Sunday, December 30, 2012
Practitioner in Residence asking for advice
I am very excited to have been chosen as the Practitioner in Residence at Melbourne Vet School for 4 months in 2013. My brief is to help prepare final year vet students for life outside vet school. I would really appreciate input from young colleagues on what they wish they were better prepared for when they left vet school (not technical skills, but life skills).
Saturday, December 29, 2012
A day in the life of a Vet
19 October 2003
Is he mentally alert? Yes, but he seems a little distressed.
Did he sleep inside last night? Yes, he slept on my bed.
Can he move his legs? Yes, but just a little.
Is he in pain? I don’t know.
I can see him now. Bring him to the surgery, I’ll meet you there.
Oh no, we don’t want to pay extra. We just wanted to know what time you open today.
I continue cleaning Minx’s ears. She has managed to stay asleep through all the pandemonium.
As I grow older, I often realize that my father was right. He said that I should be a pharmacist instead of a vet. Then I balked at the thought of spending my life between 4 walls, never getting my hands dirty. Rural veterinary practice was all I was interested in. I was going to rush about the countryside, saving lives and being eternally appreciated, not to mention well paid.
I worked the past weekend. Saturday morning at least was civilised and the rest of the afternoon was busy, but manageable. We even managed to anaesthetise and examine a raucous sulphur crested cockatoo without anyone being hurt - including the bird. But then the sun set, the moon came out and the madness began. The first caller had a dog with bloat. Now this is a life-threatening condition in dogs where minutes can make a difference. I rushed about to make sure I had everything ready for emergency treatment and surgery, and ensured that the after-hours nurse’s phone number was next to the phone. Then the wait began. The estimated time of arrival was exceeded by nearly 40 minutes.
When the dog finally arrived, it was soon apparent, that although he was seriously ill, this was not an acute stomach torsion. After some careful questioning, the owner’s claim, that his dog was fine until 24 hours ago, when it refused to eat, was replaced by the admission that his wife had noticed that the dog was unwell a month ago. Some emergency! However, the dog was quite sick and with the owner’s help, I managed to carry him to a table and set up a drip. Just when the dog was finally stable and settled and the owner appeased that the dog would not benefit from immediate emergency surgery, the phone rang again. “Doctor, my cat’s stomach just burst open”. It is late. I am not thinking clearly. My tired mind conjures up images of the fireworks at the Strand. I see a cat fired up into the sky, clawing frantically at the night sky. It explodes in a star-burst of red entrails, silhouetting a flying fox against the smoke. I collect myself, suppress a giggle, and ask with measured voice “What exactly happened? Did the skin break open?” “Yes, she was bitten by a dog a month ago, and there was a big lump. Now it has burst and there are guts poking out.” OK, this one does sound like a real emergency. “Bring her in right away!” I set up for surgery again. When the cat arrives, I find that she is called Smoky. There is a fair sized lesion on her belly where necrotic skin has sloughed off and an abscess has opened, but thank goodness, it is only through the skin. Some necrotic tissue and subcutaneous fat protrude from the lesion, but Smoky should survive the night. Her name is placed on Sunday’s lengthening surgery list. Meanwhile she goes onto a drip, pain relief and antibiotic. I clear away the surgical equipment.
The phone rings again. “We bathed our dog today and now her bottom is itchy. I think it is her anal glands”.”OK, you can bring her in, but there is an extra charge after hours”. Silence on the other end of the line, then “Umm, but do you think it is an emergency?” “Well no, it does not sound like one, she may be uncomfortable, but she should live, but you obviously think it is an emergency. Would you like me to see her tonight?” “Oh, no, we’ll see how she goes and call you tomorrow”. Sigh...
Then I went to watch World Cup rugby with the Annandale Afrikaners. The Springbucks played their hearts out and lost. I know the feeling, believe me. I get to bed just after midnight. At 6 am I am roused from a deep sleep by the insistent ringing of the phone. “My little dog is a patient of yours and you vaccinated him 6 weeks ago. Now he is paralysed.” It takes a few seconds before I even register what language is spoken at that time of morning. The innuendo is lost on me. Slowly my brain starts to function.
Is he breathing normally? Yes, but he groans a little.Is he mentally alert? Yes, but he seems a little distressed.
Did he sleep inside last night? Yes, he slept on my bed.
Can he move his legs? Yes, but just a little.
Is he in pain? I don’t know.
I can see him now. Bring him to the surgery, I’ll meet you there.
Oh no, we don’t want to pay extra. We just wanted to know what time you open today.
I am awake now anyway, so get up and make coffee. Later, at the surgery, the dog comes running into the waiting room on all 4 his paralyzed little legs. When I try to take his temperature, he spins around and nearly amputates my fingers. No neurological deficits there. He is obviously not an early riser either.
The day is busy. It takes careful planning to ensure I’ll have enough time to lance Lucky’s abscess, fix the burst cat, X ray the bloated dog and clean Minx’s sore ears with consults coming in as well. By 2 pm everything is on track. Then Susan bursts in though the door. Joan, can you come and help, please? A client who is a wildlife carer has a big trunk on the back of her truck. Inside this Pandora’s box is a hissing goanna. He thrashes his hard, rough, incredibly strong tail from side to side. I stare at him, mesmerised. Lana, the wildlife carer clambers onto the back of the truck in her miniskirt. The next moment she loses control of the situation and the goanna. He half leaps/clambers over me and rushes down the street with his ungainly side to side gait, but he is injured, and not as fast as he might be. Lana, myself and Susan, the vet nurse from Arizona, are in hot pursuit. He makes a stand, raising himself up on his hind feet. As a warning he blows up his throat and pokes out his very long eerily blue incredibly creepy tongue. Compared to this monster, a leguan is a thing of beauty and a joy forever.
The posse has now followed him into an empty lot between the road and a deep dirty ditch. If he goes down there, I’ll be blowed if I’ll follow him into the mud. Time for lateral thinking. When we were little kids, there were many leguans in Cradock. The local; people believed that they sucked your brains out with their forked tongues while you slept. They used to catch them and sell them to witchdoctors for muti (medicine). They would prop open hessian bags and herd them to the opening. The leguans went willingly, probably believing that they have found a safe hiding place. I send Susan to the surgery to look for a suitable bag. She returns with a black plastic body bag. It rattles in the wind and lifts off the ground and bears absolutely no resemblance to a cave whatsoever. The goanna makes a last stand, hissing furiously, showing his creepy blue tongue, snapping at us, and slamming his rasp like muscular tail from side to side with deadly intent. Then Lana goes in for the kill. With the aid of a net, she half grabs him. I have no choice but to help. We subdue him and carry him down the street and into the surgery. Pop him in a cage, says I, we’ll deal with him later. No way, says Lana. I am not letting him go. However, I have a commitment to finish my booked surgeries first. I will give him a tranquiliser in the meantime. If that does not work, Lana will have to hold on. She agrees, looking very dishevelled and determined.
What in the whatsisname do you use to tranquilise a goanna? There are hundreds of books in the office, but I find nothing on anaesthetising goannas. . Finally I find a reference to ketamine. The dose range given is 10 to 100mg per kg. What a range! I do not want to kill him, stressed out as he must be, and opt for 20mg per kg. This has no effect. I add 40 mg per kg. He settles down slightly. I tell Susan to give him isofluorane by mask. In the meantime I have anaesthetised Minx- a beloved 8 year old Border Collie. She is breathing too slowly and her colour is too pale. I ask vet nurse Lachlea to speed up the fluid infusion and turn down the gas. Susan panics. The goanna has stopped breathing. He is lying on his back, looking pretty dead. I roll him onto his belly. His tail flicks dangerously. We change the gas concentration and tell Lana to hold on, but keep him on his belly.
Petra gets some paper towel. She screams. A giant spider just scuttled out of the towel holder. He hides behind the endotracheal tubes, with only his long legs sticking out. The radio on the shelf belts out pop music. It suddenly penetrates my consciousness. Kill it, I scream. They all leap on the spider. No, leave him alone! Kill the radio, before it drives me insane.
I continue cleaning Minx’s ears. She has managed to stay asleep through all the pandemonium.
Finally I can get back to the goanna, who is still wriggling furiously. Iso up to maximum settles him. Lachlea is tasked to make sure that he keeps on breathing. We suture the gashes on his body and inject antibiotic. What do you call a reptile specialist, someone asks. It’s easy, I say - a madman. We put him back in the hot trunk on the hot truck before he is fully awake, urging Lana to get him to a cool , comfortable cage before he cooks.
I still have paperwork to do, and X rays to do and the first of the afternoon consults are already waiting. I phone the bloated dog’s owner about tomorrow’s plans. He has not paid anything yet. I tell him the treatment plan and estimated costs. He explodes. “I always pay your practice. I have 67 dogs, I have been a client for years, why are you talking to me about money? Just fix my dog.” I try to explain that money or not, said dog may not be fixable. I arrange a meeting and second opinion with the boss, whom he claims to know very well, for Monday, to discuss the case before we proceed with surgery. It is called pass the buck. Next I treat a sick cat. The owner waits until I am done, then informs me that she left her wallet at home. I cannot help but wonder if anyone ever does that to a pharmacist.
The last client of the day brings in his dog that swung from a fence by her hind leg and shattered the bone. He has been to another vet and the leg is splinted quite effectively in my opinion. Why is he here? Because the other vet expected payment and he is not happy. I pass the buck again. I only work here. To pay my salary, my boss likes to be paid by people like you, mate. At least we have a credit agreement arrangement to help genuine cases. When, oh when will pet’s health insurance finally take off?
Poem
The poet goes out on a limb
weaves magic with words
the truth to disguise;
but truth will out and
the ice underneath is thin.
weaves magic with words
the truth to disguise;
but truth will out and
the ice underneath is thin.
A lost lurcher.
While I was working at a small animal practice in England, a kind Samaritan dumped a lost lurcher (type of rough looking greyhound) with a broken leg on us one Wednesday. I phoned the RSPCA who referred us to the town council. On Thursday a man from council phoned back, asking us to go ahead with the required surgery. I operated on Friday - a long and difficult bone plating. With much perspiration and perseverance I achieved a pretty good fix. I did not even mind missing lunch for the 5th day that week, I felt such a warm glow of achievement.
At some point during the surgery a man arrived to empty the freezer where dead bodies are kept. We were surprised to see him as he normally arrived on a Monday before we start work. He told us there had been a change in schedule. So he collected seven dead fish, two dead budgies and a rotten rabbit and left with his loot. (We were attached to a pet superstore). Watch this space.....
The dog woke up and had a hearty meal a few hours later. I took him out to sniff the trees before closing time, but he preferred to flood the surgery floor instead. After we left, his dinner passed through his intestinal tract as all good dinners do and he spent all night smearing it across his kennel walls. The next morning I took him out for a walk, leaving the poor nurse to deal with the mess. The dog, whom I had named Pula (Setswana for blessing), because we would be blessed if anyone actually paid for his treatment, sniffed the grass, greeted the passers-by, and had a large bowel motion just after we returned to the surgery.
There was work to be done, so Pula was returned to his kennel against his wishes. He vocalized his objections very loudly. The store manager complained that his customers would complain. Every spare minute we had, we tried to console Pula. We had several walks, pleading sessions and even a few firm requests to BE QUIET! Most of the day we could not hear ourselves think. Sunday was much the same. By Monday our nerves were sufficiently frayed to resort to the use of tranquilisers for the dog - though we needed it more, especially when another freezer man arrived and declared that the Friday freezer man was a fraud. A body snatcher on the loose?
By Tuesday the pet store staff were beginning to take an interest in Pula and started taking him outside during their staggered tea breaks. The dog was delighted with his new friends and admirers and we had peace at last. When they brought him in on Tuesday evening, he was gambolling like a calf, ecstatic with all the attention. The following morning Pula was raring to go out again. We did our customary walk to the bushes resulting in Pula soiling the surgery floor on our return as usual. Then he stood quietly to have his temperature taken and bandage changed before trotting expectantly to the cupboard where his tablets are kept. He had grown accustomed to the fact that he regularly received them with a tasty snack. The only thing we could not teach him was how to be quiet in his kennel. I was delighted when the shop staff came and asked if they could take him out again. When I checked on him later he was surrounded by friends and well wishers - even the staff from the shop next door were visiting him regularly.
Late Wednesday morning the council's dog warden arrived - being towed in by a large woman from a dog sanctuary. She introduced herself. As she is named after a bodypart, let's call her Mrs Bodypart. She sailed into my consulting room uninvited, demanding to know everything about the dog's treatment. I explained that due to the initial open fracture and severe bruising, the wound was still oozing and the bandage would have to be changed every 48 hours. When I asked whether she would be comfortable doing this, she declared huffily that she had been "doing this" for 35 years. Then she said it was not normal to change a bandage so frequently, she had never come across it in 35 years of dealing with dogs and implied that we were just doing it for the money. I patiently tried to explain that no, an open fracture accompanied by severe bruising was not normal, but given the abnormal state of affairs, we had no other choice but to change the bandage frequently. I did not tell her that my salary remained the same, whether I did a lot of work or a little work, and given the choice I'd rather do a little work, but this dog was my friend in a foreign land, and hey, the way he greets me in the morning is payment enough.
Meanwhile Mrs Bodypart was in full sail and demanded to be shown said dog, who happened to be visiting the loading bay. As everyone was momentarily occupied they had chained him to a pallet in full view of where they were working. Pula wagged his tail as he heard my voice. The next moment Mrs B went ballistic about the incredible cruelty and irresponsibility of chaining this poor creature up where he is not receiving any veterinary attention, being watched over by ignorant members of the public. I tried to explain that they were not ignorant, nor members of the public and were very caring. The dog was happy, we weren't ignoring him and anyway if he was indoors he was so noisy that we had to tranquilise him. Hoo Boy, I should not have said that! Now she was off on a new tangent. I tried to defuse the situation by asking whether she would be able to bring the dog in on Friday so that I could demonstrate how I wanted the bandage change done. No, she said, she was not bringing the dog back to this terrible place where he was chained up to pallets. She wanted to see the bandage change now. I tried to explain that doing it the second time in one day would incur unnecessary expense. More ammunition for Bodypart: "This is what it is all about, money....... etc. "
By now the "ignorant members of the public" were gathering around, jaws agape. I was afraid a fist fight might ensue if Bodypart kept hurling abuse, so I managed to head her off to the relative privacy of my consulting room. As a precaution, I called a nurse in as a witness and demonstrated the bandage change. This activity calmed me a little and I was able to take a step back and let it all wash over me. I thought about becoming a ferry pilot and wondered if having an engine failure over the North Atlantic could be remotely as stressful as this. Meanwhile the nurse, who in addition to her nursing qualification, had 5 years vet nursing experience and a basic law degree, tried to placate Mrs. B. When I got my engine restarted after a nice adrenalin rush off the coast of Newfoundland and returned to the present, Mrs B was telling the nurse how young and stupid she was and that she knew nothing about anything, let alone dogs.
This enraged me, and as I my imaginary near death experience over the ocean had given me courage, I said as evenly as I could: "I appreciate your concern for the dog, but I am very offended by your attitude. We have all done our best to treat him and make him comfortable and happy and we do not deserve such treatment."
She left amidst threats of reporting us to the company and anyone else who would listen.
We have thought long and hard on how to resolve this problem and have come up with the ultimate solution. We'll lure her in on Friday when Bodysnatcher comes ......
Rhipicentor nuttali found on African wildcat
An African wild cat, Felis lybica was found dead on the road near Rondegat, Clanwilliam on 14 February 2011. It had been hit by a vehicle. The cat, a mature adult male, was in reasonable condition. The cause of death was trauma. There were no other macroscopic lesions on post mortem. Five adult ticks, identified as Rhipicentor nuttali, were found attached to the cat's neck - one engorged female, about 15 mm x 10 mm in size, one female that had not fed, one partially engorged female and two males.
An identifying feature of these ticks were paired hooks near the attachment of the front legs on the ventral aspect, and a single hook near the hind leg attachment .
The genus Rhipicentor has only two species worldwide, R. nuttali and R. bicornis and both occur only in Africa. R. nuttali is widespread in South Africa. Larvae and nymphs have only been found on elephant shrews. The Cape elephant shrew, Elephantulus edwardii occurs in the Clanwilliam district. Fourie et al found that nymphs were most numerous between March and Sept,and larvae between May and October. In the lab the life cycle takes about 214 days to complete. It is believed that in the field it is likely to take a year. Adults are mostly found on their preferred hosts: domestic dogs, leopards ( Panthera pardus) and South African hedgehogs, (Atelerix frontalis) in late summer.
These ticks have been seen (described) on dogs, cats, leopard, lion, hedgehogs, porcupines. Immatures are found on elephant shrew.
Dr. Gertrude Theiler found these ticks on dogs in the Clanwilliam district in 1962. They have not been described on Felis lybica before. They may cause paralysis in dogs.
Family Ixodidae. Resemble Dermacentor ticks.
References
Fourie LJ, Horak IG, Kok DJ, van Zyl W 2002 Hosts, seasonal ocurrence and life cycle of Rhipicentor nuttali (Acari:Ixodidae). Onderstepoort J Vet Res 69:177-87
Fourie LJ, Horak IG, Woodall PF 2005 Elephant shrews as hosts of immature ixodid ticks. Onderstepoort J vet Res 72:293-301
An identifying feature of these ticks were paired hooks near the attachment of the front legs on the ventral aspect, and a single hook near the hind leg attachment .
The genus Rhipicentor has only two species worldwide, R. nuttali and R. bicornis and both occur only in Africa. R. nuttali is widespread in South Africa. Larvae and nymphs have only been found on elephant shrews. The Cape elephant shrew, Elephantulus edwardii occurs in the Clanwilliam district. Fourie et al found that nymphs were most numerous between March and Sept,and larvae between May and October. In the lab the life cycle takes about 214 days to complete. It is believed that in the field it is likely to take a year. Adults are mostly found on their preferred hosts: domestic dogs, leopards ( Panthera pardus) and South African hedgehogs, (Atelerix frontalis) in late summer.
These ticks have been seen (described) on dogs, cats, leopard, lion, hedgehogs, porcupines. Immatures are found on elephant shrew.
Dr. Gertrude Theiler found these ticks on dogs in the Clanwilliam district in 1962. They have not been described on Felis lybica before. They may cause paralysis in dogs.
Family Ixodidae. Resemble Dermacentor ticks.
References
Fourie LJ, Horak IG, Kok DJ, van Zyl W 2002 Hosts, seasonal ocurrence and life cycle of Rhipicentor nuttali (Acari:Ixodidae). Onderstepoort J Vet Res 69:177-87
Fourie LJ, Horak IG, Woodall PF 2005 Elephant shrews as hosts of immature ixodid ticks. Onderstepoort J vet Res 72:293-301
Lymphocytes - short note
LYMPHOCYTES
Unlike granulocytes and monocytes which move unidirectionally from bone marrow to blood to tissue, blood lymphocytes recirculate. The pattern is blood to lymph node to lymph and back to blood. Transit time in the blood during each circuit is estimated to be 8 to 12 hours. Recirculating lymphocytes are long-lived cells which survive for months to years.
Function
Lymphocytes are the cells of the specific immune system. B lymphocytes differentiate into plasma cells which produce antibodies (humoral immunity).
T lymphocytes are responsible for cellular immunity through the formation and release of molecules known collectively as cytokines.
Peripheral blood lymphocytes serve as the memory cells of the immune system. As they recirculate, lymphocytes monitor for the presence of antigens to which they have been previously sensitized. When lymphocytes activated by such contact enter lymphnodes, they can initiate both the cellular and humoral immune response through selective clonal expansion.
Scabies in Humans
Scabies is a chronic skin disease caused by the mite Sarcoptes scabiei.
The mite lives in the superficial layers of the skin where it eats keratinized skin cells. As it eats, it makes tunnels. The mites are unable to live more than three to four days away from the host.
Symptoms:
Typical Scabies in humans presents as itchy papules, symmetrically distributed, mostly on the body and limbs. Vesicles and nodules are also seen. The nodules are usually inflamed and very irritating. In infants lesions commonly occur on the hands and feet. This condition can be chronic. Infectivity is low as there are only about 10 mites per gram of skin.
Occasionally secondary bacterial infection may obscure underlying scabies.
Scabies can also be transient. The reaction is mostly allergic, mite numbers are low, (10 mites per gram of skin) and the mites do not reproduce. It disappears when the person is separated from the source of the scabies.
Some people may develop Crusted Scabies. The superficial skin layer builds up and thickens. It is more likely to happen in immunocompromised individuals, such as people with HIV, leprosy, Down's syndrome, certain cancers and also some ethnic groups, such as Aboriginals in Australia.
In Crusted Scabies, there are to 2000 mites per gram of skin. It is very infectious. Where patients have been treated in hospital wards, mites were found on walls and curtains. The crusts are thick layers of keratinized skin mixed with mites, mite eggs, shed mite skins, mite faeces and bacteria.
Crusted scabies can spread all over the body, or be localized to certain areas. It is not necessarily symmetrical.
If the crusts crack, raw skin is exposed and the patient is prone to infection and septicaemia.
Diagnosis:
Diagnosis of scabies by identification of the mite can be difficult.If affected skin is coloured with a felt tip pen, and the ink then wiped off the skin surface, the tunnels in the skin will often retain the ink and be visible. The mites, if found, can be seen and identified under a microcope. Your doctor will apply some saline or mineral oil to the skin and gently scrape the superficial layers with a scalpel blade.
Diagnosis of crusted scabies by lab confirmation is easier, because of high mite numbers.
Treatment:
Typical scabies is readily cured with correct treatment.
A 5% permethrin cream (Elimite or Nix) is applied from head to foot soles and left on for 10 to 14 hours (usually overnight). Do not apply to face, eyes, or mucous membranes. The following morning the ointment is washed off by showering. The treatment is repeated after 1 week.
Ivermectin tablets (Stromectol) are very effective, but need a prescription.
Other scabies medicines are:
1% lindane (Kwell, Scabene)
Malathion 0.5% (Ovide lotion)
Crotamiton (Eurax)
Although Scabies is effectively cured within a day or two of treatment, itching may persist for up to 4 weeks. Antihistamines such as Benadryl may be used to control the itch.
In some cases Scabies is complicated by secondary infection and will require a prescription of antibiotic, eg Bactrim.
Causes of Glucosuria
Glucosuria - causes - Page numbers refer to Sodikoff except where stated otherwise.
Thrall 316, 435, 437
carbohydrate overload
corticosteroid administration
diabetes mellitus Sodikoff: 33, 115, 119, 123, 125, 161, 187,
324, 326, 328. (Thrall 434-435)
embolic nephritis 296
Fanconi’s syndrome 115, 304
feline urologic syndrome 294
lead poisoning 56, 63, 68
nephrotoxicosis 184, 288
nonsteroidal anti-inflammatory drug-induced renal disease 310
renal ischaemia 290
renal tubular defects 44, 115, 306
stress
urinary tract haemorrhage
vit C administration (false positive)
Vit D toxicity 113, 127, 364
Thrall 316, 435, 437
carbohydrate overload
corticosteroid administration
diabetes mellitus Sodikoff: 33, 115, 119, 123, 125, 161, 187,
324, 326, 328. (Thrall 434-435)
embolic nephritis 296
Fanconi’s syndrome 115, 304
feline urologic syndrome 294
lead poisoning 56, 63, 68
nephrotoxicosis 184, 288
nonsteroidal anti-inflammatory drug-induced renal disease 310
renal ischaemia 290
renal tubular defects 44, 115, 306
stress
urinary tract haemorrhage
vit C administration (false positive)
Vit D toxicity 113, 127, 364
Horses are Smart!
Published in Vetmed March 2012
According to E.B. Hanggi, at the Equine Research Foundation, Aptos, California, USA, horses are smarter than we think! They can manage ordinary daily cognitive tasks and mental challenges quite well.
In nature, food and water sources are of inconsistent quality and variable distribution. Their predators change location and habits. At the same time they must deal with interactions in the herd and need to learn and remember the identities and roles of other individuals in the herd.
Life for a domesticated horse is even more bewildering. In addition to dealing with natural situations, they often live in unsuitable environments, need to suppress instinctual behaviours and learn tasks that are not natural behaviours. They also need to co-exist with humans, who from a horses' viewpoint must be very strange indeed.
Research into the nature of cognition and perception in horses is gradually providing some fascinating insights.
Horses learn through habituation throughout their lives. In a new environment, horses are very reactive and pay attention to any stimulus perceived by any of their senses. However, when certain stimuli are insignificant and are repeated regularly, the response diminishes. Habituation is a simple form of learning, but none the less important, as it allows non-vital information to be filtered out subconsciously, enabling the horse to focus on what is significant.
When a horse is particularly sensitive or fearful, either by its nature or through learned experience, it can be desensitized. Rough handling of its ears, or a bit banging against its teeth may make a horse extremely sensitive to being bridled, for example. This leads to head shyness. Such a horse needs to be retrained by approaching its head in increments and retreating when necessary until the horse willingly accepts normal, gentle bridling.
Horses can become habituated and desensitized to almost overwhelming stressors if it is done correctly. A good trainer exposes horses in a positive manner to all sorts of sights, sounds and contacts, for instance by leaving him unrestrained in a safe corral and having humans behaving strangely around him, playing with bouncing beach balls, multicoloured balloons, umbrellas, plastic tarps, pylons, rattles etc. This makes the horse much more capable of handling novel events calmly. If desensitization is not done correctly, it has the potential to make a horse more fearful and sensitive, for instance by removing an alarming stimulus too soon.
Pavlovian conditioning does not only work for dogs.
A horse also learns effortlessly when initially unimportant stimuli or events are regularly coupled with stimuli that initiate some sort of response. This form of conditioning is used by a trainer when he places a word onto a behaviour. The word "trot" would mean nothing to an untrained horse, but if it is regularly paired with the flick of a whip (associated with invoking a flight response or pain) immediately before the horse changes gait on an upward transition, the horse soon learns to respond to the verbal cue, without the use of a whip.
The use of the word "good", when correct behaviour is carried out, followed by a food treat, informs the horse that a food reinforcer is forthcoming.
To many a veterinarians dismay, horses often learn that the sight of a syringe is associated with pain. The unconditioned horse will then attempt to escape if he has not been trained to accept such handling.
Stabled horses will learn to associate certain sounds with feeding - eg doors opening, hay being poured into a bucket, or will respond to visual cues , such as the arrival of the caretaker. They will then display sometimes unwelcome anticipatory behaviours, such as vocalizing, pawing or kicking stall doors. When reinforced, these may become conditioned behaviours. For instance, when a horse, upon hearing grain being poured, starts kicking his door, a person may feed the horse hurriedly in an attempt to get him to settle down. This positively reinforces the undesirable behaviour and if this scenario repeats itself, the horse has effectively trained the human to feed him quickly.
Operant conditioning, in contrast to classic or Pavlovian conditioning, occurs when an animal manipulates its environment to obtain reinforcement, which can be positive, when he receives something he desires, or negative - such as removing something unpleasant. Both types strengthen the relationship between stimulus and sought after response, so that when the same stimulus is given again, there is an increased chance that the horse will repeat the action.
In the early stages of learning the meaning of a new stimulus, the horse may respond randomly and hit upon the desired response by accident. Reinforcement of the response at the correct moment will cause the animal to repeat the behaviour. Horses excel at this type of learning, especially when positive reinforcement is given.
Unfortunately negative reinforcement is most often used in training. Horses are typically trained to perform actions to avoid something aversive. Under saddle they move forward when leg pressure is applied by the rider, on the ground they yield their hindquarters when pressure is applied to the flank, they back up when pressure is applied to the bridge of their nose, and they enter a trailer to avoid whips, or pressure from ropes. A good trainer refines this by reinforcing the correct and ignoring the incorrect. In this way only the slightest pressure will eventually produce the desired response, making the human/horse partnership appear effortless.
Research has been done with respect to the use of positive reinforcement principles to facilitate trailer loading of horses. It is not uncommon for a horse to be reluctant to be loaded onto a trailer. It can be very time consuming and hazardous for horse and handler. A horse may resist by rearing, pulling back, pawing, kicking or even falling over. If the owner gives up and fails to load the horse, such behaviour is reinforced. Traditional loading methods are based on negative reinforcement, often with some punishment for an uncooperative horse as well. Researchers Ferguson and Rosales-Rui found that , with positive reinforcement and target training, horses learned to load willingly and improper behaviours ceased. These effects also generalized to other novel situations. Horses that have learned to load through positive reinforcement do so eagerly, sometimes requiring only a verbal or visual signal, even when unrestrained. Positive reinforcement can also be targeted at lifting feet for hoof care, groundwork, grooming and veterinary handling.
Discrimination learning in horses has been researched since the 1930's. In discrimination tasks, horses must learn that one stimulus, and not another will result in positive reinforcement. That stimulus then begins to control behaviour, so that the horse acts in a specific manner in the presence of one stimulus, but not the other. In one study a specific horse learnt 20 pairs of discriminations. This horse also "learnt to learn" by using a general pattern to more easily solve subsequent tests. After 6 months he had also retained 77.5% of the discriminations. The "learning to learn" phenomenon has been noted in many other studies. It is a worthwhile tool in training. Often horses are restricted to performing only within a particular discipline. Racehorses don't jump; and dressage horses rarely set foot on a trail. These limitations prevent horses from learning about a variety of stimuli and such animals are less able to deal with novel situations. The more positive stimulation a horse experiences, the more readily it learns in new situations. It is also better adjusted in a variety of conditions and environments.
Spatial cues seem to be more readily discriminated by horses than any other stimuli. This is supported by observations made by vigilant horse owners of how well horses find their way around in areas they have only visited infrequently. Horses also react noticeably when objects in their environment are moved. This demonstrates an awareness of spatial surroundings.
The ease with which horses discriminate visual stimuli makes it easier for researchers to study cognition; and also to measure perceptual abilities and therefore equine vision. It has been experimentally demonstrated that a horse's visual acuity is 20/30 on the Snellen scale. (Human 20/20, dogs 20/50).
Experiments regarding colour vision in horses showed that they could discriminate red and blue from gray. Others showed that they could also discriminate between green and yellow. Recent research by Hanggi and Waggoner showed that horses responded to colour in the same manner as some red/green colour blind humans.
A myth that surfaces repeatedly is that horses cannot recognize what they have seen with one eye with the other eye. Anatomical dissections have proven that the horse's two cerebral hemispheres do indeed have a functional pathway to convey information, and a behavioural study proved that they do have inter ocular transfer. This study used multiple two choice discrimination tests with one eye blindfolded. Once the discrimination was learned, the blindfold was placed over the other eye. Horses immediately responded to the same stimulus, clearly demonstrating interocular transfer.
Horses often startle at an object they have seen before when approaching it from a different angle. This can be explained by the fact that the shape of the object appears differently when seen from another perspective. Experiments with different objects demonstrated that recognition of rotated objects was good under some but not all conditions.
With generalization a behaviour previously conditioned to one stimulus, transfers to other similar stimuli. Riding school horses regularly utilize this form of learning when making sense of a large assortment of inexact hand, leg and seat cues from riders of varying skill levels. Dressage horses, in contrast, learn to discriminate highly precise cues from their riders. As a result they go through mechanical motions that rarely enhance cognitive skills. A horse's generalization abilities can be enhanced by incorporating variety into their programs. As social animals, horses are most comfortable in the company of their own kind. Social interactions can facilitate the learning of new behaviour by observing other horses
The cognitive abilities of horses need to be understood to ensure good husbandry and treatment.
It is as harmful to confine a thinking animal to a dark, dusty stable with little or no social interaction as it is to provide inadequate feed or use abusive training methods. It is certainly in the best interests of both horses and handlers to better understand the scope of equine thinking, and enrich horses' environment. In the not too distant past little consideration was given to why horses behaved like they did. This limited the provision of adequate care and welfare. More recently research into equine cognition and perception has made noteworthy advances. This has led to a greater interest in training methodology and management. Even so, we are still a long way from fully understanding what it is to be a horse. More studies are needed to fully understand this remarkable animal and provide it with the best environment and training for its and our needs.
According to E.B. Hanggi, at the Equine Research Foundation, Aptos, California, USA, horses are smarter than we think! They can manage ordinary daily cognitive tasks and mental challenges quite well.
In nature, food and water sources are of inconsistent quality and variable distribution. Their predators change location and habits. At the same time they must deal with interactions in the herd and need to learn and remember the identities and roles of other individuals in the herd.
Life for a domesticated horse is even more bewildering. In addition to dealing with natural situations, they often live in unsuitable environments, need to suppress instinctual behaviours and learn tasks that are not natural behaviours. They also need to co-exist with humans, who from a horses' viewpoint must be very strange indeed.
Research into the nature of cognition and perception in horses is gradually providing some fascinating insights.
Horses learn through habituation throughout their lives. In a new environment, horses are very reactive and pay attention to any stimulus perceived by any of their senses. However, when certain stimuli are insignificant and are repeated regularly, the response diminishes. Habituation is a simple form of learning, but none the less important, as it allows non-vital information to be filtered out subconsciously, enabling the horse to focus on what is significant.
When a horse is particularly sensitive or fearful, either by its nature or through learned experience, it can be desensitized. Rough handling of its ears, or a bit banging against its teeth may make a horse extremely sensitive to being bridled, for example. This leads to head shyness. Such a horse needs to be retrained by approaching its head in increments and retreating when necessary until the horse willingly accepts normal, gentle bridling.
Horses can become habituated and desensitized to almost overwhelming stressors if it is done correctly. A good trainer exposes horses in a positive manner to all sorts of sights, sounds and contacts, for instance by leaving him unrestrained in a safe corral and having humans behaving strangely around him, playing with bouncing beach balls, multicoloured balloons, umbrellas, plastic tarps, pylons, rattles etc. This makes the horse much more capable of handling novel events calmly. If desensitization is not done correctly, it has the potential to make a horse more fearful and sensitive, for instance by removing an alarming stimulus too soon.
Pavlovian conditioning does not only work for dogs.
A horse also learns effortlessly when initially unimportant stimuli or events are regularly coupled with stimuli that initiate some sort of response. This form of conditioning is used by a trainer when he places a word onto a behaviour. The word "trot" would mean nothing to an untrained horse, but if it is regularly paired with the flick of a whip (associated with invoking a flight response or pain) immediately before the horse changes gait on an upward transition, the horse soon learns to respond to the verbal cue, without the use of a whip.
The use of the word "good", when correct behaviour is carried out, followed by a food treat, informs the horse that a food reinforcer is forthcoming.
To many a veterinarians dismay, horses often learn that the sight of a syringe is associated with pain. The unconditioned horse will then attempt to escape if he has not been trained to accept such handling.
Stabled horses will learn to associate certain sounds with feeding - eg doors opening, hay being poured into a bucket, or will respond to visual cues , such as the arrival of the caretaker. They will then display sometimes unwelcome anticipatory behaviours, such as vocalizing, pawing or kicking stall doors. When reinforced, these may become conditioned behaviours. For instance, when a horse, upon hearing grain being poured, starts kicking his door, a person may feed the horse hurriedly in an attempt to get him to settle down. This positively reinforces the undesirable behaviour and if this scenario repeats itself, the horse has effectively trained the human to feed him quickly.
Operant conditioning, in contrast to classic or Pavlovian conditioning, occurs when an animal manipulates its environment to obtain reinforcement, which can be positive, when he receives something he desires, or negative - such as removing something unpleasant. Both types strengthen the relationship between stimulus and sought after response, so that when the same stimulus is given again, there is an increased chance that the horse will repeat the action.
In the early stages of learning the meaning of a new stimulus, the horse may respond randomly and hit upon the desired response by accident. Reinforcement of the response at the correct moment will cause the animal to repeat the behaviour. Horses excel at this type of learning, especially when positive reinforcement is given.
Unfortunately negative reinforcement is most often used in training. Horses are typically trained to perform actions to avoid something aversive. Under saddle they move forward when leg pressure is applied by the rider, on the ground they yield their hindquarters when pressure is applied to the flank, they back up when pressure is applied to the bridge of their nose, and they enter a trailer to avoid whips, or pressure from ropes. A good trainer refines this by reinforcing the correct and ignoring the incorrect. In this way only the slightest pressure will eventually produce the desired response, making the human/horse partnership appear effortless.
Research has been done with respect to the use of positive reinforcement principles to facilitate trailer loading of horses. It is not uncommon for a horse to be reluctant to be loaded onto a trailer. It can be very time consuming and hazardous for horse and handler. A horse may resist by rearing, pulling back, pawing, kicking or even falling over. If the owner gives up and fails to load the horse, such behaviour is reinforced. Traditional loading methods are based on negative reinforcement, often with some punishment for an uncooperative horse as well. Researchers Ferguson and Rosales-Rui found that , with positive reinforcement and target training, horses learned to load willingly and improper behaviours ceased. These effects also generalized to other novel situations. Horses that have learned to load through positive reinforcement do so eagerly, sometimes requiring only a verbal or visual signal, even when unrestrained. Positive reinforcement can also be targeted at lifting feet for hoof care, groundwork, grooming and veterinary handling.
Discrimination learning in horses has been researched since the 1930's. In discrimination tasks, horses must learn that one stimulus, and not another will result in positive reinforcement. That stimulus then begins to control behaviour, so that the horse acts in a specific manner in the presence of one stimulus, but not the other. In one study a specific horse learnt 20 pairs of discriminations. This horse also "learnt to learn" by using a general pattern to more easily solve subsequent tests. After 6 months he had also retained 77.5% of the discriminations. The "learning to learn" phenomenon has been noted in many other studies. It is a worthwhile tool in training. Often horses are restricted to performing only within a particular discipline. Racehorses don't jump; and dressage horses rarely set foot on a trail. These limitations prevent horses from learning about a variety of stimuli and such animals are less able to deal with novel situations. The more positive stimulation a horse experiences, the more readily it learns in new situations. It is also better adjusted in a variety of conditions and environments.
Spatial cues seem to be more readily discriminated by horses than any other stimuli. This is supported by observations made by vigilant horse owners of how well horses find their way around in areas they have only visited infrequently. Horses also react noticeably when objects in their environment are moved. This demonstrates an awareness of spatial surroundings.
The ease with which horses discriminate visual stimuli makes it easier for researchers to study cognition; and also to measure perceptual abilities and therefore equine vision. It has been experimentally demonstrated that a horse's visual acuity is 20/30 on the Snellen scale. (Human 20/20, dogs 20/50).
Experiments regarding colour vision in horses showed that they could discriminate red and blue from gray. Others showed that they could also discriminate between green and yellow. Recent research by Hanggi and Waggoner showed that horses responded to colour in the same manner as some red/green colour blind humans.
A myth that surfaces repeatedly is that horses cannot recognize what they have seen with one eye with the other eye. Anatomical dissections have proven that the horse's two cerebral hemispheres do indeed have a functional pathway to convey information, and a behavioural study proved that they do have inter ocular transfer. This study used multiple two choice discrimination tests with one eye blindfolded. Once the discrimination was learned, the blindfold was placed over the other eye. Horses immediately responded to the same stimulus, clearly demonstrating interocular transfer.
Horses often startle at an object they have seen before when approaching it from a different angle. This can be explained by the fact that the shape of the object appears differently when seen from another perspective. Experiments with different objects demonstrated that recognition of rotated objects was good under some but not all conditions.
With generalization a behaviour previously conditioned to one stimulus, transfers to other similar stimuli. Riding school horses regularly utilize this form of learning when making sense of a large assortment of inexact hand, leg and seat cues from riders of varying skill levels. Dressage horses, in contrast, learn to discriminate highly precise cues from their riders. As a result they go through mechanical motions that rarely enhance cognitive skills. A horse's generalization abilities can be enhanced by incorporating variety into their programs. As social animals, horses are most comfortable in the company of their own kind. Social interactions can facilitate the learning of new behaviour by observing other horses
The cognitive abilities of horses need to be understood to ensure good husbandry and treatment.
It is as harmful to confine a thinking animal to a dark, dusty stable with little or no social interaction as it is to provide inadequate feed or use abusive training methods. It is certainly in the best interests of both horses and handlers to better understand the scope of equine thinking, and enrich horses' environment. In the not too distant past little consideration was given to why horses behaved like they did. This limited the provision of adequate care and welfare. More recently research into equine cognition and perception has made noteworthy advances. This has led to a greater interest in training methodology and management. Even so, we are still a long way from fully understanding what it is to be a horse. More studies are needed to fully understand this remarkable animal and provide it with the best environment and training for its and our needs.
Blue-tongue in Sheep
Wild ruminants are infected by the virus, but do not show symptoms. In Africa, some large carnivores have antibodies to bluetongue. The virus was first recognised in South Africa and has since been found in Africa, Europe, the Middle East, Australia, the South Pacific, North and South America and parts of Asia. Geographic distribution is limited by the distribution of the Culicoides midges. Twenty four serotypes have been identified world-wide. Serotypes identified by the Onderstepoort Veterinary Institute in recent years are as follows:
a). 2008 and 2009 = 1;3;4;6;8;16;18;24
b). 2009 and 2010 = 1;3;4;6
The main vectors are various species of biting Culicoides midges. Ticks or sheep keds may be mechanical vectors and the disease may be spread on veterinary equipment. Cattle are the preferred hosts of many Culicoides species. They develop a prolonged viraemia and often amplify the virus, therefore playing a major role in transmission of the virus.
Infected animals remain infectious to the insect vector for several weeks. The incubation period in sheep is between 5 and 10 days. Cattle show viraemia at 4 days post-infection. They rarely develop symptoms.
Clinical signs seen in sheep include fever, depression, salivation, dyspnea and panting. The lips, ears and eyelids may be swollen and hyperaemic. Dyspnea and panting may be seen. The tongue is often very swollen, may be cyanotic and protrude from the mouth. The mouth often has erosions and ulcerations on mucous membranes. This may be sufficiently severe to lead to necrosis and sloughing of mucous membranes. Hooves are often painful and the coronary band hyperaemic, leading to lameness. Such animals should not be moved long distances, as this may contribute to sloughing of hooves. Abortions may occur, or so-called dummy lambs may be born to affected ewes. Other signs may be seen, such as torticollis, pneumonia and conjunctivitis. Some sheep may shed their wool three to four weeks after recovery. Severity of disease and death rate is influenced by the strain of virus.
At post mortem, the following signs may be seen:
Oedema of face and ears
Crusty nasal exudate
Hyperaemia of coronary bands
Petechia, erosions and ulcers on tongue and dental pad and rest of oral cavity.
Necrotic or cyanotic oral cavity
Trachea may be hyperaemic with foam.
Hydrothorax is seen occasionally
The heart may have petechiae, ecchymoses and necrotic foci.
The reticulum and omasum may show hyperaemia and erosions.
Characteristically haemorrhage is seen at the base of the pulmonary artery.
Oedema may be seen in intermuscular fascial planes and skeletal muscles may have focal haemorrhages or necrosis.
Cattle rarely show symptoms, although clinical signs have been seen and have included nasal discharge, swelling of head and neck, conjunctivitis, swelling and ulceration of the mouth, swollen teats, lethargy and salivation.
Clinical diagnosis is based on symptoms and insect activity. In cattle the disease must be confirmed by laboratory testing. Differential diagnoses include vesicular stomatitis, foot-and-mouth disease, rinderpest, photosensitivity due to plant poisoning, malignant catarrhal fever, infectious bovine rhinotracheitis, bovine virus diarrhoea, foot rot, oestrus ovis infection.
Laboratory diagnosis includes PCR. This allows for rapid diagnosis and can identify the serogroup and serotype. Several EDTA blood samples should be collected from several live febrile animals as early in the course of disease as possible.
Serology may also be used for diagnosis. Competitive ELISA identifies IgG antibodies and will be be positive from 7 to 14 days onwards. These antibodies are persistent. Complement fixation test is positive as early as 1 to 2 days after symptoms appear and measures IgM antibodies. These antibodies start to disappear by 7 days. (Personal communication: Dr. Alison Lubisi).
Serum neutralisation tests will identify the serotype involved.
Control is based on control of the insect vector. Peak populations of Culicoides occur in late summer and autumn. Synthetic pyrethroids or organophosphates are effective against Culicoides. Housing animals from late afternoon to early morning reduces the risk of infection. Animals should also be kept away from low-lying areas near open water.
Although the virus does not affect horses, Culicoides will feed on them and breed in manure piles, so this should be considered in control of an outbreak.
A freeze dried polyvalent live attenuated vaccine is available in South Africa. The vaccine is given as a series of three separate injections with different serotypes of bluetongue virus in each bottle. The vaccine will only stimulate immunity to all serotypes after a number of annual innoculations.
(See vaccine insert for full instructions. )
Grass Tetany in Cattle
Grass Tetany
The rain of the past few weeks have caused a flush of green grass everywhere. It has coincided with the arrival of a crop of new calves throughout the district.
Though wonderful to see, this grazing is not without its risks. Cows with autumn calves can develop grass tetany on new plant growth of grass and cereal crops.
Grass tetany is an often fatal metabolic disorder of cattle. It can occur anywhere, but is prevalent on the northern, central and southern tablelands and slopes of NSW.
Although it is primarily a deficiency of magnesium, it is a complex condition. Magnesium is an important component of the cerebrospinal fluid which surrounds the brain and spinal cord and it is essential for the transmission of nerve impulses. Magnesium cannot be stored in the body and is constantly being secreted in faeces, urine and milk. Cows in milk are especially at risk. Calcium levels also play a role in the expression of symptoms.
Symptoms:
Often farmers will be unaware of a problem until they find dead cows, with froth from the nose and mouth, and signs of a struggle before death.
In mild forms of hypomagnesemia, cows may show no symptoms until they are stressed by cold, oestrus or mustering for example, when symptoms may be seen. Early symptoms include twitching of the face and ears and face, a nervous, jumpy appearance and a stiff gait. In the next phase the cow is wild, her front legs are lifted too high in a goose stepping motion, the tail is held higher than normal and she may appear blind. This progresses to excitement, bellowing, galloping and staggering. The cow goes down on her side with stiff, outstretched legs. She paddles violently, her head arches back slightly and she froths at the mouth. The cow may die within minutes.
Low magnesium levels are also implicated in lazy calving syndrome.
Treatment:
There is often not enough time to call a veterinarian, but if one arrives in time, he/she will inject a calcium and magnesium compound intravenously, followed by subcutaneous magnesium. Intravenous injections require caution as giving it too fast, or giving too much, will kill the cow.
If you treat the cow yourself, do not disturb the cow until you are ready to start. Inject one or two plastic bags of commercially available calcium and magnesium solution under the skin, followed by 60 to 100 ml of 50% magnesium sulfate under the skin. Use sterile equipment. Inject each bag into a different site. If possible warm the bags to body heat in a bucket of hot water before use.
After recovery, feed the cow sixty grams of MgO (Causmag) daily.
Prevention:
The most effective supplement is hay treated with magnesium oxide. (Causmag) Daily Causmag requirement is 60 gram per cow per day. It takes two to three days before cows are protected. If supplementation is stopped, the protection ceases too. Excess Causmag can cause scouring.
To treat hay, a slurry is made of Causmag.
Causmag 6kg
Water 2L
Molasses 3kg
This will keep for 10 days.
The prepared slurry is poured onto biscuits or rolled out hay in sufficient quantities to ensure that each adult animal will consume 60g of Causmag daily.
(For other feeding methods, see DPI Primefact 421)
Causes:
Young grass and cereals have lower magnesium levels than older grass and cereals.
Grasses and cereal have lower magnesium levels than clovers and lucerne.
More advanced pastures normally have the three critical minerals, namely magnesium )Mg), calcium (Ca) and potassium (K) in balance. However when cold conditions below 7 degrees Celsius persist for four or more consecutive days, plant roots hibernate and cease to absorb nutrients from soil. As potassium is more chemically reactive than Ca of Mg, a build-up of potassium occurs around the roots of the plant. When temperature warms up again to night temperatures above 8 degrees and 16 degree days for four days, plants switch back to active root absorption and a rapid uptake of potassium (K) relative to Mg and Ca occurs. K suppresses Mg uptake in the rumen. This can trigger hypomagnesemia (lack of magnesium in blood) and grass tetany.
After about 5 days the plant mineral balance will stabilize again.
During a drought, plants will also absorb less minerals from soil, leading to buildup of available potassium in the soil.
After germinating rain, the excess available potassium is rapidly absorbed by new plant growth. This can trigger grass tetany. Ideally stock should be kept off pasture until it has grown to at least 12 cm in length.
Yarded animals that are being hand fed are also at risk after rain. Their manure which is rich in potassium, enriches the soil with potassium. In certain circumstances where rain has germinated short pick grass, animals may consume the grass as it appears. This is not always noticed by managers until losses occur.
Heavy nitrogen or potassium fertiliser application reduces magnesium availability to plants.
Anything that reduces the animals food intake can trigger grass tetany under the right conditions.
Prevention:
Grass tetany occurs where there are acid soils and high potassium levels. Prevention of soil acidification is a long term goal.
Spring calving cows will be less susceptible than autumn/winter calving cows.
Minimise stress in last 6 weeks of pregnancy and in cows with calves.
Avoid sudden changes in food. Leave the gate open to a fresh paddock so animals can move back and forth quietly until they get used to the new pasture.
Keep hay for cows and calves and give the green crop to steers. The best hay is legume hay. It contains the right nutrients to help prevent grass tetany.
Supplement susceptible livestock with Causmag or another MgO containing supplement.
Summary:
Grass tetany is a complex condition, with magnesium, calcium and potassium ratio playing a role.
The risk of a specific pasture causing problems can be evaluated by carrying out soil tests. Plant analysis is less meaningful as levels are constantly changing in the plant and can change within days.
This article provides general information only. Consult your vet to discuss how it applies to you.
Keywords: grass, tetany, magnesium, calcium, potassium
The rain of the past few weeks have caused a flush of green grass everywhere. It has coincided with the arrival of a crop of new calves throughout the district.
Though wonderful to see, this grazing is not without its risks. Cows with autumn calves can develop grass tetany on new plant growth of grass and cereal crops.
Grass tetany is an often fatal metabolic disorder of cattle. It can occur anywhere, but is prevalent on the northern, central and southern tablelands and slopes of NSW.
Although it is primarily a deficiency of magnesium, it is a complex condition. Magnesium is an important component of the cerebrospinal fluid which surrounds the brain and spinal cord and it is essential for the transmission of nerve impulses. Magnesium cannot be stored in the body and is constantly being secreted in faeces, urine and milk. Cows in milk are especially at risk. Calcium levels also play a role in the expression of symptoms.
Symptoms:
Often farmers will be unaware of a problem until they find dead cows, with froth from the nose and mouth, and signs of a struggle before death.
In mild forms of hypomagnesemia, cows may show no symptoms until they are stressed by cold, oestrus or mustering for example, when symptoms may be seen. Early symptoms include twitching of the face and ears and face, a nervous, jumpy appearance and a stiff gait. In the next phase the cow is wild, her front legs are lifted too high in a goose stepping motion, the tail is held higher than normal and she may appear blind. This progresses to excitement, bellowing, galloping and staggering. The cow goes down on her side with stiff, outstretched legs. She paddles violently, her head arches back slightly and she froths at the mouth. The cow may die within minutes.
Low magnesium levels are also implicated in lazy calving syndrome.
Treatment:
There is often not enough time to call a veterinarian, but if one arrives in time, he/she will inject a calcium and magnesium compound intravenously, followed by subcutaneous magnesium. Intravenous injections require caution as giving it too fast, or giving too much, will kill the cow.
If you treat the cow yourself, do not disturb the cow until you are ready to start. Inject one or two plastic bags of commercially available calcium and magnesium solution under the skin, followed by 60 to 100 ml of 50% magnesium sulfate under the skin. Use sterile equipment. Inject each bag into a different site. If possible warm the bags to body heat in a bucket of hot water before use.
After recovery, feed the cow sixty grams of MgO (Causmag) daily.
Prevention:
The most effective supplement is hay treated with magnesium oxide. (Causmag) Daily Causmag requirement is 60 gram per cow per day. It takes two to three days before cows are protected. If supplementation is stopped, the protection ceases too. Excess Causmag can cause scouring.
To treat hay, a slurry is made of Causmag.
Causmag 6kg
Water 2L
Molasses 3kg
This will keep for 10 days.
The prepared slurry is poured onto biscuits or rolled out hay in sufficient quantities to ensure that each adult animal will consume 60g of Causmag daily.
(For other feeding methods, see DPI Primefact 421)
Causes:
Young grass and cereals have lower magnesium levels than older grass and cereals.
Grasses and cereal have lower magnesium levels than clovers and lucerne.
More advanced pastures normally have the three critical minerals, namely magnesium )Mg), calcium (Ca) and potassium (K) in balance. However when cold conditions below 7 degrees Celsius persist for four or more consecutive days, plant roots hibernate and cease to absorb nutrients from soil. As potassium is more chemically reactive than Ca of Mg, a build-up of potassium occurs around the roots of the plant. When temperature warms up again to night temperatures above 8 degrees and 16 degree days for four days, plants switch back to active root absorption and a rapid uptake of potassium (K) relative to Mg and Ca occurs. K suppresses Mg uptake in the rumen. This can trigger hypomagnesemia (lack of magnesium in blood) and grass tetany.
After about 5 days the plant mineral balance will stabilize again.
During a drought, plants will also absorb less minerals from soil, leading to buildup of available potassium in the soil.
After germinating rain, the excess available potassium is rapidly absorbed by new plant growth. This can trigger grass tetany. Ideally stock should be kept off pasture until it has grown to at least 12 cm in length.
Yarded animals that are being hand fed are also at risk after rain. Their manure which is rich in potassium, enriches the soil with potassium. In certain circumstances where rain has germinated short pick grass, animals may consume the grass as it appears. This is not always noticed by managers until losses occur.
Heavy nitrogen or potassium fertiliser application reduces magnesium availability to plants.
Anything that reduces the animals food intake can trigger grass tetany under the right conditions.
Prevention:
Grass tetany occurs where there are acid soils and high potassium levels. Prevention of soil acidification is a long term goal.
Spring calving cows will be less susceptible than autumn/winter calving cows.
Minimise stress in last 6 weeks of pregnancy and in cows with calves.
Avoid sudden changes in food. Leave the gate open to a fresh paddock so animals can move back and forth quietly until they get used to the new pasture.
Keep hay for cows and calves and give the green crop to steers. The best hay is legume hay. It contains the right nutrients to help prevent grass tetany.
Supplement susceptible livestock with Causmag or another MgO containing supplement.
Summary:
Grass tetany is a complex condition, with magnesium, calcium and potassium ratio playing a role.
The risk of a specific pasture causing problems can be evaluated by carrying out soil tests. Plant analysis is less meaningful as levels are constantly changing in the plant and can change within days.
This article provides general information only. Consult your vet to discuss how it applies to you.
Keywords: grass, tetany, magnesium, calcium, potassium
Nitrate Poisoning in Livestock
Significant Stock Losses caused by Drought Feeding.
Deaths were caused by drought feeding of millet silage in one case and millet hay in the other. Approximately 10% of cattle died apparently overnight after being fed the millet products.
Laboratory tests confirmed that the cause was nitrate/nitrite poisoning in both cases.
Nitrates in fodder are converted to nitrites in the rumen. Nitrates in stored fodder can also be converted to nitrites when plant materials heat up or are attacked by bacteria or fungi. Normal levels of nitrite are converted to ammonia in the rumen by bacterial action. However excessive levels of nitrate or nitrite are poisonous.
Certain soil and environmental conditions facilitate nitrate uptake and accumulation by plants, eg.:
Use of nitrogen containing fertilizers
Low soil sulfur and molybdenum
Areas where stock have congregated and urinated and defecated (stock yards)
Drought
Cloudy or cold weather
Herbicide application, esp 2.4-D
Wilting
Plant species
Stage of maturity of plant
Part of plant
Young plants have higher nitrate concentrations and most plant nitrate is located in the bottom third of the stalk.
Hays made from cereal crops, especially those grown under drought conditions and cut while "sappy" can develop toxic nitrite levels when they heat up.
Hays contain almost the same level of nitrate as the parent crop. Silage normally contains significantly less due to the fermentation process.
Sheep are less susceptible to nitrite poisoning than cattle, but can also be affected.
Stressed animals in poor health or poor condition are more susceptible and hungry animals are more likely to eat large amounts.
The risk of poisoning can be reduced by
Having feeds and forages analysed for nitrate levels.
Gradually introducing any new feeds by feeding small amounts frequently and diluting with known safe feeds.
Cattle can become acclimatized to relatively high levels of nitrate this way.
Frequent observation of stock, especially when changing food or grazing.
Don't overstock.
Prevent hungry stock from grazing on high risk fodder.
Do not graze high nitrate pastures for 7 days after rainfall, cloudy weather, frosts or high temperatures causing wilting.
Do not harvest pastures under these conditions either.
Graze these pastures during sunny afternoons above 15 degrees Celsius and remove livestock at night.
Never feed mouldy hay.
Harvest crops close to maturity and raise the cutter head selectively to avoid the bottom part of the stalk.
Keep in mind that rapidly growing weeds after rainfall may also contain excessive levels of nitrate as well as cyanide (prussic acid).
Keywords: cattle, sheep, fodder, drought, grazing, millet, nitrate, nitrite, 2.4 -D.
Deaths were caused by drought feeding of millet silage in one case and millet hay in the other. Approximately 10% of cattle died apparently overnight after being fed the millet products.
Laboratory tests confirmed that the cause was nitrate/nitrite poisoning in both cases.
Nitrates in fodder are converted to nitrites in the rumen. Nitrates in stored fodder can also be converted to nitrites when plant materials heat up or are attacked by bacteria or fungi. Normal levels of nitrite are converted to ammonia in the rumen by bacterial action. However excessive levels of nitrate or nitrite are poisonous.
Certain soil and environmental conditions facilitate nitrate uptake and accumulation by plants, eg.:
Use of nitrogen containing fertilizers
Low soil sulfur and molybdenum
Areas where stock have congregated and urinated and defecated (stock yards)
Drought
Cloudy or cold weather
Herbicide application, esp 2.4-D
Wilting
Plant species
Stage of maturity of plant
Part of plant
Young plants have higher nitrate concentrations and most plant nitrate is located in the bottom third of the stalk.
Hays made from cereal crops, especially those grown under drought conditions and cut while "sappy" can develop toxic nitrite levels when they heat up.
Hays contain almost the same level of nitrate as the parent crop. Silage normally contains significantly less due to the fermentation process.
Sheep are less susceptible to nitrite poisoning than cattle, but can also be affected.
Stressed animals in poor health or poor condition are more susceptible and hungry animals are more likely to eat large amounts.
The risk of poisoning can be reduced by
Having feeds and forages analysed for nitrate levels.
Gradually introducing any new feeds by feeding small amounts frequently and diluting with known safe feeds.
Cattle can become acclimatized to relatively high levels of nitrate this way.
Frequent observation of stock, especially when changing food or grazing.
Don't overstock.
Prevent hungry stock from grazing on high risk fodder.
Do not graze high nitrate pastures for 7 days after rainfall, cloudy weather, frosts or high temperatures causing wilting.
Do not harvest pastures under these conditions either.
Graze these pastures during sunny afternoons above 15 degrees Celsius and remove livestock at night.
Never feed mouldy hay.
Harvest crops close to maturity and raise the cutter head selectively to avoid the bottom part of the stalk.
Keep in mind that rapidly growing weeds after rainfall may also contain excessive levels of nitrate as well as cyanide (prussic acid).
Keywords: cattle, sheep, fodder, drought, grazing, millet, nitrate, nitrite, 2.4 -D.
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