isothiocyanate (mustard oil), and potassium hydrogen sulfate. Mustard oils are poisonous. The toxicity, by ingestion, of allyl isothiocyanate has been determined (in cattle) to be 0.001% of the body weight. Also, mustards occasionally contain toxic concentrations of nitrate that may complicate toxicosis.

TREATMENT
treat symptoms asw they appear, supportive therapy.

Moon-lily
Datura
Datura stramonium L.Jimson-weed; thornapple; Jamestown weed
FAMILY: Solanaceae

DISTRIBUTION:
 Jimson-weed occurs over the entire state, usually as an inhabitant of dry soil and waste places, dumps, abandoned fields, and in cultivated crops, especially soybeans and corn.

DESCRIPTION:
This is an annual plant, 1.5 m tall with a pungent, "heavy" scent, often branching in two equal forks; leaves: 2 x 1.5 dm, with a few teeth; calyx: strongly angled in cross section (prismatic) and narrowly 5-winged; petals: fused into a tube, white, opening in cloudy weather or evenings, 7-10 cm long; seed pod: 3-5 cm, ovoid, with prickles, opening by 4 valves.

TOXIC PARTS:
All parts are poisonous~ especially seeds and leaves. Lethal dosages for cattle may be 10-14 oz (0.06-0.09% of the animal's body weight). It is estimated that 4-5 g of leaf or seeds would be fatal to a child.

TOXICITY:
 In the past several years Datura is one plant reported by the U.S. National Clearinghouse for Poison Control Centers as the cause of death. Overdose can occur from excessive ingestion of the herbal medicine Stramonium U.S.P., by accidental poisonings, or intentional ingestion for illicit drug use. Symptoms vary in time of appearance (a few minutes for decoctions to several hours for ingestion of seeds). They include intense thirst, visual disturbance, fushed skin, and central nervous system hyperirritability. Victims become delirious, incoherent, and perform insensible antics. Heart beat may be rapid with elevated temperature. Subjects may be prone to violence, hallucination, convulsions, coma, and death, Ingestion of small amounts produces symptoms; larger amounts, death. Symptoms in livestock approximate those in humans Postmortem: gross and histological lesions are nonspecific.

TOXIC PRINCIPLES:
Solanaceous (tropane)  alkaloids including atropine, hyosayamine (isomeric with atropine), and hyoscine (scopolamine). Datura alkaloids are useful in medicine. Total content of alkaloids in a plant may be high, varying from 0.25-.0.7%. Concentration varies in different parts of the plant, during various stages of development, and under varied growing conditions. The alkaloids are fewer following a rainy period than during clear, dry weather, and concentration decreases during the day but increases at night.

TREATMENT:
 Gastric lavage, emesis ; treat symptoms asw they appear, supportive therapy.Artificial respiration and oxygen: Paraldehyde(2-10 cc)IM.

Indian tobacco
Lobelia inflata L
FAMILY: Lobeliaceae

 Lobelia inflata is the source of the alkaloid lobeline used medicinally as a respiratory stimulant and in veterinary science as a respiratory stimulant and ruminatonic.

DISTRIBUTION:
Lobelias are found in wet soil, along streams, ponds, shores, and in swamps. They are also cultivated for garden use.

DESCRIPTION:
 In Lobelia the corolla is characteristically split to the base on the upper side; bilabiate, having 2 lobes above and below, the upper lobes erect, the lower lobes usually spread; stamens: protrude through the split in the corolla; the 2 lower stamens bearded at the tip; inflorescence: a terminal bracteate raceme, flowers alternately inserted; leaves: decurrent.

TOXIC PARTS:
 All parts of Lobelia are poisonous. Lobelia is toxic to animals at 0.5% of body weight.

TOXICITY:
Toxicosis develops within 3 days. In livestock, symptoms are sluggishness, salivation, diarrhea, anorexia, ulceration around the mouth, nasal discharges, and eventually coma. Also, lesions of hemorrhage and mild gastroenteritis may be present. In humans, symptoms include vomiting, sweating, pain, paralysis, depressed temperature, rapid but weak pulse, collapse, coma, and death.

TOXIC PRINCIPLE:
Toxins are pyridine alkaloids, especially lobeline.

TREATMENT :-  

1.      Contact physician and /or  poison control centre.

2.      Gastric lavage, emesis ; treat symptoms as they appear, supportive therapy ;   Artficial  respiration and oxygen , atropine 2 mg IM .

Rattlebox
Crotalaria
Crotalaria sagittalis
L
 FAMILY: Fabaceae (Leguminosae)

DISTRIBUTION:
 Occurs on dry open soil, waste places, and dry forest clearings.

DESCRIPTION:
 Crotalaria sagittalis is a small plant growing to less than half a meter tall, with spreading hairs; leaf stipules: decurrent on the stem; leaves: simple, entire, sessile, lanceolate flower on the stem to linear toward the top, 3-8 cm, to l.5 cm wide; inflorescence: 2-4 flowered racemes; flowers: yellow standard, 8 mm; stamens: 10, filaments fused; fruits: oblong, sessile pods, 2-3 cm. very inflated, when dry the seeds rattling in the pods; seeds: flat, kidney-shaped, brown beans, 2.5 mm long.

TOXIC PARTS:
The herbage and seeds are considered toxic. Monocrotaline is present in the entire plant.

TOXICITY:
 Livestock show signs of stupor, labored breathing, weakness, emaciation, paralysis, and death. Postmortem: gross lesions: hemorrhag, petechiae, or large ecchymoses; organ congestion; abomasum, omasum, and gallbladder are edematous; cirrhosis of liver in prolonged cases; histological lesions: pulmonary changes, including emphysema, alternate with atelectasis and hemorrhage.

TOXIC PRINCIPLES:
The presence of pyrrolizidine alkaloid monocrotaline. The additional alkaloids, fulvine and cristpatine, have been isolated and identified as macrocyclic esters of retorsine, which is also a toxic factor in the composite genus Senecio (see Arctium).

TREATMENT:
Gastric lavage, emesis ; treat symptoms asw they appear, supportive therapy.; possibly treatment with crystalline methionine.

 

 

Rhubarb
Rheum
Rheum rhaponticum
L.
FAMILY: Polygonaceae

This family of plants contains at least 40 genera and more than 800 species, all with jointed stems. Other characters include leaf stipules: united into a tubular sheath called an ocrea; sepals: petaloid; petals: absent; fruit: an achene. The Polygonaceae are not known for their poisonous members but for useful ones such as buckwheat and various ornamental plants. Many elements in the family are weedy.

DISTRIBUTION:
 Rheum rhaponticum is a cultivated plant that occasionally escapes from the garden.

DESCRIPTION
Rhubarb can be identified by leaves: large, basal, in clumps; ovate with cordate bases; leaf blades: up to 1.5 m long, margins wavy; petioles: as long as leaf blades, often red, stout; sepals: 6, greenish, whitish, or reddish; stamens: 6 (9); fruit: a 3-winged achene.

TOXIC PARTS
The flat leaf blade is toxic.

TOXICITY
Human consumption of the rhubarb leaf results in gastroenteritis, cramps. nausea, vomiting, weakness, respiratory difficulties, irritation of the mouth and throat, poor clotting of the blood, internal hemorrhaging, coma, and death. In hogs the symptoms are staggering, salivation, convulsions, and death.

TOXIC PRINCIPLES
Oxalic acid, uncharacterized soluble oxalates, and possibly other toxins are believed responsible for poisonings.

TREATMENT:
 Gasric lavage and emesis with lime water, chalk, or calcium salts; calcium gluconate, parentral fluids; Treat symptoms as they appear, supportive therapy.

Lolium
Lolium temulentum L  
FAMILY: Gramineae (Poaceae)

DISTRIBUTION
This weed of grain fields and waste places is uncommon in Pennsylvania. Distribution records indicate sporadic occurrence in the southeastern corner of the state.

DESCRIPTION:
 Darnel is an annual grass with stems: solitary or a few clumped together, 4-8 dm tall; blades: glabrous beneath, scabrous above, 3-9 mm wide; spike: 1-2 dm; spikelets: placed edgewise to the rachis, 5-8 flowered; glume: firm, straight, 5-7 nerved, equalling or surpassing the uppermost lemma, 12-22 mm; lemmas: obtuse, awned, or awnless.

TOXIC PARTS
The seeds and seed heads are considered poisonous.

TOXICITY:
 In humans, darnel poisoning is characterized by the sensation of intoxication, ataxia, giddiness, apathy, various abnormal sensations, mydriasis, nausea, vomiting, gastroenteritis, and diarrhea. It is rarely fatal.

  TOXIC PRINCIPLES:
 The alkaloids temuline and loliine possibly are responsible for toxicity of darnel. It also has been suggested that toxicity may be due to a parasitic fungus living within the seed head.

TREATMENT: 1- Contact physician and /or  poison control centre

                             2- Gastric lavage, emesis ; treat symptoms as they appear,

                               supportive   therapy ;    Artficial  respiration and oxygen

Fly amanita; fly mushroom; fly agaric
Amanita
Amanita muscaria
(Fr.) S.F. Gray
Amanita phalloides Fries—Death cap
FAMILY: Amanitaceae

DISTRIBUTION:
 The amanitas are found singly or in numbers under hardwoods and conifers from the spring through the fall.

DESCRIPTION:
A. muscaria:
cap: 8-24 cm across, convex or flat bright yellow to orange red, surface rough with white or yellow wartlike spots; gills and stem: white; stem: 8- 15 cm long and 20-30 mm thick; base of stem: bulbous; veil: white and persistent.

A. phalloides: This species is taxonomically complex, and occasionally several species are lumped under this name, The group includes A. verna (Bull ) Quel., A. virosa (Fr.) Quel, and A, bisporiger Atk. Recent evidence suggests that A. phalloides is rare and often confused with the more common A. brunnescens, which also is poisonous. True A. phalloides has a yellowish-green to green cap and white veil and gills; it is deadly poisonous. In A. brunnescens the cap is dark brown; in the deadly poisonous A. virosa the fruiting body is pure white and the cap is devoid of warts.

TOXIC PARTS:
 All parts of the amanitas are poisonous.

TOXICITY:
The characteristic, well-defined symptoms of A. muscaria poisoning may occur within 3 hours after ingestion. They include increased secretions from salivary, lacrimal, and other glands; perspiration; and possible severe gastroenteritis; much watery diarrhea plus retching and vomiting; possible labored breathing; pupils that are rarely responsive; and possible auditory or visual hallucinations or confusion occurring before or during the digestive upset. For A. muscaria, deaths are rare, but in such cases delirium is followed by convulsions, then coma with death from respiratory failure. In some severe cases, the patient may experience a profound sleep lasting a few hours, then awake without symptoms or memory of the illness that preceded.

Symptoms for the more deadly poisonous amanitas include a 10-hour lag period (6-15 hours) before onset of conditions. They begin as sudden, severe abdominal pain. vomiting, and diarrhea. Blood, mucus, and undigested food are present in vomitus and stool. Thirst, anuria, prostration. and restlessness are also present. If quantities of mushrooms are consumed, death ensues in 2 days; more typically the disease lasts 6 to 8 days before death in adults, 4 to 6 days in children. Fever, hematuria, tachycardia, hypotension, rapid volume depletion, and fluid and electrolyte imbalance also may be present.

TOXIC PRINCIPLES:
 A. muscaria.
The toxins are choline, muscarine, and muscaridine The LD50 i.v. in mice is 0.23mg/kg. A. phalloides and other deadly amanitas contain amanitine and phalloidine (complex polypeptides). The toxins amanitin and amanin, also present, are highly toxic; the LD50, i.p. in albino mice is 0.1 mg/kg; for phalloidine it is 3 3 mg/g i.m.

TREATMENT:
 A. muscaria: (Gastric lavage with 1:2,000 tannic acid or 1:10,000 potassium permanganate) or emmesis); (5 – 0.1 to 0.5 mg either IM or IV, repeated as necessary). Atropine sulfate is antidotal.

A. phalloides: Mortality is 50-90%. First empty the stomach, then: (1-1 to 2 tablespoons in H2O): corticosteroids and both peritoneal dialysis and hemodialysis to eliminate toxins and circumvent kidney failure. A high protein diet and intravenous doses of protein hydrolysate may prevent liver damage, Antiphalloidian serum is effective only when administered at the onset of symptoms; (26); thioctic acid, charcoal hemoperfusion, and vitamin C may be useful.

Ergot
Claviceps
Claviceps
spp.
 FAMILY: Ascomycetes

OCCURRENCE:
Claviceps
parasitizes the ovary of grasses, especially rye, wheat (durum is most susceptible), barley, and some wild species. Infection occurs when host flowers begin to open.

DISTRIBUTION:
Ergot occurs on pasture land grasses or hay and cereal grains from cultivated fields.

TOXIC PARTS:
The poisonous part is the sclerotium (ergot body), a grain-shaped mass that replaces the grass ovary. This varies in size from the same as the grain to 4 times larger. The fungal mass, homogeneous and white when cut open, is shed with the grass and acts as the overwintering phase of the fungus. Federal law prohibits use of cereal grains containing more than 0.3% sclerotia by weight.

TOXICITY:
Two syndromes are produced by ingestion: 1) gangrenous, and 2) convulsive. Ingestion of small amounts daily over a short period results in necrosis of tissues in the extremities, producing dry gangrene. Gangrene is caused by constriction of the blood vessels with blockage of circulation. This results in lameness, coldness, and insensitivity to pain of the affected part. In some instances, serum seepage can cause secondary infection, which may be associated with nausea, vomiting, abdominal pain. and constipation or diarrhea. Pregnant animals spontaneously abort. Mucus membranes of the oral cavity may be inflamed or damaged. In humans gastrointestinal distress and headache may be present. Fowl may lose their combs and beaks. Convulsive ergotism results from ingestion of large quantities of ergot. In addition to the above syndrome, nervous symptoms appear, which are characterized by hyperexcitability, paranoia, rapid pulse, and belligerence. In livestock, death may result from dehydration or starvation within a few days or a month. In humans, whole body spasms and delirium may be present,.

TOXIC PRINCIPLES:
Alkaloids, amines, and other organic compounds are present in ergot. The antihemorrhagic alkaloids probably are the major problem. Chemical formulas are known for two dozen alkaloids, derivatives of lysergic acid. Compounds include ergocryptine, ergocornine, ergocristine, ergotamine, ergosine, and ergonovine.

TREATMENT: Gastric lavage, emesis ; treat symptoms asw they appear, supportive therapy.

Conium
Conium maculatum L.
FAMILY: Umbelliferae (Apiaceae)

DISTRIBUTION:
It is found in disturbed or waste areas such as roadsides and the edges of cultivated fields. Poison hemlock was introduced into North America from Europe and is and can be found in all areas of the U.S. except for dessert areas. Poison hemlock can be found growing in the same kind of habitats as the water hemlock.

DESCRIPTION
Glabrous, branching, biennial herb, to 2 m tall with smooth, purple-spotted, hollow spotted stems arising from a thick taproot. Very similar to the much more poisonous Cicuta maculata and often confused with it. However, it usually has only one fleshy taproot; there are no pithy partitions in a hollow area at the juncture of the root; stem and upper stem leaves are divided. Also, the leaf veins of the poison hemlock run to the tip of the teeth: those of the water hemlock run to the notches between the teeth. flowering umbel: 4-6 cm wide (umbels are numerous); fruit: broadly ovoid, about 3 mm, laterally constricted; petals: white

 

Toxic PARTS:
 All parts of Conium maculatum are extremely poisonous. Some studies reveal toxicosis at 0.25% (green-weight basis) of a horse's weight; 0.5% for a cow's. In contrast, experimental feeding studies on a cow showed symptoms at 2% of the animal's weight and produced death at about 4%.

TOXICITY:
Gastrointestinal irritation, bloating, rapid but feeble pulse, nervousness, trembling, staggering, coldness of thee extremities. Animals will also display evidence of muscular incoordination and appear to have great abdominal pain. In animals that die, breathing ceases due to respiratory paralysis before cardiac arrest. Unlike water hemlock convulsions do not occur after eating poison hemlock.

Teratogenic effects due to ingesting poison hemlock that occur in calves and piglets include crooked legs, cleft plate and kinked tails. Arthrogrypotic skeletal malformations occur in calves when poison hemlock is ingested by pregnant cows between 40-70 days of gestation. Similar skeletal lesions occur in pigs between days 40-61 of gestation. Cleft plates can occur in piglets if pregnant swine ingest poison hemlock between days 30-45 of gestation.

TOXIC PRINCIPLES:
 Alkaloids Gamma-coniceine, coniine, N-methylconiine, conLydrine, lambbaconiceine, and pesudoconhydrine. Toxicity levels vary with the stage of growth (time of year), plant part, and the plant's geographic location. The Conium alkaloids are similar in structure and function to nicotine. Gamma-coniceine appears to be the major alkaloid in the vegetative stage. Flowers and immature fruit contain coniine and N-methylconiine. In mature fruit the alkaloid is Nmethylconiine. The root contains the least amount of toxins; mature seeds contain the greatest. It has been shown experimentally that the toxic principles in a plant vary even from hour to hour.

TREATMENT:
 Gastric lavage, emesis ;Saline catharic;Artificial respiration and oxygen;Anti-convulsents(e.g. parental short acting barbiturates).

False hellebore
Veratrum
Veratrum viride
Ait.
FAMILY: Liliaceae

DISTRIBUTION:
This plant grows in swamps, low wet places, meadows, pastures, and open woods.

DESCRIPTION:
 Veratrum viride is a coarse, tall, unbranched herb, 3 to 6 feet, perennial from a short rhizome; leaves: large (appearing pleated), alternate in 3-ranks, broad, the bases sheathing the stems; panicle: terminal, composed of greenish-yellow to purple, hairy flowers, about 1.5 cm across; tepals: 6, narrowed at base, not glandular; stamens: 6, filaments free from the perianth; ovarv: tri-lobed, each lobe terminating in a short style; fruit: an ovoid capsule, surrounded by the withered perianth; seeds: large, flat, the embryo small and surrounded by a broad wing. See Amianthium for illustration.

TOXIC PARTS:
 All parts are poisonous, especially the young, succulent growth in spring.

TOXICITY:
Species vary in physiologically active principles, yet symptoms of acute poisoning are constant: salivation, vomiting, diarrhea, stomach pains, prostration, depressed heart action, general paralysis, spasms, and dyspnea. Death may result. In addition, hallucinations, headache, and a burning sensation of mouth and throat have been reported. A species of Veratrum from western United States is known to cause congenital malformation in lambs, including cyclopia (single median eye) and cranial and lower jaw abnormalities. Ewe embryos in the primitive streak stage (12th and 14th day of gestation) develop deformities; fetal pituitary may be absent, Postmortem: gross and histological lesions: not reported in acute toxicity.

TOXIC PRINCIPLES:
 The numerous known alkaloids exist as glyco - or ester alkaloids and include jervine, pseudojervine, rubijervine, cevadine, germitrine, germidine, veratralbine, and veratroidine. Plants also may contain cardiac glycosides.

TREATMENT: Gastric lavage, emesis ; Charcoal; Atropine; hypotensive drugs.

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Cannabis  sativa
Nomenclature:
Scientific Name: Cannabis sativa L.
Vernacular name(s): marijuana
Scientific family name: Cannabinaceae

General poisoning notes:
Accidental ingestion of marijuana (Cannabis sativa) by pets is an occasional problem. Family pets or young children may accidentally ingest the plant, which may be stored in plastic bags. A dog ingested hashish brownies and then exhibited various symptoms such as hyperactivity, vomiting, somnolence, staggering, and glazed eyes. In another case, in Edmonton, a pet ferret ingested the plant and became comatose after experiencing sneezing bouts and ataxia. Although no fatalities of humans have been reported, the effects on a young child accidentally ingesting marijuana are bound to be very disturbing to the parents (Jones 1978, Smith 1988).

Geographic Information
Alberta, British, Columbia, Manitoba, Ontario, Quebec

Toxic parts:
The resins in the leaves are psychoactive in mammals, including humans. These plants are cultivated indoors and outdoors for human use. The plants can overwinter as seed in warmer parts of the country. The most common form that may be accidentally ingested by humans and pets is marijuana that has been left in houses for illegal human use.
flowers
leaves

Toxic principles:
Delta-tetrahydrocannabinol (THC) is the chemical most often cited as causing the psychoactive compound in marijuana. This chemical affects humans and many other mammals. Any children or pets that accidentally ingest quantities of marijuana may show various symptoms, including coma.

Toxicity:-
Agitation, drowsiness, gait ,unconsciousness and vomiting.

Autumn crocus
Colchicum
Colchicum autumnale
L.—
FAMILY: Liliaceae—the Lily Family (see Amianthium)

DISTRIBUTION:
Autumn crocus is cultivated around homes and in gardens. It rarely escapes and becomes naturalized.

DESCRIPTION:
 The flowers of Colchicum are chalice-shaped, with stamens: 6; and styles: 3, long and slender. The large leaves appear in the spring with the previous season’s seed-pod and die back during summer.

TOXIC PARTS:
All parts are toxic, especially the bulb and seeds, Leaves are toxic at about 0.1 % of an animal's weight.

TOXICITY:
 Toxicosis includes vomiting; purging; weak, quick pulse; gastrointestinal irritation; burning pain in mouth, throat, and stomach; and kidney and respiratory failure.

TOXIC PRINCIPLES:
 The alkaloid colchicine and related compounds are responsible for poisonings.

AFFECTED ANIMALS:
 Children have been poisoned by eating the flowers; poisoning has been reported in all classes of livestock.

TREATMENT:
 Gastric lavage, emesis ;shock tjherapy; treat symptoms asw they appear, supportive therapy.

Poison hemlock; spotted hemlock; deadly hemlock; poison parsley

Poison ivy
Rhus
Rhus radicans L.
FAMILY: Anacardiaceae

Many readers will be surprised to learn that the edible cashew nut belongs to the same family of plants as poison ivy and poison sumac. This predominantly tropical family has leaves: alternate, compound; flowers: 5-merous, polypetalous, regular, with an annular disc between the 5 stamens and ovary; ovary: 1-celled, containing I ovule; fruit: a drupe.

DISTRIBUTION:
 Rhus radicans is commonly found in disturbed habitats, food plains, cultivated fields, cemeteries, waste places, along woodland paths, margins of woodlots, fencerows, roadbanks, along streams, and in urban situations around buildings and yards.

DESCRIPTION
The species has complex and variable forms. Some are woody vines that produce aerial roots and grow by straggling and climbing over other vegetation. Ground-forms usually spread by rhizomes and develop dense colonies with a few leaves crowded near the summit. Regardless of growth habit, poison ivy always has three leaflets per leaf, with leaflets: ovate to subrotund, varying to rhombic or elliptic, terminally acute to acuminate, basally cuneate; entire to irregularly serrate or crenate; glabrous or thinly pubescent, petiolule of the terminal leaflet longer than those of the lateral leaflets; panicles: axillary, 1 dm long, bearing greenish-yellow flowers that mature into grayish white fruits, 5-6 mm; fruits: mature August through November, conspicuous all winter; birds eat the ripe seeds with impunity.

TOXIC PARTS:
 All parts of poison ivy, with the possible exception of the pollen, contain toxins that cause dermatitis. It has been suggested that extremely sensitive persons might contract poison from wind-blown pollen in spring when the plant is flowering.

TOXICITY:
 Dermatitis ranging from minor reddened and itching skin to major swelling, blisters, and weeping wounds can result from contact. Ingestion of leaves can cause irritation of the mucosa and digestive tract; gastritis and death may result. Animals probably are not as susceptible as humans to contact dermatitis due to hair and fur. Ingestion of leaves or other plant parts by livestock could be dangerous and result in death.

TOXIC PRINCIPLES:
 The toxin 3-n-pentadecylcatechol has been isolated from Rhusradicans.

TREATMENT: For dermatitis: Antihistamines; Steroidal creams;ointments for skin inflammation;  in severe cases steroid injections can reduce the reaction.

Rattlebox
Crotalaria
Crotalaria sagittalis
L
 FAMILY: Fabaceae (Leguminosae)

DISTRIBUTION:
 Occurs on dry open soil, waste places, and dry forest clearings.

DESCRIPTION:
 Crotalaria sagittalis is a small plant growing to less than half a meter tall, with spreading hairs; leaf stipules: decurrent on the stem; leaves: simple, entire, sessile, lanceolate flower on the stem to linear toward the top, 3-8 cm, to l.5 cm wide; inflorescence: 2-4 flowered racemes; flowers: yellow standard, 8 mm; stamens: 10, filaments fused; fruits: oblong, sessile pods, 2-3 cm. very inflated, when dry the seeds rattling in the pods; seeds: flat, kidney-shaped, brown beans, 2.5 mm long.

TOXIC PARTS:
The herbage and seeds are considered toxic. Monocrotaline is present in the entire plant.

TOXICITY:
 Livestock show signs of stupor, labored breathing, weakness, emaciation, paralysis, and death. Postmortem: gross lesions: hemorrhag, petechiae, or large ecchymoses; organ congestion; abomasum, omasum, and gallbladder are edematous; cirrhosis of liver in prolonged cases; histological lesions: pulmonary changes, including emphysema, alternate with atelectasis and hemorrhage.

TOXIC PRINCIPLES:
The presence of pyrrolizidine alkaloid monocrotaline. The additional alkaloids, fulvine and cristpatine, have been isolated and identified as macrocyclic esters of retorsine, which is also a toxic factor in the composite genus Senecio (see Arctium).

TREATMENT:
Gastric lavage, emesis ; treat symptoms asw they appear, supportive therapy.; possibly treatment with crystalline methionine.

Poisonous
Plants



Vegetation helps sustain life. We eat many plants, herbs and so forth in our daily diet. But, we must remember to be choosy. Some plants, trees or shrubs are potential killers of man. Some part of the ornamental plants or flowers in your yard may contain deadly poison. Many poisonous plants are so common and seemingly innocuous you do not suspect their toxic qualities.

For example, who would expect that the beautiful oleander bush-grown indoors and outdoors all over the country-contains a deadly heart stimulant, similar to the drug digitalis?

It is easy to be deceived by plants. . .one part may be edible while another is poisonous. The following chart lists some of the more common poisonous plants.

 

PLANT

TOXIC PART

SYMPTOMS

HOUSE PLANTS

Hyacinth, Narcissus, Daffodil

Bulbs

Nausea, vomiting, diarrhea. May be fatal.

Oleander

Leaves, branches

Extremely poisonous. Affects the heart, produces severe digestive upset and has caused death.

Dieffenbachia (Dumb Cane), Elephant Ear

All parts

Intense burning and irritation of the mouth and tongue. Death can occur if base of the tongue swells enough to block the air passage of the throat.

Rosary Pea, Castor Bean

Seeds

Fatal. A single Rosary Pea seed has caused death. One or two Castor Bean seeds are near the lethal dose for adults.

FLOWER GARDEN PLANTS

Larkspur

Young plant, seeds

Digestive upset, nervous excitement, depression. May be fatal.

Monkshood

Fleshy roots

Digestive upset and nervous excitement.

Autumn Crocus, Star of Bethlehem

Bulbs

Vomiting and nervous excitement.

Lily-of-the-Valley

Leaves, flowers

Irregular heart beat and pulse, usually accompanied by digestive upset and mental confusion.

Iris

Underground stems

Severe-but not usually serious-digestive upset.

Foxglove

Leaves

Large amounts cause dangerously irregular heartbeat and pulse, usually digestive upset and mental confusion. May be fatal.

Bleeding Heart

Foliage, roots

May be poisonous in large amounts. Has proved fatal to cattle.

VEGETABLE GARDEN PLANTS

Rhubarb

Leaf blade

Fatal. Large amounts of raw or cooked leaves can cause convulsions, coma, followed rapidly by death.

ORNAMENTAL PLANTS

Daphne

Berries

Fatal. A few berries can kill a child.

Wisteria

Seeds, pods

Mild to severe digestive upset. Many children are poisoned by this plant.

Golden Chain

Bean-like capsules in which the seeds are suspended

Severe poisoning. Excitement, staggering, convulsions and coma. May be fatal.

Laurels, Rhododendrons, Azaleas

All parts

Fatal. Produces nausea and vomiting, depression, difficult breathing, prostration and coma.

Jasmine

Berries

Fatal. Digestive disturbance and nervous symptoms.

Lantana Camara (Red Sage)

Green berries

Fatal. Affects lungs, kidneys, heart and nervous system. Grows in the southern U.S. And in moderate climates.

Yew

Berries, foliage

Fatal. Foliage more toxic than berries. Death is usually sudden without warning symptoms.

TREES AND SHRUBS

Wild and cultivated cherries

Twigs, foliage

Fatal. Contains a compound that releases cyanide when eaten. Gasping, excitement and prostration are common symptoms.

Oaks

Foliage, acorns

Affects kidneys gradually. Symptoms appear only after several days or weeks. Takes a large amount for poisoning.

Elderberry

All parts, especially roots

Children have been poisoned by using pieces of the pithy stems for blowguns. Nausea and digestive upset.

Black Locust

Bark, sprouts, foliage

Children have suffered nausea, weakness and depression after chewing the bark and seeds.

PLANTS IN WOODED AREAS

Jack-in-the-Pulpit

All parts, especially roots

Like Dumb Cane, contains small needle-like crystals of calcium oxalate that cause intense irritation and burning of the mouth and tongue.

Moonseed

Berries

Blue, purple color, resembling wild grapes. May be fatal.

Mayapple

Apple, foliage, roots

Contains at least 16 active toxic principles, primarily in the roots. Children often eat the apple with no ill effects, but several apples may cause diarrhea.

Mistletoe

Berries

Fatal. Both children and adults have died from eating the berries.

PLANTS IN SWAMP OR MOIST AREAS

Water Hemlock

All parts

Fatal. Violent and painful convulsions. A number of people have died from hemlock.

PLANTS IN FIELDS

Buttercups

All parts

Irritant juices may severely injure the digestive system.

Nightshade

All parts, especially the unripened berry

Fatal. Intense digestive disturbance and nervous symptoms.

Poison Hemlock

All parts

Fatal. Resembles a large wild carrot.

Jimson Weed (Thorn Apple)

All parts

Abnormal thirst, distorted sight, delirium, incoherence and coma. Common cause of poisoning. Has proved fatal.


Treat unknown plants with respect, and teach your children to do the same.

Chart reprinted from materials provided by the Texas State Department of Health and the National Safety Council

Introduction to Poisonous Plants

Plants contain a large number of biologically active chemicals. Some of these have been found to be extremely useful for treating various human and animal diseases. However, some plant constituents produce adverse health effects following exposure. The onset of these adverse effects can be quite sudden or take some time to develop. Fortunately, there are relatively few plants that, when ingested, cause acute life-threatening illnesses.

The diversity of chemical substances in plants is quite amazing. In many instances, the role that a particular chemical plays in the normal ecology of the plant is unknown. In many cases, the presence of certain chemicals in plants is believed to confer some degree of protection from plant predators such as insects and ruminants.

There are a number of broad categories of toxicologically significant plant constituents. These include alkaloids (basic substances with nitrogen bound in a ring structure), amino acids, peptides and proteins, glycosides (chemical groups such as cyanide linked to sugars), acids (oxalic acid), terpenes (substances that contain the branched 5-carbon skeleton of isoprene), phenolics and tanlnins, and essential oils (various steam-volatile, primarily lipophilic plant metabolites stored in special plant organs and percieved by man through the stimulation of the sense of smell)

A number of factors can contribute to an animal being poisoned by plants. Fundamentally, there is the requirement that a sensitive species of animal ingest, or otherwise be exposed to, a toxic plant at an appropriate time. There are many examples of species differences with regard to sensitivity to the toxic effects of plants. In addition, it is possible for species to adapt to a potentially toxic plant if exposure is allowed to occur over a period of time. For example, ruminants adapted to oxalate-containing plants such as Halogeton glomeratus can tolerate concentrations that are lethal to non-adapted animals .

Ingestion of a potentially toxic plant is the number one route of poisoning in animals. It is important to emphasize that many, but certainly not all, toxic plants are not very palatable. Therefore, if given the choice, animals will avoid ingesting them even though they may be prevalent in the environment of the animal. In these situations, animals will often eat these plants only when other suitable feedstuffs are not available or when the animal is not able to selectively avoid the plants. The later situation may occur when toxic plants or plant parts such as seeds are inadvertently incorporated into hays, silages, or other foodstuffs

The timing of ingestion may be critical. The concentrations of toxic constituents in plants can vary from year to year, throughout the growing season of the plant, or as a result of environmental factors such as drought. As one example, the accumulation of potentially toxic concentrations of nitrate in forages most often occurs during periods of drought that prevent the normal growth of the plants (Pfister, 1984).

The diagnosis of plant poisonings can be difficult. Ingestion of many plants produce non-specific clinical signs that must be differentiated from other disease conditions. In addition, death due to toxic plant ingestion often does not result in characteristic post-mortem lesions. Relatively few tests are available to detect plant toxins in either ante-mortem or post-mortem samples. In many cases, the best way to support a diagnosis of plant poisoning is to confirm the presence of a toxic plant in the animal's environment (this will require positive identification of the suspect plant), to confirm that the plant has been ingested (noting that the candidate plants have been chewed and/or finding plant fragments in vomitus or gastrointestinal tract samples), and to correlate clinical findings, where possible, with those know to be associated with the suspect plant.

Unfortunately, there are few antidotal therapies for treating plant poisonings. The best approach for treating intoxicated animals often involves routine decontamination procedures such as induction of emesis (in appropriate species) and the administration of activated charcoal and a cathartic to hasten elimination of the plant from the gastrointestinal tract. In addition, symptomatic and supportive care need to be provided. Obviously, continued exposure to the suspect plant should be stopped. For a few plant poisonings, specific antidotes may be indicated; the treatment of cyanide or nitrate intoxicated animals are examples (see Prunus and Nitrate-Containing Plants for specific treatment protocols).

Information on poisonous plants can be found in a number of books. In addition, veterinary toxicologists at veterinary schools and/or veterinary diagnostic laboratories can provide information and identification services.

When submitted plants for identification it is important to collect specimens of the entire plant, including the roots. Wet newspaper should be wrapped around the roots of the specimen and the specimen placed in a plastic bag (it is acceptable to bend the plant along its stem so that it will fit in the plastic bag). The specimen should then be kept chilled until it arrives at the laboratory. Alternatively, plants can be dried and pressed, although this will take more time for processing.

 

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