EAR, NOSE, AND THROAT 0195-5616/94 $0.00 + .

20

PATHOGENESIS AND
TREATMENT OF
FELINE RHINITIS
Deborah R. Van Pelt, DVM, MS,
and Michael R. Lappin, DVM, PhD

As with the dog (see Van Pelt and McKiernan, this issue), evaluation
of the feline patient with rhinitis and nasal discharge may be a frustrat-
ing situation for the veterinary practitioner. Although the incidence of
specific diseases may be different, many of the same etiologies that cause
rhinitis in the dog also cause rhinitis in the cat (Table 1). Because of the
high incidence of viral upper respiratory infections in the cat population,
the diagnostic workup of cats with rhinitis often focuses on these etiolo-
gies. However, when presented with a cat with history and clinical signs
consistent with viral upper respiratory tract infection, it should be re-
membered that there are numerous other causes of feline rhinitis. This
article discusses the pathogenesis, diagnosis, and treatment of the var-
ious causes of feline rhinitis.

ANATOMY AND PHYSIOLOGY

The general structure and physiology of the nasal cavity of the cat
is very similar to that of the dog. It is essentially a bony cavity divided
in half by a cartilaginous and bony septum. The significant differences
are that the attachments of the dorsal and ventral turbinate bones are
more widely separated from each other in the cat than in the dog, and
that the turbinated portion of the ethmoid is more extensive in the cat
Text continued on page 812

From the Department of Clinical Sciences, College of Veterinary Medicine and Biomedical
Sciences, Colorado State University, Fort Collins, Colorado

VETERINARY CLINICS OF NORTH AMERICA: SMALL ANIMAL PRACTICE

VOLUME 24 • NUMBER 5 • SEPTEMBER 1994 807

~
OD

Table 1. COMMON CAUSES OF SNEEZING AND NASAL DISCHARGE IN THE DOG AND CAT
Cause Signalment History Physical Examination Discharge Diagnostic Plan Comments

CONGENITAL
Stenotic nares Brachycephalic dogs Snoring Stenotic nares Serous to mucoid Physical examination Often without
respiratory signs
Cleft palate Young, all breeds Poor suckling milk Cleft palate Food or fluid Physical examination Less common in cats
from nares Abnonmal lung sounds Mucopurulent with
Chronic discharge with aspiration secondary infection
postweaning pneumonia Usually bilateral
Elongated soft palate Brachycephalic dogs Gagging, snorting ± Elongated soft palateFood or fluid Physical examination Diagnosis may require
association with Reddened pharynx Serous to sedation
eating Inflamed tonsils mucopurulent Often without
Usually bilateral respiratory signs
DYSPHAGIA All breeds Coughing, gagging, RMdened pharynx Food or fluid Physical examination Many acquired
Congenital-young multiple swallowing Inflamed tonsils Serous to Fluoroscopy etiologies
Acquir~lder attempts Abnonmai lung sounds mucopurulent Metabolic workup Often without
with aspiration Usually bilateral Electromyography respiratory signs
pneumonia
INFECTIOUS
Viral All breeds Animal contact ± Oral ulcers Mucopurulent Direct-fluorescent Often severe
Feline viral All ages; more common Poor vaccination ± Conjunctivitis antibody staining of clinical disease;
rhinotracheitis in young history ± Dendritic ulcer conjunctival scraping abortion and
(FVR) Anorexia common. ± Abnormal lung Serology bronchopneumonia
Ptyalism sounds can occur
Fever common
Feline calicivir.us All breeds Animal contact OraVnasal ulcers Mucopurulent Diagnosis by clinical Ulcers and
All ages (more common Poor vaccination ± Conjunctivitis signs and exclusion bronchopneumonia
than FVR) history ± Abnormal lung more common than
Anorexia common sounds FVR
Ptyalism Fever common Oculonasal discharge
less common than
FVR
Reovirus Cats-all breeds and Mild symptoms Fever rare Rare Diagnosis by Generally mild
ages Often ocular signs exclusion respiratory signs
alone
 Canine distemper All breeds, all ages Poor vaccination Fever Mucopurulent Clinical signs Immunosuppressive
virus history ±. vomiting/diarrhea Complete blood cell disease with multiple
Animal contact ± Abnormal lung count (lymphopenia) system involvement
Multiple. system sounds Direct fluorescent
involvement ± CNS disease antibody staining of
(CNS, gastro- ± ophthalmologic conjunctival scraping
intestinal) changes Serology
±foot pad Characteristic
hyperkeratosis cerebrospinal fluid
BACTERIAL
Many species All breeds-dogs Chronic sneeze Decreased air flow Mucopurulent Clinical signs Generally a secondary
Common in cats Snuffling respiration Dull percussion Usually bilateral History of primary disease
All ages Often secondary to a Signs of primary etiology Often secondary to
primary inflammation etiology Culture occasionally virus, trauma,
± anorexia and. valuable fungus, congenital,
dehydration and neoplasia
Chlamydia Cats Animal contact Mild conjunctivitis Serous to Cytology Frequently recurrent
All breeds, all ages Usually no mucopurulent Exclusion Mildest feline
More frequently in· young polysystemic illness Usually bilateral History infectious upper
respiratory disease
Mycoplasma All breeds, all ages Usually no Mild conjunctivitis Rare Cytology Primarily conjunctivitis
polysystemic illness Serous, if it occurs Culture
FUNGAL
Aspergillus and Brachycephalic less Progressive Fewer-rare Mucoid, mucopurulent, Cytology Difficult to distinguish
Penicillium common Secondary to trauma Facial or palate or hemorrhagic Culture from neoplasia
All ages (15%) deformity rare One third unilateral Serology Not recognized in cats
Decreased air flow Two thirds bilateral Radiographic changes
Dull percussion
± lymphadenopathy
or anorexia
Cryptococcus . Dog and cat Upper respiratory ± lever Mucoid to Cytology Most common mycotic
neoformans All ages signs ± CNS signs mucopurulent Serology infection in cats
Polysystemic ± abnormal lung Culture
progression sounds due to
dissemination
± ophthalmologic
changes
Trichosporon sp. Nasal polyp .or Rare
granuloma
Rhinosporidium seeberi Nasal. polyp or Rare
~
I,C)
granuloma
Table continued on following page
~
0

Table 1. COMMON CAUSES OF SNEEZING AND NASAL DISCHARGE IN THE DOG AND CAT (Continued)
Cause Signalment History Physical Examination Discharge Diagnostic Plan Comments

PARASITIC
Linguatula serrata Dogs-all ages Mild sneezing None Serous to none Cytology (isolation) Often subclinical
Pneumonyssus caninum Dogs-all ages Mild sneezing None Serous to none Cytology (isolation) Often subclinical
Eucoleus hoehmi Dogs-all ages Mild signs None Mucopurulent to Biopsy Rare
hemorrhagic Fecal examination
NEOPLASTIC Dog--common Progressive Decreased air flow Progressive from Cytology Facial deformity,
Cats-rare Dull percussion mucopurulent to Radiographic changes exophthalmos,
Older animals ± exophthalmos hemorrhagic Biopsy unilateral more
± facial or palate common than fungal
deformity
ALLERGIC Dog and cat Acute, mild signs ± conjunctivitis Serous to mucoid History May predispose to
Usually young Seasonal ± dermatologic secondary bacterial
change infection
INFLAMMATORY Cats-young Gagging ± reddened pharynx Serous to Caudal pharyngeal Likely congenital and
POLYPS Dysphagia ± reddened tonsils mucopurulent examination arise from the
± respiratory signs middle ear
SYSTEMIC Generally older Dependent on Retinal vasculature Hemorrhagic Blood pressure Epistaxis is rare
HYPERTENSION primary etiology tortuous, retinal determination
hemorrhage
Abnormalities
associated with
primary etiology
 DENTAL DISEASE All animals Halitosis Fistula Unilateral Physical examination
More common in old Paroxysms of Gingival recession Mucopurulent Skull radiographs
sneezing Dental calculi Occasionally blood
Pawing face Facial abscess tinged
Halitosis
OTITIS MEDIA All animals Mild signs Keratoconjunctivitis Dry, crusty Otoscopic Damage to chorda
Otitis externa sicca examination tympani or facial
Otic lesions Aspirate and culture nerves leads to
decreased nasal
mucosal gland
secretion
TRAUMA All animals Acute Fractures often Hemorrhagic History Secondary bacterial
History of trauma palpable Unilateral or bilateral Radiographs osteomyelitis
common
FOREIGN BODY All animals Acute paroxysms Nonspecific Serous to Sedation and Secondary bacterial
Cats less likely of sneezing mucopurulent, nasal and infection common
Head-banging depending on caudopharyngeal Commonly secondary
Free-roaming chronicity examination to plant materials
Occasionally
hemorrhagic
COAGULATION All animals Hemorrhage without Pale mucous Hemorrhagic Platelet count Multiple etiologies-
ABNORMALITIES Dogs more frequently trauma membranes Activated coagulation can occur with
Hemorrhage in other ± hemothorax time thrombocytopenia,
areas ± hemoperitoneum Bleeding time platelet dysfunction,
± petechiae/ Factor VIII-related or factor deficiency
echymoses antigen
Dependent on etiology

FLV and feline immunodeficiency virus immunosuppression may be involved with recurrent upper respiratory infections.
From Lorenz MD, Cornelius LM (ed): Small Animal Medical Diagnosis. Philadelphia, JB Lippincott, t987, p 234; with permission.

QO
1-'
1-'
812 VAN PELT & LAPPIN

than in the dogY Also, the cat lacks the maxillary recess that is part of
the paranasal sinus system of the dog.30 The turbinate system (nasal
conchae) is well developed in the cat, and it is important in the filtration,
humidification, and warming of inspired air.
Turbinates are covered by ciliated pseudocolumnar epithelium. The
epithelium is primarily respiratory peripherally and olfactory caudome-
dially and caudodorsally. The lamina propria of the respiratory portion
contains serous, mucous, and mixed tubuloalveolar glands as well as
goblet cells. The nasal cavity is limited in its response to insults with
glandular hyperactivity induced by most etiologies. Initially, glandular
secretions result in the presence of a serous nasal discharge, which may
become mucoid or mucopurulent as the disease becomes chronic or
secondary bacterial infection develops.30• 41 • 47

PATIENT EVALUATION

Evaluation of the cat with rhinitis should be undertaken in a manner

similar to that in the dog, keeping in mind the differences in the various
etiologies of rhinitis. between the two species. Viral rhinitis (with or
without secondary bacterial infection) is a much more clinically signifi-
cant and common occurrence in cats than in dogs. Other potential causes
of feline rhinitis include primary bacterial or fungal infection, nasal par-
asites, allergic disease, trauma, dental disease, oronasal fistula, middle
ear disease, neoplasia, or congenital abnormalities such as cleft palate.
Again, as with the dog, the nasal cavity can only respond to insult in a
limited number of ways, regardless of the cause; therefore, the patients'
history and clinical signs are often similar.30
A thorough history is especially important in the evaluation of a cat
with chronic nasal disease. Significant attention should be directed to-
ward the environmental and vaccination history, because viral rhinitis is
much more common in catteries, multi-cat households, or immunocom-
promised cats.28 Sneezing and nasal discharges are the most common
primary presenting complaints. Owners also commonly report gagging
by their pet as discharges pool in the nasopharynx. Dysphagia and se-
vere gagging are commonly reported with nasopharyngeal polyps.37
Owners should be questioned about the presence of gastrointestinal signs
because, occasionally, diseases resulting in vomiting or regurgitation will
lead to passage of ingesta or secretions above the soft palate and predis-
pose to rhinitis. Other historical information that should be determined
includes the duration and progression of clinical signs, medications pre-
viously administered, and the response of the cat to those medications.
Nasal discharge should be characterized as unilateral or bilateral, acute
or chronic, and it's volume and character should be ascertained.
 PATHOGENESIS AND TREATMENT OF FELINE RHINITIS 813

Most conditions leading to inflammation of the nasal mucosa result

in glandular secretions that generally progress from a serous discharge
early in the course of disease to a mucoid or mucopurulent discharge as
chronicity and secondary bacterial infection develop. Hemorrhage can
occur with trauma, coagulopathies, systemic hypertension, and acute
deep insult to the richly vascularized nasal mucosa, chronic erosive or
invasive disease, or acute multiple sneezing episodes induced by any
etiology. Food or water draining from the external nares may be present
because of a communication of the oral and nasal cavities or by passage
of ingesta from the nasopharynx into the nasal cavity.
Physical examination of the cat with suspected nasal disease should
include a thorough examination of the nasal and oral cavities, as well as
a complete examination of ·an other organ systems to rule out the pres-
ence of underlying systemic disease. If the cat is obviously dyspneic, it
should immediately be placed in an oxygen-rich environment, delaying
the full examination until the cat is more stable. However, overt dyspnea
is much more common with lower respiratory tract disease than with
upper respiratory tract disease in the cat. The presence of open-mouth
breathing and dyspnea should alert the clinician to the presence of sig-
nificant lower respiratory tract or pleural space disease, rather than to
suspect upper respiratory tract disease.
The pattern of respiration should be noted and the entire length of
the respiratory tract should be auscultated. The nasal philtrum should be
evaluated for the presence of ulceration or excoriation, which may be
present in the case of chronic nasal discharge. Palpation of the nose may
aid in detection of areas of tenderness or defects resulting from bone loss
or swelling secondary to bone proliferation, neoplasia or soft tissue in-
flammation. The oral cavity should be examined and the odor of the
breath noted. Careful evaluation of the hard palate will help to rule out
congenital defects such as cleft palate or acquired oronasal fistulae. A
full dental examination should be performed to rule out the presence of
significant dental or periodontal disease (i.e., loose teeth or oronasal
fistula). Nasopharyngeal polyps can sometimes be palpated above the
soft palate. The cat tends to be much more intolerant of manipulation of
the head and mouth area than the dog, and a rapid assessment of these
areas is often necessary. Facial symmetry and the patency of nostrils
should be evaluated. The eyes should be evaluated for the presence of
epiphora, ocular discharge, or exophthalmia. A fundic examination may
provide evidence of systemic disease associated with Toxoplasma, Cryp-
tococcus, or coronavirus infection. Careful otic examination is important
in some cases to evaluate for the presence of otitis media. Otitis media
may be associated with nasopharyngeal polyps, which can induce unilat-
eral or bilateral nasal discharge and sneezing. Otitis media is commonly
associated with facial nerve dysfunction, leading to a dry nose and secon-
dary rhinitis. Horner's syndrome may occur concurrently.
814 VAN PELT & LAPPIN

SPECIFIC DISEASE CONDITIONS

Infectious Rhinitis

Viral Rhinitis
Cux;rently, more than 90% of feline upper respiratory tract infections
are thought to be caused by one of two viruses, the feline herpesvirus I
(FHV-1), also known as the feline rhinotracheitis virus, or the feline
calicivirus (FCV).3• 13• 15• 20 Epidemiologic studies indicate that as many as
50% to 75% of cats have serologic evidence of exposure to FHV-1, and
that infection rates in certain populations of cats may approach 100%.9•
13 • 29 The most common mode of transmission of FHV-I and FCV upper

respiratory infections is by direct, close contact between cats.15• 28• 33• 39

Although both viruses are shed in ocular, nasal, and pharyngeal secre-
tions for several weeks after infection, transmission via secretions is
minimal for several reasons.39 Because of their small tidal volumes, cats
do not produce effective aerosols.39 Therefore, sneezed macrodroplets
containing virus are infective, but only for distances of approximately 4
ft. 16 FHV-I is a fragile herpesvirus and is inactivated within 18 hours at
59°F in a humid environment. FCV is viable for several days at room
temperature.39 Fomites such as feeding bowls, contaminated surfaces,
and the hands and clothing of caretakers are also potential sources of
transmission.39 Transmission efficacy depends on the amount of virus
shed by the infected animal, the presence of concomitant disease, the
eat's nutritional status, the competency of the eat's immune system, and
the duration and intimacy of contact between the shedding and suscep-
tible animals. 15• 33
Although unvaccinated cats of all ages are susceptible to infection,
the highest incidence of infection and mortality is in kittens between 6
and 12 weeks of age.28• 33 This is the time when maternally derived
colostral antibodies are decreasing below protective levels. In adult cats,
the natural immunity to both FHV-I and FCV is relatively poor and
short-lived. 10• 28 Immunity derived from vaccination is incomplete; cats
vaccinated against FHV-I still develop mild signs of upper respiratory
disease when experimentally challenged with FHV-I exposure.43 Vacci-
nation reduces the duration and severity of clinical signs, but does not
prevent infection.29• 44 Local intranasal vaccine administration results in a
strong but short-lived local immunity.39
After exposure to FHV-I and FCV, virus replication occurs in the
epithelium of the upper respiratory tract, especially the nasal epitheliwn
and turbinates, tonsils, and conjunctiva.28• 29• 33• 39 An intense inflammatory
reaction of the turbinates results, with necrosis and ulceration of the
mucosa.5• 22 In young growing cats, there is a severe osteolytic reaction
with resorption of the turbinate bone.28 Oculonasal discharge results
 PATHOGENESIS AND TREATMENT OF FELINE RHINITIS 815

from excess mucous production, fibrin exudation, suppuration, and

shedding of necrotic debris.22 Secondary bacterial invasion of necrotic
areas is common.
Clinical signs of upper respiratory tract disease secondary to FHV-1
and FCV follow an incubation period of 2 to 10 days. 10• 15 Typical clinical
signs in a patient with viral rhinitis include sneezing, bilateral serous
nasal and ocular discharge, coughing, and fever. 10• 12• 13• 20• 28• 33 With devel-
opment of a secondary bacterial infection, the nasal and ocular dis-
charges may become mucopurulentY The accumulation of oculonasal
discharge may result in obstruction of the nares and matting of the
eyelids. In kittens, this may be followed by open-mouth breathing and
anorexia, as well as dehydration and pneumoniaP
The clinical signs of FHV-1 infection tend to be more severe than
those of FCV, with more severe conjunctivitis, paroxysmal sneezing, and
profuse ocular and nasal discharges.39 Cats with FCV infection often have
subclinical infections, with very mild conjunctivitis, nasal discharge, and
only occasional sneezing. Oral and lingual ulceration and corneal ulcer-
ation are more common with FCV than with FHV-1 infectionP· 39
A chronic carrier state commonly occurs after acute infection with
both FHV-1 and FCV.15• 38• 4° Carrier cats with clinical signs of persistent
upper respiratory infection are often referred to as "snufflers." As many
as 80% of cats that recover from acute viral upper respiratory infection
are likely to become chronic carriers capable of infecting susceptible cats
and kittens.10 Most commonly, FHV-1 carrier cats are latently infected
and only occasionally shed infective virus. This viral shedding typically
follows some natural or induced stress, such as parturition, lactation,
kenneling, or administration of corticosteroids. 15• 39• 40 Shedding does not
occur immediately after a stressful event but follows a lag period of
approximately 1 week, after which viral shedding may occur for up to 2
weeks.15 The site of latency of the FHV-1 virus is thought to be the
trigeminal ganglia, although in many known carriers the location of the
latent virus has not been determined.15• 39• 40
Unlike latent carriers of FHV-1, FCV carriers are persistent shedders,
shedding infective virus almost continuously.15• 39 However, the quan-
tities of virus shed in nasal and oropharyngeal secretions vary with time.
FCV persists in the tonsils and lymphoepithelial tissues of the nasophar-
ynx; tonsillectomy does not terminate the carrier state. 15• 39
Diagnosis of upper respiratory tract disease secondary to viral infec-
tion is usually made on the basis of patient signalment, history, and
clinical signs combined with exclusion of other etiologies. There are
certain findings which suggest diseases other than viral rhinitis.20 Unilat-
eral nasal discharge is more typical of nasal foreign body, tumor or
toothroot abscess. Epistaxis is rare with viral rhinitis, but is more com-
monly associated with coagulopathy, trauma, nasal foreign body, hyper-
816 VAN PELT & LAPPIN

tension, neoplasia, or fungal rhinitis. Facial deformity is most often seen

in association with neoplasia or fungal infection. Marked enlargement of
the mandibular lymphnodes is associated with neoplasia or fungal infec-
tion. Fundic abnormalities are rarely seen in association with viral upper
respiratory tract infection.
When a specific definitive diagnosis is required, as in the case of
recurrent disease or catteries with multiple animals affected, diagnostic
procedures may include hematological evaluation, conjunctival smears,
nasopharyngeal culture, or serologic testing. In the majority of cases,
hematologic abnormalities are nonspecific; a neutrophilic leukocytosis
with a mild left shift is the most common finding. 39 Fluorescent antibody
testing of cells obtained by conjunctival scraping may confirm the pres-
ence of FHV-1 infectionP' 29 Virus isolation performed on swabs collected
from the oropharyngeal region or ocultmasal discharges is a sensitive
method for the confirmation of FHV-1 and FCV infections.Z9' 39 For opti-
mal results, swabs should be collected during the first week of illness.39
A positive result, however, should be interpreted in light of the patient's
clinical signs, as isolating the virus only indicates the presence of that
specific virus in the patient and does not prove that the patient's disease
is produced by that virus. 34 Samples for serologic testing should be col-
lected early in the course of disease and again 1 to 2 weeks later.39 Virus
neutralization tests can be performed for both FHV-1 and FCV. A four-
fold or greater increase in antibody between the acute and convalescent
samples is diagnostic of active infection.39 Unfortunately, recurrent infec-
tions may not develop increasing antibody titers.
Recurrent rhinitis is common in cats infected with the feline leuke-
mia virus (FLV) or feline immunodeficiency virus.4' 49 Adult cats with
severe rhinitis or recurrent disease should be screened serologically for
antigens of FLV and antibodies against feline immunodeficiency virus.
Howeyer, seropositivity does not document immunodeficiency induced
by these agents, and both FVH-1 and FCV can induce disease primarily
in the immunocompetent host.
After the presumptive clinical or definitive diagnosis of viral rhinitis,
several treatment options exist. Unfortunately, there are no systemic
antiviral agents that are effective in cats with FHV-1 and FCV, and
treatment of these cats is aimed mainly at supportive care and treatment
of secondary bacterial infections. 15' 33 Because secondary bacterial infec-
tions are common with FHV-1 and FCV infections, use of antimicrobials
is indicated. Antibiotic selection should be based on the identity and
susceptibility of the organisms. Antibiotics that have been suggested as
first-line agents in cats with rhinitis/sinusitis include tetracyclines, chlor-
amphenicol, first-generation cephalosporins, and trimethoprim/ sulfa.6'
zo, 39 Ampicillin has been suggested as an appropriate antibiotic choice in
kittens.39 The authors have also successfully controlled secondary bacte-
 PATHOGENESIS AND TREATMENT OF FELINE RHINITIS 817

rial infections in some cats with clindamycin hydrochloride administered

at 12.5 mg/kg, once orally daily. This drug has a broad anaerobic spec-
trum, penetrates tissue well, and has been shown to be safe for use in
the cat. 19 Because the nasal cavity is colonized with anaerobic bacteria,
the authors suggest using antibiotics with anaerobic activity such as the
penicillins (amoxicillin 11-20 mg/kg orally /IV TID), clindamycin (12.5
mg/kg orally every 24 hours), metronidazole (10-15 mg/kg orally BID
to TID), or chloramphenicol (1~25 mg/kg orally TID to QID).
Because the nose is comprised of cartilage and bone, most secondary
bacterial infections probably result in osteochondritis. Thus, long-term
antibiotic administration is indicated. The authors commonly prescribe
antibiotics for 6 to 8 weeks if the initial response is positive in cats with
recurrent infections. Anecdotally, recurrence of disease has been less
common in cats receiving long-term treatment.
The use of corticosteroids in cats with viral rhinitis is controversial.
Because the clinical signs are a reflection of nasal inflammation, oral or
parenteral administration of glucocorticoids may decrease the clinical
signs.20 However, depending on the dose, glucocorticoids may decrease
the ability of the abnormal nasal cavity to deal with an underlying
infectious disease and may retard healing.15• 20 Administration of cortico-
steroids may also initiate viral shedding in cats that are carriers of FHV-
I and FCV.15• 28 Topical administration of glucocorticoids intranasally may
help clear nasal discharges and swelling, thus improving the patient's
sense of smell and appetite. The authors commonly prescribe gentacin
durafilm (Schering-Plough Animal Health, Kenilworth, NJ), one drop in
each nostril three times a day during the initial 2 to 3 days of therapy.
Administration of topical decongestants such as phenylephrine
(0.25%-0.5% solution, intranasally every 8-24 hours; NeoSynephrine,
Winthrop, New York, NY) or oxymetazoline (0.25% solution, intranasally
every 24 hours; Alfrin, Schering, Kenilworth, NJ) will aid in decreasing
the volume and tenacity of nasal discharge.39 To avoid the occurrence of
rebound nasal congestion, intranasal decongestants should be instilled
into alternate nostrils; some regimes have suggested alternating every 2
to 5 days. 11 • 20 Use of mucolytic drugs such as acetylcysteine (10% solu-
tion, nebulized at rate of 20-50 mL/h for 30 minutes, every 12 hours,
Mucomyst, Mead Johnson Laboratories, Evansville, IN) may be useful in
cats with protracted disease and thick, occlusive nasal discharge.39 Neb-
ulization using 0.9% saline often provides enough humidification to sig-
nificantly reduce the viscosity of secretions, with resultant improvement
in the eat's attitude and demeanor. Cleaning the external nares several
times daily may make the cat less distressed, as well as increasing the
ability of the cat to smell aromatic food, which potentially will increase
the eat's appetite.
In severely affected cats, close attention must be paid to prevention
818 VAN PELT & LAPPIN

of dehydration and treatment of anorexia. Mild dehydration may be

treated with the administration of subcutaneous fluids, while moderate
to severe dehydration requires the administration of intravenous fluids.
Inappetence can be addressed by offering strong smelling foods and
hand-feeding or heating the food. The use of diazepam or oxazepam
may stimulate the anorectic eat's appetite. When oral ulceration is con-
tributing to the anorexia, use of babyfood or other liquidized food may
make eating less painful,1 5 In severe, prolonged cases, use of a nasogas-
tric or gastrostomy tube may be necessary to maintain the nutritional
requirements of the patient.
The incidence of FHV-1- and FCV-induced upper respiratory dis-
ease in a given population of cats can be minimized via a combination
of vaccination and husbandry. As mentioned previously, vaccination is
effective in decreasing the severity of clinical signs, but is not totally
effective in preventing infection.43 Because viral transmission occurs
mainly by direct contact between cats, preventing the introduction of
infected cats into a noninfected colony is essential. New cats should be
quarantined for 2 to 3 weeks before introduction into a FHV-1- and FCV-
free setting. During the quarantine period, the new cats should be cul-
tured for FCV and FHV-1 after a course of glucocorticoid therapy to
detect carrier cats.3• 15• 39 For previously infected colonies or households,
kittens should be separated from their carrier mothers and other adult
cats. Weaning at 5 weeks, while maternal antibodies against FHV-I and
FCV are still present, and then separating the kittens from their mothers,
will decrease the transmission of the upper respiratory viruses. Kittens
should be vaccinated beginning at 6 weeks of age. 38• 39 Young cats can
then be re-introduced to the adult population at 12 to 16 weeks of age. 3• 39

Fungal Rhinitis
Although rhinitis secondary to Aspergillus and Penicillium infection
are being recognized with increasing frequency in the dog, feline nasal
aspergillosis and penicilliosis rarely occur.30• 41• 46 Ketoconazole (10-15
mg/kg orally every 24-48 hours) has been recommended for treatment
of cats with aspergillosis and penicilliosis.41 Whether topical clotrimazole
or enilconazole are superior to the imidazoles for the treatment of nasal
aspergillosis in the cat remains to be proven.
Cryptococcus neoformans, a saprophytic yeast, is the most common
cause of mycotic rhinitis in cats. The organism has a thick wall sur-
rounded by a refractile capsule, which may serve as a virulence factor by
inhibiting cellular ingestion by macrophages or affording resistance to
desiccation. 1• 18 The capsule also inhibits plasma cell function, phagocy-
tosis, and leukocyte migration.26 C. neoformans is most frequently found
in association with droppings and accumulated debris of pigeon roosts. 26
The most likely route of infection is via inhalation of dust contaminated
by bird droppings.1• 26 Infection can also be contracted from the gastroin-
 PATHOGENESIS AND TREATMENT OF FELINE RHINITIS 819

testinal tract or by direct inoculation of the skin.1' 12 After inhalation,

deposition of organisms in the upper respiratory tract may result in the
formation of nasal granulomas, whereas those organisms reaching the
alveoli may cause pulmonary granulomas.26 Systemic dissemination can
occur, with local extension to the central nervous system through the
cribriform plate or via hematogenous spread.26 Ocular, cutaneous and
mucocutaneous, musculoskeletal, and visceral forms of cryptococcosis
also have been described.1' 12, 24
There is no apparent breed or sex predilection for feline cryptococ-
cosis.26, 48 Age range of affected cats is broad (range, 1 to 13 years; mean,
5 years}.26' 48
Upper respiratory signs are the most common clinical findings in
cats with cryptococcosis and include sneezing, snuffling, unilateral or
bilateral nasal discharge, and respiratory stertor.1' 12' 24' 26' 48 The nasal
discharge is typically chronic and nonresponsive to antimicrobial ther-
apyY Approximately 70% of cats have a flesh-colored, polyp-like mass
visible in the nostril, or a firm, hard subcutaneous swelling over the
bridge of the nose.26 Extension of the nasal lesions may lead to destruc-
tion of facial bones.22 Although clinical evidence of pulmonary involve-
ment is rarely noticed, pulmonary lesions are present in approximately
30% of affected cats at necropsy.Z6' 48 With involvement of other organ
systems, other clinical syndromes such as uveitis, cutaneous lesions, or
neurologic signs (depression, seizures, circling, head pressing paresis)
may be observed.26 Signs of systemic illness are uncommon in affected
cats, but may include mild fever, anorexia, and listlessness.Z6, 48
Diagnosis of mycotic rhinitis is based on cytologic evaluation of
nasal exudate, with identification of the causative organism.1' s, 26 If organ
systems other than the respiratory system are involved, cytologic evalu-
ation of affected tissues (e.g., skin exudate, cerebral spinal fluid, tissue
aspirates) is also useful. India ink preparation of an impression smear of
nasal discharge is positive in approximately 60% of culture-proven infec-
tions? Diagnosis by use of India ink depends on visualization of bud-
ding, yeastlike organisms, 5 to 15 microns in diameter and surrounded
by a clear capsule.1' 26 In the absence of budding, the diagnosis is not
definitive, as lymphocytes, fat droplets and aggregated India ink parti-
cles may be confused with Cryptococcus organisms.26 New methylene blue
and Gram stains can also be used in cytologic evaluation.1' 26
The only clinically useful serologic test in the diagnosis of cryptococ-
cal infections is the latex agglutination test which detects the presence of
cryptococcal capsular antigen. 26 This test is sensitive and accurate in
detecting capsular polysaccharide antigen in serum, urine, and cerebro-
spinal fluid (CSF}.26' 48 In humans, false-negative results have been re-
ported with localized disease, while false-positive titers may be seen with
Klebsiella or Toxoplasma gondii infections or if rheumatoid factor is
820 VAN PELT & LAPPIN

present.21· 26 The latex agglutination test is considered positive with a titer

of 1:1 or greater. The cryptococcal titer during therapy can be used as a
prognostic indicator of treatment, with a good prognosis indicated by a
decrease in antigen titer during the course of therapy.26
Fungal isolation of Cryptococcus is possible, with the organism being
cultured from exudate, CSF, urine, joint fluid, and tissue samples.26 Be-
cause Cryptococcus is sensitive to cycloheximide, it will not grow on
dermatophyte test medium, but grows well on Sabouraud's agar with
antibiotics.1· 26
Several treatment regimes have been described in the treatment of
feline cryptococcosis. The combination of amphotericin B and flucytosine
has been recommended, because the sole use of amphotericin B requires
intravenous administration of high doses that are potentially nephro-
toxic.1· 10• 26 Flucytosine is well absorbed after oral administration, with
relatively few side effects.1 Used in combination, the effects of amphoter-
icin B and flucytosine are synergistic (amphotericin B 0.25-0.50 mg/kg
every 48-72 hours with total cumulative dose of 5.0 mg/kg; flucytosine
100 mg orally every 6 hours until2 months after the resolution of signs).U
Other agents reported in the successful treatment of feline cryptococcosis
include fluconazole (50 mg per cat orally every 12 hours), ketoconazole
(10 mg/kg every 12 hours), itraconazole (10 mg/kg every 24 hours), as
well as combinations of ketoconazole and amphotericin B or ketocona-
zole and flucytosine.t, t2, 24, 26, 27,48

Bacterial Rhinitis
As in the dog, primary bacterial rhinitis is uncommon in the cat,
with most bacterial infections of the upper respiratory tract representing
secondary or opportunistic infections.U The upper respiratory tract of
healthy cats is normally populated with significant bacterial flora, includ-
ing Streptococci, Staphylococci, Bacillus, and various coliforms and
anaerobes.10· 36 Culture of bronchoalveolar lavage fluid obtained from
normal healthy cats confirmed that the major bronchi of the cat are not
sterile, although the concentration of bacteria was low.35 These bacteria
are a normal component of the respiratory defense mechanisms, which
in the face of underlying viral, mycotic, or parasitic infection, may be-
come life-threatening.12
Clinical signs, diagnosis, and therapy of feline bacterial rhinitis are
similar to those in dogs (see Van Pelt and McKiernan, this issue). Anti-
biotics seemingly efficacious in the treatment of chronic feline rhinosi-
nusitis include first-generation cephalosporins, trimethoprim/ sulfa,
chloramphenicol, clindamycin, aminopenicillins, or erythromycin.6 Sev-
eral surgical approaches aimed specifically at cats with chronic bacterial
rhinosinusitis have been described.2· 32
 PATHOGENESIS AND TREATMENT OF FELINE RHINITIS 821

Noninfectious Inflammatory (Allergic) Rhinitis

Although feline allergic lung disease (bronchial asthma) is com-

monly recognized, there is little evidence for the existence of feline al-
lergic rhinitis in the veterinary literature. Although feline asthma is char-
acterized by an increased responsiveness of the lower airways to various
antigenic stimuli, its manifestations are typically those of lower airway
disease (coughing, wheezing) rather than upper airway or nasal involve-
ment.l4,44

Neoplasia-Associated Rhinitis

Intranasal tumors are uncommon in the cat, with reported incidence

rates between 1% and 5.9% of all feline tumors.8· 43 However, the 5.9%
rate is based on cats with both nasal planum and intranasal tumors, and
more than half of these cats had nasal planum squamous cell carcino-
mas.8 Therefore, the true incidence of intranasal tumors in cats is most
likely closer to 1% to 2% of all feline tumors.
Feline nasal tumors are rarely benign, with more than 90% found to
be malignant.23• 43 Local invasion is common, but distant metastasis is
infrequent.43 Compared with the dog, cats have a higher percentage of
intranasallymphoma.43· 47 Old and neutered cats of both sexes seem to be
at increased risk for nasal tumors (including those of the nose and para-
nasal sinuses).8
Common clinical signs in cats with intranasal tumors are nonspecific
for neoplasia and include sneezing, nasal or ocular discharge, and inspi-
ratory stridor.8• 22• 43 Epistaxis may also occur.43· 47 The presence of facial
deformity in association with nasal discharge should make intranasal
neoplasia a primary differential diagnosis.47
As with the dog, definitive diagnosis requires tissue biopsy, al-
though signalment, physical examination findings, and radiographs may
be highly suggestive. Diagnostic techniques are discussed elsewhere.
Treatment of cats with intranasal neoplasia is mainly by radiation
therapy.47 The lymphoid intranasal tumors of cats seem to be especially
sensitive to radiotherapy.43

Other Causes of Rhinitis

Other causes of rhinitis in the cat include nasal trauma, foreign

body, dental disease, parasitic infestation (Capillaria aerophila), nasopha-
ryngeal polyps, otitis media, and congenital abnormalities (such as cleft
822 VAN PELT & LAPPIN

palate)P· 25• 30• 31• 37 Nasal trauma and nasal foreign bodies tend to occur
less commonly in cats than in dogs. 30 Clinical signs and treatment of
these conditions are the same as those in the dog.

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Address reprint requests to

Deborah R. Van Pelt, DVM, MS
Department of Clinical Sciences
College of Veterinary Medicine
and Biomedical Sciences
Colorado State University
Fort Collins, CO 80523