Toxicon 168 (2019) 122–125

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Toxicon
journal homepage: www.elsevier.com/locate/toxicon

Case report

Acute fatal poisoning by spontaneous ingestion of Enterolobium T

contortisiliquum (Mimosidae) pods in horses
Mizael Machadoa, Marina Pacheco Miguelb, Juliano Pereira Terrac, Jair Alves Ferreira Jr.a,
Franklin Riet-Corread, Márcio Botelho de Castroa,*
a
Veterinary Pathology Laboratory, Veterinary Teaching Hospital,Via L4 Norte, Sn/, Universidade de Brasília (UnB), Campus Universitário Darcy Ribeiro, 70636-200,
Brasília, Distrito Federal, Brazil
b
Instituto de Patologia Tropical e Saúde Pública, UFG, Rua 235 S/n, Setor Universitário, 74605-050, Goiânia, Goiás, Brazil
c
Instituto Federal Catarinense, Campus Araquari, Rodovia BR 280 - Km 27 - Cx. Postal 21, Porto Grande, 89245000, Araquari, SC, Brazil
d
Instituto Nacional de Investigación Agropecuaria (INIA), Estación Experimental INIA La Estanzuela, Ruta 50 Km 11, Colonia Del Sacramento, Colonia, Uruguay

A R T I C LE I N FO A B S T R A C T

Keywords: An outbreak of acute poisoning of horses by Enterolobium contortisiliquum pods is reported in the state of Goiás,
Equine Brazil. Three horses presented apathy, hyporexia, prostration, jaundice, recumbency and died in 24–48 hours.
Hepatic necrosis The main pathological findings were a yellowish liver with an enhanced lobular pattern, multifocal hepatic
Enterolobium contortisiliquum pods necrosis mostly in the midzones of lobules and sometimes with a random distribution across the hepatic lobes
Poisonous plants
and swelling of hepatocytes. E. contortisiliquum trees has a wide distribution in South America and cases of
poisoning have not been reported in horses.

Enterolobium contortisiliquum (Leg Mimosoidae) is a leafy and fast
growing tree widely distributed in Brazil, Argentina, Uruguay and
Venezuela (Lorenzi, 2008). The tree occurs mainly in fertile soils,
reaches up to 30 m in height, producing a wide shaded area in pastures.
The production of pods begins in May, and mature pods fall between
August and November during the dry season (Lorenzi, 2008).
Mature pods are brown to black, semicircular, curved with a semi-
woody appearance, and with high levels of triterpenic and steroidal
saponins (Mimaki et al., 2003; Tokarnia et al., 2012). The consumption
of E. contortisiliquum pods has been related with toxicity in ruminants
during the dry season, when mature pods fall to the soil and pastures
are degraded and insufficient (Tokarnia et al., 2012). Poisoning out-
breaks associated with the ingestion of E. contortisiliquum pods have
been reported in cattle (Olinda et al., 2015), sheep (Bezerra et al.,
2012), and goats (Benício et al., 2005). In this report, we describe for
the first time the epidemiology and clinical-pathological findings of
horses naturally poisoned by the ingestion of E. contortisiliquum pods.
In August 2013, in the municipality of Serranópolis, Goiás state
(18°18′22.4″S 51°57′28.2″W), in the central-western region of Brazil,
during the height of the dry season, three adult crossbreed horses were
allowed to graze in a small paddock established with Cynodon dactylon
grass and which contained a leafy E. contortisiliquum tree. In this region,
the dry season is characterized by mature pastures, and the low avail-
ability of fodder, coinciding with the production of large quantities of E.
contortisiliquum pods that fall and accumulate on the ground below the
tree. The owner reported that the horses were hungry when they were
introduced to the paddock and observed the intake of large quantities of
pods (Fig. 1A) on the ground prior to the beginning of the clinical signs.
Chronological events during the outbreak are described in Table 1. Two
horses died and were buried prior to the visit by the veterinarian, after
approximately 24 hours. Blood samples were collected from an 8-year-
old male horse, for complete blood cell count (CBC) and to determine
the serum levels of aspartate aminotransferase (AST), alanine amino-
transferase (ALT), and total bilirubin.
All animals presented marked apathy, prostration, hyporexia,
jaundice, recumbency, and evolved to death in 24–48 hours. The
sampled horse presented increased serum levels of total bilirubin (18.70
mg/dL; normal range: 1.0–2.0 mg/dL), AST (455 U/L; normal range:
0–366 U/L) and ALT (50 U/L; normal range: 0–23 U/L), and no changes
in the CBC. This animal died shortly after the clinical evaluation, then a
necropsy was conducted. Samples of tissues and organs were collected,
fixed in 10% buffered formalin (pH 7.0), embedded in paraffin and
stained with hematoxylin and eosin for histological examination.
The main macroscopic findings were jaundice, hepatomegaly, an
enhanced hepatic lobular pattern (Fig. 1B), mild edema in the mesen-
tery, hyperemia and hemorrhagic multifocal areas in the mucosa of the
cecum and epicardium surface.
Histologically, the liver showed moderate multifocal hepatic

*
Corresponding author.
E-mail address: mbcastro@unb.br (M.B. de Castro).

https://doi.org/10.1016/j.toxicon.2019.07.006
Received 25 March 2019; Received in revised form 12 July 2019; Accepted 16 July 2019
Available online 19 July 2019
0041-0101/ © 2019 Elsevier Ltd. All rights reserved.
M. Machado, et al. Toxicon 168 (2019) 122–125

Fig. 1. Acute poisoning by Enterolobium contortisiliquum pods. (A) Pods of Enterolobium contortisiliquum. (B) Horse, liver. Enhanced lobular pattern and jaundice.

Table 1
Chronological events during an outbreak of acute poisoning by Enterolobium contortisiliquum pods in horses in the state of Goiás,
Brazil.
Day Events

1 Introduction of the three horses to the paddock and beginning of the consumption of the pods.
2 Two horses presented apathy, hyporexia and recumbency.
3 The two horses that developed clinical signs died. A third horse presented apathy, jaundice and recumbency.
4 The third horse was clinically evaluated and blood sample was collected. The animal died and was necropsied.

necrosis mostly in the midzones of lobules (Fig. 2A), and sometimes
with a random distribution across the hepatic lobes, surrounded by few
neutrophils (Fig. 2B). Mild to moderate multifocal swelling of the he-
patocytes with well-delimited intracytoplasmic vacuoles were also ob-
served with similar distribution of the hepatic necrosis. Mild dissocia-
tion of hepatocyte plates, moderate proliferation of bile ducts and mild
periportal inflammatory infiltrate of mononuclear cells were also ob-
served. The diagnosis of acute poisoning of horses by the ingestion of
Enterolobium contortisiliquum pods was based on clinical signs, labor-
atorial and pathological findings, and in the absence of other hepato-
toxic plants available in the paddock (assessed at local inspection).
Among the most important epidemiological findings observed in the
outbreak are the low availability of forage in the paddock, the hunger of
the horses, and the great availability of mature pods below the E.
contortisiliquum tree on the ground during the dry season. E. con-
tortisiliquum has been considered an important toxic plant for ruminants
in central-western and northeastern Brazil (Furlan et al., 2012; Olinda
et al., 2015), including southeastern Goiás state (Sant’Ana et al., 2014),
the same region where the horses were poisoned. In Brazil, natural
cases of poisoning in ruminants associated with the ingestion of E.
contortisiliquum pods always occur during the dry season with the
fructification of the tree (Tokarnia et al., 2012), as observed with these
horses.
The clinical signs presented by the animals in this outbreak are
apparently related to hepatotoxicity. Digestive, skin and reproductive
disorders, and eventually hepatotoxicity, are the main findings in nat-
ural and experimental poisonings of cattle, sheep, goats and guinea pigs
with E. contortisiliquum pods (Tokarnia et al. 1960; Grecco et al., 2002;
Benício et al., 2005; Bonel-Raposo et al., 2008; Tokarnia et al., 2012;
Bacha et al., 2017). The poisoning of ruminants by E. contortisiliquum
pods has produced different clinical presentations, such as acute rum-
inal acidosis (Pupin et al., 2017), abortion (Benício et al., 2005), he-
patogenous photosensitization and other digestive disorders (Olinda
et al., 2015; Leal et al., 2017). Although these clinical signs have been
described in natural and experimental poisonings of ruminants
(Tokarnia et al., 2012; Leal et al., 2017; Pupin et al., 2017), horses in
the outbreak did not present photosensitization, diarrhea or other en-
teric changes.
The death of horses within up to 48 h after the onset of clinical signs
were similar of acute experimental poisoning in cattle, however in these
animals, digestive disorders predominated (Tokarnia et al., 1960).
Some guinea pigs experimentally receiving 10–15g/kg of E. con-
tortisiliquum pods showed very acute poisoning and death between 12
and 18h (Bonel-Raposo et al., 2008). Despite the evidence of

123
M. Machado, et al.
Fig. 2. Acute poisoning by Enterolobium contortisiliquum pods. Horse, liver. (A) Multifocal necrosis of hepatocytes mainly distributed in the midzonal region (arrow
heads). CV: centrilobular vein; PT: portal tract; (H&E, scale bar = 250μm). (B) Focal necrosis of hepatocytes with few intralesional neutrophils. (H&E, scale
bar = 50μm).
hepatotoxicity in the horses, the absence of photosensitization may be
due to the very short course of the poisoning until death. Similarly,
acute hepatotoxicity by other photosensitizing plants such as Brachiaria
spp. grass in sheep was also characterized by rapid death of animals
without photosensitization (Castro et al., 2011).
The increase in AST and ALT activity, and bilirubin serum levels,
associated with the macroscopic and microscopic findings observed in
the poisoned animal, suggests hepatic impairment as the cause of death
of the horses. The lack of other laboratory tests related to hepatic
function and evaluation of samples of only one animal, did not allow a
complete assessment of hepatotoxicity. Fatal acute hepatic failure in
sheep experimentally poisoned with E. contortisiliquum pods was pre-
viously reported and associated with jaundice, hepatic degeneration
and necrosis (Bacha et al., 2017). Hepatotoxicity was also reported in
cattle naturally poisoned by the plant (Olinda et al., 2015). The in-
creased serum activity of liver enzymes and bilirubin levels are con-
sidered relevant for subsidizing the diagnosis of poisonous plant he-
patotoxicosis (Santos et al., 2008).
Multifocal hepatocellular necrosis mostly in the midzones of lobules
and sometimes with a random distribution across the hepatic lobes,
stands out among the main pathological findings in the necropsied
horse. As has already been pointed out, hepatic damage possibly oc-
curred following the previous swelling of hepatocytes in the same re-
gions. In cattle experimentally poisoned by E. contortisiliquum pods, a
similar midzonal hepatocellular necrosis pattern was also eventually
observed (Tokarnia et al., 1960). However, the experimental poisoning
of guinea pigs and even cattle may cause different hepatic damage
patterns, such as periportal hemorrhagic necrosis and the swelling of
centrilobular hepatocytes (Bonel-Raposo et al., 2008; Olinda et al.,
2015; Pupin et al., 2017). Multifocal coagulative necrosis of hepato-
cytes also occurred mostly in the midzones of lobules of cattle experi-
mentally poisoned by Lantana spp. (Seawright and Allen, 1972) and
was similar to that observed in the horse poisoned by E. contortisiliquum
124
Toxicon 168 (2019) 122–125
pods.
Complete midzonal hepatic necrosis is generally uncommon in hu-
mans and domestic animals (McGavin and Knake, 1977), and even
more rare in plant-poisoned animals (Tokarnia et al., 2012). Midzonal
hepatic necrosis has been reported in horses and pigs (McGavin and
Knake, 1977), and rabbits with aflatoxicosis (Newberne and Butler,
1969). This pattern of liver injury was also detected in rats that were
experimentally poisoned by Myoporum laetum (Denz and Hanger 1961)
and N-oxide derivates of lasiocarpine (Bull et al., 1958), and in cats
poisoned by hexachlorophene (Brown et al., 2017). On the other hand,
a multifocal hepatic necrosis pattern may occur in domestic animals
poisoned by plants and toxic compounds, and also due to vascular
failure and infectious agents (Cullen and Stalker, 2016). Multifocal
necrosis in the midzone regions of the hepatic lobes eventually can be
detected and explained by necrotic areas that belong to the periphery or
above the hepatic lobe due to a skewed plane of sectioning (McGavin
and Knake, 1977).
Hepatic necrosis mostly in the midzones of lobules, and eventually
with random distribution as noted in this outbreak, has not been re-
ported in cases of hepatotoxicity by plants in horses in Brazil. In Brazil,
hepatotoxic plants for horses include Crotalaria retusa and Senecio bra-
siliensis, causing chronic poisoning characterized by hepatic fibrosis,
megalocytosis, bile duct proliferation, photosensitization and hepatic
encephalopathy (Nobre et al., 2004; Santos et al., 2008; Panziera et al.,
2017). Brachiaria humidicola poisoning in horses has also been reported
to mainly cause hepatogenous photosensitization (Barbosa et al., 2006).
Acute poisoning by Senna occidentalis or Trema micranta in horses has
led to centrilobular necrosis and hepatic encephalopathy (Bandarra
et al., 2010; Oliveira-filho et al., 2012; Lorenzett et al., 2018).
The toxic compounds in the E. contortisiliquum pods are not com-
pletely elucidated (Tokarnia et al., 2012). Enterolosaponin A were de-
tected in the pods, a compound with in vitro cytotoxic activity to rat
macrophages (Mimaki et al., 2003). Other saponin-containing plants
M. Machado, et al.
such as Brachiaria sp. and Tribulus terrestris cause hepatoxicity and
death in ruminants, and also include mild hepatocyte necrosis and
apoptosis, and bile ducts damage related with accumulation of saponin
crystals (McDonough et al., 1994; Castro et al., 2011). Despite hepatic
damage and moderate proliferation of bile ducts observed in the horse,
saponin crystals were not detected in the liver. Lantana spp. is another
known hepatotoxic plant that caused death of cattle and subtle hepatic
lesions such as mild swelling and vacuolization of hepatocytes observed
at light microscopy, however, hepatic lytic necrosis could be detected
with the aid of transmission electron microscopy in these animals
(Seawright and Allen, 1972). Even with the differences between he-
patotoxic principles of Brachiaria sp., Tribulus terrestris or Lantana spp.,
the mechanisms of death in poisoned ruminants by these plants with
discrete and subtle hepatic lesions are not well known (Seawright and
Allen, 1972; McDonough et al., 1994; Castro et al., 2011; Tokarnia
et al., 2012). Therefore, our findings do not allow us to speculate about
the toxic principle involved in hepatic lesions and mechanisms of death
in horses poisoned by E. contortisiliquum pods.
Despite the limitations of our findings and the evidence of liver toxic
injury in horses, it is still necessary to study other outbreaks associated
with the intake of E. contortisiliquum pods. It is important to consider
that the known toxic plants that affect ruminants (Tokarnia et al., 2012)
could also poison horses, as observed here. Given its broad territorial
distribution and toxic potential for domestic animals, the intake of E.
contortisiliquum pods should be considered in differential diagnoses for
acute toxic hepatopathy in horses. It is recommended that animals not
be kept in paddocks containing E. contortisiliquum trees during the
period of pods production.
Ethical Statement.
Not applicable. All information and samples were obtained from
records of the Veterinary Pathology Laboratories of Jataí, Federal
University of Goiás, Brazil of horses that had natural death by acute
poisoning by Enterolobium contortisiliquum pods.
Acknowledgement
Special thanks to Rosana de Carvalho, DVM, Comigo Agricultural
Cooperative of Serranópolis, Goiás State and Sidney Aniceto Rezende
Júnior, Lab Technician at the Veterinary Clinical Analysis Laboratory,
Federal University of Jataí for the technical support and analysis of
blood and biochemical samples. This study was financed in part by the
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - Brasil
(CAPES) - Finance Code 001.
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