Fodder beet toxicity in cattle Rowan Skentelbery

Rowan Skentelbery

Fodder beet toxicity in cattle

Fodder beet has become a popular winter feed due to its high energy and low cost per kg dry matter; however, its associated health problems need to be understood by users and avoided with a combination of good education and diligent practice.

Introduction

Over the last 10 years there has been an exponential growth in the amount of fodder beet (Beta vulgaris subsp. vulgaris L.) grown and fed to production animals in New Zealand (Gibbs and Saldias, 2014), especially within the dairy industry. Fodder beet is now widely grown in New Zealand, particularly in the South Island, where its high energy and low cost per kg dry matter (DM) make it an ideal winter feed; however, there can be associated health problems which farmers need to understand. While it is generally safe to feed to cattle, with good palatability and high yields, it must be done correctly. Fodder beet is high in energy, with adequate protein, however, it is low in fibre, phosphorus and calcium (Gibbs & Hughs 2016). Therefore, supplementation of these deficient feed constituents must always be considered. A 14-day transition period is also vital to ensure that the rumen and the microbial population therein can alter and adapt to the high carbohydrate intake.

Rumen acidosis is the most common sequel to poor management during fodder beet transitioning. If an increase of >2kg DM per day is consumed relative to the previous day, the sudden increase in carbohydrates exceeds the absorption capabilities of the rumen papillae. It takes a minimum of 4 weeks for the rumen to adapt to increased carbohydrate intakes (and therefore the short chain fatty acids (SCFA) being absorbed). In the interim, some buffering capacity is

The treatment options for acute rumen acidosis are discussed later in this report, but if an affected cow is not standing within eight hours, the prognosis is grave (Gibbs 2019).

provided by bicarbonate and phosphate rich saliva, which helps minimise pH changes. However, this requires salivary production during rumination, which is stimulated by fibre; a dietary constituent that is low in fodder beet. In addition, a small amount of SCFA are also removed via the omasal orifice and by the fermentation of microbes (Gibbs 2019). These buffering capacities are overwhelmed when a steep increase in carbohydrate intake occurs, resulting in acidosis. When the rumen is adapted, SCFA are moved efficiently across the rumen mucosa via epithelial transportation into the blood.

The fall in rumen pH is the initial insult, giving this syndrome its name; however, it quickly reaches a point where the progression of the disorder is independent of rumen pH (Gibbs 2019). Once the pH drops below 5.5, the resultant rumen changes can be hard to reverse as they set up a self-perpetuating downwards spiralling cycle. The SCFA accumulation also drives increased osmolarity, causing gut stasis,

Table 1: TPR values for the three worst

Heart rate

Respiratory rate

Temperature

Cow #326

92bpm

40bpm

40.0 degrees Celsius

Cow #120

110bpm

52bpm

39.8 degrees Celsius

Cow #92

96bpm

48bpm

40.0 degrees Celsius

decreased blood flow (Gibbs 2019) and systemic dehydration (Parkinson et al. 2009). The lowered pH disrupts the rumen flora, selecting for acid resistant, lactogenic bacteria (Russel and Hino, 1985), which minimise acid transport across the stratified epithelium of the rumen wall. The high production of lactate, by the lactogenic bacteria, then drives the pH even lower, resulting in further cellular damage to the rumen. A progressive hypocalcaemia also develops, which generally manifests clinically as the first symptom of the underlying issues in the rumen. Onset of clinical signs is rapid after excessive fodder beet consumption and include anorexia, ataxia, decreased or absent rumen contractility, dehydration, diarrhoea, increased vital signs (temperature and respiratory rate may drop as the disease progresses), colic, teeth grinding, and weakness, progressing to recumbency and death (Parkinson et al. 2009).

The treatment options for acute rumen acidosis are discussed later in this report, but if an affected cow is not standing within eight hours, the prognosis is grave (Gibbs 2019). Poor prognostic indicators include heart rates >120bpm, prolonged recumbency, anuria and severe dehydration (Credille & Synder 2017). Post recovery, cows are at increased risk of developing metabolic disorders, liver abscesses, fatty liver, laminitis, abomasal displacement (Humer et al. 2018), posterior vena cava syndrome, mycotic rumenitis, rumen ulceration, polioencephalomalacia and peritonitis (Parkinson et al. 2009). Many of the conditions carry a grave or hopeless prognosis so avoiding cases should be the priority when feeding fodder beet. Rumen acidosis should no longer be a significant risk once cows have been correctly transitioned onto the crop (Gibbs and Saldias 2014); it is only during the 14-day transition period that serious health conditions are of major concern.

Clinical findings

History In April, fourteen cows were reported to be acutely recumbent after breaking through the hotwire controlling access to the mornings fodder beet allowance. A further eighteen cows were reported to be wobbly and lethargic.

Found several hours post-milking, the farmer immediately moved the rest of the herd off the fodder beet crop but had not administered any therapy to affected animals.

Herd information: There were 420 Holstein-Friesian cows in the spring calving herd; run on a twice daily milking regime. They were at day seven of the transition onto fodder beet for winter feeding and were being fed 4kg DM per day. Silage and hay were fed out two hours before the herd were put onto the crop. In addition 50g of Dicalcium Phosphate/cow/day was being supplemented via pasture dusting, to combat the relatively low calcium and phosphate in fodder beet crop.

The farmer had fed fodder beet in previous years and had always successfully transitioned cows without health issues; this incident was related to the cows breaking out rather than management failure.

Initial clinical exam On arrival nine of the initial fourteen recumbent cows were still down, the other five previously recumbent cows were now standing, but still moderately ataxic. Brief physical exams were conducted on three of the worst affected recumbent animals for prognostic indicators.

Eight out of nine recumbent cows made no efforts to stand when approached, and 7/9 had distinct ‘S’ bend of their necks and could be heard grinding their teeth.

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These results appear to be even more outstanding since no rumen alkalising drenches were used, the widely advocated treatment for rumen acidosis.

Moderate dehydration (~8%) and dull mentation was noted in all recumbent animals and decreased, or absent gut sounds were also noted on auscultation. All 14 initially presented animals had profuse, green, watery diarrhoea.

There was clear evidence in the paddock of the herd breaking through the hotwire, with approximately half of the next day’s break (4kg DM/Cow) having been partly consumed. It was also noted that the previous day’s allowance had been fully utilised, and that the break allocation appeared adequate.

Diagnosis Based on history and clinical examations, acidosis secondary to excess fodder beet ingestion was the top differential for this case.

Other differentials briefly considered, but quickly discounted, included:

Ð Hypocalcaemia – this plays an important role in rumen acidosis but was unlikely to be the primary cause of clinical signs due to the stage of lactation and calcium supplementation.

Ð Toxic mastitis or metritis

Ð Diffuse peritonitis

Ð Vagal indigestion

Ð Intestinal obstruction

Ð Listeriosis

Ð Lead poisoning

Treatment and response to treatment One bag (500ml) of calcium borogluconate (Calpro® 375; Bayer NZ Ltd) was administered to all 9 recumbent cows by slow intravenous injection (IV) using the jugular vein.

No other treatments were given, however sufficient 500ml calcium bags were left with the farmer so that treatment could be repeated, by subcutaneous injection, for any animal not standing after 4-6hrs. A poor prognosis was given to any animal not standing within 24hrs. Hay and water were made readily available to recumbent animals. The rest of the herd were not treated. The farmer was advised to continue the transitioning program but to decrease the ration to 75% of the previous days DM intake, then continue as normal.

Outcome Six of the nine recumbent cows responded to the first treatment and were standing, with mild ataxia, four hours later, and a further two responded to the second treatment given at the 4-hour mark. The remaining cow never stood and was shot the following day on welfare grounds and due to poor prognosis.

The rest of the herd recovered well, and fodder beet feeding was continued with no further issues until they reached ad-libitum intake.

Discussion

This case progressed well; anecdotal evidence would suggest that losing only 1/14 severely affected cattle from acidosis was an excellent result. These results appear to be even more outstanding since no rumen alkalising drenches were used, the widely advocated treatment for rumen acidosis. Instead the attending veterinarian focused on treating the hypocalcaemia, which was successfully resolved with calcium borogluconate treatment.

The severe dehydration that is associated with rumen acidosis often leads to hypotension. This is worsened by the acidic conditions driving Allisonellla histaminiformans overgrowth in the rumen. The histamine released by these bacteria results in vasodilation, removing the body’s ability to compensate for hypotension, and risking cardiovascular collapse. Due to the cardiotoxic effects of calcium borogluconate (Parkinson et al. 2009), there are distinct risks involved with giving this IV in such a compromised system. While issues were not seen in this case, it is generally recommended to give calcium subcutaneously.

Another aspect to consider with this case was potential administration of antibiotics. Due to rumen epithelial damage, there is high risk of bacterial translocation following rumen acidosis. Hepatic abscesses are a known risk, which may justify its use (Parkinson et al. 2009). The main bacteria involved are Fusobacterium necrophorum and Arcanobacterium pyogenes, therefore procaine penicillin is the treatment of choice (Parkinson et al. 2009). Antibiotic therapies are controversial as they may impair repopulation of gut microbiome (Credille & Synder 2017), so it becomes a balancing act regarding which is most likely to have the greater negative effects. The severity of the case will direct this decision; a more severe acidosis will result in increased epithelial damage, and therefore greater risk of bacterial translocation; whereas a milder case may retain its rumen epithelial defences. In this case, clinical exams did not demonstrate parameters exceeding crisis level, leading to the decision to exclude antibiotics from the treatment protocol.

Another ancillary treatment to consider is the use of NSAIDs to reduce inflammation and pain associated with the ruminitis, and for their antiendotoxic affects. Their use may encourage a more rapid

Fodder beet intake

>2kgDM h per day

^ CHO i Acelate, h Butyrate, Proprionate

Strep. Bovis proliferation ii pH

Allisonella histaminiformans proliferation

h Lactate production

iii pH Uncompensated metabolic acidosis i Rumen epithelial transport

h Osmotic Pressure Histamine release

Severe rumenitis and acidosis

i Myofilament contractility and change cell surface receptors, leading to i vasconstrictor responses. Tissue fluid drawn into rumen i Rumen epithelial blood flow

Rumen hypomotility/ stasis

Vasodilation

Hypotension

Systemic dehydration Diarrhoea

Anorexia

iPerfusion hHR

Figure 1: Model for pathogenesis of fodder beet toxicity in cattle

Under the Gibb’s hypothesis, the traditional treatment approach, using large amounts of alkalising agents is not only counterproductive but likely to exacerbate the condition, as the buffering agent will significantly increase the rumen osmolarity (Gibbs 2019). For example; 500g of magnesium oxide in 10 litres of water could raise the osmolarity of a 100L rumen by 40mOsm/L (Anonymous, 2017). The increase in osmolarity could be even greater, since the decreasing rumen pH increases magnesium oxide solubility, and could be up to 150mOsm/L (J. Gibbs pers. comm.). Since it is this increased osmolarity that results in rumen stasis, decreased blood flow and systemic dehydration, it is essential that this factor be controlled rather than worsened, particularly as our oath states “first do no harm”. Oral alkalisers may contribute to the death of acidotic cows. continued

continued

return to normal feed intakes and milk production, therefore reducing production checks associated with rumen acidosis.

Treating rumen pH: The major driving force for acidosis is the fall in rumen pH to below 5.5. Traditionally in mild to moderate cases of acidosis, treatment was directed at correcting the acidosis by using up to 1g/kg body weight (BW) of magnesium hydroxide or magnesium oxide, diluted in 5-10L of warm water, and given by stomach tube (Parkinson et al. 2009). As stated, this treatment was aimed at rectifying rumen pH, preventing further epithelial damage and allowing rumen flora to recover. In addition, kneading the rumen and getting the animal moving was thought to facilitate rumen emptying. Free access to grass and hay were also given to encourage saliva production. Other than the water used to suspend the alkalising agent, no further water was given for 18 hours to prevent over engorgement and fluid dilation of the gut. The alkalising agents could be repeated every 12 hours at 0.25-0.5g/kg BW if required (Parkinson et al. 2009).

For many years oral alkalisers have been the benchmark of acidosis treatment, however, a recent article challenges these recommendations, finding instead that medically correcting pH is ineffective or even counterproductive (Gibbs 2019). Gibbs (2019) states that by focusing only on treating the acidosis, practitioners are ignoring the increased osmolarity which is responsible for the rumen stasis, decreased blood supply and redox changes. Instead the focus of our treatment should be on correcting the osmolarity, since the pH will autocorrect without treatment.

Furthermore, due to the decreased gut flow and rumen stasis, anything put into the rumen will be held in suspension there. So oral alkalising remedies may have a mild, transient effect on the rumen pH, but will not treat the systemic acidosis, nor will they hold the rumen pH within normal ranges for any appreciable amount of time (Gibbs 2019). Therefore, for mild to moderate cases, Gibbs recommends ‘waiting it out’ and allowing the rumen pH to normalise through the course of the disease (Gibbs 2019). The associated inappetence will minimise further beet consumption until the rumen is recovered. Calcium may be given to those that are ataxic or acutely recumbent. Any animals that do not respond to ‘waiting it out’ and calcium treatment are likely to have severe epithelial damage and are beyond saving (Gibbs 2019).

For acute severe cases, surgery is required to remove the ingested fodder beet from the rumen. This may however only be an option for highly valuable animals and on farms with good facilities. Indications for surgery include rumen pH<5.0, dehydration >8%, heart rate >100bpm and marked rumen distension (Parkinson et al. 2009). Rumenotomy is the main line of treatment in these cases; physically emptying the bulk of the material, followed by lavage to remove the lactic acid build-up. In these cases, it has been recommended to treat the metabolic acidosis with 5-7L of 5% sodium bicarbonate solution over ~30min, followed by 1.3% isotonic sodium bicarbonate at a rate of 150ml/kg over 6-12 hours as intravenous fluids (Parkinson et al. 2009). Any animal that undergoes surgery should receive rumen-transfaunations from healthy donor animals to replenish normal bacterial flora (Credille & Synder 2017). This is especially important as these cases will generally receive antibiotics. While this method of treatment is effective, and sometimes vital for cow survival, the indicators for surgery also indicate severe disease, which increases the inherent risk of the surgery itself. It cannot always be ascertained how each animal will respond to surgery, so the farmer must be aware that losses may still occur. If surgery is to be done, it must be done immediately for the best outcome. Another option for removal of beet from the rumen is lavage through a wide bore tube (Dacharme 1990). However due to the large size of the fodder beet pieces, this method is generally not successful.

As attending veterinarians our choices for treating acute rumen acidosis simply distil down to “wait it out” or “cut it out” (Gibbs, 2019).

The wider significance of this disease comes with the increasing use of fodder beet as a winter crop in New Zealand. This is evidenced by the 150-fold increase in hectares planted with fodder beet between 2006 and 2014(Gibbs & Saldias 2014). Prevention of fodder beet toxicity is purely a management issue, and with good education and diligent practice, can be avoided. Toxicity is generally only seen in management breakdowns as in this case, or due to inherent naivety in first time uses.

Acknowledgements

Many thanks to Kevin Lawrence for his mentorship on the preparation of this case report. The help of Jim Gibbs is also gratefully acknowledged who was approached by Kevin Lawrence on behalf of Rowan Skentelbery.

REFERENCES:

Anonymous. Osmolarity Calculator – Extremely Powerful Tool. https://globalrph.com/ medcalcs/osmolarity-calculatorextremely-powerful-tool/ (Accessed 04/10/2019), Global RPH 2017.

Credille B, Synder E. Diagnosis and Treatment of Clinical Rumen Acidosis. Veterinary Clinics of North America Food Animal Practice 33 (3), 451-461, 2017.

Dacharme NG. Surgery of the Bovine Forestomach Compartments. Veterinary Clinics of North America Food Animal Practice 6 (2), 371-397, 1990.

Gibbs J. Treating Cattle with Fodder-Beet Farmer Management Disorder (Rumen Acidosis). Vetscript 32 (7), 26- 29, 2019.

Gibbs SJ, Saldias B. Fodder Beet in the New Zealand Dairy Industry. Proceedings of the South Island Dairy Event Annual Conference. Lincoln University Press 6, 2014.

Gibbs J, Hughs T. Using Fodder Beet in Lactation. New Zealand Dairy Exporter 91 (8), 46-47, 2016.

Hummer E, Petri RM, Aschenbach JR, Bradford BJ, Penner GB, Tafaj M, Sudekum KH, Zebeli Q. Invited Review: Practical Feeding Management Recommendations to Mitigate the Risk of Subacute Ruminal Acidosis in Dairy Cattle. Journal of Dairy Science 101 (2), 872- 888, 2018.

Parkinson TJ, Vermunt JJ, Malmo J. Diseases of Cattle in Australasia. 1st ed. pp.80-84. Wellington, New Zealand Veterinary Association Foundation. 2009.

Russel JB, Hino T. Regulation of Lactate Production in Streptococcus Bovis: A Spiralling Effect that Contributes to Rumen Acidosis. Journal of Dairy Science 68 (7), 1712-1721, 1985.

Dairy NZ

Fodder beet research reinforces portion control is key

New research into fodder beet shows the crop can be a key part of dairy farm systems – but should make up no more than 30 percent of lactating cows’ diet and 60 percent for non-lactating cows.

THE SUSTAINABLE USE of Fodder Beet research project looks at nutrient and mineral interactions, and impacts on long-term animal health and welfare. A literature review undertaken as part of the project has confirmed the crop’s benefits and challenges.

“Fodder beet will continue to be a key part of New Zealand dairy systems – but it should not be seen as a complete diet,” says DairyNZ senior scientist, Dawn Dalley.

“Fodder beet is widely used on South Island dairy farms and is a versatile, high energy, high yield crop which allows cows to put on body condition quickly, if transitioned correctly. This makes it an attractive option for farmers. But because of the high sugar content, careful transitioning onto the crop is critical.”

Fodder beet use has increased over the past decade and today around 55,000ha is estimated to be planted annually in New Zealand.

Most fodder beet is grown in the South Island – with the project survey showing 79 percent of Canterbury/ North Otago farms and 58 percent of South Otago/Southland dairy farms feed cows the crop.

In recent years, some farmers have become concerned about potential health effects on herds. Cows can develop ruminal acidosis, milk fever or nutrient deficiencies if fodder beet is grazed for long periods without appropriate alternative feed and mineral supplementation.

Recent research and nutritional modelling has reinforced current recommendations that - for consistent herd performance and to minimise nutrient deficiencies - fodder beet should make up no more than 30 percent of the diet for lactating cows and 60 percent for non-lactating cows.

Dr Dalley says many farmers are successfully combining fodder beet with other feeds to provide cows with a diet that meets nutritional requirements and is cost-effective.

“By using feed testing which includes mineral composition analysis of fodder beet and other feed, farmers can tailor cow diets to address any nutrient deficiencies. Using this approach, fodder beet can be a valuable feed option which contributes to a productive dairy system.”

Fodder beet is a hardy autumn and winter crop with environmental benefits. The beet’s low nitrogen content results in reduced urine nitrogen concentrations, leading to less nitrate leaching from animals grazing the crop, compared to kale. It is also an important break crop in winter rotations which use kale and swedes, and allows farmers to successfully crop areas affected by brassica disease.

Dr Dalley says that regular communication and good planning is needed between dairy farmers and graziers to develop winter feeding plans that are affordable, easy to implement and meet environmental and animal welfare regulations.

Steve Penno, Director of Investment Programmes at the Ministry for Primary Industries (MPI), which is providing $565,000 towards this million-dollar project, says this research offers an important insight into the use of fodder beet on-farm.

“Animal health and welfare is a key priority for MPI and this research will help farmers ensure their cows are eating a healthy proportion of this crop.”

The cross-sector project on the Sustainable Use of Fodder Beet on New Zealand Dairy Farms is funded by MPI’s Sustainable Farming Fund (now superseded by Sustainable Food & Fibre Futures) and from DairyNZ’s levy, and it involves PGG Wrightson Seeds, AgResearch, Plant and Food Research, farmers and vets. It is currently one year into a three-year research programme.