John R. August, BVetMed, MS, MRCVS, DACVIM
Chronic upper respiratory disease, characterized by recurring sneezing and/or snuffling that is poorly responsive to antimicrobial treatment, is one of the most frustrating clinical problems for cat owners and companion animal practitioners.1 Most of these patients are presented with signs referable primarily to the nasal cavities; however, a small cohort of these cats have clinical signs resulting from disease in the nasopharynx, creating additional diagnostic and therapeutic challenges. Successful management of upper airway diseases in cats is hampered by the following factors:
Our poor understanding of the many initiating causes of upper respiratory disease.
Our tendency to consider chronic upper respiratory disease as a single clinical entity for which antimicrobial treatment is the preferred therapy.
Our failure to recognize the changing bacterial flora of the diseased upper respiratory tract over time as the problem progresses.
Our failure to recognize that some effusive diseases of the cavities of the upper respiratory tract may not have an infectious origin.
Financial and logistical challenges that often preclude diagnostic testing necessary to accurately identify the location and extent of disease.
Our failure to recognize that many patients require adjunctive surgical therapy to address sequestered infections that are not amenable to medical management alone.
Difficulties encountered by owners in the long-term administration of oral medications to affected cats.1
Anatomic and Physiologic Relationships
The feline nasopharynx is not an isolated anatomic region, although it does have well-defined anatomic boundaries (see below). Sitting at the crossroads to the entrances to the lower respiratory tract and upper gastrointestinal tract, the nasopharynx has close anatomic relationships to the caudal nasal cavity and the nasofrontal openings, and to the pharyngeal openings of the Eustachian tubes. The contiguous nature of these structures means that epithelial dysfunction in upper respiratory disease may be widespread, leading to complications in adjoining areas.For example, 34% of cats with nasopharyngeal disease had signs of bulla effusion, especially those patients with disease primarily affecting the caudal nasopharynx--close to the openings of the Eustachian tubes.2 As noted previously, infections spreading from the nasopharynx to sequestered cavities, such as the osseous bullae, may have important implications for prognosis and choice of management strategies.1
The nasopharynx is a functional space that allows the nasal cavity to communicate with the larynx.3 The nasopharynx is located above the soft palate, bordered rostrally by the nasal choanae. On oral examination, the rostral border can be identified by palpating the paired ventrally projecting hannular processes of the pterygoid bones.4 The caudal border of the nasopharynx is defined by the intrapharyngeal ostium, with demarcations of the caudal border of the soft palate and the palatopharyngeal arches.5 In contrast, the oropharynx is located ventral to the soft palate, bordered rostrally by the palatoglossal arches and extending caudally to the base of the epiglottis. The laryngopharynx is common to the gastrointestinal and respiratory tracts, and extends from the intrapharyngeal opening to the rostral border of the esophagus.5
Microbiology of the Upper Airway
The nasal passages of healthy cats normally are colonized by a variety of gram-positive and gram-negative aerobic or facultative commensal bacteria.6 Mycoplasma species and anaerobic bacteria were isolated from the nasal passages only from cats with chronic upper respiratory disease, and not from healthy control cats.7 Less is known about the microbial flora of the healthy and diseased feline nasopharynx. Shifts in microbial flora to more pathogenic species may occur in cats with upper respiratory disease over time, and with repeated administration of non-selective antimicrobials.1 These observations deserve further investigation, because it has been the author's experience that microbiologic results from caudal nasal and nasopharyngeal cultures from cats with chronic upper respiratory disease often differ from those obtained by rostral flushing and culture. In addition to microbial cultures from nasal flushes and nasal biopsy specimens7, it also may be necessary to collect choanal cultures to properly evaluate the contribution of microbial organisms to the persistence of upper airway disease.
Diseases of the feline nasopharynx rarely occur as an isolated event; rather, involvement of contiguous structures is common due to the close anatomic and physiologic relationships within the area. Nasal, frontal and sphenoid sinus, and osseous bulla disease may accompany signs referable to the nasopharynx; the diagnostic challenge is enhanced by the occult, asymptomatic involvement of some of these complications.
Chronic Bacterial Nasopharyngitis
Because the nasopharynx is the normal conduit for the drainage of secretions from the caudal nasal cavity into the oropharynx for removal by swallowing, the region is exposed to contaminated discharges in cats with chronic rhinitis. Swelling of nasopharyngeal soft tissues with accompanying effusion is a common finding on computed tomographic (CT) evaluation of cats presented with chronic upper respiratory disease. Concurrent disease of the sphenopalatine sinuses may be noted. Retroflex endoscopic evaluation of the choanae and nasopharynx of these cats often reveals mucosal hyperemia and swelling, multifocal lymphoid follicular hyperplasia, and tenacious mucoid discharges.1 Cats with opacities in the caudal nasopharynx, as identified by CT scans, were more likely to have bulla effusion2, emphasizing once again the close anatomic and physiologic relationships between contiguous structures. As noted previously, anecdotally observed differences in the nasopharyngeal microbial flora and nasal flora of cats with chronic upper respiratory disease deserve further evaluation.
Nasopharyngeal polyps most likely originate in the middle ear cavity, and are composed of inflammatory granulation tissue covered with respiratory epithelium. The factors initiating polyp development are not well understood. Polyps may arise as a congenital defect of the first pharyngeal pouch. Conversely, the lesions may be the result of a chronic inflammatory response in the middle ear cavity induced by upper respiratory virus infection.8 With use of polymerase chain reaction (PCR) testing, no evidence of persistence of feline herpesvirus-1 (FHV-1) or feline calicivirus (FCV) was found in polyps from 21 cats, suggesting that chronic viral infection was not the cause of the lesions.9
Polyps arising in the middle ear cavity may extend by a stalk down the Eustachian tube into the nasopharynx, remain in the middle ear cavity, or migrate through the tympanic membrane into the horizontal ear canal. Clinical signs in affected cats include stertorous respiration, occasional sneezing, nasal discharges, dysphagia, weight loss, Horner's syndrome, head tilt, otic discharges, and pawing at the ears. If the polyp is large enough to cause intermittent laryngeal obstruction, respiratory stridor and syncope may occur.
Some controversy continues about the optimal method for the management of nasopharyngeal polyps. Traction and avulsion of the polyp, followed by ipsilateral ventral bulla osteotomy, has been recommended for all patients in order to minimize recurrence, irregardless of whether bulla disease was noted on CT scans.4 Conversely, polyps recurred in 5 of 9 cats with radiographic evidence of bulla disease after traction and avulsion alone, compared to 0 of 5 cats with normal bullae.9 In the latter cases, the polyps might have been arising in the Eustachian tube, rather than the bulla itself, allowing more complete removal of tissue with traction and avulsion.9 Recurrence of polyps after traction alone was reduced significantly when the affected cats were treated post-operatively with corticosteroids.10 Therefore, it might be reasonable to use traction and avulsion followed by corticosteroids as first-line treatment for cats with polyps with no radiographic evidence of bulla disease or neurologic abnormalities. Ventral bulla osteotomy should be recommended for cats with external ear canal polyps, those with radiographic signs of bulla disease and/or neurologic signs, and for patients with recurrence after traction and avulsion.
Atypical manifestations of nasopharyngeal polyps have been reported recently.11 Severe pulmonary arterial hypertension in one patient was considered to result from chronic upper airway obstruction, prompting the recommendation for routine thoracic radiographs in all cats with nasopharyngeal polyps.
The normal caudal nasopharyngeal opening is about 5 mm in diameter.12 On rare occasion, scar tissue forms a membranous web above the soft palate resulting in a pin-hole sized aperture that obstructs airflow through the nasopharynx.3 The lesion usually occurs at the junction between the nasopharynx and laryngopharynx.13 Clinical signs of upper airway obstruction in affected cats may be pronounced when they eat or sleep.14 The cause of the defect is not known. Most affected cats do not have a previous history of upper respiratory infection. Scarring might occur as a result of inflammation from gastric reflux during elective anesthetic procedures in some cats.14 Long-term clinical outcomes from balloon dilation of the strictures was reported to be very good to excellent.14
Cryptococcus species may cause mycotic rhinitis and/or nasopharyngitis. Naturally occurring cryptococcosis occurs firstly as upper respiratory infection.15 Lesions occur most commonly in the rostral nasal cavity. Sneezing, epistaxis, and nasal discharges may be noted initially, followed by the appearance of granulomatous lesions at the external nares and submandibular lymphadenopathy. Infection may penetrate the bones overlying the nasal cavity, leading to swelling of soft tissues over the bridge of the nose.15
Less commonly, the primary lesion may be present in the nasopharynx, causing typical signs of upper airway obstruction. Rostral nasal disease and signs may be absent.15 Clinical signs associated with colonization and infection of the caudal nasal cavity and nasopharynx may result from penetration of the cribriform plate and subsequent cryptococcal meningoencephalitis and optic neuritis. A thorough ocular examination, including fundic evaluation, is an important component of the comprehensive assessment of cats with nasopharyngeal masses.1 Polypoid cryptococcal granulomas can closely resemble nasopharyngeal polyps on gross observation, requiring that all such lesions be submitted for cytologic and histopathologic examination.16
Cats with signs of nasopharyngeal disease resulting from neoplasia tend to be older (average 10.7 years) than cats with polyps or cryptococcosis.4 Lymphosarcoma, adenocarcinoma, and squamous cell carcinoma are reported most commonly.3,4,12 Nasal tumors arise most commonly in the caudal one third of the nasal cavity12, facilitating convenient spread to the nasopharynx. Clinical signs of nasopharyngeal and nasal neoplasia include mucopurulent and hemorrhagic nasal discharges that initially may be temporarily responsive to antimicrobial treatment, progressive stertorous respiration, epiphora with bloody discharges, and exophthalmos and facial distortion. Similar to nasopharyngeal cryptococcosis, neoplasia in this area may cause an observable bulge at the junction of the hard and soft palates--a clinical sign that is often overlooked in the examination of older cats with upper airway obstruction and that is associated with a guarded prognosis.1 Cytological examination of squash preparations of endoscopic biopsies of nasopharyngeal masses had a diagnostic accuracy of 90%, when compared to the gold standard of histopathological examination of the same lesions.17
Other causes of nasopharyngeal disease in cats include foreign bodies (especially grass blades), nasopharyngeal abscess that may result from an extension of otitis media or the presence of a foreign body granuloma5, cystic Rathke's pouch, and tenacious mucus.15 A distorted anatomic shape of the nasopharynx in severely brachycephalic cats may affect normal physiologic function, resulting in stertorous respiration.5
The nasopharynx of cats has close contiguous contact with several surrounding structures of the upper airway. As noted previously, signs of nasopharyngitis are noted commonly on CT scans of cats undergoing comprehensive evaluation of chronic upper respiratory disease. In these cases, it is likely that posterior migration of infective caudal nasal cavity discharges results in microbial contamination of the nasopharynx. Conversely, cranial migration of infection may occur in some cats with polyps, leading to secondary bacterial rhinitis complicated by obstruction of drainage of normal nasal secretions.1
In a recent study, CT evidence of nasopharyngeal abnormalities correlated positively with the presence of bullous effusion.2 Thirteen of 46 cats (28%) with sinonasal disease had evidence of concurrent middle ear disease on CT examination. CT abnormalities in the caudal nasopharynx were most likely to be associated with concurrent middle ear disease. Few of the cats, however, had any history of otitis media. Because of the lack of clinical signs in most of these cats and the lack of thickening of the tympanic bullae, the authors proposed that the effusions probably were acute, rather than the result of ascending infection through the Eustachian tube.
In spite of these observations, owners of cats with chronic upper respiratory disease, especially patients with histories of nasopharyngeal disease, should be questioned about their cat's ability to hear. Cats with bilateral effusive otitis media tend to sleep more and to ignore trigger factors (for example, can openers) that normally attract their attention. It is not clear whether these behavioral changes are due to true deafness or to reclusiveness from underlying otic pain. Occasionally, owners of cats with otitis media report that their cats will assume positions of relief in response to the discomfort, and that they make gagging sounds, associated presumably with the drainage of nasopharyngeal or middle ear secretions into the oropharynx.1
Frontal Sinus Effusion
In a recent study, 65% of cats with chronic upper respiratory disease had CT evidence of soft-tissue opacities in the frontal sinuses.2 Additionally, 62% of cats in this study with bullous effusion had concurrent frontal and sphenoid sinus disease. Changes in surface function may predispose both areas to effusion and ascending infection in cats with chronic upper respiratory disease.
Similar to the difficulties in identifying cats with bullous effusions based on clinical signs (or lack thereof), it is impossible to predict which affected cats have sinus involvement in addition to nasopharyngitis or rhinitis, and whether one or both frontal sinuses are affected. In the author's experience, cats with frontal sinus disease present with histories identical to those cats with rhinitis alone, and show no pathognomonic historical or physical changes.1
Successful management of nasopharyngeal disease in cats depends on the recognition of 1) the wide variety of infectious and non-infectious diseases that can cause upper airway obstruction and stertorous respiration; 2) the close anatomic relationship of the nasopharynx to other airway structures and concurrent disease in those locations; 3) the need for a careful history and physical examination as the foundation for the diagnostic process; 4) a comprehensive diagnostic approach to accurately identify anatomical locations affected, primary disease processes involved, predisposing factors to infection, and secondary microbial complications; 5) the role of surgery in some patients to complement medical therapy; and 6) the changing microbial flora over time that guide choices of antimicrobial treatment in some patients.
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3. Parnell NK. In Ettinger SJ, Feldman E (eds). Textbook of Veterinary Internal Medicine, ed 6, 2005, pp1196-1204.
4. Holt DE. In King LE (ed) Textbook of Respiratory Disease in Dogs and Cats, 2004, Saunders, pp35, 328.
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6. Greene CE, Reinero CN. In Greene CE (ed): Infectious Diseases of the Dog and Cat, ed 3, 2006, Elsevier, p866.
7. Johnson LR, et al. JAVMA 2005;227(4):579.
8. Little CJL. In August JR (ed) Consultations in Feline Internal Medicine, vol 3, WB Saunders, pp310-315.
9. Veir JK, et al. J Fel Med Surg 2002;4:195.
10. Anderson DM, et al. Vet Rec 2000;147:2000.
11. MacPhail CM, et al. J Fel Med Surg 2007;9:219.
12. Rand J, Mason R. In Rand J (ed) Problem-Based Feline Medicine, 2006, Elsevier, pp 32-46.
13. Griffon DJ. Compend Contin Educ Pract Vet 2000;22(10):897.
14. Glaus T, et al. Vet Rec 2005;157(9):257.
15. Malik R, et al. Austr Vet J 1997;75:483.
16. Hunt GB, et al. Compend Contin Educ Pract Vet 2002;24(3):184.
17. De Lorenzi D. J Fel Med Surg 2007, in press.