Chronic rhinitis (Proceedings)
I have always considered this to be one of the more frustrating clinical problems to deal with in feline patients for a number of reasons. Among the key frustrations is a lack of understanding about exactly what this condition represents (i.e. Is there really a causal relationship to some form of infection? is it immune-mediated? Allergic?...). Since it is a diagnosis of exclusion, there is also always a bit of doubt about whether or not I may have missed a primary nasal disease. Lastly, it is difficult to know exactly what the best treatment for any given individual cat will be, and even if we do find a protocol that works for the cat and client, it is very unlikely that we will achieve a "cure".
The goal of this talk is to try to review the available information about chronic rhinitis in cats, and to share my experience and thoughts about diagnosis and treatment, especially in comparison (and sometimes contrast) to what I hear or read from other internists.
What can we say about etiology or pathogenesis?One key point to make is that in this talk I am making a distinction between chronic rhinitis and acute upper respiratory tract infection complex (URTI), at least in terms of clinical presentation and approach to case management. In most cases of acute URTI, there is a clear history of potential exposure to viral or bacterial pathogens, either via contact with other animals or with fomites. In contrast, many cats seem to develop clinical signs of chronic rhinitis without a similar history.
Nonetheless, it is certainly possible that the same respiratory pathogens which cause acute URTI may play a role in development of chronic rhinitis. If this is the case, feline herpesvirus type 1 (FHV-1) seems like the most likely candidate. Approximately 80% of cats infected with this virus will probably become chronic carriers (although many of these cats may be completely asymptomatic). If FHV-1 does have a role in the development of chronic rhinitis, it could be the result of damage to the nasal turbinates incurred during the more severe acute phase of infection or during reactivation of latent infections later in life, or immunosuppression or immunomodulation due to viral persistence. In either case, damage to the normal nasal tissues or modulation of normal immune responses could pave the way for secondary bacterial overgrowth or infection. However, with the high prevalence of FHV-1 in the feline population and the potential for latent infections, it is very difficult to demonstrate any specific causal relationship between the virus and the condition of chronic rhinitis.
Some authors and researchers have also proposed a more primary role for bacteria or by-products of bacterial infection. Again, however, the presence of a substantial bacterial population in the normal nose and the very common development of secondary overgrowth or infection make it very difficult to clarify what role, if any, bacterial might play in the initiation of this disease.
Lastly, there is a possibility that, disease is not related to any primary infectious agent. It is possible that the inflammation observed in these cases is a response to inhaled particulates that act as irritants, toxins, or allergens. I have had a number of cases in which substantial clinical improvement has been achieved simply by removing potential irritants/allergens from the environment. One of the most common offending agents is cigarette smoke, but there are certainly other potential environmental causes as well.