Julie Nuttall, Author at Oakhill Vets

Poisonous toxins to be aware of on Autumn dog walks

Autumn is the season for muddy woodland walks, kicking through piles of crunchy golden leaves and wrapping yourself up, ready to battle the wet and windy weather. Although autumnal walks with your dog can be beautiful, it’s important to be aware of the seasonal dangers that could be harmful to them.

Acorns

Acorns contain a type of toxin called tannic acid that can make your dog sick or give them a stomach upset. In larger amounts, or if eaten regularly, tannins can also cause kidney and liver failure. Green acorns contain the highest amounts of tannins and are more poisonous than brown ones. As well as being poisonous, acorns can also block your dog’s stomach, causing further complications.

Conkers

These hard shiny seeds contain a toxin called aesculin, which can make your dog sick or give them an upset stomach. Conkers have a bitter taste that might put some dogs off eating a lot of them. When eaten in larger amounts, aesculin can cause more serious effects, and in rare cases can even be deadly.

Clinical signs are usually seen between one and six hours after ingestion, although they can be delayed for up to two days.

Symptoms of conker poisoning include:

Vomiting, which may contain blood
Diarrhoea
Drooling
Abdominal pain
Increased thirst and reduced appetite.
Signs of restlessness, wobbliness and muscle tremors may also be seen.

Poisoning is not the only risk – Conkers are large and hard and may cause your dog to choke on them, or could cause a blockage in your dog’s intestines.

Fallen fruits

As the temperature begins to cool in autumn, many trees start to drop their fruits. Some seeds, pips and fruit stones (apples, cherries, plums etc.) contain toxins that can make your dog ill.

These fruits can also make your dog unwell if they’re eaten when mouldy or after they’ve begun to ferment.

Case Report: Acorn toxicity

In mid-October we were called to examine two 14 month-old beef heifers which had exhibited a sudden onset of foul smelling diarrhoea, inappetence and abdominal pain whilst at grass. Despite symptomatic treatment both animals died within 48 hours. Faecal samples were analysed at the practice but did not reveal a significant parasite burden. One heifer was submitted to the laboratory for a full post mortem investigation.

The post mortem revealed significant kidney damage which raised suspicion of the ingestion of a poisonous substance. On further investigation the field in which the heifers were grazed had 3 oak trees and an abundance of acorns. Acorns contain high levels of tannins which cause acute kidney damage.

Cattle and sheep can exhibit clinical signs of foul-smelling diarrhoea which may contain blood, weakness, inappetence, weight loss and may appear hunched up due to abdominal pain. They may die relatively suddenly. Those animals which survive exhibit weight loss and anaemia as the result of kidney failure.

It is advisable to prevent stock having access to acorns by removing them from fields with oak trees in the autumn or erecting a temporary electric fence. Stock are more likely to ingest acorns if grazing is in short supply.

Interestingly one of the laboratories that we use has reported over 20 cases of acorn toxicity this year, in comparison to only one last year.

Look out for Lungworm

Lungworm outbreaks are unpredictable but are more prevalent following warm wet weather spells (thankfully not at the time of writing!). Immunity requires repeated exposure, therefore older cattle may become susceptible if they have not been exposed to sufficient challenge within the last 2-3 years.

Suspect lungworm infection if there is widespread coughing or respiratory distress in grazing calves or adult cattle. Coughing may be more noticeable when cattle are gathered. Milk drop is seen in dairy herds experiencing a lungworm outbreak.

Affected cattle should be treated as early as possible. Severely affected cattle may not respond to treatment due to the large number of dead larvae blocking the lower airways and secondary bacterial pneumonia. Treated cattle should be removed from infected pasture and transferred to clean pasture if available or well-ventilated housing.

All available anthelmintics are effective against lungworm. To date, there are no confirmed resistance issues. Anthelmintics vary in their duration of residual activity. For example, Enovex is active against lungworm for 28 days.

Bought-in calves or adult cattle may introduce lungworm onto a farm, so quarantine and treat all incoming cattle. If you have a known problem on your farm then purchased cattle should be vaccinated prior to grazing.

Respiratory tract health

Does your horse cough at the beginning of an exercise session? Do you often find accumulations of mucus outside your horse’s stable door? These subtle signs can indicate lung inflammation.

Formerly known as COPD or RAO, Equine Asthma is commonly seen in equine practice. For the purpose of simplicity, two forms are recognised- Summer asthma and the more traditional dust-induced form.

Both forms of the disease occur when a susceptible horse inhales either an allergen, to which they are allergic, or dust into their airway. This results in the airway spasming and the production of increased amounts of both inflammatory cells and mucus within the airway.

Affected horses present with clinical signs of varying degrees of severity. Some horses present with the subtle signs mentioned above or with a history of poor performance, whereas others present in respiratory distress and struggling to breathe.

On examination affected horses will generally have an increased breathing rate and effort combined with nostril flare. Mucoid nasal discharge may also be present. More severely affected horses may cough, have abdominal effort to their breathing and may have a ‘heave-line.’ A horse’s history combined with clinical examination findings will point towards a diagnosis of asthma but for definitive confirmation, airway endoscopy, to visualise the airway and grade airway mucus combined with laboratory analysis of respiratory tract samples is required. This will also rule in/out secondary bacterial infection.

Treatment of asthma should be based on environmental modifications plus drug therapy on an as needed basis. Horses affected by dust-induced asthma should be turned out in so far as possible. The stable environment should be closely examined. Ideally, the stable will have an inlet and outlet for airflow. Forage should not be stored adjacent to the stable to minimise the dust to which the patient is exposed. Horses should be groomed outside of the stable and fresh bedding laid when your horse is not in the stable environment. If your horse’s stable is unsuitable, try find an alternate stable on your yard that has better airflow. If feeding hay or ‘dry’ haylage, steaming is optimal to reduce dust particles but if not available, soaking should be considered. Managing Summer asthma is more challenging, but the measures outlined above should be followed to ensure stable ‘air hygiene’ is a good as possible.

Drug therapy, when needed, is based on relieving airway spasm (bronchodilators) and reducing airway inflammation and mucus production (steroids and mucolytics). Drug therapy can be provided by the oral or inhalatory routes. Oral medication includes bronchodilators, steroids and mucolytics (which serve to break-up airway mucus). From an inhalatory medication perspective, three options are available- the Equihaler, MDIs and nebulisation. The Equihaler is a licensed, steroid based product which utilises a fine mist to deliver steroid directly to the lungs. The product is very safe as the steroid acts at the lung surface only. We have had some great success using this product in cases of severe asthma and in those that did not respond to other forms of medication. MDIs, human asthma inhalers administered via a baby asthma face mask, have been utilised in equine practice for many years. These are probably most useful in relatively mild cases. Drug delivery via a nebuliser is the third inhalatory option but arguably used less frequently these days.

If you have any questions regarding asthma or think your horse may be affected, please do not hesitate to contact the team for guidance.

Are your tup’s up to the job?

Reduced fertility performance in tups can have a detrimental effect on scanning percentages and can lead to an extended lambing period. Often subfertile tups are only noticed well into the breeding period when ewes are returning.

A pre-breeding examination can rule out common health problems, assess the genitalia, and check semen quality. It can take 6 weeks for sperm production to recover after a problem (stress, lameness, disease etc), so it is important to schedule the pre-breeding exam at least 8 weeks before the planned start of breeding.

The 5 T’s of the tup exam

Teeth – Check for under or overshot jaw and dental health. It is important that he can eat well during the breeding season to maintain his energy status and body condition.
Toes – Check for any signs of lameness, infectious disease, or arthritis. Assess his locomotion.
Tone – Assess his body condition score. Aim for 3.5-4.
Testicles – Measure scrotal size, check firmness and feel for any lumps.
Treatment – Chance to give any treatments e.g. vaccinations or parasite products.

Assessing the semen quality

If the tup passes the first half of the test then a semen sample will be taken with the aid of an electro-ejaculator and examined under the microscope. The motility and number of abnormal sperm will be assessed.

What is MRI used for?

Our standing MRI scanner can be used to assess injuries from the hoof, up to and including the hock and carpus (knee). The scanner is specifically designed to image the lower limb in the standing horse, as this is the most common site of lameness. It has revolutionized our understanding of the structures of the hoof, and we can now differentiate between the multiple conditions that were encompassed as ‘navicular syndrome’.

Previously, a horse with forelimb lameness that was localized to the foot, was diagnosed with ‘navicular syndrome’. However, a lot of the time, the severity of the lameness did not fit with the mild observations noted on radiographs (X-rays). We now know, through the use of MRI, that there are many other anatomical structures that could be injured and causing the lameness. With forelimb lameness being a common problem in horses, this diagnostic imaging tool means we can target rehabilitation, farriery, and treatment more specifically.

Injuries identifiable on MRI would include deep digital flexor tendon lesions within the hoof. Without the use of MRI this condition would have been misdiagnosed, leading to inaccurate management and unsoundness. MRI can also assess ligaments within the hoof capsule, such as the collateral ligaments of the coffin joint, which are often painful when horses are lunged in a circle. This amazing imaging modality also shows us the degree of inflammation within synovial structures such as the coffin joint and navicular bursa of the foot which cannot be visualized in any other way. Not only does MRI allow us to diagnose more accurately, but it allows us to monitor the progression of conditions and carefully assess the horse’s response to treatments.

X-ray imaging is used to assess bone pathology as an initial tool. However, it can take up to 2 weeks following injury before the bone pathology is noticeable on radiographs, and sometimes it is not visualized at all. MRI is the only imaging modality that can assess inflammation within bones such as bone bruising or cysts. These can cause severe lameness and require long periods of rest but would not be diagnosed without the use of MRI.

As equine vets we are eternally grateful for these advancements in technology which have enabled us to achieve an accurate diagnosis much faster than ever before, and as we know, a faster diagnosis leads to more precise treatment and management protocols to get your horse feeling in tip-top shape again.

Heat Stress in Cattle

Cattle are particularly susceptible to heat stress as they carry a fermentation tank (their rumen!) around with them which is constantly producing heat (the equivalent to a 1.4 kW heater in ambient temperatures). Cows may be subjected to heat stress under housed conditions or at grass.

For lactating cows, the greater the milk yield, the more heat is produced. For example, irrespective of the environmental temperature, a cow yielding 31 litres a day produces 48% more body heat than a dry cow!

There is evidence that heat stress is most marked when it comes in short bursts (as we (un)commonly see in Lancashire!) with no time for the cow to adapt to the rising temperatures.

Factors affecting the likelihood of heat stress include:

Air temperature
Solar radiation
Air velocity
Relative humidity

Cattle are likely to experience heat stress once the temperature reaches 24°C, particularly if the humidity is >70%. Calves are susceptible to heat stress from 25°C, as they have a larger surface area to body weight ratio.

The effects heat stress in dairy cattle include:

10-30% reduction in dry matter intake. Cows reduce their feed intake as a means to limiting their own heat production by the rumen. Cows will be more selective in what they eat and will avoid roughages if they are able to sort their diet. Less roughage = reduced rumination, and a reduction in heat production.
Negative energy balance. A reduction in DMI will have a negative effect on the cows’ metabolic status.
8-37% reduction in milk yield. Butterfats will reduce if fibre intake is decreased.
Negative impact on fertility. A reduction in heat expression and increased embryo mortality.
Increased lameness. Heat-stressed cows prefer to stand in an attempt to keep cool. They may congregate in cooler areas of the shed. Increased standing puts greater pressures on feet.
Increase in somatic cell count and clinical mastitis. This is due to a combination of compromised immune function, increased standing times, reduced fibre intake leading to thinner slurry, and a reduction in cubicle hygiene (sweaty skin and warm humid bedding materials are the perfect recipe for mastitis!)

Cows suffering from heat stress exhibit increased breathing rates. In extreme cases cows may be seen panting and open-mouth breathing in an attempt to cool down. You may notice cows clustering in cooler areas of the shed or in shaded areas. Respiration rates and body temperature are both good ways to assess whether cows are affected by heat stress. A normal respiratory rate is 26-50 breaths per minute. Rectal temperature should be <39.3. It is not advisable to wait for a reduction in milk yield as there is a lag time of 2-4 days.

Managing heat stress:

Ensure sufficient water sources – cows may drink in excess of 200 litres in hot weather. Provide at least 10cm linear trough space per cow, from multiple troughs to minimise competition.
Reduce solar radiation – ensure cows at grass have sufficient shade and assess the effect of solar radiation from sky lights. Try painting south-facing sky lights to reduce sunlight entering buildings.
Modify existing buildings to maximise ventilation. This could include opening up the ridge and creating more air inlets along the side of buildings. For adult cattle the outlet in the ridge needs 0.1m² per animal. Inlets in each sidewall need to be 1.5-2x the outlet area.
If the ventilation is still inadequate, consider installing fans.
Reduce the stocking density in buildings.
It may be appropriate to house grazed cattle.
Only handle cattle at cooler times of the day and minimise time spent in holding pens.
Feed at cooler times of the day (8pm-8am).
Ensure good fly control as flies are more active in hot weather and contribute cows’ frustration.
Move calf hutches to shaded areas where there is good air flow.

Don’t forget collecting yards and the milking parlour. If it’s uncomfortable for you it certainly will be for your cows!

What is kissing spines?

What is kissing spines and why has it suddenly become more common?

Kissing spines or more correctly termed ‘impinging dorsal spinous processes’ (IDSPs) is where there is over-crowding of the summits of the 18 spines that the horse has, usually in the saddle region of the spine. This leads to bone friction and pain which spreads along the muscles either side of the spine. In our years of experience of dealing with this disorder, by far the most common clinical signs are (in order):

Bucking
Being ‘Cold-backed’ on mounting
Hunching or arching of the spine
Sudden shooting/scurrying under saddle particularly on mounting
Bolting

Yes, some young (and old!) horses will buck when they are excited, these horses usually have their ears pricked and they are ready to go!! Horses who buck due to pain will have their ears pinned back and they are not ready to go, they just want to get rid of the pain (unfortunately that’s usually the rider on board!).

The problem we have in diagnosing this condition is that many horses will have kissing spines on X-rays of their spine, in fact up to 86% of thoroughbred horses will have x-rays consistent with IDSPs! That does not mean that they are all painful! To determine whether or not the x-ray findings are causing discomfort relies on 3 methods of diagnosis (in order of our preference!):

Medication of the spine with steroids (potent anti-inflammatory drugs) which lasts several weeks in this region in severe cases, so you can tell if your horse feels better over this prolonged period of time.
Infiltration of the spine with local anaesthetic and seeing if the clinical signs resolve when the horse is re-evaluated ridden.
A ‘bute’ trial, whereby we administer systemic anti-inflammatory drugs to see if the clinical signs improve.

Only then can we be sure if the X-ray findings are consistent with pain in the horse. So your horse is diagnosed with kissing spines, what can we do? Is it hopeless? NO, in fact, this condition can be treated fairly successfully in most cases either with conservative management and altered training techniques, including physiotherapy or with different surgical methods. If your horse is suffering with kissing spines, we are equipped to help you every step of the way with your journey back into the saddle.

And in answer to the original question, IDSPs is NOT more common than it was years ago…….we just have X-ray machines that are capable of seeing the spine now. We are also more aware than ever that our horses are generally not a naughty bunch, and are often just asking for our help because something hurts!

Endometritis

Clinical endometritis or “whites” is defined as the presence of pus in the vagina from 21 days after calving. The greatest impact and cost of endometritis is due to its detrimental effect on fertility, which persists way beyond the duration of the disease itself. In addition to creating a uterine environment which is unfavourable for embryo development, endometritis also disrupts follicle growth, leading to reduced egg quality. This is particularly important for eggs which are ovulated between 60-120 days in milk.

The impact of endometritis on fertility:

Calving to first service interval was extended by 11 days
Conception was delayed by 32 days
Cattle were 1.7 times more likely to be culled for reproductive failure

From a study of over 10,000 dairy cattle

80-90% of cows have bacterial contamination of the uterus post-calving.

So why do some cows develop endometritis and others don’t?

Risk factors associated with endometritis:

Trauma of the reproductive tract:
- Retained fetal membranes
- Twins
- Large calves
- Dystocia
- Caesarean section
- Stillbirth
Reduced immune function around calving:
- Metabolic disease
- Negative energy balance
- Ketosis
Poor hygiene

A healthy immune system is needed to clear bacterial contamination of the uterus. Anything which causes uterine damage, even on a microscopic level, will compromise the cows ability to clear uterine infections. A lack of energy or metabolic stress will further hinder the cows immune response.

The weight of the uterus changes from 9kg at calving to 1kg by 30 days in milk. This process of involution requires a healthy immune system, energy and essential nutrients. Cows experiencing metabolic stress post-calving will have a compromised immune response are more likely to develop endometritis.

Up to 80% of cows with endometritis show no vulval discharge. Checking cows for “whites” after 21 days post calving will help to identify affected cows so that they can be treated promptly. A target for the incidence of clinical endometritis is <5%.

Coccidiosis

Almost all cattle will be infected with coccidia during calfhood but disease only occurs if they are exposed to a heavy parasite challenge or if their resistance is lowered through stress, poor nutrition or concurrent disease. Calves between 3 weeks – 6 months of age are most at risk. Over 95% of the losses associated with coccidiosis are not immediately obvious:

→ reduced feed conversion efficiency and reduced growth rate

→ Delayed time to service

→ Reduced conception rate

Did you know? Less than 5% of affected calves exhibit clinical disease:
• Dehydration
• Inappetence, weight loss
• Diarrhoea, possibly bloody, straining
• Impaired absorption of water and nutrients
• Rough coat
• Death

Cocci oocysts (eggs) can survive for over 1 year in the environment between -30 and +40°C and are resistant to most disinfectants. Only a few oocyts need to be ingested to cause disease and the parasite multiplies rapidly in the gut. A single infected calf can shed millions of oocysts in its faeces therefore the environment can become heavily contaminated very quickly.

Effective control relies upon treating infected animals during the early stages of parasite development. This allows calves to acquire immunity to the parasite whilst avoiding the negative consequences of disease. Good hygiene practices alone are insufficient to manage coccidiosis as environmental contamination is inevitable. However, improving shed hygiene can aid in reducing the infection pressure.

Control of Coccidiosis:

Dosing calf groups 10-14 days after they have been moved to contaminated pasture or housing. This prevents disease and reduces oocyte shedding. Treatment during an outbreak is of limited value as the damage to the small intestine has already occurred.
Minimise oocyst intake. Prevent feed and water sources becoming contaminated with faeces. Feed from clean, elevated troughs. Avoid the transfer of faeces between older and younger groups of calves.
Ensure calves have a healthy immune system. Provide optimal nutrition and prevent concurrent disease (pneumonia, BVD, salmonella) which will make them more likely to succumb to coccidiosis.
Minimise stress such as re-grouping, dietary change and overstocking.

Preventative Treatment

A single treatment with Tolracol (toltrazuril) is effective against all stages of the parasite. Products containing diclazuril (Vecoxan, Dycoxan) only treat certain stages of the parasite. These products are usually slightly cheaper, but calves may need to be dosed twice. Alternatively, decoquinate can be used as an in-feed medication. Decoquinate must be fed continuously for as long as calves are at risk as it only stops the initial phase of the coccidia life cycle. Calves may succumb to coccidiosis once they stop receiving the medicated feed. Lick buckets containing decoquinate are not recommended as not all animals will consume the required amount to be effective.