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PLANTS-LANTANA

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Classification   |    Detailed evidence-based information

Substances Included Synonyms

Therapeutic Toxic Class

    A) Lantana camara is a garden plant/weed which has produced toxicity in both humans and animals. There are very limited reports of human toxicity reported in the literature. Historically, unripe berries were associated with increased toxicity; however, in one pediatric case series, children developed primarily mild gastrointestinal illness following ingestion of all parts of the plant. Animal poisonings are typically due to grazing on the foliage.
    B) Not all varieties of Lantana are equally toxic to animals. Varieties such as 'Common Pink' contain triterpenes that are different than lantadene A or B. Since the toxic substance in the berries is unknown, the effect of unripe berries from this variety is unknown (Frohne & Pfander, 1984).

Specific Substances

    A) Lantana camara
    1) Wild Sage
    2) Bunchberry
    3) Lantana
    4) Red Sage
    5) Yellow Sage
    Lantadene A
    1) 22-beta-angeloxy-3-oxooloean-12-en-28-oic
    2) acid
    3) Rehmannic acid
    Lantadene B
    1) 22-beta-dimethylacryloyloxy-3-oxoolean-12-
    2) en-28-oic acid

Available Forms Sources

    A) FORMS
    1) Lantana camara is a woody, shrub plant and a member of the Verbenaceae family. It has a variety of flower colors including reds, orange, white, yellow, pink, and violet. It is a common plant in tropical areas where it is more or less a weed (Gopinath & Ford, 1969). Some varieties have prickles or spines along the stems and branches (Ghisalberti, 2000). It is considered one of the 10 most noxious weeds in the world (Sharma et al, 1988). One study in India illustrated that a variety of Lantana camara with red flowers (Lantana camara var aculeata) was more toxic to animals (Thirunavukkarasu et al, 2000).
    B) USES
    1) Uses of Lantana camara include (Ghisalberti, 2000):
    1) Cancers and tumors
    2) Fever, influenza, stomachache (tea of the leaves and flowers)
    3) Sores, chicken pox, measles (poultice of leaves and flowers in Central America)
    4) Bronchitis (infusion of whole plant in Ghana)
    5) Vermifuge, ulcer treatment (leaves)
    6) Hypertension
    7) Leprosy and scabies
    2) Lantana camara is also much used as a garden and pot ornamental.

Overview

Life Support

    A) This overview assumes that basic life support measures have been instituted.

Clinical Effects

    0.2.1) SUMMARY OF EXPOSURE
    A) BACKGROUND: The species Lanta camara is part of the Verbenaceae family. The plant is a sprawling shrub with squarish prickly stems. The leaves are rough and have an aromatic odor when crushed. The flowers are brightly colored and appear in clusters. The fruit is small and turns purple-black when mature. DISTRIBUTION: The plant grows in warm weather and is found in Australia, New Zealand, India, South Africa and commonly grows in the southern United States. It some areas it may be thought of as a noxious weed.
    B) TOXICOLOGY: The leaves contain a mixture of flavonoids, lantadene A and icterogenin, while the roots contain both toxic and nontoxic taxa and oleanolic acid. The leaves and flowers may contain small amounts of bisabolene, traces of monterpenes, and sesquiterpenes. It is not known what substance produces toxic effects in humans, but it does not appear that the phototoxin or lantadene A are responsible. In animals, toxicity is likely due to lantadene A and the leaves appear to be poisonous.
    C) EPIDEMIOLOGY: Reports of human toxicity are rare. In one pediatric case series, most patient were asymptomatic and a minority developed minor effects. All parts of the plant (ripe and unripe berries, leaves, flower, stem, seeds) were associated with mild toxic effects.
    D) WITH POISONING/EXPOSURE
    1) CLINICAL EFFECTS: COMMON: Most children with exploratory exposures remain asymptomatic. In the minority that develop mild effects, gastrointestinal irritation is most common, including vomiting, nausea, abdominal pain/cramping, diarrhea, and throat/mouth irritation.
    2) SEVERE: Very rarely drowsiness, lethargy, respiratory distress, dilated pupils, ataxia, weakness and cyanosis have been reported. A single fatality has been reported but exposure was not confirmed.
    3) ONSET: 2.5 to 6 hours.

Laboratory Monitoring

    A) No routine laboratory measures are indicated for human exposures.
    B) Monitor fluid status and electrolytes in patients that develop significant vomiting or diarrhea.

Treatment Overview

    0.4.2) ORAL/PARENTERAL EXPOSURE
    A) MANAGEMENT OF MILD TO MODERATE TOXICITY
    1) Limited human data. Treatment is symptomatic and supportive. Mild gastrointestinal events including vomiting, abdominal pain or diarrhea are likely to occur. Monitor fluid status. Rehydrate with oral or IV fluids, replace electrolytes and antiemetics as needed. Monitor CNS and respiratory function.
    B) MANAGEMENT OF SEVERE TOXICITY
    1) Limited human data. Treatment is symptomatic and supportive. Based on current literature, severe toxicity is unlikely to occur. Monitor for significant CNS or respiratory insufficiency. Support airway as indicated.
    C) DECONTAMINATION
    1) PREHOSPITAL: Gastric decontamination is generally not indicated as toxicity is limited.
    2) HOSPITAL: Gastric decontamination is generally not indicated as toxicity is limited.
    3) DERMAL: Wash skin with soap and water following contact to avoid irritation from the leaves.
    D) ANTIDOTE
    1) No known antidote.
    E) AIRWAY MANAGEMENT
    1) Airway support is unlikely to be necessary. Clinical events are usually mild. Severe toxicity may produce respiratory insufficiency; support airway as needed.
    F) MONITORING OF PATIENT
    1) Routine labs are not usually necessary. Monitor fluid status and electrolytes as indicated. Monitor neurologic and respiratory function.
    G) ENHANCED ELIMINATION
    1) Enhanced elimination is unlikely to be necessary and the benefits are unknown.
    H) PATIENT DISPOSITION
    1) HOME CRITERIA: An asymptomatic child or a child with mild gastrointestinal symptoms can be managed at home with adult supervision. Symptoms maybe delayed for 2 to 6 hours after ingestion.
    2) OBSERVATION CRITERIA: Patients with persistent clinical effects (eg, vomiting or diarrhea) or more than mild toxicity should be referred to a healthcare facility. They may require supportive measures including IV fluids, electrolyte replacement and antiemetics.
    3) ADMISSION CRITERIA: Due to the minimal effects reported with most exposures, it is unlikely that patients would require hospital admission following a L camara exposure. Patients with evidence of significant neurologic toxicity (i.e., lethargy, weakness or coma) or respiratory dysfunction should be admitted.
    4) CONSULT CRITERIA: Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    I) PITFALLS
    1) Toxicity is limited, do not over treat. Limited clinical information available in the literature. Other potential unknown ingestions in a young child.
    0.4.4) EYE EXPOSURE
    A) DECONTAMINATION: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, the patient should be seen in a healthcare facility.
    0.4.5) DERMAL EXPOSURE
    A) OVERVIEW
    1) DECONTAMINATION: Remove contaminated clothing and jewelry and place them in plastic bags. Wash exposed areas with soap and water for 10 to 15 minutes with gentle sponging to avoid skin breakdown. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Range Of Toxicity

    A) TOXICITY: No specific toxic dose has been established. Limited human data. In one case series, most children remained asymptomatic and those that did not developed only mild symptoms (eg, mainly gastrointestinal) following exposure to all parts of the Lantana plant. A toddler died about 7 hours after ingesting an unknown amount of unripe Lantana berries. In 17 cases, no ingested amounts were known; however, only 4 developed symptoms.

Clinical Effects

Summary Of Exposure

    A) BACKGROUND: The species Lanta camara is part of the Verbenaceae family. The plant is a sprawling shrub with squarish prickly stems. The leaves are rough and have an aromatic odor when crushed. The flowers are brightly colored and appear in clusters. The fruit is small and turns purple-black when mature. DISTRIBUTION: The plant grows in warm weather and is found in Australia, New Zealand, India, South Africa and commonly grows in the southern United States. It some areas it may be thought of as a noxious weed.
    B) TOXICOLOGY: The leaves contain a mixture of flavonoids, lantadene A and icterogenin, while the roots contain both toxic and nontoxic taxa and oleanolic acid. The leaves and flowers may contain small amounts of bisabolene, traces of monterpenes, and sesquiterpenes. It is not known what substance produces toxic effects in humans, but it does not appear that the phototoxin or lantadene A are responsible. In animals, toxicity is likely due to lantadene A and the leaves appear to be poisonous.
    C) EPIDEMIOLOGY: Reports of human toxicity are rare. In one pediatric case series, most patient were asymptomatic and a minority developed minor effects. All parts of the plant (ripe and unripe berries, leaves, flower, stem, seeds) were associated with mild toxic effects.
    D) WITH POISONING/EXPOSURE
    1) CLINICAL EFFECTS: COMMON: Most children with exploratory exposures remain asymptomatic. In the minority that develop mild effects, gastrointestinal irritation is most common, including vomiting, nausea, abdominal pain/cramping, diarrhea, and throat/mouth irritation.
    2) SEVERE: Very rarely drowsiness, lethargy, respiratory distress, dilated pupils, ataxia, weakness and cyanosis have been reported. A single fatality has been reported but exposure was not confirmed.
    3) ONSET: 2.5 to 6 hours.

Heent

    3.4.3) EYES
    A) MYDRIASIS may be seen after eating unripe berries (Wolfson & Solomons, 1964).
    1) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara for the years 1997 to 2008, 57 children developed symptoms. Of those cases, 1 developed mydriasis after ingesting all plant parts and 1 case was unknown (Carstairs et al, 2010).
    B) PHOTOPHOBIA may be present after eating berries that are not ripe (Wolfson & Solomons, 1964).

Respiratory

    3.6.2) CLINICAL EFFECTS
    A) CYANOSIS
    1) WITH POISONING/EXPOSURE
    a) Cyanosis was reported in a patient who ingested the unripe berries (Wolfson & Solomons, 1964).
    B) DYSPNEA
    1) WITH POISONING/EXPOSURE
    a) Respirations may be slow and labored after eating berries that are not ripe (Wolfson & Solomons, 1964).

Neurologic

    3.7.2) CLINICAL EFFECTS
    A) DROWSY
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara for the years 1997 to 2008, 57 children developed symptoms. Of those cases, 3 developed drowsiness after ingesting all plant parts and 1 from ingesting ripe berries (Carstairs et al, 2010).
    B) PSYCHOMOTOR AGITATION
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara for the years 1997 to 2008, 57 children developed symptoms. Of those cases, 6 developed agitation after ingesting all plant parts, 1 from ingesting unripe berries and 2 were unknown (Carstairs et al, 2010).
    C) ATAXIA
    1) WITH POISONING/EXPOSURE
    a) Weakness and lethargy may lead to ataxia after ingestion of the unripe berries (Wolfson & Solomons, 1964; Lampe & Fagerstrom, 1968).
    D) COMA
    1) WITH POISONING/EXPOSURE
    a) Coma was reported in one fatal case of ingestion of unripe berries (Wolfson & Solomons, 1964).
    E) HYPOREFLEXIA
    1) WITH POISONING/EXPOSURE
    a) Deep tendon reflexes may be depressed after eating unripe berries (Wolfson & Solomons, 1964).

Gastrointestinal

    3.8.2) CLINICAL EFFECTS
    A) VOMITING
    1) WITH POISONING/EXPOSURE
    a) Vomiting is seen consistently with ingestion of unripe berries (Wolfson & Solomons, 1964). Ripened berries are often eaten without clinical effects (Sharma et al, 1988).
    b) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara for the years 1997 to 2008, 57 children developed symptoms. Of those cases, 30 developed vomiting after ingesting all plant parts, 13 from ripe berries, 1 from unripe berries and 5 were unknown. Vomiting was the most common clinical event observed. Overall, nausea was an infrequent finding (Carstairs et al, 2010).
    B) ABDOMINAL PAIN
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara for the years 1997 to 2008, 57 children developed symptoms. Of those cases, 8 developed abdominal pain after ingesting all plant parts, 1 from ripe berries, 2 from unripe berries and 2 were unknown. Overall, abdominal pain was a frequent clinical symptom (Carstairs et al, 2010).
    C) DIARRHEA
    1) WITH POISONING/EXPOSURE
    a) Diarrhea with green berries present in the stool may be seen after ingestion (Wolfson & Solomons, 1964).
    b) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara for the years 1997 to 2008, 57 children developed symptoms. Of those cases, 6 developed diarrhea after ingesting all plant parts and 1 from ingesting ripe berries (Carstairs et al, 2010).
    D) DISORDER OF MUCOUS MEMBRANE
    1) WITH POISONING/EXPOSURE
    a) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara for the years 1997 to 2008, 57 children developed symptoms. Of those cases, 5 developed throat/mouth irritation after ingesting all plant parts and 2 from ingesting ripe berries (Carstairs et al, 2010).

Dermatologic

    3.14.2) CLINICAL EFFECTS
    A) DERMATITIS
    1) WITH POISONING/EXPOSURE
    a) MECHANICAL DAMAGE: The leaves are rough, causing skin irritation (Morton, 1982).

Laboratory Monitoring

Monitoring Parameters Levels

    4.1.1) SUMMARY
    A) No routine laboratory measures are indicated for human exposures.
    B) Monitor fluid status and electrolytes in patients that develop significant vomiting or diarrhea.

Treatment

Life Support

    A) Support respiratory and cardiovascular function.

Patient Disposition

    6.3.1) DISPOSITION/ORAL EXPOSURE
    6.3.1.1) ADMISSION CRITERIA/ORAL
    A) Due to the minimal effects reported with most exposures, it is unlikely that patients would require hospital admission following a L camara exposure. Patients with evidence of significant neurologic toxicity (i.e., lethargy, weakness or coma) or respiratory dysfunction should be admitted.
    6.3.1.2) HOME CRITERIA/ORAL
    A) An asymptomatic child or a child with mild gastrointestinal symptoms can be managed at home with adult supervision. Symptoms maybe delayed for 2 to 6 hours after ingestion (Nelson et al, 2007).
    1) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara exposure for the years 1997 to 2008, 57 children developed symptoms. There was no statistically significant differences between the parts of the plant that were ingested or whether the berries were ripe or unripe in producing symptoms. Overall, symptoms were mild and were primarily gastrointestinal. Other symptoms included agitation, drowsiness and mydriasis. Most patients (n=590) were treated at home, only 2 patients were admitted. Of all the patients, 584 developed no symptoms, 57 had minor effects and no moderate or severe effects were reported (Carstairs et al, 2010).
    6.3.1.3) CONSULT CRITERIA/ORAL
    A) Consult a poison center or medical toxicologist for assistance in managing patients with severe toxicity or in whom the diagnosis is not clear.
    6.3.1.5) OBSERVATION CRITERIA/ORAL
    A) Patients with persistent clinical effects (eg, vomiting or diarrhea) or more than mild toxicity should be referred to a healthcare facility. They may require supportive measures including IV fluids, electrolyte replacement and antiemetics.

Monitoring

    A) No routine laboratory measures are indicated for human exposures.
    B) Monitor fluid status and electrolytes in patients that develop significant vomiting or diarrhea.

Oral Exposure

    6.5.1) PREVENTION OF ABSORPTION/PREHOSPITAL
    A) Gastric decontamination is generally not indicated as toxicity is limited.
    B) DERMAL: Wash skin with soap and water following contact to avoid irritation from the leaves.
    6.5.2) PREVENTION OF ABSORPTION
    A) GI decontamination is generally not indicated as toxicity is limited.
    6.5.3) TREATMENT
    A) SUPPORT
    1) SUMMARY
    a) Limited clinical information. Treatment is symptomatic and supportive. There is no specific antidote.
    2) CASE SERIES
    a) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara exposure for the years 1997 to 2008, only 57 children developed symptoms. There was no statistically significant differences between the parts of the plant that were ingested or whether the berries were ripe or unripe in producing symptoms. Overall, symptoms were mild and were primarily gastrointestinal (eg, vomiting, abdominal pain, nausea, mucosal irritation). Other symptoms included agitation, drowsiness and mydriasis. Seven patients developed tachycardia. Most patients (n=590) were treated at home, only 2 patients were admitted. Of all the patients, 584 developed no symptoms, 57 had minor effects and no moderate or severe effects were reported (Carstairs et al, 2010).

Eye Exposure

    6.8.1) DECONTAMINATION
    A) EYE IRRIGATION, ROUTINE: Remove contact lenses and irrigate exposed eyes with copious amounts of room temperature 0.9% saline or water for at least 15 minutes. If irritation, pain, swelling, lacrimation, or photophobia persist after 15 minutes of irrigation, an ophthalmologic examination should be performed (Peate, 2007; Naradzay & Barish, 2006).

Dermal Exposure

    6.9.1) DECONTAMINATION
    A) DECONTAMINATION: Remove contaminated clothing and wash exposed area thoroughly with soap and water for 10 to 15 minutes. A physician may need to examine the area if irritation or pain persists (Burgess et al, 1999).

Abstracts

Case Reports

    A) PEDIATRIC
    1) A 2.5-year-old, 35 pound, healthy girl was known to have eaten an unknown number of unripe Lantana berries. About 6 hours after ingestion she became lethargic, weak, vomited, ataxic and unconscious. In the emergency department, she was found to be comatose with depressed respiration, pinpoint pupils and cyanosis. She was not lavaged, but was given adrenal steroids, epinephrine, oxygen and provided supportive care. She died about 90 minutes after arrival (Wolfson & Solomons, 1964).

Range Of Toxicity

Summary

    A) TOXICITY: No specific toxic dose has been established. Limited human data. In one case series, most children remained asymptomatic and those that did not developed only mild symptoms (eg, mainly gastrointestinal) following exposure to all parts of the Lantana plant. A toddler died about 7 hours after ingesting an unknown amount of unripe Lantana berries. In 17 cases, no ingested amounts were known; however, only 4 developed symptoms.

Minimum Lethal Exposure

    A) SUMMARY
    1) No specific toxic dose has been established in humans.
    B) CASE REPORT
    1) A 2.5-year-old, 35 pound, healthy girl was known to have eaten an unknown number of unripe Lantana berries. About 6 hours after ingestion she became lethargic, weak, vomited, became ataxic and then unconscious. In the emergency department, she was found to be comatose with depressed respiration, pinpoint pupils and cyanosis. She was not lavaged, but was given adrenal steroids, epinephrine, oxygen and provided supportive care. She died about 90 minutes after arrival (Wolfson & Solomons, 1964).

Maximum Tolerated Exposure

    A) SUMMARY
    1) The amount of lantadenes found in a toxic dose of Lantana leaves is estimated to be 3 mg/kg (Ghisalberti, 2000).
    B) CASE SERIES
    1) CASE SERIES: In a retrospective review of the California Poison Control System database of pediatric (ages 1 to 16 years; mean 2.5 years) cases (n=641) of L. camara exposure for the years 1997 to 2008, only 57 children (9%) developed symptoms. There was no statistically significant differences between the parts of the plant that were ingested or whether the berries were ripe or unripe in producing symptoms. Overall, symptoms were mild and were primarily gastrointestinal (eg, vomiting, abdominal pain, nausea, mucosal irritation). Other symptoms included agitation, drowsiness and mydriasis. Seven patients developed tachycardia. Most patients (n=590) were treated at home, only 2 patients were admitted. Of all the patients, 584 developed no symptoms, 57 had minor effects and no moderate or severe effects were reported (Carstairs et al, 2010).
    2) In a case series (n=17), the amount of Lantana ingested was unknown; however, only 4 cases went on to develop symptoms (Wolfson & Solomons, 1964).

Pharmacology Toxicology

Pharmacologic Mechanism

    A) Lantana camara has been shown to have antimalarial properties (Weenen et al, 1990).
    B) An alkaloid fraction from the leaves decreased blood pressure, accelerated deep respirations, and caused shivering in dogs. However, these claims have not been verified (Ghisalberti, 2000).
    C) Pentacyclic triterpenes have antibacterial, antiviral, antiinflammatory, and cyclooxygenase isoenzyme inhibiting activity (Ghisalberti, 2000).
    D) Tetracyclic triterpenes experimentally show increased coagulation time and prothrombin time, decreased blood sedimentation time, and decreased plasma protein and fibrinogen (Ghisalberti, 2000).
    E) Iridoid glycosides experimentally show cardiovascular, antihepatotoxic, choleretic, hypoglycemic, antiinflammatory, antispasmolytic, antitumor, and antiviral actions (Ghisalberti, 2000).
    F) Furanonaphthoquinones are cytotoxic to various tumor cell lines (Ghisalberti, 2000).
    G) Phenyl ethanoid glycosides are inhibitors of protein kinase C and aldolase reductase and lipid peroxidation. These compounds may have immunomodulating activity, immunosuppressive properties, and anti-tremor effects (Ghisalberti, 2000).

Toxicologic Mechanism

    A) TOXIC COMPONENTS
    1) TOXICOLOGY: The toxin is UNKNOWN. It does not appear that the phototoxin or lantadene A produce toxicity in humans as reported in some publications. In animals, toxicity is likely due to lantadene A and the leaves appear to be poisonous (Nelson et al, 2007).
    2) There have been limited case reports that the unripe berries contain an atropine-like substance (lantadene), which may result in acute symptoms resembling anticholinergic poisoning. However, these compounds have not been isolated from lantana. TOXIC PART: Unripened or immature berries are poisonous (Nelson et al, 2007). In one study only 57 of 641 children exposed to lantana developed even mild symptoms, and there was no difference in the frequency or severity of effects between those that ingested ripe and unripe berries. In addition, all parts of the plant (ie, leaves, flower, stem, seeds) produced similar rates and types symptoms which were mainly gastrointestinal or mucosal irritation (Carstairs et al, 2010).
    3) Lantadenes: Lantadene A and B have both been identified, but depending on the study they have been shown either to be hepatotoxic or non-hepatotoxic. It would appear that purified lantadene A and B are not toxic, whereas reduced lantadene A may be. It may be that another impurity is the liver toxin, since some studies showed that even reduce lantadene A is not hepatotoxic (Sharma et al, 1988; Sharma, 1986).
    4) Lantadene A has 2 polymorphic forms. Form I was non-toxic when given to guinea pigs orally, form 2 induced icterus, hepatomegaly, and increased plasma bilirubin and acid phosphatase activity (Sharma et al, 1991).
    5) Lancamarone: Is a fish poison that has not been studied in regard to its hepatotoxicity or mammalian toxicity (Nigam et al, 1957).

Physicochemical

Physical Characteristics

    A) Lantadene A: needle shaped crystals
    B) Lantadene B: prism-like crystals.
    C) Lantana toxins are similar to cholesterol in both polarity and chromatographic profiles (Sharma et al, 1988; Sharma, 1986; Sharma & Makkar, 1980).

Molecular Weight

    A) Not applicable

Animal Toxicology

Clinical Effects

    11.1.2) BOVINE/CATTLE
    A) SUMMARY - Toxicity, following Lantana camara ingestions, occur primarily in cattle, sheep, and goats. Not all species of L. camara are toxic. In general, photosensitive dermatitis is the most prominent clinical sign following intoxication and may occur within 1 to 2 days and may progress to skin necrosis. Jaundice may occur with 2 to 3 days post-ingestion and anorexia may occur with 1 day post-ingestion. Severely poisoned animals may die within 2 days post-ingestion, although death usually occurs 1 to 3 weeks after poisoning (Ghisalberti, 2000).
    B) Cattle poisoned by Lantana showed osmotic fragility of erythrocytes. Bilirubin content in fatal cases was 5 to 50 times the normal value (Sharma et al, 1981).
    C) Ten of 91 cattle died after grazing, for several days, in a field containing Lantana camara. The affected animals exhibited signs of anorexia, severe depression, ruminal stasis, black soft feces, and yellow discoloration of mucus membranes. Necropsies showed swollen and discolored livers, edematous gallbladders containing pale green bile, bilateral perirenal edema, moderately congested and edematous abomasal and intestinal mucosa, with dark brown to black discoloration of the contents of the abomasum and the small and large intestines (Fourie et al, 1987).
    11.1.4) CAPRINE/GOAT
    A) SUMMARY - Toxicity, following Lantana camara ingestions, occur primarily in goats, cattle, and sheep. Not all species of L. camara are toxic. In general, photosensitive dermatitis is the most prominent clinical sign following intoxication and may occur within 1 to 2 days and may progress to skin necrosis. Jaundice may occur with 2 to 3 days post-ingestion and anorexia may occur with 1 day post-ingestion. Severely poisoned animals may die within 2 days post-ingestion, although death usually occurs 1 to 3 weeks after poisoning (Ghisalberti, 2000).
    B) A Boer goat kid, not previoulsy exposed to Lantana, was exposed to the plant in a new pasture and subsequently died from Lantana poisoning. Necropsy showed distention of the gall bladder, nephrosis, single cell necrosis of the liver, bile statis, icterus, constipation, and dehydration. Skin lesions were NOT noted. The amount ingested was unknown. Effects in other cases of ingestion by goats were similar. Onset, in goats, is usually within 1 to 4 days of ingesting the plant (Ide & Tutt, 1998).
    11.1.7) ICHTHYOID/FISH
    A) LANCAMARONE - A component of Lantana camara is a fish poison, even in very low doses (Nigam & Kaul, 1958).
    11.1.9) OVINE/SHEEP
    A) SUMMARY - Toxicity, following Lantana camara ingestions, occur primarily in sheep, cattle, and goats. Not all species of L. camara are toxic. In general, photosensitive dermatitis is the most prominent clinical sign following intoxication and may occur within 1 to 2 days and may progress to skin necrosis. Jaundice may occur with 2 to 3 days post-ingestion and anorexia may occur with 1 day post-ingestion. Severely poisoned animals may die within 2 days post-ingestion, although death usually occurs 1 to 3 weeks after poisoning (Ghisalberti, 2000).
    B) ACUTE - Sheep fed powdered Lantana (10 gram/kg) acutely, developed anorexia within 48 hours, and were icteric by the fourth day. By day 7, there was swelling of the eyelids, ears, and face, as well as lacrimation. Icterus lasted until the 10th day (Gopinath & Ford, 1969).
    C) Histologically, there was degeneration of the parenchymal cells of the periportal regions of the liver. The liver enzymes which appeared in the serum in highest concentrations were sorbitol dehydrogenase and arginase (Gopinath & Ford, 1969).
    D) IMMUNOLOGY - A significant reduction in both cellular and humoral immunity was observed in Lantana-toxic sheep. The non-specific phagocytic activity of splenic reticulo-endothelial cells was also reduced. In this study, one group was doused with water while the other group was drenched with a Lantana solution (200 milligrams/kilograms) daily for 110 days. Cell-mediated immunity was evaluated using 2,4-dinitrofluorobenzene skin sensitivity and graft versus host reaction. Antibody-producing potential was evaluated using hemagglutination against chicken red blood cells antigen (Ganai & Jha, 1991).
    11.1.13) OTHER
    A) OTHER
    1) Livestock poisoning has occurred in at least 9 countries spread over 5 continents (Sharma et al, 1988; Kingsbury, 1964). In general, animals who eat Lantana become constipated and anorexic within 2 hours. Over the next one to two days they become photosensitive, sedated, and develop swelling on eyelids, muzzles, or other hairless parts (Yadava & Verma, 1978; (Sharma et al, 1981a).
    2) Buffaloes, sheep, cattle, and goats have become toxic (Sharma et al, 1988; Lai & Kalra, 1960). There is some species susceptibility variation, with goats being somewhat less sensitive. Similar liver and skin toxicity has been reported in the red kangaroo (Megaleia rufus) after ingestion of Lantana (Johnson & Jensen, 1998).

Treatment

    11.2.1) SUMMARY
    A) GENERAL TREATMENT
    1) Treatment should only be attempted under the guidance and control of a licensed veterinarian.
    2) Attempts have been made to use olegenic purgatives to remove the Lantana prior to absorption and to increase gastrointestinal movement. They have not been very successful (McSweeney & Pass, 1982; Sharma et al, 1981a).
    3) Lantana in the rumen becomes more toxic as time passes, possibly due to it becoming more liquid and being better absorbed. Rumentotomy followed by removal and replacement of rumen contents is possible, but could only be used for valuable animals (McSweeney & Pass, 1982).
    4) Activated charcoal was found to be effective if administered early after an ingestion, prior to adsorption of the toxins (Sharma et al, 1988).
    5) In a study,conducted to compare the efficacy of activated charcoal versus bentonite in the treatment of Lantana camara poisoning in cattle, bentonite administration, at a dose of 5 grams/kilogram, was shown to be equally effective in reducing plasma total bilirubin concentrations in the poisoned animals. Bentonite's action appeared to be slower than activated charcoal, taking an average of 3 days longer for the plasma bilirubin to normalize (McKenzie, 1991).
    a) Five of the six calves who did not receive any treatment following intoxication with L. camara died, whereas 5 of the six calves who received either bentonite or activated charcoal recovered.
    11.2.2) LIFE SUPPORT
    A) GENERAL
    1) MAINTAIN VITAL FUNCTIONS: Secure airway, supply oxygen, and begin supportive fluid therapy if necessary.
    11.2.5) TREATMENT
    A) GENERAL TREATMENT
    1) ACTIVATED CHARCOAL -
    a) Cattle - 2 kilograms of activated charcoal in 20 liters of electrolyte solution is effective in preventing Lantana poisoning in cattle if given early after an ingestion (Pass & Stewart, 1984).
    b) Sheep - 500 grams of activated charcoal in 4 liters of electrolyte solution was likewise effective in sheep (Pass & Stewart, 1984).
    2) INEFFECTIVE TREATMENTS -
    a) COBALT - Administration of cobalt pellets was ineffective (Seawright, 1963).
    b) A mixture of glucose, saline, anthisan, liver extract, and the herbal preparation liv-52 was given to buffalo calves. It did increase the survival time, but only a little (Hari et al, 1973).
    3) EXPERIMENTAL TREATMENTS -
    a) VACCINATION - Only a mild protective effect was noted in sheep and cattle vaccinated with lantadene A & B conjugates. Lantadene A & B were conjugated with bovine serum albumin or hemocyanin. When these conjugates were injected into sheep and cattle, antibodies developed against the conjugates. These animals were then exposed to toxic amounts of the lantadene toxins. A mild protective effect against hepatotoxicity and cholestasis was noted (Stewart et al, 1988).
    b) DEGRADATION VIA MICROORGANISMS - Lantadene A was extracted from Lantana camara var. aculeata. The organism Alcaligenes faecalis was obtained from the soil under the Lantana bushes. The microorganism was fermented with the toxin and the resultant mixture fed to guinea pigs. A. faecalis appeared to detoxify the lantadene without producing toxic by-products. Animals fed the mixture had reduced liver weights and total bilirubin. In practice, the organism might be added to feed to create a culture in the rumen (Singh et al, 2001).

Range Of Toxicity

    11.3.2) MINIMAL TOXIC DOSE
    A) SPECIFIC TOXIN
    1) Lantadenes A, B, D, compound 9, and icterogenic acid are toxic to sheep, cattle, and goats (Ghisalberti, 2000).
    2) Lantadene A in intravenous doses of 1 to 3 milligrams/kilogram has produced hepatotoxicity in animals (Ghisalberti, 2000; Sharma et al, 1981a). It is not entirely clear if it is the lanthadene A, a metabolite, or a chemical associated with the lantadene A which produces the reaction (Sharma et al, 1988).
    3) The toxic dose in sheep, following ingestion of lantadene A, is 60 to 80 milligrams/kilogram and that of lantadene B is 200 milligrams/kilogram (Ghisalberti, 2000).

Continuing Care

    11.4.1) SUMMARY
    11.4.1.2) DECONTAMINATION/TREATMENT
    A) GENERAL TREATMENT
    1) Treatment should only be attempted under the guidance and control of a licensed veterinarian.
    2) Attempts have been made to use olegenic purgatives to remove the Lantana prior to absorption and to increase gastrointestinal movement. They have not been very successful (McSweeney & Pass, 1982; Sharma et al, 1981a).
    3) Lantana in the rumen becomes more toxic as time passes, possibly due to it becoming more liquid and being better absorbed. Rumentotomy followed by removal and replacement of rumen contents is possible, but could only be used for valuable animals (McSweeney & Pass, 1982).
    4) Activated charcoal was found to be effective if administered early after an ingestion, prior to adsorption of the toxins (Sharma et al, 1988).
    5) In a study,conducted to compare the efficacy of activated charcoal versus bentonite in the treatment of Lantana camara poisoning in cattle, bentonite administration, at a dose of 5 grams/kilogram, was shown to be equally effective in reducing plasma total bilirubin concentrations in the poisoned animals. Bentonite's action appeared to be slower than activated charcoal, taking an average of 3 days longer for the plasma bilirubin to normalize (McKenzie, 1991).
    a) Five of the six calves who did not receive any treatment following intoxication with L. camara died, whereas 5 of the six calves who received either bentonite or activated charcoal recovered.

Pharmacology Toxicology

    A) GENERAL
    1) Ingestion produces a paralysis of the gall bladder and closure of bile canaliculi (Pass & Goosem, 1982; Pass et al, 1978; Pass & Heath, 1977). Biochemical lesions are not found in any one particular place within the liver, but are seen in microsomes, mitochondria, lysosomes, and canalicular plasma membranes (Sharma, 1984b).

References

General Bibliography

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