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Information For Farmers

Subclinical Mastitis in Cows

The most important economic loss from mastitis is subclinical mastitis, for every clinical case of mastitis in a dairy herd there can be 25 or more subclinical cases. These subclinical cases are the main cause of increased cell counts:

Mastitis Risk Factors - Five Point Plan

The main risk factors for mastitis are shown below:

The Five Point Plan

The five point plan was established by the Milk Marketing Board in the 1950’s in order to counteract the mastitis risk factors – the points are still valid today:

  • Hygiene: i.e. improving operator hygiene during milking such as the wearing of gloves and using disposable teat wipes.

  • The correct maintenance of milking machine equipment.
  • Post-milking teat disinfection.
  • The prompt identification of clinical cases, veterinary treatment and the culling of chronic recurrent cases.
  • Dry Cow Therapy.

Diagnosis of Mastitis in Cows

Early identification of all cases of clinical mastitis is a key weapon in preventing further outbreaks of mastitis and is a key part of the overall mastitis control programme, ensuring maximum herd health, milk quality and dairy farm profitability.

The organisms that cause mastitis in dairy cows are divided into 2 main groups; contagious and environmental mastitis. There is some degree of interplay between these two types, for example strep uberis is primarily an environmental organism that can become ‘cow adapted’ and change into a contagious organism.

Each type of mastitis may present in an entirely different way. For example as infection with Staphylococcus aureus progresses through a herd the incidence of clinical mastitis may be quite low but the herd cell count continues to rise.
Streptococcus uberis may present with a high level of clinical cases and fluctuating bactoscans and herd somatic cell counts. Once ‘cow adapted’ strains of Strep uberis develop the herd cell count will increase rapidly due to the contagious transfer of infection.

Each farm has its own mastitis profile and the first task when investigating a problem is to establish the main organisms involved.

This can be assessed in two ways:

  1. Take a bulk milk sample under strict conditions and submit it for specialist examination.
  2. Take samples from each case of mastitis and store them in the freezer. These can then be analysed at a later date for the causative organisms.

Fertility

On-farm conception rates in the UK have been declining at a rate of 1% per year over the last 20 years. There are many reasons given for this decline and many different views expressed. The high yielding Holstein cow seems to have suffered the most from a drop in fertility performance.

One factor without doubt is that the steady increase in milk yields has seen a similar decrease in fertility performance. This is probably not surprising given the energy demands on a high yielding Holstein cow.

So are we wasting our time in trying to improve fertility performance? The answer is no but the solution requires a large investment in the environment, nutrition and management of the modern dairy cow.

Three Rivers Veterinary Group use a fertility control program and a 100 day contract scheme to improve fertility performance.

The main factors which must be brought together to improve fertility are:

1. Nutrition

This covers the areas of ration formulation, mineral supplementation, correct transition diets and correct mixing and delivery of the ration to the cow.

2. Environment and Housing

This subject covers the areas of good comfortable housing, with yards or modern cubicles which allow good levels of cow comfort. Wide, well lit passageways and good flooring help to reduce injuries and lameness.

3. Breeding

There is thought to be a genetic relationship between yield and fertility and that genetic selection for yield has partly contributed to this decline in fertility. Whether or not this is the case selection for longevity is now seen as being more important than yield.

4. Good Quality Records

This is essential to fertility performance. On farm records may be manual or computerised; this does not matter provided they are accurate and easy to use.

5. Good Heat Detection

This is probably the area where many farms struggle to get the best performance. The modern Holstein may only show oestrus activity for 6 hours and she may only ride other cows a few times during this period. On dairy farms the rise in cow numbers has been accompanied by a reduction in staffing levels. This has resulted in a requirement for heat detection aids such as Kamars, chalk, paint, pedometers, HeatTime etc. all with varying degrees of success.

6. Reliable Insemination of Cows

If DIY AI is used then it is essential that the semen straws are stored correctly and that a good technique is used for thawing and delivering the semen. Generally good quality DIY AI is superior to the use of outside AI where cows can only be served once a day. Three Rivers Veterinary Group can provide refresher AI courses on an individual basis; please contact us for details.

7. A Reliable Veterinary Fertility Control Program

Three Rivers Veterinary Group operate a Fertility Control program which is designed to ensure that all cows are prepared correctly for the start of the service period and that any non-cycling or non-pregnant cows are picked up as quickly as possible. Monitoring of herd performance using herd records, metabolic profiles and bulk milk quality results in conjunction with Interherd and Herd Companion ensures a quick response to any problems that arise.

8. 100 Day Contract

The 100 day contract is a revolutionary dairy management program to optimize early pregnancies.

Norfolk & Suffolk BVD Eradication Campaign

Mike Bardsley is a member of the steering commitee for this exciting project. The project was started by The members of the Norfolk and Suffolk Holstein Club because of their concern regarding the severe economic impact of this disease.

East Anglia has traditionally had a lower number of infected farms (c 75%) than the national average (c 95%0).

Our aim is to eradicate BVD virus from our region, it does not matter if you currently vaccinate, you can still join. Previous BVD-free schemes have not been able to allow vaccination. However our main priority is to eliminate the virus from the region and if farmers have to vaccinate for biosecurity reasons this is quite OK.

Our first target is to reach 100 farms in the region which are free of BVD virus.

BVD virus is carried by persistently infected cattle (PI’s) and these animals eventually die from Mucosal Disease or secondary infections. BVD cannot survive without these PI’s as a source of infection, therefore by tracking these animals down and removing them from the herd them we will remove the threat of this diseae.

The testing is done by SAC and is subsidised by funding from EBLEX and Holstein UK. For dairy farmers an initial screen involves a bulk milk test plus 5 blood samples from each separately managed group of 9 – 18 month old heifers.

New tests have allowed us to detect virus in bulk milk samples from up to 300 cows. In addition we are now able to screen calves for infection at 1 month of age rather than waiting until they are 9 months or older.

We are very fortunate to have Professor Joe Brownlie from the Royal Vet College, London to design and oversee this project. Prof Brownlie was instrumental in making the discoveries that have led to our understanding the mechanism of infection

Many farmers don’t realise their herds are infected with BVD, Conversely many farmers do not know if their herd is naive. Those farmers that are not infected may be at significant risk of becoming so with potentially disastrous consequences.

The main risk factors for aquiring BVD infection are:

  • Hiring of bulls.
  • Purchasing Cattle.
  • Contact with sheep.
  • Contact with neighboring stock - escaped animals or over the fence.

Interherd

Interherd is a flexible and detailed computer program that is able to analyse your milk records be they from NMR of CIS.
These records are downloadable on the Internet with your permission from NMR or CIS.

As a result of this analysis we can quickly see if there are any underlying problems regarding the performance of your herd with regard to:

  • Fertility
  • Mastitis
  • Somatic cell counts
  • Milk quality
  • Health parameters

The analysis allows us to act quickly and put in place measures to improve the situation.

In addition farmers are able to purchase their own Interherd program for the storage and analysis of all mastitis, health, fertility, movement and medicine records. The farmers Interherd program can be directly linked to their veterinary surgeons Interherd program. This will allow the production of action lists for your vet visits.

Bluetongue in Cows

In the autumn of 2006 Bluetongue (serotype 8) was found in the Netherlands, Belgium, Luxemburg, Western Germany and in parts of North Eastern France. The outbreak was identified as a new incursion in the EU. How Bluetongue entered Europe is still subject to investigation.

In August 2008 the first case of Bluetongue serotype 8 was diagnosed in East Anglia in a cow.

Bluetongue was first described in South Africa but has since been recognised in most countries in the tropics and sub-tropics. Since 1999 there have been widespread outbreaks of Bluetongue in Greece, Italy, Corsica (France) and the Balearic Islands (Spain). Cases also occurred in Europe in Bulgaria, Croatia, Macedonia, Kosovo and Yugoslavia. Serotypes 8, 1, 2, 4, 9 and 16 have been involved. These cases have been well north and west of its normal distribution. It appears that the virus has spread from both Turkey and North Africa. Bluetongue does not affect humans. A virus within the Orbivirus genus of the family Reorvirades causes bluetongue. At present 24 distinct serotypes have been identified as a result of serum neutralisation tests.

The virus is transmitted by a small number of species of biting midges of the genus Culicoides. Bluetongue virus cannot naturally be transmitted directly between animals. Virus transmission between animals occurs via the midges. However mechanical transmission of the virus between herds/flocks and within a herd/flock by unhygienic practices (e.g. use of contaminated hypodermic needles) is possible.

When a midge bites an infected animal, the virus passes to the midge in the blood meal and the virus multiples in the midge. The cycle of replication of the virus in the insect vector and in the ruminant host, results in amplification of the amount of virus available to naïve hosts and vectors. Peak populations of vector Culicoides occur in the late summer and autumn and therefore this is the time when Bluetongue is most commonly seen.

Clinical signs can vary by species – although symptoms are generally more severe in sheep, cattle are important in epidemiology of the bluetongue as they act as an often silent source of BTV – a reservoir for disease and keep the infection circulating.

There is a wide variation in the clinical signs seen in cattle

The initial signs in lactating cows are that the animal becomes slower and stiff with a reduced appetite and a fall in milk yield. There is usually a nasal discharge, clear at first with the mucosa inside the nostril noticeably redder than usual; this is accompanied by red eyes due to the inflammation of the conjunctivae. Over the following days erosions and crusting develop around the entrance to the nose; there may be crusty scabs on the teats. There may be some foamy saliva around the mouth. On opening the mouth there are erosive lesions on the upper gum (dental pad) which develop a yellowy skin of necrotic tissue over them, there may also be lesions on the hard palate and tongue. It is important to note that these are erosive lesions not vesicles as in Foot and Mouth! The lameness is due to a coronitis (i.e. inflammation of the coronary band which runs around the top of the hoof); if the foot is washed and cleaned the coronary band can be seen to be red and inflamed. Sometimes the leg above the coronary band may become secondarily infected and swell up.

There are problems with transplacental infection; pregnant cattle infected with Bluetongue will pass the infection on to their calf in utero. The calf may be aborted, die in the first few days of life or recover. It is believed that colostrum from recovered cows is valuable in helping weak calves to recover. These calves, their placentas and fluids will also act as a focus of infection on the farm, allowing the disease to flare up again in unvaccinated animals. The dams that have carried infected foetuses are likely to have lower milk production and fertility in their next lactation, reinforcing the point that prevention is the key in controlling this disease. If the disease spreads to a herd with a large number of pregnant animals the effects will be much more severe.

Bluetongue UK Situation 2011

On 12th June 2010, Scotland, England and Wales moved into a Lower Risk Protection Zone (LRZ) for BTV-8.

This LRZ provides some increased protection against imports from higher risk zones and is being viewed as the first move towards disease freedom.

There were no outbreaks of BTV in the UK in 2010 and no evidence of bluetongue virus circulation in the winter of 2009. Further testing was to be carried out in 2010 but the results have not yet been reported.

Between April and October 2010, new outbreaks of BTV were reported in Greece, Cyprus, Italy, Portugal and Spain.

In the UK We must not be complacent. We need to continue to take steps to keep disease out, so that we maintain a good chance of becoming free and removing our BTV zones and trade restrictions.
Vaccination played a key role in keeping us free from circulating bluetongue disease in 2008 – 2010 and will provide the greatest security against loss, should there be a resurgence of disease in 2011.

Vaccination before the start of the risk period or when the midges and disease become active is still being recommended by NFU and DEFRA.. For those who vaccinated last year, a reminder that only a single vaccination booster is required in both cattle and sheep.

It is vital that we continue to remain vigilant for signs of disease. Suspicion of disease must be notified immediately to your local DEFRA Animal Health Office.

Bovine Respiratory Disease (BRD) Pneumonia

The total UK calf population is 3.3 million and of these 30% get pneumonia (1million) each year; mortality varies from 3-50% (average ~5% or 157,000 calves a year).

Economic studies highlight the cost to national herd estimated of approximately £80 million; there are welfare costs too.

Three Rivers Veterinary Group pneumonia control program:

  • Reducing the risk of disease by quality advice regarding housing and environment solutions.
  • Good biosecurity and health planning.
  • Advice re vaccination programs.
  • Reduction of the necessity for on farm treatment
  • Reduction in antibiotic usage.
  • Achieving high quality farm assurance standards.

Environmental factors involved in calf pneumonia:

  • Poor ventilation
  • High humidity
  • Stress
  • Mixing age groups
  • Handling
  • Housing
  • Transport

The 'calf factors' in pneumonia incidence are:

  • Poor colostral intake
  • Nutritional status
  • Concurrent disease
  • Lung capacity

The viruses involved are:

  • Para-influenza 3 (PI)
  • Respiratory Syncytial virus (RSV)
  • Infectious Rhinotracheitis (IBR)
  • Bovine Viral Diarrhoea Virus (BVDV)

The bacteria involved are:

  • Pasturella multocida
  • Histophilus somnus
  • Mycoplasma Bovis

How do all these factors work together?

What are the common housing problems?

  • Lack of high level outlet for waste air.
  • Inadequate inlet areas for fresh air.
  • Shared airspace with older animals (who may carry the disease).
  • Low heat production from calves at low stocking levels.
  • High moisture levels (humidity above 70% is at a critical level for calves).
  • Poor design or location of mechanical ventilation.

Good ventilation is vital for the following reasons:

  • Removal of excess water vapour.
  • Removal of excess heat.
  • Removal of micro-organisms, dust and gases.
  • Provision of uniform distribution of air.
  • Provision of correct air speed for stock.

Lameness in Dairy Cows

After infertility and mastitis, lameness is the third most common reason for culling cows on dairy farms.  In the average dairy herd 38 out of every 100 cows is affected by lameness per year, some cows being affected more than once.  90% of lameness cases involve the feet and 90% of these involve the rear feet, the majority affect the outside claw. Lameness prevention is much better than treatment from both an animal welfare and an economic point of view. Locomotion scoring can be used to asses the progress of a lameness action plan, which is likely to include regular foot bathing and foot trimming.

This costs the average 100-cow dairy herd almost £4,595 per year (i.e. approximately 1pence per litre of milk produced) these losses are a result of:

  • Reduced milk yield
  • Increased calving interval
  • Increased inseminations per pregnancy
  • Increased culling rate
  • Cost of treatments, inc. herdsman’s time

Types of lameness:

  • Digital dermatitis.
  • Laminitis.
  • Sole ulcer.
  • White line disease.
  • Slurry heel erosion.
  • Foul of the foot.
  • Toe necrosis.
  • Horizontal vertical wall fissures.
  • Hock lesions.
  • Trauma, injury and foreign body penetration of the sole.

Johne's Disease

Johne’s Disease is most commonly thought of as a cattle disease; however it can have a significant impact in sheep flocks as well. The main clinical sign is chronic progressive weight loss rather than the pipe-stem diarrhoea seen in cattle.

As many other diseases, such as poor dentition, chronic liver fluke, Jaagsiekte and Maedi are characterised by chronic weight loss, Johne’s cannot be diagnosed on clinical signs alone. A diagnosis of Johne’s is generally only made as the result of investigation into ill-thrift, and, because ill-thrift is not routinely investigated, Johne’s disease is almost certainly under diagnosed in sheep.

Despite this under diagnosis, most National Animal Disease Information Service (NADIS) monthly reports contain a reference to Johne’s in sheep, with most of these reports coming from flocks in the south-east of Scotland.

In the NADIS database 2.7% of flocks have recorded cases of Johne’s. Taking the under diagnosis into account, this suggests that the level of disease in the UK flock is likely to be as high as, if not higher than, the level of 5% recorded in New Zealand where investigation of ill-thrift is more common.

The NADIS data show a clear difference between lowland and upland flocks in the rate of diagnosis, with none of the lowland flocks in the NADIS database having recorded Johne’s disease, whereas the rate in the upland and hill flocks is 4% of farms. So take care when buying in stock that you don’t introduce it into your flock.

Sheep Scab

Sheep scab is a skin disease of sheep caused by a mite called Psoroptes ovis. It is present in several sheep producing countries, including the UK. It causes severe itching in affected sheep if left untreated. Scaly lesions develop on the woolly parts of the body and sheep often bite themselves and rub against objects to relieve the irritation causing loss of wool. Untreated sheep may lose weight.

Maedi Visna

Maedi Visna (Caprine Arthritis Encephalitis)

Maedi Visna (MV) is a disease of sheep present in most sheep producing countries, including GB. It is caused by a lentivirus. A closely related virus, Caprine Arthritis Encephalitis CAE), causes a similar disease in goats. The name of the disease is formed by the two Icelandic words that describe the clinical signs it produces – maedi (‘laboured breathing’ affecting the lungs) and visna (‘shrinking’ or ‘wasting’ affecting the central nervous system). The virus can infect sheep at any age, but signs of the disease are not usually seen until at least 3 years of age. These may include pneumonia, weight loss, joint problems, mastitis and nervous signs. In goats the main clinical sign of CAE is lameness. Weight loss and shrinkage of the udder may also be present. The nervous form of the disease occurs rarely and generally only in young kids. The disease spreads easily between sheep and can cause high economic losses. A MV/CAE accreditation scheme is run by the Scottish Agricultural College.

Urinary Calculi

A hard mass of mineral salts in the urinary tract caused by dietary imbalance; seen in male animals it causes blockage of the penis and subsequent death due to renal failure if not treated. The disease is most common in castrated males on a high cereal diet. The signs are restlessness, straining to urinate, pawing the ground, constantly looking at its own abdomen, vocal signs of pain.

Treatment involves surgery to remove the blocked penis and create a new opening for the urethra which is the tube that carries urine from the bladder to the outside.

Tetanus

Infection of wounds by the bacterium Clostridium tetani results in tetanus. A general increase in muscle stiffness is seen, causing a rigid, unsteady gait. The goat develops bloat and has an anxious look. The symptoms get progressively worse and convulsions may occur. The goat dies because it is unable to eat or breathe.

Vaccination with Lambivac will prevent the disease; an initial course of two injections is required followed by 6 monthly boosters.

Enterotoxaemia

Clostridium perfringens type D bacteria produce the toxins responsible for enterotoxaemia. The condition results in rapid death from a bowel infection with death often coming before the goat shows signs of diarrhoea. The common signs are sudden loss of appetite, depression and a drunken appearance. A high temperature and diarrhoea may be seen; the animal becomes recumbent and rapidly deteriorates before death occurs.

Vaccination with Lambivac will prevent the disease; an initial course of two injections is required followed by 6 monthly boosters.

Cloudburst or Pseudopregnancy in Goats

This is a common condition in female goats. Female goats sometimes cycle, mate and display all the attributes of being pregnant, but in fact are not pregnant. In many cases they have not even been mated. The uterus fills with large amounts of fluid but no foetus or placenta develops. This condition has several names:

  • False pregnancy
  • Cloudburst pregnancy
  • Pseudopregnancy
  • Hydrometra

When a doe is treated for the condition or if it resolves itself a ‘cloudburst’ of liquid materials comes out of the doe’s body.

The precise causes of false pregnancy are not completely understood, however we can treat the condition effectively.

Caprine Arthritis Encephalitis (Maedi Visna)

Maedi Visna (MV) is a disease of sheep present in most sheep producing countries, including GB. It is caused by a lentivirus. A closely related virus, Caprine Arthritis Encephalitis CAE), causes a similar disease in goats. The name of the disease is formed by the two Icelandic words that describe the clinical signs it produces – maedi (‘laboured breathing’ affecting the lungs) and visna (‘shrinking’ or ‘wasting’ affecting the central nervous system). The virus can infect sheep at any age, but signs of the disease are not usually seen until at least 3 years of age. These may include pneumonia, weight loss, joint problems, mastitis and nervous signs. In goats the main clinical sign of CAE is lameness. Weight loss and shrinkage of the udder may also be present. The nervous form of the disease occurs rarely and generally only in young kids. The disease spreads easily between sheep and can cause high economic losses. A MV/CAE accreditation scheme is run by the Scottish Agricultural College.

common diseases

Coccidiosis

Coccidiosis is caused by a host specific species of Eimeria and it is a protozoon common in chickens and less often in turkeys it also occurs occasionally in geese, guineas, pigeons, pheasants, quail, and many other birds. It is usually seen in young birds under conditions of warmth and high humidity or conditions that lead to wet litter.

The infective oocysts are present in the litter having been deposited there by infected chickens. Oocysts are easily transported by blowing dust, boots, clothing, crates, vehicle wheels, other animals, and people.

Susceptible chickens ingest sporulated oocysts in feed, water, litter and become infected. If exposure is moderate, the chickens become immune to that species of coccidia. Outbreaks occur when susceptible chickens ingest massive numbers of oocysts.

Coccidia produce lesions by destruction of epithelial cells in which they develop and multiply and by trauma to the intestinal mucosa and submucosa.

The clinical signs vary with species of coccidia. Pathogenic species cause diarrhoea which may be mucoid or bloody, dehydration, ruffled feathers, anaemia, listlessness, weakness, retraction of the head and neck. In turkeys, the signs are the same except the diarrhoea isn’t bloody.

The prevention of Coccidiosis is usually by the incorporation of anticoccidials in the feed. A low level exposure allows immunity to develop. Various products are available for treatment.

Hexamitiasis

This is seen in 1-9 week old turkey poults. It is caused by a motile protozoon Hexamita meleagridis (Hexamita columbae in pigeons).

Recovered birds often are carriers and shed the parasite in their faeces which contaminate feed, water and range. Susceptible birds get the organism by ingestion.

Initially birds are very nervous and active. They shiver, crowd around any heat source and have subnormal temps. There is watery or foamy diarrhoea and the birds dehydrate rapidly. Later on the birds are depressed, stand with their heads retracted, feathers ruffled and wings drooping before going into coma, and dying.

Diagnosis is by post mortem.

Hygiene is the most important factor in the prevention of outbreaks. Various treatments are available.

Trichomoniasis

This occurs in pigeons and doves and raptors that feed on them and also in turkeys, chickens, and game birds. Outbreaks usually occur in warm weather.

The disease is caused by Trichomonas gallinae, a motile protozoon. Pigeons are carriers and contaminate surface water or water containers. Pigeons can transmit trichomonads to their young during feeding. Raptors expose themselves and their young by feeding them infected doves and pigeons.

The main clinical sign in pigeons, doves, and raptors is that they have trouble closing their mouth due to oral lesions. There is drooling and repeated swallowing movements with watery eyes in birds and lesions in the sinuses or periorbital area. In rare cases with penetrating cranial lesions may show CNS signs. Turkeys have a gaunt appearance with a hollowed area over the crop.

Histomoniasis (Blackhead)

This is caused by Histomonas meleagidis, a protozoon and it occurs most frequently in exposed, unmedicated turkeys, especially under 3 months; it also occurs in chickens. Young birds are more frequently and severely affected.

It is transmitted by the ingestion of fresh faeces containing the infected ova of Heterakis gallinarum that are within earthworms.

The clinical signs initially are listlessness, anorexia, drooping wings and yellow faeces the head may be cyanotic. In chickens there may be bloody faeces. In the later stages there is depression, drooping wings, eyes closed, head drawn close to the body, and emaciation. Mortality may be 100% in young turkeys.

Diagnosis is by post mortem. Prevention is by practising good hygiene and not mixing turkeys with other species of birds. Also it is important to de-worm regularly. There is no treatment available.

Mycoplasmosis

The clinical signs observed in birds with mycoplasmosis are red, swollen eyelids and conjunctival tissue with a clear ocular discharge. The condition can become more severe resulting in extreme swelling of the eyelid and conjunctiva, crust formation along the eyelid margins resulting in ulcerations on the cornea and purulent discharge and loss of sight. Inflammation of the sinuses may occur resulting in discharge flowing from the nares. The birds may also display wet, matted feathers on the face (especially around the eyes), fluffed body feathers, inactivity, weight loss, loss of appetite and death due to starvation, exposure or predation.

Domestic poultry display respiratory symptoms such as coughing, sneezing and nasal discharge. They are lethargic, stop feeding and undergo severe weight loss. In turkeys, the sinus under the eye becomes swollen.

A diagnosis can be made using blood samples and post mortem. There are a number of treatments available once a diagnosis has been made. The response to treatment often depends upon how early the disease was identified and treatment started.

Marek's Disease

This occurs in Chickens between 12 to 25 weeks of age; occasionally pheasants, quail, game fowl and turkeys can be infected. Marek’s disease is a type of avian cancer; tumours in nerves cause lameness and paralysis. Tumours can occur in the eyes and cause irregularly shaped pupils and blindness. Tumours of the liver, kidney, spleen, gonads, pancreas, proventriculus, lungs, muscles, and skin can cause incoordination; unthriftiness, weak laboured breathing, and enlarged feather follicles. In terminal stages, the birds are emaciated with pale, scaly combs and greenish diarrhoea.

Marek’s disease is very similar to Lymphoid Leucosis, but Marek’s usually occurs in chickens 12 to 25 weeks of age and Lymphoid Leucosis usually starts at 16 weeks of age. Transmission: The Marek’s virus is transmitted by air within the poultry house. It is in the feather dander, chicken house dust, faeces and saliva. Infected birds carry the virus in their blood for life and are a source of infection for susceptible birds. Treatment: none Prevention: Chicks can be vaccinated at the hatchery. While the vaccination prevents tumour formation, it does not prevent infection by the virus.

Common Game Bird Diseases

Coccidiosis

Coccidiosis is caused by a host specific species of Eimeria and it is a protozoon common in chickens and less often in turkeys it also occurs occasionally in geese, guineas, pigeons, pheasants, quail, and many other birds. It is usually seen in young birds under conditions of warmth and high humidity or conditions that lead to wet litter.

The infective oocysts are present in the litter having been deposited there by infected chickens. Oocysts are easily transported by blowing dust, boots, clothing, crates, vehicle wheels, other animals, and people.

Susceptible chickens ingest sporulated oocysts in feed, water, litter and become infected. If exposure is moderate, the chickens become immune to that species of coccidia. Outbreaks occur when susceptible chickens ingest massive numbers of oocysts.

Coccidia produce lesions by destruction of epithelial cells in which they develop and multiply and by trauma to the intestinal mucosa and submucosa.

The clinical signs vary with species of coccidia. Pathogenic species cause diarrhoea which may be mucoid or bloody, dehydration, ruffled feathers, anaemia, listlessness, weakness, retraction of the head and neck. In turkeys, the signs are the same except the diarrhoea isn’t bloody.

The prevention of Coccidiosis is usually by the incorporation of anticoccidials in the feed. A low level exposure allows immunity to develop. Various products are available for treatment.

Hexamitiasis

This is seen in 1-9 week old turkey poults. Also occurs in gamebirds, peafowl, ducks, and pigeons. It is caused by a motile protozoon Hexamita meleagridis (Hexamita columbae in pigeons).
Recovered birds often are carriers and shed the parasite in their faeces which contaminate feed, water and range. Susceptible birds get the organism by ingestion.

Initially birds are very nervous and active. They shiver, crowd around any heat source and have subnormal temps. There is watery or foamy diarrhoea and the birds dehydrate rapidly. Later on the birds are depressed, stand with their heads retracted, feathers ruffled and wings drooping before going into coma, and dying.

Diagnosis is by post mortem.

Hygiene is the most important factor in the prevention of outbreaks. Various treatments are available.

Trichomoniasis

This occurs in pigeons and doves and raptors that feed on them and also in turkeys, chickens, and game birds. Outbreaks usually occur in warm weather.

The disease is caused by Trichomonas gallinae, a motile protozoon. Pigeons are carriers and contaminate surface water or water containers. Pigeons can transmit trichomonads to their young during feeding. Raptors expose themselves and their young by feeding them infected doves and pigeons.

The main clinical sign in pigeons, doves, and raptors is that they have trouble closing their mouth due to oral lesions. There is drooling and repeated swallowing movements with watery eyes in birds and lesions in the sinuses or periorbital area. In rare cases with penetrating cranial lesions may show CNS signs. Turkeys have a gaunt appearance with a hollowed area over the crop.

In game birds Trichomonas is a normal inhabitant of the bird’s gut but when present in large numbers it can cause disease. Affected birds become depressed and pass yellow, frothy caecal droppings, disease is usually seen in birds under stress and the removal of stress together with treatment with re-hydration salts and possibly an antibiotic should be effective in reducing losses.

Histomoniasis (Blackhead)

This is caused by Histomonas meleagidis, a protozoon and it occurs most frequently in exposed, unmedicated turkeys, esp. under 3 mths. It also occurs in chickens and captive game birds. Young birds are more frequently and severely affected.

It is transmitted by the ingestion of fresh faeces containing the infected ova of Heterakis gallinarum that are within earthworms.

The clinical signs initially are listlessness, anorexia, drooping wings and yellow faeces the head may be cyanotic. In chickens there may be bloody faeces. In the later stages there is depression, drooping wings, eyes closed, head drawn close to the body, and emaciation. Mortality may be 100% in young turkeys.

Diagnosis is by post mortem. Pr3vention is by practising good hygiene and not mixing turkeys with other species of birds. Also it is important to de-worm regularly. There is no treatment available.

Gapes

Gapes is caused by the gapeworm Syngamus trachea. The adult worms live in the trachea (windpipe) of game birds, poultry and several other birds such as rooks, crows and starlings. The female and male are permanently attached to each other forming the typical Y shape.

The gapeworm eggs are coughed up, swallowed and passed out in the droppings. Game birds may be infected by eating the eggs, larvae, or by eating earthworms that have themselves eaten eggs or larvae. The larvae may remain infective in the earthworm for up to 5 years, thus release pen can build up a large reservoir of infection. When swallowed by the game bird the larvae migrate through the body or bloodstream to the trachea via the lungs.

Respiratory signs, such as coughing and snicking, are caused by irritation of the trachea by the worms. Death occurs by respiratory failure when worms block the airways. Partridges seem to be especially susceptible and mortality can be rapid and high.

Flubenvet is effective and can be added to the feed, either in proprietary feeds on prescription or by mixing food on site.

Prevention means rotating pens, hygiene of feeders and drinkers, discouraging wild birds from entering pens, avoiding high stocking densities and preventative medication.

Rotavirus

This virus causes an intestinal infection in birds up to 14 days of age will often produce a very watery, frothy scour. Affected birds will huddle to keep warm and deaths may occur.

The infection is easily transmitted by people moving about the site and viruses spread rapidly within a hut once introduced. Overcrowding of chicks, excess humidity and poor temperature control all contribute to making conditions more severe.

There is no specific treatment for viral infections but treating with re-hydration preparations and antibiotics to control secondary bacterial infection can cut down losses markedly.

Contagious Mastitis

The main contagious organisms are listed below:

  • Staphylococcus aureus
  • ‘Cow-adapted’ Streptococcus uberis
  • Coagulase negative staph (CNS)

Other organisms which are quite rare but cause serious outbreaks of contagious mastitis are:

  • Streptococcus agalactia
  • Mycoplasma
  • Control of contagious mastitis

Staphylococcus Aureus (S. aureus)

This bacterium is extremely difficult to control by treatment alone, because the response to antibiotic treatment is poor. Successful control is achieved by prevention of new infections and culling infected cows. S. aureus organisms colonize damaged teat ends or teat lesions. The infection is spread form cow to cow by a number of factors e.g. milkers’ hands, wash cloths, teat cup liners, and flies. The organisms probably penetrate the teat canal during milking. Irregular vacuum fluctuations impact milk droplets and bacteria against the teat end with sufficient force to cause teat canal penetration and possible development of new infection. Infected cows must either be culled, segregated from the milking herd and milked last or milked with separate milking units, or teat cup liners must be rinsed and sanitized after milking infected cows. The development of automatic dipping and flushing through the cluster has the potential to revolutionise the control of S. aureus mastitis.

Staphylococcus aureus causes chronic mastitis, often it is subclinical, where there is neither abnormal milk nor detectable change in the udder, but somatic cell count has increased. Some cows may flare-up with clinical mastitis, especially after calving. The bacteria persist in mammary glands, teat canals, and teat lesions of infected cows and are considered contagious. The infection is spread at milking time, when S. aureus contaminated milk from infected cows comes into contact with teats of uninfected cows, and the bacteria penetrate the teat canal. Once established, S. aureus often does not respond to antibiotic treatment, and infected cows eventually must be segregated or culled from the herd. Eradication of S. aureus, has proved to be almost impossible; however control is possible by practicing the highest level of hygiene and milking techniques.

Cows infected with S.aureus do not necessarily have high SCCs. Only 60% of infections are found in cows producing milk with more than 200,000 SCC. In several research trials, 3-8% of first lactation cows were found infected with S. aureus at calving. Many remain infected throughout the first lactation and are reservoirs for infecting other cows in the herd. Although as many as half of the cows with high SCC may be infected with S. aureus, somatic cell counts alone are not sensitive enough to positively diagnose S. aureus infections.

Streptococcus Uberis. (Strep Uberis)

Strepuberis mastitis is probably the most important organism with regard to mastitis in the modern dairy cow. It is an environmental organism (Control of environmental mastitis) that lives in faeces, the rumen and in all areas where there is cow contact. Whilst it is an easy organism to kill in a petri dish it is very difficult to eradicate from an infected udder. The organism may progress from being an environmental cause of infection to a contagious cause by becoming cow-adapted (Control of contagious mastitis). In other words the organism lives in the udder and transmits to other cows during the milking process in the same way as S.aureus. Large clinical outbreaks of strep uberis can result in high and fluctuating bactoscans as well as raised herd SCC.

Treatment of Strep uberis mastitis must be aggressive and targeted with specific treatment protocols. If treatment is not aggressive then there is more likelihood of cow-adapted infections developing. This is why many farms fail in their attempts to control and treat strep uberis mastitis.

coagulase negative staph (CNS)

Coccidiosis

Coccidiosis is caused by a host specific species of Eimeria and it is a protozoon common in chickens and less often in turkeys it also occurs occasionally in geese, guineas, pigeons, pheasants, quail, and many other birds. It is usually seen in young birds under conditions of warmth and high humidity or conditions that lead to wet litter.

The infective oocysts are present in the litter having been deposited there by infected chickens. Oocysts are easily transported by blowing dust, boots, clothing, crates, vehicle wheels, other animals, and people.

Susceptible chickens ingest sporulated oocysts in feed, water, litter and become infected. If exposure is moderate, the chickens become immune to that species of coccidia. Outbreaks occur when susceptible chickens ingest massive numbers of oocysts.

Coccidia produce lesions by destruction of epithelial cells in which they develop and multiply and by trauma to the intestinal mucosa and submucosa.

The clinical signs vary with species of coccidia. Pathogenic species cause diarrhoea which may be mucoid or bloody, dehydration, ruffled feathers, anaemia, listlessness, weakness, retraction of the head and neck. In turkeys, the signs are the same except the diarrhoea isn’t bloody.

The prevention of Coccidiosis is usually by the incorporation of anticoccidials in the feed. A low level exposure allows immunity to develop. Various products are available for treatment.

Hexamitiasis

This is seen in 1-9 week old turkey poults. It is caused by a motile protozoon Hexamita meleagridis (Hexamita columbae in pigeons).

Recovered birds often are carriers and shed the parasite in their faeces which contaminate feed, water and range. Susceptible birds get the organism by ingestion.

Initially birds are very nervous and active. They shiver, crowd around any heat source and have subnormal temps. There is watery or foamy diarrhoea and the birds dehydrate rapidly. Later on the birds are depressed, stand with their heads retracted, feathers ruffled and wings drooping before going into coma, and dying.

Diagnosis is by post mortem.

Hygiene is the most important factor in the prevention of outbreaks. Various treatments are available.

Trichomoniasis

This occurs in pigeons and doves and raptors that feed on them and also in turkeys, chickens, and game birds. Outbreaks usually occur in warm weather.

The disease is caused by Trichomonas gallinae, a motile protozoon. Pigeons are carriers and contaminate surface water or water containers. Pigeons can transmit trichomonads to their young during feeding. Raptors expose themselves and their young by feeding them infected doves and pigeons.

The main clinical sign in pigeons, doves, and raptors is that they have trouble closing their mouth due to oral lesions. There is drooling and repeated swallowing movements with watery eyes in birds and lesions in the sinuses or periorbital area. In rare cases with penetrating cranial lesions may show CNS signs. Turkeys have a gaunt appearance with a hollowed area over the crop.

Histomoniasis (Blackhead)

This is caused by Histomonas meleagidis, a protozoon and it occurs most frequently in exposed, unmedicated turkeys, especially under 3 months; it also occurs in chickens. Young birds are more frequently and severely affected.

It is transmitted by the ingestion of fresh faeces containing the infected ova of Heterakis gallinarum that are within earthworms.

The clinical signs initially are listlessness, anorexia, drooping wings and yellow faeces the head may be cyanotic. In chickens there may be bloody faeces. In the later stages there is depression, drooping wings, eyes closed, head drawn close to the body, and emaciation. Mortality may be 100% in young turkeys.

Diagnosis is by post mortem. Prevention is by practising good hygiene and not mixing turkeys with other species of birds. Also it is important to de-worm regularly. There is no treatment available.

Mycoplasmosis

The clinical signs observed in birds with mycoplasmosis are red, swollen eyelids and conjunctival tissue with a clear ocular discharge. The condition can become more severe resulting in extreme swelling of the eyelid and conjunctiva, crust formation along the eyelid margins resulting in ulcerations on the cornea and purulent discharge and loss of sight. Inflammation of the sinuses may occur resulting in discharge flowing from the nares. The birds may also display wet, matted feathers on the face (especially around the eyes), fluffed body feathers, inactivity, weight loss, loss of appetite and death due to starvation, exposure or predation.

Domestic poultry display respiratory symptoms such as coughing, sneezing and nasal discharge. They are lethargic, stop feeding and undergo severe weight loss. In turkeys, the sinus under the eye becomes swollen.

A diagnosis can be made using blood samples and post mortem. There are a number of treatments available once a diagnosis has been made. The response to treatment often depends upon how early the disease was identified and treatment started.

Marek's Disease

This occurs in Chickens between 12 to 25 weeks of age; occasionally pheasants, quail, game fowl and turkeys can be infected. Marek’s disease is a type of avian cancer; tumours in nerves cause lameness and paralysis. Tumours can occur in the eyes and cause irregularly shaped pupils and blindness. Tumours of the liver, kidney, spleen, gonads, pancreas, proventriculus, lungs, muscles, and skin can cause incoordination; unthriftiness, weak laboured breathing, and enlarged feather follicles. In terminal stages, the birds are emaciated with pale, scaly combs and greenish diarrhoea.

Marek’s disease is very similar to Lymphoid Leucosis, but Marek’s usually occurs in chickens 12 to 25 weeks of age and Lymphoid Leucosis usually starts at 16 weeks of age. Transmission: The Marek’s virus is transmitted by air within the poultry house. It is in the feather dander, chicken house dust, faeces and saliva. Infected birds carry the virus in their blood for life and are a source of infection for susceptible birds. Treatment: none Prevention: Chicks can be vaccinated at the hatchery. While the vaccination prevents tumour formation, it does not prevent infection by the virus.

Streptococcus agalactiae

This infection is now quite rare; it is caused by poor hygiene and milking plant maintenance. Take care not to buy it in with replacements!

Since 2000 there has been a small rise in incidence due to corner cutting as a result of poor milk prices.

The infection causes massive bacterial counts 10 million or more in a cow!

The organism inhabits ducts and cisterns in the mammary gland, however it does not survive in environment and can be eliminated by simultaneous herd treatment.

The infection causes inflammation which blocks ducts and leads to decreased milk production and increased somatic cell counts.

control of contagious mastitis

Quarantine Infected Cows

Keep infected cows in a separate treatment group and milk them last or use a separate claw and bucket.

Teat Dipping - Germicidal Dips

Postmilking teat dipping with germicidal dips is recommended. Barrier dips are useful against environmental infection but their effect against the contagious pathogens appears to be lower than that of germicidal dips.

Dry Cow Therapy

Treat all quarters with dry cow antibiotics at end of lactation, this is essential.

Special Treatments at Drying off

Some cows with a history of mastitis or raised cell counts require special additional treatment t drying off.

ADF (auto dip/fush) - (backflushing)

The cost of these units is coming down all the time; probably the best way of stopping transfer of infection.

Flush milk claws (hot water or germicide) after milking infected cows

If using a germicide ensure that it is licenced for this purpose.

Use individual cloth/paper towels to wash/dry teats

Hygiene

Clean hands (wear gloves). good hygiene and teat preparation.

Milking Machine Maintainence

Malfunctioning milking machines that result in frequent liner slips and teat impacts can increase cases of environmental mastitis. Ensure your machine is cheched by a technician regularly and any faults rectified as soon as possible. Also make sure your liners are replaced at the correct time – a simple calculation is shown below:

Liner life = 2,500 x number of milking units
Number of cows x 2*
* milked twice daily.

A poorly maintained milking plant will cause teat end lesions which allow infections to enter the teat canal.

Avoid buying infected cows

Always check cell count history of individual cows and the herd of origin as a minimum requirement.

Cull persistently infected cows

environmental mastitis

The main causes of environmental mastitis are:

  • Escherichia coli (E.Coli)
  • Streptococcus uberis
  • Pseudomonas species

pseudomonas

The clinical signs are similar to E. coli. Pseudomonas mastitis is usually a result of a hygiene problem in the parlour. It generally causes infection from contaminated water, pipes, heater, wash hoses, teat dip. It is often resistant to many antibiotics

Control of environmental mastitis

1. Housing and Environment

Housed cows are at greater risk for environmental mastitis than cows on pasture. However in the summer oubreaks of environmental mastitis often occur, these are due to either high rainfall or very hot weather which causes the cows to shelter under trees and produce a very contaminated area. Sources of environmental pathogens include manure, bedding, feedstuffs, dust, dirt, mud, and water.

Bedding materials are a significant source of teat end exposure to environmental pathogens. The number of bacteria in bedding fluctuates depending on contamination (and, therefore, availability of nutrients), available moisture, and temperature. Low-moisture inorganic materials, such as sand or crushed limestone, are preferable to finely chopped organic materials. In general, drier bedding materials are associated with lower numbers of pathogens. Warmer environmental temperatures favor growth of pathogens; lower temperatures tend to reduce growth.

Finely chopped organic bedding materials, such as sawdust, shavings, recycled manure, pelleted corncobs, peanut hulls, and chopped straw, frequently contain very high coliform and streptococcal numbers. With clean, long straw, coliform numbers are generally low; but the environmental streptococcal numbers may be high.

Attempts to maintain low coliform numbers by applying chemical disinfectants or lime are generally impractical because frequent, if not daily, application is required to achieve results. Total daily replacement of organic bedding in the back third of stalls has been shown to reduce exposure of teat ends to coliform bacteria.

Environmental conditions that can increase exposure include: overcrowding; poor ventilation; inadequate manure removal from the back of stalls, alleyways, feeding areas and exercise lots; poorly maintained (hollowed out) free stalls; access to farm ponds or muddy exercise lots; dirty maternity stalls or calving areas; and general lack of farm cleanliness and sanitation.

Control of environmental mastitis is achieved by decreasing teat end exposure to potential pathogens or by increasing the cow’s resistance to mastitis pathogens.

2. Teat Dipping - Germicidal Dips

Premilking dipping is advocated for the control of environmental pathogens and is certainly recommended in herds where there is a high risk of either E.coli or Strep uberius infections.

Postmilking teat dipping with germicidal dips is recommended. A degree of control over the environmental streptococci is exerted, but there is no control of coliform intramammary infection.

3. Teat Dipping - Barrier Dips

Barrier dips, postmilking, are reported to reduce new coliform intramammary infections. Their efficacy against the environmental streptococci and the contagious pathogens appears to be lower than that of germicidal dips.

4. Dry cow therapy and teat sealants

Dry cow therapy with the use of teat sealants of all quarters of all cows is recommended. Dry cow antibiotic therapy significantly reduces any infections carried over from the previous lactation and the teat sealant prevents new environmental infections.

5. Backflushing or use of germicidal sprays between cows

Ensure the product you are using is licenced to be used in this way. This proceedure is usefull in preventing the spread of cow-adapted strep uberis infection, However it does not prevent initial environmental mastitis infection.

6. Milking machine problems

Malfunctioning milking machines that result in frequent liner slips and teat impacts can increase cases of environmental mastitis. Ensure your machine is cheched by a technician regularly and any faults rectified as soon as possible. Also make sure your liners are replaced at the correct time – a simple calculation is shown below:

Liner life = 2,500 x number of milking units
Number of cows x 2*
* milked twice daily.
A poorly maintained milking plant will cause teat end lesions which allow infections to enter the teat canal.

7. Udder preparation

Milking cows with wet udders and teats is likely to increase the incidence of environmental mastitis. Teats should be clean and dry prior to attaching the milking unit. Washing the teats, not the udder, is recommended.

8. Vaccination

There is a vaccine available for mmunizing cows during the dry period against Escherichia coli J-5 bacterin. This vaccine will reduce the number and severity of E.coli clinical mastitis cases during early lactation.

9. Diet

Feeding diets deficient in vitamins A or E, beta-carotene, or the trace minerals selenium, copper, and zinc will result in an increased incidence of environmental mastitis. The supplementation of the dry cow diet with Selenium has been shown to be of benefit.

Fertility Control Program

The Three Rivers Veterinary Group fertility control program covers the following areas:

  • Post calving period. All cows are checked post calving to ensure that there is no uterine infection, cystic ovaries or post calving damage which might affect fertility.
  • Oestrus detection target period of 42 days post calving. Any cows not observed in oestrus by day 42 post calving are examined and treated to get them cycling again.
  • Early detection of anoestrus cows with the use of target dates (i.e. those cows which cycle once post calving and then go quiet).
  • Early pregnancy and non pregnancy detection. We are able to perform early pregnancy diagnosis by ultrasound from day 28 and manual pregnancy diagnosis from day 35.
  • Monitoring of Body condition scores. This is routinely done in conjunction with Interherd to provide feedback to the nutritionist regarding dietary balance.
  • Metabolic profiles taken at an early stage of lactation in conjunction with samples from cows about to calve and mid lactation cows provides valuable information about the state of the cows with regard to energy and protein balance and allows for alterations in the ration in time to affect fertility performance.
  • Regular monitoring of Interherd and Herd Companion information in conjunction with the farm record to ensure a quick response to any problems.
  • Monitoring of bulk milk samples for disease e.g.:
  • Bovine Virus Diarrhoea (BVD)
  • Leptospira hardjo
  • Infectious Bovine Rhinotracheitis (IBR)
  • Liver Fluke
  • Gastro-intestinal worms

100 day contract

Three Rivers Veterinary Group use the 100 day contract to improve yield, fertility performance and health in dairy herds. The 100 day contract is a revolutionary dairy management program to optimize early pregnancies. For each cow, the 100-Day Contract focuses on the critical period of 30 days before calving to 70 days after.

The aims of the 100 day contract are:

  • High fertility at first breeding
  • 100 percent service rate for the first oestrous cycle after the voluntary waiting period
  • Significantly increased pregnancy rates
  • Improved cow health
  • Improved calf health
  • Improved peak milk
  • Improved fertility at first breeding

The components of the 100 day contract are:

  • The Dry Cow program
  • The Fresh Cow program
  • The Breeding Cow program

Lameness Prevention

Any lameness action plan must take into account the factors below if it is to be successful.

1. Environmental Factors

  • Enable the cow to enter and leave cubicles easily
  • Ensure the cow can lie down and rise without interference
  • Ensure the cow can stand or lie in the stall comfortably
  • Avoid the rear feet constantly being in contact with slurry and urine
  • Take care with slurry cleaning and scraping
  • Provide soft dry bedding – particularly for pre-calving heifers
  • Check flooring condition –? renew poor concrete, concrete grooving, avoid variable heights
  • Observe cows daily – watch for foot injuries
  • Treat cows promptly and place in straw yard/ pen for recovery
  • Regular foot bathing greatly reduces lameness in most cases
  • Regular foot trimming is also important

2. Nutritional Factors

  • Avoid Rumen acidosis
  • Take care in heifer rearing to avoid laminitis

3. Inherited Factors

  • Avoid selecting replacement heifers from cows with poor conformation, gait or hoof type
  • Use Bulls with good classification for leg and hoof conformation
  • Locomotion scoring can be used to assess the progress of a lameness action plan.

Locomotion Scoring

There are a number of different systems for locomotion scoring, however as long as the same method of assessment is used each time, worthwhile results will be obtained. The system shown in this link is a very effective method.

Locomotion scoring can be repeated between once and four times a year depending upon the lameness problem on the unit. It is a very effective way of monitoring lameness and the response to preventative measures and treatments.

Rumenal Acidosis

Clinical acidosis is relatively easy to spot and correct:

  • Decreased rumen movement
  • Erratic appetite
  • Loss of body weight
  • Scouring
  • Lameness

Sub-clinical acidosis is much more of a problem – less clear cut, drain on productivity:

  • Reduced rumination (cud chewing)
  • Great daily variation in feed intake of individual animals
  • Faeces in the same feeding group varies from firm to diarrhea (feed sorting)
  • Faeces foamy, contains gas bubbles
  • Appearance of mucous/fibrin casts in faeces
  • Increase in fiber particle size (> 0.5 inch) in faeces
  • Appearance of undigested fiber/feed in faeces
  • Appearance of undigested, ground (≤ 1/4 inch) grain in faeces
  • Decreased milk production
  • Reduced fat test
  • Poor body condition – despite adequate energy intake
  • High culling rate
  • Unexplained scouring
  • Lameness

Dairy farmers with high yielding cows walk a fine line between maximising milk production/profits and having sick lame cows. Here are some tips to reducing acidosis problems in your herd:

  • Retain the services of a good nutritionist and take his/her advice
  • Meet or exceed dietary fibre minimums of 18-21% acid detergent fibre (DM basis) and 27-30% NDF (DM basis)
  • Meet or exceed dietary NDF from forage minimums of 18-21% (DM basis) for grass silage based diets and 21-23% (DM basis) for maize silage based diets
  • Do not exceed 35-40% NFC (DM basis)
  • Provide TMR with 8-10% of as-fed particles on the top screen of Penn state/Nasco shaker box
  • Monitor and prevent over-mixing or over-processing of the TMR
  • Monitor and minimize separation during feed mixing and delivery
  • Monitor and minimize sorting in the feed bins
  • Periodically calibrate TMR scales
  • Monitor and control daily variation in amounts of individual feed ingredients added to the TMR
  • Routinely check moisture content of wet feeds and adjust rations accordingly to ensure correct DM ratio of forage to concentrate
  • Limit maize silage as a percent of forage DM to 75% or less for lactating cow diets and 50% or less for dry cow diets
  • Feed close-up dry cows 35-40% NFC diets (DM basis) to adapt the rumen microbial population and develop the rumen papillae prior introducing the high-group diet
  • Do not feed less than 50% forage (DM basis) in the close-up dry cow diet; this diet may benefit from addition of baled haylidge
  • Feed a post-fresh transition diet that contains more total NDF and NDF from forage than the high-group diet; this diet may benefit from addition of baled haylidge
  • Feed buffers
  • In component feeding situations, increase concentrate feeding to peak amounts gradually over the first six weeks of lactation and feed grain 3 to 4 times daily
  • In component feeding or partial TMR situations, monitor and control selective consumption of concentrate vs. forage or maize silage vs. grass silage
  • Minimize effects of heat stress on selective consumption of grain vs. forage

Key: Non fibre carbohydrate (NFC)
Neutral detergent fiber (NDF)
Dry matter – intake (DM – DMI)

Foot Bathing

Footbathing is an important part of the management and control of lameness – particularly digital dermatitis and slurry heel. Foot baths are best situated near the parlour exit – far enough not to reduce flow of cows.

Two baths are ideally required, the first for washing the feet and the second to apply the treatment. Foot baths may be concrete or plastic, they should be easy to set-up and clean out and near water and drainage. Some authorities recommend straw in first bath to produce better cleaning. If there is only one bath available then the feet should be power washed in the parlour before the cows leave.

Foot bath requirements:

  • Min. length 3 m, depth 20 cm
  • Flush to wall or rails of race
  • Non-slip floor, + ridges along long axis?
  • Standing room beyond bath

It is important to stick to a routine and locomotion score regularly.

The most common ingredients used in cattle footbaths contain one or more of the following chemicals:

1. Copper sulphate, 2.5 to 12.5

  • Proven efficacy
  • Can be expensive
  • Easy to use
  • Disposal is a serious environmental concern

2. New copper sulphate delivery system. Healthy Hooves

  • Reduces the copper sulphate used by 70%
  • Reduces the cost
  • More effective control of Digital Dermatitis
  • See our fact sheet (this links to fact sheet attached)
  • Link to Healthy hooves Web site http://www.healthyhooves.eu
  • Three Rivers Veterinary Group are stockists for Healthy Hooves products

3. Antibiotics

  • Expensive and not recommended from a farm assurance point of view
  • Only used in extreme circumstances
  • Withdrawal period issues

4. Organic acids

  • Have an antibacterial effect
  • Can be used with copper sulphate to prevent binding of copper sulphate by organic material on the foot

5. Zinc sulphate

  • Usually used in combination with copper
  • Good for healthy hoof horn

Foot Trimming

This is a vital part of a lameness control program.

For routine herd foot trimming you will need the services of a qualified foot trimmer. However for individual cases that occur between the foot trimmer’s visits you will need to treat them yourself or ask for our help.

We are happy to give individual tuition on foot trimming and corrective paring of diseased hooves, please contact us.

The following reference is a concise guide to foot trimming including the Dutch method, please log on to it.

Digital Dematitis

Digital dermatitis appeared in the UK around 1987 and has since become one of the most serious causes of lameness (>25%), 90% of cases occur on the hind feet.

Digital dermatitis is caused by 3-5 different spirochaete bacteria (Treponema spp.) and it is most common on the underside of the hind foot above the heel. The infection causes circumscribed, eroded, painful lesions surrounded by hyperkeratosis and hypertrophied hairs. In long standing cases these hairs can become very marked and are known as ‘hairy warts’.

Affected cows are lame and slow and often stand and constantly lift the foot as is the pain appears to be sharp and stinging. Slurry heel or heel/horn erosion often progresses from the initial lesion.

The spirocheates thrive in wet conditions especially slurry; it is likely that the irritant effect of urine in slurry allows the organism to attack the skin. Cattle from affected farms carry the infection and most farms became infected due to the purchase of infected cows. Contaminated foot trimming equipment can also spread the disease.

The disease is controlled on a herd scale by foot bathing. Individual treatment may be required in more severe cases; we treat these with our ‘digital dermatitis cream’ and bandage plus in some cases antibiotic treatment.

The cost of each case of digital dermatitis is approx £106 Young, S., MDC Study. An average 38% incidence in a 100 cow herd gives a total annual cost of around £4,028.

laminitis

Laminitis is the route cause of many herd lameness problems and it’s control can make spectacular savings to the annual lameness treatment costs.

There are three types of laminitis:

1. Acute Laminitis

  • Sudden onset
  • Severe pain
  • All four legs affected
  • Difficulty in standing – or cow will kneel only
  • Not common

2. Sub-acute Laminitis

  • Most common form of laminitis on farm
  • No obvious signs
  • Frequent nutritional and environmental stress
  • Heifers on high cereal/silage diets
  • Cows on hard standing for long periods
  • Hoof weakened through abnormal growth
  • Yellow sole, haemorrhaging and sole ulcers

The following are associated with sub-acute laminitis:

  • Sole ulcer
  • White-Line Disease
  • Toe necrosis
  • Double or false sole

3. Chronic Laminitis

  • If left untreated, sub-acute laminitis will progress to chronic laminitis
  • Breakdown of blood supply to the corium and damage to the internal structure of the foot
  • Irreversible damage, culling

The link between nutrition and laminitis is acidosis which results in poor blood supply to the corium. The severity depends upon frequency and length of each period of rumen acidosis.

sole ulcer

Sole ulcers are caused by the uneven distribution of weight in the foot. The increased pressure on the inside of the sole causes damage and necrosis of the tissues below the horn and an ulcer develops. Sole ulcers are preventable by regular foot trimming and hoof care; they are a major cause of economic loss. Often the opposite claw requires a block glued on to it to take the weight off the affected claw and allow it to heal. The healing process takes some considerable time and there is always a weakness there afterwards.

Sole ulcers are one of the 3 most common causes of lameness; the others are digital dermatitis and white-line disease. Sole ulcers cause the most-severe lameness and they are also expensive the average cost of a case is £314.08 (Esselmont).

Regular foot bathing helps to improve horn quality and reduce the incidence of sole ulcers.

white line disease

The white line lies between the hard side wall of the hoof and the more pliable sole. It allows some elasticity and mobility within the hoof and the line is part of the lamellae which lock the hoof onto the pedal bone. Reduced horn quality and hardness leaves the structure more susceptible to damage and vascular disturbances. It is known that when the white line is weakened foreign material (grit) may be caught in it and gradually work its way into the foot with the pressure and shearing forces as the cow moves along especially on hard surfaces. If foreign material ascends the white line and penetrates the sensitive tissue of corium, infection will most likely occur, which leads to lameness and further damage to the white line at the point of origin.

A regular hoof trimming program and attention to the hoof quality with regular foot bathing of the herd will assist in spotting potential white line disease. The elimination of standing water and maintenance of high quality walkways will help to ensure healthy hoof horn structure. Old damaged concrete surfaces are a source of hard grit and this often causes white line disease.

slurry/heel erosion

Slurry heel or heel erosion is associated with interdigital dermatitis. The cause is multifactorial with a bacterial component superficial. The skin becomes greyish, sweaty, smelly with no obvious lameness. The inflammation extends to the heel and erodes it, V-shaped fissures appear and poor-quality black horn is produced.

There is a reduction of horn production at the heel and an increase in horn production elsewhere in the hoof: lengthening, sometimes with elevation. Regular foot bathing helps to improve horn quality and reduce the incidence of slurry/heel erosion.

Mild lameness may appear and various complications arise such as:

  • Double or false sole
  • Bruised sole
  • Sole ulcer

foul of the foot

Foul of the foot is a contagious disease of cattle characterized by the development of a necrotic lesion in the interdigital skin. The accompanying infection extends into the soft tissues of the foot causing swelling and lameness. The lesion has a typically foul smell which some find helpful in distinguishing it from other conditions.Incidence appears to be higher during the winter months and in confinement-housed cattle.

Recently a new more severe form of the disease has been observed. It has been termed “Super Foul” which is believed to result from a combined infection with the spirochaetes that cause digital dermatitis; very prompt aggressive treatment is required in these cases if the cow is to be saved.

Environmental factors may cause foul of the foot such as walking through or standing in manure slurry for extended periods or flints and stones in gateways or walkways. The condition is caused by Fusobacterium necrophorus and it lives in the gastrointestinal tract of the cow.

Improving the quality of walkways and alleyways and eliminating debris in these areas to avoid interdigital skin lesions and keeping the cattle environment as dry as possible are major considerations in the prevention of foot rot problems.

Treatment requires systemic antibiotic therapy and simple cases will usually respond to penicillin alone.

Regular foot bathing helps to control the infection reduce the incidence of foul of the foot.

toe necrosis

This is a serious infection of the toe with the spirochaete organisms that cause digital dermatitis. The infection has a gangrenous smell and gradually eats away the toe; initially the cow may not be too lame. Regular paring can ease the problem in the early stages but as the disease progresses the animal will have to be culled.

horizontal and vertical wall fissures

Horizontal fissures in the outside wall of the hoof are usually a result of a severe illness or metabolic disorder which affected hoof production from the coronary bane for a period of time. These fissures will grow out but they can be painful at times, corrective paring of the fissure to make it shallower often helps.

Horizontal fissures are often a result of either weak horn due to inherited or nutritional factors or they may be caused by a traumatic event e.g the foot becoming wedged somewhere.

Provided the horn has the capacity to regrow good quality, hard horn these defects will resolve themselves; however because of the slow growth rate of horn this takes a considerable time.

hock lesions

Hock lesions are associated with cubicle design problems. The type of bedding material also affects the incidence of hock lesions. Hock lesions and swellings may become infected and spread to the joint and it is difficult to save these cows.

On some farms poor cubicle design and maintenance may lead to a high number of cows with hock lesions and a herd welfare issue.

NEWS LETTER SEPTEMBER 2018

Practice information

Beccles

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    8:00am - 7:30pm
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    8:00am - 6:00pm
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01502 712169
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The Veterinary Clinic London Road Beccles Suffolk NR34 9YU
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01502 712169

Loddon

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01508 520247
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The Veterinary Surgery 19 Beccles Road Loddon Norfolk NR14 6JQ
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01508 520247

Poringland

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01508 492834
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The Veterinary Surgery 113 The Street Poringland Norfolk NR14 7RP
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01508 492834

Kessingland

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01502 741988
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The Veterinary Surgery 81 High Street Kessingland Lowestoft NR33 7QQ
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01502 741988

Norwich

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Emergency Details

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01603 765897
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The Veterinary Surgery 70 Hall Road Norwich Norfolk NR1 3HP Great parking directly outside practice with reserved spaces
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01603 765897

Mulbarton

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    8:30am - 5:30pm, Closed 1:00pm - 2:00pm
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01508 570960
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The Veterinary Surgery Norwich Road Mulbarton Norwich NR14 8DE
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01508 570960