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Veterinary Journal
The Veterinary Journal 181 (2009) 90–96
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Review

New aspects in the pathogenesis of abomasal displacement

Klaus Doll *, Marlene Sickinger, Torsten Seeger
Clinic for Ruminants and Swine, Faculty of Veterinary Medicine, University of Giessen, Frankfurter Str. 110, 35392 Giessen, Germany

Accepted 20 January 2008

Abstract

Impaired abomasal motility and an increased accumulation of gas are prerequisites for displacement of the abomasum in the cow.
Predisposing factors are the breed (e.g. Holstein–Friesian, Simmental–Red-Holstein cross breeds and Guernsey), genetic background,
twin pregnancy, first weeks of lactation, metabolic disorders (ketosis, increased lipomobilisation, insulin resistance), high-concentrate
and low-fibre diets, as well as other concomitant diseases, such as endometritis, mastitis and claw disorders. There does not appear
to be a strong correlation between increased milk yield or endotoxaemia and abomasal displacement.
Recent studies have focused on possible functional disorders of the enteric nervous system within the abomasal wall, since cattle with
abomasal displacement have an increased activity of neuronal nitric oxide synthase, as well as decreased acetylcholine sensitivity. In addi-
tion, there appear to be significant differences between breeds in the levels of the neurotransmitters substance P (SP) and vasoactive intes-
tinal peptide (VIP) in the abomasal wall. For example, SP (stimulatory) was significantly less in German Holsteins in comparison to the
German Fleckvieh, whereas VIP (inhibitory) was markedly increased. These risk factors may explain why Holstein cows are more sus-
ceptible to abomasal displacement than other breeds.
Ó 2008 Elsevier Ltd. All rights reserved.

Keywords: Cattle; Abomasal displacement; Risk factors; Pathogenesis; Heritability

Introduction
The first reports of abomasal displacement (AD) in cat-
tle were published in the 1950s (Begg, 1950; Moore et al.,
1954) and, since then, the occurrence of the condition has
continued to increase. In recent studies in North America,
the mean lactation incidence of AD was estimated to range
between 3% and 5% (Gröhn et al., 1998; Zwald et al.,
2004a; LeBlanc et al., 2005) although an incidence rate of
10%, even up to 20%, has been observed in individual herds
(Dawson et al., 1992; Pehrson and Stengärde, 2000). In
Germany, the mean lactation incidence in German Hol-
stein herds has been estimated at 1.6% (Wolf et al.,
2001a) and up to 7.5% in individual herds (Poike and Fürll,
2000).
The economic losses from AD include reduced milk pro-
duction and the cost of treatment or culling. Studies using a
*
Corresponding author. Tel.: +49 641 99 38670; fax: +49 641 99 38679.
E-mail address: Klaus.Doll@vetmed.unigiessen.de (K. Doll).
305 day milk yield have estimated average milk loss from
left AD of 11% (Martin et al., 1978) and 7.5% (Dohoo
and Martin, 1984). Compared to healthy cows, cows with
left AD in parity, particularly with twins, lost an average
of 700 kg of milk, with the highest losses occurring in high
yielding cows (Detilleux et al., 1997).
Evidence from epidemiological and experimental studies
over the last 50 years have identified a variety of risk fac-
tors associated with the occurrence of AD. However, the
primary cause of the disease remains unknown. In 1961,
Dirksen postulated that an abomasal motility disorder
(hypotony or atony) occurred prior to inflation of the
organ (Dirksen, 1961), a hypothesis that has been sup-
ported by other researchers. Impaired motility prevented
gases (mainly methane and CO2 produced either in the
abomasum or passed into it from the forestomachs) from
escaping via the omasal or the intestinal pathway, in turn
causing the organ to distend. As the abomasum enlarges,
it slides, so that in the case of left-side displacement it will
move leftwards, beneath the ruminal atrium and ventral

1090-0233/$ - see front matter Ó 2008 Elsevier Ltd. All rights reserved.
doi:10.1016/j.tvjl.2008.01.013
 K. Doll et al. / The Veterinary Journal 181 (2009) 90–96
ruminal sac, ultimately rising (like a balloon) between the
rumen and the abdominal wall.
In the less common right-side displacement, the accu-
mulation of fluid and gas leads to a caudo-dorsal dilata-
tion. The abomasum then has the potential to twist on
the lesser omentum, creating an abomasal volvulus. This
can cause acute obstruction with local circulatory impair-
ment and ischaemic necrosis of the abomasal wall leading
to a worse prognosis, with mean survival rates of only
61–74% (Constable et al., 1991; Fubini et al., 1991; Mey-
lan, 1999; Sattler et al., 2000). In contrast to left-side dis-
placements, which occur primarily within the first 4 weeks
after calving, only 50–70% of right displacements are
found in this period, while the rest occur independent
of the stage of gestation or lactation (Hof, 1999; Dirksen,
2002).
The majority of studies have focused on factors that pre-
dispose to left AD, although the aetiopathogenesis of right
AD and abomasal volvulus are thought to be similar (Dirk-
sen, 2002; Trent, 2004). This review will give an overview of
the current knowledge of the aetiology and pathogenesis of
AD in dairy cows.
Epidemiological and experimental data referring to the
causes of abomasal displacement
Breed, age and milk yield
AD occurs primarily in the classical dairy breeds, such
as the Holstein Friesian and German Holstein (Martin
et al., 1978; Geishauser et al., 1996; Wolf et al., 2001a,b)
as well as on Simmental–Red-Holstein crossbreeds (Eicher
et al., 1999), Brown Swiss, Ayrshires, Guernseys (Consta-
ble et al., 1992) and Jerseys (Jubb et al., 1991). In contrast,
left AD is still a rare finding in German Fleckvieh cows
(lactation incidence 0.15%; Berchtold and Prechtl, 2007),
despite an increase in the average milk yield/herdbook
cow in this breed (from 5689 kg to 6854 kg between 1995
and 2006; ADR, 2007).
Similar differences in the incidence of AD between
breeds have also been found in other countries, such as
Switzerland, where the Holstein–Friesian was compared
to the Brown Swiss (Eicher et al., 1999), or in Sweden
between Swedish Friesian and Swedish Red and White
(Stengärde and Pehrson, 2002). Studies have suggested
that selection for a tall stature and deep body depth in
breeding herds may explain this observed breed predispo-
sition (Stöber and Saratsis, 1974; Mahoney et al., 1986;
Wittek et al., 2007). These traits may increase the risk of
AD because the higher vertical distance between the
abomasum and the descending duodenum will impair
abomasal emptying.
Further differences between breeds can be observed
when investigating the ratio of left and right AD. In the
case of Holstein Friesian cows, this ratio is thought to
range between 3:1 and 7:1 (personal observations; Whit-
lock, 1969; Markusfeld, 1986; Constable et al., 1992). In
91
German Fleckvieh herds, however, right AD seemed to
occur slightly more often than left displacements. A study
of 139 Fleckvieh cows with AD admitted to the Clinic
for Ruminants of Munich University yielded a ratio of left-
to right-side displacement of 0.9:1 (G. Dirksen, personal
communication).
It has been reported that the risk of AD increased with
age (Constable et al., 1992; Detilleux et al., 1997). Accord-
ing to Wolf et al. (2001a,b), cows beyond the third lacta-
tion were more frequently affected than younger animals.
In contrast, data collected by our group have indicated that
in first calf heifers there is an increased occurrence of 28%
of all cases (Seeger, 2004). The age distribution of cows
with AD in our patient population correlated with the
age distribution within the Holstein herds in Hesse, Ger-
many. Other reports from the United States and Eastern
Germany have also noted a higher incidence in younger
animals. For example, Pehrson and Stengärde (2000) ana-
lysed 71 dairy herds in Wisconsin and found that 54% of
the animals with AD were first calf heifers. In East German
herds, 31–58% of affected animals were first calf heifers
(Poike and Fürll, 2000).
The relationship between high milk yield (as a predis-
posing factor) and AD is controversial. Zwald et al.
(2004b) observed a positive relationship (product-moment
correlation) of 0.09 between predicted transmitting ability
(PTA) for milk and AD. Similar findings were reported
in earlier publications (Dirksen, 1961; Grymer et al.,
1982; Kuiper, 1991; Lotthammer, 1992), although other
authors have been unable to verify this finding (Cameron
et al., 1998; Rohrbach et al., 1999; Wolf et al., 2001b). Ric-
ken et al. (2004) identified a significant additive genetic cor-
relation of the trait ‘milk yield’ and left but not right AD.
However, analysis of both abomasal disorders as one fac-
tor revealed a correlation close to zero.
Genetics
The observation that AD is associated with certain sires
and dams led to the proposal that it may depend on
genetic predisposition (Stöber et al., 1974; Jubb et al.,
1991). In a population of daughters that were descended
from two bulls, Poike and Fürll (2000) calculated an
abomasal incidence of 29.4% and 22.6%, respectively.
Each bull had served as a sire in the investigated herds
over 100 times.
It is generally accepted that genetic predisposition is an
important risk factor for the occurrence of AD (Jubb et al.,
1991; Lyons et al., 1991; Constable et al., 1992; Uribe et al.,
1995; Geishauser et al., 1996; Wolf et al., 2001a,b; Ricken
et al., 2004; Zwald et al., 2004a). The heritability (h2) is esti-
mated to range between 0.11 and 0.41, with only few
researchers disagreeing with this correlation (Van Dorp
et al., 1998). According to Wolf et al. (2001a), both left
and right AD are highly genetically correlated and they
concluded that both forms of the disease are determined
by the same genes.
92 K. Doll et al. / The Veterinary Journal 181 (2009) 90–96
Nutrition
The predominant occurrence of left AD (80%), either
shortly prior to calving or within the first 4 weeks post par-
tum, is striking (Constable et al., 1992; Gröhn et al., 1998;
Wolf et al., 2001a,b; Seeger, 2004). This time period is asso-
ciated with hormonal changes and a high metabolic stress,
as well as changes in feed. Epidemiological studies have
shown a correlation of high-concentrate and low-fibre diets
with the incidence of AD (Grymer et al., 1981; Jacobsen
and Riddell, 1995; Shaver, 1997; Fürll and Krüger, 1999;
Van Winden, 2002). In experimental studies, an increase
in the fraction of concentrates resulted in a dramatic
decrease in abomasal motility (Svendsen, 1969; Neu-Zuber,
2005), as well as an increase in AD (Coppock et al., 1972;
Van Winden et al., 2003, 2004). Furthermore, decreased
abomasal motility has been observed in sheep fed with a
high-concentrate diet (Lester and Bolton, 1994). In con-
trast, feeding highly digestible diets with low neutral deter-
gent fibre (NDF) content may be a more important risk
factor than the amount of concentrate in the ration (Sten-
gärde and Pehrson, 2002). However, Jacobsen and Riddell
(1995) concluded that an increased occurrence of AD is
related to a decreased feed intake observed in cows receiv-
ing roughage feed of inferior quality.
The data regarding the impact of total mixed rations
(TMR) is contradictory. The majority of studies have sug-
gested that this feeding technique increased the incidence of
AD (Poike and Fürll, 2000; Stengärde and Pehrson, 2002),
while Østergaard and Gröhn (2000) reported that TMR
diets reduced the risk of developing this disease. Taken
together, the key factor in this discussion is the composi-
tion of the TMR. An unbalanced mixture, too high milling
and a high fraction of corn silage generally resulted in a
diet with inadequate physical structure which may lead to
AD (Shaver, 1997; Poike and Fürll, 2000). Adequate
roughage of sufficient particle size is needed to maintain
a good rumen function and prevent AD. A proportion of
at least 16–25% crude fibre content is recommended in
order to minimise the risk of AD (Grymer et al., 1981;
Van Winden and Kuiper, 2003; Shaver, 1997). Moreover,
processing and mixing feed causes a reduction in size of
all particles and is directly related to TMR mixing time
(Heinrichs et al., 1999).
Although many studies have stressed the impact of
physical structure of food in dairy nutrition, until recently
there has not been a standardised tool to characterise the
particle size of forages. However, the Pennsylvania State
– Nasco shaker box (Lammers et al., 1996) has recom-
mended diets with 8–10% of particles from the top screen
for both pre-fresh and post-fresh cows (R.D. Shaver,
undated1).
The pathophysiological relationship between feeding
high energy/low structure diets and the occurrence of AD
1
See: http://www.uwex.edu/ces/ag/teams/dairy/tristateda011.pdf.
can be summarised by the fact that a high concentration
of short chain fatty acids (SCFAs) will inhibit abomasal
motility (Svendsen, 1969). However, it should be kept in
mind that the author infused the abomasum with solutions
containing five times more SCFA than the normal physio-
logical levels in the organ (Breukink and de Ruyter, 1976).
Martens (2000) suggested that abomasal atony may be
caused by an overload of water and electrolytes resulting
in distension of the abomasal wall. During the first weeks
of lactation, the forestomachs are not fully adapted to
the high energy diet. This results in an increased concentra-
tion of volatile fatty acids and a decrease in pH, which sub-
sequently leads to an increase in osmotic pressure and the
influx of water. The water and electrolytes not yet absorbed
then pass into the omasum and the abomasum. Concur-
rently, an increase in the development of gas occurs in
the abomasum. This is related to either an increase in
CO2 or methane. An increase in CO2 is associated with a
high level of SCFAs and an impaired ructus, which will
lead to an increase of bicarbonate in the abomasum. Bicar-
bonate will then react with hydrogen ions to release CO2.
The increase in methane is also associated with the increase
of SCFAs and pH, which will stimulate methane producing
microorganisms (Breves, 2006). In fact, the gas mixture col-
lected from displaced abomasa is usually high in methane
(up to 70%) and comparable to the mixture found in gas
collected from the rumen (Dirksen, 1961; Svendsen, 1969;
Sarashina et al., 1990; Krey, 2005).
These findings suggest that the abomasal gas originated
from the rumen. However, a further possibility is ‘post fer-
mentation’ occurring in the abomasum. In contrast to the
commonly cited opinion, the numbers and variety of bacte-
ria situated in the abomasum of the dairy cow are high,
with 103–105 aerobes and 103–104 anaerobes/mL (Krey,
2005). In particular, incubation of abomasal fluid from
cases of right AD reveals gas production comparable with
the amounts produced from the incubation of ruminal con-
tents. However, these experiments also demonstrated that
the amount of methane that is produced in the abomasum
is low, leading to the conclusion that most of the methane
found in gas collected from ADs is actually produced by
ruminal microflora (Krey, 2005).
Several recent studies have suggested that abomasal
atony may be related to an increased concentration of
endotoxins (Fürll and Krüger, 1999; Poike and Fürll,
2000), which can inhibit abomasal motility, either directly
or indirectly via the induction of hypocalcaemia. Vlaminck
et al. (1985) and Sustronck (2000) demonstrated a dose-
dependent reduction and inhibition of abomasal motility
following application of Escherichia coli endotoxin IV or
via a duodenal fistula. In vitro, muscle tissue derived from
the abomasal antrum of cows treated with endotoxins
showed a significant decrease in contractility (Kaze et al.,
2004).
Apart from bacterial infections such as endometritis or
mastitis, the cause of endotoxaemia has been thought to
arise from gastro-intestinal translocation or a decrease in
 K. Doll et al. / The Veterinary Journal 181 (2009) 90–96
liver clearance (Poike and Fürll, 2000). In addition, feed
containing endotoxins (e.g. rapeseed cake, rapeseed meal,
brewers’ grain contaminated with yeasts, or poor quality
corn silages) are thought to play a role in the pathogenesis
of the disease (Krüger and Röpke, 2000). However, recent
publications have demonstrated that endotoxaemia does
not occur more often in cows with AD than in healthy con-
trols during the postpartum period (Wittek et al., 2004).
Feeding experiments in our clinic demonstrated a signifi-
cant decrease in abomasal and duodenal myoelectrical
activity after an abrupt change to a high-concentrate diet
(65% dry matter). However, endotoxin and cytokine
(TNF-a, interleukin-6) concentrations in blood samples
obtained from the jugular and portal vein remained within
the reference ranges in each animal (Schulz, 2005).
Stress, metabolic disorders and other diseases
Stress as a risk factor for AD has been frequently sug-
gested. Epidemiological studies concluded that poor ani-
mal husbandry, ranking problems (especially after the
introduction of heifers into the herd) and parturition may
induce enough stress to increase the risk of developing
AD (Hultgren and Pehrson, 1996; Fürll and Krüger,
1999). This increased risk has been statistically proven in
cases of multiple pregnancies, dystocia, retention of the
fetal membranes or metritis (Poike and Fürll, 2000; Wolf
et al., 2001a,b; Stengärde and Pehrson, 2002; LeBlanc
et al., 2005).
There are indications that seasonal and meteorological
events can also induce the disease. Although there are some
field reports that may indicate an influence of heat stress on
the incidence of AD, nearly all epidemiological studies
show an increased incidence in winter and early spring,
which cannot only be attributed to a higher calving fre-
quency (Wallace, 1975; Constable et al., 1992; Cameron
et al., 1998; Cannas da Silva et al., 2004). A study in Por-
tugal, which included 372 cases of AD, reported an
increased occurrence of AD during the change from sunny,
warm and dry weather to humid and cold conditions (Can-
nas da Silva et al., 2004). The hypothesised reason for the
higher incidence in the winter months, in addition to the
seasonal difference, was the declining quality of the stored
roughage and reduced intake (Cannas da Silva et al., 2004).
It was assumed that all factors that lead to a decreased
rumen volume predisposed to left AD (Dirksen, 1961,
2002; Van Winden et al., 2002).
Low blood calcium is known to inhibit abomasal motil-
ity. According to Madison and Troutt (1988), the total cal-
cium concentration should fall below 1.2 mmol/L but this
is seldom the case in cows suffering from AD. In a study
performed by Stengärde and Pehrson (2002), 96.5% of
the cows with AD had calcium values of P2.0 mmol/L.
Furthermore, Bajcsy et al. (1997) and LeBlanc et al.
(2005) observed no correlation between hypocalcaemia
and AD. In contrast, Massey et al. (1993) demonstrated
that during parturition hypocalcemic cows had a 4.8 times
93
greater risk of developing the disease than normocalcemic
animals.
Several studies have shown that peripartum cows with a
marked negative energy balance (increased NEFA and b-
hydroxybutyrate values) have an increased risk for left
AD (Geishauser et al., 1997; Cameron et al., 1998; LeBlanc
et al., 2005). Furthermore, a significant positive genetic
correlation between ketosis and AD has been observed
(Uribe et al., 1995; Shaver, 1997; Zwald et al., 2004b). Insu-
lin resistance has been discussed as one possible pathogenic
explanation for these findings. Some animals with AD
show high glucose and insulin concentrations even though
their metabolism is catabolic (Kuiper, 1991; Smith et al.,
1997; Pravettoni et al., 2004). Measurements of the electro-
myographic activity of the abomasum have shown that
abomasal motility in these cows is decreased for up to 7
days post surgery, a condition which is not observed in ani-
mals without insulin resistance (Pravettoni et al., 2004). In
addition, experimental studies have shown an association
between high insulin concentrations and delayed abomasal
emptying, an effect which is independent of blood glucose
levels (Holtenius et al., 1998, 2000; Sustronck, 2000). In
contrast, Van Winden et al. (2003) observed low insulin
and glucose in cows suffering from AD at a later point in
time. This finding corresponded to the condition normally
expected to be present in cows with postpartum negative
energy balances. Therefore Van Winden and Kuiper
(2003) concluded that the increased glucose and insulin lev-
els found in cows with AD may be the result of the disease
rather than the cause.
Cows with a high body condition score at parturition are
particularly predisposed for increased lipomobilisation, and
therefore AD (Kuiper, 1991; Fürll and Krüger, 1999; Van
Winden et al., 2003). In addition, all animals with a
decreased feed intake due to other illnesses are more affected,
as an adequately filled rumen serves as a natural barrier in
preventing left AD (Dirksen, 1961; Constable et al., 1992;
Fürll et al., 1999). Concomitant diseases, such as retention
of the fetal membranes, endometritis, mastitis or lameness,
are a common finding in cows with AD (Wallace, 1975;
Markusfeld, 1986; Schmidt et al., 1996; Rohrbach et al.,
1999; Zwald et al., 2004a,b). Animals suffering from these
diseases had a significantly higher risk of developing AD in
comparison to healthy controls (Detilleux et al., 1997; Poike
and Fürll, 2000; Stengärde and Pehrson, 2002).
Neuronal disorders
The contractility of the stomach and the abomasum is
regulated by sympathetic and parasympathetic pathways
and, particularly, by the enteric nervous system (Wong
and McLeay, 1988; Malbert and Ruckebusch, 1989; Grun-
dy and Schemann, 1992). Recent studies have therefore
focused on possible disorders of the abomasal enteric ner-
vous system. As in other species, the contraction of the
abomasum is mainly governed by cholinergic neurotrans-
mission. Stoffel et al. (2006) identified the muscarinic recep-
94 K. Doll et al. / The Veterinary Journal 181 (2009) 90–96
tor subtypes M1, M3 and M5, as well as the interstitial cells
of Cajal, which play an important role in motility. Further
studies focused on the role of serotonin (5-HT) in abomasal
motility, while Meylan et al. (2004) located the 5-HT recep-
tors 1B and 2B as well as the subtypes 1F, 2A and 1F.
Geishauser et al. (1998) examined tissue samples from the
abomasal wall and suggested that a dysfunction of the
enteric neurons may be present in cows with AD. These neu-
rons exhibited an increased activity of neuronal nitric oxide
synthase as well as a decreased sensitivity to acetylcholine.
Thus, abomasal hypomotility and impaired emptying may
be related to an abnormal increased activity of inhibiting
neurons of the enteric nervous system as well as a decreased
cholinergic sensitivity of the abomasal muscle (Geishauser
et al., 1998; Reiche, 2000). However, it remains unclear
whether these findings are primary causes of AD or second-
ary to impaired circulation in the inflated organ.
Current research in our clinic has focused on other neu-
rotransmitters in the abomasal wall (Sickinger, 2007).
Biopsies of this compartment from 20 healthy German
Holstein and 20 healthy German Fleckvieh cows were
assessed immunohistochemically. Significant differences
were found between the breeds, regarding the content of
substance P (SP) and total innervation density (detection
of neurofilament 200), even though there was a consider-
able inter-individual variation. The concentration of SP
(stimulating neurotransmitter) in the abomasal wall was
significantly lower in German Holsteins and was accompa-
nied by markedly higher (although not significant) levels of
the inhibiting neurotransmitter vasoactive intestinal poly-
peptide (VIP). This could explain why German Holstein
cows are more frequently affected by AD than the German
Fleckvieh.
Conclusions
Based on current data, it can be assumed that an inhibi-
tion of abomasal motility is the key event in the majority of
cases of AD. Most likely this is due to an impaired function
of the enteric nervous system in this organ. In addition, the
genetic background is an important risk factor for the
development of the disease. Thus, inter-individual predis-
positions within the breeds should be considered when rais-
ing cattle. At the present time, cattle farmers should try to
avoid all risk factors which may lead to AD. Adequate feed
with a sufficient crude-fibre fraction during the transition
phase is pivotal. The basic principle is to ensure that the
rumen is adequately filled prior to and post calving. Fur-
thermore, optimising husbandry conditions as well as pro-
phylaxis or early recognition and treatment of metabolic
disorders and other concomitant diseases can contribute
to decrease the risk of AD.
Conflict of Interest Statement
None of the authors of this paper has a financial or per-
sonal relationship with other people or organisations that
could inappropriately influence or bias the content of the
paper.
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