Lantana 

and Lippia spp.
Lantana camara - Largeleaf Lantana

L. involucrata

L. aculeata

L. ovalifolia

L. sellowiana

Lippia ligustrina - White brush

Major Species Usual Time of Onset Usual Duration (if survives)

Herbivores Days to chronic Weeks to permanent damage; often lethal

Family

Verbenaceae (Verbena Family)

Images

 Lantana (Lantana camara) . Knight A.P. and Walter R.G. (Eds.). A Guide to Plant Poisoning of
Animals in North America. Ithaca: International Veterinary Information Service (www.ivis.org),
2003 

 Lantana, Red Sage, Yellow Sage, or West Indian Lantana, Lantana camara.. Source: Cornell
University, Poisonous Plants Informational Database (www.ansci.cornell.edu/plants/index.html) 

 Largeleaf Lantana, Lantana camara - Google Image Search 

 Lantana involucrata - Google Image Search 

 Lantana aculeata - Google Image Search 

 Lantana sellowiana - Google Image Search 

Description

Lantana spp.

 Plant - Erect or spreading shrub.

 Stem - Ridged, angular, prickly.

 Leaves - Opposite, ovate, crenated or serrated margin, veined from base, spreading hairs, 1.5 - 5
inches long.

 Flowers - Small, tubular, spreading lobes, long axillary peduncles, yellow or pink changing to orange
or bright red.

 Fruit - Fleshy, drupe-like, 2-celled or 2 one-seeded.

L. camara

 Plant - Low, perennial shrub, 3 - 6 ft tall.

 Stem - Square, sparse weak spines, occasionally vine-like, hairy.

  Leaves - Opposite or in whorls of 3, ovate, petioled, crenatedentate, 2 - 4 inches long, 1.2 - 2.4
inches wide, toothed, aromatic, rough above, hairy beneath; leaf stalks, 0.4 - 0.8 inches long.

 Flowers - Small, tubular, yellow or pink changing to bright red, 0.4 - 0.5 inches long, 0.24 - 0.31
inches across; in flat-topped clusters, axillary umbels, 1.6 - 2.4 inches across.

 Fruit - Greenish-blue or black, fleshy, berry-like, 0.24 - 0.31 inches diameter, glossy; seeds, oval,
0.16  -0.2 inches long, 0.12 - 0.14 inches thick, grooved on 2 sides, brown, rough, irregular.

Lippia liqustrina

 Plant - Shrub, often spiny, 0.4-1.2 ft high.

 Leaves - Opposite, lanceolate to oblong, veinless, 0.2-1 inch long.

 Flowers - In slender, naked spikes.

 Fruit - 2-celled nutlets; 1 seed per cell nutlets, greenish-blue or black 1/4 inch in diameter.

Habitat

 General - Southern Africa; Australia; India.

 L. camara - Central and Southern Florida; Northern USA and Canada as an ornamental; Australia;
Mexico.

 Fence rows, ditch banks, fields, waste areas, pastures, sandy soils, potted; cultivated as outdoor
annual, dry woods.

 Lippia spp. - Southwest Texas to Mexico

 Also grown as a potted plant in Central and other parts of USA.

Toxic Principle

 Pentacyclic triterpene acids, including lantadene A and B, reduced lantadene A, dihydrolantadene

A, and icterogenin.

 Hepatogenous photosensitizer.

 Gastrointestinal irritants.

Susceptible Species

 Lantana camara - Sheep, cattle, children.

 Lippia spp. - Cattle, sheep, goats, horses.

Toxicity

 Lantana camara.

 Foliage and ripe berries contain toxic substance.

 Green berries have a higher concentration of the toxin.

 Berries may be lethal to children. However, some dark skinned people eat ripe berries without
noticing ill effects.

 Lantana is one of the main causes of poisoning in Florida.

 Three-fourths to 1 lb of dry leaves may cause toxicosis of a 400 lb bovine (1% of animals weight)
(green weight basis).
  Two percent of sheep's weight produced fatal results in 5 days.

 Toxicity of individual plants is genetically determined.

 Fifty to 90% of animals newly exposed are affected.

 High mortality of affected animals (90%).

 All species of Lantana should be considered poisonous.

 Poisoning commonly occurs among grazing animals.

 Lantadene A.

 One dose of lantadene A, 1 - 3 mg/kg, produces mild liver injury, increased SGOT and SDH; but
serum bilirubin does not increase.

 One dose at 3 mg/kg or 7 doses at 1 mg/kg over 3 days causes cholestasis, elevated SGOT, SDH,
and bilirubin; green discoloration of the liver; enlarged gallbladder; dry impacted feces may be
found in rectum; renal tubular necrosis.

 One dose of 4 - 8 mg/kg causes centrilobular, midzonal, and massive hepatic necrosis; hemorrhage
into the intestinal tract is common.

 One dose at 60 mg/kg given orally is toxic to sheep.

Mechanism of Action

 Hepatogenic photosensitizer; hepatotoxic; cholestasis.

 The toxins have effects on both hepatocytes and bile canaliculi.

 Decrease in canaliculi ATPase activity.

 Collapse of canaliculi.

 Secretory function of hepatocytes is lost; metabolizing function is retained.

 Literature is in disagreement as to whether or not normal bilirubin conjugation is retained.

Signs

 Lantana.

 Acute toxicosis:

 The major clinical effect of Lantana toxicosis is photosensitization, the onset of which often takes
place in 1 to 2 days after consumption of a toxic dose (1% or more of animal's body weight).

 Jaundice is usually prominent, animals usually become inappetent, and they often exhibit
decreased digestive tract motility and constipation.

 Other signs may include: sluggishness, weakness, and transient, sometimes bloody diarrhea. In
acute cases, death occurs in 2 to 4 days.

 Subacute and chronic toxicosis:

 Subacute poisoning is more common.

 Raw photosensitized surface areas are susceptible to invasions by blow fly maggots and bacteria.

 In severely affected cattle, lesions may appear at the muzzle, mouth, and nostrils.
  Ulceration may be present in the cheeks, tongue, and gums, while swelling, hardening, peeling of
mucous membranes, and deeper tissues occur in the nostrils.

 Death may occur after 1 to 3 weeks of illness and weight loss.

 Lippia spp.

 Emaciation.

 Leg weakness.

 Incoordination.

Lesions

 General.

 Highly pigmented liver.

 Icterus, general edema.

 Gallbladder paralysis and distention.

 Necrosis of renal tubules.

 Hemorrhages in some organs.

 Myocardial damage and intestinal paralysis has been suggested, but conclusive supportive
evidence is lacking.

 Cattle (severe cases).

 Lesions from muzzle to mouth and nostrils, ulceration of cheeks, tongue, and gums.

 Swelling, hardening, peeling of mucous membranes and deeper tissues in the nostrils.

 Human.

 Acute pulmonary edema and "neurocirculatory collapse" has been reported in a 2 1/2 year old girl.

Diagnosis

Identification of Lantana or Lippia, evidence of consumption and appropriate clinical signs and lesions
(browsing might be overlooked because of the small amount necessary to cause toxicosis).

Treatment

 Treat for 12 -24 hours to overcome reduction in gut motility.

 Physostigmine may initiate dramatic reversal of some of the signs within minutes.

 Contraindications for the use of physostigmine include: asthma, gangrene, cardiovascular disease,

mechanical obstruction of the gastrointestinal or urogenital tracts.

Prevention

 Grubbing and destruction of plants is most practical.

 Herbicides.
Lantana - The oval, toothed, and veiny leaves; the square prickly stems; the terminal flower clusters; and
the black berries are characteristic of this attractive ornamental shrub.

Alpha-Naphthyl Thiourea (ANTU)

Major Species Usual Time of Onset Usual Duration (if survives)

Dogs, cats 6 - 12 hours Days, highlty lethal

Sources

 Alpha-naphthyl thiourea is a fine gray insoluble powder possessing almost no odor

or taste.
 The compound is extremely stable and does not deteriorate on prolonged storage.
 It finds primary use as a rodenticide and in doses less than 100 mg/kg has been
found to be toxic only to the Norway rat, cats, dogs, mice and pigs.
 Usually baits are prepared by including 2% ANTU in cereals, meats or bread
mashes.
 Baits containing ANTU are readily accepted by animals, but they are able to
develop a tolerance towards the substance.
 ANTU is only rarely used at the present time.
 ANTU
a-(1-Naphthyl)-2-thiourea

Toxicity

Dogs are the domestic species most often poisoned with ANTU. The LD50 is influenced by
species and age. Comparative LD50s of ANTU in mature animals are presented in the following
table.

Species Route of Administration LD, mg/kg Body Weight

Norway rat, wild Oral 6.9 + .05
Dog Oral 38
Mouse Oral 19
Guinea pig Oral 143
Cat Oral 75 - 100
Pig Oral 25 - 50

 Aged dogs are more susceptible to ANTU poisoning than young ones.
 An identical effect of age has been demonstrated in wild rats; suckling rats were 5
- 7 times more resistant to the effects of ANTU than old rats.
 The route of administering ANTU influences its toxicity in the dog and cat
because emesis often occurs following oral administration.

Mechanism of Action

ANTU kills by producing a marked hydrothorax and pulmonary edema. The animal literally
drowns in its own fluids. The accumulation of fluids is due to an increase in the permeability of
capillaries in the lungs. When lymph flow from the lungs was monitored following the
administration of ANTU to dogs, increases were noted within 90 minutes following dosing. At
the eighth hour after dosing, the lymph flow had increased to 80 times its original value. The
exact mechanism resulting in increased capillary permeability has not been determined. Reaction
of ANTU with sulfhydryl groups may be a necessary part of the mechanism of toxic action, since
it has been reported that sulfhydryl group blocking agents are effective antidotes in rats in some
experimental conditions.

Signs

 Vomiting is one of the first signs noted, occurring a few minutes to a few hours
following ingestion of ANTU.
 Breathing becomes rapid (short, jerky inspirations) and a shallow hacking cough
may be noted. Moist rales can be detected in the lung fields.
 The extremities are cold to the touch and the visible mucous membranes appear
cyanotic. The peripheral pulse is almost imperceptible while the cardiac impulse is
accelerated and weak.
  Normal or subnormal temperatures are the rule in poisoned animals.
 Animals continue to vomit as the disease progresses and the vomitus may consist
entirely of blood.
 A watery fluid diarrhea becomes hemorrhagic if the patient survives the acute
symptoms.
 The affected animal remains standing or sits on its haunches to relieve thoracic
pressure. As the animals become weaker, they assume a position of sternal
recumbency.
 In the terminal stages, the lungs are congested or filled with fluid and fluid may
escape from the mouth.
 The animal becomes comatose and fails to respond to external stimuli. Most deaths
occur in 2 - 4 hours after symptoms appear. If the animal survives for 12 hours
after ANTU exposure, the prognosis becomes more favorable.

Lesions

 The most apparent change noted at necropsy is hydrothorax. The thoracic cavity is
often completely filled with a clear, colorless fluid. Severe edema of the lungs is a
consistent finding and, in some instances, fluid will actually flow from the trachea
when the lungs are removed from their cavity.
 The poison is moderately irritating to the stomach and intestines, and catarrhal
inflammation is usually present in these organs.
 In many instances, the kidneys assume a blood red color as a result of intense
hyperemia or congestion.

Diagnosis

Since chemical tests for ANTU are usually inconclusive, diagnosis is dependent upon history,
characteristic clinical signs and necropsy findings.

Treatment

Emetics such as apomorphine (in the dog) may be of value if animals are presented early in the
course of the poisoning and if the ingestion of baits containing ANTU is suspected. Because of
the seriousness of ANTU toxicosis, measures to eliminate the gastrointestinal tract contents
should be followed as soon as possible after exposure. Activated charcoal may possibly be of
value in the lavage solutions and should be left in the lumen thereafter. If a thorough
enterogastric lavage is not performed, then a saline cathartic should also be administered. Some
authors suggest that mineral oil fats can enhance absorption of ANTU and should be avoided.
Although silicone aerosols may prevent foaming of excessive bronchial fluids, there is no
specific treatment for ANTU poisoning. Experimental evidence indicates that providing thiol
groups may reduce mortality. Potential thiol-containing compounds include N-amyl
mercaptan, N-acetyl cysteine, or thyacetyl cysteine. Atropine has not been helpful in controlling
the pulmonary edema. The prognosis for animals suffering from clinically significant ANTU
poisoning is poor.