Canine Chronic Inflammatory Rhinitis

Canine Chronic Inflammatory Rhinitis
Rebecca C. Windsor, DVM*, and Lynelle R. Johnson, DVM, PhD, DACVIM †
Chronic inflammatory rhinitis is commonly found in dogs with chronic nasal disease and is
characterized by lymphoplasmacytic infiltrates in the nasal mucosa in the absence of an
obvious etiologic process. The pathogenesis of lymphoplasmacytic rhinitis remains unknown.
Animals respond poorly to antibiotics, oral glucocorticoids, and antihistamines,
making primary infectious, immune-mediated, or allergic etiologies unlikely. Aberrant immune
response to inhaled organisms or allergens may induce inflammation in some
animals. Common clinical signs include nasal discharge, sneezing, coughing, epistaxis,
and stertor. Diagnosis is made by performing a thorough history, physical examination,
radiography or advanced imaging (via computed tomography or magnetic resonance imaging),
rhinoscopy, and nasal mucosal biopsy to rule out primary etiologies of nasal
discharge. Treatment strategies have included various antibiotics, antihistamines, oral and
inhalant steroids, nonsteroidal antiinflammatories, and antifungal medications. Some dogs
may respond partially to doxycycline or azithromycin, although it is unclear whether
response is related to antimicrobial or antiinflammatory properties of these drugs. Hydration
of the nasal cavity through nasal drops or aerosols may limit nasal discharge, and some
animals may improve with inhalant (but rarely oral) glucocorticoids.
Clin Tech Small Anim Pract 21:76-81 © 2006 Elsevier Inc. All rights reserved.
Keywords rhinitis, nasal, canine, inflammatory, lymphoplasmacytic
The most common causes of chronic nasal discharge in
dogs include nasal neoplasia, fungal rhinitis, and lymphoplasmacytic
rhinitis (LPR), also referred to as inflammatory
rhinitis. Other causes of chronic nasal disease include
nasal foreign body, rhinitis secondary to dental disease, parasitic
rhinitis (Pneumonyssoides caninum), and primary ciliary
dyskinesia. Idiopathic LPR is recognized with increasing frequency
in the canine population and may be more common
in certain geographic locations. Diagnosis is made via histopathologic
identification of a lymphoplasmacytic infiltrate
in the nasal mucosa with exclusion of specific causes of
chronic inflammation. An effective therapeutic regimen for
dogs with LPR has not been established, largely because the
underlying pathogenesis is still unknown.
Etiology
The etiology of LPR has not been determined, although infectious,
allergic, and immune-mediated mechanisms have
*Department of Clinical Sciences at North Carolina State University, Raleigh,
NC.
†Diplomate of the American College of Veterinary Internal Medicine, Department
of Medicine and Epidemiology at the University of California,
Davis, CA.
Supported in part by the Bailey Wrigley Fund and the American Kennel Club
Grant 0389, and the Joseph and Mable Howe Research Scholarship.
Address reprint requests to: Department of Clinical Sciences, North Carolina
State University, 4700 Hillsborough Street, Raleigh, NC 27606.E-mail:
rebecca_windsor@ncsu.edu.
76 1096-2867/06/$-see front matter © 2006 Elsevier Inc. All rights reserved.
doi:10.1053/j.ctsap.2005.12.014
been suggested. LPR may have a multifactorial etiology in
some dogs and/or different etiologies in different dogs, making
it difficult to develop general treatment guidelines.
Primary Infection
Primary bacterial infection of the nasal cavity is rare, and no
single infectious organism has been identified in dogs with
LPR. However some dogs respond anecdotally to certain antibiotics
including doxycycline and azithromycin, leading to
the speculation that certain bacterial organisms such as
Chlamydophila, Mycoplasma, orBartonella could be involved
in the pathogenesis of LPR. Chlamydophila is a primary upper
respiratory pathogen in humans, cats, and other species. Bartonella
has been associated with nasal discharge, 1 granulomatous
rhinitis, 2 and epistaxis2,3 in dogs. A recent study investigating
the role of infectious organisms in LPR quantified
DNA loads of Chlamydophila, Bartonella, Canine-adenovirus
2 (CAV-2), and Parainfluenza virus 3 (PI-3) in biopsy samples
from dogs with LPR by the use of quantitative PCR, and
a role for these organisms could not be established. 4 In addition,
endpoint PCR was used to examine nasal biopsy samples
for evidence of Mycoplasma spp. and this also failed to
identify a specific pathogen in DNA extracted from formalinfixed
nasal biopsy samples. 4 The poor long-term response to
multiple antibiotics in dogs with LPR suggests that a primary
bacterial infectious etiology is unlikely, although ongoing
studies investigating serologic evidence of Bartonella in dogs

Canine chronic inflammatory rhinitis 77
with LPR may provide valuable information on the role of this
organism in the syndrome.
Table 1 Common Clinical Signs in 37 Dogs with Idiopathic
Rhinitis 5
Secondary Infection
Secondary bacterial infection is common in dogs with
chronic nasal disease, which may explain the transient response
to antibiotics seen in some dogs with LPR. Nasal
cultures from dogs with LPR yield mixed bacterial growth of
normal nasal flora including Staphylococcus, Streptococcus,
Escherichia coli, Proteus, Pasteurella, Corynebacterium, Bordetella,
and Pseudomonas. 5-7 A recent study demonstrated no
significant difference in bacterial DNA loads among dogs
with LPR, fungal rhinitis, and nasal neoplasia; however, all
three disease groups had significantly higher bacterial loads
than did healthy control dogs. 4 Accumulation of bacterial
organisms in dogs with chronic nasal disease could result
from mucus trapping and decreased nasal mucosal defense
mechanisms.
Role of Fungal Organisms
Aspergillus and Penicillium spp. are common inhabitants of
the canine nasal cavity, 6 and a positive fungal culture can be
found in the absence of primary fungal rhinitis. Candida,
Trichosporum, and Cladosporidium have also been cultured
from dogs with LPR. 5 In the study assessing molecular con -
tent of paraffin-embedded nasal tissue from dogs, higher fungal
DNA loads were reported in dogs with LPR than in
healthy control dogs and dogs with nasal neoplasia. 4 Mucus
trapping and decreased nasal defense mechanisms alone cannot
explain this difference because dogs with nasal neoplasia
would be expected to have similar mucosal compromise to
dogs with LPR. Further research is required to determine the
significance of increased fungal DNA in dogs with LPR. Fungal
hypersensitivity characterized by an aberrant immune
response has been identified in human chronic rhinosinusitis
(CRS) patients. 8-14 Humans with CRS exhibit a humoral and
cellular (Th1 and Th2) response to airborne fungi. 8 T-cell
sensitization to fungus leads to production of T-helper 2
cytokine release, namely Interleukin-5. 11 Fungal hypersensitivity
in humans appears to be characterized by IgG3 rather
than IgE production, suggesting that the hypersensitivity is
not a true allergic response, 8,12 although humans with CRS
do exhibit a predominantly eosinophilic infiltration. 13 In humans,
the quantity of fungal DNA does not correlate with
disease severity. 15 Further research is needed to assess the
immune response of affected dogs to resident fungal organisms.
Allergy
There is some speculation that respiratory allergy may manifest
with signs of chronic rhinitis as is seen in humans, although
evidence of allergic rhinitis as a recognized disease
entity in dogs has yet to be established. It is possible that dogs
with LPR exhibit a heightened immune response to inhaled
environmental allergens; however, no published studies to
date have demonstrated an allergic inflammatory pattern in
dogs with naturally occurring LPR. Experimentally, nasal
congestion has been induced using ragweed pollen in Beagle
colonies, 16-18 Th2 immune response was identified in the peripheral blood
mononuclear cells of three dogs with rhinitis. 19 Nasal mucosal
biopsies were not collected from dogs in these studies so it
is not known whether lymphoplasmacytic infiltration characterized
the disease. Dogs with LPR generally respond
poorly to antihistamines and glucocorticoids, making an allergic
etiology unlikely.
Immune-Mediated
The initial report describing LPR suggested that the disease
was likely immune-mediated because three of five dogs in
that study demonstrated a favorable response to glucocorticoids.
and evidence of allergic response to house dustmite
antigen characterized by increased IL-4 expression and
20 Historically, in our experience, most dogs with LPR
have exhibited a poor response to oral glucocorticoid treatment,
suggesting that a primary immune-mediated etiology
is unlikely. Cats with nasal inflammation exhibit a heightened
Th1 immune response that is more pronounced as inflammation
becomes more severe 21 Mucopurulent, mucoid, or serous
35/37 (95%)
nasal discharge
Sneezing
Coughing
Epistaxis
Reverse sneezing
Stertor
Ocular discharge
Pawing at the muzzle
19/37 (51%)
15/37 (41%)
15/37 (41%)
6/37 (16%)
5/37 (14%)
4/37 (11%)
2/37 (5%)
; however, information is
not available in dogs. Further studies evaluating the immunoregulatory
patterns in the nasal mucosa of dogs with LPR
are required to determine the role of immune dysregulation
in disease.
History
Important historical features in dogs with chronic rhinitis
include duration and progression of clinical signs, character
and laterality of nasal discharge, and response to previous
medical therapies. LPR can be seen in any breed but occurs
most commonly in large-breed dogs. There is no apparent
age or sex predilection. Duration of clinical signs may range
from weeks to years at the time of diagnostic evaluation. The
most common clinical signs include nasal discharge, sneezing,
coughing (likely secondary to pharyngitis caused by
swallowing irritant nasal secretions), and episodes of epistaxis
(Table 1). Although signs related to LPR are often bilateral,
many dogs with LPR have unilateral or lateralizing
signs on presentation. Laterality of clinical signs based on
history and physical examination correlates poorly with computed
tomography, rhinoscopy, and biopsy findings. 5 Therefore,
while unilateral nasal discharge is classically considered
more typical of nasal neoplasia, fungal rhinitis, foreign body
rhinitis, or an oronasal fistula, LPR remains a consideration,
and all dogs with unilateral nasal discharge historically or on
physical examination should be evaluated for bilateral nasal
disease. Other clinical signs of LPR may include reverse
sneezing, stertor, ocular discharge, and pawing/rubbing at
the muzzle.

78 R.C. Windsor and L.R. Johnson
Dogs with LPR typically have a history of poor or transient
response to medical treatment. Many animals demonstrate
little improvement with antibiotics, antihistamines, and glucocorticoids
alone or in combination, while some demonstrate
a transient response with return of clinical signs when
medications are discontinued.
Physical Examination
The most common physical examination findings in dogs
with LPR include fresh or dry nasal discharge or crusting
around the nares. Most animals have mucoid or mucopurulent
discharge, but hemorrhagic or serous discharge may be
seen. Nasal airflow should be assessed using a microscope
slide or cotton ball wisp. When assessing the patency of airflow,
each nostril should be manually occluded to watch for
a stress response, indicating occluded nasal airflow in the
contralateral nostril. Nasal airflow is normally preserved in
dogs with LPR, since obstruction would be more typical of a
mass lesion.
Facial palpation is often unremarkable in patients with
LPR, which may be helpful in differentiating it from fungal
rhinitis and nasal neoplasia, where facial pain is more common.
Dogs with nasal neoplasia may also exhibit facial or
skull deformity, which is not seen in dogs with LPR. Ocular
retropulsion should be performed to detect retrobulbar
masses or abscesses as a cause for nasal discharge. Nasal
planar depigmentation may rarely be noted in dogs with
severe and long-standing discharge associated with LPR but
is more commonly exhibited in dogs with fungal rhinitis or
immune-mediated dermatologic diseases such as discoid lupus
erythematosus. Assessment of regional lymph nodes is
important in animals with nasal discharge due to the tendency
for neoplastic processes to metastasize locally. Lymph
nodes are often enlarged in dogs with LPR or fungal rhinitis,
but aspiration cytology reveals a reactive inflammatory process
rather than neoplasia.
Diagnostic Evaluation
Laboratory Evaluation
Complete blood count, chemistry panel, and urinalysis are often
unremarkable in patients with chronic rhinitis. Dogs with epistaxis
should be evaluated for clotting abnormalities by performing
a platelet count OSPT, APTT, and BMBT to rule out coagulopathies,
thrombocytopenias, and/or thrombocytopathias.
Dogs presenting primarily for epistaxis should also have blood
pressure measured for detection of systemic hypertension.
Imaging Techniques
Radiography has been used in some cases to help differentiate
LPR from nasal neoplasia but has become less popular due to
the availability of superior imaging techniques. Some dogs
with LPR have radiographic evidence of lucent foci and multifocal
lesions, which are not typically seen in dogs with nasal
neoplasia. 22 Neoplastic lesions are more likely to invade - sur
rounding bone22 ; however, neoplastic lesions without obvi -
ous osteolysis may be difficult to differentiate from chronic
rhinitis cases as both diseases cause soft-tissue opacification.
Although one study identified the absence of frontal sinus
Figure 1 Computed tomographic images through the rostral nasal
cavity of two dogs with idiopathic LPR. In the panel on the left,
soft-tissue or fluid opacity is noted between nasal turbinates and is
worse on the right than on the left. In the panel on the right, more
extensive soft-tissue or fluid opacity is noted bilaterally.
involvement on radiographs as a positive predictive indicator
for LPR compared with neoplasia, 22 a recent study showed
that a high percentage of dogs with LPR have frontal sinus
fluid accumulation. 5 LPR is difficult to differentiate from -fun
gal rhinitis via radiography as both can cause turbinate destruction
and frontal sinus accumulation.
Recent studies have demonstrated that computed tomography
(CT) is more sensitive and specific than radiography in
differentiating LPR, nasal neoplasia, and fungal rhinitis. 23-25
The most common CT findings in dogs with LPR include
fluid accumulation within the nasal passages, soft-tissue
opacification, turbinate destruction, frontal sinus accumulation,
and gas pocketing 5 (Figs. 1 and and 2 Table 2) Imaging
abnormalities noted on CT are often diffusely distributed
throughout the nasal cavity, but rostral or caudal localization
may be observed. Turbinate destruction tends to be less severe
in dogs with LPR compared with dogs with nasal neoplasia
or fungal rhinitis. 23 Dogs with nasal neoplasia com -
monly exhibit a soft-tissue density with extensive turbinate
destruction, while those with fungal rhinitis exhibit extensive
turbinate destruction and hyperlucency of the nasal passages. 23
Magnetic resonance imaging (MRI) is another excellent
imaging modality for the nasal cavity, providing superior
soft-tissue detail compared with CT. However no studies to
date have compared the sensitivity and specificity of CT and
MRI for differentiating causes of chronic nasal disease, and
CT is currently the most popular imaging technique due to its
lower cost compared with MRI.
Rhinoscopy
Rhinoscopic evaluation of patients with chronic nasal disease
is essential. For complete assessment of the nasal mucosa and
turbinates, a rigid or flexible endoscope is required. The most
common rhinoscopic features in dogs with inflammatory rhinitis
include mucoid or mucopurulent discharge, hyperemic,
edematous, and/or friable nasal mucosa, and mild turbinate
atrophy or destruction 5 (Fig. 3 and Table 3). Indistinct softtissue
opacities noted on CT can be visualized rhinoscopically,
allowing differentiation among nasal masses, nasal polyps,
and mucus plugs. Fungal plaques or nasal mites may
also be observed rhinoscopically, thus providing a primary
etiology for nasal discharge. Representative biopsy specimens
are best obtained by rhinoscopic identification of areas of

Canine chronic inflammatory rhinitis 79
Figure 2 Sequential computed tomographic images through the
frontal sinus of a dog with idiopathic LPR. The top panel shows
soft-tissue or fluid opacification in the left frontal sinus. In the next
7-mm slice, the frontal sinus has filled more completely and an
air–fluid meniscus is present, suggesting that fluid is filling the
frontal sinus.
significant nasal mucosal pathology and visualization of the
area sampled for histopathology.
Other diagnostic techniques to perform after rhinoscopy
are examination of the nasopharyngeal region using a
dental mirror or retroflexed endoscope to look for nasopharyngeal
polyps and dental probing to rule out oronasal
fistula or dental disease as a cause for unilateral nasal
discharge.
Histopathology
Nasal biopsy samples of dogs with chronic, idiopathic, inflammatory
rhinitis are characterized by a primarily lymphoplasmacytic
infiltrate, but concurrent neutrophilic or less
commonly eosinophilic infiltrate may also be seen. Epithelial
Table 2 Computed Tomography in 33 Dogs with Idiopathic
Rhinitis 5
Normal 4/33 (12%)
Unilateral lesions 8/33 (24%)
Bilateral lesions 21/33 (64%)
Fluid accumulation 27/33 (82%)
Soft-tissue opacification 25/33 (78%)
Plaque-like lesions 24/33 (73%)
Turbinate destruction 23/33 (70%)
Gas pocketing 23/33 (70%)
Frontal sinus opacification 14/33 (42%)
Figure 3 Rhinoscopic image of a dog with idiopathic LPR. Marked
hyperemia and mucus accumulation are evident. (Color version of
figure is available online.)
changes are usually mild but may include epithelial hyperplasia
and erosion. Turbinate remodeling or destruction can
also be evident. The majority of dogs with unilateral clinical
signs have bilateral nasal mucosal pathology, and severity of
inflammation between the two sides of the nasal cavity often
varies.
Culture and Cytology
Obtaining a positive culture of bacterial and/or fungal organisms
in dogs with inflammatory rhinitis is not uncommon
and likely reflects normal nasal mucosal flora or secondary
infection rather than primary infectious rhinitis. Culture results
from the rostral nasal cavity may differ from the caudal
nasal cavity. 26 Similarly, brush or lavage samples from super -
ficial epithelium may not adequately reflect bacterial and fungal
infiltration into the nasal mucosa. When culture is desired,
collection of a deep nasal lavage using a protected
catheter brush or submission of a nasal biopsy sample for
culture should be considered.
Nasal mucosal cytology may be used to identify fungal or
neoplastic lesions in some cases; however, cytology has poor
sensitivity and specificity compared with histology in nasal
mucosal samples27-29 and is often unreliable for detecting
chronic changes. 29
Table 3 Rhinoscopic Findings in 37 Dogs with Idiopathic Rhinitis
5
Normal 1/37 (3%)
Unilateral lesions 7/37 (19%)
Bilateral lesions 21/37 (57%)
Mucoid or mucopurulent discharge 29/37 (78%)
Hyperemic, or inflamed mucosa 26/37 (70%)
Mucosal edema 8/37 (22%)
Turbinate atrophy, destruction, or loss 8/37 (22%)
Hemorrhage or blood clots 5/37 (14%)
Mucosal friability 4/37 (11%)

80 R.C. Windsor and L.R. Johnson
Treatment
No effective treatment regimen for LPR has been established;
therefore, animals are commonly treated with a variety of
medications including antibiotics, antiinflammatory drugs
(glucocorticoids: oral or topical, or nonsteroidal antiinflammatory
drugs), antihistamines, and antifungal medications.
Antibiotics
Dogs with mucopurulent nasal discharge likely have some
degree of secondary bacterial contamination. Antibiotic treatment
in these animals may help to reduce the severity of the
nasal discharge and alter the character of discharge from
mucopurulent to serous, but complete sustained resolution
of nasal discharge is rarely achieved. Most nasal bacterial
infections are susceptible to multiple antibiotics. Some dogs
respond well to doxycycline (3 to 5 mg/kg PO twice per day),
which may be attributed partially to its antiinflammatory
effects. Macrolides such as azithromycin (5 mg/kg daily for 5
days, then twice weekly) have also been effective in some
dogs.
Although the long-term response to antibiotics has not
been reported, it is unlikely that such treatment results in
cure of disease. Extended courses of suppressive antibiotic
therapy or intermittent treatment with such drugs may be
required for control of signs. If the severity of the nasal discharge
worsens when antibiotics are discontinued, it is advisable
to reinstitute therapy with the same antibiotic to avoid
development of antibiotic resistance by use of multiple antibiotics.
Anti-Inflammatory Agents
Oral glucocorticoids have not proven effective in treating
most dogs with LPR; therefore, long-term use of oral steroids
should be avoided because of systemic side effects. Topical
nasal steroid drops may be applied if the dog will tolerate
administration. Topical glucocorticoid sprays such as fluticasone
propionate have been used with variable success in human
chronic rhinosinusitis patients 30-32 and have shown an -
ecdotal promise in some dogs and cats with chronic nasal
discharge. Although typically used to treat lower airway disease,
metered dose inhalers (MDIs) containing fluticasone
may also benefit animals with rhinitis as the drug must first
pass through the nasal passages before reaching the lower
respiratory tract. Aerosolized steroids can be administered
using MDIs attached to a spacer and tightly fitting facemask.
The MDI must be well-shaken before actuation into the
spacer, and the animal must take 8 to 10 breaths without
panting to carry the drug into the respiratory tract. A commercially
available spacer with facemask designed for cats
(Aerokat) works well in brachycephalic dogs. For larger,
dolicocephalic dogs, human pediatric spacers must be obtained,
and appropriate face masks must be acquired from a
local pharmacy or anesthetic supply company.
Nonsteroidal antiinflammatory drugs may be somewhat
efficacious in reducing nasal inflammation in certain cases.
These drugs are also sometimes used in feline nonspecific
rhinitis, when it is unclear whether an infectious etiology
might be present. The most commonly used drug is likely
piroxicam. Like all nonsteroidal agents, this drug can be as-
sociated with gastrointestinal effects associated with GI ulceration
and with renal dysfunction. When used at 0.3 mg/kg
PO daily in healthy animals, it is unlikely to have untoward
side effects, although owners should be instructed to watch
for anorexia, vomiting, or abdominal pain.
Antihistamines
Antihistamines are occasionally used in LPR dogs, although
response is typically poor, and the sedative effects of some
antihistamines may outweigh any therapeutic benefit. Also,
antihistamines may have the undesirable side effect of drying
nasal secretions and worsening mucus accumulation. However,
if sneezing and nasal discharge worsen seasonally and
an inhaled environmental allergen is suspected, an antihistamine
trial may be employed.
Antifungal Therapy
A few dogs with LPR have been treated empirically with
topical antifungal medications (clotrimazole, enilconazole)
to treat a possible undiagnosed fungal rhinitis; however, improvement
in clinical signs was not noted. 5 Response to oral
antifungals has not been reported. Variable results have been
reported in human chronic rhinusinusitis patients with suspected
fungal hypersensitivity. Nasal amphotericin B resulted
in deterioration of symptoms in one study, 33 while
proving safe and effective in another. 34
Other Therapies
Some dogs with LPR may present with signs of reverse sneezing.
Reverse sneezing occurs in response to irritation of the
nasal mucosa, which may be caused by inhaled irritants or
occasionally by the nasal mite, P. caninum. Dogs that exhibit
reverse sneezing should be treated empirically with ivermectin
(or milbemycin in Collie breeds) to rule out parasitic
infestation as a cause of rhinitis before pursuing aggressive
diagnostics.
Increasing nasal hydration through the use of topical saline
drops or with saline inhalation or nebulization can aid in
evacuation of the nasal cavity. Dogs are variably tolerant of
having saline nasal drops administered to the nasal cavity,
but this is the least expensive alternative for liquefying nasal
secretions and encouraging removal from the nasal cavity.
Conclusion
Inflammatory rhinitis is commonly found in dogs with
chronic nasal disease. The etiology of this disorder remains
unknown and may involve different pathogenic mechanisms
in different dogs with chronic nasal disease. Some dogs may
exhibit an aberrant immune response to commensal fungal
organisms or other inhaled pathogens or irritants. The diagnosis
of LPR requires a thorough history and physical examination,
advanced imaging (CT or MRI), rhinoscopic evaluation,
and biopsy. Culture and cytology may occasionally
prove useful in differentiating LPR from other causes of rhinitis
(ie, fungal rhinitis and neoplasia). The poor response to
treatment with antibiotics, glucocorticoids, and antihistamines
makes LPR a frustrating condition to treat. Current
recommendations to be considered include the use of doxycycline
or azithromycin for their antiinflammatory as well as

Canine chronic inflammatory rhinitis 81
antibacterial effects, and trial therapy with piroxicam. Owners
should be advised that antibiotics only treat secondary
bacterial infections and nasal discharge will likely return
once antibiotics are discontinued. Use of multiple antibiotics
should be avoided. Oral corticosteroids have shown little
therapeutic benefit and should be avoided due to unwanted
systemic effects. However, inhalant corticosteroids may be
effective in some patients. Further research is required to
identify the pathogenesis of LPR with the aim of developing
an effective treatment regimen.
References
1. Henn JB, Liu CH, Kasten RW, et al: Seroprevalence of antibodies
against Bartonella species and evaluation of risk factors and clinical
signs associated with seropositivity in dogs. Am J Vet Res 66(4):688-
694, 2005
2. Pappalardo BL, Brown T, Gookin JL, et al: Granulomatous disease
associated with Bartonella infection in 2 dogs. J Vet Intern Med 14(1):
37-42, 2000
3. Breitschwerdt EB, Hegarty BC, Maggi R, et al: Bartonella species as a
potential cause of epistaxis in dogs. J Clin Microbiol 43(5):2529-2533,
2005
4. Windsor RC, Johnson LR, Sykes JE, et al: Molecular detection of microbes
in nasal biopsies of dogs with idiopathic lymphoplasmacytic
rhinitis. J Vet Int Med (in press)
5. Windsor RC, Johnson LR, Herrgesell EJ, et al: Idiopathic lymphoplasmacytic
rhinitis in 37 dogs: 1997-2002. J Am Vet Med Assoc 224(12):
1952-1957, 2004
6. Norris AM, Laing EJ: Diseases of the nose and sinuses. Vet Clin North
Am (Small Anim Pract) 15:865, 1985
7. Greene CE: Bacterial infections of the upper respiratory system. In
Greene CE (ed): Infectious Diseases of the Dog and Cat. Philadelphia,
PA, WB Saunders, 1998, pp 583-584
8. Shin SH, Ponikau JU, Sherris DA, et al: Chronic rhinosinusitis: an
enhanced immune response to ubiquitous airborne fungi. J Allergy Clin
Immunol 114(6):1369-1375, 2004
9. Gosepath J, Brieger J, Vlachtsis K, et al: Fungal DNA is present in tissue
specimens of patients with chronic rhinosinusitis. Am J Rhinol 18(1):
9-13, 2004
10. Gosepath J, Mann WJ: Role of fungus in eosinophilic sinusitis. Curr
Opin Otolaryngol Head Neck Surg 13(1):9-13, 2005
11. Hamilos DL, Lunf VJ: Etiology of chronic rhinosinusitis: the role of
fungus. Ann Otol Rhinol Laryngol Suppl 193:27-31, 2004
12. Pant H, Kette FE, Smith WB, et al: Fungal-specific humoral response in
eosinophilic mucus chronic rhinosinusitis. Laryngoscope 115(4):601-
606, 2005
13. Sasama J, Sherris DA, Shin SH, et al: New paradigm for the roles of fungi
and eosinophils in chronic rhinosinusitis. Curr Opin Otolaryngol Head
Neck Surg 13(1):2-8, 2005
14. Polzehl D, Weschta M, Podbielski A, et al: Fungus culture and PCR in
nasal lavage samples of patients with chronic rhinosinusitis. J Med
Microbiol 54:31-37, 2005
15. Schueller MC, Murr AH, Goldberg AN, et al: Quantitative analysis of
fungal DNA in chronic rhinosinusitis. Laryngoscope 114(3):467-471,
2004
16. Rudolph K, Bice DE, Hey JA, et al: A model of allergic nasal congestion
in dogs sensitized to ragweed. Am J Rhinol 17(4):227-232, 2003
17. Cardell LO, Agusti C, Nadel JA: Nasal secretion in ragweed-sensitized
dogs: effect of leukotriene synthesis inhibition. Acta Otolaryngol
120(6):757-760, 2000
18. Tiniakov RL, Tiniakova OP, McLeod RL, et al: Canine model of nasal
congestion and allergic rhinitis. J Appl Physiol 94(5):1921-1928, 2003
19. Kurata K, Maeda S, Yasunaga S, et al: Immunological findings in 3 dogs
clinically diagnosed with allergic rhinitis. J Vet Med Sci 66(1):25-29,
2004
20. Burgener DC, Slocombe RF, Zerbe CA: Lymphoplasmacytic rhinitis in
five dogs. J Am Hosp Assoc 23:565-568, 1987
21. Johnson LR, DeCock HE, Sykes HE, et al: Cytokine gene transcription
in feline nasal tissue with histologic evidence of inflammation. Am J Vet
Res 66(6):996-1001, 2005
22. Russo M, Lamb CR, Jakovljevic S: Distinguishing rhinitis and nasal
neoplasia by radiography. Vet Radiol Ultrasound 41(2):118-124, 2000
23. Lefebvre J, Kuehn NF, Wortinger A: Computed tomography as an aid
in the diagnosis of chronic nasal disease in dogs. J Small Anim Pract
46(6):280-285, 2005
24. Saunders JH, van Bree H, Gielen I, et al: Diagnostic value of computed
tomography in dogs with chronic nasal disease. Vet Radiol Ultrasound
44(4):409-413, 2003
25. Codner EC, Lurus AG, Miller JB, et al: Comparison of CT with radiography
as a noninvasive diagnostic technique for chronic nasal disease in
dogs. J Am Vet Med Assoc 202(7):1106-1110, 1993
26. Abramson AL, Isenberg HD, McDermott LM: Microbiology of the canine
nasal cavities. Rhinology 18:143, 1980
27. Cohen M, Bohling MW, Wright JC, et al: Evaluation of sensitivity and
specificity of cytologic examination: 269 cases (1999-2000). J Am Vet
Med Assoc 222(7):964-967, 2003
28. Lin R, Nahal A, Lee M, et al: Cytologic distinctions between clinical
groups using curette-probe compared to cytology brush. Ann Allergy
Asthma Immunol 86:226-231, 2001
29. Michiels L, Day MJ, Snaps F, et al: A retrospective study of non-specific
rhinitis in 22 cats and the value of nasal cytology and histopathology. J
Fel Med Surg 5:279-285, 2003
30. Parikh A, Scadding GK, Darby Y, et al: Topical corticosteroids in
chronic rhinosinusitis: a randomized double-blind, placebo-controlled
trial using fluticasone proprionate aqueous nasal spray. Rhinology
39(2):75-79, 2001
31. Dolor RJ, Witsell DL, Hellkamp AS, et al: Comparison of cefuroxime
with or without intranasal fluticasone for the treatment of rhinosinusitis.
The CAFFS Trial: a randomized controlled trial. J Am Med Assoc
286(24):3097-3105, 2001
32. Dijkstra MD, Ebbens FA, Poublon RM, et al: Fluticasone propionate
aqueous nasal spray does not influence the recurrence rate of chronic
rhinosinusitis and nasal polyps 1 year after functional endoscopic sinus
surgery. Clin Exp Allergy 34(9):1395-1400, 2004
33. Weschta M, Rimek D, Formanek M, et al: Topical antifungal treatment
of chronic rhinosinusitis with nasal polyps: a randomized, doubleblind
clinical trial. J Allergy Clin Immunol 113(6):1122-1128, 2004
34. Ponikau JU, Sherris DA, Kita H, et al: Intranasal antifungal treatment in
51 patients with chronic rhinosinusitis. J Allergy Clin Immunol 111(5):
1137-1138, 2003