Feline Upper Respiratory Tract Infection

Chapter 152


Feline Upper Respiratory Tract Infection




Feline upper respiratory tract infection (URI) is frequently identified in high-density populations, including those in breeding catteries and animal shelters. This clinical syndrome is inextricably linked to stress, crowding, and poor husbandry. Consequently, adopting effective preventive strategies is essential to combatting this disease in both household pets and large feline populations.



Causes and Primary Agents


Feline URI is a multifactorial disease with a primarily viral origin and secondary bacterial components. Feline herpesvirus type 1 (FHV-1) and feline calicivirus (FCV) cause approximately 80% of all URIs in cats, but the relative importance of each contributing pathogen varies with context. FHV-1 is an antigenically stable DNA virus, whereas FCV is an RNA virus with multiple strains of varying virulence. Both viruses maintain carrier states, both are readily spread by fomites, and droplets can be transmitted up to 5 ft by forceful sneezing.


FHV-1 shedding is closely associated with stress. In the United States, FHV-1 is the principal pathogen causing most shelter-acquired URIs, and once infected, most cats develop latent chronic infections. In one study, the percentage of cats shedding FHV-1 increased from 4% of cats on day 1 to more than 50% on day 7 of their shelter stay (Pedersen et al, 2004). Accordingly, cats are most commonly diagnosed with URI during their second week in a shelter. Intermittent shedding occurs after stress-induced reactivation of FHV-1. URI signs are manifest during recrudescence in 50% of cats.


In contrast, FCV shedding is not linked to stress and has greater prevalence in long-term sanctuaries and large, stable populations, including hoarding situations. One recent study documented the prevalence of FCV in long-term sanctuary cats with and without clinical signs to be more than double that in shelter cats with and without clinical signs (McManus et al, 2011). The relative importance of FCV in sanctuary settings is likely due in part to dissemination of multiple mutating strains in a constant population.


Less commonly, the bacterial agents Chlamydophila felis, Bordetella bronchiseptica, Mycoplasma spp., and Streptococcus canis have been implicated in primary disease. Respiratory pathogens have a synergistic effect, and there is increased likelihood that cats harbor multiple pathogens when clinically ill. However, all pathogens associated with URI have been isolated from both healthy and clinically affected cats, so identification of a microorganism does not necessarily implicate it as the primary cause of illness.



Risk Factors


Any factor that elicits stress has the potential cause clinical signs of URI by reactivating latent feline herpesvirus. For the household pet, the addition of a new animal, a recent move, or a trip to the veterinarian could be enough to cause recrudescence.


For cats entering animal shelters, the cumulative effect of many stressors compounded with a new environment, can lead to viral shedding. A cat’s length of stay, or time spent in the shelter, is directly linked to development of URI, and, conversely, development of URI leads to increased lengths of stay. Crowded conditions, poor housing, loud noises, and new foods make cats more susceptible to illness. Notably, the single-compartment feline cages commonly used in shelters are directly linked to stress and, by extension, illness (Kessler and Turner, 1999). These housing units provide insufficient floor space, which limits a cat’s ability to exhibit normal feline behaviors (e.g., stretching, hiding, grooming), and lack sufficient separation of bedding, food, and litter.


Cats in animal hoarding situations often manifest clinical signs of feline URI. When multiple cats from a single household are diagnosed with severe or chronic URI over an extended period, the clinician should obtain a thorough history and evaluate the housing environment.



Clinical Signs


The magnitude of evidenced clinical signs depends on the immune status of the cat, the specific pathogens or strains involved, infecting dose, presence of coinfections, and the environment. A list of clinical signs associated with the most common URI pathogens is provided in Table 152-1. The organisms listed in this table can cause overlapping clinical signs. Thus a particular clinical manifestation does not implicate a specific pathogen as the cause of disease. Synergism among pathogens may lead to more severe clinical signs in cats harboring multiple pathogens.




Diagnosis


The diagnosis of acute feline URI is based on clinical signs often coupled to a triggering event. Diagnostic testing is warranted in individual cats, in cases of chronic disease, and in populations in which disease manifestations are unusually severe or frequent. It is important to consider noninfectious differential diagnoses for URI signs, including neoplasia, inflammatory polyp, foreign body, trauma, cleft palate, chronic rhinosinusitis, oronasal fistula, and fungal infection. Preexisting immunosuppression caused by feline leukemia virus or feline immunodeficiency virus infection should be considered in previously untested cats. It is also emphasized that although viral or bacterial culture or DNA detection can be used to confirm the presence of a potential pathogen, a positive test result does not confirm causality. Additionally, oculonasal or oropharyngeal swabs submitted for sampling are likely to contain some normal flora.


Real-time polymerase chain reaction (RT-PCR) is one test used to evaluate potential infectious primary causes of URI. However, RT-PCR results must be interpreted with caution, especially in individual cases. Currently, a positive PCR test result cannot distinguish between the inciting cause of disease, commensals, and vaccine strains. In the future, quantitative RT-PCR tests may be available to differentiate acute infection from carrier states. A negative test result helps rule out an acute infection with a particular infective agent but not a carrier state, because shedding can be sporadic.


In group settings, sampling a minimum of 5 to 10 affected cats or 10% of the population early in the course of disease should be considered. Positive test results should be interpreted in the context of the expected prevalence of the organism in that population. In severe outbreaks, in which cats are euthanized or are dying from disease, histopathologic analysis and necropsy should be performed to determine the underlying cause and guide risk assessment. Monitoring of disease prevalence, incidence, duration, and severity is critical for assessing the success of URI control measures. These data also provide a baseline for comparison. In this manner, URI incidence, prevalence, and rates serve as overall indicators of the welfare of a cat population (Hurley, 2004).

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Jul 18, 2016 | Posted by in PHARMACOLOGY, TOXICOLOGY & THERAPEUTICS | Comments Off on Feline Upper Respiratory Tract Infection
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