In this issue
- Lameness in heifers - should we be worried?
- Q-Fever - can you help with bulk tank PCR testing?
- Jejunal Haemorrhage Syndrome (JHS) in cows - what you need to know
- Bluetongue - an update on cases in the South East
- Schmallenburg - a reminder for lambing time
- Huskvac - protecting your youngstock against lungworm for 2024
Lameness in milking heifers - should we be worried?
What does the research say?
Maxwell et al. (2015) reported that 95% of the 139 milking heifers in the study that were foot trimmed at 50-80 days in milk had some disease in at least one claw.
Capion et al. (2009) looked at 147 milking heifers and found that 80 of them had moderate to severe sole bruising and 105 of them had a white line lesion.
Randall et al. (2016) found that milking heifers that were lame between 60-100 days in milk gave nearly 3 litres less milk per day compared to milking heifers with no lesions. They also found that heifers that had Digital Dermatitis (DD) in their first lactation were culled from the herd 341 days earlier than those without DD and had a lifetime reduction in milk yield of 3,513kg.
Why are heifers particularly at risk?
The 6 week period around calving poses a massive risk of lameness for cattle of all ages, but particularly for heifers. Heifers have multiple group and diet changes around calving, have to learn about how to lie in cubicles and how to dodge more senior bully cows. They also have to get used to standing on concrete, are often waiting the longest to be milked, and get exposed to the bacteria causing Digital Dermatitis.
The 60 day trim.
If heifers are calving in and being housed for the first few months of lactation, the 60 day trim becomes a really important tool to protect her foot health for her lifetime. A routine trim at this point gets her foot rebalanced, takes the pressure off the sole ulcer site by removing excess sole and redistributing her weight correctly, and can stop a bruise developing into an ulcer which she would otherwise end up dealing with her whole life.
Have you heard of EDPET?
Early Detection and Prompt Effective Treatment
EDPET is one of the cornerstones of successfully treating a new case of lameness. EDPET means all new, mild cases of lameness should be picked up and trimmed within 48 hours of first going lame - using pain relief and blocks at this point maximises her chance of a full recovery. Sometimes it is easy to get stuck in a cycle of presenting the same old cows with foot issues to the foot trimmer and never managing to get to the new, fresh, mild cases that have a much better chance of a cure.
Next time you're making your list of cows to foot trim - pull out some 60 day heifer trims and see what their feet tell you - if they're perfect and balanced you can relax a bit and concentrate on other areas for foot health - but if you're finding bruises or early Digi lesions then know it is a valuable trim that is protecting her future in your herd.
Is there anything we can do to protect heifers and their feet as they join the milking herd?
- Make sure heifers have had contact with concrete before they calve to develop the fat pads in their feet - this internal cushioning is critical to keeping heifers sound
- Make sure heifers have comfy cubicles and lie in quickly - if they're refusing a cubicle that first day after joining the milkers, help them into the cubicle and give them pain relief to minimise the damage to the inside of the foot
- Make sure there are spare cubicles so heifers have options where to lie and don't have to squeeze in between two dominant cows
- Make sure there is at least 80cm feed space per cow in the milkers so less dominant heifers can feed easily and minimise weight loss
- Make sure dry cows and heifers are footbathed as often you footbath the milkers - this means the skin around the hoof is more resilient against the bacteria causing DD in freshly calved cows
How do we test for Q fever?
There are a few different ways of testing for Q fever - any abortion samples going to the VLA at Shrewsbury will be automatically tested as part of the submission but on a herd level we either look at levels of immunity (antibodies) in the bulk tank or we can look for evidence of the bacteria itself in the bulk tank (PCR test).
When we look at samples taken across the South West of the UK it seems that almost half of the herds tested had antibodies to Q fever in the bulk tank - but this doesn't tell us about current infection status, just that there's been some exposure in the past.
The Q Test is a PCR test that is looking for the bacteria that causes Q fever and can be used on a bulk tank sample as a screening test for current or active infection.
What about your herd?
We've started testing "at-risk" herds with the Q Test to look for active/current infection and all herds tested at HFV have so far come back negative with repeat rounds of testing scheduled in 3 months time.
We now have the opportunity to widen our bulk tank testing as part of a UK wide study by a vet at the University of Liverpool - the Q Test PCR bulk milk test will be free for herds that are eligible to join the study.
Are you eligible to be part of the study?
- Herds must have 12 months of milk recording data or 12 months of good quality fertility data (calvings, all serves, any PDs)
- Herds must be recording which cows had held cleansings and the ID of cows treated for "whites" after calving for the last 12 months
- Herds must know their status for BVD, IBR and Lepto
Want to get involved?
Get in touch with Paula on 07764 747855 or via email: paula@haywoodfarmvets.com
Jejunal Haemorrhagic Syndrome (JHS) in cows - what you need to know
JHS causes sepsis and a sudden, severe blood loss into the gut of the cow - more than 95% of affected cows die within a few days.
The disease has been increasingly diagnosed over the past few decades in USA, across Europe and in the Middle East. JHS seems to affect dairy cows more than beef cattle, and affected cattle tend to be older cows, especially high producing animals that are fed on high energy diets in the first third of lactation. JHS tends to be a problem in bigger herds, and more cases happen between December and May - JHS is less of a problem in grazing herds.
What does JHS look like?
- sudden drop in yield
- very dull and slow; last in the parlour
- quiet guts and a drop in rumination if cows have collars or tags
- teeth grinding
- no muck coming through (some may have bloody muck)
- high heart rate
- cold
- won't eat
- dehydration
- wobbly
- collapse
- sudden death
What's happening inside the cow affected by JHS?
A cow affected with JHS has a massive bleed in a part of their intestine called the jejunum - the blood clots in the jejunum and causes a complete blockage which means food backs up the system, the cow goes into sepsis, rapidly deteriorate and die.
Can we treat JHS?
Some cattle with early signs of JHS have been treated surgically in the USA - the affected intestine can be removed or the huge blood clot can be "milked through" but even when caught early and operated on in a University teaching hospital environment, these cows seem to have a very poor chance of survival.
Vets have attempted various medical treatments using anti-inflammatories, antibiotics, intravenous fluids, Clostridia antitoxin, steroids, gut relaxants, oral fluids, calcium - but there doesn't seem to be an effective treatment so far.
What causes JHS?
There are a number of risk factors found, but no definite cause yet.
The role of Clostridia:
A bacteria called Clostridia perfringens has been isolated from the intestines of lots of JHS cases, and found in feed on farms affected by JHS but when researchers have tried to cause JHS by putting Clostridia perfringens into the intestines of healthy cattle, no cattle have then gone on to develop JHS so it's role remains unclear.
Clostridia perfringens is found in normal cattle guts but you can see an overgrowth if there's an overflow of gut contents from the rumen/abomasum into the intestines so any risk of overfeeding concentrate or poor rumen health can predispose herds to JHS.
Risk factors for Clostridia perfringens overgrowth:
- Low fibre levels in the diet
- Poor cudding levels
- Cows sorting their ration
- Feeding a lot of concentrates
The role of moulds:
The DNA of moulds such as Aspergillus have also been found in the gut contents of JHS cases - and this isn't something that is found in normal cattle guts so could be playing a role in the disease. Aspergillus can produce mycotoxins which not only disrupt the gut lining, but also cause localised immunosuppression so may allow secondary invaders such as Clostridia perfringens in.
So, what can we do about JHS?
As the cause of JHS is yet unknown, there are some general preventative measures:
- Using Clostridia vaccines in affected herds may help to reduce the chance of secondary invaders
- Make sure Mycotoxin binders are being fed and that you are really careful to remove any visible moulds on clamps or stored feed
- Promote good rumen health as much as possible: include short chop length fibre, avoid slug feeding concentrates and make sure all cows have truly ad lib access 24/7.
Don't forget the value of an on farm post-mortem if you have an animal that doesn't recover or you find as a sudden death - often opening these cases up means we all learn a bit more about the diseases on your farm and that means we're better able to focus our preventative measures.
Bluetongue - an update on the situation in the South East
Many of you will have heard there have been a number of Bluetongue cases picked up by routine blood sampling in the SE of England (Kent and Norfolk).
Bluetongue is a notifiable disease, spread by midges that can affect cattle, sheep and other ruminants. There are currently 51 BTV cases on 27 premises in Kent and Norfolk - these are likely to have been caused by midges blowing across the channel last autumn. There's no sign of bluetongue currently circulating in midge populations in the UK but this will change as we head into Spring and warmer weather.
This time the serotype is BTV-3 which causes more severe disease than the previous strain BTV-8 in 2007, and it is a strain that we don't have a vaccine for.
Schmallenburg - a reminder for lambing time
Schmallenberg is affecting hundreds of early lambing flocks across the south of England, with vets and farmers seeing a sharp rise in cases of abnormal lambs being born with fixed/fused/abnormal legs and twisted necks.
The disease is transmitted through bites from infected midges, and creates these deformities when animals are infected during the mid stages of pregnancy; about four to eight weeks into gestation.
Ewes lambing at the moment would have been served in the middle of August and so been susceptible to the disease from mid-September to mid-October.
Keep Schmallenburg in mind when you put your hand inside to assist a ewe - whilst most affected lambs can be delivered, especially in multiple births, we need to minimise any damage to the ewes so they can breed again next year; so more lubrication, patience, and pain relief after assistance will be really beneficial.
APHA Free Testing for Schmallenburg Virus
APHA will continue to offer free of charge testing in 2024 on samples from lambs, kids, and calves born with abnormal/fixed/fused legs or other deformities. We will need a fresh brain sample from the affected lamb - get in touch if you have any suspect cases.
Huskvac -protecting your youngstock against lungworm for 2024
It’s a lovely reminder that spring turnout is just around the corner when we see Huskvac start coming in and going out of the practice. Formerly known as Dictol, vaccination is our preventative tool when it comes to lungworm control.
Lungworm is caused by a parasite called Dictyocaulus viviparus which is found on a lot of cattle farms in the UK, but not all. Disease patterns can be unpredictable as weather affects how quickly the lifecycle progresses; lungworm like gut worms prefer warm wet weather.
Infected cattle pass live larvae, not eggs, in their muck and the larvae develop over a few days inside the cowpat before wriggling out onto surrounding grass or being fired out by a fungus called "Pilobolus". These larvae are eaten by other cattle and migrate through the gut, ending up in the lungs where they become adults and sit in the main airways producing eggs. These eggs are coughed up and swallowed into the gut where they hatch and are passed out in her muck.
In the UK we used to see disease from July to September but milder winters mean more extended grazing seasons and we now see disease as early as May and as late as December. Lungworm can be quite dramatic if the airways are full of adults - you can get severe coughing, head outstretched, mouth breathing and deaths, but in earlier cases you hear coughing, especially when being moved.
Huskvac Vaccination
Huskvac is one of the ways we can protect cattle from lungworm - the vaccine is an oral dose of 1000 larvae that have been damaged by radiation - this means the larvae are alive but harmless and exposure builds immunity safely. It's a two dose vaccine, given 4-6 weeks apart with the second dose at least 2 weeks before turn out.
Grazing & worming after vaccination:
Immunity to lungworm is short lived so it is vital that vaccinated animals are exposed to pasture larvae in that first grazing season - don't use slow release worming boluses or long acting wormers as this can stop the natural immunity boost that is needed.
What about sheep?
Sheep can become infested with a different species of lungworm called Dictyocaulus filaria. Unlike in cattle, this parasite is rarely of clinical significance but do get in contact if you have any concerns.
Get in touch
Paula: 07764 747855 paula@haywoodfarmvets.com
Tom: 07837 291097 tom@haywoodfarmvets.com
Katie: 07507 656747 katie@haywoodfarmvets.com
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