Page 446 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

Arsenic Chapter | 23 413

VetBooks.ir gens in people, this has not been the case in animals. hair coat as well as dry, brick-red mucous membranes.
Although arsenicals have been classified as carcino-
Cattle are described as having enlarged joints.
Clinical signs of phenylarsenic poisoning occur within
Experimentally, there have been attempts to document
arsenic-related cancer in animals, but the experiments 3 days of a high dose or after chronic exposure. Most
have been unsuccessful (Chan and Huff, 1997; Agency noticeable are the neurological signs. The animal is gener-
for Toxic Substances and Disease Registry, 2007; Hughes ally bright and alert but uncoordinated. The animal may
et al., 2011). or may not be blind, and these animals may have ery-
thema in the skin. Some of the neurological damage may
be reversible unless the nerves are damaged.
TOXICITY
Lesions are often dependent upon the dose and survival
Inorganic arsenicals are up to ten times more toxic than times. There may be no lesions at all in animals dying
pentavalent arsenicals. The order of toxicity from greatest from peracute poisoning. However, even these animals
to least follows this schematic: inorganic As 13 have some degree of GI irritation. With the exception of
15
(arsenite) . inorganic As (arsenate) . trivalent orga- peracute deaths, most of the other animals dying from
13 15
nics . pentavalent organics (I As . I As . O some form of arsenic poisoning may have excess fluid in
13 15
As . OAs ). In other metal toxicities, the organics the GI tract. In cattle, there is hyperemia of the aboma-
are more toxic, but with arsenicals the inorganics are the sum, and this may be the only finding. This “paint brush”
more toxic. hyperemic lesion is characteristic of arsenic poisoning. If
Toxicity is also influenced by many factors, including there are other lesions in cattle, it is often necrosis of the
particle size. The more finely ground, the more surface rumen mucosal epithelium. Ruminants have gelatinous
area there is for reactions. Solutions, such as dips and serosal edema in the rumen, reticulum, omasum, and
defoliants, are the most dangerous. However, the causes abomasum. The GI tract may have indications of irritation
of the poisonings are varied. Debilitated animals are more and be hemorrhagic. Lesions are indicative of capillary
sensitive. Since arsenic is not biodegradable, the soil and damage, and the liver is usually soft and yellow.
the old corrals around old dipping vats are still sources The phenylarsonics (15) were previously used in feed
for arsenic poisoning. The area around smelters is also a additives, and lesions would be expected to be associated
source of poisoning, similar to that of dipping vats. with overdoses in the feed mixture. A “downer pig”
Human mistakes and carelessness are the largest contrib- would have severe abrasions with muscle atrophy.
uting factors to toxic events. For example, feeding a prod- Microscopic lesions indicate there was demyelination in
uct known as gin trash instead of cotton seed hulls has the optic nerve and the posterior cord. The FDA
resulted in numerous animals being poisoned. announced in 2013 the voluntary withdrawal of roxarson,
Clinical signs caused by either inorganic or trivalent arsanilic acid, and carbarsone by Zoetis and Fleming
aliphatic arsenicals are similar. Peracute toxicities often Laboratories, leaving only nitarsone approvals in place
result in sudden death within minutes to a few hours if (CFSAN).
the dose of dissolved arsenic ingestion is high. Acute poi-
sonings have more clinical signs: abdominal pain or colic, TREATMENT
vomiting (in those animals capable of vomiting), a stag-
gering gait and weakness, incoordination, rapid weak A diagnosis of arsenic poisoning is important and is based
pulse and shock, diarrhea, followed by collapse and death. upon clinical history and clinical signs. If more than one
If the acute poisoning is through dermal contact, then the animal is involved, then lesions may also be important.
arsenic will also be systemic. The skin will have blisters Diagnostic arsenic levels in the kidney and liver are usu-
and edema and may be cracked and bleeding, leaving the ally more than 8 10 parts per million (ppm) unless sev-
skin susceptible to secondary infection (National eral days have lapsed since exposure, in which case it
Academy of Science, 1977; Evinger and Blakemaore, would likely be 2 4 ppm. Diagnostic levels of arsenic in
1984). Those receiving a lower dose over a period of time the urine and feces are greater, between 10 and 20 ppm.
may have subacute poisonings and will likely live several Arsenic should not be found in phenylarsonic acid
days, developing depression and anorexia. Movements intoxications.
may be difficult, stiff, and uncoordinated. Diarrhea is Removal of the source of arsenic from the animal is
dark and possibly hemorrhagic and very fluid. Hematuria critical. Treatment must be directed toward the clinical
may be present, or the urine may contain protein and casts signs of the patient. There are no specific treatments for
(National Academy of Science, 1977; Osweiler et al., organic arsenicals. However, the neurotoxic effects are
1985). However, those suffering chronic poisoning are usually reversible. This involves removing any offending
easily fatigued and have dyspnea when they are moved. feed early in the process, within 2 3 days of the onset of
These animals display intense thirst and have a rough dry ataxia. If there is paralysis and nerve damage, then the