Review
New aspects in the pathogenesis of abomasal displacement

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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 addition, there appear to be significant differences between breeds in the levels of the neurotransmitters substance P (SP) and vasoactive intestinal 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 susceptible to abomasal displacement than other breeds.

Introduction

The first reports of abomasal displacement (AD) in cattle 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 Holstein 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 production and the cost of treatment or culling. Studies using a 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 factors 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 supported 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 ruminal sac, ultimately rising (like a balloon) between the rumen and the abdominal wall.

In the less common right-side displacement, the accumulation of fluid and gas leads to a caudo-dorsal dilatation. The abomasum then has the potential to twist on the lesser omentum, creating an abomasal volvulus. This can cause acute obstruction with local circulatory impairment 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, Meylan, 1999, Sattler et al., 2000). In contrast to left-side displacements, 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 predispose to left AD, although the aetiopathogenesis of right AD and abomasal volvulus are thought to be similar (Dirksen, 2002, Trent, 2004). This review will give an overview of the current knowledge of the aetiology and pathogenesis of AD in dairy cows.

Section snippets

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, Wolf et al., 2001b) as well as on Simmental–Red-Holstein crossbreeds (Eicher et al., 1999), Brown Swiss, Ayrshires, Guernseys (Constable 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

Conclusions

Based on current data, it can be assumed that an inhibition 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 predispositions within the breeds should be considered when raising cattle. At the present time, cattle farmers should try to avoid all risk factors

Conflict of Interest Statement

None of the authors of this paper has a financial or personal relationship with other people or organisations that could inappropriately influence or bias the content of the paper.

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