Feline respiratory disease complex includes those illnesses typified by rhinosinusitis, conjunctivitis, lacrimation, salivation, and oral ulcerations. The principal diseases, feline viral rhinotracheitis (FVR; feline herpesvirus type 1), feline calicivirus (FCV), Chlamydia felis, or combinations of these infections affect exotic as well as domestic species. Feline pneumonitis (Chlamydophila psittaci) and mycoplasmal infections appear to be of lesser importance. Feline infectious peritonitis (see Feline Infectious Peritonitis) typically causes a more generalized condition but may cause signs of mild upper respiratory tract infection.
FVR and caliciviruses are host-specific and pose no known human risk. Human conjunctivitis caused by the feline chlamydial agent has been reported.
Most acute feline upper respiratory infections are caused by FVR virus, although FCV may be more prevalent in some populations. Dual infections with these viruses may occur. Other organisms such as C felis, Mycoplasma spp, and reoviruses are believed to account for most of the remaining infections or further complicate FVR or FCV infection. Concurrent Bartonella henselae also may further complicate infection.
Natural transmission of these agents occurs via aerosol droplets and fomites, which can be carried to a susceptible cat by a handler. Convalescent cats may harbor virus for many months. Calicivirus is shed continuously, while infectious FVR virus is released intermittently. Stress may precipitate a secondary course of illness. The incubation period is 2–6 days for FVR and FCV, and 5–10 days for pneumonitis.
The onset of FVR is marked by fever, frequent sneezing, conjunctivitis, rhinitis, and often salivation. Excitement or movement may induce sneezing. The fever may reach 105°F (40.5°C) but subsides and tends to fluctuate from normal to 103°F (39°C). Initially, a serous nasal and ocular discharge occurs; it soon becomes mucopurulent and copious, at which time depression and anorexia are evident. Severely debilitated cats may develop ulcerative stomatitis, and ulcerative keratitis occurs in some. Signs may persist for 5–10 days in milder cases and up to 6 wk in severe cases. Generally, the mortality is low and prognosis good except for young kittens and aged cats. The illness often is prolonged, and weight loss may be marked. FVR often is complicated by secondary bacterial infections; abortions and generalized infections also have been associated with disease.
There are many serologically related strains of feline caliciviruses. They appear to have a predilection for the epithelium of the oral cavity and the deep tissues of the lungs. Some caliciviruses are nonpathogenic. Some induce little more than salivation and ulceration of the tongue, hard palate, or nostrils; others produce pulmonary edema and interstitial pneumonia. Clinically, it is often impossible to differentiate FVR from FCV infection. Two strains may produce a transient “limping syndrome” without signs of oral ulceration or pneumonia. These strains produce a transient fever, alternating leg lameness, and pain on palpation of affected joints. Signs occur most often in 8- to 12-wk-old kittens and usually resolve without treatment. The syndrome may occur in kittens vaccinated against FCV; no vaccine protects against both of the strains that produce the “limping syndrome.”
Calicivirus has also been found in cats with lymphocytic-plasmacytic gingivitis and stomatitis (see Feline Caudal Stomatitis). The superficial lesions heal rapidly, and appetite returns 2–3 days after onset. The clinical course usually is 7–10 days. An acute febrile response, inappetence, and depression are common signs. Serous rhinitis and conjunctivitis also can occur.
C felis infections characteristically produce conjunctivitis (see Chlamydial Conjunctivitis); infected cats sneeze occasionally. Fever may occur as the disease progresses beyond serous lacrimal discharge to mucopurulent conjunctivitis, lymphoid infiltration, and epithelial hyperplasia. Convalescent cats may undergo relapses.
Mycoplasma may infect the eyes and upper respiratory passages, characteristically producing severe edema of the conjunctiva and a less severe rhinitis.
The occurrence of severe viral upper respiratory disease is rare in adult, properly vaccinated cats. These cats should be tested for other upper respiratory diseases and, less commonly, concurrent immunodeficiency diseases, including feline leukemia virus and feline immunodeficiency virus.
Lesions generally are confined to the respiratory tract, conjunctivae, and oral cavity. In FVR, the conjunctivae and nasal mucous membranes are reddened, swollen, and covered with a serous to purulent exudate. In severe cases, focal necrosis of these membranes may occur. The larynx and trachea may be mildly inflamed. The lungs may be congested, with small areas of consolidation; however, pulmonary changes are rarely remarkable in FVR except possibly in stressed, young kittens. The characteristic histologic lesion of FVR is the acidophilic intranuclear inclusion body. During the early stage of illness, inclusions may be present in sites of epithelial necrosis on the tongue, nasal membranes, tonsils, epiglottis, trachea, and nictitating membranes. Inclusion bodies are transitory. Inclusions are not seen in calicivirus infections.
The characteristic lesion caused by FCV is ulceration of the oral mucosa. Lesions on the tongue or hard palate initially may appear as vesicles, which subsequently rupture. Ulcerations are occasionally found on the epithelium covering the median nasal septum. The more virulent caliciviruses destroy epithelial cells of the bronchioles and alveoli, which causes acute pulmonary edema that progresses through seropurulent bronchiolar hyperplasia and interstitial pneumonia.
Early in the clinical course of feline pneumonitis, the causative organism may be identified in Giemsa-stained conjunctival smears or scrapings. The elementary bodies are intracytoplasmic. Mycoplasmas occur as extracellular coccoid bodies often seen on the surface of conjunctival epithelial cells.
The presumptive diagnosis is based on such typical signs as sneezing, conjunctivitis, rhinitis, lacrimation, salivation, oral ulcers, and dyspnea. FVR tends to affect the conjunctivae and nasal passages, caliciviruses the oral mucosa and lower respiratory tract. Chlamydial infections result in chronic, low-grade conjunctivitis. These characteristics may be obscured in mixed infections. Cytologic examination of Giemsa-stained conjunctival scrapings is of value for the identification of chlamydiae and mycoplasmas. A definitive diagnosis is based on isolation and identification of the agent. The oropharyngeal mucosa, external nares, and conjunctival sacs are the preferred sampling sites. However, diagnosis of FVR may be difficult due to intermittent shedding of virus and to similar seroprevalence and virus isolation rates in ill and clinically normal cats.
Treatment is largely symptomatic and supportive, but broad-spectrum antibiotics are useful against secondary bacterial invaders (eg, amoxicillin with clavulanic acid, cephalosporins, trimethoprim/sulfa, fluoroquinolones, tetracyclines, chloramphenicol) as well as directly against C felis. Tetracyclines are the most effective against C felis. Nasal and ocular discharges should be removed frequently for the comfort of the cat. Nebulization or saline nose drops may aid in the removal of tenacious secretions. Nose drops containing a vasoconstrictor (eg, 2 drops of ephedrine sulfate [0.25% solution] in each nostril, bid) and antibiotics may be helpful in reducing the amount of nasal exudate. Prolonged use of nasal decongestants, however, may result in rebound nasal congestion and worsening of clinical signs. A bland ophthalmic ointment containing antibiotics (tetracyclines in C felis infections) is indicated 5–6 times daily to prevent corneal irritation produced by dried exudate. If corneal ulcers occur in FVR infections (herpetic keratitis), ophthalmic preparations containing idoxuridine or acyclovir are indicated in addition to other antibiotic ophthalmic preparations. Lysine (250 mg, PO, bid-tid) interferes with herpetic viral replication and may reduce the severity of FVR infection. If dyspnea is severe, the cat can be placed in an oxygen tent. Fluids may be indicated to correct dehydration, and force-feeding may be necessary. Esophagostomy and gavage may be appropriate for alimentation of severely debilitated cats. Antihistamines (eg, chlorpheniramine maleate, PO, bid [8 mg for adults, 4 mg for kittens]) may be beneficial early in the course of the disease.
Two types of modified live virus FVR-FCV vaccines are available. The first type is intended for parenteral administration; cats >9 wk old should be vaccinated twice, with a 3-wk interval. Kittens should be vaccinated at intervals of 3–4 wk until they are ≥12 wk old. In adult cats, revaccination with a single dose every 1–3 yr is indicated.
The second type of vaccine is administered to healthy cats by instillation into the conjunctival culdesacs and nasal passages. Owners should be advised that cats inoculated oronasally may sneeze frequently 4–7 days after vaccination. Kittens vaccinated when <12 wk old should be revaccinated on reaching this age. Annual revaccination with a single dose is recommended.
Modified live virus FVR-FCV vaccines intended for parenteral administration are available in combination with either chemically inactivated or modified live virus feline panleukopenia vaccines. A parenterally administered vaccine composed entirely of inactivated viruses also is available.
Vaccines containing either chick-embryo- or cell-line-origin C felis are administered parenterally. A single dose is recommended for cats >12 wk old; younger kittens should be revaccinated when they reach 16 wk. All should be revaccinated annually. These vaccines are indicated in catteries or on premises where C felis infection has been confirmed. The chlamydial vaccines are available in combination with FVR-FCV and panleukopenia vaccines. Systematic vaccination and control of environmental factors (such as exposure to sick cats, overcrowding, and stress) provide good protection against upper respiratory disease.
Last full review/revision March 2012 by Ned F. Kuehn, DVM, MS, DACVIM; Steven L. Marks, BVSc, MS, MRCVS, DACVIM