Equine Respiratory Disease Part 2: The Lower Airway

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Equine Respiratory Disease Part 2: The Lower Airway

by: Ball, DVM

August 1998 Article # 533

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http://www.thehorse.com/viewarticle.aspx?ID=533

The lower airway consists of the lungs and the air tubing (bronchi)

that supplies them. The lungs have some very interesting and unique

protective mechanisms that put forth a great effort to prevent

infection. Obviously, the air we breathe is not sterile and contains

many contaminants such as dirt, dust, pollen, chemicals, and

particles of a million other things as well as bacteria, viruses,

and fungal elements.

MICHAEL A. BALL, DVM PHOTO

A horse with pleuritis and indwelling drains into the thoracic

cavity allowing for continuous drainage of inflammatory material.

The protection actually starts in the upper airway with filtering,

humidifying, and warming of the inspired air. The upper respiratory

system, trachea, and bronchi are lined with tissue that always is

covered with a wet/sticky mucus to which contaminants in the air

will stick. To take the process one step further, the tissue lining

the trachea and bronchi has a billion or so cells with extremely

small hair-like fibers sticking out into the airway (these hair-like

fibers are called cilia).

The cilia increase the surface area of the filtering surface and

play an active role in airway protection. Through a process called

mucociliary transport, the debris that is collected on the surface

of the airways actually is transported away from the lungs. Also

called the mucociliary escalator, the small fibers " beat " in a

coordinated manner to move the thin layer of mucus that floats on

top of the cilia (and the debris stuck to it) out of the lungs and

up the trachea, where the horse (and we) swallow it. Absolutely

disgusting--and you aren't even aware that it is happening. But it

is essential for the maintenance of the lungs' normal health.

Anything that decreases the effectiveness of the mucociliary

escalator increases the chance for the development of respiratory

disease. Factors such as cold air, smoke or chemicals in the air

(like ammonia fumes from poorly cleaned stalls or because of bad

barn ventilation), and inflammatory conditions of the airways (such

as bronchitis/asthma) can decrease the defense mechanism of the

mucociliary escalator.

Another very important way by which the mucociliary clearance

mechanism can be overwhelmed and rendered less effective is forced

head posture during transport. In fact, the transportation process

can stress the defense mechanism of the lungs in several ways. The

exhaust fumes from a poorly maintained or designed truck or van can

have a negative effect on the mucociliary escalator. In addition, a

trailer or van that has poor drainage can allow for the buildup of

ammonia fumes during the ride, thus adding another negative factor.

And finally, if the ventilation within the trailer or van is bad, it

can worsen all of the aforementioned negative factors regarding lung

health during transportation.

There have been several scientific papers evaluating the effects of

transportation and head posture on lung health. One such paper by

Dr. S. L. Raidal, from the Department of Veterinary Pathology,

University of Sydney, entitled " Effects of posture and accumulated

airway secretions on tracheal mucociliary transport in the horse, "

was published in a 1996 issue of the Australian Veterinary Journal.

Raidal demonstrated that horses confined with their heads elevated

for 24 hours developed an accumulation of inflammatory airway

secretions that was associated with increased numbers of bacteria in

the lower respiratory tract. These findings " have implications for

management practices where horses are prevented from lowering their

heads, such as transportation and cross-tying, which may therefore

contribute to lower respiratory tract disease in horses. "

Great attention should be devoted to ensuring that head posture is

not restricted to such a degree that the respiratory system is

compromised.

In addition to the mucociliary clearance system, there are other

protective mechanisms in place to protect the respiratory system

against infection. There are millions of special cells deep within

the tissues of the lung that can kill bacteria and inactivate

viruses. Going back to last year's article on the immune system (The

Horse of December 1997), you'll remember the special white blood

cells that have the ability to engulf and kill invading organisms.

These cells are plentiful within the lungs and play a vital role in

the local immune system. It should be noted that the normal function

of these cells can be impaired by a number of factors. Many of the

factors that decrease the effectiveness of the mucociliary transport

also can have a negative effect on the cellular immunity within the

lungs. In addition, the cellular defense mechanisms can simply be

overwhelmed by high concentrations of environmental contaminants.

Should infection occur, the respiratory tissue easily can be flooded

with extra white blood cells from the blood.

Pneumonia

Pneumonia is a vague term that simply means " inflammation of the

lung. " It does not define the actual cause of the inflammation. As

we will explore here, the causes of pneumonia are numerous.

Viral Pneumonia

We will briefly return to the upper airway when we discuss the viral

respiratory diseases since many of the viral entities affecting the

lungs also affect the upper airway.

Equine Adenovirus--The equine adenoviruses can be found all over the

world. It must be noted that infection with the virus is not always

associated with the development of disease. In adult horses,

infection is more likely to go unnoticed, whereas foals are more

likely to develop clinical signs. Infection with the adenoviruses

commonly involve the respiratory tract and conjunctiva of the ocular

tissues. Clinical signs can include coughing, nasal discharge,

shortness of breath, inflammation of the pink tissue surrounding the

eyes, and fever. Infection with the adenovirus, if clinical signs

develop, generally does not require any significant treatment.

Foals, however, might be more severely affected.

Equine Influenza--The equine influenza virus is in the same family

as that which causes the " flu " in people, although it is different

enough that human infection with the equine flu virus does not

naturally occur. The flu viruses contain a chemical that very

effectively damages the mucociliary transport mechanism, allowing

for evasion of the immune system. In addition, the damage to the

mucociliary transport system can take several days or longer to

repair, leaving the defense mechanisms decreased and opening the

horse up to the possibility of secondary bacterial infection. The

disease can be extremely contagious, especially in conditions of

crowding and poor ventilation--some racetracks have an " outbreak "

several times per year.

Influenza most commonly affects two- and three-year-olds. Stresses

on the respiratory tract's immune system, and inadequate vaccination

can be predisposing factors. The incubation period is one to three

days, with the virus typically affecting the upper respiratory tract

to a greater extent than the lungs. Clinical signs typically appear

three to five days following exposure to the virus. The clinical

signs include fever, anorexia, depression, a clear nasal discharge,

and a deep, dry cough. Some horses experience muscle pain (they

might be reluctant to walk) and have swollen legs (edema). The

course of infection is typically from two to 10 days if there are no

complications; secondary bacterial infection is a common

complication of equine influenza. Horses can shed virus for three to

six days after the last signs of illness and should be kept in

isolation for that period of time.

The treatment generally involves symptomatic care and the use of

antibiotics only if a secondary bacterial infection is suspected.

One of the greatest risks is that an affected animal will be put

back in work too soon. The nature of the virus is to cause a

significant amount of tissue damage that requires time to regenerate

and heal. Should the horse be placed back in work too soon, the

likelihood of complications developing is great. In some horses with

severe infections, there might be the need for one to two months of

rest prior to resumption of training--always adhere to your

veterinarian's advice regarding the convalescent time.

Young foals can suffer more severely from equine influenza,

developing extensive pneumonia that has the potential to be fatal.

Foals exhibiting signs of respiratory disease should receive

veterinary attention as soon as possible.

Regular vaccination can significantly reduce the population at risk

and is recommended. For younger athletic horses which might be at

greater risk, it is suggested that they be vaccinated at four- to

six- month intervals as opposed to the older horses, which should

receive their boosters at nine- to 12-month intervals.

Equine Herpesvirus (Rhino)--Equine herpesvirus, equine rhino, rhino,

and rhinopneumonitis are all synonyms for the equine herpesvirus.

Rhino implies the upper airway and rhinopneumonitis means

inflammation of the upper airways and lungs. There are four

currently known strains of the equine herpesvirus known as 1, 2, 3,

and 4. It is strains 1 and 4 that are associated with respiratory

disease in the horse.

Respiratory disease related to the herpesvirus most commonly occurs

in foals, weanlings, and yearlings. The immunity to herpesvirus

infection is short-lived and reinfection is thought to occur; re-

exposure generally results in a milder or subclinical (undetected)

infection. In broodmares, there can be abortion related to

infection. The equine herpesvirus type 1 has the ability to cause

respiratory disease, abortion, and neurologic disease. Foals can

essentially be born suffering from extensive pneumonia (if they are

not aborted) and die within 72 hours. Any signs of respiratory

distress in a newborn should be evaluated by your veterinarian

immediately.

The infection occurs via the inhalation of the virus. The virus does

not tolerate being outside of the body for extended periods of time,

so close contact with an infected animal or tissues is probably

important for transmission. The clinical signs appear one to three

days following infection and include fever, anorexia, depression, a

clear nasal discharge, and a deep dry cough--they cannot be

distinguished from influenza.

The treatment is largely supportive and, as with influenza, the

convalescent period of rest is extremely important for reducing the

complication rate. Vaccination will not prevent the disease, but can

reduce the severity of the disease. If you have any pregnant mares,

they might need to be vaccinated accordingly to prevent abortion.

You should check with your veterinarian regarding the vaccination of

a pregnant mare for protection against the herpesvirus.

Equine Rhinovirus--There are several equine rhinoviruses that

primarily cause mild upper respiratory disease. The

equine " rhinovirus " should not be confused with equine " rhino "

or " rhinopneumonitis, " which is caused by the equine herpesvirus.

Equine Viral Arteritis--The equine arteritis virus, as offered by

its name, causes inflammation of the blood vessels. Transmission of

this virus can occur via inhalation or sexual contact. The virus

rapidly spreads throughout many of the body's organs and the disease

can produce signs of respiratory distress. The disease also can

cause abortion anywhere from 10 to 34 days following exposure.

The incubation period is three to 14 days (six to eight days if

passed by the veneral route). The main clinical signs include fever,

anorexia, depression, and potentially a cough. In addition, a clear

nasal discharge, a bright reddening of the nasal and ocular tissue,

and excessive tear production can be associated with EVA.

The treatment, as with all the other viral diseases, consists mainly

of supportive therapy and observation for any secondary bacterial

infection. Convalescent rest is extremely important, and isolation

should be maintained for three to four weeks past the last

observation of clinical signs to prevent transmission. Most horses

recover uneventfully, but occasionally young foals suffer a

fatality.

Viral Diagnosis

As you now know, the clinical signs for most of the viral

respiratory diseases are very similar. In many cases, the exact

cause does not have a significant bearing on the treatment, but

knowing the specific cause can provide valuable information with

respect to management and the future. A nasal swab can be acquired

for an attempt to grow and identify the virus in the laboratory.

This is the most common way to confirm a diagnosis. In addition,

there are several advanced laboratory techniques used in the

identification of a virus present in a laboratory sample. Another is

to evaluate the concentration of antibodies in the blood for the

suspected virus. Remember that the antibodies are proteins

manufactured by the body when the immune system is stimulated. These

tests unfortunately take time for the antibody levels to rise in

response to disease, and therefore require two samples a week or so

apart in order to demonstrate a " rise " in the titer proving that the

immune system was being stimulated by a particular virus.

Vaccination also can increase the antibody titer (concentration),

which sometimes makes interpreting the test results more difficult.

Bacterial pneumonia

As has been stated, the air we breathe is not sterile, and neither

are many parts of the upper respiratory system. There is a constant

source of bacteria that could potentially invade the lung. There are

more than a dozen types of bacteria that have been identified as

being involved in pneumonia in the horse. Most of these bacteria

either are common to the environment of the horse, or are a normal

inhabitant of the upper airway or throat area. In most cases of

pneumonia, there is some predisposing cause.

Bacterial pneumonia often follows viral pneumonia due to the damage

to the normal protective mechanisms and disruption of the local

immune system. This situation often is the result of bringing a

horse back into work too soon after suffering from a viral

respiratory disease. Other stressful events that can lead to the

development of bacterial pneumonia include any intense athletic

exercise, transportation, poor nutrition (leading to a decrease in

immune function), and overcrowding. Realistically, many horses

experience these factors on a daily basis without problem, but they

all can potentially contribute to respiratory disease. Also, primary

immune dysfunction (such as Arabian foals afflicted with CID), the

aspiration of feed material due to neurologic dysfunction or choke,

or inflammation due to parasitic disease can contribute to the

development of bacterial pneumonia.

The clinical signs associated with bacterial pneumonia include

fever, depression, inappetence, nasal discharge, coughing,

respiratory distress, and the presence of abnormal lung sounds. In

more chronic cases, the onset can be slow and vague, with exercise

intolerance and weight loss being the only clinical signs.

In some cases, the infection might be localized and walled off in

the form of an abscess. If the development of the abscess is

insidious enough, the first recognition of the disease can be severe

acute respiratory distress during exercise. The exacerbation of the

disease occurs when the lung abscess ruptures or leaks during the

stress of exercise.

The diagnosis of bacterial pneumonia often is made based on history,

clinical signs, and what the lungs sound like. Ultrasound and

radiographs might be necessary to assess completely the extent of

the infection. If the clinical signs are severe or antibiotic

therapy has been unsuccessful, a transtracheal wash can provide very

important information and might help direct therapy. (See article on

transtracheal wash in The Horse of March 1997.)

The treatment of bacterial pneumonia generally consists of long-term

antibiotic therapy, any supportive therapy necessary, and rest. The

outcome of bacterial pneumonia can be extremely variable and depends

on the predisposing causes, duration of infection, amount of lung

tissue involved, the specific type(s) of bacteria involved, and the

existence of additional complications. Again, it is important to

follow your veterinarian's instructions regarding convalescent time

and antibiotic therapy in order to prevent a relapse.

Shipping Fever

With respect to the respiratory system, there are a number of known

factors that can predispose an individual horse to respiratory

disease. Many of these factors have been heavily researched, and

others are just hypothetical but make good sense and have been

distilled from the wisdom of generations of horse trainers and

people specializing in horse transport.

There have been several studies evaluating the direct effects of

transportation on the internal environment of the lungs. In the June

1997 issue of the Australian Veterinarian Journal, Dr. S. L. Raidal,

et al. from the Department of Veterinary Pathology, University of

Sydney, New South Wales, published a paper entitled " Effect of

transportation on lower respiratory tract contamination and

peripheral blood neutrophil function. " The study looked at six

horses which had been transported by road for 12 hours. A sample of

fluid was obtained from within the trachea (windpipe) both prior to

and immediately following transport. When compared to the pre-

transport controls, the post-transport tracheal fluid contained

signs of inflammation and an increased number of bacteria. The

sample also showed that of the bacteria a Streptococcus species was

the most predominant (Streptococcus is a common pneumonia-causing

bacteria in the horse).

In addition to the evaluation of the tracheal fluid, the researchers

also evaluated the function of a type of white blood cell--the

neutrophil. The neutrophil will migrate out of the blood to sites of

infection and, in a Pac Man-like way, surround and kill invading

bacteria. Raidal demonstrated that after transport, the neutrophils

from the blood of these horses had a significantly reduced ability

to devour and kill bacteria. The conclusion was that " bacterial

contamination of the lower respiratory tract occurs as a routine

consequence of transportation of horses and is likely to be an

important determinant in the development of transport-associated

respiratory disease. "

Another study that carried this research a little deeper was

reported in the May 1997 issue of the American Journal of Veterinary

Research. A paper by S. Hobo, et al. from the Equine Research

Institute, Japan Racing Association, Tokyo, Japan, entitled " Effect

of transportation on the composition of bronchoalveolar lavage fluid

obtained from horses " presented research evaluating the pulmonary

effects of 41 hours of transport in 20 horses.

The bronchoalveolar lavage is a technique that evaluates the state

very deep within the lung. This technique, therefore, reflects the

health of a small portion of lung tissue itself. What Hobo

demonstrated was that there were four times the number of cells

indicating inflammation in the samples from transported horses as

compared to controls. In addition, the research also demonstrated a

decrease in the concentration of a protein that " may reduce the

pulmonary defense mechanisms in the alveolar region, possibly

resulting in infection. "

Pleuropneumonia

Remember that the pleura is the thin covering of the lung or the

thin lining of the thoracic cavity. Pleuritis is an inflammation of

the pleura (essentially the space between the body wall and the

lung). Pleuropneumonia is inflammation both within the lung and

within the pleural cavity. In most cases, pleuritis is secondary or

occurs in conjunction with pneumonia or a ruptured lung abscess that

infects the pleural space.

All of the factors that predispose to the development of pneumonia

also are thought to predispose to the development of pleuritis, but

anything specific leading to the development of pleuritis is

unknown. The development of pleuritis in conjunction with pneumonia

can greatly complicate and prolong treatment; successful treatment

can take up to six months, and there can be fatalities. A variety of

bacteria can infect the pleural space. The type of individual

bacteria that cause disease can have a great impact on the overall

outcome.

The clinical signs of pleuritis/pleuropneumonia include fever,

depression, nasal discharge, and being off feed. In addition,

pleuritis is an extremely painful disease process--these horses

often hurt between the ribs. There also will be a reluctance to walk

with some of these horses, presumably due to the chest pain. In

chronic cases, weight loss can be a prominent clinical sign.

One of the hallmark clinical signs of pleuritis is the buildup of

fluid within the thoracic cavity. This fluid muffles the lung sounds

in such a way that there is a straight line (a fluid line) of

silence parallel to the ground at the junction between fluid and

lung. There also are " sandpaper rubbing " sounds heard with the

stethoscope called pleural friction rubs. These abnormalities can be

confirmed and further defined with the aid of ultrasonography. The

fluid within the pleural cavity generally is cultured and evaluated

microscopically for the presence of bacteria; there are some forms

of thoracic cancer that can produce all of the clinical signs

associated with pleuritis.

The treatment of pleuritis can be very difficult and relies on long-

term antibiotics, supportive therapy, and drainage of the fluid from

the thoracic cavity should it become necessary. There are numerous

complications that can occur on the road to recovery for these

horses, but if no complications occur, treatment can be successful.

In a 1996 issue of the Journal of The American Veterinary Medical

Association, Krista Seltzer, DVM, Diplomate ACVS, and Doug Byars,

DVM, Diplomate ACVIM, from Hagyard-son-McGee in Lexington, Ky.,

reported on the " Prognosis for return to racing after recovery from

infectious pleuropneumonia in Thoroughbred racehorses: 70 cases

(1984-1989). " Their study indicated that 61% of horses having

suffered from pleuropneumonia raced following recovery.

Parasitic Pneumonia

There are several different parasites that can end up in the lung.

The first of these is the common intestinal roundworm--the ascarid.

The ascarid is a unique little creature that has a life cycle that

goes something like this. After being swallowed, the worms migrate

out of the intestine and into the abdominal cavity, where they

migrate through the liver and the lung. Once they have finished the

lung migration, they come out in the airways, get coughed up and

swallowed, where they end up back in the intestine. There they

become adults and produce eggs.

If the parasite infection is great and the number of worms within

the lungs is high, you will see clinical disease. This case scenario

is most typically seen in young horses (four to six months of age),

with the main clinical sign a moist cough.

The second lung parasite is the true " lungworm " of horses. Donkeys

and mules are carriers for the equine lungworm and do not show any

clinical signs. The horse develops pneumonia and will show clinical

signs (chronic coughing) two to three months after being infected.

Horses with chronic coughs which have been exposed to donkeys or

mules should be evaluated for the presence of lungworms.

COPD

The term COPD stands for chronic obstructive pulmonary disease,

otherwise known as " heaves. " Other names for this disease

include " chronic pulmonary disease, " " chronic airway

reactivity, " " hyperactive airway disease, " " hay sickness, "

and " broken wind. " This disease is characterized by airway

obstruction at the level of the bronchi, primarily due to airway

constriction similar to asthma in people.

The specific causes of heaves are as yet unknown. There are

suspicions that a variety of allergic reactions might be involved.

Many clinicians consider heaves to be a hypersensitivity reaction to

dusts and molds. The incriminated molds, Aspergillus and

Micropolyspora, are commonly found in poorly cured hay. There appear

to be two categories of affected horses. One group appears to be

reacting to allergens within the barn and gets better when kept

outside; another group (more commonly located in the Southeast)

appears to be reacting to allergens in the pasture and gets better

when kept inside.

The clinical signs include a chronic cough, a cloudy nasal

discharge, and difficulty in expiring air; these horses usually take

in air relatively well--it is on exhalation where there is

difficulty. Because COPD is primarily an allergic reaction without

the presence of infection, there is generally no fever (unless there

is the development of a secondary bacterial infection). In addition,

exercise intolerance, weight loss, and not eating are additional

clinical signs. Sometimes these horses can get into trouble because

they are so focused on breathing they will not (cannot) take the

time out from the effort of breathing to eat or drink. Sometimes

older horses with chronic heaves will have a hypertrophy of the

external abdominal oblique muscle noted along the body wall as an

indication of the long-standing disease process.

The diagnosis of heaves generally is based on history and

examination of the respiratory system. Sometimes other diagnostic

tests, including a transtracheal washing, might be necessary to rule

out other secondary problems. However, a bronchoalveolar lavage is

preferred to a transtracheal wash for diagnosis of COPD.

The treatment of heaves involves altering the horse's environment.

If a horse is worse outside, then keep him inside, and vice versa.

Often wetting of the hay (or occasionally complete removal of hay

from the diet) is necessary, along with bedding on non-dusty wood

chips or newspaper. Should it become necessary to remove hay

completely from the diet, there are several fermented hay products

and other complete feed products on the market (see the Nutrition

column on haylage and processed hay feeds in The Horse of July 1998,

article #513). In my experience, the management changes are very

important and must occur in addition to the medical management of

heaves. Approximately 50% of the horses I have worked on which had

heaves respond favorably to management changes.

Medical therapy typically involves making sure there is no secondary

bacterial infection either by diagnostic testing or by a short

course of antibiotic therapy. The main focus of therapy is to

decrease the inflammation associated with the allergic reaction

going on within the lungs. The drugs of choice for this--as it is

for people with asthma--are corticosteroids and/or bronchodilators.

Steroids decrease inflammation and bronchodilators relieve

respiratory distress by opening obstructed airways. During a severe

crisis, the main problem is the constricted small airways within the

lungs. The use of drugs that function to dilate the airways can be a

great benefit, if not lifesaving. With respect to systemic therapy,

caution must be used as these drugs can have significant side

effects. The corticosteroids suppress the immune system and can

predispose to infection. Their use also has been associated with the

development of founder (laminitis).

One of the most potent bronchodilator drugs, atropine, can have

great and negative impact on gastrointestinal motility and can

induce colic if used in excess or if the horse is sensitive to it.

Many of the other bronchodilator drugs have a narrow range between

therapeutic and toxic and have to be administered frequently, making

them less useful in the horse. The drug albuterol (common human

asthma drug) has been used in the horse, but our clinical

pharmacology laboratory has just recently determined that albuterol

is not absorbed well out of the horse's gastrointestinal system and

therefore has no benefit when given orally.

One drug that recently was approved by the FDA should offer a needed

therapy for horses with heaves. The drug " clenbuterol " (trade named

Ventipulmin Syrup) has been used outside of the United States for

some time now with reported success--the drug can be given orally

and is absorbed well from the gastrointestinal tract. (See The

Horse, July 1998, pg. 19 for more information on Ventipulmin.)

Another method of therapy is the use of inhalers. The inhaler is

probably the main line of defense for the maintenance of asthma in

people and has, until recently, posed a unique problem with respect

to use in the horse. The development of the Aeromask, by Trudell

Medical in Ontario, Canada, now allows veterinarians effectively to

utilize inhalant medication in the horse. The system is quite unique

and allows for the use of some great human asthma drugs in the form

of inhaled steroids, bronchodilators, and other drugs to control

allergic inflammation. These drugs have been used successfully with

minimal effort to control advanced cases of COPD, but the main

drawback is the expense. Without the $5 insurance co-pay offered by

human insurance, many of these drugs cost in excess of $50 per

inhaler, which might only last a few weeks in the horse.

Nonetheless, these provide another option for the effective

treatment of heaves. As newer inhalant drugs are developed for

people, the cost of some of the older drugs has become significantly

less.

See more on COPD in article #618.

EIPH

Exercised-induced pulmonary hemorrhage is a disease of athletic

horses in which there is hemorrhage originating from within the

lungs (the exact location is unknown). The hemorrhage can be subtle

enough to be seen only by microscope evaluation of a bronchial

aspirate, or frank enough to be observed pouring from the nostrils.

Some additional clinical signs include exercise intolerance,

respiratory distress, coughing, and excessive swallowing. The

diagnosis generally is made by evaluation with the endoscope within

90 minutes of exercise; examination of aspirates from the trachea or

bronchi allow the veterinarian to look for white blood cells that

have ingested red blood cells as evidence of EIPH.

Treatment of EIPH involves ruling out the presence of infection. The

use of the diuretic drug Lasix (furosemide) to combat EIPH in

athletic horses might be restricted by whatever authority governs

the individual horse's activities; different states also have

different regulations.

[Guest guest]

n-acetyl-cysteine and massive doses of vitamin C both seem to help

clear my airways..

I bet you could give both to a horse in water.. n-acetyl-cysteine

helps loosten up the mucous membranes and I am pretty sure is helpful

for athsmatics..

(oral) Choline supplementation might help as well, especially if the

infection is from stachybotrys.. as stachy also effects the mucous

membranes in the lungs and choline is involved in acting as a

" surfactacent " maintaining moisture and cellular integrity at that

interface.. (I'm just guessing here on that, but it works for me)

With horses, you have to give them these things in bulk.. Talk to your

vet about it and dosages.... search PubMed...

Mold disease is probably as common in horses environments as it is in

humans.. Horses are beautiful, often affectionate and gentle animals..

They don't deserve it...

On 1/16/06, tigerpaw2c <tigerpaw2c@...> wrote:

> Equine Respiratory Disease Part 2: The Lower Airway

> by: Ball, DVM

> August 1998 Article # 533

>

> Article Tools

>

> http://www.thehorse.com/viewarticle.aspx?ID=533

>

> The lower airway consists of the lungs and the air tubing (bronchi)

> that supplies them. The lungs have some very interesting and unique

> protective mechanisms that put forth a great effort to prevent

> infection. Obviously, the air we breathe is not sterile and contains

> many contaminants such as dirt, dust, pollen, chemicals, and

> particles of a million other things as well as bacteria, viruses,

> and fungal elements.

>

>

> MICHAEL A. BALL, DVM PHOTO

>

> A horse with pleuritis and indwelling drains into the thoracic

> cavity allowing for continuous drainage of inflammatory material.

>

> The protection actually starts in the upper airway with filtering,

> humidifying, and warming of the inspired air. The upper respiratory

> system, trachea, and bronchi are lined with tissue that always is

> covered with a wet/sticky mucus to which contaminants in the air

> will stick. To take the process one step further, the tissue lining

> the trachea and bronchi has a billion or so cells with extremely

> small hair-like fibers sticking out into the airway (these hair-like

> fibers are called cilia).

>

> The cilia increase the surface area of the filtering surface and

> play an active role in airway protection. Through a process called

> mucociliary transport, the debris that is collected on the surface

> of the airways actually is transported away from the lungs. Also

> called the mucociliary escalator, the small fibers " beat " in a

> coordinated manner to move the thin layer of mucus that floats on

> top of the cilia (and the debris stuck to it) out of the lungs and

> up the trachea, where the horse (and we) swallow it. Absolutely

> disgusting--and you aren't even aware that it is happening. But it

> is essential for the maintenance of the lungs' normal health.

>

> Anything that decreases the effectiveness of the mucociliary

> escalator increases the chance for the development of respiratory

> disease. Factors such as cold air, smoke or chemicals in the air

> (like ammonia fumes from poorly cleaned stalls or because of bad

> barn ventilation), and inflammatory conditions of the airways (such

> as bronchitis/asthma) can decrease the defense mechanism of the

> mucociliary escalator.

>