Canine Infectious Respiratory

Disease Complex
Jonathan Dear, DVM, MAS, DACVIM (SAIM), University of California, Davis

INFECTIOUS DISEASE | NOVEMBER/DECEMBER 2020 | PEER REVIEWED | WEB-EXCLUSIVE

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Background & Pathophysiology

Canine infectious respiratory disease complex (CIRDC) is complex and multifactorial. Host,
pathogens, and environment contribute to development of respiratory disease, which is
primarily characterized by cough. In most instances, viral infection results in injury to the
respiratory epithelium, which increases susceptibility to infection with bacteria, Mycoplasma
spp, or other organisms that compound damage to the respiratory tract and contribute to
progressive clinical signs.1

The disease has been referred to as kennel cough and infectious tracheobronchitis, but CIRDC is
now preferred, as this term highlights both the involvement of multiple infectious agents and
that disease susceptibility depends on host immunity and environmental factors. Moreover,
although the term kennel cough may be useful in discussion with pet owners, it has become
somewhat synonymous with Bordetella bronchiseptica and can cause confusion because dogs
with appropriate vaccination history and robust immunity can still become infected with other
CIRDC pathogens. Further, clinicians and owners should understand that antibacterial drugs are
not effective when CIRDC is caused by a virus.

Although B bronchiseptica was the most commonly isolated bacterium in some previous
studies,2-4 recent research has suggested numerous organisms likely play a role in CIRDC.5
Molecular techniques and virus isolation have identified mycoplasmal organisms,6 previously
recognized viruses known to cause disease (eg, canine adenovirus-2, canine herpesvirus-1,7
canine parainfluenza virus,4 canine distemper virus [less frequent], canine respiratory
coronavirus,8 various canine influenza viruses9), and emerging and novel viruses in which the
link to clinical disease is not well-recognized (eg, canine reovirus,10 canine bocavirus, canine
hepacivirus, canine pneumovirus11).

CIRDC has been documented worldwide, and no host-susceptibility–related genetic factors have
been identified. Seasonal patterns of CIRDC have been observed; B bronchiseptica infections
have been more commonly identified in dogs during cold months.5 Any dog can be infected with
CIRDC-associated pathogens; however, young dogs and those with pre-existing airway disease
(eg, bronchiectasis, airway collapse, ciliary dyskinesia) may be more susceptible due to impaired
airway clearance. In addition, dogs in high-density environments12 or those that are
immunologically naive or immunocompromised (endogenous or exogenous) are at increased
risk and appear to develop more severe disease.13

History
In dogs presented with signs of upper respiratory tract disease, it is important to determine travel
history and exposure to densely housed dog populations. Certain diseases (eg, canine influenza)
have historically appeared to be geographically restricted, and travel to or contact with animals
from these locations can raise suspicion for the primary pathogen. Similarly, a clue to the
infectious pathogen may be related to the patient being recently boarded at a kennel (see
Bordetella Bronchiseptica Pneumonia Treated with Glucocorticoids due to Chronic Cough),
shelter, or veterinary hospital, as well as exposure to recent addition of animals to the
household.14,15
Immunization history does not rule out CIRDC, but patients with up-to-date vaccinations
against B bronchiseptica and parainfluenza virus appear to have attenuated clinical signs.
Vaccines are not available for many viruses implicated in CIRDC.

BORDETELLA BRONCHISEPTICA PNEUMONIA TREATED WITH

GLUCOCORTICOIDS DUE TO CHRONIC COUGH
An 11-year-old intact female Pomeranian was presented for collapse refractory to previous
therapy. She and her housemate had developed an acute cough after being boarded at a
kennel. The housemate recovered without treatment. The patient had previously been given
amoxicillin, enrofloxacin, prednisone, acepromazine, and hydrocodone to treat her cough, but
no appreciable improvement was observed.

On examination, the dog was panting with expiratory effort and crackles auscultated diffusely.
She exhibited an occasional goose-honking cough and retch. Her body temperature was
normal. Radiography (Figures 1 and 2), fluoroscopy (Figure 3), and bronchoscopy (Figures 4
and 5) were performed.

Bronchoscopy revealed moderate grade 2 (40%-50%) extra-thoracic airway collapse, with

grade 4 (100%) collapse of the intrathoracic airway (most severe at the carina). Marked diffuse
purulent discharge was observed throughout the trachea and mainstem bronchi along with
grade 3 to 4 (75%-100%) collapse of proximal bronchi (left cranial, right cranial, and right
middle), with thickened mucosa and blunted airway divisions throughout. The caudal airways
(left and right) were less affected distally.

Bronchoalveolar lavage samples revealed marked septic suppurative inflammation. The

patient was initially treated with nebulization and empiric enrofloxacin (10 mg/kg PO once
daily for 3 weeks) and amoxicillin/clavulanic acid (13.5 mg/kg PO twice daily for 3 weeks)
pending culture and susceptibility results. Both B bronchiseptica and Mycoplasma spp were
cultured from the bronchoalveolar lavage samples. B bronchiseptica was susceptible to most
antimicrobials; a susceptibility panel was not performed for Mycoplasma spp. A recheck 2
weeks later revealed improved but persistent disease; the patient was subsequently
transitioned to doxycycline (5 mg/kg PO twice daily for 2 weeks) for possible clinical activity
against Mycoplasma spp.17

Because of her concurrent airway collapse, the patient was at risk for chronic cough without
lifestyle modification. This case illustrates the need for comprehensive evaluation of dogs with
acute or chronic cough, as many therapies (eg, glucocorticoids, cough suppressants, airway
stenting) can prolong or exacerbate disease.

FIGURE 1 Left lateral radiograph showing dynamic collapse of the

intrathoracic trachea from the level of the thoracic inlet to the
mainstem bronchi. A small amount of esophageal gas is observed
(asterisk), and the lungs are hypoinflated, which is likely secondary to
increased respiratory effort. Mild, generalized cardiomegaly and
hepatomegaly are also evident in the thorax (arrows) and abdomen
(arrowheads), respectively.
FIGURE 2 Dorsoventral radiograph revealing hypoinflation, as seen by
the tented diaphragm (asterisks), and mild, generalized cardiomegaly
(arrows)
FIGURE 3 Fluoroscopic image with the patient in right lateral
recumbency with a plexiglass paddle (asterisk) compressing the
trachea to incite cough. Collapse of both the trachea and lower airways
can be seen. Dynamic collapse of the intrathoracic trachea during
normal respiration and elicitation of cough was also revealed. Collapse
was most marked at the level of the thoracic inlet (arrows), where
complete loss of visible lumen was observed.

FIGURE 4 Left mainstem bronchus revealing pale mucosa with

inapparent mucosal blood vessels and profuse yellow to green
purulent exudate
 FIGURE 5 Right middle lobar bronchus with marked suppurative
exudate

Clinical Signs
Clinical signs of CIRDC are generally based on the degree of respiratory tract involvement,
severity of damage, patient age, and pathogen virulence. CIRDC can be characterized as
uncomplicated or complicated, depending on the severity of clinical signs. Uncomplicated
disease generally results in an acute, self-resolving cough that can be triggered by exercise or
excitement or occur spontaneously; retching and expectoration of clear mucoid respiratory
secretions typically follows, but this is not specific for CIRDC or any specific organism.
Complicated disease can progress to pneumonia, which manifests as the aforementioned cough
and is often accompanied by hyporexia, fever, lethargy, hemoptysis, and difficulty breathing.

Physical examination of dogs with uncomplicated disease can be unremarkable or may include
the presence of an inducible cough on tracheal palpation; however, this is not specific for CIRDC
and it is possible to induce a cough with tracheal palpation in dogs with other respiratory
disease. In dogs with complicated disease, a low-grade fever (103°F-104°F [39.4°C-40°C]) is not
uncommon, respiratory rate and/or effort might be increased, and increased bronchovesicular
sounds or crackles may be auscultated.

Diagnosis
Uncomplicated Disease
Diagnostic examination in dogs with uncomplicated disease can be unrewarding and
unnecessary, as CBC, thoracic radiography, and arterial blood oxygen concentrations are
generally within normal limits. Diagnosis is accomplished via a combination of compatible
history and clinical signs, physical examination, and spontaneous resolution of disease.

Complicated Disease
In dogs with pneumonia as a result of complicated disease, CBC can reveal neutrophilic
leukocytosis with a left shift; thoracic radiographs may show an interstitial to alveolar pattern
with cranioventral distribution (characteristic of bacterial pneumonia), diffuse interstitial
pneumonia (observed with viral disease), or a mixed pattern; and radiographs can help
investigate differential diagnoses (eg, fungal pneumonia, pyothorax, congestive heart failure).

Ideally, airway samples from dogs with complicated disease should be submitted for cytologic
evaluation and culture and susceptibility testing (aerobic and mycoplasmal culture). PCR can be
performed on airway washes when specific viral diseases (ie, distemper, influenza, canine
parainfluenza virus) are suspected, but caution should be used when interpreting respiratory
PCR panels because the sensitivity and specificity of these tests are unknown.16

Treatment & Management

Uncomplicated Disease
Outpatient therapy and isolation from other dogs for 2 to 3 weeks is recommended to minimize
the risk for transmission. Therapy should include adequate nutrition, hydration, and hygiene.
Cough suppressants (eg, hydrocodone [0.22 mg/kg PO every 8-12 hours] or butorphanol [0.1-0.4
mg/kg PO every 8-12 hours]) can be used when bacterial pneumonia is unlikely. Antimicrobial
therapy is not typically needed, but doxycycline (5 mg/kg PO every 12 hours for 7-10 days) can
be administered if disease persists >10 days or as a first-line antimicrobial if clinical signs
progress to systemic signs (ie, fever, lethargy, decreased appetite).17

Complicated Disease
Inpatient therapy should be considered for dogs with bacterial pneumonia if hydration would be
inadequate with outpatient therapy or if oxygen therapy is necessary. In these dogs, IV fluid
therapy and parenteral antibiotics are generally warranted; empiric antimicrobial therapy with
either doxycycline (5 mg/kg IV every 12 hours) or a combination of clindamycin (5-10 mg/kg IV
every 8 hours) or ampicillin (10-20 mg/kg IV every 8 hours) and a fluoroquinolone (ie,
enrofloxacin [10 mg/kg IV every 24 hours]) can be considered. At discharge, enteral therapy can
be continued with doxycycline (5 mg/kg PO every 12 hours) or amoxicillin/clavulanate (12-20
mg/kg PO every 12 hours), ideally, based on culture and susceptibility testing.17 These patients
should be strictly isolated from other patients, and veterinary staff should use personal
protective equipment and proper hygiene to prevent transmission via fomites. Patients with
significant respiratory compromise should be provided with supplemental oxygen in an oxygen
cage (if available) or through a nasal cannula.

Bronchodilators (eg, theophylline [5-10 mg/kg PO every 12 hours], terbutaline [0.625-5 mg/dog
SC every 8-12 hours]) are rarely indicated in dogs with CIRDC but can be administered in
patients suspected to have bronchospasm that is impairing appropriate ventilation. If used
concurrently with medications metabolized by cytochrome P450 enzyme system, the dosage
should be altered. In the case of fluoroquinolones, the theophylline dose should be reduced due
to drug interactions that can lead to reduced metabolism and subsequent increase in plasma
levels, which might result in adverse effects.

Prognosis & Prevention

Complete resolution of uncomplicated disease typically occurs within 10 to 14 days after onset of
clinical signs. Complicated disease can require treatment for 2 to 6 weeks, and, although
prognosis is generally good, subsequent development of severe pneumonia can progress to
sepsis or multiple organ dysfunction due to systemic inflammatory response syndrome.

According to AAHA vaccination guidelines,18 immunization is against core (eg, canine distemper
virus, canine adenovirus-2) and noncore (eg, B bronchiseptica, canine influenza virus, canine
parainfluenza virus) CIRDC pathogens. When administered appropriately, core vaccines
provide robust immunity against these viruses. Immunization with noncore vaccines may not
prevent infection but does appear to limit the severity of clinical signs and duration of shedding
postinfection. Oral, intranasal, and parenteral B bronchiseptica (modified-live and killed)
vaccines are commercially available. In general, parenteral vaccines produce a profound
serologic response, but oral and intranasal vaccines appear to provide more effective mucosal
immunity, with intranasal vaccines resulting in less severe disease in dogs challenged with
infection in experimental studies19,20; thus, intranasal vaccination has been shown to produce
protective immunity for at least 1 year. To the author’s knowledge, these studies have not been
published for oral or parenteral B bronchiseptica vaccines. Vaccines are available as monovalent
products or in combination with other respiratory pathogens (eg, canine parainfluenza virus,
canine adenovirus-2). Vaccines are available for 2 strains of canine influenza (ie, H3N2, H3N8)
as both monovalent and bivalent formulations. As killed vaccines, they induce a less robust
immune response than avirulent live viruses and are likely to reduce severity of disease rather
than prevent infection.

Clinical Follow-up/Monitoring
Recheck of dogs with uncomplicated disease is often unnecessary. In dogs with suspected
bacterial pneumonia as a result of complicated disease, radiography should ideally be
performed every 2 to 3 weeks while monitoring for resolution of clinical signs. Previously,
antimicrobials were administered for 3 to 6 weeks or at least 1 to 2 weeks beyond resolution of
clinical and/or radiographic signs of disease. The International Society for Companion Animal
Infectious Diseases guidelines suggest that a shorter duration may be adequate; thus, the
decision to continue antimicrobials should be made on a case-by-case basis using clinical,
hematologic, and radiographic findings to guide treatment.17

Following onset of signs, dogs should be isolated for 2 to 3 weeks, and care should be taken to
avoid sharing of bedding, bowls, and other husbandry items to prevent transmission to
susceptible dogs.

Conclusion
CIRDC is a common cause of acute cough in dogs, especially those cohoused with or exposed to
other dogs (eg, shelters, dog shows, grooming facilities). Generally, this condition is self-limiting
with supportive care, but some dogs need more advanced intervention, including
hospitalization or antimicrobial therapy if bacterial or mycoplasmal pneumonia develop.

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vaccines against Bordetella bronchiseptica in dogs. Vet J. 2016;212:71-77.

20. Ellis JA, Gow SP, Lee LB, Lacoste S, Ball EC. Comparative efficacy of intranasal and
injectable vaccines in stimulating Bordetella bronchiseptica-reactive anamnestic
antibody responses in household dogs. Can Vet J. 2017;58(8):809-815.

AUTHOR
Jonathan Dear
DVM, MAS, DACVIM (SAIM)
University of California, Davis

Jonathan Dear, DVM, MAS, DACVIM (SAIM), is a small animal internal medicine
specialist at University of California, Davis, where he also completed his MAS in clinical
research and a residency in small animal internal medicine. Dr. Dear is also president of
the International Society for Companion Animal Infectious Disease. He earned his
DVM from University of Georgia. His clinical interests include urinary and respiratory
medicine, and his research interests include small animal infectious diseases.

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