Page 919 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

874 SECTION | XIV Poisonous Plants

VetBooks.ir teristic histologic lesions. For example, pyrrolizidine alka-
Plant-induced hepatopathy generally results in charac-
loids generally cause bridging portal fibrosis with
hepatocellular necrosis, biliary proliferation, and mega-
locytosis. Panicum and Tribulus species generally produce
a crystalline cholangiohepatitis. Liver biopsy also provides
prognostic information. The degree of damage is correlated
directly with the animal’s ability to compensate, recover,
and provide useful production. Note that the liver reacts to
insult in a limited number of ways, and most histologic
changes are not pathognomonic. Hepatic cirrhosis (necro-
sis, fibrosis, and biliary proliferation) involves nonspecific
changes that can be initiated by a variety of toxic and
infectious agents (Stegelmeier et al., 1999).

DEATH CAMAS
All death camas species are assumed to be toxic; how-
ever, variation in toxicity exists between species and even
FIGURE 61.8 Foothill death camas with leaf structure, flower head,
within species depending on season, climate, soils, and and bulb.
geographical locations. Poisoning in sheep, cattle, horses,
pigs, fowl, and humans has been reported. The largest cavitied capsule, separating into three members and open-
losses generally occur in sheep. Sheep are primarily ing inwardly at maturity. Death camas is easily confused
affected because of their tendency to select forbs, particu- with wild onion, mariposa lily, or common camas particu-
larly in early spring when they are turned onto range larly before flowering. Wild onions are distinguished by
before grasses have emerged. tubular leaves and their onion-like odor. The leaves of
Death camas is generally not palatable to livestock but mariposa lilies are more U-shaped in cross section, and
is one of the earliest species to emerge in the spring. common camas has a blue flower. Death camas is preva-
Poisoning most frequently occurs in spring when other lent in western North America and is native to the open
more palatable forage is not available, or on overgrazed plains and foothills of the United States.
ranges where there is a lack of more desirable forage.
Poisonings have resulted due to management errors in
which hungry animals were placed in death camas- Toxicity of Death Camas to Livestock
infested areas (Panter et al., 1987).
The toxins in death camas are of the cevanine steroidal
alkaloid type that is, zigacine (11). Zigacine is a very
Description, Habitat, and Geographical
Distribution H

Foothill death camas is typical of the 15 20 species of
H
Zigadenus in North America and Asia (Figure 61.8).
N
A list of death camas species and their habitats, distribu-
tions, and growth periods is provided in Table 61.10.It is
H
difficult to distinguish between species because they are OH
taxonomically similar. A member of the lily family, death
camas is a perennial, glabrous herb with basal V-shaped H H H
grass-like leaves growing from an onion-like bulb with a
dark-colored outer coat. Stems produced at flowering are OH
O OH
single, unbranched, sparingly leafed, and terminated by a
OH
terminal raceme of greenish-white, cream-colored, or pink
CH 3 C O
inflorescence. The perianth is six-membered, consisting
H
of three lanceolate or ovate sepals and three petals sepa-
O OH
rate or united below, with one or two glands just above (11)
the base; six stamens; and three styles. Floral parts are Zigacine
persistent as the fruits develop. The seed is a three-