DOI: 10.1111/j.1439-0396.2012.01309.
REVIEW ARTICLE
A review of oxalate poisoning in domestic animals: tolerance
and performance aspects
M. M. Rahman, R. B. Abdullah and W. E. Wan Khadijah
Institute of Biological Sciences, Faculty of Science, University of Malaya, Kuala Lumpur, Malaysia
Keywords
adaptation, oxalate, performance, tolerance
Correspondence
M. M. Rahman, Institute of Biological
Sciences, Faculty of Science, University of
Malaya, 50603 Kuala Lumpur, Malaysia.
Tel: +603-79674366; Fax: +603-79674374;
E-mail: mijanur04@yahoo.co.uk
Received: 4 November 2011;
accepted: 23 March 2012
Introduction
Oxalic acid is a common constituent of plants that
occurs in two forms: soluble and insoluble oxalates.
Soluble oxalate usually forms with monovalent
counterions such as sodium (Na+), potassium (K+)
and ammonium (NH4+), whereas insoluble oxalate
forms with divalent calcium (Ca2+), magnesium
(Mg2+) and iron (Fe2+) ions (Savage et al., 2000).
Journal of Animal Physiology and Animal Nutrition 97 (2013) 605–614 ª 2012 Blackwell Verlag GmbH
Summary
Published data on oxalate poisoning in domestic animals are reviewed,
with a focus on tolerance and performance. Oxalic acid is one of a num-
ber of anti-nutrients found in forage. It can bind with dietary calcium
(Ca) or magnesium (Mg) to form insoluble Ca or Mg oxalate, which
then may lead to low serum Ca or Mg levels as well as to renal failure
because of precipitation of these salts in the kidneys. Dietary oxalate
plays an important role in the formation of Ca oxalate, and a high die-
tary intake of Ca may decrease oxalate absorption and its subsequent
urinary excretion. Oxalate-rich plants can be supplemented with other
plants as forage for domestic animals, which may help to reduce the
overall intake of oxalate-rich plants. Non-ruminants appear to be more
sensitive to oxalate than ruminants because in the latter, rumen bacteria
help to degrade oxalate. If ruminants are slowly exposed to a diet high
in oxalate, the population of oxalate-degrading bacteria in the rumen
increases sufficiently to prevent oxalate poisoning. However, if large
quantities of oxalate-rich plants are eaten, the rumen is overwhelmed
and unable to metabolize the oxalate and oxalate-poisoning results.
Based on published data, we consider that <2.0% soluble oxalate would
be an appropriate level to avoid oxalate poisoning in ruminants,
although blood Ca level may decrease. In the case of non-ruminants,
<0.5% soluble oxalate may be acceptable. However, these proposed safe
levels of soluble oxalate should be regarded as preliminary. Further
studies, especially long-term studies, are needed to validate and improve
the recommended safe levels in animals. This review will encourage fur-
ther research on the relationships between dietary oxalate, other dietary
factors and renal failure in domestic animals.
Several pathways for oxalate production have been
proposed, which include photorespiratory glyoxylate
oxidation, cleavage of ascorbate and isocitrate, and
hydrolysis of oxaloacetate (Nakata, 2003). Glyoxy-
late oxidation has been considered to be a more
direct and efficient precursor for oxalate formation
in oxalate-accumulating plants (Fujii et al., 1993).
Soluble oxalate is one of a number of anti-nutri-
ents in forage plants. It exerts its effects by binding
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Oxalate poisoning in animals
calcium (Ca), magnesium (Mg) and other trace min-
erals such as iron (Fe), making them unavailable for
assimilation (Talapatra et al., 1948; Watts, 1959a,b;
Gorb and Maksakow, 1962). This leads to distur-
bances in Ca and phosphorus (P) metabolism and
causes excessive mobilization of bone mineral. The
demineralized bones become fibrotic and misshapen,
causing lameness and ‘bighead’ in horses (McKenzie
et al., 1981). Ruminant animals are less affected, but
prolonged grazing by cattle and sheep on some tropi-
cal grasses can result in severe hypocalcaemia (Sea-
wright et al., 1970). High levels of oxalate in pasture
plants were considered as a major factor in urolith
formation in grazing animals (McIntosh et al., 1974).
In another study, high levels of oxalate in beet tops
were related to the occurrence of hypocalcaemia and
hypomagnesaemia in ewes (El-Khodery et al., 2008).
When a ruminant consumes an oxalate-containing
plant, the oxalate is metabolized in four possible
ways. First, soluble oxalate may be degraded by
rumen bacteria (Allison et al., 1977). Secondly,
when Ca is taken with dietary feed that is high in
soluble oxalate, oxalate ions in the rumen or intes-
tine combine with Ca2+ or Mg2+ to form insoluble
oxalate crystals, which are then eliminated in the
faeces. This form of oxalate cannot be absorbed into
the body. Thirdly, when Ca is low in the diet, solu-
ble oxalate remains soluble in the liquid portion of
the intestine contents and is readily absorbed from
the intestine into the bloodstream. If the oxalate ion
concentration becomes very high in the blood being
filtered by the kidney, it may combine with Ca2+ or
Mg2+ to form insoluble oxalate crystals that may
block urine flow and cause kidney failure (Lincoln
and Black, 1980; Blaney et al., 1982). Fourthly,
insoluble oxalate from ingested plants may pass
through the digestive tract without any harmful
effect on the body metabolism (Ward et al., 1979).
In general, oxalate poisoning is a complex issue.
Induction of acute oxalate intoxication depends on
several factors including the chemical form of oxa-
late, the age of animal, the rate of consumption, the
amount and quality of other feed consumed concur-
rently, the total amount of oxalate consumed and
adaptation to a diet containing oxalate (Burrows and
Tyrl, 1989; Pickrell and Oehme, 2004; Radositits
et al., 2007). Dietary oxalate, if consumed in large
quantities, is well known to have potential toxicity
(Panciera et al., 1990; Sidhu et al., 1996). The
rumen is overwhelmed and unable to metabolize
the oxalate, which is absorbed into the blood. In the
blood, the oxalate forms an insoluble salt that pre-
cipitates in the kidney, causing kidney failure.
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M. M. Rahman, R. B. Abdullah and W. E. Wan Khadijah
The earlier knowledge on oxalate toxicosis has
been summarized by James (1972). Studies on oxa-
late feeding in animals have been carried out from
time to time, but the amount of oxalate that could
be included in feeds without reducing the availabil-
ity of Ca is not clear. The purpose of the present
study is to review published scientific literature on
the effects of oxalate in terms of the tolerance and
performance of domestic animals, in order to estab-
lish preliminary safe levels of oxalate for domestic
animals. Toxicity data from different authors were
more directly compared by expressing all contents
and levels of oxalate as percentage of dry matter
(DM).
Oxalate tolerance
Ruminant vs. non-ruminant
Ruminants (e.g. goats) tend to be more tolerant of
oxalate than non-ruminants (e.g. horses), because
rumen bacteria degrade oxalate into harmless formic
acid and carbon dioxide. Allison et al. (1977)
adapted cattle and sheep gradually to increasing
amounts of oxalate and demonstrated an enhanced
degradation by rumen bacteria. Later work with
horses indicated that oxalate-degrading bacteria were
also found in the intestines, but were not always
present (Allison and Cook, 1981).
Although rumen bacteria can readily metabolize
soluble oxalate (Davies, 1979), most of the ingested
Ca oxalate appear to pass intact through the rumi-
nant digestive tract (McKenzie and Schultz, 1983) as
oxalate cannot be degraded by most rumen or intes-
tinal bacteria. The gut bacterium that appears capa-
ble of degrading oxalate is Oxalobacter formigenes; this
is a slow-growing bacterium that cannot utilize other
substrates. The ability of other intestinal organisms
to degrade oxalate has been less well studied, but
Enterococcus faecalis as well as some lactic acid bacte-
ria can degrade oxalate (Hokama et al., 2000;
Campieri et al., 2001), and their contribution to oxa-
late elimination in the gut may be significant.
Adaptation
Hungry and unadapted ruminants are the ones most
susceptible to oxalate intoxication. If ruminants are
slowly exposed to a diet high in oxalate (over an
approximately 4-day period), the population of oxa-
late-degrading bacteria in the rumen will increase to
a level sufficient to prevent oxalate poisoning (Alli-
son et al., 1977; Burrows and Tyrl, 1989; Radositits
et al., 2007). The increased rate of oxalate degrada-
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M. M. Rahman, R. B. Abdullah and W. E. Wan Khadijah
tion during adaptation may be maintained by con-
tinued oxalate ingestion, but the rate drops rapidly
when oxalate intake is reduced. James and Butcher
(1972) suggested that range sheep may efficiently
utilize up to 6% oxalate if proper management prac-
tices are followed. A study with sheep and goats
showed that administration of free oxalic acid led to
changes in the rate of oxalic acid breakdown in the
rumen, particularly in goats, thereby protecting the
host animal from toxic symptoms (Duncan et al.,
1997). It seems that ruminants, when adapted to
oxalate-rich diets, are able to eat a wide array of
plants without ingesting a harmful dose of oxalate.
Frutos et al. (1998) observed that goats could be
adapted to oxalic acid by daily oral administration of
0.6 mM/kg live weight/day of free oxalic acid, which
successfully generated an active oxalic acid–degrad-
ing rumen bacterial population, although the goats
showed a chronic mild hypocalcaemia. Therefore,
ruminants adapted to diets with high oxalate content
can tolerate oxalate levels that may be toxic or lethal
to unadapted ruminants.
Natural resistance
The oxalate tolerance may also differ depending on
the animal species. For example, Duncan et al.
(1997) reported that a goat’s rumen is a special place
for a bacterial population that degrades oxalic acid
more rapidly than in sheep. Goats, when compared
to sheep, are known to consume shrubby vegetation
and to browse plants that are usually rich in second-
ary metabolic compounds (e.g. oxalic acid). Libert
and Franceschi (1987) reported that a substantial
portion of Ca oxalate in the feed ingested by rumi-
nants could be dissolved during digestion. Horses are
completely unable to utilize the Ca oxalate in tropi-
cal grasses (Blaney et al., 1981; McKenzie and
Schultz, 1983), although pigs appear to be able to
utilize up to 80% of this Ca oxalate (Brune and
Bredehorn, 1961).
Age of animals
Young animals are generally more susceptible to tox-
icants than adults. Mortality of cattle and buffalo
calves have been reported following feeding on
Napier grass (cv. Pusa giant) (Dhillon et al., 1971;
Sidhu et al., 1996). No comparative data are avail-
able on oxalate poisoning with regard to age of ani-
mals. Additional research is required to understand
the effect of age on oxalate poisoning in animals.
Journal of Animal Physiology and Animal Nutrition. ª 2012 Blackwell Verlag GmbH
Oxalate poisoning in animals
Sex of animals
Urolithiasis commonly occurs in ruminant animals
and invariably results in blockage of the urethra in
male animals (Tiruneh, 2004). In females, calculi are
formed, but are more readily excreted owing to ana-
tomical differences in the male and female urinary
tract. Therefore, males are most likely to exhibit dis-
ease symptoms; however, females may also form uri-
nary stones.
Growth stage of animals
Lactating ruminants may be more susceptible than
non-lactating ruminants to oxalate poisoning,
because of the amount of Ca excreted from the body
through the milk. In this situation, lactating animals
are always under Ca deficiency. For example, lactat-
ing ewes were more frequently affected by hypo-
calcaemia than pregnant and dry, non-pregnant
ewes (El-Khodery et al., 2008). In contrast, previous
studies reported that hypocalcaemia was more fre-
quent in pregnant ewes, especially those fed concen-
trated rations (Tindall, 1986; Sweeney and
Cuddeford, 1987; Pickard et al., 1988). Radositits
et al. (2007) suggested that pregnant and lactating
animals are probably more susceptible than other
animals. Little is known about the effect of oxalate
on the performance at different stages of ruminant
growth, and more research is needed in this regard.
State of nutrition
In general, most forages contain sufficient Ca for
animal production (Minson, 1990). However, owing
to the low solubility of Ca oxalate, extremely little
soluble Ca can exist in forages in the presence of ox-
alic acid. Because of its low solubility, the Ca in Ca
oxalate is poorly available to grazing herbivores and
it passes through the digestive tract to be excreted in
the faeces (Ward et al., 1979).
Some oxalate-rich plants contain abundant Ca
(e.g. Medicago sativa), meaning that they are safe to
feed despite their high oxalate content. For a grass
of this nature to be safe for feeding, even to horses,
without the risk of causing Ca deficiency, it must
have a Ca to oxalate ratio of at least 0.5:1 (Gardner,
2002).
Maximum tolerable levels
Previous research indicated that diets containing low
levels of halogeton (Halogeton glomeratus) (3.2%
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Oxalate poisoning in animals
oxalate) induced a mild hypocalcaemia, increased
water intake and caused an increase in rumen pH
(James et al., 1968). James and Butcher (1972)
reported that feeding diets containing 0%, 4%, 5%
and 6% soluble oxalate to sheep caused a slight hyp-
ocalcaemia, increased serum P and decreased serum
Mg (Table 1). Rankins and Smith (1991) suggested
that kochia (Kochia scoparia) hay (4.8% oxalate)
could be fed at levels up to 50% of total DM intake
to maintain sheep without any overt sign of toxico-
sis. A mild degree of hypocalcaemia was observed in
sheep fed at a dose of 0.12 g oxalic acid/kg live
weight/d (Kyriazakis et al., 1997). Panda and Sahu
(2002) observed that the total oxalate intake at the
level of 0.58% of the DM intake was harmless to
bulls, but an increase to 1.19% created a negative
balance of Ca (Table 2). WeinChang et al. (2004)
and Rahman et al. (2011a) reported that ruminants
(cattle, goats and sheep) fed on a high oxalate-con-
taining grass had lower blood Ca levels when com-
pared to animals fed on a low oxalate-containing
grass (Table 3). These data indicate that ruminant
animals may efficiently utilize large amounts of oxa-
late without causing ill effects (although blood Ca
level is reduced), if proper management practices are
followed.
Cattle mortality owing to oxalate poisoning
and resulting acute hypocalcaemia has occurred on
Table 1 Effects of various levels of dietary oxalate on blood Ca, P
and Mg values in sheep (derived from James and Butcher, 1972)
Oxalate Ca (mg/ P (mg/
(%) in diet 100 ml) 100 ml)
0 10.8* 3.3**
4 10.6 3.3
5 10.2 3.7
6 9.9 4.2
Ca, calcium; P, phosphorus; Mg, magnesium.*p < 0.05; **p < 0.01.
Table 2 Balances of calcium (Ca) with respect to oxalic acid intake in
crossbred bulls (derived from Panda and Sahu, 2002)
Oxalic acid intake (% DM)
Parameter 0.21 0.58
Ca intake (g/d) 12.10 12.20
Ca excretion via 10.89 11.83
faeces and urine (g/d)
Ca balance (g/d) +1.21a +0.37b
Mean values with different superscripts in a raw differ significantly
(p < 0.05).
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M. M. Rahman, R. B. Abdullah and W. E. Wan Khadijah
setaria (Setaria sphacelata) pastures (Jones et al.,
1970). Instances of sheep poisoning have been docu-
mented owing to high oxalate contents in Buffel
grass (Cenchrus ciliaris) pastures (McKenzie et al.,
1988). Higher mortality in cattle and buffalo calves
has been reported following feeding on Napier grass
(Pennisetum purpureum cv. Pusa giant) that contained
high levels of oxalic acid (3.01%) and low levels of
Ca, when compared to other varieties of Napier grass
(Dhillon et al., 1971; Sidhu et al., 1996). An out-
break of acute oxalate intoxication in a flock of
sheep was associated with consumption of Seidlitzia
rosmarinus (Chenopodiaceae), with a mortality rate
of about 19% (Aslani et al., 2011). Soluble oxalate
levels of 2.0% or more may lead to acute toxicosis
in ruminants, while levels of 0.5% or more may
induce nutritional hyperparathyroidism in horses
(McKenzie et al., 1988). Compared to what is
known concerning ruminants, information on maxi-
mum tolerable levels of oxalate for non-ruminants is
still lacking.
The literature covered in this review does not
point to any agreement regarding potentially safe
levels for oxalate content in plants because toxicity
is affected by a multitude of factors, such as rate of
ingestion and adaptation. However, we consider that
<2.0% soluble oxalate in the diet would be appropri-
ate for protecting ruminants from oxalate poisoning,
although blood Ca level may decrease. In case of
non-ruminants, we consider that <0.5% soluble oxa-
late in a diet may be acceptable. The critical levels
reported in the literature for oxalate in animals are
Mg (mg/
summarized in Table 4.
100 ml)
2.5** Toxicosis
2.3
The importance of oxalic acid in limiting the utiliza-
2.3
2.3
tion of dietary Ca was first realized by McClugage
and Mendel (1918), who observed that dogs retained
less Ca from diets based on spinach than on carrots.
Since this observation, many animal studies have
been conducted showing that soluble oxalate rapidly
combines with serum Ca or Mg, causing a sudden
decrease in the availability of these minerals (Oswe-
iler et al., 1969; Dickie et al., 1978; James, 1978;
Allison et al., 1985). Acute oxalate poisoning causes
1.19 1.59
a sudden decrease in serum Ca, which impairs nor-
10.42 10.66 mal cell function and causes animals to develop
12.21 12.69 muscle tremors and weakness, leading to collapse
and eventual death. In chronic oxalate poisoning,
)1.79c )2.03d
filtration of insoluble Ca oxalate by the kidneys
causes severe damage to the kidney tubules. If ani-
mals do not die from the acute effects of the low
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M. M. Rahman, R. B. Abdullah and W. E. Wan Khadijah Oxalate poisoning in animals

Table 3 Blood calcium (Ca) level of animals consuming grasses with different soluble oxalate contents

Soluble oxalate Blood Ca

Animal Type of feed Trial No. in grass (% DM) level (mg/dl) Reference
b a
Cattle Napier grass (cv. TLG2) Trial 1 0.95 6.8 WeinChang et al. (2004)
Napier grass (line 7439) 1.76a 5.8b
Goat Napier grass (cv. TLG2) Trial 2 1.26b 8.5a
Napier grass (line 7439) 1.74a 8.1b
Sheep Guinea grass Trial 1 0.47* 13.7a Rahman et al. (2011a)
Setaria 1.34 11.7b
Sheep Guinea grass Trial 2 0.47* 12.4a
Guinea grass  3.47 11.0b

*No statistical analysis was performed.

a,b
 Guinea grass was treated with 3% oxalic acid; Means in the same column with different superscripts under each trial differ significantly
(p < 0.05).

Table 4 Animal responses as affected by dif-

ferent levels of soluble oxalate (% DM) Critical level Incidence Reference

4.0% or more Toxic or even fatal to the cattle Moir (1953)

2.0% Negative calcium balance in cattle Morris and Garcia-Rivera (1955)
6.9% Acute toxicity in cattle Seawright et al. (1970)
3.01% Toxicity in buffalo calves Dhillon et al. (1971)
3.5% Increased blood clotting time in calves James (1978)
1.3–1.8% Sub-clinical bone diseases in ponies Cymbaluk et al. (1986)
2.0% or more Acute toxicity in ruminants McKenzie et al. (1988)
3.01% Toxicity in cattle and buffalo calves Sidhu et al. (1996)
0.39–2.44% Acute toxicity in ruminants Marais (2001)
2.66–2.75% Reduced serum calcium level in WeinChang et al. (2004)
cattle and goat

blood Ca levels and impaired cellular energy metab-
olism, death results from kidney failure.
Parathyroid hormone (PTH) is secreted in response
to low blood Ca levels, causing bone to release Ca
into the blood stream. Low levels of this hormone
are secreted even when blood Ca levels are high, but
there is a steep increase in the secretion of PTH
when Ca levels fall below the normal range (Martin
et al., 1996). Several syndromes related to PTH may
arise following oxalate ingestion by ruminants. They
include an acute syndrome in which hypocalcaemia
and death occurs soon after high intake of oxalate; a
less acute syndrome in which neither serum Ca
reductions nor renal damages are sufficient to cause
death; a chronic syndrome caused by deposition of
oxalate in the renal tubules, which leads to nephron
damage, renal fibrosis, and renal insufficiency; and
urolithiasis (James and Seawright, 1971; Waltner-
Toews and Meadows, 1980). Symptoms of oxalate
poisoning in cattle and buffalo calves are character-
ized by severe inappetence, straining, constipation,
dryness of muzzle, dullness, increased blood clotting
time, dyspnoea with normal water intake and zero
rumen motility (Sidhu et al., 1996). Symptoms of
oxalate poisoning in sheep dying from acute bassia
intoxication included weakness, incoordination, tet-
any and coma (Williams et al., 1976). Osteodystro-
phy in horses has been associated with prolonged
ingestion of Setaria sphacelata containing moderate
(5%) concentrations of oxalate (Groenendyk and
Seawright, 1974).
Oxalate also interferes with energy metabolism
and plasma glucose levels (Knight and Walter,
2003). A lethal dose of Halogeton glomeratus resulted
in hyperglycaemia in sheep (James, 1999). Experi-
mental-induced hypocalcaemia in ewes resulted in
lower plasma glucose and lower endogenous glucose
production (Schlumbohm and Harmeyer, 2003).
Animal performance
Palatability and voluntary feed intake
Preference for an oxalate-rich plant may be affected
by taste or texture. For example, the oxalate level
may determine the acidity of the plant material.
Similarly, the presence of Ca oxalate crystals may
cause irritation and burning sensations owing to
mechanical penetration (Franceschi and Horner,
1980). Feed intake is very important for the promo-
tion of productivity in animals. James and Butcher

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Oxalate poisoning in animals
(1972) observed that as the dietary oxalate
increased, daily feed intake decreased, water intake
increased, faeces production decreased and urine
excretion increased. Kyriazakis et al. (1998) reported
that voluntary feed intake in sheep decreased as
oxalate in the ration increased. Burritt and Provenza
(2000) also observed that voluntary feed intake in
sheep was significantly depressed by the inclusion of
3% oxalate, perhaps because of reduced palatability.
In contrast, Wang and Provenza (1997) reported that
the presence of a toxin does not necessarily prevent
sheep from eating a food, especially if the food con-
tains needed nutrients. Rahman et al. (2011a)
observed that feed intake in sheep appeared to
decrease as the amount of oxalate in the ration
increased, but the difference was not statistically sig-
nificant.
Live weight gain
The depression in voluntary feed intake owing to
oxalate consumption may have an adverse effect on
live weight gain. However, no data are available in
the literature in terms of any influence on live
weight gain by oxalate consumption.
Milk production
Excess levels of oxalate in plants may have a nega-
tive impact on milk production and fat content (Rai
et al., 2004). In addition, milk Ca level might also be
depressed following feeding of oxalate-rich plants.
However, no data are available regarding the effect
of oxalate feeding on milk production and milk com-
position in animals.
Physiological parameters
Feeding of oxalate-containing Napier grass decreased
the concentration of rumen protozoa in buffalo
calves and decreased rumen motility, but it increased
plasma creatinine and blood urea nitrogen (Bajaj
et al., 2011). The leucocyte count of the calves also
increased significantly, but the packed cell volume
decreased. More research is required to understand
the role of oxalate on these types of physiological
parameters.
Oxalate producing forage plants
Plants with high contents of oxalate include rice
(found in the straw), the leaves of Acacia spp., and
species of grasses in the genera Cenchrus, Panicum
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M. M. Rahman, R. B. Abdullah and W. E. Wan Khadijah
and Setaria, which are widely cultivated in tropical
and subtropical areas (Rahman and Kawamura,
2011). The most important plants involved in oxa-
late intoxication in ruminants include halogeton,
soursob (Oxalis spp.), rhubarb (Rheum rhaponticum),
curly dock (Rumex crispus), purslane (Portulaca olera-
cea), lamb’s quarters (Chenopodium album), bassia
(Bassia hyssopifolia), greasewood (Sarcobatus vermicula-
tus), pigweed (Amaranthus spp.), Russian thistle (Sal-
sola kalis) and sugar beets (Beta vulgaris) (Pickrell and
Oehme, 2004; Maxie and Newman, 2007; Sargison
and Angus, 2007; Angus, 2008). The factors affecting
oxalate accumulation in forage plants have been
reviewed and summarized by Rahman and Kawam-
ura (2011). Forage species or cultivars having a
lower tendency to accumulate oxalate should be
selected for cultivation. Many oxalate-containing
plants accumulate the highest amount of oxalate
during the young, rapidly growing stages and this
amount decreases with maturity and drying of the
plant (Pickrell and Oehme, 2004; Radositits et al.,
2007).
Prevention
Feeding large quantities of oxalate-rich forage to
ruminants is inadvisable unless the animals are grad-
ually introduced to the forage to allow the build-up
of oxalate-degrading bacteria. Horses should not be
fed a diet of predominantly oxalate-rich forage as
nutritional disorders can result. Animals should not
be allowed to become hungry or thirsty while feed-
ing or grazing on oxalate-rich plants. Supplementary
dicalcium phosphate in the diet before and during
high-risk oxalate exposure is an effective means of
reducing losses. High levels of dietary Ca bind with
oxalate in the rumen as insoluble, non-absorbable
Ca oxalate. Animals may be provided Ca in a salt
mixture.
Rahman et al. (2011b) observed lower blood Ca
level (12.5 vs. 13.4 mg/dl) in sheep-fed control
(without Ca-fertilization) grass than in sheep-fed Ca-
fertilized grass, which suggested that feeding of Ca-
fertilized grass can minimize the negative effects of
oxalate. Diets can also be supplemented with other
low oxalate-containing plants to help reduce the
overall intake of oxalate-containing plants. Soaking
the feed in water and then straining off the water
can also reduce the oxalate content of the feed and
help to reduce its toxicity. Silage making may be
another option to reduce oxalate content in forage
plants. However, Das et al. (2010) reported that bulls
that fed Napier silage diets showed a significant
Journal of Animal Physiology and Animal Nutrition. ª 2012 Blackwell Verlag GmbH
M. M. Rahman, R. B. Abdullah and W. E. Wan Khadijah
(p < 0.05) reduction in Ca and P balances. Although
the intakes of these two minerals were adequate,
they showed linear inverse relationships with the
increases in oxalate intake from Napier silage.
Adequate water intake is also necessary to prevent
the formation of urinary calculi. Inadequate water
intake causes the urine to be more concentrated,
which increases the likelihood of stone formation.
Animals that drink more will excrete more diluted
urine, which will further tend to reduce the likeli-
hood of calculi formation (Tiruneh, 2004).
Research methods
Most studies on ruminants reported in the literature
have been conducted by artificially administering
oxalic acid, either with the ground ration or in a
capsule form (Duncan et al., 1997; Kyriazakis et al.,
1998; Burritt and Provenza, 2000; Duncan et al.,
2000), which can readily taken by animals within a
short period. More research is needed to focus on
direct feeding of oxalate-rich plants to animals. As
described earlier, the effect of oxalate feeding on
performance (both productive and reproductive) of
domestic animals is far from clear, and more long-
term research is needed in this regard.
Concluding remarks
The data presented in this review provide clear evi-
dence that dietary oxalate may result in oxalate poi-
soning in domestic animals. The literature reviewed
here leads us to consider that limiting oxalate inges-
tion to <2.0% soluble oxalate would be appropriate
for protecting the ruminants from oxalate poisoning,
even though blood Ca level may decrease. In case of
non-ruminants, levels of <0.5% soluble oxalate may
be acceptable. These proposed safe levels for soluble
oxalate ingestion for domestic animals, however, are
only preliminary. Further studies, especially long-
term studies, are required to validate and improve
these recommended safe levels. Additional studies
must also examine the influence of dietary oxalate
on feed intake and on productive and reproductive
performances of animals. We hope that this review
will encourage further research regarding the rela-
tionships between dietary oxalate, other dietary fac-
tors and renal failure in domestic animals.
Acknowledgement
This study was financially supported by the Univer-
sity of Malaya.
Journal of Animal Physiology and Animal Nutrition. ª 2012 Blackwell Verlag GmbH
Oxalate poisoning in animals
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