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Controlling lameness for a more productive flock

Controlling lameness for a more productive flock

It is estimated that the UK flock contains over 3 million lame sheep. Staggeringly over 60% of the total amount of antibiotic used in flocks is used to treat lameness. Footrot and Contagious Ovine Digital Dermatitis (CODD) are two important highly infectious causes of lameness. Each flock should have a control strategy in place with the aim of reducing the number of new cases to improve flock welfare and efficiency. Control plans should centre on improving under-foot hygiene, culling chronic cases, improving biosecurity, ensuring prompt treatment, and using the footrot vaccine.

Footrot is the most common cause of lameness in sheep. Damaged interdigital skin, poor claw hygiene, and moist environmental conditions promote the spread and development of infection. Chronic cases can lead to overgrown and permanently misshapen hooves. Treatment has the best results when initiated early. Affected sheep should be isolated from the rest of the flock and treated with long-acting amoxicillin and Metacam.

CODD is caused by spirochaete bacteria (same family as digital dermatitis in cattle). CODD lesions start at the coronary band and progress down the hoof wall towards the toe. The hoof capsule eventually comes away to expose the sensitive underlying tissues. Affected sheep should be isolated and treated promptly.

Purchased sheep should be quarantined and have their feet examined carefully as around 30% of infected sheep show no signs of lameness. A randomised controlled trial found that a single dose of long-acting amoxicillin resulted in a 71% cure rate. Some cases may require a second treatment 3 days later. Tulathromycin (Draxxin) and tilmicosin (Micotil – vet-only) may be used in refractory cases.

Footrot bacteria have been isolated in 71% of CODD lesions and sheep with footrot are 3.8 times more likely to develop CODD. Therefore, controlling footrot is an important aspect of controlling CODD. In addition to significantly reducing the impact of footrot, the Footvax vaccine was found to reduce the number of CODD cases by 32%. Annual Footvax vaccination may provide sufficient control in most flocks. An additional booster may be given 4 weeks prior to risk periods (e.g. housing for lambing). The vaccine can also be used in the face of an outbreak.

Parasite management at housing time

Parasite management at housing time

At this time of year parasites take on a dormant state and “overwinter” within the stomach lining. It is important to remove this inhibited stage of the parasite because if left they can cause significant damage and disease when they emerge en masse in spring. Affected animals develop rapid clinical signs of weight loss, scour and dehydration, which may be fatal.

Parasites which survive over winter in the stomach lining will contribute to larval pasture burdens when they emerge the following spring.

 

1st and 2nd season grazed youngstock

This age group are most susceptible to gut and lung worms as cattle have not had time to develop a protective immune response until after their 2nd grazing season. Treat all youngstock at housing with a Group 3-ML (clear drench/injection/pour-on – ivermectin e.g. Enovex) that will remove all inhibited larvae. Avoid Group 1-BZ (white drenches – albendazole, fenbendazole) and Group 2-LV (yellow drenches – Levamisole) products are these will not remove all inhibited larval stages

The winter housing period will soon be upon us, which means that many of you will now be planning to treat your animals for gut parasites. Purchasing worm and fluke products can be a bit of a minefield, but this guide aims to help you choose the most appropriate product for your stock. The aim being to effectively remove parasites whilst minimising the likelihood of selection for resistance.

Purchased 1st lactation dairy/ 1st lactation beef cattle

The immune status of these animals is unknown with respect to lungworm. It is worth paying particular attention to this group of animals and treating them if they are coughing or under conditioned. Dairy cattle can be treated with an eprinomectin product (e.g. Eprizero -zero milk withdrawal). A Group 3-ML (e.g. Enovex) would be a good choice in beef cattle.

Adult dairy/beef cattle

Adult cattle should not require any treatment for gut worms as they will have built up protective immunity. However, it may be beneficial to perform faecal egg counts in any animals in poor condition so that they can be treated if necessary.

All age groups

Cattle (and sheep) are unable to develop a protective immune response to fluke infection. Therefore fluke control should encompass all ages of cattle. A bulk milk test can be used to monitor the infection level in milking herds and faecal tests can be used to test individual or small groups of animals.

In contrast to sheep, cattle typically only suffer from the chronic form of fluke infection. After a dry summer like we have just had, even if autumn is wet, cattle will only be harbouring immature flukes at the time of housing. Therefore, it is best to wait at least 10 weeks before treating with a product which targets adult fluke (e.g. Distocur). A nice job to look forward to at Christmas time!

 

Products containing Oxyclozanide (e.g. Distocur) or albendazole (e.g. Tramazole) may be used in milking herds (usually at dry-off) as they have a short milk withhold (Oxyclozanide = 108hrs and albendazole = 60hrs). Resistance to triclabendazole is becoming more widespread. Whenever possible we should avoid the use of triclabendazole products in cattle as this drug targets immature fluke which are more significant in sheep.

Combination products

Combination products are more costly as you are paying for the “convenience” of a 2-in-1 product. However, it is often the case that the two drugs which are combined should not ideally be given together at housing.

For example, if you used a product containing ivermectin and closantel at housing, you will remove all worms, but very few fluke as closantel will only kill fluke that were ingested over 7 weeks ago. Therefore, another fluke treatment would be needed later on. If you waited until the cattle had been housed for at least 7 weeks before dosing they will have carried their worm burden for an extra 7 weeks+. Adult cattle do not need treating with combination products as their worm burden will be low and does not require treatment. So overall, combination products are a more costly option and may increase the risk of resistance to these drugs.

 

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

Parasite management at housing time

At this time of year parasites take on a dormant state and “overwinter” within the stomach lining. It is important to remove this inhibited stage of the parasite because if left they can cause significant damage and disease when they emerge en masse in spring. Affected animals develop rapid clinical signs of weight loss, scour and dehydration, which may be fatal.

Parasites which survive over winter in the stomach lining will contribute to larval pasture burdens when they emerge the following spring.

 

1st and 2nd season grazed youngstock

This age group are most susceptible to gut and lung worms as cattle have not had time to develop a protective immune response until after their 2nd grazing season. Treat all youngstock at housing with a Group 3-ML (clear drench/injection/pour-on – ivermectin e.g. Enovex) that will remove all inhibited larvae. Avoid Group 1-BZ (white drenches – albendazole, fenbendazole) and Group 2-LV (yellow drenches – Levamisole) products are these will not remove all inhibited larval stages

The winter housing period will soon be upon us, which means that many of you will now be planning to treat your animals for gut parasites. Purchasing worm and fluke products can be a bit of a minefield, but this guide aims to help you choose the most appropriate product for your stock. The aim being to effectively remove parasites whilst minimising the likelihood of selection for resistance.

Purchased 1st lactation dairy/ 1st lactation beef cattle

The immune status of these animals is unknown with respect to lungworm. It is worth paying particular attention to this group of animals and treating them if they are coughing or under conditioned. Dairy cattle can be treated with an eprinomectin product (e.g. Eprizero -zero milk withdrawal). A Group 3-ML (e.g. Enovex) would be a good choice in beef cattle.

Adult dairy/beef cattle

Adult cattle should not require any treatment for gut worms as they will have built up protective immunity. However, it may be beneficial to perform faecal egg counts in any animals in poor condition so that they can be treated if necessary.

All age groups

Cattle (and sheep) are unable to develop a protective immune response to fluke infection. Therefore fluke control should encompass all ages of cattle. A bulk milk test can be used to monitor the infection level in milking herds and faecal tests can be used to test individual or small groups of animals.

In contrast to sheep, cattle typically only suffer from the chronic form of fluke infection. After a dry summer like we have just had, even if autumn is wet, cattle will only be harbouring immature flukes at the time of housing. Therefore, it is best to wait at least 10 weeks before treating with a product which targets adult fluke (e.g. Distocur). A nice job to look forward to at Christmas time!

 

Products containing Oxyclozanide (e.g. Distocur) or albendazole (e.g. Tramazole) may be used in milking herds (usually at dry-off) as they have a short milk withhold (Oxyclozanide = 108hrs and albendazole = 60hrs). Resistance to triclabendazole is becoming more widespread. Whenever possible we should avoid the use of triclabendazole products in cattle as this drug targets immature fluke which are more significant in sheep.

Combination products

Combination products are more costly as you are paying for the “convenience” of a 2-in-1 product. However, it is often the case that the two drugs which are combined should not ideally be given together at housing.

For example, if you used a product containing ivermectin and closantel at housing, you will remove all worms, but very few fluke as closantel will only kill fluke that were ingested over 7 weeks ago. Therefore, another fluke treatment would be needed later on. If you waited until the cattle had been housed for at least 7 weeks before dosing they will have carried their worm burden for an extra 7 weeks+. Adult cattle do not need treating with combination products as their worm burden will be low and does not require treatment. So overall, combination products are a more costly option and may increase the risk of resistance to these drugs.

 

Are your tup’s up to the job?

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

  1. 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.
  2. Toes – Check for any signs of lameness, infectious disease, or arthritis. Assess his locomotion.
  3. Tone – Assess his body condition score. Aim for 3.5-4.
  4. Testicles – Measure scrotal size, check firmness and feel for any lumps.
  5. 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.

Heat Stress in Cattle

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!

Endometritis

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

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.

Garden plants poisonous to livestock

Livestock may eat toxic plant species when they are dried in forages such as hay. So even if you think your livestock can’t access garden plants it’s still important to be aware of which ones are poisonous. Here are a few of the most common toxic garden plants.

Yew

Yew is commonly found in church yards and even small amounts are fatal. It contains highly toxic alkaloids which affect the heart, causing an irregular heartbeat and rapid death. Yew clippings must be disposed of appropriately and good fencing should prevent cattle from entering church yards and gardens.

Rhododendron

Rhododendrons contain a poison (Grayanotoxin) that slows the heart rate and lowers blood pressure. Affected livestock are weak, often recumbent, bloated and may vomit, which is unusual for ruminants. Goats in particular my exhibit dramatic projectile vomiting with rhododendron poisoning. Animals show signs of abdominal pain such as groaning and teeth-grinding. Death may be rapid. As a prevention, ensure stock have access to adequate silage or hay at these times to reduce the likelihood of livestock browsing. Pastures bordering woodland should be inspected for rhododendron and fenced accordingly. Ensure clippings are disposed of appropriately.

Pieris

Ornamental garden shrub. Most commonly nibbled over a garden fence or ingested when hungry animals break into a garden. This plant contains the same toxin as the Rhododendron (Grayanotoxin) and produces similar gastro-intestinal signs and is often fatal.

Laurel

Laurel contains cyanide, one of the most rapidly acting toxins affecting cattle. Cyanide prevents haemoglobin in red blood cells from releasing oxygen, effectively starving the tissues of oxygen. Affected animals initially show excitement, increased breathing and heart rate, and increased salivation. The mucous membranes are bright red, eventually turning blue. Muscle spasm, coma and death follow. Laurel should not be planted where animals can reach.

Wild plants poisonous to livestock

During the grazing months it’s important to look out for cases of plant toxicity. Many poisonous plants are bitter and unpalatable while they are growing and will not be eaten by livestock under normal circumstances. However, if grazing is scarce, such as after a period of dry weather, or when pastures are overstocked it can be more likely. Here are a few of the most common wild toxic plants to look out for.

Ragwort

Ragwort poisoning is seen less commonly, as pasture management usually prevents this plant colonising grazing land. Poisoning can occur from ingestion of the live plant or from conserved forages containing Ragwort. Clinical signs of ragwort poisoning include depression, chronic weight loss, diarrhoea, jaundice and accumulation of fluid under the jaw and brisket caused by liver disease. Sheep are much less susceptible to ragwort than cattle. There is no effective treatment once the liver damage has occurred.

Bracken

Bracken poisoning often occurs when alternative forage is in short supply and animals have little else to eat, additionally some animals develop a taste for the young shoots in the spring. Bracken poisoning requires long-term exposure, over weeks to years. The outcome of ingestion is related to the time period and the quantity ingested. Haematuria (blood in the urine) primarily affects cattle (less commonly sheep) and is often accompanied by anaemia. The toxins cause bone marrow suppression and depletion of white blood cells resulting in immunosuppression. Affected cattle may be weak, exhibit rapid weight loss, high temperature (40°C+), pale mucous membranes, spontaneous bleeding or prolonged bleeding from minor wounds, and blood clots in the faeces. Affected sheep may be blind.

Lower doses of bracken fern ingested over several years are more likely to be carcinogenic and may result in bladder tumours. Poisonings are prevented by not allowing access to bracken, particularly in spring when the young more palatable fronds are emerging. Alternatively, ensure animals have adequate nutrition at all times, so they are not forced to eat bracken as an alternative.

Oak (Acorn)

Acorns contain tannins which cause serious, often fatal, kidney damage. Mass ingestion of acorns may occur following stormy weather. Rumen microbes break down the tannins, producing gallic acid, which causes damage to kidney cells. Animals may show abdominal pain and bloat due to ruminal stasis. They are anorexic, depressed and often recumbent. Constipation may be followed by foetid tarry diarrhoea. Death may occur within hours to several days depending on the number of acorns eaten. It is prudent to fence off oak trees on grazing pastures.

Hemlock water-dropwart

Cattle are particularly at risk of hemlock poisoning after ditches have been cleared out, exposing the most toxic part of the plant, the roots (“dead man’s fingers”). Animals show signs of salivation, dilated pupils, difficulty breathing, collapse and spasmodic convulsions. The majority of affected cattle die.