Category: FARM

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.

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.

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.

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!

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%.

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.