Nasal disorders in the dog and cat (Proceedings)


Lymphocytic-plasmacytic rhinitis (L-PR) is a nonspecific inflammatory condition associated with antigenic and irritant stimulation. This disorder is most commonly found in dogs. and has a predisposition for Dachshunds. The clinical signs are those commonly seen with nasal diseases, including sneezing and nasal discharge of varying character.

Lymphocytic-Plasmacytic Rhinitis

Lymphocytic-plasmacytic rhinitis (L-PR) is a nonspecific inflammatory condition associated with antigenic and irritant stimulation. This disorder is most commonly found in dogs. and has a predisposition for Dachshunds. The clinical signs are those commonly seen with nasal diseases, including sneezing and nasal discharge of varying character. Although the origin of this disorder is typically idiopathic, fungal, parasitic, and neoplastic diseases are sometimes associated with the chronic inflammatory infiltrates observed with L-PR. One theory concerning the origin of L-PR speculates that some affected individuals may not have actual fungal infection but acquire this disorder as a result of a hypersensitivity to fungal organisms, including commensal fungal organisms residing within the nose. Rhinoscopy in patients with L-PR generally reveals evidence of nonspecific inflammation. Diagnostic imaging often shows fluid density In the nasal cavity and frontal sinuses and may show mild to moderate lysis of the turbinates, especially rostrally. Histopathology of the nasal mucosa most commonly reveals mixed inflammatory cells with lymphocytes and plasma cells predominating. Immunohistochemical staining for B- and T- cell markers should be considered in patients, especially cats, with marked lymphoplasmacytic inflammation to rule out lymphoma. Therapeutic options for L-PR of idiopathic origin include:

     1. Trial therapy with ivermectin (0.2 mg/kg subQ or PO, 2 treatments 3 weeks apart) for nasal mites

     2. Trial therapy with itraconazole (5 mg/kg PO q12hrs for a minimum of 3-6 months) for possible low grade fungal infection or fungal-triggered hypersensitivity reactions

     3. Immunosuppressive steroid therapy (prednisone, 1 mg/kg q12 hours PO initially) or topical steroid administration with nasal drops or aerosolized preparations via metered dose inhaler

     4. Alternative immunosuppressive therapy with azathioprine (1 - 2 mg/kg/day PO)

     5. Antiinflammatory therapy with piroxicam (0.3 mg/kg/day PO)

     6. Immunomodulating antibiotics such as doxycycline (3 – 5 mg/kg q12 hrs) or azithromycin (5 mg/kg q24 hrs PO) in combination with daily piroxicam; if improvement is noted,combination therapy is continued but with a reduction in frequency of antibiotic administration (doxycycline – SID or azithromycin – twice weekly)

     7. Ancillary therapy with humidification of airways, elimination of environmental irritants, and intranasal saline

Most dogs with L-PR have some degree of persistent clinical signs although the majority of patients can be managed successfully long-term with medical treatment.

Foreign Bodies

Nasal foreign bodies should be suspected with the following circumstances:

     1. Known opportunity for foreign body inhalation with a sudden onset of compatible signs

     2. Sudden onset of paroxysmal sneezing

     3. Pawing at the nose

     4. Unilateral nasal discharge, especially mucopurulent discharge with occasional hemorrhage

     5. Persistent gagging, retching, or reverse sneezing

     6. Persistent nasal discharge which follows an acute onset of sneezing

It should be remembered that acute and persistent sneezing in the cat is more often associated with viral upper respiratory infection than with foreign body inhalation.

Foreign bodies within the nasal cavity usually enter via the caudal nares following gagging or vomiting episodes. Plant material is the most common type of foreign body usually encountered. Patients with appropriate history and clinical signs for nasal foreign body should undergo rhinoscopy, including examination of the caudal nasopharynx, as an initial diagnostic procedure and are an exception to the general rule of performing imaging prior to rhinoscopy. If a nasal foreign body is suspected but not seen with rhinoscopy or cannot be removed with a grasping instrument, extensive nasal flushing should be performed to try to dislodge any hidden foreign material. When flushing, the patient's nose should be directed downward with the endotracheal tube cuff inflated and the caudal oropharynx packed with gauze to prevent tracheal aspiration. If a foreign body is removed, the remainder of the nasal cavity and caudal nasopharynx should be examined to be sure that all foreign material has been eliminated. Granulomas may develop when foreign material has been present for an extended period of time, making identification and nonsurgical removal of the foreign matter difficult.

Feline Upper Respiratory Infection and Chronic Rhinosinusitis

Feline upper respiratory infection (URI) and chronic rhinosinusitis are commonly associated with infection with feline herpesvirus (FHV) and feline calicivirus (FCV) with a lesser frequency of infection related to Bordetella bronchiseptica, Chlamydophilia felis, and Mycoplasma. Infection is transmitted through contact with infected or carrier cats and fomites. Infected cats may become chronic carriers of FHV, FCV, and Bordetella. Feline URI may be acute or chronic.


Acute URI is more common than the chronic form. Typical signs include fever, sneezing, serous or mucopurulent nasal discharge, conjunctivitis, ocular discharge, anorexia, dehydration and cough (Bordetella). Additional signs may be seen with FHV (corneal ulceration, abortion, and neonatal death) and FCV (oral ulceration, interstitial pneumonia, and polyarthritis). The diagnosis of acute URI is usually made based on appropriate historical and physical findings. Specific etiology may be determined by viral isolation, cytology, and bacterial culture but is most useful in multiple cat situations. Supportive care is an important part of therapy, including providing appropriate hydration, nutrition, hygiene, humidification and decongestion. Antibiotics such as amoxicillin are often indicated for secondary bacterial infections; doxycycline or azithromycin (5 – 10 mg/kg q24 hrs PO for 3 days, then q72 hrs) are good choices for Bordetella, Chlamydophilia, and Mycoplasma. Ophthalmic ointment may be needed in some cases, especially, when Chlamydophilia is suspected (e.g., ocular preparations containing tetracycline or chloramphenicol) and should be applied for at least 14 days post-resolution of clinical signs. When FHV etiology is suspected, antiviral eye drops (trifluridine, idoxuridine, adenine arabinoside) may be helpful along with routine corneal ulcer management. The prognosis for acute URI is generally good.

Chronic rhinosinusitis is characterized by persistent clinical signs similar to acute URI. Serous to mucopurulent nasal discharge is the most prominent clinical sign. The developmentt of chronic rhinosinusitis may be related to previous acute infection with FHV1, FCV or Chlamydia felis infection or permanent damage to the turbinates and mucosa, predisposing to secondary bacterial infection. Diagnosis is best made by eliminating other causes of chronic nasal discharge. Viral isolation, bacterial culture, PCR, or antibody titers may identify a specific microbial agent, but microbes are thought to be only a part of the etiology for chronic rhinosinusitis.. Imaging results include fluid density opacity within the nasal cavity, sinuses and, occasionally, tympanic bullae, and mild to moderate lysis involving the turbinates, nasal, and frontal bones. Typical rhinoscopic findings are nonspecific inflammation, mucoid to mucopurulent nasal discharge, and mild to moderate turbinate erosion. Histopathologic results can include neutrophilic and/or lymphocytic inflammation, turbinate destruction, fibrosis, and necrosis. Nasal biopsies and/or nasal fluid from deep aspiration should be cultured for aerobic, anaerobic, and Mycoplasma. Therapeutic approach should include treating the underlying disease when possible and supportive care, including humidification, saline drops, topical decongestants, and nasal flushing under anesthesia. Long-term intermittent or continuous antibiotic therapy is usually needed to help control the clinical signs. Lysine administration (250-mg/cat q12 hours PO with food) may be beneficial where recrudescence of FHV is involved. Antiinflammatory therapy with glucocorticoids at the lowest dose needed to control clinical signs or administration of piroxicam (0.3 mg/kg q24 hrs PO) can be helpful in managing the disease. Turbinectomy and frontal sinus ablation can be considered in cases unable to be maintained successfully with medical management alone. The prognosis is poor for cure but fair to good for medical management and a good quality of life with appropriate supportive care.


Nasal Neoplasia

Nasal neoplasia can be found in both older dogs and cats. The majority of nasal tumors are malignant.. Adenocarcinoma, squamous cell carcinoma and undifferentiated sarcomas are commonly found in the dog. The cat most commonly is affected by lymphoma and adenocarcinoma. Patients are typically older adults of either sex. Chronic nasal discharge is a frequent clinical sign and may progress from unilateral to bilateral. The character of the discharge can be serous, mucoid, mucopurulent, or hemorrhagic. Other clinical signs include sneezing, decreased air flow through the nares, deformity of the facial bones, hard palate, or maxillary dental arcade. Additional signs may include CNS signs with brain invasion, exophthalmos with orbit invasion, and systemic signs such as weight loss and anorexia. Diagnosis often involves imaging which may reveal soft tissue opacity in the nasal cavity, varying degrees of destruction of turbinates, vomer bone, and facial bones, and soft tissue swelling external to the facial bones. Rhinoscopic findings include nonspecific inflammation, a mass lesion, and turbinate erosion. Extent of disease should be assessed through fine needle aspirate (FNA) of submandibular lymph nodes and thoracic radiographs. FIV/FeLV status should be determined in cats. Radiation therapy is the treatment of choice for most malignant nasal tumors. Surgical excision of benign tumors is recommended, if possible. Chemotherapy may be indicated for nasal lymphoma. Palliative therapy potentially includes photodynamic therapy (PDT), piroxicam (especially for carcinomas), or glucocorticoids. The prognosis is poor for untreated patients. Patients receiving radiation therapy ± surgical debulking may live 1 – 2 years. Depending on the type of neoplasia, treatment with chemotherapy, PDT, and antiinflammatories may produce improvement for several weeks to months.

Nasal Fungal Infections

Nasal fungal infection most commonly involves Cryptococcus in the cat and Aspergillus in the dog although either fungus can occur in both species. Aspergillus may develop as a primary disease or as an opportunistic infection secondary to other disease. Rhinosporidium seeberi can occasionally cause a granulomatous mass in the rostral nasal cavity of the dog, which may be diagnosed by cytology or histopathology. Rarely rostral ulcerative lesions with nasal discharge and/or an intranasal granulomatous mass can result from Sporothrix schenckii infection in the dog. Sporothrix infection in the dog often requires histopathology for diagnosis. Cryptococcus causes typical signs of nasal disease, CNS signs, and signs related to infection of the eyes, skin, and subcutaneous tissues. Aspergillus infection occurs most frequently in young to middle-aged, dolichocephalic male dogs. Clinical signs include sneezing, sensitivity to facial palpation, depigmentation and ulceration of the external nares, and nasal discharge which can be mucoid, mucopurulent, or hemorrhagic in character.

Rhinosporidium nasal infection is generally best treated by surgical resection of the associated granulomatous mass. Sporothrix infection can be treated with potassium iodide (40 mg/kg PO q8 hrs for 1 month beyond clinical resolution) or itraconazole (5 – 8 mg/kg PO q 12 hrs until 1 month beyond clinical resolution).

Nasal Cryptococcus infection is often diagnosed by identification of the organism through cytologic examination of nasal exudates or a swab from a granulomatous lesion. Imaging typically reveals soft tissue opacity in the nasal cavity, lysis of turbinates, facial bone destruction, and a possible soft tissue mass external to the facial bones. Gross rhinoscopic findings include nonspecific inflammation, granulomatous masses, and turbinate erosion. Nasal biopsies generally reveal inflammation and Cryptococcus organisms. The organism may be grown by culture from biopsies or a swab of nasal exudate. Antigen testing may also be useful in diagnosing this disorder. Therapeutic options may include debridement of any granulomatous mass present in conjunction with administering antifungal agents such as itraconzole (50 – 100 mg/cat PO q24 hrs and 5 mg/kg PO q12 hrs for 4 days, then 5 mg/kg q24 hrs in the dog) or fluconazole (50 mg/cat PO q12 hrs). Therapy should continue for at least 1 month post-resolution of clinical signs. The prognosis is generally good for nasal and cutaneous forms if treated early enough in the course of the disease.

Nasal Aspergillus infection is most frequently diagnosed by histopathology of nasal mucosal biopsies, which usually reveal a mixed inflammatory response and the presence of fungal organisms. Culture of biopsied tissue can help confirm the presence of Aspergillus. Imaging results can include radiolucent areas within the nasal cavity, especially rostrally, increased fluid opacity of the nasal cavity and frontal sinuses, and mild destruction of the vomer or facial bones. Rhinoscopic findings may include erosion of the nasal turbinates, white- to green- colored fungal plaques, and nonspecific inflammation. In addition, fungal titers and antigen testing are useful adjunctive diagnostic procedures. Therapy most often involves infusion of clotrimazole into the nasal cavity and/or frontal sinuses. The most recent treatment approach with clotrimazole involves flushing 1% clotrimazole solution (Lotrimin) into the frontal sinuses through an opening created by trephination followed by instillation of 1% clotrimazole cream. Oral itraconazole (5 mg/kg PO q12 hrs), terbinafine (5 – 10 mg/kg q12 hrs), or fluconazole (2.5 -5 mg/kg q12 hrs – dog; 50 mg/cat q 12 hrs- cat) for a minimum of 3 – 6 months) may be recommended for patients that have complicating factors such as erosion of the cribiform plate. The prognosis ranges from guarded to good, depending upon the extent of involvement.

Nasal Parasites

Nasal parasites include mites (Pneumonyssoides caninum) and nematodes (Capillaria boehmi) that are occasionally found in dogs. Dogs affected by nasal mites may be asymptomatic but sometimes exhibit clinical signs such as sneezing, pawing at the nose, reverse sneezing, chronic nasal discharge, and epistaxis. Diagnosis is generally made by visualization of the mites via rhinoscopy or examination of material obtained by nasal flushing. Therapy consists of administration of milbemycin oxime (0.5 – 1 mg/kg PO q7 -10 days for 3 treatments) or ivermectin (0.2 mg/kg subQ or PO administered twice at a 3-week interval). It is advisable to treat all dogs in direct contact with the patient. The prognosis is excellent for eradication of nasal mites. Capillaria boehmi, a small, thin nematode which lives on the nasal and frontal sinus mucosa, is sometimes found in dogs. The eggs of this nematode are shed in the feces. Clinical signs include sneezing, mucopurulent discharge, and occasional epistaxis. Diagnosis can be made by identifying the parasite eggs on fecal flotation or the adult parasite on rhinoscopy. Therapeutic options include administration of ivermectin (0.2 mg/kg PO or subQ once) or fenbendazole (25 -50 mg/kg q24 hrs for 10 – 14 days). Retreatment depends upon resolution of clinical signs along with negative fecal examinations. The prognosis is good for eradication of the nematode provided reinfection from contaminated soil does not occur.

Allergic Rhinitis

Allergic rhinitis is related to a hypersensitivity reaction to airborne antigens within the nasal cavity and sinuses. Clinical signs generally consist of sneezing and serous or mucopurulent nasal discharge that can be related to environmental factors and which may be seasonal, continuous or intermittent, and acute or chronic. Improvement in clinical signs following removal of a suspected offending antigen is highly suggestive of this disorder. Imaging frequently shows increased soft tissue opacity of the nasal cavity with minimal turbinate destruction. Nonspecific inflammation is the most common rhinoscopic finding with eosinophilic inflammation identified on nasal mucosal biopsy. Besides removal of the offending antigen therapy with antihistamines and glucocorticoids. The problem is often recurring, but the prognosis for control of clinical signs is usually good.

Bacterial Rhinitis

Bacterial rhinitis in the dog and cat can be an acute process caused by a primary pathogen such as Mycoplasma Occasionally in the cat and rarely in the dog Bordetella bronchiseptica can also be a primary cause of acute rhinitis. However, bacterial rhinitis occurs most commonly as a consequence of another underlying disease. Whether acute or chronic the most consistent clinical sign is mucopurulent nasal discharge. Other than fluid in the nasal cavity. imaging and rhinoscopic findings will vary according to the nature of the underlying disease process. Material for culture is best obtained by well placed swabs or mucosa taken from deep within the nasal cavity. Normal nasal flora include a variety of bacteria and Aspergillus. Growth of multiple colonies of one or two organisms is usually more significant than growth of a few colonies of several different organisms. Ideally the antibiotics used in therapy should be chosen based on culture and sensitivity results and be administered for 7 – 10 days in acute disease and a minimum of 4 – 6 weeks in chronic disease. The patient should also be treated concurrently for any underlying disease identified. Prognosis is generally dependent upon the ability to successfully treat underlying diease.

Feline Nasopharyngeal Polyps

Nasopharyngeal polyps are benign growths that can occur in kittens and young cats. Generally a single polyp is present which has a stalk and is often attached to the base of the eustachian tube or originates in the middle ear and enters the nasopharyngeal area through the eustachian tube. Clinical signs include stertor, decreased movement of air through the nasal passages, gagging, serous to mucopurulent nasal discharge, and occasionally signs of otitis externa, media, or interna. Bacterial rhinitis often develops secondary to the nasopharyngeal obstruction. Diagnosis is achieved by identification of a soft tissue opacity above the palate on imaging and/or visual inspection. Visual inspection should include looking above the soft palate with an endoscope or by pulling the soft palate forward with a spay hook. The ear canals should also be examined with an otoscope to identify inflammation and extension of the mass into the ear canal. Imaging of the bullae is also recommended. Histopathology of the mass will confirm the diagnosis. The mass can be removed with surgical excision or by applying gentle traction on the mass with a basket or other grasping instrument. In some cases bulla osteotomy is indicated. The prognosis is generally excellent with complete excision; however, recurrence of the polyp may occur, especially without bulla osteotomy on the side of polyp origin.

Nasopharyngeal Turbinates and Nasopharyngeal Stenosis

Nasopharyngeal obstruction can occasionally be caused in both the dog and the cat by nasopharyngeal turbinates and nasopharyneal stenosis. Although nasopharyngeal turbinates can occur in cats, particularly Himalayan and Persians, this disorder is most commonly seen as part of the brachycephalic airway syndrome in dogs, notably Pugs, French and English bullodogs, and Pekingese. Stertor is one of the most consistent signs resulting from the nasal turbinates extending caudally from the nose into the rostral nasopharynx. No practical therapeutic option is available for this disorder. Nasopharyngeal stenosis is an obstructive airway problem that develops as a result of congenital narrowing or scar tissue formation that restricts air flow above the soft palate. Acquired nasopharyngeal stenosis may develop as a consequence of URI or vomiting. After identification of the strictured area through nasopharyngoscopy ± imaging, stretching of the affected area through techniques such as balloon dilation may provide relief. Re-stricturing is a common complication, requiring multiple balloonings, concurrent corticosteroid therapy, surgical intervention, or stent placement.

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