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Allium species poisoning in dogs and cats
Salgado BS (1), Monteiro LN (2), Rocha NS (1, 2)
(1) Department of Pathology, Botucatu Medical School, São Paulo State University (UNESP – Univ Estadual Paulista),
Botucatu, São Paulo State, Brazil; (2) Department of Veterinary Clinical Sciences, Veterinary Pathology Service, School of
Veterinary Medicine and Animal Husbandry, São Paulo State University (UNESP – Univ Estadual Paulista), Botucatu, São
Paulo State, Brazil.
Abstract: Dogs and cats are the animals that owners most frequently seek assistance for potential
poisonings, and these species are frequently involved with toxicoses due to ingestion of poisonous food.
Feeding human foodstu to pets may prove itself dangerous for their health, similarly to what is observed
in Allium species toxicosis. Allium species toxicosis is reported worldwide in several animal species, and
the toxic principles present in them causes the transformation of hemoglobin into methemoglobin,
consequently resulting in hemolytic anemia with Heinz body formation. The aim of this review is to analyze
the clinicopathologic aspects and therapeutic approach of this serious toxicosis of dogs and cats in order to
give knowledge to veterinarians about Allium species toxicosis, and subsequently allow them to correctly
diagnose this disease when facing it; and to educate pet owners to not feed their animals with Allium-
containg food in order to better control this particular life-threatening toxicosis.
Key words: Allium spp., poisonous plants, hemolytic anemia, Heinz bodies.
Review A Rticle
The Journal of Venomous Animals and Toxins including Tropical Diseases
ISSN 1678-9199 | 2011 | volume 17 | issue 1 | pages 4-11
INTRODUCTION
e genus Allium includes onion, garlic, leek,
chives, shallots, and scallions, and was previously
classied in the family Alliaceae (1). However, in
the new classication of Angiosperm Phylogeny
Group, Alliaceae is now the subfamily Allioideae
of the family Amaryllidaceae (2). Some botanical
authorities have also previously included it in the
lily family (Lilliaceae) (3, 4).
e Allium genus comprises biannual bulbous
plants that grow in the north hemisphere except
for a few species found in South America and
Tropical Africa (5) (Table 1). ese plants form
solitary or clustered bulbs and are strongly
aromatic, with a characteristic odor when
crushed. is distinctive aroma is thought to be
related to allicin and other oil-soluble sulfur-
containing organic compounds that allow us to
dierentiate them from other morphologically
similar poisonous plants (6, 7).
Wild and domestic Allium species have been
used as ingredients in many dishes and with
ethnomedical purposes for many years. is
plant is rich in two chemical groups that are
thought to provide benets to human health:
avonoids and alk(en)yl cysteine sulfoxides.
Apart from its culinary uses (fresh, cooked or
dehydrated), medicinal properties have been
attributed it since ancient times, prompting in
recent years an accurate chemical analysis of its
most characteristic active components (7-10).
Compounds from onions have a range of health
benets such as anticarcinogenic, antiplatelet,
antithrombotic, antiasthmatic, antidiabetic,
brinolytic and hypocholesterolemic properties,
and other various biological actions including
antibiotic eects (11-13).
Salgado BS, et al. Allium species poisoning in dogs and cats
J Venom Anim Toxins incl Trop Dis | 2011 | volume 17 | issue 1 5
All Allium species and their derivatives can
be toxic to dogs and cats (14-20). However,
relatively few Allium species are of important
toxicological interest. Domestic species that
are more commonly involved in poisoning are
onion (Allium cepa) (Figure 1), garlic (Allium
sativum) (Figure 2), leek (Allium porum) (Figure
3), and chives (Allium schoenoprasum) (Figure
4). Onions contain toxic components that may
damage red blood cells and provoke hemolytic
anemia accompanied by the formation of Heinz
bodies in erythrocytes of animals such as cattle,
water bualoes, sheep, horses, dogs, and cats
(14-29).
Plant poisoning is not a usual disease in
dogs and cats, since plants are not a common
compound of their diet. However, they oen
cause acute life-threatening conditions and
represent an imminent cause of death in those
animals. Accordingly, the present review aim to
discuss aspects related to one particular plant
poisoning: Allium species toxicosis.
Since those plants are culturally present in the
Brazilian gastronomy and can be easily accessible
to pets, consequently leading to the development
of important clinical problems, essential features
of Allium species toxicosis are discussed herein in
order to sensitize veterinarians to the possibility
of facing similar cases and to prepare them for
readily diagnose and treat aected animals.
Table 1. Subdivision, horticultural names, and origin of important cultivated Allium species
Species Subdivision Horticultural name Origin
Allium cepa
cepa Bulb onion
Asia
ascalonium Shallot
aggregatum Potato onion
proliferum Tree onion
Allium sativum – Garlic Asia
Allium ampeloprasum porrum Leek Eurasia and
Africa
aegyptiacum Kurrat
Allium schoenoprasum – Chives Europe
Allium chinense – Rakkyo Asia
Allium stulosum –Japanese bunching (Welsh
onion) Asia
Allium tuberosum – Chinese chives Asia
Figure 1. Bulb onion (Allium cepa). Figure 2. Garlic (Allium sativum).
Salgado BS, et al. Allium species poisoning in dogs and cats
J Venom Anim Toxins incl Trop Dis | 2011 | volume 17 | issue 1 6
TOXICITY
Allium species contain various
organosulfoxides, particularly alk(en)yl cysteine
sulfoxides, some of which are responsible for
their characteristic odor (7, 9). Plant trauma (e.g.
chewing or cutting) converts the organosulfoxides
to a complex mixture of sulfur-containing
organic compounds that are responsible for the
avor and eects of these plants on animals (30).
Many Allium organosulfur compounds appear to
be readily absorbed through the gastrointestinal
tract and are metabolized to highly reactive
oxidants (6).
Di-propyl-disulde (H7C3S2C3H7) and allyl
propylisulde (H5C3S2C3H7) have been implicated
in onion-induced hemolytic anemia (30-34).
However, recently, more active oxidizing sulfur-
containing compounds have been discovered
and proposed as causative agents, either in onion
or garlic poisoning episodes (20, 35). Sodium
n-propylthiosulfate, isolated from boiled onions,
was proven to cause an increase of Heinz body
formation in erythrocytes and subsequent
hemolytic anemia in dogs (36).
Garlic, on the other hand, is considered to be
less toxic and safe for dogs than onion when used
in moderation (37).
ACTION MECHANISM
e primary toxicological mechanism of
Allium-derived organosulfur compounds is
oxidative hemolysis, which occurs when the
concentration of oxidants in the erythrocyte
exceeds the capacity of the antioxidant metabolic
pathways. Catalase antioxidant activity in dog
erythrocytes is low, and normal hemoglobin in
cats is about two to three times more susceptible
to oxidative damage than the hemoglobin in
other species (38, 39).
N-propyl disulfide and sodium
n-propylthiosulfate are very poisonous
organosulfur compounds present in onions.
e former may cause a marked decrease in the
activity of glucose-6-phosphate dehydrogenase
(G6PD), whereas the latter can increase the
methemoglobin concentration and Heinz body
count in erythrocytes, and reduce glutathione
concentration in the erythrocyte (30, 40, 41).
In erythrocytes, G6PD oxidizes glutathione to
a reduced form through the pentose phosphate
pathway (39, 42, 43). When the activity of G6PD
is decreased, the content of glutathione also
drops, leading to increased levels of hydrogen
peroxide. It is known that lipid peroxidation can
be determined by malondialdehyde formation
(44). Consequently, hydrogen peroxide and
malondialdehyde oxidize the sulydryl groups
of hemoglobin, resulting in the denaturation of
hemoglobin (30).
Additionally, oxidation of the exposed β-93
cysteine residues present in hemoglobin results in
sulemoglobin formation (45). Sulemoglobin
and denatured hemoglobin are less soluble than
normal hemoglobin, so they precipitate, aggregate,
and bind to the cell membrane and form Heinz
bodies. Other types of oxidation of hemoglobin
globin chains result in membrane cross-linking
reactions and eccentrocyte formation (46). e
formation of Heinz bodies and eccentrocytes
increases erythrocyte fragility and extravascular
hemolysis, since erythrocytes that contain
Heinz bodies are removed from the circulation
by the reticuloendothelial system, thus causing
Figure 3. Leek (Allium porrum).
Figure 4. Chives (Allium schoenoprasum).
Salgado BS, et al. Allium species poisoning in dogs and cats
J Venom Anim Toxins incl Trop Dis | 2011 | volume 17 | issue 1 7
anemia. Damaged erythrocytes are removed
from circulation, causing hemoglobinemia and
hemoglobinuria (6, 47).
Direct oxidative damage to the erythrocyte
cell membrane and its sodium-potassium pump
or the oxidative production of hemin also
contribute to cell lysis. Oxidation of the heme ion
and associated methemoglobinemia result in a
le shi of the hemoglobin-oxygen dissociation
curve, decreased blood oxygen transportation
capacity, and, ultimately, impaired delivery of
oxygen to tissues (48, 49).
us, the result of the oxidative hemolytic
process induced by Allium consumption is the
onset of anemia, methemoglobinemia, and
impaired oxygen transportation. Although
marked Heinz body formation may be present
within a day aer onions are ingested, the anemic
nadir typically develops several days later (49).
Allicin and ajoene, pharmacologically
active agents in garlic, are potent cardiac and
smooth muscle relaxants, vasodilators, and
hypotensive agents (50-52). Also, ajoene and
other organosulfur compounds derived from
onions are potent antithrombotic agents (53).
us, hypotensive and antithrombotic properties
can exacerbate the physiologic eects of anemia
and impaired oxygen transportation. Garlic
preparations that have not been aged cause direct
damage to the gastric and ileal mucosa, resulting
in pain and diarrhea (54).
EXPOSURE AND SUSCEPTIBILITY
Allium toxicosis commonly occurs aer
ingestion. In addition to consuming fresh plant
material, juice, fresh and dietary supplements,
powdered cooking preparations, dehydrated
material, or food preparations derived from or
containing Allium species can be potentially toxic
to dogs and cats (37, 49). is type of toxicosis
is typically caused by consumption of a single
large quantity of plant material or repeated small
amounts. Dogs and cats are highly susceptible to
onion toxicosis, consumption of as little as 5 g/kg
of onions for cats or 15 to 30 g/kg for dogs resulted
in clinically important hematologic changes.
Onion toxicosis is consistently noted in animals
that ingest more than 0.5% of their body weight
in onions at one time (49). A relatively high dose
(600-800 g) in one meal or spread apart over a
few days can damage red blood cells and cause
hemolytic anemia accompanied by the formation
of Heinz bodies in erythrocytes (37).
Dogs with hereditary high erythrocyte reduced
glutathione and circulating potassium level are
more susceptible to the hematologic eects of
onions (36, 55). is trait is relatively common in
Japanese breeds, such as Akita inu and Shiba inu.
Other inborn errors in metabolism or nutritional
deciencies that result in decreased erythrocyte
antioxidant defenses, such as glucose-6-phosphate
dehydrogenase deciency or zinc deciency,
could increase an animal’s susceptibility to Allium
toxicosis (56).
e oral administration of 500 mmol
per kilogram of body weight of sodium
n-propylthiosulfate to dogs results in hemolytic
anemia associated with increased Heinz body
formation in erythrocytes, which is more
severe in dogs with the hereditary condition,
which, in turns, results in erythrocytes with
high concentrations of reduced glutathione and
potassium than in normal dogs. In aected dogs
there is a ten-fold increase in the concentration
of oxidized glutathione in their erythrocytes 12
hours aer the administration of the compound,
whereas in normal dogs there is almost no
change (36).
Humans are the most resistant species studied.
On the other hand, there is some concern about
the susceptibility of certain ethnic groups that
have a genetic deciency of glucose-6-phosphate
dehydrogenase. Although dogs appear to be one
of the most susceptible species, there are a few
reports in the literature concerning accidental
canine poisoning associated with onion ingestion.
Cats are more susceptible than dogs. Since
baby food is oen oered to sick animals that are
not eating (to stimulate their appetite), there is
some concern that the onion powder would cause
a Heinz body anemia in these cats (57). Several
baby food manufacturers add onions or onion
powder to increase palatability.
It is generally accepted that sheep, goats, rats
and mice are more resistant to onion toxicosis
than other domestic animals (27, 48). e safety of
feeding onions to livestock depends upon animal
susceptibility and the toxic potential of the plant
species. Sheep can be maintained on diets of up
to 50% onions with no clinical abnormalities or
detrimental eects on growth. Even when onions
are fed free choice, sheep have only transient
hemoglobinuria and anemia, with few deaths
Salgado BS, et al. Allium species poisoning in dogs and cats
J Venom Anim Toxins incl Trop Dis | 2011 | volume 17 | issue 1 8
reported. In contrast, cattle should be fed onions
with caution, due to the relative susceptibility
of their erythrocytes to oxidative damage. Daily
feeding of onions could have a cumulative eect
due to ongoing formation of Heinz bodies versus
a single exposure with awide gap until the next
exposure, allowing the bone marrow to regenerate
the prematurely destroyed red cells (37).
Concurrent treatment with xenobiotics,
drugs, or dietary factors that induce erythrocyte
oxidative injury (e.g. propofol, propylene glycol,
dl-methionine, sulfonamides, sulfapyridine,
large doses of vitamin K3, benzocaine) or
diminish erythrocyte oxidative defenses (e.g.
acetaminophen) is likely to increase an animal’s
susceptibility to Allium species toxicosis (49).
CLINICAL SIGNS
In dogs and cats, clinical signs of Allium
species toxicosis may appear within one day of
consumption if large amounts of material have
been ingested. However, it is more common
the development of clinical signs aer a lag of
several days (49). e rst signs are usually of
gastroenteritis: vomiting, diarrhea, abdominal
pain, loss of appetite, depression and dehydration.
It will take a few days for the dog to display the
signs associated with the loss of red blood cells:
pale mucous membranes, rapid respiratory rate,
diculty to breathe, lethargy, dark colored urine
(reddish or brown), jaundice, weakness, and rapid
heart rate (37). Depression, hemosiderin in urine,
exercise intolerance and cold sensitivity may also
be observed (49). In cases of recent ingestion, the
breath of the aected dog or cat may smell like
onions or garlic (16).
CLINICAL PATHOLOGY
Clinical pathology ndings are consistent
with intravascular and extravascular hemolysis,
anemia, hemoglobinemia, hemoglobinuria
associated with hemoglobin casts in urine
and hemosiderin, hyperbilirubinemia,
methemoglobinemia, and, if the animal survives
long enough, an accompanying regenerative
response (49). Hematologic tests may reveal
neutrophilia, lymphopenia, Heinz-body anemia
and methemoglobinamia (37).
Heinz body formation, eccentrocytosis, and
a decrease in erythrocyte glutathione levels can
also be detected. Additionally, eccentrocytosis
appear to be one of the major diagnostic features
of garlic-induced hemolysis in dogs (20, 46).
ANATOMIC PATHOLOGY
Necropsy and histological ndings typically
indicate hemolytic anemia. Because of the
lag of several days between ingestion and the
development of clinical signs, gastrointestinal
erosion or Allium in the gut content may not be
seen (49). Necropsy ndings basically consists
of splenomegaly due to hemosiderosis and
increased hemocatheresis, and jaundice due
to the hemolytic anemia provoked, in turn, by
extravascular hemolysis (19, 58, 59).
Histopathologic ndings, although consistent
with hemolytic anemia, are not specic for
Allium toxicosis and may include deposition of
hemosiderin in the phagocytic cells of the liver,
spleen, and renal tubular epithelium; renal tubular
pigment necrosis; and nephrotubular casts and
hemoglobin casts in the renal tubules (58, 59).
DIFFERENTIAL DIAGNOSES
Heinz bodies comprise an uncommon
nding in dogs that can only be induced by a
few other toxicoses, such as methilen blue,
acetaminophen, benzocaine, vitamin K3, zinc
and phenylhidrazine (32, 60, 61). In such cases,
Allium toxicosis should always be included in
the dierential diagnosis (34).
Common feline disorders associated with
Heinz body formation include diabetes mellitus,
particularly if ketoacidosis is present; hepatic
lipidosis, hyperthyroidism; and neoplasms such
as lymphoma (49). Jaundice-causing infections
such as babesiosis and leptospirosis should also be
included in the dierentials. Additionally, post-
hepatic obstructions should also be speculated
due to its jaundice-causing eects.
TREATMENT
No specic antidote is available for Allium
toxicosis; however, supportive care may be
helpful including hospitalization, administration
of intravenous uids and blood transfusions.
Treatment is indicated aer ingestion of any
quantity (37). Several therapeutic approaches have
been suggested to treat onion-poisoned animals,
Salgado BS, et al. Allium species poisoning in dogs and cats
J Venom Anim Toxins incl Trop Dis | 2011 | volume 17 | issue 1 9
including gastrointestinal decontamination,
administration of antioxidant vitamins (C and E)
(in dogs, ascorbic acid – 30 mg/kg of body weight
intravenously, each 6 to 8 hours) or N-acetyl-
cysteine, and intravenous uid therapy or blood
transfusions, but none has proven really eective
(31, 34, 62). Nevertheless, even taking into
account that lethal eects are infrequent in dogs,
avoiding animal exposure to any kind of onion
seems to be the best preventive health strategy
(15, 31, 34).
Induction of emesis (e.g. apomorphine 0.08
mg/kg intramuscularly or subcutaneously, or 3%
hydrogen peroxidase 2 mL/kg, no more than 45
mL) can be valuable in asymptomatic dogs and
cats that showed no complicating factors one or
two hours aer the ingestion. Administration of
activated charcoal (1 to 4 g/kg per oral) is indicated
aer emesis. In severely aected animals, a blood
transfusion and supplemental oxygen therapy
may be required. Administration of intravenous
crystalloids is indicated if extensive vomiting
and diarrhea occurred or if hemoglobinuria or
hypotension is evident (49).
CONCLUDING REMARKS
e ingestion of Allium species by various
animals may lead to toxicosis; however, dogs
and cats deserve special attention since they are
most susceptible. Allium toxicosis is typically
diagnosed through a combination of history,
clinical signs, and microscopic conrmation of
a Heinz body-type hemolytic anemia that if is
quickly performed can allow veterinarians to
give a support treatment in order to avoid animal
death. It is important to carefully monitor the
erythron of aected animals for several days aer
ingestion since it is when the anemic nadir usually
occurs. Antioxidants – such as sodium ascorbate,
vitamin E, and acetylcysteine – have minimal
protective eects on onion powder toxicosis in
cats (62). Diets with low potential oxidants are
recommended; semimoist food that contains
propylene glycol should be avoided, particularly
for cats (63).
Additionally, it is also important to educate
pet owners to not feed their animals with Allium-
containg food and not to store Allium in places
accessible to their pets; these measures may lead,
in long term, to a better control of this particular
life-threatening toxicosis.
COPYRIGHT
© CEVAP 2011
SUBMISSION STATUS
Received: June 11, 2010.
Accepted: October 26, 2010.
Abstract published online: November 5, 2010.
Full paper published online: February 28, 2011.
CONFLICTS OF INTEREST
ere is no conict.
CORRESPONDENCE TO
BRENO SOUZA SALGADO, Departamento de
Patologia, Faculdade de Medicina de Botucatu,
UNESP, Distrito de Rubião Jr., s/n, Botucatu, São
Paulo, SP, 18618-970, Brasil. Phone/fax: +55 14
3811 6293. Email: brenosalgado@globo.com.
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