Chronic inflammatory rhinitis represents a significant cause of chronic nasal disease in the dog and is characterised by lymphocytic-plasmacytic infiltration of the nasal mucosa in the absence of an obvious underlying aetiology. Importantly, therefore, chronic idiopathic lymphocytic-plasmacytic rhinitis (LPR) can only be diagnosed following exclusion of known causes of chronic nasal disease and discharge such as nasal neoplasia and sinonasal aspergillosis (SNA).

The aetiopathogenesis of LPR is poorly understood, although infectious, allergic and immune-mediated mechanisms have all been proposed. The suggestion that infectious agents may be involved stems in part from the clinical observation that some cases of LPR appear to respond, albeit transiently, to antimicrobial therapy. A recent investigation of microbial involvement in LPR failed, however, to demonstrate differences in the bacterial load of nasal tissues from dogs with LPR, fungal rhinitis and nasal neoplasia using molecular detection methods, and also failed to detect DNA or RNA for Chlamydophila, Bartonella, Mycoplasma, canine adenovirus 2 (CAV-2) or parainfluenza 3 (PI-3). It is unclear whether these findings were influenced by the methodology of the study. It has also been postulated that LPR represents undiagnosed SNA, particularly as Aspergillus infection may be restricted to the frontal sinuses in some cases. Although higher levels of fungal DNA have been demonstrated in nasal tissue from dogs with LPR compared to dogs with nasal neoplasia and healthy controls, cytokine and chemokine expression profiles in SNA and LPR differ, implying two very distinct disease entities.

The most common clinical sign of LPR is nasal discharge and, although in the majority of cases inflammation is bilateral, up to 40% of cases present with unilateral discharge. Nasal discharge is typically mucoid or mucopurulent; haemorrhagic/blood-tinged and serous discharge is also observed less commonly. Other clinical signs include sneezing, epistaxis, reverse sneezing, stertor and ocular discharge. Although these signs are typical of chronic nasal disease they are not specific for LPR.

As, by definition, LPR is a diagnosis of exclusion, investigation should be designed to rule out known causes of chronic nasal disease. Investigation should therefore include imaging of the nasal cavities and frontal sinuses, direct visualisation of the nasal mucosa by endoscopy, and biopsy of the nasal mucosa.

Although traditionally radiography has been used to aid differentiation of LPR from other chronic nasal diseases such as nasal neoplasia and fungal rhinitis, computed tomography (CT) represents the imaging modality of choice due to superior sensitivity and specificity. A variety of tomographic abnormalities have been described including fluid accumulation, soft tissue opacification, turbinate destruction and gas pocketing; in the majority of cases lesions are diffuse. Sinus involvement has also been reported in over 40% of cases, and bilateral changes are most commonly observed even in dogs presenting with unilateral nasal discharge. It should be noted that CT may be normal in some cases of LPR.

Rhinoscopy (anterograde) often reveals a combination of the following abnormalities: presence of mucoid or mucopurulent nasal discharge; erythema/hyperaemia/oedema of the mucosa; turbinate atrophy, loss and/or destruction; presence of haemorrhage. Retroflexed rhinoscopy is typically unremarkable.

Direct visualisation of mucosal pathology allows targeted biopsies to be performed. In addition to submission of nasal mucosal tissue for histopathology, nasal biopsy specimens and/or brushings of the nasal mucosa should be submitted for bacterial and fungal culture, particularly to rule out significant fungal infections (i.e., SNA). However, in view of our poor understanding of the contribution that these organisms make to the pathogenesis of LPR, positive cultures should be interpreted with caution, and in the light of histopathological findings.

LPR is a particularly frustrating condition to treat and no effective treatment protocols have been established; controlled clinical trials are lacking. Transient improvements in the character and quantity of nasal discharge may be observed with antibiotic therapy, although this is likely to reflect resolution of secondary bacterial infection, and recurrence is often observed. Oral glucocorticoids appear not to be effective in the treatment of LPR. Anecdotally, local therapy, e.g., with fluticasone, may be more efficacious although further evaluation is required. Alternatively some authors recommend the combination of antibiotics (in particular doxycycline or azithromycin) and non-steroidal antiinflammatory drugs such as piroxicam, but again demonstration of clinical efficacy is lacking.

References

1.  Lefebvre J, Kuehn NF, Wortinger A. Computed tomography as an aid in the diagnosis of chronic nasal disease in dogs. Journal of Small Animal Practice 2005; 46(6): 280-285.

2.  Peeters D, Peters IR, et al. Distinct tissue cytokine and chemokine mRNA expression in canine sino-nasal aspergillosis and idiopathic lymphoplasmacytic rhinitis. Veterinary Immunology and Immunopathology 2007; 117(1-2): 95-105.

3.  Tasker S, Knottenbelt CM, et al. Aetiology and diagnosis of persistent nasal disease in the dog: a retrospective study of 42 cases. Journal of Small Animal Practice 1999; 40(10): 473-478.

4.  Windsor RC, Johnson LR, et al. Idiopathic lymphoplasmacytic rhinitis in dogs: 37 cases (1997-2002). Journal of the American Veterinary Medical Association 2004; 224(12): 1952-1957.

5.  Windsor RC, Johnson LR, et al. Molecular detection of microbes in nasal tissue of dogs with idiopathic lymphoplasmacytic rhinitis. Journal of Veterinary Internal Medicine 2006; 20(2): 250-256.