Chronic bronchitis (CB) is an inflammatory airway disease,
which, in association with tracheobronchial collapse, is probably
the most common chronic canine airway disorder. Inflammation
within airways causes chronic cough and excessive mucus production.
Because, dogs can’t expectorate (spit), it is not always easy
to know if the dog is making increased airway mucus. Therefore,
the diagnosis of CB is usually based on chronic cough alone.
Because we diagnose CB on the basis of a daily cough, we need
to be sure that other causes of chronic cough such as heart
failure, heartworm infestation, pneumonia, lung tumor, etc.,
have been ruled out. This can be complicated, in part, because
CB is a disease of older dogs, and these animals may have
any of these other, co-existing disorders, which can by themselves,
cause cough. Additionally, certain drugs used to treat CB
in dogs may be inappropriate and even contraindicated for
disorders other than CB. Importantly then, the diagnosis of
CB must be made with some degree of certainty to avoid potential
complications related to therapy.
CLINICAL FINDINGS IN
DOGS WITH CHRONIC BRONCHITIS
Dogs diagnosed with CB are generally > 6 years of age. There
does not seem to be a clear sex or breed predilection although
lots of small and toy breeds such as Poodles and Pomeranians
have been clinically diagnosed with CB.
By definition, dogs with CB have a chronic cough. This cough
is generally deeper and “throatier” than the high pitched
“honking” cough caused by extrathoracic tracheal collapse,
and yet harsher than the “soft moist” cough caused by pneumonia.
To figure out if increased mucus production is associated
with the cough, ask the client if the cough terminates in
gagging, swallowing or choking. If so, the dog is coughing
up and then swallowing the mucus.
Some dogs with CB may be otherwise absolutely normal while
others will be severely exercise-limited by their disease.
The difference is probably due to the amount of cartilage
weakening that is present, and the resulting airway collapse
that occurs when the easily fatigued dog begins to exercise.
These animals are otherwise bright, alert, and in all other
respects, systemically well. Chronic bronchitis in dogs does
not cause depression, lethargy, anorexia, etc. If these signs
are present, you should consider other disorders that cause
The only consistent auscultable finding in dogs with CB is
inspiratory and expiratory crackles. Heart rate is generally
normal for the breed and age, and may be a bit slower than
anticipated. A sinus arrhythmia is very common and can be
appreciated by palpating the femoral pulse in time with the
breathing pattern of the dog.
Because the diagnosis of CB is based on a history of chronic
cough, it is only necessary to perform those diagnostic tests
that help to determine the presence of other disorders that
Thoracic Radiographs. Thoracic radiographs of dogs
with CB may appear normal. This finding does not rule out
CB! More commonly however, thoracic radiographs reveal the
presence of “doughnuts” and/or “tram lines” which are prominent
and thickened bronchial walls seen on end or in parallel,
Bronchopulmonary Cytology. Neutrophils are usually
the predominant cell recovered from specimens taken by tracheal
wash; these cells do not independently indicate current or
past infection. Intracellular bacteria and/or a toxic appearance
of neutrophils would of course suggest the presence of bacterial
infection. Mucus is generally abundant even when a relatively
small volume of fluid is recovered. Small numbers of lymphocytes,
eosinophils, and epithelial cells are recovered in most samples.
Alveolar macrophages may be found in various morphologic stages,
from relatively quiescent to “activated” in all normal animals
as well as in dogs with CB. Techniques such as bronchoalveolar
lavage allow the wash fluid to come into contact with the
lung surface and result in retrieval of a higher percentage
of alveolar macrophages compared to tracheal washing. Regardless
of the techniques used, the alveolar macrophage is an absolutely
normal finding and should not be interpreted as a sign of
bronchopulmonary inflammation or pathology.
CB may sometimes be associated with airway eosophilia in dogs.
In my experience, this is more common in “snow dogs” (Malamutes,
Huskies etc). These pets commonly are symptomatic on a seasonal
basis only (suggesting an environmental source of the offending
antigen and cause for the subsequent cough). These cases also
seem to respond most dramatically to anti-inflammatory therapy
(see Glucocorticoid Therapy below).
Tracheobronchial Culture. A presumptive diagnosis of
“bacterial” bronchitis is most commonly made when cultured
airway samples grow a mixed population of aerobic bacteria.
Remember though, airways of all species studied, including
dogs, cats and people, retain small numbers of bacteria throughout
the day. That is one of the reasons we cough and clear our
throat. In my experience, bacteria recovered from the airways
of bronchitic dogs reflect innocuous colonization rather than
Bronchoscopy. The airways of dogs with CB are universally
erythematous and usually have a roughened or granular appearance.
The mucosa is often thickened, irregular and edematous. Excessive
and thick mucus may span the lumen of an airway or gather
as a mucus plug, which can occlude smaller airways.
Collapse of the dorsal tracheal membrane into the lumen of
the airway is common in dogs with CB. This finding does not
rule out CB, but instead reflects concurrent tracheal collapse
in association with CB. A striking finding in some dogs with
CB is the collapse of intrathoracic airways during passive
exhalation. This may not be apparent on thoracic radiographs
and in any case is much more dramatic when visualized endoscopically
in dynamic motion. In my experience, dogs with intrathoracic
airway collapse respond only marginally to therapy, and in
general, have a less fortunate prognosis.
Biopsy and Histopathology. Chronic bronchitis is a
clinical diagnosis and does not require tissue biopsy for
confirmation. Nevertheless, certain histologic features of
chronic bronchial disease are characteristic and include goblet
cell hypertrophy and hyperplasia, mononuclear cell infiltration,
and increased connective tissue within the lamina propria.
Chronic bronchial inflammation, regardless of cause, causes
mucosal and airway wall thickening, mucus hypersecretion,
and some degree of airway smooth muscle constriction. The
resulting signs are the defining features of canine CB and
include cough and exercise intolerance. The primary treatment
of CB is based entirely on controlling airway inflammation.
The guiding principle of any therapy must always be “if in
doubt, do no harm.”
Glucocorticoids have been used to treat humans with bronchial
disease for over 50 years. They are clearly the most effective
treatment for this disorder, although potentially debilitating
side effects limit their use in this clinical setting. Even
though steroids are not primary antitussives, by decreasing
inflammation they may decrease stimulation of airway sensory
nerves that are responsible for initiating cough in canine
CB. Additionally, steroids decrease the volume of mucus produced
by bronchitic airways. In my experience, steroids are the
most effective drugs available to treat dogs with CB, and
should be considered the mainstay of chronic therapy. I generally
begin treatment with prednisone 1 mg/kg q12h PO for one week,
then 0.5 mg/kg q12h PO for an additional week. The first week
or two of treatment will cause the most dramatic decrease
in clinical signs and this is usually as good as the dog will
ever get on prednisone. Tapering continues to the lowest effective
dose that controls > 75% of the cough. If the cough returns
using a dose of prednisone that causes significant side effects
(as determined by you and the owner), I introduce inhaled
steroids (flovent, 220 mcg q12h; see article on inhaled medications
elsewhere in these Proceedings).
It would make sense to use bronchodilators to treat dogs with
CB if some degree of bronchoconstriction existed which led
to clinical signs. There is very little reason to believe
that this is true for most dogs with CB. Only one non-anecdotal
study has collected objective data to determine the effect
of bronchodilator therapy in dogs with CB. In that report,
and in our later experience, only about one in seven dogs
had a positive therapeutic response. On the other hand, bronchodilator
therapy by inhalation is safe and easy to administer (see
article on inhaled medications elsewhere in these Proceedings).
Because it is not clear which dogs with CB will benefit from
bronchodilator therapy, it can be attempted in any dog with
CB that does not have a great response to steroids.
Bacterial infection probably doesn’t play a significant role
in most cases of canine CB. A positive culture result obtained
from a tracheobronchial wash does not necessarily imply the
presence of a clinically significant airway infection and
should not lead to antibiotic therapy, unless there was a
pure bacterial culture on a primary culture plate. This is
because aerobic bacteria recovered from the airways of healthy
cats, dogs, and humans, does not exceed 5 X 103 organisms/ml.
In contrast, growth of a single organism recovered without
the use of enrichment broth implies >105 organisms/ml; this
is consistent with an “infected” airway. Of course, if a primary
culture is returned, antibiotic treatment should begin based
on culture and sensitivity data.
Chronic airway inflammation causes production of lots of thick
mucus, probably as a protective mechanism to trap the offending
irritant from reaching the lung. Coughing is very important
to clear this mucus and should be thought of as a protective
physiologic reflex. However, there are many cases in which
the cough is dry and non-productive. In these situations,
the cough is not protective and serves to further irritate
the airway, leading to a vicious cycle of cough-irritation-cough.
In addition, some dogs with chronic cough are unable to sleep
and may awaken their owners at night. Occasionally, some dogs
with chronic cough may become syncopal. In each of these clinical
settings, cough suppression may be indicated. I use hydrocodone
bitartrate, 0.22 mg/kg PO q6-12h as needed. This is a starting
dose, and I increase the dose and the frequency until the
cough is greatly reduced or the dog is asleep. Literally!
In practice, the most common side effects of high doses of
hydrocodone in dogs are drowsiness and constipation. I use
1 teaspoon of metamucil for the constipation and I reduce
the dose of hydrocodone during the day to decrease the somnolence.
Mucolytics have been suggested as a form of therapy for dogs
with airway disease associated with excessive secretion of
mucus. While drugs such as acetylcysteine are capable of breaking
the disulphide bonds that are partially responsible for the
particularly viscid nature of airway mucus, in practice, aerosolized
acetlycysteine is irritating to airway epithelium and can
promote significant bronchoconstriction.
PROGNOSIS AND CONCLUSIONS
Canine CB is a common, progressive, and chronic airway disorder.
Signs can be greatly improved but the disease is not curable.
Establishment of excellent client communications is critical
so that client expectations are realistic and so that the
therapeutic regime established by the clinician is adhered
Philip Padrid United States