Page 301 - Veterinary Toxicology, Basic and Clinical Principles, 3rd Edition

268 SECTION | II Organ Toxicity

VetBooks.ir glomerulonephritis. Extra-renal effects of cadmium recumbency, paralysis and coma; death occurs within
1 2 days of onset of signs. Gross lesions of pigweed tox-
include osteoporosis and osteopenia, hepatocellular
icosis include widespread edema, most prominently
testicular
injury.
and
injury
myocardial
necrosis,
Cadmium is a mutagen and putative carcinogen. around the kidneys, rectum and omentum. Kidneys are
pale and normal to swollen in size. Histopathologic
Lead changes within the kidney include interstitial edema, scat-
tered hemorrhages and proximal tubular degeneration and
The incidence of lead toxicosis has declined in the United
necrosis. Dilated tubules and tubules filled with necrotic
States since the banning of lead-based paints in residential
debris are often present and interstitial fibrosis may be
domicilesin1977andleadedgasolinein1996(with signifi-
present in chronic cases. Extra-renal lesions include
cant reductions in use of leaded gasoline for the prior 20
edema and ulceration of the digestive tract.
years). However, lead is still present in the paint of many
older homes as well as common household items such as
toys, artists’ paints, linoleum, lead weights, lead fishing sin- Lilium spp. and Hemerocallis spp.
kers and ornaments. Additionally, despite bans on the use of Ingestion of some species of the genera Lilium and
lead shot for hunting waterfowl, lead ammunition is still Hemerocallis by cats has resulted in potentially fatal renal
widely used on upland game, and lead toxicosis is still a sig- dysfunction that has not been successfully reproduced in
nificant cause of death among scavengers such as eagles and other species including dogs, rats, and rabbits (Rumbeiha
condors (Hunt et al., 2009; Stauber et al., 2010). Birds with et al., 2004). Although the toxic principle remains
lead toxicosis frequently present with emaciation and evi- unknown, Rumbeiha et al. (2004) were able to demonstrate
dence of renal tubular degeneration (Pattee et al., 2006). that the toxic effects originated from an aqueous floral
Acute lead toxicosis is most commonly associated with neu- extract of the Easter lily. All parts of the plant, including
rological signs in mammals, while chronic lead toxicosis can pollen, are toxic, and even small ingestions can result in
result in dysfunction of a variety of organ systems including significant renal injury (Fitzgerald, 2010). Prevention of
gastrointestinal, neuromuscular, central nervous, hematologi- serious renal injury can often be achieved if aggressive
cal and renal (Gwaltney-Brant, 2002). Degeneration and intravenous fluid therapy is instituted within the first 18 h
necrosis of proximal renal tubules results in oliguria, amino following exposure. Clinical effects include vomiting,
aciduria, glucosuria and altered tubular ion transport. Acute depression, polyuria, polydipsia, azotemia, glucosuria, pro-
renalfailure mayoccur followingexposuretolead, but CRF teinuria and isosthenuria. Serum creatinine levels tend to
is more common. Dense, homogeneous, eosinophilic intra- elevate disproportionately to blood urea nitrogen.
nuclear inclusion bodies may be visualized in affected renal Histopathologic lesions include proximal convoluted tubule
tubular cells; although suggestive for lead toxicosis, these degeneration and necrosis with denudation of basement
inclusions are not pathognomonic as they can occur follow- membrane and filling of tubular lumens with cellular debris
ing exposure to other metals such as bismuth. (Rumbeiha et al., 2004). Extra-renal lesions include vacuo-
lar degeneration of pancreatic acinar cells.
Plants
Quercus spp.
Amaranthus spp. Oak foliage and acorns provide forage to a variety of wild-
The pigweed family includes several different species life and livestock, but when oak is the primary source of
capable of producing toxicosis, but Amaranthus retro- feed for more than a few days, toxicosis can develop
flexus is the species most commonly associated with dis- (Burrows and Tyrl, 2001). Oak buds, acorns and young
ease in domestic animals (Burrows and Tyrl, 2001). Renal leaves are involved in the majority of reported livestock
injury from pigweed has been reported in pigs, cattle and poisonings, and most oak species have, at one time or
sheep. Other herbivorous species are likely susceptible, another, been implicated in animal poisonings. Cattle are
although the disease was not able to be reproduced in rab- most commonly affected, and reports in other species such
bits fed A. retroflexus (Schamber and Misek, 1985). The as horses, goats and sheep are rare. The primary toxic prin-
toxic principle is not known. Although pigweeds do con- ciples in oak are tannins, phenolic and polyphenolic com-
tain some oxalates, the levels are low and the clinical syn- pounds such as ellagic and gallic acids, and tannin
drome and lesions caused by pigweed toxicosis are not metabolites such as pyrogallol. At toxic doses, oak tannins
consistent with those seen in oxalate nephrosis (Burrows precipitate proteins in the digestive tract, causing erosions
and Tyrl, 2001). Clinical signs generally begin following and ulcerations as well as altering mucosal absorption bar-
several days of ingesting the plant, although renal lesions riers. Increased absorption of polyphenolic tannins via
have been identified within 24 h of ingestion. Clinical injured mucosa results in damage to the liver and kidney; in
signs include weakness, ataxia, knuckling of pasterns, rats, gallic acid was identified as the compound responsible