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---Poisoning by metals---
lead poisoning
(plumbism)
Lead poisoning is associated with the
accidental ingestion of sources of lead
metal or compounds or the ingestion of
feed, usually forage, containing lead usually
from pollution of the environment.
Epidemiology
Occurrence
Lead is one of the most common poisonings
in farm animals, especially young cattle.
Sheep and horses are also affected but not as
commonly.
Cattle.
lead poisoning is the most common toxicosis in
cattle.
The disease occurred most commonly in younger
cattle with 52% of the cases reported in animals 6
months of age or less.
Approximately 60% of the cases occurred during the
summer months from May to August, when the
cattle have ready access to lead –containing
materials such as crankcase oil and batteries that
are being changed in agricultural machinery.
In many countries the incidence of the disease is
highest in cattle in the spring of the year a few
days after the animals have been turned out onto
pasture.
Lead poisoning occurs most commonly in
young cattle soon after spring turnout when
animals gain access to discarded waste
materials including batteries, dump oil, oil
paint containers, and bonfire ash where
painted lumber has been burned.
In ruminants there is a tendency for metallic
lead particles to settle in the reticulum and
poisoning results from the gradual conversion
of lead particles to soluble lead acetate.
Animals eating vegetation in these areas may
accumulate amounts of lead sufficient to produce
clinical signs of lead poisoning.
Sheep…
are usually affected by eating forage
contaminated by environmental sources of
lead
Horses.
Lead poisoning in horses occurs most
commonly when they graze lead
contaminated pastures rather than by the
accidental ingestion of a toxic amount of
lead. Young horses are particularly more
susceptible than older horses. some cases
in horses have been due to ingestion of
paint chips from a fence on pasture.
Sources of lead
1-Lead poisoning may occurs in cattle at
pasture, particularly if the pasture is poor
and the animals are allowed to forage in
unusual places, such as rubbish dumps.
Phosphorus deficiency may also be a
predisposing factor, in that affected animals
will chew solid objects as a manifestation of
osteophagia. However, cattle on lush pasture
may also seek out foreign material to chew.
Confined housing of calves with or without
overcrowding is often followed by the
appearance of pica which may be associated
with mineral deficiency.
2-Lead paint and lead batteries.
The common sources of lead are lead-bearing paints
and metallic lead. Discarded lead batteries are one
of the most common sources of lead poisoning in
cattle. the batteries freeze during the winter
months and break open, exposing the plates which
are attractive and palatable for cattle to lick and
chew.
3-Lead contaminated feed.
The contamination of forage supplies with shotgun lead
pellets used in hunting and shooting exercises, can serve
as a source of lead for cattle grazing the pasture or
consuming silage made from the contaminated field.
Automobile batteries have been accidentally added to feed
mixers where they are ground by powerful augers and
mixed into the feed supply of cattle.
4-Industrial lead.
Metallic lead in the form of lead shot, solder, or
leaded windows has been associated with
mortalities.
5- Lead parasiticide sprays, particularly those
containing lead arsenate, was once associated with
heavy losses in cattle grazing in recently sprayed
orchards or vegetable crops.
6- Environmental pollution with lead
a-Environmental pollution with lead is a common
occurrence in cities and on their edges. highways
buldings
b- Environmental pollution from processing factories
can result in varying degrees of poisoning with
lead,
Toxic levels of lead
The toxic level of lead varies between species
and the chemical composition of the
compound containing lead may influence its
toxicity. Lead acetate is very soluble and
more toxic than insoluble lead oxide, or solid
lead sheeting.
Acute lethal single doses
In calves, acute single lethal doses range
from 400 to 600 mg/kg body weight
in adult cattle 600-800 mg/kg
for goats 400 mglkg.
The acute dose for horses is more than 1000 mg/ kg
Pathogenesis….
1-Regardless of the chemical form of the ingested
lead, only a small proportion is absorbed because
of the formation in the alimentary tract of insoluble
lead complexes which are excreted in the feces.
2-The toxic effects of lead are manifested in three
main ways:
Lead encephalopathy
Gastroenteritis
Degeneration of peripheral nerves.
3- In general, acute nervous system involvement
occurs following the ingestion of large doses in
susceptible animals such as calves, alimentary
tract irritation following moderate doses, and
peripheral nerve lesions following long-term
ingestion of small amounts of lead.
4-The nervous signs of encephalopathy and
the lesions of peripheral nerve degeneration
are due to the degenerative changes of
nervous system tissue.
5- Gastroenteritis is associated with the
caustic action of lead salts on the
alimentary mucosa.
Ruminal atony occurs in cattle and sheep
and initially is associated with scant
feces,followed later in some cases by
diarrhea due to gastroenteritis. The rumen
protozoa in cattle with acute lead poisoning
are commonly absent or inactive.
6- Peripheral nerve degeneration occurs
principally in horses.
7- The lesions, including degeneration of the
liver and kidney, vary in their severity with
the tissue levels of lead.
8- The blue 'lead-line' at the gum-tooth
junction, which is seen in man and the dog,
does not commonly occur in ruminants
because of failure to form tartar but may be
present in the horse. The 'lead line' is a
deposit of lead sulfide formed by the
combination of lead with sulfide from the
tartar.
9-Lead is transferred across the placental
barrier. Calves born from cows
experimentally poisoned with lead have
elevated levels of lead in bone, kidney, and
liver.
10-Anemia may occur in chronic lead
poisoning. The erythrocytes are microcytic
or normocytic and hypochromic,or
normochromic and reticulocytosis and
basophilic stippling may be observed.
The anemia in chronic lead poisoning is
associated with two basic defects: a
shortened erythrocyte lifespan and
impairment of heme synthesis.
Clinical findings…
Cattle…
In the acute form
there is usually a sudden onset of signs and a
short course of 12-24 hours so that many
animals,especially those at pasture, are
found dead without signs having been
observed.
Staggering, and muscle tremors particularly of
the head and neck, with champing of the
jaws frothing at the mouth are obvious.
Snapping of the eyelids, rolling of the eyes
and bellowing are common
Blindness and cervical, facial and auricular
twitching are consistent in acute lead
poisoning of cattle.
The animal eventually falls and intermittent
tonic-clonic convulsions occur and may
continue until death.
Pupillary dilatation
opisthotonos and muscle tremor are marked
and persist between the convulsive
episodes.
There is hyperesthesia to touch and
sound,and the heart and respiratory rates
are increased.
In some cases, particularly in adults, the
animal remains standing, but appearing
blind,
attempts to jump over walls
Head-presses strongly against walls or
fences
Frenzy is common and some animals appear
to attack humans but the gait is stiff and
jerky and progress is impeded.
Death usually occurs during a convulsion and
is due to respiratory failure.
In the subacute form
the animal remains alive for 3-4 days. There is
dullness, total anorexia, blindness, and
some abnormality of gait including
incoordination and staggering, and
sometimes circling.
The circling is intennittent and not always in
the same direction and usually occurs when
the animal is confined in a small space like
a box stall. Muscle tremor and
hyperesthesia are common but not as
pronounced as in the acute form.
Grinding of the teeth is common,
Excessive salivation may occur
Mild abdominal pain may be seen
occasionally.
Alimentary tract dysfunction is one of the
most common abnormalities. Ruminal atony
is accompanied by constipation in the early
stages. Later a fetid diarrhea occurs in most
cases.
Experimental lead poisoning in young
milk-feed calves
initially is characterized by severe
depression and hypoglossal paresis
which interferes with sucking.
Within the next 12-24 hours, the calves
become unsteady, ataxic, and exhibit
muscular tremors of the head and
forelimbs and finally convulsions,
opisthotonos
they die in respiratory failure during a
state of epilepsy .
Sheep…
Lead poisoning in sheep is usually
manifested by a subacute syndrome similar
to that seen in adult cattle.
There is anorexia and scant feces followed
by the passage of dark, foul-smelling feces.
Weakness and ataxia follow, often with
abdominal pain, but there is no excitement,
tetany, or convulsions. Polyuria occurs
when the intake of lead is small but with
large amounts there is oliguria.
Chronic ingestion of metallic lead by pregnant sheep
can be associated with abortion and transitory infertility.
Horses
Horses are not commonly affected by lead
poisoning, although the chronic form
occurred occasionally in the vicinity of lead
mines and processing works.
The clinical findings are extremely variable.A
rough hair coat, pharyngeal dysfunction, and
weight loss were the most common clinical
findings.
Inspiratory dyspnea associated with paralysis
of the recurrent laryngeal nerve is the most
common finding. This may be accompanied
by pharyngeal paralysis in which recurrent
choke and regurgitation of food and water
through the nostrils occur
Aspiration pneumonia may result after
inhalation of ingesta through the
paralyzed larynx.
Paralysis of the lips occasionally
accompanies the other signs.
General muscle weakness and stiffness
of the joints occur commonly and the
hair coat is usually harsh and dry.
Sub clinical lead poisoning
Because of the present concern about
environmental pollution, the effects of the
chronic low-level intake of lead have been
examined and defined.
In cattle, at intake levels below those which
are associated with clinical signs, there are
metabolic changes and changes in blood
variables accompanied by a decreased rate
of growth.
One concern is that continuous low-level
consumption by pregnant females will result
in teratogenic effects in the newborn.
Clinical pathology….
In the living animal which has ingested lead,
the element can be detected in blood, feces,
urine, and milk.
1- Blood lead…
Whole blood levels of lead in normal
ruminants are usually below 0.05-0.25 ppm;
poisoned animals usually have levels above
0.35 ppm and deaths begin at 1.0 ppm.
2- Milk lead….
Lead levels of 0.13 mg/L of milk have occurred in natural
cases with a half life of 4-6 days. In acute lead poisoning
lead concentrations in milk
were 1.13 ppm.
3-Fecal lead….
Fecal levels of lead represent
unabsorbed and excreted lead deriving
from the bones, and are of limited
value unless considered in conjunction
with blood levels because ingested
lead may have been in an insoluble
form and harmless to the animal.
When fecal levels are high it can be proposed
that the lead has been ingested in the
preceding 2-3 weeks but high blood levels
may be maintained for months after
ingestion. Thus high blood and low fecal
levels indicate that the lead was taken in
some weeks previously but high blood and
high fecal levels suggest recent ingestion
and significant absorption.
4-Urinary lead…
Urine lead levels are variable, rarely high (0.2-
0.3 mg/L), and although elevated urine levels
are usually associated with high blood levels.
5-Estimation of delta-aminolevulinic acid
dehydratase (Delta-ALA-D) in blood used to
supplement blood lead determinations.
6- Erythrocyte protoporphyrin
The levels of free erythrocyte zinc protoporphyrin
increase in lead poisoning and this is indicative of
the chronic metabolic effect of lead on the erythroid
cells being released from bone marrow into the
peripheral circulation.
7-Hematology
In chronic lead poisoning, hematological
examination may reveal
a normocytic, normochromic anemia
however basophilic stippling might seen
but may be not enough to be diagnostic.
Moreover poikilocytosis and anisocytosis
were marked some times.
8-50 g of liver ,kidney and reticulum for assay
of lead.
9-Histopathological examination
Necropsy findings…
In most acute cases there are no gross lesions at
necropsy. In cases of longer standing there may be
some degree of abomasitis and enteritis, diffuse
congestion of the lungs and degeneration of the
liver and kidney.
Epicardial hemorrhages are common. Congestion of
meningeal and cerebral vessels may also be
observed and hemorrhages may be present in the
meninges.
An increase in cerebrospinal fluid is often recorded
but is of minor degree in most cases.
In chronic cases gross lesions are recorded in cattle. These
include cerebrocortical softening, cavitation and yellow
discoloration with most severe lesions in the occipital lobes.
DD….
In all animals the disease must be differentiated
from
Rabies
Polioencephalomalacia
Hypovitaminosis-A
nervous acteonemia
arsenic poisoning
meningio-encephalomylitis
Treatment…
1-Sedation and care …by IV injection of
pentobarbital sodium in calves and chloral hydrate
in adults temporarily relieves the convulsions.
2-Calcium versenate (calcium disodium
ethylenediamine tetra-acetate, CaEDTA).
CaEDTA is available as a 6.6% solution for
IV administration. at a dose of 110-220
mg/kg BW over 12 hours, which is
approached by rapid IV injections of two
doses of 110 mglkg BW weight, 6 hours
apart. This can be done daily for 3-5 days.
Note:1…CaEDTA removes lead directly from
bone-sensitive sites and not from
parenchymatous organs because cell
membranes form a barrier to the therapeutic
removal of intracellular lead.
3-Thiamin hydrochloride….
Are used in combination with Ca EDTA to
reduced the deposition of lead in most
tissues especially liver, kidney. and the
central and peripheral nervous system.
thiamin at 25 mg/kg BW SC BID is
recommended .
Arsenic poisoning
Arsenic compounds likely to be encountered
by large animals are as follows:
Inorganic compounds used as insecticidal
dips or as herbicides such as arsenic
trioxide, sodium arsenite,sodium arsenate.
Organic compounds such as
Aliphatic organic arsenicals:such as
cacodylic and phenylarsonic
acids,monosodium, and disodium
methanearsonates (MSMA & DSMA) .
Relative toxicities.
1-Toxic oral doses may range from 1 to 25
mg/kg for the arsenite, 30-100 mg/kg for the
arsenate, cacodylic acid 25 mg/kg daily for
8-10 days, and 10-25 mg/kg for 5-6 days for
the methanearsonates.
2-Aromatic organic arsenicals are toxic when
the recommended accumulative dose is
exceeded by 2-4 times the recommended
dose, delivered by either exceeding the
recommended percentage in the feed or
feeding it for too long.
Epidemiology….
Source of toxin
Arsenic is remains in the environment permanently
so that the source may not be recorded in natural
history.
1-Dips and sprays.
Fluids used for dipping and spraying of animals to
control ectoparasites are the commonest source.
Animals may swallow the solution while in the dip
or in the draining yards after dipping. Animals that
are not allowed to drain completely and faulty
disposal of drainage from yards and dips may
contaminate the pasture.
Opened containers of dipping solutions or
powders may accidentally contaminate feed
or be mistakenly applied as a skin dressing
thus amounts of arsenic are absorbed
through the skin after dipping in sodium
arsenite.
The absorption is increased if the animals are
dipped when hot, if the fleece is long, if they
are crowded too tightly in draining yards or
driven too soon after dipping
There is some danger in dipping rams at
mating time when erythema of the skin of
the thighs and scrotum is present.
Dipping immediately after shearing and
jetting at too high pressure or with
excessively strong solutions may also be
associated with increased absorption.
2-Herbicides include sodium or potassium
arsenite, arsenic pentoxide, and
monosodium or disodium acid methane
arsonate sprays used to kill potato prior to
mechanical harvesting
3-Insecticidal sprays used in orchards and
pasture contaminated by calcium arsenate
applied to kill beetle grubs are sources.
In most instances poisoning occurs when
animals accidentally gain access to recently
sprayed areas, although drifting of
windblown spray may result in accidental
contamination of pasture.
Grass clippings from lawn areas treated with
arsenical herbicides 6 months earlier may
carry 15 000 mg/kg arsenic. With lead
arsenate the major effects are usually
ascribed to the effects of the lead but this
does not always appear to be so.
4-Insect baits may contain Paris green (cupric
acetoarsenite) mixed with bran and when
these are laid over large areas of land in an
attempt to control grasshopper plagues
they constitute a major hazard to livestock.
5-Wood preservatives especially arsenic
copper- chromiun are used to treat pine in
wooden calf pens. The compound has a
salty taste and is licked avidly. Ashes from
burned treated pine posts are also palatable
to cattle.
6-Some metal-bearing ore deposits including
iron, arsenic pyrites in volcanic soils, gold
and copper ores contain large quantities of
arsenic which may be licked.
7-Pharmaceuticals and growth stimulants
including arsanilic acid and sodium
arsanilate, and phenylarsonic acid
preparations such as roxarsone, nitarsone,
are used both as feed additives and in the
control and treatment of dysentery in
animals, and as antidotes to selenium
poisoning. Overdosing with them can occur
accidentally by carrying on the administration for
too long or when there is an error in mixing a
batch of feed.
Route of poisoning
Arsenic poisoning usually occurs after
ingestion of the toxic substance but per
cutaneous absorption can occur especially if
the skin is abraded or hyperemic and
percutaneous toxic dose is much lower.
Poison risk factors
Soluble salts are highly poisonous; arsenic
trioxide and sodium arsenate are much less
soluble and thus less toxic than sodium
arsenite. Organic chemicals used as
weedicides are as poisonous as the arsenite
but organic arsenicals used as growth
stimulants are less toxic, although they are
absorbed rapidly
Host risk factors.
The LD50 of sodium arsenite varies between
species with pigs, horses, cattle, and sheep
requiring increasing doses to be affected.
Pathogenesis….
1-Mode of action.
Arsenic is a general tissue poison. The
inorganic salts and the enteric-oriented
organic compounds exert their toxic effects
by combining with and inactivating the
sulfuydryl groups in tissue enzymes.
2- Tissue susceptibility.
Although all tissues are affected, deposition and
toxic effects are greatest in those tissues which
are rich in oxidative enzyme systems.Thus
alimentary tract wall, liver, kidney,spleen, and lung
are most susceptible to the general depression of
metabolic activity which results.
A-Alimentary tract lesions produce the most
obvious clinical signs due to the extensive
damage to capillaries causing increased
permeability and exudation of serum into
tissue spaces. The mucosa lifts from the
underlying muscle coat and is shed with the
resulting loss of large quantities of body
fluids.
B- Percutaneous absorption. Arsenic
absorbed from the skin may be associated
with local necrosis without systemic signs if
the peripheral circulation is poor or the
concentration of arsenic is excessively
high, but if the cutaneous circulation is
good, the arsenic is quickly carried away
and is associated with a systemic disease
without skin necrosis.
C- Chronic poisoning. The chronic toxicity of
arsenic at low levels of intake is due to its
accumulation in particular organs,especially
the liver, kidney, alimentary tract wall,
epidermis, spleen, and lung.
D- Nervous tissue lesions. The nervous
signs associated with organic
arsenicals are the result of inhibition of
dehydrogenase enzyme systems
causing degenerative changes in
peripheral nerves. These appear as
demyelination and axonal degeneration
in prolonged cases.
Animals recumbent longer than 7 days are
unlikely to recover and will remain
paralyzed until death from other associated
conditions.
In poisoning with the arsanilic acid
compounds the lesions are mostly in the
optic nerves, causing blindness. In
poisoning with the phenylarsonic acid
group the nerves to the limbs appear to be
affected most.
Clinical findings….
Peracute cases
show little except depression and
prostration and die before signs of
enteritis develop. A fluid sound in
the abdomen can be elicited by
shaking the animal. Death occurs
3-4 hours after commencement of
the illness and is usually preceded
by clonic convulsions and diarrhea
Acute cases (Ruminant gastroenteritis
syndromes)
are the commonest syndromes in ruminants;
the onset of signs of illness is delayed 20-50
hours from the intake of the poison,
Distress develops suddenly, commencing
with severe abdominal pain, restlessness,
groaning, an increased respiratory rate,
salivation, grinding of the teeth, complete
ruminal stasis, and vomiting, even in cattle.
A fluid and fetid diarrhea develops later. The
heart rate is greatly increased, the pulse
small in amplitude; dehydration, and
oliguria are marked.
Subacute cases
give the same signs as acute cases
but the course may extend over 2-7
days. Nervous signs of muscle
tremor, incoordination, and clonic
convulsions are followed by
terminal coma.
Chronic cases.
Commonly observed signs include low body
weight, a dry, staring coat which is easily
shed, loss of vigor and spirit,capricious
appetite, indigestion,conjunctival and
mucosal erythema, eyelid edema and
conjunctivitis. Buccal mucosal ulceration
may extend to the muzzle. Milk yield is
seriously reduced and abortions and
stillbirths may occur. Local skin lesions
include initial hyperemia followed by
necrosis and sloughing leaving indolent
lesions which are extremely slow to heal.
Horses…
Signs include marked congestion of
the mucosae and a very sudden
onset of severe colic which passes
off in a few hours in horses which
survive . Severe diarrhea may be
followed by a period of complete
stasis of the alimentary tract with
diarrhea recurring just before
death.
Nervous syndromes in pigs and lambs
Chronic poisoning resulting from overdosing
with arsanilic acid is manifested by
incoordination and blindness appearing
about 7 days after the compound is first fed.
Consciousness, body temperature,and
appetite are unaffected. If feeding is
continued the signs gradually worsen but
disappear within a few days if the feed is
changed. Some pigs remain permanently
blind or paralyzed.
Clinical pathology….
1-Arsenic can be detected in the
urine, feces, and milk for
periods of up to about 10 days,
beginning shortly after the toxic
material is ingested.
2- Histopathological examination
Necropsy findings….
In acute and subacute cases of inorganic arsenic
poisoning there are pronounced hyperemia and
patchy submucosal hemorrhage in the stomach,
duodenum,and cecum. Hemorrhage and multifocal
ulceration of the cecum and large colon have been
observed in horses.
In ruminants the forestomachs are unaffected but
typical lesions are present in the abomasum. The
gut contents are very fluid, and contain much
mucus and shreds of mucosa.
Profuse subendocardial hemorrhages are common
and ulceration of the gallbladder mucosa is often
observed in sheep
DD….
Lead poisoning
Bovine malignant catarrh
Salmonellosis
Poisonous plants
internal parasitism
Organic mercury poisoning
Salt poisoning
Encephalitis
Treatment….
1-In acute cases treatment is of little value because
of the large amounts ingested and the delay
between ingestion and the appearance of illness,
but affected animals are unsuitable for human
consumption so that treatment is not usually
undertaken
2- BAL (2,3-dimercaptopropranol) is an
efficient antidote for poisoning by organic
arsenicals, but is often disappointing in
cases of poisoning by inorganic salts,
unless therapy is begun before clinical
signs appear. Dosing at 4- hourly intervals
is necessary and the oily injection is
associated with some local pain. Although
BAL has a general beneficial effect and is
recommended as a treatment, the drug is
quite toxic itself and in the doses required
may be associated with deaths in sheep. It
also is associated with a reaction at the
injection site sometimes serious enough to
warrant the animal's destruction.
3- Sodium thiosulfate is a practicable and
frequently used treatment. The compound is
almost completely non-toxic and can be
given in large amounts and without
accurate measurement.Intravenous
injection is desirable as an initial treatment
using 15-30 g of the salt in 100-200 mL of
water and this should be followed by oral
dosing of 30-60 g at 6-hour intervals.
Treatment should be continued until
recovery occurs which may require 3-4
days.
4- Supportive treatment
a- The antioxidants zinc, methionine, and
cysteine,used with chelation therapy, have been
reported to enhance excretion of arsenic
b- Attempts should be made to adsorb the residual
arsenic in the gut by administering charcoal (1-4
g/kg BW per os), and then removed by the
administration of an oil demulcent, or osmotic
aperient like magnesium sulfate
c-fluid therapy and Astringent preparations given by
mouth may help to reduce the loss of body fluids.
Recovering animals should receive a
bland diet and high-quality protein.