Guest Blog: Ready for Spring

By Paula Carnell: Creating a Buzz About Health

To wake up listening to birdsong is truly a magical experience and something that, having always lived in the countryside, I could too easily take for granted.

This year, spring seems to have come all of a sudden and surprised us all with the sunshine and the warm, sunny, longer days.

Since working with Bees, my awareness and appreciation of the natural cycle in the order of things has changed. I used to dread the long dark nights of autumn. October, November and December would be very difficult months for me. With my birthday in November, what I would do is always organise a big party; a big celebration to distract from the depression that would set in as the days grew shorter.

After spending seven long years of my forties in bed and wheelchair bound, I had to learn to appreciate the small things in life: a blue tit sitting on my bedroom window ledge; watching spiders weaving webs in the roof lantern above my bed; and watching the bees from the hive I could see through the bedroom window.

Recovery has taught me to appreciate the small things, every day, and not to take wellness or health for granted. We are all merely a breath away from disease or disability.

I’ve learned that the winter months, as for the bees, are my rest time. They are my chance for hibernation and the time for my body to heal. After a busy season with long summer days where I’m enjoying every ounce of daylight, either with work or play, I then need the long winter nights to sleep.

Back in February we suddenly had warm days which were getting longer, and I didn’t feel ready. It felt too early to be busy with Bees. They were awakening with the sunshine, and the plants were slowly awakening too, but were they quick enough for the bees? Was there enough food for them? I wondered about us: had we had enough time to rest and recuperate before another busy summer?

A bee research project found that healthy bees in a colony that is lined with propolis and filled with honey, spend the majority of their time resting.

So, when we say ‘busy as a bee’, we are not referring to them being busy all the time, but just when they need to be busy, pollinating flowers, collecting nectar or building wax comb. The rest of the time they are together in the hive doing nothing, maybe Meditating?

In contrast, an unhealthy hive which has its honey taken away and replaced with sugar syrup, (lacking the trace minerals essential for healthy life), this colony spends none of its time resting.

The bees emerge from the cocoons and begin a busy race for survival. Each of the phases of life is shortened and sped up: cleaning their cells as they emerge; nursing the new bees; and, finally, whilst still immature, they begin their foraging flights to collect nectar and pollen for the rest of the colony.

These bees, living a life shortened by almost half, are found shivering and twitching with their wings in tatters exhausted from life without rest.

This behaviour is caused by the toxins that the bees are exposed to. A cocktail of insecticides and pesticides and environmental poisons sprayed on our plants, leeched into our soil, drawn up by the flowers and given to the bees through the nectar and pollen. These toxins are then deposited in the honey or used to make the wax cells that they lay their eggs in.

Keeping their colony at a constant 35° ensures that the vapours from these toxins vaporises, allowing the bees to inhale this man-made mix of poison from the moment they emerge.

These toxic fumes affect the nervous system, preventing the bees from pausing between each nerve impulse. Each cell in their body is constantly bombarded with stimulation. Without these important pauses, the muscles are exhausted, the brain is exhausted, no organ in the body has been able to repair itself which it can only do during rest and sleep.

Could we be seeing parallels in our own lives?

What if the same poisons we use on our land and in our homes to keep us pest free, have now poisoned the water we drink and the air we breathe, and are now affecting our own nervous systems, pressurising us to work and play hard, not to rest or meditate.

We haven’t yet reached the ‘silent spring’ that biologist Rachel Carson wrote about in the 1960s. I can still hear birds and I do have bees in my garden, but there are places in the world where insects are scarce, and birds are scarcer. As we dispose of unwanted nature are we slowly disposing of ourselves?

As we have this respite from winter with bright sunshine, clear skies and dry feet, let’s use it to enjoy nature and to care for the wildlife around us, using this time to nurture ourselves and the environment we live in. Should more of winter return, let’s use that time to rest so that when we have the longer days and we need more work to be done, we have the energy reserves, and the strength to make the world a better place.


Bio

Paula’s book ‘Artist to Bees’ was published in February 2019 and is available from her website and local independent bookshops. www.paulacarnell.com

Paula Carnell was born in Dorset, England and has spent much of her adult life living in Castle Cary Somerset. Forming ‘Possi’ in 1990 as part of the Prince’s Youth Business Trust’ scheme, she soon had a successful enterprise selling her original paintings on silk, and printed greeting cards of her work in over seven hundred shops across the UK and exporting to eleven countries worldwide. Opening a gallery in Castle Cary in 1995 established her as a familiar face in the town, until she ‘retired’ from retail in 2004 and focused on her personal painting career. Exhibiting in London and the USA, Paula was fulfilling her dream as a globe travelling artist. Then in 2008, she began to fall ill, becoming bed and wheelchair bound with Ehlers Danlos Syndrome in 2009. The following seven years were spent on a personal quest to find meaning in life, transforming from an artist to a bee speaker. Achieving a full recovery in 2016, she is studying as a medical herbalist with the IRCH, runs her business ‘Creating a Buzz about Health’, working as a Global beekeeping consultant, writer and speaker. She lives in Castle Cary with her husband Greg and three sons.

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Grass sickness

grass sickness

This is a piece that I wrote some time ago about the little understood condition of ‘grass sickness’.  It tends to appear in the Spring and so I thought it might be timely to share it now.

The medical name for grass sickness is ‘equine dysautonomia’.  It is a rare but predominantly fatal illness which can affect all types of horse, pony and donkey.  It is caused by damage to the central, peripheral and intestinal nervous systems.  The most obvious symptoms are related to the consequent paralysis within the digestive tract, however nerves throughout the body are affected.

There are three forms of grass sickness:

  • acute grass sickness (AGS) – horses require euthanasia or die within 48 hours
  • subacute grass sickness (SAGS) – horses display clinical signs similar to AGS but with less severity and may survive up to 7 days
  • chronic grass sickness (CGS) – horses present with severe and rapid weight loss and a selected portion of these cases may survive.

In the acute form of the disease the gut paralysis leads to signs of colic including rolling, pawing at the ground and looking at the flanks, difficulty in swallowing and drooling of saliva.  The stomach might become grossly distended with foul-smelling fluid which can start to pour down the nose. Further down the gut, constipation occurs. If any dung is passed, the pellets are small, hard and may show a ‘cheesy’ coating of mucus. Fine muscle tremors and patchy sweating may occur. In this form, the disease is fatal and the horse should be put down once the diagnosis is made.

In subacute grass sickness, the symptoms are similar to those of the acute disease but are less severe. Accumulation of fluid in the stomach may not occur but the horse is likely to show difficulty swallowing, mild to moderate colic, sweating, muscle tremors and rapid weight loss. Small amounts of food may still be consumed. Such cases may die or need to be put down within a week.

In chronic grass sickness, the symptoms come on more slowly and only some cases show mild, intermittent colic. The appetite is likely to be reduced and there will be varying degrees of difficulty in swallowing but salivation, accumulation of fluid in the stomach and severe constipation are not a feature. One of the major symptoms is rapid and severe weight loss which may lead to emaciation. Previously, it was thought that nearly all such cases died and that the few which survived made only a partial recovery and were subsequently useless for work. This is now known to be incorrect if appropriate treatment and care are provided.

Grass sickness is difficult to diagnose as not all affected animals show all the signs and it can be difficult for the vet to distinguish this from other causes of colic, swallowing difficulties and weight loss.  The symptoms can also be confused with those of several other illnesses including colic, tying-up (azoturia), laminitis, botulism, and choke.  In addition there is no non-invasive test for grass sickness, although certain blood tests and examination of peritoneal fluid can be helpful, when considered together with the symptoms.  A definite diagnosis can only be given after biopsies of the gut have been taken, or if the horse has already died, biopsies of the nerves can be used.  There is currently research into a possible test involving application of 0.5% phenylephrine eye drops, which reverses the drooping eyelids seen in grass sickness, as this has shown potential for use in the live horse.

At this time there is no treatment for this condition.  A small proportion of horses suffering with the chronic form can survive if they are given intensive nursing care, however this is expensive, time consuming and their survival is not guaranteed.  Overall mortality rate is considered to be over 95%.

The disease was first recognised in about 1907 following an outbreak in army remount horses near Dundee. The incidence increased significantly and, at least in Scotland, hundreds of horses, mainly draught animals, died annually from grass sickness in the 1920s. In the 21st century, grass sickness continues to kill horses of all breeds and it has been estimated that approximately 1 in 200 die annually from the disease in some parts of the UK.

The cause of grass sickness is unknown and so research is ongoing to see if a culprit can be identified.  This research has included the development of a nationwide surveillance scheme across Great Britain which hopes to identify all cases of grass sickness occurring from the year 2000 onwards. The scheme is run by the Animal Health Trust, in collaboration with the Equine Grass Sickness Fund, the University of Edinburgh and the University of Liverpool, following funding from The Horse Trust.  (The Equine Grass Sickness Fund are a dedicated charity, raising funds to tackle the disease.) Present research seems to suggest that toxin production from the bacterium Clostridium botulinum type C may be involved.

Clostridium botulinum is a soil-borne bacterium, which may be better known for producing clinical signs of botulism. Research has suggested that Clostridium botulinum may cause grass sickness when the spores of are ingested and produce their toxin locally within the intestine.  It has been discovered that the concentration of this toxin is high in the intestine of acute cases and that horses with low levels of antibody to the bacteria and its toxin are at increased risk from the disease.

The incidence of grass sickness in Great Britain is higher than in any other part of the world.  It can be found in most areas of England, Wales and Scotland with some areas being more affected than others.  For some reason eastern counties seem to be particularly at risk.  There have also been reported incidents in several other countries.  It is well known in northern Europe, although for some reason there seem to have been fewer cases in France.  It has also been seen in Ireland and North America.  There have been no confirmed incidents in Africa, Australia or Asia but an apparently identical illness known as mal seco (dry sickness) can be found in Argentina, the Falklands, Colombia and Chile.

All breeds seem to be equally susceptible and cases have even been seen among captive zebra and Przewalski’s horse.  In the early 1990s an almost identical disease was spotted in hares, some of which had been living in pastures where horses had been diagnosed with the illness.  Shortly after this it was discovered that the disease also affects wild and domestic rabbits, however there is no evidence that it can be passed from one species to the other.  Dogs and cats can also develop a similar disease but there is no human equivalent.

Any horse from the age of 4 months to over 20 years old can get grass sickness however it is most common in animals from 2-7 years old, and particularly in those aged 3-4 years.  It has been suggested that the lower incidence in older horses, and the fact that some horses in a group survive even though others have succumbed, could be due to the ability of some animals to develop a degree of resistance.

Cases can occur at any time of the year however there is an increase between April and July with a peak in May.  In some years a second, smaller, peak occurs in the autumn or winter months.  In Scotland the lowest incidence is in August which suggests that there might be a weather associated effect.

Grass sickness, unsurprisingly, is strongly associated with grazing, however there have been a small number of cases in animals who have had no access to pasture.  In these rare cases, hay has been blamed for the disease.  Most incidents have been in horses who have been at grass full-time, or at least for all of the day, however it has also occurred in horses who only have a few minutes’ access each day.  Feeding of concentrates as a supplement to horses’ diet does not seem to have any protective effect however in one study, giving hay seemed to reduce the risk.

It can be common for only one horse in a group to be affected at a time but it has also been known for ‘outbreaks’ to occur where several cases appear over a period of a few weeks.  Certain areas, or even particular fields have been associated with grass sickness cases, and it seems that animals which have been on affected premises for less than 2 months (have newly joined the herd) are more likely to develop the disease. (http://www.grasssickness.org.uk/advice/grass-sickness-in-horses/)

No clear connection has been found between type of pasture and number of incidents however recent evidence suggests that high nitrogen content of the soil, and soil disturbance, could be high risk factors.  While it was previously thought that grass sickness was more common in pastures with a high clover content, recent studies indicate that it can also occur on pastures with no clover. Thus clover is not the sole cause of the disease, and at worst may be a trigger for a bacterium such as Clostridium botulinum.

Other possible risk factors include having high numbers of horses grazing together, mechanised methods of poo-picking and the presence of domesticated birds on the fields.  Stress also appears to leave horses more susceptible to contracting the disease.  It has been discovered that many of the animals who have become ill have had a history of recent stress including recent purchase, mixing with strange horses, travelling a long distance, breaking and castration. Animals in good to fat condition also appear to be more likely to get grass sickness.

Some horse owners believe that weather conditions play a part in the disease.  In a survey of weather conditions in the two weeks preceding multiple-case outbreaks, it was found that cool, dry weather with a temperature between 7 and 11°C was recorded in a statistically significant number of instances. This may partly explain the higher incidence of the disease in the eastern side of Britain where such conditions are more prevalent.

Results of two surveys suggest that the risk of developing grass sickness is slightly higher in horses which are wormed more frequently with Ivermectin based dewormers.  However as the consequences of not worming can be very serious or even fatal it is not advisable to stop worming altogether.  Other wormers could be considered and alternative methods of worm control such as field clearing and worm counts used alongside to create a more effective regime. There is also no indication that wormers themselves contain the toxin that causes grass sickness.

Despite almost one hundred years of investigation the cause of grass sickness is still unknown.  Many possibilities have been explored including poisonous plants, chemicals, bacteria, viruses, insects and metabolic upsets.  Horse owners often feel that a mineral or vitamin deficiency could be to blame.  To date no definite link has been proven although selenium deficiency, which results in reduced levels of protective antioxidants in the body, may have some role to play.  Grass sickness does not appear to be contagious and the type of damage to the body seems to suggest some form of neurotoxin is likely to be the cause.  This is why Clostridium botulinum is the current favourite.

Treatment should not be considered for horses suffering the acute or subacute forms of the disease as both are fatal and the horses’ suffering should not be prolonged.  However, in chronic cases, if the animals are not in much pain, can still eat at least a small amount and are still interested in life, treatment can be attempted.  This is not the case for all chronic cases and so the opinion of an experienced vet should be sought.

Treatment of chronic cases involves provision of palatable, easily swallowed food, for example chopped vegetables, grass and high energy concentrates soaked in molasses. It is essential that high energy foods are consumed as chronic cases fed roughages and succulents alone will invariably die. Nursing is also vital with the patients requiring constant stimulation by human contact, frequent grooming to prevent them becoming scurfy and sticky with sweat and, in some cases, rugging which has been found to reduce sweating and prevent hypothermia.

Previously it was believed that horses never made a full recovery after grass sickness however a follow-up study has shown that 41% of the recovered cases were back to work including hunting, racing, and eventing.  33% were being hacked, preparing for competitive work or being used for breeding and the other 26% (the more recent cases) were still gaining weight and recovering at the time of the survey. None of the survivors were described as being of no use. This represents a major improvement in the prognosis for such cases compared with the situation before the late 1980s.

Without a proven cause for this disease it is difficult to give advice around prevention. If certain fields are ‘bad’ for the disease, they can be grazed by other stock, especially in spring and summer. If a case occurs amongst a group of horses, it is probably best to move the others out of that field provided this does not involve too much stress associated with transportation or mixing with strange horses.

References