Journal of Feline Medicine and Surgery (2003) 5, 249–255

doi:10.1016/S1098-612X(03)00047-0

REVIEW
Lead toxicosis in cats—a review
TE Knight*, MSA Kumar

Department of Biomedical Sciences,
Tufts University School of
Veterinary Medicine,
200 Westboro Road,
North Grafton, MA 01536, USA
Date accepted: 8 May 2003
Although the incidence of lead toxicosis in small animals continues to decrease, it
remains a significant malady. We have reviewed the literature of the past
45 years, which revealed 70 cases involving cats. Sources, signs, diagnosis,
pathology and treatment of feline lead toxicosis are reviewed.
In 84% of these cases the source of lead was old paint usually from home
renovation. The most common signs in cats are anorexia, vomiting, and seizures.
The younger individuals seem more likely to show CNS signs. Since signs are
often vague, lead toxicosis may be significantly under diagnosed in cats. The
gold standard of diagnostic tests is blood lead concentration, although it does not
necessarily correlate with total body burden of lead or with metabolic effects
including clinical signs. Diagnostic tests including erythropoietic protoporphyrin
(EPP), urine aminolevulinic acid, and others are discussed. Gross findings on
necropsy are few and include a yellow-brown discoloration of the liver often
with a nutmeg-like appearance. Histological examination may reveal
pathognomonic inclusion bodies in liver and renal tissues. Characteristic
histological changes in the CNS include neuronal necrosis and demyelination.
Treatment of lead toxicosis in cats, as in any species, involves removing the
exposure, decontaminating the individual and the environment, supportive care
and chelation therapy. The most recently available chelator is succimer (meso
2,3-dimercaptosuccinic acid). Succimer given orally is well tolerated and has a
wide margin of safety.
A high index of suspicion of lead toxicosis is warranted in cats since they often
present with vague and non-specific signs. With any consistent history owners
need to be asked about home renovation. Early diagnosis and treatment affords a
good prognosis.
© 2003 Published by Elsevier Ltd on behalf of ESFM and AAFP.

Introduction rodenticides, antifreeze, insecticides, and human

pain relievers such as ibuprofen and aceta-

A
t one time lead toxicosis was considered
the most common accidental poisoning
in small animals (Zook et al 1969, 1972,
Clark 1973, Hamir 1986, Bratton and Kowalczyk
1989). Federal regulations enacted in the 1970s led
to decrease in the amount of lead allowed in
residential paints, leaded gasoline, and other
household products, and a significant decrease in
incidence of lead toxicosis in humans and
domestic species has been seen over the past two
decades (Morgan et al 1991a, Graeme and Pollac
1998). Lead now ranks behind more common
accidental poisons in small animals such as
*Corresponding author. 14080 Hwy 98N, Kathleen, FL 33849,
USA. Tel: 1-863-859-3502; Fax: 1-863-853-8352. E-mail:
tknight327@aol.com
minophen in cats (Bratton and Kowalczyk 1989,
Berny et al 1992). Reports of lead poisoning repre-
sented approximately 0.5% of the calls received at
the National Animal Poison Control Center
(NAPCC) from 1985 to 1989 (Berny et al 1992).
Nevertheless, lead remains an important source
of toxicity in small animals.
Lead toxicosis in cats is infrequently reported.
Review of the literature from the past 45 years
has revealed 70 cases (Valler and Virat 1956,
Scott 1963, Priester and Hayes 1974, Zook and
Carpenter 1977, Turner and Fairburn 1979,
McLeavey 1980, Jacobs 1981, Watson 1981,
Prescott 1983, Hoffheimer 1988, Maddison and
Allan 1990, Morgan et al 1991a, Hawke and
Maddison 1992, Miller and Bauk 1992, Maddison

1098-612X/03/050249+07 $30.00/0 © 2003 Published by Elsevier Ltd on behalf of ESFM and AAFP.
250 TE Knight and MSA Kumar
et al 1993, Van Alstine et al 1993, Knight et al
2001). Incomplete data precluded analysis of an
additional report of 64 cats (Anonymous 1979).
This compares with over 800 cases of lead poison-
ing reported in dogs in the same time period
(Scott 1963, Zook et al 1969, 1972, Schrimsher
1971, Priester and Hayes 1974, Kowalczyk 1976,
Knecht et al 1979, Hamir 1981, O’Brien 1981,
Hamir and Handson 1982, Prescott 1983, Koh
1985, Hamir et al 1986, Morgan et al 1991a,
Khanna et al 1992, Ramsey et al 1996). This dis-
parity has traditionally been ascribed to the more
fastidious dietary habits in felines (Aronson 1972,
Van Alstine et al 1993). Constant grooming, how-
ever, makes cats more susceptible to ingestion of
paint dust or soil contamination on the coat and
footpads. Other factors which may help explain
this disparity include physiological differences in
susceptibility between species, although, to our
knowledge, no data concerning cats are available;
under diagnosis due to the often vague, non-
specific presenting signs in cats (Priester and
Hayes 1974, Miller and Bauk 1992, Maddison et al
1993); and historically more households have
owned dogs as pets (AVMA, 1997). In the follow-
ing paragraphs we review sources, signs, diag-
nosis, pathology, and treatment of lead toxicosis
in cats.
Sources
Numerous sources of lead exposure for small
animals include old paint and other building
materials such as linoleum, caulking compounds,
plumbers solder, carpet padding, and roofing
materials (Bratton and Kowalczyk 1989). Auto-
motive related sources include storage batteries,
wheel weights, used motor oil, and emissions
from gasoline engines. Sporting goods such as
golf balls, ammunition, and fishing weights are
also potential sources (Zook et al 1972, McLeavey
1980, Bratton and Kowalczyk 1989, Morgan et al
1991a,b, Van Alstine et al 1993). Miscellaneous
sources are contaminated water or soil (Scott
1963), newspaper and magazine print (Hankin
et al 1974), pottery glazes (Schrimsher 1971,
Turner and Fairburn 1979), lead dust from shoot-
ing galleries (Khanna et al 1992), and leaded
glass artwork and curtain weights (Fenner 1989,
Morgan et al 1991b). In our review of studies
specifically involving cats the source of lead
exposure was determined in 74% of cases (32/43)
with old paint being responsible 84% of the
time (27/32) (Scott 1963, Turner and Fairburn
1979, Jacobs 1981, Watson 1981, Prescott 1983,
Hoffheimer 1988, Maddison and Allan 1990,
Morgan et al 1991a, Miller and Bauk 1992, Van
Alstine et al 1993). Old paint is the most com-
monly identified source not only in lead poisoned
cats, but dogs and humans as well (Maddison et al
1993). Renovation of older houses involving the
sanding and scraping of lead-based paint is the
primary means of exposure (Maddison et al 1993).
Federal regulations have limited the lead content
of residential paint to <0.06% since 1977 (Morgan
et al 1991a, Ramsey et al 1996). However, 74% of
the occupied houses in the United States built
before 1980 still contain hazardous quantities of
lead paint (Graeme and Pollac 1998). Other
sources of exposure were contaminated soil from
a nearby lead mine in at least three cats (Scott
1963) and contamination of the integument of a
cat with lead silicate used in pottery glazing
(Turner and Fairburn 1979).
Signs
Lead toxicosis in domestic species character-
istically involves the gastrointestinal and neuro-
logical systems. Ingested lead is distributed first
to soft tissues including blood, liver, kidneys, and
the central nervous system with clinical signs
reflecting dysfunction of these organs. With
more chronic exposure bone becomes the primary
reservoir (Bratton and Kowalczyk 1989, Hong
and Han 1994). The most common clinical signs in
cats are anorexia, which may be the only present-
ing sign (McLeavey 1980, Miller and Bauk 1992,
Maddison et al 1993), vomiting, and seizures
(Table 1). Constitutional signs of lethargy and
weight loss are common. Among the more
unusual signs reported are ataxia of cerebellar
(Hoffheimer 1988) or vestibular (Knight et al
2001) origin, vertical nystagmus indicating
central vestibular dysfunction (Knight et al 2001),
polyuria/polydipsia (Valler and Virat 1956,
Morgan et al 1991a) presumably from renal
tubular damage, and megaesophagus with dys-
phagia which resolved 8–10 weeks following
treatment (Maddison and Allan 1990) (Table 1).
The age of the cat may affect which organ system
is involved. For example, in a report of 10 cats
(mean age 3.5 years) from Boston the most fre-
quent signs were anorexia, vomiting, and seizures
(Morgan et al 1991a), while a study of 13 cats from
Australia (mean age 8.8 years) reported vomiting
and anorexia but no neurological signs. This was
ascribed to the older age of the cats in that report
(Maddison et al 1993). In our review the average
age of cats with lead toxicosis, in reports where
 Lead toxicosis in cats—a review 251

Table 1. Signs of lead toxicosis in cats

Signs No. of cats References
Anorexia 48 Valler and Virat (1956), Turner and Fairburn (1979), McLeavey (1980), Jacobs
(1981), Watson (1981), Prescott (1983), Hoffheimer (1988), Maddison and Allan
(1990), Morgan et al (1991a), Miller and Bauk (1992), Hawke and Maddison
(1992),
Van Alstine et al (1993), Maddison et al (1993), and Knight et al (2001)
Vomiting 30 Valler and Virat (1956), Turner and Fairburn (1979), Watson (1981), Jacobs
(1981), Prescott (1983), Hoffheimer (1988), Morgan et al (1991a), Maddison et al
(1993), and Van Alstine et al (1993)
Seizures 23 Valler and Virat (1956), McLeavey (1980), Prescott (1983), Hoffheimer (1988),
Morgan et al (1991a), Van Alstine et al (1993), and Knight et al (2001)
Lethargy 17 Morgan et al (1991a), Van Alstine et al (1993), Hawke and Maddison (1992),
Jacobs (1981), and Maddison et al (1993)
Weight loss 17 Morgan et al (1991a), Van Alstine et al (1993), Hawke and Maddison (1992),
Jacobs (1981), Maddison et al (1993), and Knight et al (2001)
Ptyalism 10 Van Alstine et al (1993), and Hoffheimer (1988)
Depression 7 Maddison and Allan (1990), Turner and Fairburn (1979), and Maddison et al
(1993)
Hyperexcitability 7 Valler and Virat (1956), Maddison and Allan (1990), McLeavey (1980),
Maddison et al (1993), and Knight et al (2001)
Hysteria 5 Morgan et al (1991a) and Valler and Virat (1956)
Colic 4 Morgan et al (1991a), Maddison and Allan (1990), Hawke and Maddison (1992),
and Maddison et al (1993)
Constipation 4 Valler and Virat (1956), Prescott (1983), and Turner and Fairburn (1979)
Ataxia 3 Hoffheimer (1988) and Knight et al (2001)
PU/PD 3 Morgan et al (1991a) and Valler and Virat (1956)
Dysphagia 2 Valler and Virat (1956) and Maddison and Allan (1990)
Diarrhea 2 Morgan et al (1991a) and Maddison et al (1993)
Vertical nystagmus 2 Knight et al (2001)
Head tremor 2 Knight et al (2001)
Regurgitation 1 Hawke and Maddison (1992)
Hypermetria 1 Hoffheimer (1988)
Failure to groom 1 Hawke and Maddison (1992)
Third eyelid prolapse 1 Maddison et al (1993)
Megaesophagus 1 Maddison and Allan (1990)
Blindness 1 Hawke and Maddison (1992)
Circling NS McLeavey (1980)
Mydriasis NS McLeavey (1980)
NS=not stated.

the age was given, was 6.1 years (median age
4.5 years, n⫽35). Cats presenting with CNS signs
(seizures, ataxia, and hysteria) with or without
gastrointestinal signs had an average age of
4.1 years, and cats presenting with gastrointesti-
nal signs (vomiting, colic, constipation, diarrhea,
and regurgitation) without CNS signs had an
average age of 8.3 years. The trend of this small
number of cases indicates that younger cats may
develop CNS signs more readily. The explanation
may be that younger individuals of any domestic
species have increased permeability of the blood–
brain barrier (O’Brien 1981, Reid and Oehme
1989, Maddison et al 1993), greater gastrointesti-
nal absorption of ingested lead (Bratton and
Kowalczyk 1989, Reid and Oehme 1989), and less
efficient detoxification and excretory pathways
(Prescott 1983, Bratton and Kowalczyk 1989,
Maddison et al 1993), all resulting in higher lead
concentrations in the CNS.
Diagnosis
Blood lead concentrations are considered the
best diagnostic test for lead toxicosis. Toxic blood
levels in cats are >30–35 µg/dl (Fenner 1989, Van
Alstine et al 1993, Puls 1994) or >60 µg/dl (Reid
and Oehme 1989). However, it is important to be
aware that blood lead concentrations fluctuate
and due to sequestration in other organs do not
necessarily correlate with total body burden of
lead or with metabolic effects including clinical
252 TE Knight and MSA Kumar
signs (Bratton and Kowalczyk 1989, Hong and
Han 1993, Maddison et al 1993). Some animals
with clinical lead toxicosis will not have a diag-
nostic elevation of blood lead while some animals
may have elevated blood concentrations with few
if any clinical signs (Maddison et al 1993). Making
the diagnosis of lead toxicosis in cats requires
consistent physical examination findings with
confirmatory concentrations of blood lead. Lead
concentration in the blood should not be the sole
basis for diagnosis.
Less reliable diagnostic laboratory tests include
urine lead or urine
-aminolevulinic acid (ALA)
concentrations and blood zinc protoporphyrin
(ZPP) levels. Although urine lead concentrations
diagnostic for lead toxicosis have not been estab-
lished for cats, some authors suggest concen-
trations >50 µg/dl should be considered toxic
with background concentrations in cats being
<20 µg/dl (Scott 1963, Van Alstine et al 1993).
Enzymes of the heme synthetic pathway are
especially sensitive to lead and their substrate
concentrations may aid in the diagnosis of lead
toxicosis. Erythropoietic protoporphyrin (EPP)
accumulates in red blood cells (RBCs) residing in
the bone marrow due to inhibition of ferroche-
latase by lead. The majority of EPP in the cat will
bind zinc and exist as ZPP. Blood levels of ZPP
>50–54 µg/100 ml (Hawke and Maddison 1992,
Hong and Han 1993) indicate lead toxicosis. Since
elevated ZPP will be found only in those RBCs
which have left the bone marrow subsequent to
exposure, ZPP levels are not a good indicator of
acute lead exposure. Likewise, the ZPP remains in
the RBCs even after chelation therapy has been
completed, and is thus not a good indicator for
following the success of treatment. Additionally,
elevated ZPP is not specific to lead toxicosis. Iron
deficiency, for example, gives similar results
(Hawke and Maddison 1992). Inhibition of

-aminolevulinic dehydrase results in accumula-
tion of the substrate
-ALA in blood and urine.
Urinary ALA increases acutely with exposure to
lead but is not specific for lead toxicosis and may
be elevated in chronic liver disease and some por-
phyrias. A value greater than 87 µmol/l is sug-
gestive of lead toxicosis, although wide variation
in urinary ALA concentration in healthy cats
requires correlation with clinical signs and
blood lead levels (Hawke and Maddison 1992,
Maddison et al 1993).
‘Lead lines’ on radiographs are caused by lead
sequestration in the metaphyses of long bones in
growing animals and can potentially be helpful
diagnostically (Bratton and Kowalczyk 1989). The
term ‘lead lines’ also refers to a dark blue linear
discoloration of the gingiva near the teeth caused
by hydrogen sulfide of decaying food particles
reacting with blood borne lead to form a lead
sulfide precipitate (Jones et al 1997). To our
knowledge, radiographic or gingival ‘lead lines’
have not been reported in cats. Perhaps the most
valuable use of radiography to diagnose lead
poisoning in cats is to reveal radiodense specks of
lead in the gastrointestinal tract, although bone
chips may appear similar.
Hemogram evaluation for lead toxicosis in cats
is usually normal and not helpful. The abnormali-
ties most commonly found are nucleated RBCs
(McLeavey 1980, Prescott 1983, Bratton and
Kowalczyk 1989), followed by anemia (Valler and
Virat 1956, Scott 1963, Priester and Hayes 1974,
Zook and Carpenter 1977) and then basophilic
stippling (Priester and Hayes 1974, Bratton and
Kowalczyk 1989). Although nucleated RBCs
(normoblastemia) in the absence of anemia are
regarded as classic hemograms in lead poisoned
animals, this finding is unusual in cats.
Lead causes toxic effects primarily in the
hepatocytes and renal tubular epithelial cells by
forming complexes with sulfhydryl groups in
crucial sulhydryl-dependent proteins resulting in
enzyme inhibition and ultimately cell death
(Graeme and Pollac 1998). This results in elevated
liver enzymes on serum chemistry analysis and
glycosuria, proteinuria, and granular cast forma-
tion on urinalysis (Hoffheimer 1988, Bratton and
Kowalczyk 1989, Morgan et al 1991a). A post-
mortem diagnosis can be made by analyzing lead
concentration in tissues. The liver and kidneys are
primary soft tissue organs of distribution with
lead toxicosis. Higher doses and more acute
exposure increase the proportion of lead found in
the liver, kidneys, and brain (eg 36, 20, and 1%,
respectively) relative to amounts found in bone
(eg 42%). With chronic exposure bone may con-
tain higher levels (eg 82%), with smaller amounts
in the liver, kidney, and brain (eg 7, 8, and 2%,
respectively) (Hong and Han 1994). Analysis of
lead concentration in the liver is used most fre-
quently. Levels >3.6–10 µg/g by wet weight of
liver tissue is diagnostic of lead toxicosis (Bratton
and Kowalczyk 1989, Puls 1994, Jones et al 1997).
Pathology
Reports of pathology findings in cats with lead
toxicosis are rare. Experimental lead poisoning in
a study of 30 cats revealed on gross necropsy
examination yellow-brown discoloration of the
 Lead toxicosis in cats—a review
liver in 11 cats often with a nutmeg-like appear-
ance. Enlarged mesenteric lymph nodes were also
seen in five cats although no specific histological
changes were found (Hong and Han 1994).
Pathognomonic, intranuclear, acid fast inclusion
bodies or intranuclear or cytoplasmic inclusion
bodies seen on H&E and orcein stained specimens
may be seen in hepatocytes and in epithelial cells
of the proximal renal tubules (Jubb et al 1993,
Hong and Han 1994, Jones et al 1997). Lesions of
the CNS are not found on gross necropsy (Van
Alstine et al 1993, Hong and Han 1994), but
histological findings include neuronal necrosis,
demyelination, and astrocyte proliferation in the
gray matter of the cerebrum. The cerebellum may
have degeneration of Purkinje cells (Hong and
Han 1994). Brain stem histology may reveal multi-
focal hemorrhages, vacuolated and dilated
periaxonal spaces, eosinophilic shrunken nerve
cell bodies with astrocytosis and microgliosis
(Van Alstine et al 1993), and demyelination with
neuronal necrosis (Hong and Han 1994).
Neurological signs correlate with necropsy
findings in the CNS. Seizures, the most commonly
reported neurological sign, as well as hyper-
exciteability, hysteria, and depression are consist-
ent with abnormalities in the cerebral cortex.
Hypermetria, ataxia, and head tremor may
reflect cerebellar dysfunction while brainstem
lesions could result in ataxia, nystagmus, dys-
phagia, and ptyalism. Anorexia, vomiting, and
ptyalism may result from CNS or gastrointestinal
dysfunction.
Treatment
Treatment of lead toxicosis in the cat, as in other
species, involves prevention of further exposure,
decontamination of the environment and the indi-
vidual (ie bathing, cathartics, and/or enemas),
supportive therapy, and chelation teatment.
Magnesium sulfate (epsom salt) or sodium sulfate
cathartics are preferred since lead will precipitate
in the gastrointestinal tract as lead sulfate which is
not absorbed (Bratton and Kowalczyk 1989). The
recommended dose in cats is 2–5 g given orally
while enema solutions of these agents should
be avoided in cats due to possible electrolyte
imbalances (Plumb 1999). The first chelating
agent available was calcium disodium ethyl-
enediaminetetraacetic acid (CaNa2EDTA, cal-
cium edetate, CaEDTA; Calcium Disodium
Versenate, 3M Pharma., St. Paul, MN). This agent
has the advantage of a proven track record in
many species and can be administered by any
253
route. For cats CaEDTA may be given subcutane-
ously at 27.5 mg/kg in 15 ml of D5W qid for
5 days, and repeated in 2 or 3 weeks if blood lead
concentration remains >0.2 ppm. CaEDTA may
also be given slowly IV at a dose of 5 mg/kg in
divided daily doses (Reid and Oehme 1989).
CaEDTA acts primarily on lead sequestered in
bone which may be from 42 to 82% of total body
lead burden depending on length of exposure and
concentration of ingested lead. With lower doses
and longer exposures proportionately more lead
is sequestered in bone (Jubb et al 1993, Hong and
Han 1994). The lead chelator complex is then
excreted in the urine. Significant side effects of
CaEDTA include pain at injection sites (especially
when given IM), potential nephrotoxicity, and
depletion of essential minerals like calcium, zinc,
and iron. Also, when given alone it may para-
doxically worsen lead encephalopathy within the
first 2 days of therapy (Graziano et al 1978, 1985,
Fikes and Dorman 1994, Ramsey et al 1996). This
is apparently caused by lead being redistributed
from soft tissue to the brain. Some authors recom-
mend that British anti-lewisite (dimercaprol,
BAL; BAL in Oil, Becton Dickinson) be given as an
intramuscular (IM) injection before instituting
CaEDTA therapy. BAL, a dithiol agent, works
primarily by chelating lead from soft tissue with
excretion of the complex in urine and bile. BAL
therapy prior to calcium edetate helps prevent
exacerbation of encephalopathy (Fikes and
Dorman 1994, Ramsey et al 1996, Graeme and
Pollac 1998) and the two agents act synergisti-
cally. CaEDTA is given parenterally or, if neces-
sary, may be given orally in dogs (Hamir et al
1986) while BAL is given by IM injection. Because
the therapeutic index is low for both agents they
are best given in a hospital setting (Graziano et al
1978, 1985). BAL in veterinary medicine is pri-
marily used in arsenic toxicosis. In our review we
found no reports of use in cats, and we have no
experience treating lead toxicosis in cats with
BAL. The dosage for arsenic toxicosis in cats (and
presumably for lead toxicosis) is 2.5–5 mg/kg IM
q 4 h for 48 h, then q 12 h until recovery. The drug
causes pain with IM injection and should be used
cautiously in patients with renal compromise and
always with IV fluid support (Reid and Oehme
1989). D-penicillamine (Cuprimine, Merck, West
Point, PA) is a monothiol, oral chelating agent
which is often given (125 mg q 12 h. p.o. for
5 days) as an outpatient drug to follow-up
CaEDTA therapy in cats particularly if the
blood lead concentration remains >0.2 ppm at
3–4 weeks after CaEDTA therapy (Reid and
254 TE Knight and MSA Kumar
Oehme 1989). Vomiting is a common side effect
but may be cirvumvented by giving with food or
giving smaller, more frequent dosing (same total
dose). Cuprimine may also increase the amount
of lead absorbed from the gastrointestinal tract.
Enemas or purgatives should therefore be given
prior to use, especially if radiodense specks are
seen in the gastrointestinal tract on radiographs.
CaEDTA, Cuprimine and BAL are all potentially
nephrotoxic (Fikes and Dorman 1994, Graeme
and Pollac 1998).
Succimer (meso 2,3-dimercaptosuccinic acid,
DMSA; Chemet, Sanofi-Synthelabo, New York,
NY), an analog of BAL, is the most recent chelat-
ing agent to become available. Succimer has been
used for decades in other countries but was first
approved for human use in the United States in
the mid-1990s. Oral dosing is an advantage, and it
may be given rectally as a solution in vomiting
patients. Excretion is via bile and urine (Graziano
et al 1978, Ramsey et al 1996). Succimer has been
used successfully in dogs (Ramsey et al 1996) and
cats (Knight et al 2001), but does not have FDA
approval for use in veterinary patients. In the only
report of use in cats, two 5-year-old female litter-
mate cats with lead toxicosis presented with
anorexia, head tremors, central vestibular signs,
and developed seizures soon after admission.
They were successfully treated with oral succimer
and suffered no side effects from the drug. Within
48 h of beginning treatment the signs began to
resolve and blood lead concentrations were nor-
mal after 1 week of therapy. The cats were clini-
cally normal 3 weeks after discharge (Knight et al
2001). Succimer appears to be a safe drug with no
potential for nephrotoxicity. Toxicity studies with
beagles given three times the recommended dose
(105 mg/kg/day) for 15 times the recommended
duration (22 weeks) showed no adverse effects
and no clinical, biochemical, or pathological
abnormalities (Graziano et al 1978). Standard dos-
age for dogs and cats is 10 mg/kg, p.o., q 8 h for 10
days (Graziano et al 1978, Knight et al 2001).
Maximal response to succimer, in terms of
amount of lead excreted, can be expected in the
first day of treatment (Graziano et al 1978, 1985,
Knight et al 2001). A rebound in blood lead levels
after completion of the first course of therapy may
necessitate a subsequent course (Graziano et al
1985, Ramsey et al, 1996).
Conclusions
Lead toxicosis remains a significant malady in
feline patients and warrants a high index of sus-
picion since cats often present with vague, non-
specific signs. With any consistent history,
owners should be asked specifically about home
renovations. Making the diagnosis is usually
straightforward by finding elevated blood lead
concentrations with consistent clinical signs.
Supportive therapy, eliminating the source of
lead and early treatment with chelating agents
afford a good prognosis. Succimer has worked
well in dogs and appears to work well in cats.
More experience with this drug in cats will be
helpful in determining safety profile, alternate
routes of administration (eg efficacy when given
per rectum in cats), and potential for rebound of
lead concentrations after treatment.
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