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IN DEPTH: INFLAMMATORY AIRWAY DISEASE
IAD: Cough, Poor Performance, Mucus in the
Airways—What Is So Important About That?
Laurent L. Couëtil, DVM, Diplomate ACVIM
Author’s address: Department of Veterinary Clinical Sciences, Purdue University School of Veterinary Medicine. West Lafayette, IN 47907-1248. © 2002 AAEP.
1.
Introduction
The lower respiratory tract responds to a variety of
inhaled irritants in a stereotypical way by coughing,
increasing mucus secretion, and bronchospasm.
The purpose of such response is to limit further
inhalation of irritants and to accelerate their removal from the respiratory tract. Additional defense mechanisms involve alveolar macrophages,
airway-associated lymphoid tissue, and systemic
immunity.1,2 Substances irritant to the airways
may be infectious agents (viruses, bacteria, mycoplasma, fungi), parasites, endotoxins, molds, dust,
noxious gases, or pollutants.1 Airway inflammation may result if exposure to the irritant is of sufficient magnitude.
Lower airway inflammatory diseases include infectious and parasitic diseases, interstitial pneumonia, recurrent airway obstruction (RAO) or heaves,
and inflammatory airway disease (IAD).3– 6 Inflammatory airway disease is an incompletely characterized pulmonary disorder that is most
commonly observed in young, athletic horses.7
Contrary to other lower airway inflammatory diseases, clinical signs of IAD are subtle and include
chronic cough, excess mucus in the trachea, and poor
performance; otherwise, horses have a normal atti-
tude and appetite, are not febrile, and do not exhibit
increased respiratory effort at rest.8 –10
Recently, a panel of international experts recommended using the term IAD instead of small-airway
inflammatory disease, small-airway disease, and
bronchitis/bronchiolitis, which have been used in the
past to describe the disease.5,11–13 In addition to
terminology issues, confusion may result from
horses with IAD being included in broader disease
categories such as undifferentiated pulmonary disorders, chronic obstructive pulmonary disease, and
lower airway disease.3,7,8,14
The purpose of the following discussion is to clarify our current understanding of IAD focusing on
clinical characteristics.
2.
Historical Findings
RAO or “heaves” is an allergic disease characterized
by cough, accumulation of mucopurulent secretions
in the tracheobronchial tree, abnormal breath
sounds, increased respiratory efforts, and exercise
intolerance.15 Clinical signs result from small-airway obstruction secondary to airway inflammation,
bronchospasm, mucus plugging of airways, and
thickening of the airway wall. Cytologic examination of respiratory secretions usually reveals moderate to severe neutrophilia.16 Clinical signs resolve
NOTES
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IN DEPTH: INFLAMMATORY AIRWAY DISEASE
Table 1. Summary Comparison Between Recurrent Airway
Obstruction (RAO) and Inflammatory Airway Disease (IAD).
Heaves/RAO
IAD
• Older horses
• Chronic cough, mucopurulent
exudate, abnormal lung
sounds, increased
respiratory efforts, marked
exercise intolerance
• Chronic inflammation
• Allergic etiology
• Moderate to severe airway
obstruction
• Recurrent disease
• Bronchitis/bronchiolitis
• Young performing horses
• Chronic cough,
mucopurulent exudate,
mild exercise intolerance
• Chronic inflammation
• Multifactorial etiology
• Mild airway obstruction
• Not recurrent
• Bronchitis/bronchiolitis
within a few days after implementation of environmental changes such as reducing organic dusts, conversely susceptible horses housed indoors and
exposed to moldy hay develop clinical signs within a
few hours to a few days.17,18 Horses with RAO tend
to be mature to old animals with obvious clinical
signs of respiratory disease and severe exercise intolerance during period of disease exacerbation.
A mild form of lower airway inflammatory disease
commonly encountered in young athletic horses has
been recognized recently as a separate entity from
RAO and termed “inflammatory airway disease.”19 –21
In the majority of cases, RAO and IAD may be differentiated based on clinical grounds (Table 1); however, some have argued that, over time, horses with
IAD may progress into RAO.5 The incidence of IAD
in racehorses may vary between 11% and 65% depending on the diagnostic criteria used (endoscopy,
cytology) and the conditions of examination (i.e.,
pre- versus post-exercise).7–9 Horses with IAD
usually have a history of decreased performance,
mild exercise intolerance, cough, and increased respiratory secretions.14,19 Foals and older horses
may also suffer from IAD.22,23 In these cases, the
diagnosis is often reached by excluding infectious
and other non-infectious causes of lower airway inflammation. The possibility of IAD should be considered in horses with signs of respiratory disease
including tracheobronchial mucopurulent exudate
that do not respond, or relapse, after antimicrobial
therapy and further diagnostic tests should be pursued (e.g., bronchoalveolar lavage).
Duration of IAD is 7 wk on average with a range
of 4 –22 wk, which is longer than most infectious
respiratory diseases.14,24 In a study involving 170
thoroughbred horses in training over a 2-yr-period,
it was estimated that during 8 of the 24 mo, horses
had some degree of IAD.14 IAD appears to be more
common in young, athletic horses with the incidence
decreasing with increasing age.7,25 IAD is particularly common in thoroughbred and standardbred
racehorses, but has been also reported in a variety of
other breeds such as Quarter Horse, Warmblood,
Appaloosa, and American Saddlebred.8,14,23,26,27
In fact, horses of any breed may be affected but
racehorses are over-represented because of several
factors. First, the major limiting factor to performance in a racehorse is pulmonary gas exchanges;28
therefore, even a mild degree of respiratory disease
may have a profound negative impact on performance, whereas the same problem in a dressage
horse would be considered clinically insignificant.
Second, most racehorses are kept in an environment
that is particularly challenging for the respiratory
tract. They are often confined in stables with suboptimal ventilation 24 h/d (except for the training
session), exposed to high levels of respirable irritants (e.g., dust and endotoxins from straw and hay),
and commingle in large population of horses originating from various locations.1,29 Third, racehorse
training and racing schedule and frequent traveling
are often stressful impairing body’s immune response and commonly resulting in lower airway
disease.
The most common complaints reported by owners
of athletic horses with IAD, other than racehorses,
are chronic cough and prolonged recovery after exercise. These horses may be involved in a variety of
activities such as barrel racing, three-day event,
dressage, or simply trail riding. Owners often report a history of infectious respiratory disease in the
months preceding the diagnosis of IAD with several
horses in the barn being affected. The typical history is that all horses recovered except for the one
with IAD, which continued to cough intermittently
while in the stall and/or during riding.
3.
Clinical Signs
The most common clinical signs associated with IAD
are increased respiratory secretions, cough, and decreased performance.8,19,30 Estimation of the
quantity of mucus present in the trachea by endoscopy reveals that horses free of respiratory disease
have either no mucus or a few isolated flecks and
horses with IAD have a pool of mucus at the thoracic
inlet or a continuous stream of variable width (Fig.
1).7,9 In addition, the severity of IAD is related to
the amount of mucopus and the percentage of neutrophils in tracheal wash or in bronchoalveolar lavage (BAL) fluid.7,23 The incidence of tracheal
exudate has been found to increase after strenuous exercise by some investigators9 but not by
others.31 In healthy horses, the amount of tracheal
mucus is not affected by age.32
Cough is only present in 38% of horses with IAD,
however 85% of coughing horses have IAD.10,14
Daily observation of horses in training showed that
coughing is not noted 62% of the time during which
they have IAD.14 Epidemiologic studies of thoroughbred racehorses in training found a strong association between coughing, the amount of mucus
present in the upper airways, and pharyngeal lymphoid hyperplasia.10,25 Also, a strong association
exists between coughing, isolation of bacteria, and
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IN DEPTH: INFLAMMATORY AIRWAY DISEASE
Fig. 1. Endoscopic examination of the distal trachea in a horse diagnosed with IAD.
ventral aspect of the trachea.
the degree of inflammation in tracheal wash
fluid.7,10 Nevertheless, bacteriological examination of tracheal wash samples reveals that 35–58%
of horses with IAD do not contain significant amount
of bacteria.
Other clinical signs of respiratory disease such as
nasal discharge and fever do not appear to be associated with the disease.14 Thoracic auscultation is
usually normal; however, some horses may exhibit
increased breath sounds or wheezes. Horses with
severe IAD may have a slightly increased respiratory rate and abdominal contraction on expiration. For the most part, IAD is subclinical and may
go undetected unless coughing is present or tracheal
exudate is detected by endoscopy.23
Exercise intolerance and poor performance in
racehorses have been associated with presence of
mucopurulent exudate in the tracheobronchial tree
and increased percentage of neutrophils in BAL
fluid.8,30 Other signs associated with exercise intolerance are delayed recovery of normal respiratory
rate after exercise and respiratory embarrassment.20 The latter signs are more likely to be recognized in athletic horses other than racehorses
because most of their activities do not require exercising at or above maximal aerobic capacity.
Poor performance may result from a variety of
causes such as lameness, exertional rhabdomyolysis, and cardiac and neurologic diseases. More im202
Mucopurulent secretions are pooling on the
portantly, it is common to diagnose several problems
in the same horse.33 In a retrospective study performed on 163 horses presented for poor performance evaluation at Purdue’s Equine Sports
Medicine Center, 20% of cases were diagnosed with
a combination of respiratory disease and at least one
other problem involving a different body system. These findings underscore the importance of
performing a comprehensive evaluation of poorly
performing horses.
Further characterization of the type of inflammatory process may be achieved with BAL fluid
cytology. Cytological analysis of BAL fluid allows
recognition of three types of inflammatory profiles in
IAD.6 Type 1 is the most commonly encountered
and is characterized by an increased total nucleated
cell count with mild neutrophilia (5–20% cells), lymphocytosis, and monocytosis (Fig. 2). Increased
percentages of mast cells (⬎ 2%, Fig. 3) and eosinophils (⬎ 3%, Fig. 4) are observed in IAD type 2
and 3, respectively. In contrast, BAL of horses
with RAO show moderate to severe neutrophilia
(⬎20% cells), lymphopenia, and decreased alveolar
macrophages.16,23,34 Cytology of BALF collected
from horses with RAO in clinical remission may be
normal if sufficient time away from offended allergens has been allowed. Some RAO cases may be
clinically normal but still exhibit some degree of
pulmonary neutrophilia and, therefore, may be dif-
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Fig. 2.
Bronchoalveolar lavage fluid cytology from a horse diagnosed with IAD (Wright’s stain).
ficult to differentiate from IAD. A practical way to
discriminate RAO from IAD is by performing a hay
challenge and monitoring clinical signs of respiratory disease, which should develop within a few
Fig. 3.
hours to a few days in RAO affected horses.3,18
Horses with IAD exposed to moldy hay may exhibit
a worsening of coughing and pulmonary neutrophilia; however, they do not develop increased respi-
Bronchoalveolar lavage fluid cytology from a horse diagnosed with IAD (Wright’s stain).
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Fig. 4.
Bronchoalveolar lavage fluid cytology from a horse diagnosed with IAD (Wright’s stain).
ratory efforts or nostril flaring like RAO affected
horses do.
4.
Suspected Etiology
Putative causes of IAD include bacteria, viruses,
and inhaled environmental pollutants with a modu-
latory role played by factors such as the horse’s
immune response and genetic make-up.
The likelihood of isolating bacteria from tracheal
wash samples is strongly associated with the cytologic degree of inflammation.7,10,14 Bacterial species most frequently isolated are Streptococcus spp.,
Fig. 5. Forced expiratory flow after 95% of the vital capacity has been exhaled (FEF95%) in healthy horses (normal), horses with IAD,
and horses with recurrent airway obstruction or heaves during period of disease exacerbation (crisis) or clinical remission. Values are
expressed as mean ⫾ SD (vertical bar).
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Pasteurella/Actinobacillus spp., and Bordetella spp.
Mycoplasma organisms have not been isolated in
horses with IAD. However, the role of bacteria in
the pathogenesis of the disease is unclear. First, no
bacteria are cultured in more than one third of
horses with IAD.7 Second, the presence of bacteria
in the airways may result from decreased clearance
capacity and not from primary infection. Third, the
trachea is not a sterile environment and potentially
pathogenic bacteria may be isolated by tracheal
wash in 8 –25% of healthy horses with isolation of
non-pathogenic organisms in as many as 75% of
those horses.35,36 Fourth, successful treatment of
IAD with oral interferon-alpha or inhaled glucocorticoids suggests that infectious agents may not be
causative agents but rather opportunistic invaders
of the lower respiratory tract.5,6,37
Contrary to a common belief, respiratory viruses
do not appear to play an important role in IAD.
Several reports have shown no evidence of viral
infections in horses with IAD based on serology or
virus isolation aimed at detecting equine herpes, influenza, adenovirus, and rhinoviruses.9,10,14 These
findings are consistent with the fact that no relationship has been found between presence of fever and
IAD.14
The role of exposure to dust in the pathogenesis of
IAD is suggested by several studies. Healthy yearlings fed hay demonstrate BAL fluid neutrophilia
and a higher airway inflammation score when
housed in a stable than when kept on pasture.38
Natural exposure of healthy horses to moldy hay or
controlled exposure to organic molds and endotoxins
to levels encountered during natural exposure result
in BAL fluid neutrophilia.34,39,40 Also, horses in
training kept on straw bedding experience episodes
of IAD that last longer than in horses bedded on
paper.14 These findings are consistent with data
showing that conventional horse management consisting of indoor housing with straw bedding and
feeding of hay result in much larger dust exposure
levels than housing of horses on wood shavings and
pelleted feed or keeping them on pasture.29,41
Some horses with IAD demonstrate increased eosinophil or metachromatic cell counts in BAL fluid suggesting hypersensitivity response of the lower
airways to inhaled allergens.5,19,20,42
Ozone inhalation may result in lower airway inflammation; however, levels encountered during
natural exposure are unlikely to induce IAD.43,44
Several additional factors commonly encountered
in athletic horses may contribute to the pathogenesis of IAD. Transportation of horses over long distances may induce airway inflammation and
colonization of the tracheobronchial tree by bacteria.45,46 Strenuous exercise results in a large increase in the number of bacteria (10- to 100-fold)
penetrating the lower airways.47 Finally, airway
response to environmental challenges is likely under
the influence of certain genes as it is the case for
heaves.48
5.
Functional Significance
Horses with clinical signs of IAD are more likely to
perform poorly; nevertheless, the mechanism of exercise intolerance is speculative.8,19,49 Mild degree
of airway obstruction is evident in some horses with
IAD and may result in impaired gas exchanges (Fig.
2).23,50 Horses with marked airway obstruction
such as RAO exhibit abnormal gas exchanges at rest
characterized by increased ventilation/perfusion
mismatching, arterial hypoxemia, and increased
work of breathing at rest and exercise induces a
marked deterioration of these parameters.51,52
Findings with IAD are equivocal since some investigators have found a more pronounced exerciseinduced hypoxemia in affected horses than in
healthy controls during standardized treadmill exercise, and others have reported no differences in
pulmonary gas exchanges.13,53
Airway hyperresponsiveness is a feature of IAD in
horses with increased BALF eosinophil and mast
cell counts.42,54 This increased bronchoconstriction
in response to inhaled irritants plays an important
role in the pathogenesis of the cough.
6.
Case 1
Signalment
10-yr-old Quarter Horse gelding used for barrel
racing.
History
The horse was evaluated for chronic coughing and
exercise intolerance. Coughing started ⬃2 yr ago;
however, exercise intolerance has only been observed since last year. Various treatments have
been attempted with little success. Clinical signs
are worse during spring-summer and tend to improve during the winter. The horse competed 2 wk
ago and the owner observed epistaxis from the right
nostril.
Clinical examination
Physical examination findings were T ⫽ 100.5°F,
heart rate of 42 BPM, and respiratory rate of 24
BPM. Bilateral serous nasal discharge was observed and cough could be elicited by compression of
the trachea. Thoracic auscultation revealed normal breath sounds; however, presence of mucus in
the trachea was suspected.
Upper airway endoscopy revealed moderate
amounts of mucopurulent and blood tinged secretions in the trachea. Tracheal wash cytology
findings were mild macrophagic/neutrophilic inflammation with minimal blood contamination.
Bronchoalveolar lavage cytology results were: total nucleated cell count (TNCC) ⫽ 428/␮l, eosinophils ⫽ 0%, epithelial cells ⫽ 1%, mast cells ⫽ 0%,
neutrophils ⫽ 6%, lymphocytes ⫽ 44%, macrophages ⫽ 49%.
Pulmonary function tests, treatment, and case
management will be discussed.
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IN DEPTH: INFLAMMATORY AIRWAY DISEASE
7.
Case 2
Signalment
10-yr-old Standardbred gelding racehorse.
History
The horse presented for evaluation of poor performance. The horse had a 3-mo history of tracheal
pus and decreased performance, had been coughing
intermittently for 6 – 8 mo, and was considered a
“bleeder.” The horse was treated with antibiotics
for the last 6 wk with no apparent improvement.
Clinical examination
Physical examination findings were T ⫽ 100°F, P ⫽
30 BPM, R ⫽ 18 BPM, bilateral serous nasal discharge, no inducible cough, and normal thoracic
auscultation.
Endoscopy revealed a mild amount of mucopurulent discharge in the trachea. Bronchoalveolar lavage cytology results were: total nucleated cell
count (TNCC) ⫽ 494/␮l, eosinophils ⫽ 9%, epithelial
cells ⫽ 1%, mast cells ⫽ 2%, neutrophils ⫽ 3%,
lymphocytes ⫽ 9%, macrophages ⫽ 83%.
Pulmonary function tests, treatment, and case
management will be discussed.
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