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2018 Peanut Oil Intoxication in Bovine – A Clinical Study
Article in The Indian veterinary journal · December 2018
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Saravanan Mani
Ranjithkumar Muthusamy
Tamil Nadu Veterinary and Animal Sciences University
Tamil Nadu Veterinary and Animal Sciences University
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C. Balan et al.
Summary
The period of birth, season and sex of lambs
highly signicant variation which in turn inuence the absolute growth rate at all the age
intervals of the lambs born.
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Indian Vet. J., November 2018, 95 (11) : 15 - 18
Peanut Oil Intoxication in Bovine – A Clinical Study
M. Ranjithkumar1, S. Krishnakumar, R. Saahithya, M. Saravanan and H. Pushkin Raj
Teaching Veterinary Clinical Complex, Veterinary College and Research Institute, Orathanadu 614625, Tamilnadu.
(Received : April, 2018 124/18
Abstract
Edible oils particularly peanut oil is part of
staple food in India. Unsaturated fatty acids
have more potent antimicrobial effects and
inhibit ruminal fermentation than saturated
fatty acids. Hence, excessive quantity of peanut
oil may produce ruminal disturbance and clinical illness. Six animals with history of peanut oil
intoxication were presented with clinical signs
suggestive of anorexia, cessation of rumination,
ruminal atony, watery to semi solid diarrhoea
1
Corresponding author : Email : clmranjith@gmail.com
Accepted : June, 2018)
with mucosal shreds in the dung, ruminal putrefaction, chronic inanition and death. Signicant
leukocytosis and neutrophilia were observed
in affected animals. Among the intoxicated
animals, one recovered completely after 15 days
of therapy but no clinical recovery was noticed
in another ve animals. The peanut oil intoxication produces ruminal disturbances and severe
clinical illness in cows which may be due to
direct toxicity of PUFA to ruminal microbes, and
decreased calcium absorption.
Key words: Peanut oil, Intoxication, Bovines,
Fatty acids
The Indian Veterinary Journal (November, 2018)
15
Peanut Oil Intoxication in Bovine ...
Edible oils particularly peanut oil (also
called as groundnut oil) is part of staple food
to India as it provides characteristic avour
and texture to food as integral diet components (Odoemelam, 2005) and can also serve
as a source of oleo chemicals (Morrison et al.,
1995). Peanut oil contains a high proportion of
unsaturated fatty acids in particular linoleic
acid (13-35%). Vegetable oils with unsaturated fatty acids when fed excessive amounts
to ruminants have the potential to inhibit the
ruminal fermentation (Jenkins, 1993). Feeding
of polyunsaturated fatty acids (PUFA) has
been found to decrease the protozoa number in
rumen. Cellulolytic bacteria and fungi present
in rumen are the most sensitive ora to PUFA
than others (Maia et al., 2007). Linoleic acid is
the most abundant PUFA present in peanut
oil. Hence, it is postulated that consumption of
excessive quantity of peanut oil may produce
clinical illness through disturbance in ruminal
fermentation. To our knowledge, this may be the
rst report in peanut oil intoxication of cattle.
Materials and Methods
The clinical study was carried out at Teaching Hospital of Veterinary College Research
Institute, Orathanadu during March 2014 to
April, 2017. Six animals were reported with the
history of peanut oil intoxication and admitted to large animal outpatient unit at various
periods mostly in summer. It is the habit of
the rural farmers of delta region in Tamilnadu
to crush peanuts oil seeds by rotary type and
cured in sunlight. Animals particularly cattle,
returning from common grazing area are thirsty
and drink liquids. This situation conjugates
this clinical work as edible oil intoxication. The
various signs exhibited by the clinically sick
animals were carefully noted and are presented
Table I. Mean ± SE values of haematological parameters in Peanut oil intoxicated animals
16
S.No.
Parameters
Intoxicated group (n=6)
1.
Total leukocyte counts (x103/µl)
13.56 ± 1.12
2.
Lymphocytes (x103/µl)
4.22 ± 0.80
3.
Monocytes (x103/µl)
0.15 ± 0.04
4.
Neutrophils (x103/µl)
8.84 ± 1.80
5.
Eosinophils (x103/µl)
16.40 ± 2.07
6.
Basophils (x103/µl)
0.09 ± 0.03
7.
Total Erythocyte Counts (x106/µl)
5.82 ± 0.39
8.
Hemoglobin (g/dl)
8.51 ± 0.73
9.
Hematocrit (%)
24.96 ± 2.54
10.
Mean Corpuscular Volume (fl)
42.50 ± 2.11
11.
Mean Corpuscular Hemoglobin (pg)
14.62 ± 0.57
12.
Mean Cell Hemoglobin Concentration (g/dl)
34.42 ± 0.88
13.
Red Cell Distribution width c (%)
23.60 ± 1.72
14.
Red Cell Distribution width s (fl)
39.37 ± 1.98
The Indian Veterinary Journal (November, 2018)
M. Ranjithkumar et al.
Fig 1. Mucosal shreds excreted inside feces
Fig 2. Encapsulation of protozoa by oil droplets in rumen fluid
in this paper. The rumen uid was collected by
using rumen pump. The complete blood count
was carried out using automated hematology
analyzer (Vet Scan HM5). All the animals were
treated with polyionic uids, oral and parenteral
sodium bicarbonate, calcium borogluconate,
light kaolin, ruminotorics and multivitamins. In
four animals, rumen uid transplantation was
attempted. Sodium bicarbonate was administered orally @ 100-200 gms as total dose according to the clinical recovery. Strepto-penicillin
2.5 gm/animal, i/m was administered with
commercial preparations of ruminal buffers
(Powder Bufzone*). One animal having an intestinal mucosal shred in dung was treated with
light kaolin. Owners were encouraged to administer oral rehydration therapy with polyionic
solutions (Electrobest**). Mean with standard
error was calculated in intoxicated animals for
haematological parameters.
Fatty acid analysis in our cases was not done on
rumen uid because of lack of facilities. Unsaturated fatty acids have more potent antimicrobial effects and promote greater inhibition of
ruminal fermentation than saturated fatty acids
(Maia et al., loc. cit). Accumulation of 18:2n-6
in the rumen inhibits complete biohydrogenation (Jenkins and Adams, 2002). The oleic and
linoleic acids have 18:1 and 18:2 carbons respectively. The presence of large amount of linoleic
acid (18:2) in the rumen, irreversibly inhibits
the hydrogenation to stearic acid (Jenkins, loc.
cit).
Results and Discussion
The common clinical signs were anorexia, cessation of rumination, mild bloat, ruminal atony,
initially semi solid dung and latter diarrhoea
with mucus shreds (Fig 1), pasting dung with
heavy foetid smell, chronic inanition and nally
death. Muscle tremor was noticed in fore
quarters, particularly on severe cases (>4 litres
of oil). After four days, two animals developed
cud droppings. Out of six cases, one animal was
sent to emergency slaughter and another four
died. This might be due to polyunsaturated fatty
acid present in oil, particularly of linoleic acid.
Fatty acids have bacteriostatic and
bacteriocidal effects (Maia et al., loc. cit). Hence,
the increase in these fatty acids in rumen might
be one of the reasons for microbial death and
reduced fermentation. Ruminant diets containing more than 2 to 4% added lipid from plant
oils is likely to demoralize ber digestion in
the rumen (Jenkins, 1994). Further, increase
in unsaturated fatty acids within the rumen
decreases the acetate:propionate ratio. This
decrease is accompanied by reduced digestion
of organic matter, particularly brous fraction
(Doreau and Chilliard, 1997; Jenkins and Adams,
loc. cit). Maia et al., (loc. cit) reported that the
cellulolytic bacteria and fungi were most sensitive to toxic effect of PUFA in rumen than others.
The kinked unsaturated fatty acids disrupt the
lipid bilayer structure of microora and thus
cause toxicity (Keweloh and Heipeiper, 1996).
The exogenous lipids inhibit amino acid uptake
and energy metabolism in bacterial protoblast.
The Indian Veterinary Journal (November, 2018)
17
Peanut Oil Intoxication in Bovine ...
The other toxicity mechanism is increased fatty
acids decreases calcium and magnesium absorption for about 25 to 40% and 15 % respectively
(Emery and Thomas, 1991). Several authors have
already proved that a reduced serum/plasma
calcium level reduces the ruminal, abomasal
and intestinal motility in ruminants (Jorgensen
et al., 1999). The denudation of gastrointestinal
epithelium might be due to direct action of
fatty acids on membrane function of ruminal
as well as intestinal epithelium. The epithelial
damage in the rumen produces rumenitis which
paved way for cud dropping in two cases. In
our cases, four out of six animals died inspite
of parenteral administration of calcium and
magnesium along with oral sodium bicarbonate
as buffer. The mean heamatological parameters
for the intoxicated animals are given in table
1. The total leukocyte count increase might be
due to gastrointestinal damage subsequent to
bacteremia. Similarly, leukocytosis with neutrophilia is common nding in haemorrhagic bowel
syndrome in bovines (Elhanafy et al. 2013). The
rumen uid examination revealed no protozoal
activity, except in two animals. These animals
had oil bubbles encapsulated with protozoa (Fig
2). The reason for this is not known.
Summary
The accidental consumption of excess quantity
of peanut oil produces clinical illness and death
in cattle. The major clinical signs were anorexia,
cessation of rumination, ruminal atony, watery to
semi solid diarrhoea with mucosal shreds in the
dung, chronic inanition and death. One peanut
oil intoxicated animal recovered completely
after 15 days of therapy while no clinical recovery was noticed in another ve animals. Linoleic
acid present in the peanut oil may inhibit the
biohydrogenation and cellulolytic bacteria in
rumen and produces toxicity in cattle.
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