Grass tetany is a metabolic disease caused by low concentrations of magnesium (Mg) in the blood and cerebrospinal fluid. Mg is not stored in the body; therefore, a constant source in the diet is required. It occurs due to insufficient dietary Mg or excessive dietary potassium and/or nitrogen. Risk factors for this include:

• Animals in late gestation/early lactation because they have higher Mg demand
• Stock grazing lush pasture with low dry matter content (reducing cud chewing and digestion time).
• Pasture fertilized with nitrogen and/or potassium is a risk as it will inhibit Mg uptake

Typically, we see grass tetany in cattle grazing on fresh, rapidly growing pasture after periods of reduced feed intake, for example after poor weather, yarding/transport, or over the calving period. This lush pasture moves through the gut much quicker than hay, which reduces the opportunity for magnesium to be absorbed. Sudden death with signs of struggling (disturbed ground surrounding the animal) can be the first sign of grass tetany in the herd and often stress can trigger clinical signs.

What does it look like?

Mg is required for normal nerve conduction, muscle function and bone mineralization, hence most visible clinical signs are attributed to nerve and muscle function.

Grass tetany can present in different ways;

1. Peracute – staggering, collapse, convulsions, paddling and death
2. Acute – twitching ears, grinding teeth, salivation or frothing at the mouth, muscle tremors, aggression (including charging), hyper-responsiveness, bellowing. The animal can become progressively uncoordinated and develop muscle spasms and can die within hours.
3. Sub-acute – slight inappetence and agitation over 3-4 day period, reduced milk yield, diarrhoea, tucked abdomen, stiff gait, hyper-responsiveness to noise/handling
4. Chronic – usually seen around 6 weeks after calving and is associated with long term Mg deficiency. Often animals will have thin/rough coats, pale gums due to anaemia and possibly udder oedema/swelling and wasting. Often chronic hypomagnesaemia is also associated with hypocalcaemia (milk fever) and decreased milk yield.

Note the salivation and frothing at the mouth, dilation of nostrils and retracted eyeballs

_{Credit: Disease of Cattle in Australasia}

Note the flattened and disturbed dirt around the legs of this cow.

_{Credit: Disease of Cattle in Australasia}

Grass tetany can be confused with the early signs of hypocalcemia (milk fever), nervous ketosis, clostridial infections or lead poisoning. Diagnosis is often made on clinical signs and confirmed with blood testing.

If a dead animal is found on farm and grass tetany is suspected, we can test the fluid in the eye for magnesium levels. Please call and speak to us should this situation arise.

How is it treated/prevented?

To increase chances of successful treatment, intervention is necessary as soon as clinical signs are noticed. Ideally, this involves slow administration of intravenous magnesium and calcium (4in1 flowpacks). In cases where this isn’t possible, a flowpack under the skin is advisable. Note that on some occasions, additional sedations are needed to stop the cow convulsing.

Other treatment options include:  

• Magnesium sulphate fluids given under the skin
• Oral magnesium supplements

After treatment, it is common for a cow to take approximately 30mins to stand. There is no need to rush her.

There are a multitude of methods that can be used to prevent grass tetany including:

• Feeding hay
• Mg lick blocks (some better than others!).
• Pasture dusting with Mg
• Adding Mg to water troughs, although this is unpalatable
• Using rumen Mg bullets

A good starting point for prevention is ensuring stock have access to 4kg/head/day of hay as feed during times of lush pasture growth, plus Mg lick blocks.

Depending on your situation, one supplement may be more practical than others, for this reason, feel free to call the clinic and discuss the best option.

The outdated approach of routinely drenching (blindly) without any knowledge of worm burden status or a pasture management plan is likely to lead to long term issues like drench resistance and poor production, which can be costly. Routine FECs offer an opportunity to determine if drenching is even necessary, and if so, which mobs or age groups require it. A more strategic approach also allows us to monitor drench effectiveness, reducing the stress, costs and health issues that are associated with drench resistance. Carrying out FEC before drenching and following up with a second tests approximately 10-12 days after drenching allows us to objectively measure how well the drench has been at eradicating the parasites. If egg levels do not drop by the expected >95% after treatment, this is a clear indicator that the drench has been ineffective, the parasites are likely resistance to the active ingredient used, an alternative drench program should be adopted. Be sure to check your dosing gun is correctly calibrated prior to use to prevent underdosing.

Environmental conditions such as rainfall, temperature and pasture condition can all play a role in worm lifecycles, risk periods and pasture contamination. These vary from year to year so understanding your real time situation, and having a record of previous year’s patterns gives you the knowledge to create tailored herd health/ property management strategies that are effective for your stock’s situation.

Some individuals can carry a surprisingly high worm burden without presenting with any noticeable symptoms. These high shedding, silent carriers can cause havoc in a mob, and animals that are less resistant are put at risk. FECs are an important and helpful tool in detecting emerging issues and allowing for early intervention. So, what does a worm burden need to be at to warrant treatment? Season, age, body condition, pregnancy status and worm species are all factors that contribute to determining at what point a worm burden starts to cause issues for individual stock. While these figures are a useful starting point, they are a guide only and your veterinarian should be consulted when determining the best parasite management plan.

The McMaster technique is a simple quantitative faecal egg count test used to estimate eggs per gram (represented as e.p.g) in a known volume of faecal suspension to the nearest 50 e.p.g. X2 0.15ml of solution is placed into the counting chambers and the sample is examined under a microscope. Systematically, eggs lying within the chambers are counted and an e.p.g result calculated using the following formula;

EPG = total eggs counted in both chambers x50.

This quick method allows us to accurately monitor strongyle type eggs, Nematodirus, tapeworm (to an extent) and coccidia burdens. Some species like Lungworm, encysted tapeworm and Liver Fluke require additional testing and should not use the McMaster technique as a sole means of determining status. To minimise the chance of missing potential eggs, always used a fresh faecal sample, ideally less than 24 hours old. If samples are being pooled, bring in samples from individual animals (with clearly labelled ID). The lab will pool the samples. Refrigerate the sample if there is going to be a delay in getting it to the lab. It is important to point out that if no eggs are seen, it does not guarantee an animal or mob are parasite free, it just means that no eggs were detected in that particular sample. If a result comes back low or negative but an animal is still presenting with symptoms, consult your veterinarian.

There are several parasite species that we look for on worm egg counts, and a burden can present differently depending on the species. Remember, targeted selective treatment, when used in conjunction with pasture rotation and routine testing will ensure effective parasite control. Consult your veterinarian to discuss the most appropriate, safe and effective treatment group.

Parasite	Host Species	Symptoms	Notes
StronStrgyles (roundworms)	Cattle, sheep, goats and alpacas	Weight loss, poor coat condition, scours. Can cause death suddenly.
Nematodirus spp.	Youngstock – lambs, kids, calves	Scours, dehydration, poor growth rates	Adult stock generally have an acquired immunity to Nematodirus infection because of previous exposure.
Coccidia (oocysts)	Calves, lambs, kids and alpacas	Scours sometimes with blood or mucous, dehydration, weight loss, poor coat condition	Protazoan parasite.  These are counted separately from other eggs seen in a sample. Treatment is also different.
Tapeworm	Sheep, goats, cows, camelids	Often subclinical, but high burdens can present with lethargy, anaemia, poor growth or pastey scours.	Encysted tapeworm will not be detected in a FEC. Additional blood testing may be required along with observation of clinical signs.
Liver Fluke	Sheep, goats, cows, camelids	Anaemia, bottle jaw, weight loss, reduced production.	Specific sedimentation test is required as shedding is sporadic and eggs can be easily missed. Antigen testing is also accurate and detects infections sooner.
Lungworm	Sheep, goats, cows, camelids	Persistent cough, increased respiratory rate and difficulty breathing poor growth rate in youngstock, reduced milk production in adult cows.	Baerman Test is preferred as FEC can be unreliable is these cases.

References:

Morgan. E. & Williams. D., 2023, COWS – Control of Lungworm in Cattle, Queen’s University (Belfast)

Loughman. T., et al., 2024, Faecal Egg Counts in Australian Pasture Based Dairy herds, Veterinary Parasitology: regional Studies & Reports, Vol 51 101028

Hutchinson. G., 2009, Nematode Parasites of Small Ruminants, Camelids & Cattle Diagnosis with Emphasis on Anthelmintic Efficacy & Resistance Testing, EMAI, Australia & NZ Standard Diagnostic Procedures

Sabantini. G., et al., 2023, Practical Guide to the Diagnostics of Ruminant Gastrointestinal Nematodes, Like Fluke & Lungworm Infection: Interpretation & Usability of Results, Parasites and Vectors, Vol 8 (16)

StronStrgyles

Nemarodirus spp.

Coccidia (oocysts)

Tapeworm

Liver Fluke

Lungworm

The signs of fly strike are often subtle without close inspection as strike lesions start off being small. Sheep will show signs of discomfort and irritation such as leg stamping and bowing of the head. As cases progress, fleece will become darker and wet as the struck areas increase in size.

As the disease worsens, animals become depressed, they stop eating and drinking leading to weight loss. These animals are reluctant to stand or walk and become separated from the group. By this time the maggots will be quite large and tracts within the fleece will be see as they migrate towards healthy tissue. If left untreated, these cases will die quickly and so early detection and intervention is paramount. Flocks that have had clinical cases are more likely to have further cases so increased monitoring of the flock is advised.

Treatment of fly strike requires the wool to be sheared with a minimum of a 6cm margin of unaffected fleece. Applying a registered flystrike dressing such as Extinosad can kill the maggots but may need reapplying as any remaining eggs on the fleece hatch. Struck sheep should be removed from groups as they will remain attractive to the blowfly, and so this will reduce the risk to others.

Prevention of flystrike is based around insecticides, culling, management tools and breeding strategies. The insecticides need rotating to prevent resistance and the same product should not be used within the same wool cycle. Breeding strategies should be as such that animals that have been struck should not be bred from again and decision making about retaining high-wrinkle sheep should be well thought through. Crutching, dagging and shearing should be part of your annual management strategy in addition to avoiding faecal staining by monitoring internal parasite burdens with regular faecal egg counts. By ensuring crutching has been completed 6 weeks before the risk period for flies will help reduce the numbers of flies that hatch and thus minimise your risk.

If you have any concerns about the best approach, please contact us at the clinic.

image from https://www.lls.nsw.gov.au