Page 917 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

872 SECTION | XIV Poisonous Plants

VetBooks.ir metabolism has been shown to be high in those species people. Their distribution in the western United States,
common names, and toxins are listed in Table 61.9.
that are most susceptible and lowest in animals of least sus-
ceptibility. In addition, in in vivo studies, it was demon-
strated that a higher pyrrole production rate occurred in Toxicology
cattle compared to sheep. Simple induction of liver micro-
somal enzymes by phenobarbitone increased pyrrole pro- Primary
duction and increased PA toxicity (LD 50 in guinea pigs
In primary photosensitization, the photoreactive agent is
from .800 to 216 mg/kg). PA toxicity may disrupt other
absorbed directly from the plant and reaches the periph-
hepatic functions. Abnormal copper metabolism coagula-
eral circulation and skin, where it reacts with the ultravio-
tion, NH 3 metabolism, protein metabolism, etc. may be
let rays of the sun and results in sunburn, particularly of
affected in PA poisoning.
unprotected areas of the body. Hypericin and fagopyrin
are polyphenolic derivatives from St. John’s wort and
Prevention and Treatment buckwheat, respectively, and are primary photodynamic
agents (Cheeke and Shull, 1985). By definition, primary
Because there are no proven effective methods of preven-
photosensitization does not induce hepatic damage. Most
tion or treatment, avoidance of the plant and controlling
agents are ingested, but some may induce lesions through
plant populations with herbicides or biological control is
skin contact. Several of these plants are weedy in nature
essential. Resistance to PA toxicosis in some species sug-
and can contaminate pastures and feed. Exposure to some
gests that the possibility may exist to increase resistance
plants is increasing as they are becoming widely used as
to PAs. Dietary factors such as increased protein, particu-
herbal remedies and holistic medicines. In most cases, the
larly those high in sulfur amino acids, had minor protec-
photodynamic agent is absorbed from the digestive tract
tive effects in some species. Antioxidants such as BHT
unchanged and reaches the skin in its “native” form
and ethoxyquin induced increased detoxifying enzymes
(Stegelmeier, 2002).
such as glutathione S-transferase and epoxide hydrolase.
There are drugs and other toxins known to cause pri-
Zinc salts have been shown to provide some protection
mary photosensitization, and these should be considered in
against hepatotoxicosis from sporidesmin or lupinosis in
the differential diagnosis. Phenothiazine-induced photosen-
New Zealand and Australia, and zinc supplementation
sitization is most common in ruminants because the photo-
reduced toxicity in rats from Senecio alkaloids (Burrows
dynamic agent is phenothiazine sulfoxide, a rumen
and Tyrl, 2001; Knight and Walter, 2001).
metabolite. Clinical signs in addition to photosensitivity
Many of these plants were introduced either inadver-
include corneal edema and kerato conjunctivitis from the
tently or intentionally. Without natural predators to keep
phenothiazine sulfoxide excreted in tears and the aqueous
populations in check, they experienced explosive growth
humor. Other toxins associated with primary photosensitiv-
and distribution followed by epidemic proportions of tox-
ity include thiazides, acriflavins, sulfonamides, tetracy-
icity. Introduction of biological controls and natural popu-
clines, methylene blue, coal-tar derivatives, furosemide,
lation controls have reduced many of the plant
promazine, chlorpromazine, quinindine, and some antimi-
populations and thus toxicoses have declined. Sheep, a
crobial soaps (Stegelmeier, 2002).
resistant species, have been used to graze plants, particu-
larly S. jacobaea.
Secondary
In secondary or hepatogenous photosensitization, the
PHOTOSENSITIZING PLANTS
photoreactive agent is phylloerythrin, a degradation product
Numerous plants cause photosensitization resulting in of chlorophyll. Phylloerythrin is produced in the stomach
losses to the livestock industry. Photosensitization is the of animals, especially ruminants, and absorbed into the
development of abnormally high reactivity to ultra-violet bloodstream. In normal animals, the hepatocytes conjugate
radiation or natural sunlight in the skin or mucous mem- phylloerythrin and excrete it in the bile. However, if the
branes. Primarily induced in livestock by various poison- liver is damaged or bile secretion is impaired, phylloery-
ous plants, the syndrome in livestock has been defined as thrin accumulates in the liver, the blood, and subsequently
primary and secondary photosensitization. the skin, causing photosensitivity. This is the most com-
mon cause of photosensitization in livestock and horses
(Knight and Walter, 2001). Because chlorophyll is almost
Description and Distribution
always present in the diet of livestock, the etiologic agent
Photosensitizing plants are too numerous to describe indi- of secondary photosensitization is the hepatotoxic agent.
vidually, and readers are referred to taxonomic texts for The dermatologic signs of photosensitization in live-
plant description. Photosensitizing plants occur throughout stock are similar regardless of the plant or toxicant
the world and are common in the diets of livestock and involved. Degree of severity varies, depending on the