Diagnosing and managing feline respiratory disease (Proceedings) - Veterinary Healthcare


Diagnosing and managing feline respiratory disease (Proceedings)


Acute upper respiratory tract disease (URTD) is a source of major morbidity and, less frequently, mortality in the domestic cat. It has been reported to be a major financial burden (Foley and Bannasch 2004) and a leading cause of euthanasia in shelters (Pedersen et al 2004). The syndrome is characterized by nasal discharge, conjunctivitis, ocular discharge, sinusitis, dyspnea, coughing, inappetence, lethargy, and in kittens or debilitated animals, death. Many pathogens are associated with the syndrome, including feline herpesvirus-1 (FHV-1), feline calicivirus (FCV), Chlamydophila felis, and Bordetella bronchiseptica. Additionally, several species of Mycoplasma have been isolated from cats with URTD (Campbell et al 1973, Haesebrouck et al 1991, Johnson et al 2004, Tan et al 1977), however, the role of this group of organisms as primary pathogens in respiratory disease remains contentious, as, similar to the above pathogens, some studies have isolated Mycoplasma species from the respiratory tract of healthy cats at a frequency similar to that found in cats with URTD (Foster et al 2004b, Haesebrouck et al 1991, Tan et al 1977, Tan and Miles 1974).

As expected, the relative frequency of organisms associated with URTD in cats varies from study to study. This fact can be attributed to differences in entry criteria (conjunctivitis compared to nasal discharge), geographic distribution, populations sampled (shelter vs. privately owned), detection methods (microbiological culture compared to nucleic acid amplification), and anatomic sampling site. Additionally, most studies to date have examined only a single class of pathogens (i.e. viral or bacterial), pathogens detected by a single detection method (virus isolation or nucleic acid detection), or a single sampling site (nasal, pharyngeal, or ocular), making identification of co-infections compared to primary infection and comparisons across studies difficult. Therefore, our laboratory examined the prevalence of all proven primary pathogens (FCV, FHV-1, Chlamydophila) as well as Mycoplasma species in shelter cats with URTD by both microbiologic culture techniques as well as nucleic acid amplification from two anatomic sampling sites (nasal and pharyngeal).

In most prevalence studies of URTD, including the aforementioned study, FHV-1 emerges as a major pathogen. Feline herpesvirus-1 was first identified as an organism associated with URTD in cats by Crandell et al in 1958 after in vitro culture of nasopharyngeal swabs from both diseased and healthy cats resulted in characteristic cytopathic effects in host feline cells. Primary sites of replication are epithelial cells, as is typical for the α-herpesviruses. These sites in the cat include corneal epithelial cells, conjunctiva, and nasal and pharyngeal epithelium (Gaskell and Povey 1979). The organism is a cause of neonatal death in cats and can be associated with the chronic sequelae of herpetic stromal keratitis (HSK), which is similar to the disease in man (Stiles 2003). Like herpes simplex virus-1 (HSV-1), the causative agent of HSK, FHV-1 is a classic alpha-herpesvirus and as such, readily establishes neuronal latency in the trigeminal ganglia with an incidence of up to 80% (Gaskell et al 1985, Nasisse et al 1992, Ohmura et al 1993) and can cause disease secondary to reactivation (Gaskell and Povey 1977). Latency is associated with transcription of short RNA transcripts termed latency associated transcripts (LAT) in infected neurons in experimentally infected animals (Daheshia et al 1998) and in naturally infected cats (Townsend et al 2004). This makes detection and isolation or removal of carriers difficult. Additionally, the virus is easily spread from cat to cat (Pedersen et al 2004) making spread of the virus from stressed, reactivated carriers to healthy animals in isolation or holding areas of shelters a significant problem. In one shelter study, the prevalence of FHV-1 shedding as detected by virus isolation increased from just 4% at admission to over 50% after just one week of housing at the shelter (Pedersen et al 2004).


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