MEDICAL ARCHIVES

08.02.2006

Lower Airway Disease - More Common than You Think!

Optimum airway function is essential for all levels of athletic activity in performance horses. The horse has 18 ribs for a large respiratory capacity for fast exercise, providing up to 1200 square metres of lung surface area when the 3 million air sacs in the lungs are fully inflated. Horses take 140 breaths per minute at the gallop, inhaling 15-20 litres of air in each breath. Racehorses inhale up to 2250 litres per minute at the gallop, with airflow of 70 litres per second into the lungs. Up to 70 litres of oxygen are absorbed per minute at the gallop in a racehorse to fuel energy metabolism in the muscles.

A horse has a high oxygen uptake of 165mL oxygen per kg of body weight per minute, compared to greyhounds at 100mL/kg/min and human sprinters at 55ml_/100kg body weight/minute. 80% of the energy is metabolised aerobically in the muscles at the full gallop, with 80% of this energy being lost as heat during exercise. This illustrates the horse's high reliance on airway function for maximum performance.

Lower Airway Disease

Lower airway disease in the bronchi and air sacs (alveoli) is primarily a chronic inflammatory reaction within the airway lining cells, resulting in accumulation of increased amounts of mucus and fluid, often with build-up of inflammatory and allergic white blood cells. This leads to narrowing and blockage of airways, with reduced air transport function, oxygen uptake and loss of speed, stamina and performance.

The severe allergic reaction with airway constriction (bronchoconstriction) or shutdown is often referred to as the "Heaves" or Chronic Obstructive Pulmonary Disease (COPD). The "Heaves" or COPD is a common condition in stabled horses in the Northern Hemisphere that are fed on hay containing allergic moulds with the risk increased when straw is used as bedding.

Lower airway disease may also lead to increased risk of lung bleeding in racing and performance horses, resulting in subsequent loss of stamina and performance (See "Lung Bleeding" below).

"Facts and Stats"

• 63% of horses that have a loss of performance have underlying airway disease as the cause.
• 40% of airway disease is caused by viral and bacterial infections.
• 60% of airway disease is caused by inflammatory allergic reaction to dust and moulds inhaled from feed and bedding.
• 20% of horses suffer from an asthma like allergy with narrowing of the airways from inhaling dust, pollens and moulds in the feed.
• 90% of fast gaited horses bleed in the lower airways and airsacs.

Upper airway infection with the stable virus (EHV-1 virus), and EHV-4 and other respiratory viruses can cause loss of airway cleaning function and accumulation of fluid, mucus and inflammatory cells in the lower airways. A horse that is 'tied short' during travelling also accumulates more fluid in its lungs if its head is held above chest bar height, increasing the risk of airway disease and reduced performance.

Recent research has shown that the highest risk of airway disease is related to fine dust and allergies to moulds and pollens inhaled from the feed, bedding or stable environment, as well as airway irritation from inhaled ammonia in a poorly ventilated stable environment.

High protein diets increase the level of ammonia produced by fermentation of nitrogen compounds in the urine and manure within the warm bedding environment.

The type of bedding and the quality of the hay relative to its curing process and content of dust and mould has a direct influence on the incidence of lower airway disease and the development of COPD or the "Heaves" in stabled horses.

Bedding

Recycled plant materials, such as cereal straw, grain and rice hulls and poor quality wood shavings contain the highest level of allergic moulds, dust and other fine particulate matter that can become suspended in the air and then into the lower airways.

Very absorbent materials such as peat moss and shredded paper have the lowest content of allergic dust and mould but, when wet with urine, they become very heavy to muck out.

The size of the dust particles has a direct influence on the incidence and risk of airway disease and allergic reaction. Dust and fibre particles from bedding that you can see suspended in the air are greater than 10 microns in diameter and settle out in the nasal passages, windpipe and upper airways. These are removed using the normal mucocilary cleaning mechanisms by ciliated cells (cells with hair like projections) that move as a 'wave' or in an escalator motion to carry mucus and larger particles up the windpipe into the throat (at 2.5cms per minute), where they are swallowed with feed. Horses that have suffered from a respiratory virus will lose their ciliated cell airway lining and the cleaning mechanism for up to 30-35 days, increasing the risk of lower airway accumulation of fluid, mucus and allergic dust particles.

Normal airway cleaning mechanisms can be assisted by allowing a horse to put its head down to feed below chest height, or preferably from a safe feed bin located in the corner of the stable on the floor. However, dust that is less than 10 microns in diameter, and mould particles less than 5 microns in size in particular, have the highest risk of causing allergic and inflammatory reaction in the lower airways. When suspended in the air under conditions of little air movement, they are inhaled deep into the lungs in a horse with a normal breathing depth at rest. Risk of inhalation is increased when horses are returned to a stable after exercise, or moved to a new stable, and become excited and disturb the bedding to create suspended dust and mould particles.

Studies have indicated that horses that lay down a lot in stable bedding have a higher incidence of lower airway disease than horses that stand for long periods or when occupied by 3-4 feeds per day.

Studies have shown that when straw bedding is cleaned and "fluffed up" to make a soft bed for the horse, small mould particles become suspended in the air within the stable space for up to 48 hours.

It is important to avoid disturbing the straw bedding by quick energetic mucking out procedures - the fastest stable clean-out is not the best in terms of maintaining good air quality.

Sawdust and shavings, although they contain large visible dust particles, are not a high risk bedding if they originate from virgin new wood and are not left out in the rain to start mould growth. Always cover stored sawdust and shavings, and if necessary, dampen the surface of new shavings and mix them into the bedding carefully.

Bedding should absorb urine to reduce the risk of moisture build-up leading to breakdown of nitrogenous wastes to ammonia by bacteria on the bedding floor.

Ammonia irritates the airway lining and causes an inflammatory reaction, narrowing the airways and causing reduced oxygen uptake and performance. High levels of ammonia gas have been shown to:

• inhibit the 'escalator' clearing function in the airways.
• stimulate increased mucus production.
• absorb onto dust and mould particles and release the irritant amonia the lower airways.
• increase in concentration under hot, humid conditions, or in poorly ventilated stables.
• reach highest levels overnight, especially at floor level on cold mornings and within 30cms of the bedding surface in poorly ventilated stables.

The concentration of ammonia in a stable can be reduced by removing urine "damp spots" twice daily and providing absorbent bedding such as saw dust, hemp fibre or shredded paper. Straw is the least absorbent of the common bedding materials and has the highest content of dust and moulds. Ammonia is absorbed onto the dust and can be inhaled deep into the lungs. After cleaning out the bedding, wet spots on the floor can be sprinkled with calcium carbonate (fine limestone) to absorb and neutralise the acid in the urine.

Diets that contain higher levels of protein, such as lucerne based diets (lucerne contains 15-17% crude protein), will result in excretion of more concentrated nitrogen wastes in the urine (not protein) and droppings. The urine of healthy horses is usually alkaline on pasture, but is slightly acid on high grain diets in training containing up to 30% mucus in its precipitate, providing an ideal acidic environment and substrate for bacterial attack of urine and higher protein droppings accumulated in the bedding and soaked into the stable floor.

When the amount of Lucerne is reduced and replaced in part with clover or grass hay with lower protein content, the 'smell' of ammonia in the stable air space is dramatically reduced.

Ensuring adequate airflow by providing roof ventilation outlets and mesh dividing walls will help remove accumulated ammonia and other gas from the stable space.

Studies have shown that, where hay is 'musty' with mould and dusty due to poor curing and long term storage, within an area of 60cms of a hay net as a horse is pulling hay out to eat it (up to 50% is dropped onto the bedding), up to 1 million particles are suspended in the air around the net.

If the hay is dampened before feeding by soaking in water for 5 minutes and draining, the concentration of mould and dust particles drops from 93,000 per litre of air to 3,500 per litre of air.

Research indicates that 15 minutes after hard exercise the contamination of aerobic bacteria inhaled from the nose, throat and mouth secretions increase by 10 times in the lower airways, from 45 to 440 cfu and the number of anaerobic bacteria increase by 40 times from 15 to 600 cfu. Therefore it is important to allow a horse to put its head down to eat for 1-2 hours after hard exercise to assist airway drainage and removal of high levels of bacteria that could cause infection if the airways are irritated or inflamed.

When travelling over long distances for more than 3-4 hours with the head held above chest height, the amount of fluid and mucous secretion trapped in the lungs increases by 7 times in the lower airways. This provides an ideal growth media for bacteria, especially of a horse has been exercised hard within the 8 hours prior to travelling and has not been given the opportunity to put its head down to drain its airways.

Lung Bleeding

Over the last 20 years, bleeding in the lower airways related to exercise (termed Exercise Induced Pulmonary Haemorrhage or EIPH) due to rupture of pulmonary capillary vessels has been shown to occur in over 90% of Thoroughbred racehorses, 89% of trotting racehorses, 60% racing Appaloosas, 40% eventing horses, 12% Polo horses and 0% in endurance horses each time they exercise to sustained maximum intensity during competition. The incidence of lung bleeding is directly related to the speed and intensity of exercise.

Blood is seen at the nostrils in only about 2% of "bleeders", but up to 90% are "hidden bleeders" each time they race. However, concurrent airway disease, inhalation of cold air, hard swimming and repeated exertion by hard racing can all contribute to the risk of "bleeding".

The exact cause of lung bleeding has not been proven, but it is possible that excessively high blood pressures generated in the pulmonary arteries (up to 120mm mercury pressure at the gallop as compared to 40mm pressure at the medium trot) weakens the thin blood vessels that expand with a pulse wave at up to 250 times per minute relative to the heart beat and are stretched to thin their walls 140 times as the lung airsacs expand at the gallop.

It is also postulated that concussive waves generated by the front limbs hitting the ground at 42 times per minute at the gallop are transmitted up the front limb and focus to a rebound point at the rear of the chest cavity. This is an area where the highest amount of lung haemorrhage has been found to occur.

Surveys have shown that 21% of racing greyhounds bleed in the lungs in distance races over 700 metres or longer, and a similar percentage of racing camels in the Middle East bleed in races over 7kms. Once a horse bleeds in a race, the blood cells are removed by scavenging white blood cells (called phagocytes). However, in a severe bleed, the red cells trapped in the airways develop an allergic and inflammatory reaction, causing long term airway disease, which in turn increases the risk of chronic allergic and reactive airway disease (RAD).

If a horse bleeds severely once, it has a 70% increase in the chance that it will bleed badly again, especially for horses over 6 years of age in high risk sports such as racing, eventing and polo.

Once a horse has bled, an adequate time of 2-3 months must be given for blood vessel and lung sac wall repair. Any concurrent airway disease must be treated with antibiotics and other appropriate therapy. There are a number of therapies that are advocated to assist in healing, strengthening and improving the elasticity of lower airway structures.
Reducing the Risk of Lung Bleeding

There are a number of measures that can be taken to reduce the incidence of lung bleeding, but because of the inherent stress on lung arteries by high blood pressure generated during exercise and damaging concussion waves resonating within the chest cavity, bleeding cannot be completely prevented.

On return to training:

• Avoid hard swimming as a part of the training program - high blood pressures and restricted chest expansion by the surrounding water pressure can increase the internal pressures within the lungs, increasing the risk of recurrence of a bleeding episode. However, controlled swimming a horse to cool it off for 1 - 1 V2 minutes or to reduce leg concussion where a horse has joint problems is unlikely to result in bleeding.
• Warm the horse up thoroughly for 10-15 minutes prior to all-out galloping to improve blood perfusion, open lung airways and increase vessel elasticity and 'stretch'. Work a 'bleeder' last in a morning session when the inhaled air is likely to be warmer. This will help to reduce airway narrowing (bronchoconstriction) in response to inhalation of cold air and will avoid airway and airsac chilling under cold conditions.
• Instigate a program of short, sharp sprints over 350-400 metres to maintain maximum aerobic fitness and capacity. Repeat twice on a fast work morning, with a 600-800 metre trot (loose rein) in between the all-out sprints. This will control the stress associated with high blood pressure over long, sustained galloping and concussion waves into the chest cavity on the already damaged airsacs and lung tissues.
• After a hard gallop, warm down over 7-10 minutes with a slow to medium trotting exercise program. If possible, turn the horse out for a green pick for a minimum of 4-6 hours or allow it to eat from a bin at ground level on the day after strenuous or all-out exercise to facilitate airway drainage.
• Provide a suitable "bleeding" control medication based on reducing lung artery blood pressure (drug free medication), fluid build-up in the tissue spaces between the airsacs (frusemide (Lasix®) drug) or herbal preparations to assist airsac and blood vessel wall healing. Benefits from Vitamin K and Vitamin A supplementation in preventing bleeding are based on anecdotal evidence only.
• Maintain adequate ventilation in the stable area (without risking cold breezes or chilling) to remove dust and accumulated ammonia levels in the air, which a horse breathes when stabled and fed on dry feeds. Remember to feed below chest height to encourage lower airway drainage and dampen the feed to reduce dust and moulds that cause irritation and airway reaction. Use low dust bedding to reduce risk of lower airway reaction and weakening of the lung sac walls.

Reducing the Risk of Airway Disease

There a number of measures that can be adopted to reduce the risk of lower airway disease and is subsequent adverse effects on performance.

Respiratory Viral Infection

Recognise symptoms early - early symptoms include elevated temperature, decreased appetite, depression and lower exercise tolerance for 2-4 days prior to evidence of more obvious signs such as a runny nose, coughing or noisy respiration. Cease fast work and lightly work the horse for 2-3 days to observe whether these typical symptoms develop. If symptoms develop, isolate the horse and treat accordingly. Provide feed in bins at below chest height and access to daytime grazing to encourage airway clearance.

The natural immunity created following infection with Equine Herpes Virus only lasts for 30 days after an infection. A large number of horses in training have a reduced immunity due to physical stress, and can become "carriers' of the Equine Herpes Virus, harbouring viable virus particles in their throat tonsil area. They do not show symptoms, but can spread aerosol droplets into the stable air space, which are likely to infect other horses, particularly those with low immune defence against the virus when first brought into work.

Vaccination against common respiratory viruses is important to reduce the risk of infection and subsequent chronic upper and lower airway disease conditions. Booster shots should be given as prescribed and all horses vaccinated at least 2-3 weeks prior to entering the stable for training. Consult your own vet for more specific advice.
Pharyngeal Lymphoid Hyperplasia (PLH)

This is a common low grade reaction that often develops in the large tonsil area at the back of the pharynx or throat of young 2-3 year old horses following Equine Herpes Viral infection. The tonsil tissue become reactive and inflamed as monocyte phagocytic (engulf cleaning cells) and other white cells accumulate to control the viral infection and local tissue damage within the tonsil lymphoid structures.

Infective viral particles can be harboured within the lymphoid tissue providing a source of reinfection and developing into a "carrier" state as the immune defence is not strong enough in young horses as they adapt to training. It is also considered that dust, ammonia and inhalation of cold air creates ongoing irritation and low grade infection.

Although PLH condition has not been associated with reduced performance in 2-3 year old horses, tonsil enlargement could restrict the upper airways and result in interference with laryngeal function in the throat. Some horses develop symptoms of a "sore" throat, reduced appetite and occasional coughing, especially when cold air is inhaled in early morning training when they are exercising to warm-up. In most cases, when young horses are turned out to rest after a preparation, the reduced stress and airway insult with dust etc enables the tonsil tissue to become less reactive and the condition resolves.

There is no recommended treatment for PLH, although administration of cortisone and immune booster preparations such as Equimmune and Immunovet have been claimed to be of clinical benefit. Administering a mixture of 30mL of glycerine containing 6 drops of weak iodine solution (2.5% iodine) over the tongue daily about 10 minutes prior to working the horse is widely used by trainers. It is administered daily for 7-10 days and provide a soothing, lubricating and antiseptic action to the throat and tonsil area, and can assist in limiting PLH and symptons of coughing.