CE Article #1

Bronchiectasis
Angela J. Marolf, DVM*
Margaret A. Blaik, DVM, MS, DAVCR
University of Florida

ABSTRACT: Bronchiectasis refers to irreversible dilation of diseased bronchi. Chronic inflammation

and infection cause irreversible bronchial wall changes. Cylindrical and saccular forms are recognized
in veterinary medicine. Bronchiectasis is defined morphologically, and diagnostic imaging is essential
to identify the condition. Local pulmonary, diffuse pulmonary, and systemic diseases are implicated in
bronchiectasis. An underlying cause should be diagnosed, if possible, to guide treatment planning and
provide a prognosis.The aim of clinical treatment is to slow the progression of bronchiectasis for as
long as possible.

T
he term bronchiectasis is derived from
the Greek words broncos, meaning wind-
pipe, and ektasis, meaning stretching or
extension.1 Bronchiectasis refers to chronic irre-
versible dilation of diseased bronchi. Bron-
chiectasis has many causes and should be
considered the end stage of a number of mecha-
nisms rather than a discrete disease entity. The
condition can be the pulmonary manifestation
of bronchial obstruction or untreated infection,
diffuse pulmonary pathology, or a systemic dis-
order. 2 Thoracic radiography and computed
tomography (CT) have key roles in the identifi-
cation of bronchiectasis.2–5 This article reviews
the pathophysiology, clinical signs, diagnostics,
and conditions associated with bronchiectasis.
PATHOPHYSIOLOGY
The respiratory tract has ciliated epithelium
from the nasal cavity to the terminal bronchi-
oles, and through a coordinat-
Send comments/questions via email to ed beat, the cilia clear the
editor@CompendiumVet.com airways of mucus, inhaled par-
or fax 800-556-3288. ticles, and cellular debris.2 Un-
Visit CompendiumVet.com for der conditions of prolonged
full-text articles, CE testing, and CE *Dr. Marolf is now affiliated with
test answers. Colorado State University.
inflammation or infection, the normal pul-
monary clearance system becomes overwhelmed,
and cellular debris, inflammatory cells, and mu-
cus accumulate in the airways. As a result, de-
struction of the ciliated respiratory epithelium
and submucosa occurs.6
Impaired patient pulmonary clearance mech-
anisms initiate the classic pathway of bronchi-
ectasis.2 As a consequence, mucosal secretions
stagnate and endoluminal pressures rise, propa-
gating an environment for infection.6 Once
infection has been initiated, bacteria and patho-
gens remain in the bronchi for prolonged peri-
ods, inflaming the bronchial walls.6 Chronic
infection and inflammation harm the respira-
tory epithelium and submucosa, predisposing
patients to future infection.6 Thus the entire
cycle repeats itself, causing further damage to
the epithelium and submucosa and subsequent
bronchial dilation (Figure 1). However, not all
dogs with chronic infection or inflammatory
lung disease develop bronchiectasis, indicating
that preexisting abnormalities in immune and
inflammatory host responses or the pulmonary
clearance mechanism play a role in the develop-
ment of bronchiectasis.7
In all forms of bronchiectasis, the aforemen-

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 Bronchiectasis CE 767

tioned dilation is identified

in the proximal subdivisions Cycle of Normal host
bronchiectasis response
of bronchi containing carti-
laginous walls. This dilation Insult
is due to destruction of the Inflammation Infection
Cytokines
elastic and muscular layers of Underlying
Neutrophil enzymes
the bronchial wall.2,6 The sur- Microbial condition
colonization/ Bacterial products
rounding healthy lung tissue infection
exerts a contractile force that
Bronchiectasis Bronchial
expands the bronchi, creating drainage Health

the dilation, as observed via Mucociliary

radiography. 2,6 Subsequent clearance further
impaired Mucociliary
bronchial wall thicken- clearance

ing develops as a result of Impaired Normal

mucosal hypertrophy and Mucous hypersecretion
hyperplasia. 2,6 In chronic obstruction
bronchiectasis, peribronchial
alveolar tissue is damaged Figure 1. Persistent cycle of bronchiectasis. (Adapted from Angeli MC: Bronchiectasie.
and fibrosis and/or squamous Accessed May 2005 at www.chirurgiatoracica.org/bronchiectasie1.htm)
metaplasia occurs. 2 Long-
term inflammation obliter-
ates distal bronchi and terminal bronchioles, reducing SIGNALMENT/CLINICAL SIGNS
lung segmentation.8 Bronchiectasis is most common in old dogs (>10 years
Bronchiectasis can be classified morphologically or spa- of age); however, an age range of 4 months to 18 years
tially. Two morphologic forms are recognized in veteri- has been reported.7 The incidence of bronchiectasis is
nary medicine and correspond to radiographic changes: low, with 0.05% of dogs affected in a multicenter hospi-
tal population in a recent retrospective study.7 In com-
• Cylindrical bronchiectasis, the more common type, paring the incidence of bronchiectasis with other lower
refers to uniform tubular dilation of proximal bron- respiratory diseases, 10 of 109 (9.2%) cases of bron-
chial tree segments.3,7,9 chiectasis were identified.11 Common diagnostic differ-
• Saccular (cystic) bronchiectasis is a ballon-like dila- entials identified with or without bronchiectasis included
tion of distal/terminal branch bronchi.3,7,9 The saccu- chronic bronchitis, bronchopneumonia, eosinophilic
lar form represents a more advanced manifestation of bronchopneumopathy, parasitic bronchitis, bronchial
cylindrical bronchiectasis.5 foreign body, and primary neoplasia.11,12 The most com-
mon breeds included the American cocker spaniel,
A single case report10 in the veterinary literature identified miniature poodle, West Highland white terrier, Siberian
cystic bronchiectasis, which is considered the end stage of husky, and English springer spaniel.7 Neutered males
saccular bronchiectasis. Varicose bronchiectasis, a third appear to be predisposed.7 Bronchiectasis is considered a
form described in humans, consists of focally dilated rare manifestation of bronchial disease in cats, in which
bronchial segments interposed between normal or nar- it occurs predominantly in old (i.e., >7 years of age),
rowed bronchial segments.6 neutered males. 9 The most common clinical sign is
The spatial classification of bronchiectasis designates a chronic coughing7,9; other signs include tachypnea, dys-
focal, multifocal, or diffuse distribution pattern through- pnea, and posttussive retching. A lack of clinical signs is
out the lungs. 7,8 This categorization scheme aids in less common.9
developing the differential diagnosis when attempting to
determine the underlying cause.6,8 Causes of focal bron- DIAGNOSTICS
chiectasis include infection or obstruction, whereas dif- Bronchiectasis is primarily an imaging diagnosis.
fuse causes indicate congenital or acquired deficiencies in Thoracic radiography, bronchography, and CT can be
host defense mechanisms.6 used to further delineate the location and type of

November 2006 COMPENDIUM

768 CE Bronchiectasis
Figure 2. Ventrodorsal projection of the thorax with an
affected region in the left caudal lung lobe magnified (inset).
Multiple, thickened, dilated end-on bronchi (arrows) are
noted throughout the thorax.
bronchiectasis.5,7 Imaging is essential in making a diag-
nosis and monitoring patient progress during treatment.
Thoracic Radiography
Thoracic radiography is considered the first-line diag-
nostic tool in bronchial disorders. However, it is relatively
insensitive to early bronchial changes in humans.4,5 Early
thoracic radiographic changes, such as peribronchial
inflammation, which can obscure adjacent vessels, is often
nonspecific for bronchiectasis.5,7 However, other radi-
ographic changes are more apparent. Thickening and
dilation of the bronchial walls appear as ring shadows
(i.e., “doughnuts”) or tram tracks when seen end-on or
longitudinally, respectively5,6 (Figure 2). “Honeycombing”
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Figure 3. Lateral projection of the thorax. Cylindrical
bronchiectasis is identified in the proximal aspect of the left
cranial lobar bronchus (arrows in inset). Note how the bronchus is
dilated and fails to taper toward the periphery.
describes a confluence of multiple thickened, dilated
bronchi as seen via radiography.6 More advanced changes
include roentgen signs, which parallel the previously
described morphologic bronchiectatic changes. Cylindri-
cal bronchiectasis is tubular dilation of the more proximal
bronchial segments that fail to taper toward the peri-
phery 2,3,5 (Figure 3). The cylindrical form is by far the
more common manifestation of bronchiectasis, represent-
ing 70% of cases in a recent retrospective study.7 The
saccular form appears as multiple circumscribed outpock-
etings of distal and terminal bronchi and can be described
as a “cluster of grapes”5 (Figure 4).
Additional nonspecific radiographic changes have
been identified. Mixed pulmonary patterns (e.g., combi-
nations of interstitial, bronchial, and alveolar pulmonary
infiltrates; mucous plugs; atelectasis) often coincide with
the previously described bronchiectatic changes (Figures
5 and 6). These radiographic changes are secondary to
purulent or mucus-filled bronchi and extension into
interstitial tissues.7,11,12 Mild narrowing or dilation of the
trachea may be observed in some cases.7
Spatial evaluation of bronchiectatic changes denotes
the extent of bronchial pathology. Multiple-lobe involve-
ment is more common (89%) than single-lobe disease.7
The right cranial lung is predisposed (i.e., affected in
93% of cases) to bronchiectatic changes.7 The predomi-
nance of this affected lobe is likely secondary to its cran-
ioventral location and to subsequent gravitational effects,
which hamper clearance of bronchial exudates.
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 Bronchiectasis CE 769

Bronchography
Bronchography, which entails administration of non-
ionic water-soluble contrast via catheter or broncho-
scope, was commonly performed to confirm the
presence and extent of bronchiectasis.2,5,13 The dilated
bronchial walls are coated with contrast, delineating
their outline (Figure 7). However, with the advent of
CT, bronchography is rarely performed today. Several
complications are associated with bronchography,
including decreased breathing capacity secondary to
bronchial obstruction from contrast and alveolization of
contrast, leading to granuloma formation and scarring.13
In humans, bronchography is considered nonessential
unless surgical resection of the affected lung lobe(s) is
recommended.2,14

Computed Tomography
Evaluation of thoracic structures via CT has virtually
replaced bronchography in diagnosing bronchiectasis in
humans and animals. CT allows depiction of a “slice”
(i.e., section) of the body free from superimposition of
overlying structures. The computer assigns a gray-scale
value to each pixel based on attenuation of the x-ray
beam through tissue.15,16 With the advent of high-resolu-
tion CT, the specificity and sensitivity (i.e., 80% to 90%)
of CT to diagnose bronchiectasis in humans are excel-
lent.5,6 High-resolution CT uses a tightly collimated x-ray
beam, decreased field of view, high spatial frequency algo-
rithms, and thin slices (1 to 1.5 mm), rendering excellent
spatial resolution.5,16 High-resolution CT enhances accu-
rate identification of subtle pulmonary disease. In veteri-
nary medicine, volumetric scanning with thinly
collimated slices enables evaluation of the bronchial tree
and adjacent pulmonary parenchyma.16 The most widely
accepted criterion for evaluating bronchiectasis in CT
imaging is the size of the bronchus relative to its adjacent
pulmonary artery.5 In healthy individuals, the overall
diameter of the bronchus is the same, at any level of
branching, as that of its adjacent artery.5 With CT, mild
dilation and thickening of bronchi can be detected earlier
in the disease process (Figure 8).
Nonimaging Diagnostics
Adjunctive diagnostic tests are used for further evalu-
ation of bronchiectasis. Bronchoalveolar lavage and
transtracheal washes provide samples for cytologic and
culture results. Cytologic analysis often demonstrates
neutrophilic and eosinophilic inflammation and in-
creased mucus.7 Bacterial cultures can guide future ther-
Figure 4. Lateral projection of the thorax. Saccular
bronchiectasis is noted in the distal and terminal portions
of the left cranial lobar bronchus (inset).Well-circumscribed
outpocketings are evident.
apies and treat current infections. In humans,
bronchiectatic sputum includes a large quantity of
mucus and inflammatory cells with or without blood.2
Sputum samples are generally not taken in dogs because
of excessive contamination from the oral cavity. In
humans, hemoptysis commonly occurs because of rup-
tured anastomotic vessels bleeding into the bronchial
lumen.2 The extensive anastomoses that occur between
bronchial and pulmonary arteries secondary to chronic
inflammation in humans do not occur in dogs.17 Conse-
quently, hemoptysis is not a recognized finding in dogs
with bronchiectasis.17
ASSOCIATED CONDITIONS
As previously emphasized, bronchiectasis is associated
with multiple conditions and warrants further diagnos-
tics to determine the underlying cause. Local pulmonary
disease, generalized pulmonary disorders, and systemic
disease processes have been implicated and will be
reviewed in this section.
Local Pulmonary Diseases
Local conditions most commonly include pulmonary
infection by viral, bacterial, protozoal, parasitic, or fungal

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770 CE Bronchiectasis
Figure 5. Lateral projection of the thorax. Cylindrical
bronchiectasis is identified in the right cranial and middle lobar
bronchi (small arrows). A large mucus plug is noted in the terminal
portion of the right cranial bronchus (large arrow).
organisms. Recurrent or chronic pneumonia is the most
common cause of bronchiectasis in both animals and
humans.2,6,7,9,11 Incomplete treatment of pneumonia can
lead to low-grade infection and exaggerated inflamma-
tory response, which irreversibly damages bronchial
walls.6 Endobronchial obstruction secondary to foreign
bodies, broncholiths, or neoplasia is a less common cause
of localized bronchiectasis. Bronchial foreign bodies,
including inhaled grass awns and aspiration of teeth,
have been reported.18,19 Broncholithiasis describes any
calcified material within a bronchial lumen and includes
extrusion of calcified adjacent lymph nodes and aspira-
tion of calcified foreign material.20 Pulmonary neoplasms
can arise from or invade the bronchial lumen or cause
extraluminal compression, leading to bronchiectasis.2,6,7,11
Generalized Pulmonary Disorders
Generalized pulmonary disorders affect the lung
parenchyma diffusely and include chronic bronchitis,
eosinophilic bronchopneumopathy, tracheal collapse
(chondromalacia), and fibrotic pulmonary disease.
Spontaneous chronic bronchitis in dogs is poorly
understood. The clinically accepted definition of chronic
bronchitis is a chronic cough occurring for two consecu-
tive months that is not attributable to another
cause.11,12,21,22 The inciting cause is rarely elucidated, but
inhaled irritants, recurrent low-grade infection, and
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Figure 6. Ventrodorsal projection of the thorax. Focal dense
interstitial pulmonary infiltrates are noted in the midzone of
the left caudal lung lobe (inset).
smoldering inflammation have been implicated.12 As the
disease progresses, irreversible pathologic changes
caused by inflammation can occur in the bronchial
walls, resulting in dilation of the bronchi.12,22 Chronic
bronchitis and asthma are the most common systemic
causes of bronchiectasis in cats.9
Eosinophilic bronchopneumopathy, traditionally
called pulmonary infiltrates with eosinophilia, is associ-
ated with eosinophilic infiltration of the lungs and
bronchial mucosa.23–25 A wide range of disease entities
varying from mild to severe in clinical presentation have
been implicated and related to manifestations of
immune hypersensitivity.23,24 The underlying causes of
these exaggerated immune responses are not clearly
understood in humans or animals. Suspected and known
causes in humans and animals include fungi, molds,
drugs, bacteria, and parasites.2,23 The inciting antigens
are often unidentified. Heartworm infestation is the
most common cause of eosinophilic bronchopneumopa-
thy in animals. 24,25 Alaskan malamutes and Siberian
huskies are most frequently affected.23 Eosinophilic pul-
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772 CE Bronchiectasis
Figure 7. Bronchogram.
Lateral projection demonstrating saccular bronchiectasis within
the right cranial lobar bronchus (arrow in inset) and normal left
cranial lobar bronchus dorsally (arrowheads).
monary granulomatosis, which is considered a more
severe form of eosinophilic bronchopneumopathy, is
characterized by multiple lung nodules or masses with
or without thoracic lymph node involvement.23,26,27 This
condition is associated with more severe clinical signs
and a poorer prognosis.23
Chronic pulmonary fibrosis is defined as fibrosis of
the lung interstitium and alveoli, with minimal changes
to the bronchial walls, and is similar to idiopathic pul-
monary fibrosis in humans.28,29 Multiple causes, includ-
ing underlying connective tissue diseases, dust or
inhaled irritants, and previous lung injury, have been
identified. 29 West Highland white, Parson Russell,
Staffordshire bull, and cairn terriers are predisposed.28
Bronchiectasis is inconsistently found with chronic pul-
monary fibrosis, which is progressive and fatal.7,28,29
Tracheal collapse, which is characterized by flat, weak
cartilaginous arcs and a flaccid tracheal membrane, is
commonly found in miniature and chondrodystrophic
breeds of dogs.30 This malformation has been described as
chondromalacia or achondrodysplasia and is associated
with a primary cartilage deficiency and dysplasia.7,30,31 The
trachea and bronchial components containing cartilage
dilate and narrow with inspiration and expiration, ulti-
mately resulting in end-stage collapse.7 Bronchiectatic
changes have been associated with this condition in
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Ventrodorsal projection showing the severely dilated bronchus
(arrow in inset).
humans.2 However, no such association in dogs has been
firmly established, and whether chronic bronchial inflam-
mation and bronchiectasis cause chondromalacia (or the
reverse) warrants further study.8,30,31
Systemic Conditions
Congenital or acquired impairment of host defenses is
the underlying mechanism behind systemic conditions as-
sociated with bronchiectasis. These conditions include pri-
mary ciliary dyskinesis and primary immunodeficiencies.
Primary ciliary dyskinesis is a hereditary disorder char-
acterized by absent or defective mucociliary clear-
ance.32–34 This syndrome is associated with ultrastructural
defects within the ciliary axonemes and appears to be a
recessive autosomal inheritance defect.34 Electron micro-
scopic findings include abnormal ciliary orientation and
microtubular abnormalities with subsequent functional
immotility.32,33 The impaired mucociliary clearance hin-
ders one of the primary defense mechanisms of the res-
November 2006

piratory system—trapping inhaled particulates and
expectoration through ciliary action.32 As a consequence,
secretions are retained, and recurrent infections develop,
leading to bronchiectasis. A subset of patients with pri-
mary ciliary dyskinesis have Kartagener’s syndrome,
which is associated with a triad of signs: rhinosinusitis,
bronchiectasis, and situs inversus.35,36 The incidence of
this condition is well documented in humans—approxi-
mately half of all patients with primary ciliary dyskinesis
have Kartagener’s syndrome.8 The incidence in veteri-
nary medicine is unknown.
Primary immunodeficiencies, predominantly the IgG
subclass, rarely cause bronchiectasis in humans.37 An
impaired IgG antibody response has been demonstrated
in these patients when other underlying causes of
bronchiectasis have been eliminated.37 In veterinary
medicine, multiple primary immunodeficiencies have
been identified. 38,39 A canine-selective IgA and IgG
deficiency similar to the condition in humans is typified
by recurrent infections (i.e., usually upper respiratory
infection, otitis, and dermatitis).39 These hereditary defi-
ciencies have been established in the German shepherd,
beagle, and shar-pei.39 Further investigation is needed to
determine the incidence of canine primary immunodefi-
ciencies and concurrent bronchiectasis.
CLINICAL MANAGEMENT
The clinical management of a patient with suspected
bronchiectasis can be summarized as follows5:
• Confirm a diagnosis of bronchiectasis
• Identify the cause, if possible
• Define the severity and location of disease
• Initiate treatment
• Monitor the patient
The foundations of therapy include administration of
antibiotics when acute exacerbations of lung disease
occur; treatment of underlying conditions; reduction of
the inflammatory response through administration of
corticosteroids; enhancement of bronchial clearance of
secretions with physiotherapy, mucolytics, and bron-
chodilators; and surgical removal of diseased lung
lobes.8,14 In humans, lung lobectomy is considered a pal-
liative approach limited to patients who are resistant to
medical therapy or who experience other complications,
such as severe hemoptysis.14 Lung lobectomy is a thera-
peutic option in animals with focal bronchiectasis and
may be curative.10,40
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Bronchiectasis CE 773
Figure 8. CT lung scan (transverse image). Note the
thickened, dilated bronchus adjacent to the normally sized
bronchial artery (red arrowheads). Yellow arrowheads identify
normal peripheral bronchus/bronchial artery pairs.
Treatment of recurrent bacterial infections is essential
to disrupt the persistent cycle of host inflammatory
response to pathogens and further damage to the
bronchial walls. Dogs with pneumonia should be treated
with broad-spectrum antibiotics efficacious against both
aerobes and anaerobes.41 Culture and sensitivity test
results can further guide the antibiotic choice.40 Airway
samples for culture, sensitivity, and cytology may be
obtained through bronchoalveolar lavage or transtracheal
wash.12 Bronchoscopy with bronchoalveolar lavage is the
preferred method to obtain samples. With bronchoscopy,
the airways can be visually evaluated and samples can be
obtained from the lower airways.12 Recurrent infections
may be treated with chronic suppressive therapy or
administration of antibiotics for 1 week each month.41
Bronchodilators may be beneficial; however, irre-
versible impaired airflow may limit their effectiveness.41
If inflammation resulting in some degree of bron-
chospasm is suspected, bronchodilator therapy may be
beneficial. 12 Cough suppressants should be avoided
because they exacerbate the already decreased mucocil-
iary clearance.41
If the underlying disease is inflammatory in nature,
antiinflammatory drugs are recommended. Cortico-
steroids are the most commonly prescribed antiinflamma-
tory for inflammatory lung conditions.12,40 The use of
systemic corticosteroids warrants caution because of pos-
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774 CE Bronchiectasis
Key Points
• Impaired pulmonary clearance mechanisms (e.g.,
stagnant mucosal secretions and bacteria) are the
classic cause of bronchiectatic changes.
• The most common clinical sign reported in animals is
chronic coughing.
• To initiate appropriate treatment of bronchiectasis, the
underlying cause should be determined, if possible.
sible immunosuppression and the risk for new infection.
These doses usually start in the inflammatory range and
are tapered as low as possible to control the patient’s
signs.12 Inhaled steroids have been used in humans with
bronchiectasis12,40; however, similar studies are warranted
in veterinary medicine. Metered-dose inhalers of steroids,
which can be administered via face mask, have been used
to treat asthma in cats.41 The actual dosing and amount of
steroid administered via inhalation are not well substanti-
ated in veterinary medicine.12
Bronchiectasis is a progressive condition, and the treat-
ment goal is to maintain baseline radiographic changes
for as long as possible. Saccular bronchiectasis is consid-
ered a more advanced form, and its radiographic presence
indicates more severe disease.5,10 Because most patients
are geriatric at diagnosis (median age: 12 years), the long-
term prognosis for patients with bronchiectasis is gener-
ally fair to good, with a median survival time of 16
months.7 Thus early diagnosis of bronchiectasis is vital to
treatment initiation, improved quality of life, and maxi-
mum survival time after diagnosis.
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1. Bronchiectasis is 6. Which is a hereditary disorder characterized by

a. a distinct disease entity. the absence of defective mucociliary clearance?
b. a pulmonary manifestation of an underlying disorder. a. chondromalacia
c. transient and reversible as documented via radiogra- b. chronic pulmonary fibrosis
phy. c. primary ciliary dyskinesis
d. always associated with pneumonia. d. IgG subclass immunodeficiency

2. Saccular bronchiectasis is
a. a more advanced form of bronchiectasis. 7. The most common cause of eosinophilic broncho-
b. associated only with local disease conditions. pneumopathy is
c. identifiable via radiography by its “cluster of grapes” a. heartworm disease.
appearance. b. inhaled allergens.
d. a and c c. drug reaction.
d. fungal infection.
3. The _________ lung lobe is most often affected by
bronchiectasis.
a. right middle 8. Clinical management of bronchiectasis involves
b. left caudal a. diagnosis of the underlying cause.
c. right cranial b. definition of the severity and location of disease.
d. right caudal c. monitoring the patient.
d. all of the above
4. The advantage(s) of CT in diagnosing bronchiec-
tasis include(s)
a. increased sensitivity in detecting early pulmonary 9. Local conditions, such as pneumonia, that cause
changes. bronchiectasis
b. depiction of a section of the body free from superim- a. are more common than systemic conditions.
position of overlying structures. b. occur equally in dogs and cats.
c. decreased morbidity compared with that associated c. are usually associated with broncholithiasis.
with bronchography. d. are less common than systemic conditions.
d. all of the above

5. Which clinical finding is not associated with 10. Which is not associated with Kartagener’s syn-
bronchiectasis in animals? drome?
a. coughing a. situs inversus
b. hemoptysis b. hydrocephalus
c. dyspnea c. rhinosinusitis
d. posttussive retching d. bronchiectasis

November 2006 COMPENDIUM