The chronic feline snuffler is a frustrating patient to treat. The longer the course, the more severe the consequences to
affected tissues are and the more debilitating it is to the patient. A logical diagnostic plan to differentiate probable etiologies
and to rule-out non-viral causes results in appropriate therapeutic choices. Even with a viral etiology, therapies to reduce
the pathological consequences of the infection may modulate and help control the clinical signs. Novel choices and drug combinations
are discussed.
History and Presentation
Chronic, recurrent rhinosinusitis can occur in cats of any age. Cats are presented because of sneezing, nasal discharge, and
noisy breathing with or without inappetance. Sneezing occurs because of stimulation of irritant receptors in the nasal and
sinus subepithelium. Knowing the timing, onset, duration and frequency of sneezing can be helpful. With chronicity, inflammatory
changes this response may be abolished resulting in accumulation of discharge. Nasal discharge may be serous, mucoid, purulent,
or sanguinous. It is helpful to know whether the discharge has changed, whether it changes throughout the day or season, and
especially whether it is unilateral or bilateral.
Respiratory patterns and sounds may be abnormal. Clients may comment on the cat sounding hoarse or even silent when meowing
or that his/her purr is different. In general, sounds heard on inspiration are associated with larger airways whereas expiratory
sounds are associated with smaller, lower airways. Snorting occurs with accumulation of discharges in the nasal passages or
with secretions coughed into the oropharynx (e.g., from pneumonia). A snoring, stertorous sound is associated with proximal
upper respiratory occlusion, such as with a polyp or foreign body obstruction or functional inflammatory obstruction. Stridor
is an inspiratory wheeze that reflects changes in the larynx. An expiratory wheeze, crackles and rales reflect small airway
involvement. A complete lack of bronchovesicular sounds occurs when there is pulmonary consolidation or inflammation.
If the breathing is "worse at night" this could reflect bronchitis or merely the time that the client is at home to observe
the cat. Sounds that are worse after exercise or at rest may reflect the severity of the respiratory interference or the movement
of secretions. Some cats have seasonal flare-ups suggesting an allergic or contact irritant component.
Assess facial symmetry both face on and from above the head. Palpate the face to further look for swelling, invagination or
discomfort. Thoroughly evaluate teeth and alveolar bone for evidence of periodontal disease, abscessation or inflammation.
Look at and palpate the hard and soft palate, where feasible, looking for oronasal fistula or mass lesions or ulceration.
If a cat retches or yawns, the tonsils may be visualized. By opening the mouth we can evaluate neurologic competency: jaw
tone (motor V), position, movements and symmetry of the tongue (XII), and gag reflex (IX, X).
Evaluate nasal passage patency using a small mirror (compact or dental) or a glass slide that has been kept in the freezer.
Wisps of cotton are also helpful. Palpate the trachea to see if this elicts a cough. It is helpful to auscult the trachea
as well as three locations (dorsal cranial and caudal and craniaoventral) bilaterally to define the primary location of the
lesion. Occasionally auscultation of the frontal sinuses may be revealing. For this, a small pediatric bell is used. For pulmonary
auscultation, use two heads, the standard bell and a plexiglass scope (e.g., Ultrascop) as they provide different sensitivities
and frequencies.
A thorough physical examination should be performed. Fundic examination should be performed to look for Cryptococcus and other
signs of systemic disease. Enlargement of regional lymph nodes or generalized node enlargement should be assessed.
Etiologies and Pathogenesis
Chronic rhinitis may be a sequel to acute rhinitis but it may be a separate condition, all together. It may represent an ineffective
immune response to persistent viral infection (1). Feline herpesvirus 1 (FHV-1) may be the common denominator initiating turbinate
resorption, with subsequent secondary bacterial infections and unchecked inflammation exacerbating the problem. This is especially
bad in anatomically predisposed individuals (conformation, anomalies). Irreversible destruction of the turbinates may result
in viral or inflammatory mediator-induced cytolysis. Reactivation of herpesvirus from infected trigeminal ganglion may result
in recurrent destruction. All of these are possible pathogenic strategies; it is not possible to determine the course/cause
in a given individual.
Caliciviruses infection results in a carrier state with continuous shedding for variable periods of time. FHV-1, like other
herpesviruses, results in a state of latency and approximately 80% of infected cats are permanent carriers. Latency accounts
for recurrence of clinical signs during periods of physiological or psychological stress.
