Lymphoplasmacytic
rhinitis (LPR) is a common histologic finding in dogs with chronic
nasal disease; however, potential etiologies of this disorder have not been examined. We investigated the hypothesis that specific microbes contribute to clinical disease in dogs with LPR.
Paraffin-embedded nasal biopsies were obtained from 19 dogs with LPR, 10 dogs with nasal
neoplasia, and 10 dogs with nasal
aspergillosis.
Nucleic acids were extracted from
paraffin blocks, and real-time quantitative polymerase chain reaction (PCR) was employed for detection of target genes for bacterial and
fungal DNA, canine adenovirus 2 (CAV-2),
parainfluenza virus 3 (PI-3), Chlamydial Chlamydophila spp., and Bartonella spp. Conventional PCR was used for detection of Mycoplasma spp. Statistical analysis was performed using the Mann-Whitney U-test for nonparametric data, and significance was set at P < 0.05.
DNA or
RNA for CAV-2, PI-3, Bartonella, Mycoplasma, and Chlamydophila was not detected in any nasal biopsy.
DNA loads for
bacterial DNA did not differ among disease groups. Detection of
fungal DNA in nasal biopsies was highest in dogs with
aspergillosis (P < 0.0001); however, nasal biopsies of LPR dogs also displayed higher
fungal DNA levels than samples from dogs with nasal
neoplasia (P = 0.016). Detection of high levels of
fungal DNA in nasal biopsies of dogs with LPR suggests that fungal organisms may be causally associated with the
inflammation observed, although the possibility of entrapment or accumulation of fungi in the nasal cavity due to chronic
inflammation cannot be excluded. Further investigations are required to elucidate the underlying etiopathogenesis of LPR.