Both young and aged animals are at increased risk of developing respiratory disease

 Both young and aged animals are at increased risk of developing respiratory disease

 At birth, the respiratory and immune systems are incompletely developed; this facilitates the introduction and spread of pathogens within the lungs, and alveolar flooding may occur.

 In aged animals, chronic degenerative changes that disrupt normal mucociliary

clearance and immunologic anergy may render the lungs more vulnerable to

airborne pathogens and toxic particulates.

 A varying flora of indigenous commensal organisms (including Pasteurella multocida, Bordetella bronchiseptica, streptococci, staphylococci, pseudomonads, and coliform bacteria) normally reside in the canine and feline nasal passages, nasopharynx, and upper trachea, and at least intermittently in the lungs, without causing clinical signs. 

 Opportunistic infections by these bacteria may occur when respiratory

defense mechanisms are compromised by infection with a primary

pathogen (eg, distemper, parainfluenza virus, or canine type 2 adenovirus

in dogs, and rhinotracheitis virus or calicivirus in cats), other insults (eg,

inhalation of smoke or noxious gases), or diseases such as congestive

heart failure and pulmonary neoplasia.

Congenital abnormalities, such as stenotic nares, elongation of the soft palate, nasopharyngeal turbinates, and tracheal stenosis, can cause respiratory dysfunction. Neoplastic masses, degenerative changes of the airways, and tracheal collapse can result in dyspnea and other clinical manifestations of respiratory disease.

Tracheal collapse is most common in toy and miniature breeds of dogs

and rare in cats. The cause is unknown.

Lung Flukes in Small Animals

 Paragonimus kellicotti and P westermani usually are found in cysts, primarily in the lungs of dogs, cats, and several other domestic and wild animals

 They also have been found rarely in other viscera or the brain.

 The life cycle includes several snails as the first intermediate host, and crayfish or crabs as the second. Dogs and cats become infected by eating raw crayfish or crabs that contain the encysted cercariae. After penetrating the intestinal wall and wandering in the peritoneal

cavity, the young flukes pass through the diaphragm to the lungs, where they become

established

Infected animals may have a chronic, deep, intermittent cough and eventually become weak and lethargic, although many infections pass unnoticed.

Finding the characteristic eggs in feces or sputum is diagnostic. The location in the lungs is ascertained by radiography. Aberrant infections can be identified serologically.

Fenbendazole (50 mg/kg/day, PO, for 10–14 days) or less

preferably albendazole (25 mg/kg, PO, bid for 14 days) reduce the number of

eggs deposited and eventually kill the parasites. Praziquantel (25 mg/kg, PO,

tid for 3 days) may also eliminate lung flukes in dogs.

Allergic Pneumonitis in Small Animals

 An underlying cause is rarely determined in pulmonary hypersensitivity reactions in dogs and cats. 

 Type I or immediate hypersensitivity is probably the most common

mechanism, although Type III and IV mechanisms may also be involved

 The cellular infiltrate is typically eosinophilic; however, mixed

inflammatory infiltrates consisting of mononuclear cells, eosinophils,

and neutrophils, or predominantly lymphocytic infiltrates can be seen

 PIE is a group of diseases associated with both pulmonary-associated and peripheral eosinophilia.

 Causes of eosinophilic bronchopneumopathy include migrating parasites, reaction to microfilariae of heartworms, lungworms, chronic bacterial or fungal infections (eg, histoplasmosis, aspergillosis), viruses, external antigens, and unknown precipitating factors.

Eosinophilic bronchopneumopathy (formerly

pulmonary infiltration with eosinophilia [PIE]

Pulmonary nodular eosinophilic granulomatous syndrome

 Rare

 Severe eosinophilic bronchopneumopathy–like syndrome that occurs in dogs and is most often associated with heartworm infection or possibly an uncontrollable progressive form of eosinophilic bronchopneumopathy

 a severe granulomatous hypersensitivity reaction to microfilariae (or other antigen)

results in mixed alveolar and interstitial pulmonary infiltrates plus variably sized,

multiple pulmonary nodules scattered throughout the lung fields.

Clinical Findings

 Chronic cough (mild or severe, productive or nonproductive, and progressive or nonprogressive.)

 Weight loss, tachypnea, dyspnea, wheezing, exercise intolerance, and occasionally hemoptysis may be seen. 

 moderate to severe dyspnea and cyanosis at rest

 Auscultation varies from unremarkable to increased breath sounds, crackles, or wheezes. Fever is usually absent. 

 The degree of dyspnea and coughing is related to the severity of

inflammation within the airways and alveoli.

Diagnosis

 This is based largely on history and on radiographic and clinicopathologic findings

 Thoracic radiographs frequently show irregular patchy alveolar infiltrates and increased bronchial and interstitial markings. 

 Typical hematologic changes are mild leukocytosis, variable peripheral eosinophilia (4%–50%), and occasionally basophilia

  Fecal analysis and an occult heartworm test are indicated when lung parasitism or heartworm disease is suspected

 Bronchoalveolar lavage for cytologic analysis, culture, and detection of larval forms is often helpful. In allergic pneumonitis, bronchoalveolar lavage cytology generally reveals a predominance of

eosinophils. Bacterial cultures of aseptically collected lavage specimens are commonly negative.

Treatment

 When an underlying cause can be found, elimination of the offending agent and a short-term course of glucocorticoids resolves the problem

 Prednisolone beginning at 1–2 mg/kg, PO, tapered over 10–14 days is often sufficient. 

 When eosinophilic bronchopneumopathy is secondary to heartworm disease or pulmonary parasites, treatment with prednisolone before or during treatment for the parasite controls the pulmonary signs.

 When an underlying cause cannot be determined, prolonged therapy with prednisolone for

3–12 wk is often required. When severe bronchoconstriction is suspected, bronchodilators or

β

-agonists may be helpful. Severely dyspneic animals may require short-term oxygen

therapy.

Canine Influenza (Flu)

 Two strains of the canine influenza virus (CIV) have been identified, H3N8 and H3N2. 

 Outbreaks are most common when dogs are in close contact, eg, kennels, shelters, dog parks.

 CIV is spread via respiratory secretions, contaminated objects (eg, water bowls), and people moving between infected and uninfected dogs.

 The incubation period is usually 2–4 days from exposure to onset of clinical signs, when dogs

are most contagious; ~20% of infected dogs remain asymptomatic but can still shed virus.

Clinical Findings and Diagnosis

 Most exposed dogs (80%) develop mild infection, with a cough that persists 1–3 wk and may be similar to the cough of canine infectious tracheobronchitis

 Other possible clinical signs include ocular and nasal discharge, sneezing, fever, lethargy, and anorexia. Some dogs become severely ill, with high fever (104º–106ºF), pneumonia, and secondary bacterial infection. The mortality rate is <10%.

 There is no rapid test for specific diagnosis. Nasal or pharyngeal swabs from dogs ill for <3 days can be submitted for PCR testing. After 4 days of illness, PCR testing may result in false- negatives, because the time of maximal virus shedding has passed

 Serum antibodies to CIV may be detected as early as 7 days after onset of clinical signs. The

best method for confirmation of infection is serologic testing with acute and convalescent

serum samples.

Treatment, Prevention, and Control

 Treatment is largely supportive; most dogs recover in 2–3 wk.

 Additional treatment (eg, antimicrobials, NSAIDs) is warranted to combat secondary bacterial infection, pneumonia, and other complications

 H3N8 canine influenza vaccines are available, but whether they protect against the H3N2 strain is unknown. 

  CIV can persist in the environment for 1–2 days but is readily killed by common

disinfectants. 

Canine Nasal Mites

 Pneumonyssoides caninum or Pneumonyssus caninum

 There does not seem to be a breed, age, or sex predilection, although one report suggested that dogs >3 yr old were affected more often and that large-breed dogs had a higher incidence than small-breed dogs.

 The most common clinical signs associated with nasal mite infestation include epistaxis, sneezing, reverse sneezing, impaired scenting ability, facial pruritus, nasal discharge, head shaking, and stridor

 coughing, restlessness, and collapse

Treatment

 No drugs are currently approved for the treatment of P caninum;

however, ivermectin(200–400 mcg/kg, SC or PO), milbemycin oxime (1 mg/kg, PO,

three times at 10-day intervals), and selamectin (topical) have been suggested.

Feline Respiratory Disease Complex

 Feline respiratory disease complex includes those illnesses typified by rhinosinusitis, conjunctivitis, lacrimation, salivation, and oral ulcerations.

 The principal diseases, feline viral rhinotracheitis (FVR; feline herpesvirus type 1),

feline calicivirus (FCV), Chlamydia felis, Mycoplasma felis, or combinations of these

infections, affect exotic as well as domestic species.

 Natural transmission of these agents occurs via aerosol droplets and fomites, which can be carried to a susceptible cat by a handler.

 Convalescent cats may harbor virus for many months.

 Calicivirus is shed continually, while infectious FVR virus is released

intermittently. Stress may precipitate a secondary course of illness. The

incubation period is 2–6 days for FVR and FCV, and 5–10 days for

pneumonitis.

Clinical Findings

 Fever, frequent sneezing, conjunctivitis, rhinitis, and often salivation

 The fever may reach 105°F (40.5°C) but subsides and tends to fluctuate from normal to 103°F (39°C)

 Initially, a serous nasal and ocular discharge occurs; it soon becomes mucopurulent and copious, at which time depression and anorexia are evident

 Severely debilitated cats may develop ulcerative stomatitis, and ulcerative keratitis develops in some. 

 Signs may persist for 5–10 days in milder cases and as long as 6 wk in severe cases.

 FVR often is complicated by secondary bacterial infections; abortions and generalized

infections also have been associated with disease.

 Clinically, it is often impossible to differentiate FVR from FCV infection. Two strains may produce a transient “limping syndrome” without signs of oral ulceration or pneumonia. 

 These strains produce a transient fever, alternating leg lameness, and pain on palpation of affected joints. Signs occur most often in 8- to 12-wk-old kittens and usually resolve without treatment.

 The syndrome may occur in kittens vaccinated against FCV; no vaccine

protects against both of the strains that produce the “limping syndrome

 C felis infections characteristically produce conjunctivitis

 Mycoplasma spp may infect the eyes and upper respiratory passages, characteristically producing severe edema of the conjunctiva and a less severe rhinitis

  FVR tends to affect the conjunctivae and nasal passages, caliciviruses the oral mucosa and lower respiratory tract

 Chlamydial infections result in chronic, low-grade conjunctivitis

Cytologic examination of Giemsa-stained conjunctival scrapings is of value for the identification of chlamydiae and mycoplasmas

Diagnosis of FVR may be difficult, because virus is shed intermittently and because seroprevalence and virus isolation rates are similar in ill and clinically normal cats.

Samples of ocular, nasal, or caudal pharyngeal secretions for PCR may help establish a

diagnosis and causative agent.

Treatment:

 Largely symptomatic and supportive

 Broad-spectrum antibiotics are useful against secondary bacterial invaders (eg, amoxicillin with clavulanic acid, cephalosporins, trimethoprim-sulfa, fluoroquinolones, tetracyclines, chloramphenicol) as well as directly against C felis and M felis

 Nasal and ocular discharges should be removed frequently for the comfort of the cat.

 Nebulization or saline nose drops may aid in the removal of tenacious secretions. Nose drops

containing a vasoconstrictor (eg, two drops of ephedrine sulfate [0.25% solution] in each

nostril, bid) and antibiotics may help reduce the amount of nasal exudate. 

 A bland ophthalmic ointment containing antibiotics (tetracyclines in C felis infections) is indicated 5–6 times daily to prevent corneal irritation produced by dried exudate.

 If corneal ulcers develop in FVR infections (herpetic keratitis), ophthalmic preparations containing idoxuridine or acyclovir are indicated in addition to other antibiotic ophthalmic preparations

 Antihistamines (eg, chlorpheniramine maleate, PO, bid [8 mg for adults, 4 mg for

kittens]) may be beneficial early in the course of the disease

Prevention:

 The chlamydial vaccines are available in combination with FVR-FCV

and panleukopenia vaccines. Systematic vaccination and control of

environmental factors (such as exposure to sick cats, overcrowding,

and stress) provide good protection against upper respiratory disease.

Lung Nematodes in Small Animals

Click icon to add picture

Click icon to add picture

Aelurostrongylus abstrusus

 Aelurostrongylus abstrusus, the most common lungworm of cats

 They are small parasites (males 7 mm, females 10 mm), deeply embedded in the lung tissues. 

  The eggs are forced into alveolar ducts and adjacent alveoli, where they form small nodules and hatch

 Once the larvae escape, they are coughed up, swallowed, and passed

in the feces

 The life cycle includes snails or slugs as first intermediate hosts, and frogs, lizards, birds, or rodents as transport hosts of encysted larvae.

 When one of these transport hosts is eaten, the larvae migrate from the stomach to the lungs via the peritoneal and thoracic cavities.

 They reach the lungs within 24 hr and are seen in the feces in ~1 mo.

 Fenbendazole (50 mg/kg/day, PO, for 10–14 days)

or ivermectin (400 mcg/kg, SC, twice at a 3-wk interval)

Capillaria aerophila

 Although usually parasites of the frontal sinuses, trachea, bronchi, and rarely nasal cavities of foxes, C aerophila are found in dogs and other carnivores. 

 The eggs are laid in the lungs, coughed up and swallowed, and passed in the feces.

 The eggs can be identified from either tracheal washes and bronchoalveolar lavage

or fecal flotation

 The life cycle is direct; dogs become infected through consumption of feed or water contaminated with larvated eggs. After hatching in the intestine, the larvae reach the lungs and bronchi via the circulatory system. They mature ~40 days after infection.

 Clinical signs include coughing, sneezing, and nasal discharge. Treatment may be

attempted using fenbendazole (50 mg/kg/day, PO, for 10–14 days) or ivermectin (200

mcg/kg, SC, twice at a 3-wk interval).

Filarids

 Oslerus osleri are tracheal worms of dogs, usually found in thin-walled nodules around the bronchial bifurcation. 

 The life cycle is direct, and an infected bitch can transfer larvae in her saliva to her pups while licking and cleaning them. On ingestion, the larvae pass to the blood and are carried to the lungs and bronchi.

 A persistent , dry cough is the most common clinical sign. Coughing may later become severe, with respiratory distress. 

 Finding larvae in the feces is diagnostic, but because these larvae are lethargic and

few in number, bronchoscopy is a better method. 

 Surgical excision of the nodules combined with administration of fenbendazole, levamisole, or thiabendazole has effectively treated infected dogs. Chemotherapy alone can be successful but does not always result in a complete cure.

 Filaroides hirthi is similar to O osleri but is found in the lung parenchyma. 

 Treatment with fenbendazole (50 mg/kg/day, PO, for 10–14 days) or

less preferably albendazole (25 mg/kg, PO, bid for 5 days and repeated

in 2 wk) has reportedly been effective. Ivermectin (200 mcg/kg, SC,

twice at a 3-wk interval) may also be effective

Pneumonia in Small Animals

 Pneumonia is an acute or chronic inflammation of the lungs and bronchi characterized by disturbance in respiration and hypoxemia and complicated by the systemic effects of associated toxins. The usual cause is primary viral infection of the lower respiratory tract

 Canine distemper virus, adenovirus types 1 and 2, parainfluenza virus, and feline

calicivirus cause lesions in the distal airways and predispose to secondary bacterial

invasion of the lungs. 

 Parasitic invasion of the bronchi, as by Filaroides, Aelurostrongylus, or Paragonimus spp may result in pneumonia.

 Protozoan involvement, eg, by Toxoplasma gondii (see Toxoplasmosis) or Pneumocystis jiroveci, is rarely seen.

 Tuberculous pneumonia, although uncommon, is seen more often in dogs

than in cats. The incidence of mycotic granulomatous pneumonias is also

higher in dogs than in cats.

 Cryptococcal pneumonia has been described in cats. Injury to the bronchial mucosa and inhalation or aspiration of irritants may cause pneumonia directly and predispose to secondary bacterial invasion.

 Aspiration pneumonia (see Aspiration Pneumonia) may result from persistent vomiting,

abnormal esophageal motility, or improperly administered medications (eg, oil or

barium) or food (forced feeding); it may also follow suckling in a neonate with a cleft

palate.

Clinical Findings

 The initial signs are usually those of the primary disease.

 Lethargy and anorexia are common.

 A deep cough

 Progressive dyspnea, “blowing” of the lips, and cyanosis may be evident, especially on exercise. 

 Body temperature is increased moderately, and there may be leukocytosis.

 Auscultation usually reveals consolidation, which may be patchy but more commonly is diffuse. 

 In the later stages of pneumonia, the increased lung density and peribronchial consolidation caused by the inflammatory process can be visualized radiographically.

 Complications such as pleuritis, mediastinitis, or invasion by opportunistic

organisms may occur

Diagnosis:

 Analysis of bronchoalveolar lavage fluid is valuable for the diagnosis of bacterial infections

 anaerobe and mycoplasma culture

 A viral etiology generally results in an initial body temperature of 104°–106°F (40°–41°C).

Leukopenia, often expected, may not be seen in many viral respiratory infections (eg, canine infectious tracheobronchitis, feline calicivirus pneumonia, feline infectious peritonitis

pneumonia).

 A history of recent anesthesia or severe vomiting indicates the possibility of aspiration pneumonia

  Mycotic pneumonias are usually chronic in nature. Miliary nodules seen at necropsy may

suggest protozoal pneumonia.

Treatment

 The animal should be placed in a warm, dry environment.

 Anemia, if present, should be corrected.

 If cyanosis is severe, oxygen therapy may be used, administered by means of an oxygen cage, with a concentration of 30%–50%. 

  Empirical antimicrobial chemotherapy should be initiated and changed if needed based on results of culture of bronchoalveolar lavage fluid

 Antimicrobial chemotherapy should be continued 1 wk after clinical and radiographic signs

resolve

Pulmonary Thromboembolism in Small Animals

 Pulmonary thromboembolism (PTE) is an obstruction of one or more pulmonary vessels by a blood clot

 Immune-mediated hemolytic anemia, corticosteroid administration, bacterial

infections, protein-losing enteropathy or nephropathy, neoplasia, trauma, feline

infectious peritonitis, diabetes mellitus, hyperadrenocorticism, hypothyroidism,

disseminated intravascular coagulation, dirofilariasis

 The acute pulmonary consequences of PTE include ventilation-perfusion mismatch,

hypoxemia, hyperventilation, and bronchoconstriction. Hemodynamic consequences

of PTE are related to the magnitude of the obstruction and presence of coexisting

cardiopulmonary disease. Myocardial ischemia, arrhythmias, or right ventricular

failure may result. Decreased cardiac output may ensue with severe obstruction to

pulmonary arterial blood flow as a result of decreased venous cardiac return.

Clinical Findings:

 Clinical signs are nonspecific and most often subclinical or may be mild to profound, reflecting the severity of cardiorespiratory compromise.

Dyspnea, tachypnea, and depression are commonly seen. Coughing,

cyanosis, hemoptysis, collapse, shock, and sudden death can occur.

Diagnosis:

 Diagnosis is often difficult because PTE can resemble many other conditions, including pneumonia, pulmonary edema or hemorrhage, neoplasia, or pleural effusion. Routine diagnostic tests such as thoracic radiography or arterial blood gas analysis are nonspecific and rarely confirm diagnosis. Arterial blood gas analysis will identify hypoxemia

present in 80% of dogs, although response to oxygen is variable. Thoracic radiographs can be normal in 9%–27% of dogs and in 9% of cats with PTE.

Abnormal radiographic findings with PTE include alveolar or interstitial pulmonary infiltrates or regional hypovascular lung areas.

  Spiral CT angiography or selective pulmonary angiography remain gold

standards for diagnosis of PTE in people, but these advanced imaging

studies are available at few veterinary institutions.

Rhinitis and Sinusitis in Small Animals

 Viral infection is the most common cause of acute rhinitis or sinusitis in dogs and cats. Feline viral rhinotracheitis (FVR), feline calicivirus (FCV), canine distemper, canine adenovirus types 1 and 2, and canine parainfluenza are most frequently incriminated. Chronic states exist for FVR and FCV, with intermittent shedding associated with stress. 

 Primary bacterial rhinitis is extremely rare in dogs. It may result from infection with Bordetella bronchiseptica in dogs. Bacterial rhinitis appears to be a common complicating factor in cats with chronic rhinosinusitis, although exposure to

environmental aeroallergens may also play a role. Allergic rhinitis or sinusitis is a poorly defined atopy that may occur seasonally, possibly in association with

pollen production, or perennially, probably in association with house dusts and

molds. Smoke aspiration, inhalation of irritant gases and dusts, or foreign bodies

lodged in the nasal passages also may cause acute rhinitis

 Underlying causes of chronic rhinitis include idiopathic chronic

inflammatory disease (lymphoplasmacytic rhinitis), trauma, parasites (Cuterebra), foreign bodies, neoplasia, or mycotic infection.

 Mycotic rhinosinusitis may be caused by Cryptococcus

neoformans,  Aspergillus spp, and Penicillium spp. Cats are more often affected with Cryptococcus spp than dogs, whereas aspergillosis is

frequent in dogs but rare in cats.

Clinical Finding

 Acute rhinitis is characterized by nasal discharge, sneezing, pawing at the face, respiratory stertor, open-mouth breathing, and/or inspiratory dyspnea. Lacrimation and conjunctivitis often accompany inflammation of the upper respiratory passages

 Affected tissues are often hyperemic and edematous. The nasal discharge is serous but becomes mucoid as a result of secondary bacterial infection. If inflammatory cells infiltrate the mucosa, the discharge may become mucopurulent.

 Approximately 35% of cats with nasal cryptococcosis have facial

deformity (dorsal lump) of the rostral aspect of the nose. Head shyness

or facial pain is more commonly associated with fungal rhinitis in dogs.

Diagnosis

 Diagnosis is based on history, physical examination, radiographic findings (especially CT), rhinoscopy, nasal biopsy, deep nasal tissue culture, and elimination of other causes of nasal discharge and sneezing

 Serum titer for cryptococcal antigen is a very specific and sensitive test for nasal cryptococcosis. Serologic evaluation for aspergillosis is more

problematic in that negative test results do not exclude infection. Nasal tissue culture for Aspergillus may also result in false-positive results; as many as 30% of normal dogs and 40% of dogs with nasal neoplasia have positive

culture results. The combination of seropositivity for and culture identification

of Aspergillus is highly suggestive of infection, although negative test results

do not exclude nasal aspergillosis. Direct sampling of visualized suspected

fungal plaques may potentially yield Aspergillus hyphae in all cases.

Treatment:

 Mycotic rhinosinusitis requires antifungal therapy based on identification of a fungal etiologic agent. Fluconazole (50–100 mg/day, PO) or itraconazole (50–100 mg/day, PO) may be effective for treatment of nasal cryptococcosis in cats.

 Oral antifungal agents have variable efficacy in treatment of dogs with nasal aspergillosis, although voriconazole (4 mg/kg, PO, bid) alone or in combination with terbinafine (15 mg/kg, PO, bid for 1 mo) may be effective. 

 Topical intranasal infusions of enilconazole or clotrimazole or

combined clotrimazole solution and cream depot therapy instilled via the frontal

sinuses have success rates as high as 50% for the first treatment and 90% with

two treatments, although reinfection or relapse may occur

Tracheobronchitis in Small Animals

 Canine infectious tracheobronchitis (kennel cough, see 

Infectious Tracheobronchitis of Dogs) is often secondary to viral infection of the respiratory system. Other causes of tracheobronchitis in dogs include parasites,

eg, Aelurostrongylus abstrusus (also in cats), Capillaria aerophila, Crenosoma vulpis, and Oslerus osleri.

 smoke aspiration and exposure to noxious chemical fumes

 Feline bronchial asthma (allergic bronchitis) is a syndrome in cats with similarities to asthma in people. Young cats and Siamese and Himalayan breeds are most affected.

Feline asthma is associated with airway hyperresponsiveness, airflow obstruction,

airway remodeling, and eosinophilic airway inflammation.

Infectious Tracheobronchitis of Dogs

 Infectious tracheobronchitis results from inflammation of the upper airways. It is a mild, self-limiting disease but may progress to fatal

bronchopneumonia in puppies or to chronic bronchitis in debilitated adult or aged dogs.

 Canine parainfluenza virus, canine adenovirus 2 (CAV-2), or canine distemper virus can be the primary or sole pathogen involved. Canine reoviruses (types 1, 2, and 3), canine herpesvirus, and canine adenovirus 1 (CAV-1) are of questionable significance in this syndrome. Bordetella bronchiseptica may act as a primary pathogen, especially in dogs <6 mo old; however, it and other bacteria (usually gram-negative organisms such as Pseudomonas sp, Escherichia coli, and Klebsiella pneumoniae) may

cause secondary infections after viral injury to the respiratory tract.

Treatment

 Cough suppressants containing codeine derivatives, such as hydrocodone (0.25 mg/kg, PO, bid-qid) or butorphanol (0.05–0.1 mg/kg, PO or SC, bid-qid), should be used only as needed to control persistent nonproductive coughing.

Antibiotics are usually not needed except in severe chronic cases;

cephalosporins, quinolones, chloramphenicol, and tetracycline are preferable because they reach effective concentrations in the tracheobronchial mucosa

 Antibiotics given PO or IM may not significantly reduce the numbers of B

bronchiseptica in the distal trachea or major bronchi. Thus, in severely affected dogs that are not responsive to parenteral antibiotics, kanamycin sulfate (250 mg) or gentamicin sulfate (50 mg) diluted in 3 mL of saline may be

administered by aerosolization bid for 3 days. Aerosolization treatment should

be preceded by administration of bronchodilators.