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Feline Viral Upper Respiratory Diseases Barbara J Volume 46 | Issue 2 Article 4 1984 Feline Viral Upper Respiratory Diseases Barbara J. Hill Iowa State University Susan O'Brien Iowa State University Follow this and additional works at: https://lib.dr.iastate.edu/iowastate_veterinarian Part of the Respiratory Tract Diseases Commons, and the Small or Companion Animal Medicine Commons Recommended Citation Hill, Barbara J. and O'Brien, Susan (1984) "Feline Viral Upper Respiratory Diseases," Iowa State University Veterinarian: Vol. 46 : Iss. 2 , Article 4. Available at: https://lib.dr.iastate.edu/iowastate_veterinarian/vol46/iss2/4 This Article is brought to you for free and open access by the Journals at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected]. Feline Viral Upper Respiratory Diseases Barbara J. Hill, BS, DVM* Susan O'Brien, DVM* * Infectious upper respiratory disease is the tion takes place in the mucosa of the nose, most common and probably the most devas­ turbinates and conjunctiva. The principal le­ tating respiratory syndrome recognized in sions in FVR are necrosis of epithelium and cats. 1 Three infectious diseases are responsi­ associated purulent inflamn1ation. 5 The sub­ ble: feline viral rhinotracheitis (FVR), feline sequent exudates may cause dyspnea and calicivirus infection, and feline pneumonitis paroxysmal coughing and sneezing. Lesions (Chlamydia psittaci). Feline Viral Rhinotra­ do not usually extend to the bronchi, bronchi­ cheitis and caliciviral infection account for the oles, or alveoli. Intranuclear inclusion bodies majority of clinical cases and will be reviewed can be demonstrated in n1ucosal epithelium here. These two viral diseases comprise 80 to for up to 7 days after infection. 90 % of infectious upper respiratory disease in Feline calicivirus strains vary in their viru­ domestic cats and are isolated in approxi­ lence. Viral replication occurs in the oral and mately equal frequency. Both affect the feline respiratory mucosa and the conjunctiva. For­ respiratory tract and conjunctival membranes merly, it was thought that the virus affected and cause a variety of clinical signs in infected mainly the upper respiratory tract, as in cats. Both FVR and feline calicivirus have a FVR, but it has been more recently demon­ widespread distribution throughout the strated that while calicivirus does affect the world; serological studies have shown specific conjunctiva and upper airways, the lung is antibodies present in 80 % or greater of adult also an important target for the more virulent cat populations. 2 strains. The Agents Transmission The etiologic agent of FVR is feline herpes­ Transmission of both viruses is most com­ virus, which causes characteristic intranuclear monly by direct contact with infectious oral, inclusion bodies in infected cells. The virus is nasal, or ocular secretions, or by contact with fragile and is susceptible to heat, acid and contaminated fomites. Aerosol transmission is common disinfectants (e. g. hypochlorite or uncommon and appears to be much less im­ quaternary ammonium compounds).4 Feline portant in the spread of the disease than ear­ 6 herpesvirus appears to be highly species-spe­ lier postulated. ,7 Route of infection may be cific for the domestic cat. intranasal, oral, or conjunctival. Feline calicivirus is composed of a number of serologic variants, or strains. It is slightly Clinical Syndromes hardier than FVR, but is susceptible to the Cats of any age can be affected by viral res­ same disinfectants as FVR. piratory disease, but the morbidity and mor­ tality is highest in young cats and kittens. Pathogenesis and Lesions Anorexia, fever and depression are common The mucosal surfaces of the upper respira­ with both viral infections. Feline viral rhino­ tory tract and conjunctiva are predilection tracheitis produces a characteristic syndrome sites for feline herpesvirus, and viral replica- in susceptible cats. After a 2 to 8-day incuba­ *Dr. Hill is a 1984 graduate of the Iowa State Univer­ tion period, early signs include hypersaliva­ sity College of Veterinary Medicine. **Dr. O'Brien is an assistant professor in Clinical tion, sneezing, and clear, serous, ocular and Sciences at Iowa State University nasal discharges. As the disease progresses, vol. 46) No. 2 97 conjunctIvItIS and coughing may develop. therapy, general anesthesia, cat shows, etc. Ocular and nasal secretions may become mu­ An estimate of up to 80 % of FVR-recovered copurulent, especially with secondary bacter­ cats remain carriers for a variable period of ial invasion. The ocular manifestations of fe­ time. 4 Cats may spontaneously clear the virus line herpesvirus primarily involve the con­ after months or years, but some animals re­ junctiva, but ulcerative keratitis may de­ main carriers for life. velop.8 A leukocytosis is generally present Unlike FVR, carrier cats of feline cali­ throughout the course of the disease. The ma­ civirus excrete virus more or less continuously jority of clinical signs have usually resolved from the orophrynx. Such animals are there­ within 10 to 20 days, but some animals may fore a constant hazard to susceptible cats. In a be left with chronic sequelae such as persistant survey of 1500 clinically healthy cats, sampled conjunctivitis or rhinitis. The recurrent clini­ with a single oro-pharyngeal swab, feline cali­ cal signs seen in these chronically affected cats civirus was found to be widespread; 8 % of is most often due to secondary bacterial inva­ single household pets, 24 % of cats attending sion of mucosal surfaces originally damaged cat shows and 41.5% of cats in institutional by the virus. 4 colonies were found to be excreting the In general, the disease produced by feline virus. 12 calicivirus is similar to but rnilder than FVR, although the range of clinical signs varies Diagnosis greatly among the various strains of the virus. Differentiation of FVR and feline cali­ The majority of strains, after a 2 to 10-day civirus infection on the basis of clinical signs incubation period, produce a mild upper res­ alone is difficult and generally not recom­ piratory disease with ocular and nasal dis­ mended. Clinical differentiation is possible charge and ulceration of the tongue, hard pa­ based on the principle that while some mani­ late, and nostrils. In some cases mouth festations (e. g. fever, depression, anorexia) ulcerations n1ay be the only clinical sign of are common to both diseases, others signs are infection. The more virulent strains of cali­ more frequently associated with one infection civirus may produce a primary interstitial or the other. Rhinitis and conjunctivitis with pneumonia with resulting dyspnea. serous to mucopurulent discharges, keratitis, Involvement of systems other than the res­ blepharospasm, sneezing, coughing, hypersa­ piratory tract can occur with FVR. Feline livation and oral respiration are signs most viral rhinotracheitis has been associated with suggestive of FVR, while ulcers of the tongue, central nervous system dysfunction and liver hard palate and nostrils, occasionally asso­ disease, but only in very young, old, or im~ ciated with signs of pneumonia are more con­ munosuppressed animals. 13 Feline herpes­ sistent with feline calicivirus. Unfortunately, virus has also been associated with ulcerations differentiation of the two viral infections is not of the skin. 9 always as simple as descriptions suggest, due to overlap and variation in clinical signs and The Carrier State severity of infection and complications with As stated previously, both feline respiratory secondary infections. Therefore, definitive viruses are relatively fragile, and thus they diagnosis is best made serologically or by must rely for their continued survival on their virus isolation. However, because treatment ability to persist in the cat. In both FVR and of both viral diseases is symptomatic in the feline calicivirus infections most of the clinical majority of clinical cases, etiologic diagnosis signs regress over a period of 10 -12 days. Af­ of upper respiratory viral disease in cats is ter this time any animal which remains per­ generally not necessary or economically war­ sistently infected with the virus is termed a ranted. "carrier." The carrier animal may be asympto­ matic or show chronic symptoms of the dis­ Treatment ease. The carrier state of FVR is character­ The intensity of treatment of viral respira­ ized by latent periods with only intermittent tory disease is dependent on the severity of episodes of virus shedding. During such epi­ clinical signs. In some cases clinical manifes­ sodes the carrier is highly infectious to other tations are so mild and the cat so relatively cats. 4 Carriers may shed spontaneously or unaffected that no treatment is required. 10 In subsequent to stresses such as corticosteroid the case of the more severely affected cat, 98 Iowa State Veterinarian however, prompt and vigorous therapy is nec­ during the course of the infection. essary. Therapy is for the most part sympto­ The chronic rhinitis and/or sinusitis that is matic and supportive. Good nursing care is sometimes a sequelae to viral upper respira­ extremely imporant in the treatment of these tory disease presents a therapeutic challenge cats, as respiratory arrest secondary to airway for the veterinarian. The more chronic the obstruction and/or pneumonia, dehydration, condition becomes, the more unlikely it is
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