Thursday 30 April 2015

PHYSITIS

Physitis is a common condition in rapidly growing horses.It causes painful swelling of the physes, or growth plates, just above the knees, hocks, or fetlocks.It can be a component of osteochondrosis

Causes
  • malnutrition,
  • conformational defects, 
  • faulty hoof growth, 
  • excessive exercise, 
  • obesity, and toxicosis
  • Nutritional factors play a key role.
  • Physitis is most common in large, rapidly growing foals.
  • stud farms where the calcium:phosphorus ratio in the diet is imbalanced.
  • These foals are fed more carbohydrate than they need.
  • Physitis most commonly involves the distal extremities of the radius, tibia, third metacarpal or metatarsal bone, and the proximal aspect of the first phalanx. 
  • overload of the physeal area due to excessive loading or weakened bone and/or cartilage
First, high carbohydrate diets suppress thyroid hormone production, which, limits nutrients supply to cartilage cells.

Second increase body weight is to early to accommodate.

When the demands on the growth cartilage exceed its ability to produce new bone, problems develop.

Signs

Swelling of the affected physes.
This swelling is firm, warm, and painful.
One side of physics is more  swollen than other.
The condition is usually bilateral.
Foals and young horses with physitis may be stiff-gaited or lame.

Treatment

Treatment consists of reducing food intake to reduce body weight or at least growth rate; confining exercise to a yard or a large, well-ventilated loose box with a soft surface

The calcium:phosphorus ratio should be adjusted to 1.6:1, and protein content limited to <10% of dry matter. 

In general terms, bran should not be fed, and dicalcium phosphate or bone flour (10–30 g daily) should be added to the diet. 

Limiting the young horse's activity to daily short periods of voluntary exercise.
Complete restriction may result in flexural limb deformities, so some forms of light exercise should be encouraged each day.

The diet should be examined and any imbalances corrected.

In particular, the amount of carbohydrate should be reduced to a maintanence level.
NSAIDs should be given to reduce pain.

References

http://www.merckvetmanual.com/mvm/musculoskeletal_system/lameness_in_horses/physitis_in_horses.html

Lameness
Equine Research by Christine King and Richard Mansmann

PREVENTION OF COLIC

Steps to reduce the risk of colic

1. Always have fresh, clean water available

Horses without water for as little as 1-2 hours, were at increased risk of colic in one study. The risk was especially high for horses over 6 years of age. Additionally, horses have been shown to prefer to drink out of buckets compared to automatic waterers, likely due to the ability to ingest large quantities quickly. In the winter, it is important to ensure automatic waterers and other water sources have free flowing water. In colder weather, horses drink more water if it is warmed. Twice daily addition of hot water to buckets works as well as continuous warm water. When traveling on longer trips, stop to let horses drink and/or have a veterinarian pretreat them with mineral oil before starting.

2. Allow pasture turnout

Horses that have access to pastures have been shown to have a lower colic risk than those without pasture access. Feeding from round bales increased the risk of colic in one study. This increased risk may have been related to decrease in quality in the round bales due to exposure and storage (stored outside), types of hay baled, and/or uncontrolled ingestion of certain types of hay.

3. Avoid feeding on the ground in sandy areas.

Horses may ingest enough sand to irritate their intestines. Feed in tubs or hay racks. Place rubber mats or catch pans underneath racks to enable horses to get the scraps without getting sand.

4. Feed grain and pelleted feeds only as needed.

Colic risk increased 70% for each pound increase in whole grain or corn fed in some studies. Horses eating pelleted feeds and sweet feeds are also at increased risk for colic compared to horses on a 100% hay diet.

5. Watch horses carefully for colic following changes in exercise, stabling, or diet.

Colic risk increases during the two weeks that follow changes. Farms that make more than four changes in feed in one year have three times the incidence of colic than farms with less than four feed changes. Even changing the batch of hay can increase the risk of colic. Make only gradual changes in diet, housing, and exercise whenever possible. To make changes in feed, mix ¼ new with ¾ old for about seven days, then increase the percent of new feed gradually.

6. Horse's teeth should be floated every six months.

This ensures good ability to properly and thoroughly chew hay and other feed stuffs.

7. Control parasites.

Horses on a daily wormer or horses regularly dewormed are less likely to colic.

8. Closely monitor your horse and care for it as much as possible yourself.

Owners who take great interest in their horse's care on a day-to-day basis have fewer incidences of colic. Early signs of impaction colic include dry fecal balls or fecal balls that are smaller than usual. Some horses with impactions, may go slightly off feed (particularly off grain) or change drinking habits during the early stages of colic. Subtle signs will be picked up more quickly if you are familiar with what is normal for your horse.

9. Watch broodmares and horses who have colicked previously.

Watch broodmares closely in the two months following foaling. Monitor any horses that have been ill or have colicked before as all are at an increased risk of colic, and early treatment is essential. Treatment with phenylbutazone (bute) can also make horses prone to types of colic and can hide early signs of colic. Discuss the appropriate levels of bute with your veterinarian and avoid using large amounts or prolonged treatment whenever possible.
Above all, be a proactive owner. If your horse is being placed at unnecessary risk for colic, try to adjust the situation. If your horse does colic, appropriate and timely care makes a great deal of difference in the outcome.


Reviewers: Brenda Postels and Betsy Gilkerson Wieland, and Krishona Martinson, PhD, University of Minnesota Extension; Abby Duncanson, Indigo Acres; Harlan Anderson, DVM; and Missie Schwartz, MN Horse Council and Tucker Road Stables.

ENTEROLITHS

Enteroliths are concretions composed of magnesium ammonium phosphate salts that forms slowly around a nidus such as a small metallic object or stone.

Enteroliths are single or multiple and usually do not cause any clinical signs unless they become lodged in the transverse or small colon.

It is commonly seen in middle aged horses,with Arabians, Morgans , Saddlebreeds and Miniature horses.

A large percentage of affected horses are on an Alfalfa diet with a high magnesium and protein content

That foreign object can be as insignificant as a sliver of wood or a piece of binder twine that didn’t get sorted out from the hay.

In the rare instance that the body fails to expel the indigestible particle, it tries to protect the gut instead, by encasing the object in layers of mineral deposits

Small ones are generally passed in the manure (eventually), but larger ones can be responsible for mysterious, recurrent colic and need to be removed surgically before they cause a fatal intestinal rupture.

Clinical signs

  • Decreased faecal passage,colic and weight loss.
  • If enteroliths is in colonic mucosa, the obstruction is complete and gas and ingesta accumulates leads to severe acute abdominal pain.
  • Tachycardia
  • Abdominal distension
  • Nasogastric reflux


Diagnosis

Diagnosing enteroliths is usually done by a combination of radiographs and surgical exploration

Preventions

  • Eliminate, as much as possible, the chance that your horse will ingest a foreign object by removing binder twine from hay and checking his surroundings and paddocks for debris and garbage.
  • Feeding on the ground should be avoided.
  • Feed grass hay. Most horses that develop enteroliths have a diet of at least 50% alfalfa hay, which has much higher levels of calcium, magnesium, and protein than grass hay.
  • Reduce the amount of wheat bran in your horse’s diet. Bran provides high levels of phosphorus, which could contribute to enterolith formation.
  • Provide free-choice hay or increase the number of feedings each horse gets per day. This will help keep the digestive system occupied because when the gut isn’t actively moving feed material along its length, it could be providing a favorable environment for enteroliths to incubate and grow.
  • Provide daily exercise and avoid prolonged stall confinement. Inactivity also contributes to reduced intestinal movement of feed.

References


The Equine Manual by Andrew J.Higgins and Jack R.Snyder
thehorse.com

Wednesday 29 April 2015

CONTAGIOUS EQUINE METRITIS

Contagious equine metritis (CEM) is an extremely contagious venereal disease that is acquired primarily via breeding. While this disease can be carried by either mares or stallions, it is the mare that suffers the ill effects of the infection. Stallions do not show any symptoms of CEM, but mares often will have a thick discharge from the vagina, and will be unable to conceive during the point at which the infection is active.

Etiology
The causative agent of CEM is a microaerophilic gram-negative coccobacillus Taylorella equigenitalis in the family Alcaligenaceae.


Symptoms


Stallions are asymptomatic (no symptoms), but may carry the bacterium on their external genitalia for years, and therefore be persistent carriers and transmitters of the disease.

In fact, to be technical, the stallion does not become "infected" with the CEMO, but rather harbours it in the manner of a commensal organism.

One of the first symptoms in a mare is likely to be that she is not pregnant after one or more breeding cycles. 

It should be noted that although failure to establish pregnancy is a common sequela of infection, abortion is rare.

There are three categories of infection in the mare:


The acutely infected mare: This mare will present with an actively inflamed uterus, with an obvious milky-mucoid (pus) discharge from the external genitalia when she returns to estrus (and the cervix relaxes) - and quite often that return to estrus is earlier than anticipated


The chronically infected mare: This mare shows a lesser level of uterine inflammation, and an associated lower level of vulval discharge. It is likely that mares in this category will be more difficult to treat in order to clear the organism.

The carrier mare: This mare shows no symptoms of the disease, but is harbouring the CEMO in the reproductive tract. This mare is more difficult yet to clear, and as a result of no obvious external signs represents a greater risk to the non-identified at-risk population

The incubation period in the mare from the time of exposure to the onset of active symptoms (or diagnostic ability) is 2-12 days.

Transmission

The following includes practices that may result in, or increase, the likelihood of transmission in the face of T. equigenitalis presence:
  • Not using a disposable AV liner;
  • Sharing AV's between stallions;
  • Not cleaning AV's adequately between use;
  • Not using a disposable protective barrier on the rear of the breeding mount (where the penis contacts) during collection and changing it between stallions;
  • Not washing the breeding mount with a suitable agent (e.g. Chlorhexidine) between stallions;
  • Not using an antibiotic extender (or an antibiotic to which the organism is not sensitive) - it should be noted that even with the use of a suitable antibiotic, transmission may still occur;
  • Sharing of penis washing equipment without sterilization in between stallions or good aseptic technique (this includes hands - e.g. use of disposable latex gloves when washing and/or guiding the penis that are then discarded, or thorough scrubbing of the hands in between collections/breedings with a suitable bactericide);
  • Other poor sterility or aseptic technique associated with the collection/breeding process.

    Treatment
    Treatment for both sexes is primarily topical with the intent of removing the offending organism and any smegma in which it may be located.
    Scrubbing the clitoral sinuses and fossa in the mare with a 4% solution of chlorhexidine for 5 consecutive days, following each daily treatment with packing of the area with a 0.2% nitrofurazone ointment (such as Furacin) is one protocol.
    An alternative treatment is 5 days of scrubbing with Betadine, followed by packing with Silvidine cream.
    Systemic antibiotic treatment may be provided in conjunction with the topical cleansing. It should be noted that until the acutely infected mare has resolved internal tract presence of T. equigenitalis, there is little point in implementing external treatment.
    Repeated treatment of the mare is often required to eradicate the bacterium, so the mare is tested again 28 days after the last treatment, and if still positive a repeat of the treatment and testing is performed until found to be clear.
    In rare cases of persistent infection in the mare, surgical removal of the clitoral sinuses may be necessary. This was once a common part of treatment of the infected mare, but is now only used in extreme cases.

    Treatment for the stallion is similar, consisting of thorough cleansing of the external genitalia, with the penis fully extended and erect. Additionally the urethral fossa and sinus are cleansed.
    A 2% Chlorhexidine solution is adequate for the stallion. It is recommended by some that following the Chlorhexidine wash, the penis be rinsed with sterile saline to avoid irritation, this is not however included in other protocol recommendations.
    Following this washing, the region is coated with 0.2% nitrofurazone cream or a similar ointment. Again, these treatments are continued for five consecutive days.
    Systemic antibiotics may also be used, oral Trimethoprim-Sulfa being suitable. Once treated and tested clear, a stallion that previously tested positive for presence of T. equigenitalis will be required to test-breed two mares that were confirmed clear of the pathogen prior to that breeding.
    The mares are subsequently tested following breeding as discussed above under "diagnosis" to confirm absence of a carrier state in the stallion.
    If a mare tests positive for T. equigenitalis during the post-breeding testing, treatment and further testing of the stallion is recommenced, as well as treatment of the test mare. Most stallions however typically respond favourably to a single course of treatment, and are found to be clear upon the post-treatment test breeding.

References

1: Eaglesome MD, Garcia MM (1979) Contagious Equine Metritis: A Review; Canadian Vet. J. 20:8 201-2062: Powell DG. Contagious Equine Metritis. (1978) Equine vet. J. 10: 1-43:O'Driscoll JG, Troy PT, Geoghan FJ. (1977) An epidemic of venereal infection in Thoroughbreds. Vet. Rec. 101: 359-3604: Taylor CED, Rosenthal RO, Brown DFJ, Lapage SP, Hill LR, Legros RM. (1978) The causative organism of contagious equine metritis 1977: proposal for a new species to be known as Haemophilus equigenitalis. Equine Vet. J. 10: 136-1445: Jang SS, Donahue JM, Arata AB, Goris J, Hansen LM, Earley DL, Vandamme PA, Timoney PJ, Hirsh DC. (2001) Taylorella asinigenitalis sp. nov., a bacterium isolated from the genital tract of male donkeys (Equus asinus); Int J. Syst. Evol. Microbiol. 51(Pt 3):971-66: Båveruda V, Nyströmb C, Johansson K-E. (2006) Isolation and identification of Taylorella asinigenitalis from the genital tract of a stallion, first case of a natural infection; Veterinary Microbiology 116:4, 294-3007: USDA-Aphis CEM Factsheet, 2005.8: Swerczek, T.W. 1979. Contagious equine metritis - - outbreak of the disease in Kentucky and laboratory methods for diagnosing the disease. J. Reprod. Fertil. (Suppl), 27:361-365.9: Simpson, D.J., and Eaton-Evans, W.E. 1978. Sites of CEM infection. Vet. Rec., 102:488.10: Swerczek, T.W. 1984. Unpublished data.11: Swerczek, T.W. 1978. The first occurrence of contagious metritis in the United States. J. Am. Vet. Med. Assoc., 173:405-407.12: Wakeley PR, Errington J, Hannon S, Roest HIJ, Carson T, Hunt B, Sawyer J, Heath P. (2006) Development of a real time PCR for the detection of Taylorella equigenitalis directly from genital swabs and discrimination from Taylorella asinigenitalis; Vet. Microbiology 118:3-4; 247 – 254,13: KY Department of Agriculture recommendations for CEM-exposed stallions. 12/19/0814: AclandHM, Kenney RM. (1983) Lesions of contagious equine metritis in mares. Vet. Pathol., 20:330-34115: Platt H, Atherton JG, Simpson DJ. (1978) The experimental infection of ponies with contagious equine metritis. Equine Vet. J., 10:153-15916: Timoney PJ. (2003) The Continuing Threat to the US Horse Population Posed by CEM; Proc. NIAA Annual Meeting Proceedings

ULCERATIVE LYMPHANGITIS

  • Ulcerative lymphangitis is inflammation of the lymphatic vessels, usually as a result of bacterial invasion.
  • In most cases the bacteria enter the lymphatic vessels through a wound on the lower leg.
  • This condition is more likely when the normal lymphatic flow is slowed by inactivity or obstructed by injury.
  • The inflammation results from bacterial infection further obstructs lymphatic flow.
  • This process may obstruct the vein which causes further leakage of fluids into the tissues.
  • As the result the leg become swollen ,which is why the common name "big leg".
  • If the immune system cannot control the infection the abcess break open in several places and giving the ulcerative conditions.
Treatment
  • Often the invading bacteria is staphylococcus aureus .
  • This organism is difficult to kill because it has become resistant to most antibiotics
  • Bacterial culture and Antibiotic sensitivity testing is important to identity which organism is causing inflections.
  • Oral antibiotics, poulticing and physical therapy help to resolve the infection.
  • NSAIDs are commonly given to reduce the inflammation and pain .
Reference
Lameness
Equine Research
Christine King and Richard Mansmann

PREVENTION OF TENDINITIS


  • Regular trimming and shoeing by an experienced farrier so that a normal hoof pastern angle is maintained and the heels are always well supported.
  • Using exercise bandages that restrict fetlock overextension.
  • Always warm up before giving any work.
  • Correct conditioning-with a base of long,slow distance work and a fitness shedule that is not increased too rapidly.
  • Walk the horse 10 to 15 minutes before giving work.
  • Feeling the tendons for swelling,pain,or heat before and after each training session or competition.
  • Suspending training at the first sign of swelling ,pain,or heat in a tendon.
  • Ensuring that slow,distance work is the basis of the horse training schedule,no matter what the sport or activity.

Reference
Lameness
Equine Research by Christine King and Richard Mansmann

ENDOMETRITIS

Endometritis is infection of the endometrium.
Endometritis is a common cause of poor fertility in the mare.It occurs following uterine contamination during covering, artificial insemination, reproductive examination, parturition and as a result of poor conformation.

History and signs
  • Failure to concieve
  • mucopurulent discharge from the vagina
  • Early embroynic loss
  • Short oestrus cycles
Clinical findings
  • Signs of vulval discharge and in some cases failure to concieve.
  • Definitive diagnosis is by collection of bacteriological swabs from the cervix or endometrium,which should be under taken under strict aceptic conditions.
  • The mere presence of bacteria is not enough to diagnose infections.
  • Examination with speculum is an important of the workup and can be performed when the bacteriologic and cytologic swabs are collected
Types
  • Venereal Infectious Endometritis
  • Non-venereal Infectious Endometritis
  • Persistent Post-mating Endometritis
  • Chronic Degenerative Endometritis
  • Chronic Infectious Endometritis

Venereal Infectious Endometritis

Three major pathogens cause venereal endometritis in the mare:
  • Taylorella equigenitalis - causing the notifiable Contagious Equine Metritis (CEM)
  • Klebsiella pneumoniae - tests can be performed to identify capsule types 1, 2 and 5 which are sexually transmitted
  • Pseudomonas aeruginosa - there is no available test to differentiate strains so all must be treated as pathogenic
The mare may present with vaginal discharge in anacute infection. However she may also present in acarrier state, in which case there may be no outward clinical signs. Stallions are usually sub-clinical carriers of disease. All three bacteria prevent conception.
Equine Viral Arteritis (EAV) and Equine Herpes Virus 3 (EHV-3) are also classified as venereal infections however they do not cause endometritis or prevent conception.
Detailed guidelines on the diagnosis, treatment and prevention of all these infections can be found in the of Practice which are followed by Thoroughbred breeders in the UK.

Non-venereal Infectious Endometritis

This occurs following infection during covering, reproductive examination or foaling. The mare will normally present with a history ofinfertility or early embryonic death and short cycles. There may also be evidence of vaginal discharge. Infection may be caused by:

Persistent Post-mating Endometritis

This is more common in older and multiparous mares. They present with a history of short cycling and often an vaginal discharge approximately two weeks post-cover.
A transient inflammatory response is normal in the mare post-cover, however a normal immunological response is mounted and the infection cleared before the embryo exits the fallopian tube. In the cases of persistent post-mating endometritis the inflammation persists longer than 72-96 hours so that when the embryo enters the uterus the environment is still unsuitable for embryonic development, resulting in early embryonic death.

Chronic Degenerative Endometritis

Chronic degenerative endometritis aka endometriosis is degenerative change that occurs in older mares or following repeated inflammation of the uterus. If the condition is severe it may result in delayed clearance of the uterus post-cover. Definitive diagnosis can only be achieved by biopsy, which will show degenerative change of the uterus histologically.

Chronic Infectious Endometritis

Normally an underlying conformational condition such as pneumovagina predisposes the mare to chronic infectious endometritis. Definitive diagnosis is again by biopsy which should show infiltration of the endometrium with lymphocytes and plasma cells. Infection may be:
Prognosis is guarded due to the chronic nature of the infection and the anatomical faults predisposing to infection. Surgical correction of the conformational abnormalities may be attempted using Caslicks procedure.

Diagnosis
  • Vaginal examination
  • Ultrasound
  • Clitoral and endometrial swabs
  • Uterine flush
  • Endometrial endoscopy
  • Uterine biopsy diagnose
Treatment


(1) Uterine lavage with copious amounts of fluid. This is beneficial because it:
removes contaminants such as bacteria and purulent material
stimulates uterine contractions to aid clearance
causes mechanical irritation to the endometrium aiding healthy neutrophil recruitment
2-3 litres of saline or lactated ringers solution should be administered using a uterine flushing catheter and then drained back into the bag and inspected. Dilute Povidone iodine can also be used as a cheap alternative.

(2) Antibiotics (intrauterine or systemic). Antibiotic type should be guided by culture and sensitivity and activity of the drug in the uterus where possible. The length of the treatment should be proportional to the severity of infection.

(3) Administration of ecbolics to stimulate uterine contractility and clearance of infection - oxytocin and prostaglandin analogues
Reference

Manual of Equine Practice by Reuben J.Rose and David R.Hodgson
Pycock, JF (1997) Self-Assessment Colour Review Equine Reproduction and Stud Medicine Manson
Pycock, JF (2004) Pre-breeding checks for mares In Practice 2004 26: 78-85
Ricketts, S (1987) Vaginal discharge in the mare In Practice 1987 9: 117-123
RVC staff (2009) Urogenital system RVC Intergrated BVetMed Course, Royal Veterinary College







Tuesday 28 April 2015

HIRSUTISM


  • Hirsutism is a condition in which the horse has an excessive growth of hair,resulting in a long wavy haircoat.
  • The hair is often 4-5 inches in length, and may remain long throughout the year.
  • The horse may fail to shed in the spring,or it may shed its coat normally and then have an abnormally abundant regrowth of hair.
  • The presence of an abnormally long hair coat in an older horse is very strong evidence of Pituitary Pars Intermedia Dysfunction (PPID)
  • The skin may be dry and scaly,or slightly greasy.
  • The horse occasionnaly drenched in sweat
  • It is caused by tumor of the pituitary gland.
  • The condition is due to over-activity of one part of the pituitary gland the excessive release of certain metabolically active proteins and hormones

Sunday 26 April 2015

BLEPHARITIS

Blepharitis is inflammation of the eyelids, and is commonly seen in general practice.

The owner will report eye irritation and a discharge may be present. 
The condition is most likely to be insidious in onset and gradually progressive, although acute presentations do occur.
There are many underlying causes for blepharitis, and it can occur along with conjunctival hyperaemia. 

The most common cause is bacterial infection of the eyelids, most often with Staphylococcal species, followed by an inappropriate allergic or sensitivity reaction to the bacterial toxins.

 Dermatological conditions such as atopy, Leishmania or puppy strangles can also be responsible.
In horses, primary bacterial infection is rare, and more common causes include trauma, allergic reactions to insect bites, exposure to intense solar radiation, ringworm and cutaneous habronemiasis.


Clinical Signs

Many forms of blepharitis are part of a general dermatological condition, and so skin changes are common.
Ophthalmic examination will reveal eyelid swelling and hyperaemia, possibly with crusting or exudative erosions close to the eyelid margins. Some lesions are erosive and a serosanguinous discharge may be present.
Periorbital hyperaemia and alopecia may be signs of self-trauma.
Conjunctival hyperaemia will accompany most cases of blepharitis, and corneal ulceration may develop.
Normally there is no intraocular involvement with blepharitis, but if uveitis is present this may suggest either the uveodermatological syndrome, or Leishmania infection.

Diagnosis

Swabs for bacterial culture and sensitivity should be taken from the ocular discharge and the lid margins themselves. The contents of the meibomian glands at the eyelid margins can be expressed for sampling.
Impression smears of the lid margins can be useful, as can hair plucks and scrapes to look for parasites.
If Leishmania is suspected, serological testing should be performed.
Biopsy may be considered if a more generalised condition is suspected, and the sample should include the eyelid margin wherever possible.

Treatment

The specific treatment regime will depend upon the underlying aetiology for the blepharitis.
General hygiene and preventing self-trauma will apply to all cases.
For a primary bacterial blepharitis, broad-spectrum systemic antibiotics for 2-4 weeks are advised. Eyelids are part of the skin and require systemic medication.
A topical lubricant can be considered as involvement of the meibomian glands will affect the lipid layer of the tear film and there will be increased evaporation, leading to qualitative tear film abnormalities.
If inflammation is particularly severe, an anti-inflammatory such as a NSAIDs can be administered systemically. If an immune-mediated condition is suspected, systemic steroids can be administered at immuno-suppressive levels until signs resolve.

Reference

Slatter, D. (2001) Fundamentals of veterinary ophthalmology Elsevier Health Sciences
Gelatt, K. (2000) Essentials of veterinary ophthalmology Wiley-Blackwell
Turner, S. (2008) Small animal ophthalmology Elsevier Health Sciences

BIG HEAD DISEASE IN HORSES

Nutritional secondary hyperparathyroidism is a metabolic bone disease --a disease that affects bone metabolism.
It is often called  big head or bran disease.It has also been called Miller's disease.

Causes
  • Insufficient calcium intake
  • Excess phosphorus intake
  • Eating plants which contains oxalates
Nutritional Secondary Hyperparathyroidism is seen mostly in horses grazing exclusively on grasses containing high levels of oxalate that locks up calcium, making it unabsorbable by the horse's intestines.

An excess of phosphorus affects the body stores of calcium in a few ways.

1.High levels of dietary phosphorus reduce calcium absorbtion from the intestine.
2.Excess intake of phosphorus results in the blood phosphate concentration.The phosphorus bind to the calcium in the blood stream,causing the blood calcium concentration to drop.
3.A high blood phosphates concntration also interfers with the conversion of inactive vitamin D to its active form.

Signs
  • Enlargement of facial bones
  • lameness
  • Gait is stiff and stilted
  • Physitis in young horses
  • Neck pain
  • Poor body or coat condition
  • lethargy
  • Poor growth
  • In severe cases tearing of tendon,
  • Bone fracture


Treatment and prevention
  • Horses grazing oxalate containing pastures and those affected with clinical signs of bighead should be provided with daily calcium supplementation.
  • Because NSH is a condition that results from dietary imbalance,treatment  and prevention must focus on correcting the diet
  • Mineral and supplement mixtures that will provide the required amount of calcium and phosphorus for horses for a week include 1 kg rock phosphate mixed with 1.5 kg molasses plus 1 kg of a mixture of 1/3 ground limestone and 2/3 dicalcium phosphate mixed with 1.5 kg molasses.
  • Calcium supplements
  • Supplementation should be continued for 6 months or indefinitely if the horse is to be kept on the offending pasture. Lucerne hay is also high in calcium and should be given in addition to the calcium supplements.
  • calcium can be provided through a variety of sources.
  • But supplements also contains phosphorus ,such as dicalcium phosphate.
  • Alfalfa is a very good natural source of calcium.
  • In severe cases, affected horses should be confined to a stall .
  • NSAIDS should be used with caution because reducing pain may inspire an increase in the horse's level of activity,which increases the risk of bone damage.
  • The horse should not allow for a vigorous exercise even after recovery.


Reference

Lameness
Equine Research
by Christine King and Richard Mansmann









Saturday 25 April 2015

CANKER

  • Canker is an unusual condition of the horse's foot that affects the frog, bars, and sole.
  • The name comes from the early belief that the condition was of a cancerous nature.
  • However, to the best of our knowledge, canker is an anaerobic (grows in the absence of oxygen) infection in the superficial epithelium of the hoof (the outermost tissues, which produce the horn).
  • The causative bacterium is unknown, but some researchers have suggested the organism is a part of the Bacteroides species, which is similar to what causes "foot rot" in sheep.
  • In a more recent study researchers found spirochete (spiral-shaped) bacteria in the epithelium, which was similar to findings in cows and sheep with digital dermatitis.

Causes
  • The microorganism associated with canker causes abnormal keratin production, or overgrowth of the horn. This excessive proliferation occurs underneath the horn, as the infection spreads throughout the epithelial layer. 
  • Commonly, an affected horse will have white or gray matter that is moist and spongy appearing in the sulci region (grooves on either side and in the center of the frog) of the hoof. This characteristic growth's appearance has been described as similar to wet cauliflower with cottage cheeselike exudates. If there is extensive infection, heat might be felt in the hoof, but usually only in extreme situations.
  •  In attempts to recreate the disease, I and others have packed the frog with manure after injecting what we believe are the causative bacteria, but we still have been unable to prove that unsanitary conditions contribute to canker's onset. Development might instead be influenced by how the horse is used. 
  • In contrast to thrush, which is a necrotic or tissue-destroying process, canker creates abnormal tissue growth and is described as a hypertrophic pododermatitis. 
  • Both thrush and canker are found in the same region of the foot, but thrush resembles a tarlike substance. While thrush eats at tissue, the inner tissues of the digit are protected until bacteria get deep enough to deteriorate more sensitive structures. 
  • Canker, on the other hand, spreads in live tissue, without the help of oxygen

Treatment

1. Superficial debridement (cutting away abnormal tissue) over the entire affected area. This can be done using either general anesthesia or a nerve block. Only the superficial layer of infected tissue should be removed, as excising too deeply can retard healing and might also drive the infection into deeper tissues. Some veterinarians follow the debridement with two to three superficial freezes of the affected area to further kill off the diseased tissue.

2. Canker prefers moist conditions, so keep the treated area very clean and dry.

3. Topical treatments. Two most effective topical therapies are the antimicrobial drug metronidazole and 10% benzyl peroxide solution. 

Metronidazole is usually ground into a powder and spread over the affected area. Benzyl peroxide is a potent astringent commonly found in acne medicine. It is soaked into gauze sponges and applied as a wound dressing. Systemically, no medicine will cure canker if superficial debridement is not performed.

After applying the topical medication, apply a clean, dry, waterproof bandage. Many veterinarians recommend using shoes with treatment plates, which are more convenient than bandaging the hoof.
Horses have variable responses to treatment. Some cases heal within a week or 10 days, and some cases last for months. Given good, aggressive treatment, a week to 10 days of intensive therapy should control the canker. Once the tissue has healed, it is very rare for the disease to recur. However, before healing is complete, canker might return--a trait that led many to believe it was a cancerous disease.


Reference
http://www.thehorse.com/articles/28652/equine-canker

BURSITIS

  • Bursitis is defined as an inflammatory reaction within a bursa. This can range from mild inflammation to septic bursitis.It is most common and important in the horse.
  • A bursa is present on a limb or at specific areas of the body that generally have limited movement but with pressure against a portion of bone, tendon or ligament. A bursa can also be found in areas to facilitate the gliding action of a tendon.
  • True or natural bursae are located in a predictable position and examples include: navicular bursa prepatellar bursa, cunean bursa, bicipital bursa, trochanteric bursa and the subtendinous bursa of the common calcaneal tendon.
  • Acquired bursa develop subcutaneously in response to pressure and friction. Tearing of the subcutaneous tissue allows fluid to accumulate and become encapsulated by fibrous tissue. These include: olecranon bursa (capped elbow), subcutaneous calcaneal bursa (capped hock) and carpal hygroma.
  • Bursa may communicate with a joint or tendon sheath and may become clinically apparent because effusion from the joint or sheath cases filling of the bursa.
  • True bursitis involves a natural bursa and is caused by direct trauma or associated with the stress of racing or performance. This form of bursitis is called traumatic bursitis.
  • Acquired bursitis is either the development of a subcutaneous bursa or inflammation of that bursa.
  • If a bursa becomes infected, septic bursitis occurs and this is commonly following a puncture wound.

Signs

Bicipital, trochanteric and cunean bursitis are characterised by lameness. 
Pain can be elicited through palpation in bicipital and trochanteric bursitis, but cunean bursitis needs local blocking to define.
Acquired bursae do not usually lead to lameness and are characterised by a local, fluctuant swelling in the region. 
With chronicity they become firm and can cause mechanical limitation to flexion of the corresponding joint.
Septic bursitis, such as septic navicular bursitis is characterised by severe lameness and the recognition of foreign body penetration.

Treatment


The treatment methods vary considerably depending on the bursa.
Rest is the method of choice for bicipital bursitis. 
Cold applications can be used in all cases in the early acute stages.
For cunean tendon bursitis, options include cunean tenectomy, rest, local anti-inflammatory injections or phenylbutazone.
Acquired bursae of the elbow, hock or carpus should firstly be treated by preventing further trauma to the region. Local corticosteroid injections and pressure bandaging have been used in the past.
The contents of the bursa can be aspirated, or drains implanted.
For more chronic cases, surgical removal and primary closure is the treatment of choice. If immobilisation of the region can be performed, results can be good.
In septic bursitis, treatment requires systemic antibiotics as well as local drainage. The prognosis for complete recovery is guarded.



References

Kahn, C. (2005) Merck Veterinary Manual Merck and Co
Stashak, T. (1996) Practical guide to lameness in horses Wiley-Blackwell

McKinnon, A. (1998) Equine diagnostic ultrasonography Wiley-Blackwell

Friday 24 April 2015

FEEDING FOR IMMUNITY


Allergies, heaves, thrush, insect bite reactions, and hives all can reflect a struggling immune system, as can the more obvious signs of respiratory disease.
Some infections and diseases are beyond your control, but you can influence the outcome by boosting your horse's immune response nutritionally. 

Stress and the Immune System
One of the best things you can do for your horse is pay attention to his stress level and adjust activities accordingly. 
Chronic stress, whether physical or mental, weakens his immune system. When cortisol, the stress hormone, becomes elevated, disease agents that don't normally faze your horse might make him sick--for example, equine herpesvirus (EHV). 
Did you know that your horse might already be infected? This opportunistic organism can remain latent until something (e.g., stress) triggers it, giving it the "opportunity" to cause clinical signs.
Encountering some stressors is inevitable: Horses travel long distances, congregate in strange settings with unfamiliar horses, and are subject to performance stress and other factors. But one of the most common stressors--an empty stomach--is easy to fix. Horses are "trickle feeders" that evolved to roam and graze freely. Not being permitted to graze at will works against a horse's physiology. This is because the horse's stomach, unlike our own, secretes acid continuously, even when empty. Chewing produces saliva, a natural antacid, but it can't help neutralize stomach acid if the horse is left with nothing to chew. Exercising on an empty stomach causes acid to slosh onto the unprotected areas of the stomach's lining, potentially causing ulcers.

Nutrients to Protect Your Horse

Healthy, well-managed pastures supply your horse with many important nutrients, including vitamins E, A (as beta carotene), and C.
 Grasses are also high in omega-3 fatty acids in the proper proportion to omega-6s. 
And if a variety of grasses and clover grow in your pasture, you can expect the protein quality to be good.
While free access to pasture often provides all the nutrients a horse at maintenance requires to remain healthy, many horses rely on hay as their main forage source during winter.
 Hay loses some of its vitamins and omega-3s in storage, so horses consuming only hay for prolonged periods of time (more than three or four months without fresh pasture) might require additional feed supplementation.
 Most horses do well on a fortified commercial feed in recommended amounts. But if your horse exhibits signs of suppressed immune function (e.g., signs of respiratory infections including a runny nose, coughing, and fever; recurrent thrush; bacterial infections; fever; allergic reactions; and general malaise), it's time to boost his diet's nutrient content.
Your horse might need the following vitamins and minerals to fill nutritional gaps and maintain a healthy immune system:
Vitamin E is a powerful antioxidant. Antioxidants protect against disease by neutralizing the damaging free radicals (unstable molecules with an unpaired electron that pull electrons from other molecules) that mental and physical stress produce.
Rhode Island's Department of Fisheries, Animal and Veterinary Sciences, and colleagues examined the impact of vitamin E dosages 15 times the National Research Council's recommended levels on aging horses' immune systems. They found that horses supplemented with vitamin E were more capable of fighting bacteria and produced increased amounts of the antibody immunoglobulin. However, Carey Williams, PhD, associate extension specialist and associate professor at Rutgers University's Department of Animal Science, discovered that just 10 times the recommended dose of vitamin E in otherwise healthy horses interfered with Vitamin A absorption. Gross excess supplementation is not recommended, therefore, even in chronically stressed horses.
"The benefits of vitamin E as an antioxidant and its ability to improve immune function have been known for years--vitamin E impacts several key components of immune function," says Stacy Oke, DVM, MSc, president of Rolling Thunder Scientific, in Ontario, Canada. "There are four different types of vitamin E: α, β, γ, and ? tocopherols. What remains to be known is which types are the most effective."
Many different tocopherols exist in forages and other sources. The form manufacturers most commonly add to commercial feeds and supplements is α- tocopherol. When added in its natural state manufacturers note it as d-α tocopherol in the ingredients, and in its synthetic version they list it as dl-α tocopheryl acetate. Natural vitamin E is more effective as an immune system booster than the manufactured vitamin; however, the synthetic form is more stable and, therefore, has a longer shelf-life.
Vitamin E works parallel to selenium compounds that also serve as antioxidants. University of Kentucky researchers found that a low blood selenium status experienced a delayed immune response to vaccinations. However, selenium can be toxic in high amounts, so horses should only be supplemented if veterinarians document a deficit, and supplement levels should be kept low (below 5 mg/day for an average-sized horse). Vitamin E and selenium are commonly packaged together; evaluate the diet's total selenium content before adding more. For therapeutic doses, it might be better to purchase vitamin E alone.

Vitamin A, in humans, is necessary for normal regeneration of mucosal barriers damaged by infection, and it enhances the function of neutrophils, macrophages, and natural killer cells--three types of white blood cells critical to the immune system. Plants contain beta carotene, which the body uses to produce vitamin A. Beta carotene, vitamin E, and vitamin C work synergistically to reduce inflammation and protect lipids in cell membranes against free radicals' damaging effects.
Boon Chew, PhD, of Washington State University's Department of Animal Science, explains that beta carotene has been reported to modulate the immune system in humans and animals. It increases the ability of specialized white blood cells to damage harmful cells. The resulting inflammation helps eradicate bacterial and viral pathogens and stimulates production of various cytokines, which are messenger cells in the immune system. Beta carotene also stimulates blood neutrophils' phagocytic ability, by which they engulf and eliminate bacteria.
Since most vitamin/mineral supplements and feeds are fortified with vitamin A, it is important to monitor levels before supplementing. The active form of vitamin A (Retinol, retinyl compounds) is toxic at five times the National Research Council's recommended level.

Vitamin C neutralizes free radicals through its ability to donate electrons. The horse's liver normally synthesizes vitamin C in more than adequate amounts and releases and excretes it during periods of prolonged stress. Sarah L. Ralston, VMD, PhD, Dipl. ACVN, associate professor in Rutgers' Department of Animal Science, theorizes that older horses' increased susceptibility to infections might be due to the chronically elevated cortisol secretion associated with pituitary dysfunction (equine Cushing's disease). Ralston finds vitamin C to be an effective supplement in reducing the effects of stressful travel. "We verified that after prolonged transportation stress, oral supplementation (with) vitamin C twice a day was beneficial for the horses the first few days after arrival," she explains.

Omega-3 fatty acids have been shown to reduce inflammation as well as allergic inflammatory response in other species. Researchers at the University of Guelph's Equine Research Centre found evidence that the fatty acid source flaxseed can potentially reduce the allergic inflammatory response in horses susceptible to biting midges (Culicoides). Omega-6 fatty acids can exacerbate inflammatory responses if fed in large amounts, but omega-3s do just the opposite--they help inflammation subside. Omega-6 fatty acids are the predominant form in edible oils such as corn and soybean that are commonly used as calorie supplements. If given in reasonable amounts (less than 2 cups per day to an average-sized horse), they should not pose a threat to a horse's inflammatory system. Some omega-6 activity is beneficial, since inflammation is another way the body combats infections.

High-Quality Protein
At least 8% of a horse's diet should be high-quality total crude protein. A high-quality protein has all the essential amino acids in their proper proportion to allow for adequate body protein synthesis. This enables the immune system to produce antibodies and enzymes and to repair tissues. High-quality protein sources for horses include legumes such as alfalfa, clover, and soybeans. For horses fed lower-quality grass hays, add legume hay pellets or cubes to provide high-quality protein. If you feed a commercial product, check for alfalfa or soybean meal on its list of ingredients.

Other Supporting Nutrients
Some veterinarians and manufacturers have said the following supplements further boost immune support, though these claims haven't been scientifically proven:
  • Bioflavonoids These supposedly work with vitamin C to enhance antioxidant capability.
  • Coenzyme Q10 Used primarily in humans, nutritionists are just starting to recognize this substance as a potent player on the antioxidant team.
  • Water soluble vitamins Thiamine, niacin, panthotenic acid, B-6, riboflavin, and cyanocobalamin work together to support digestion, skin, hooves, hair, blood vessels, protein synthesis, nervous system health, and energy production in all species, and their use and excretion is enhanced during periods of stress. However, in horses only thiamine has been clinically proven to be necessary during periods of prolonged stress. Scientists have not documented deficits of the others in horses.
  • Spirulina Blue/green algae reportedly reduces allergy signs and improves respiratory function in other animals
Reference

http://www.thehorse.com/articles/30983/feeding-for-immunity