UPPER RESPIRATORY INFECTION IN CATS Dr. Max Rust WHAT IS IT? Although many causes of upper respiratory symptoms in cats have been identified, we are most concerned with three infectious agents: Feline Herpesvirus, Type I (FHV-I), Feline Calicivirus (FCV), and Feline Chlamydia (Chlamydia psittaci). All three are known to have a prolonged and sometimes asymptomatic carrier state that makes control a difficult proposition. FHV-I generally produces the most severe disease (Feline Viral Rhinotracheitis) in susceptible cats, and many infected become lifelong carriers, shedding virus after "stressful" events - and often without overt upper respiratory signs. Symptoms of acute FHV-I infection often include profuse ocular and nasal discharge, bouts of sneezing, and small ulcers in the eyes and mouth. Eight to ten week old kittens are most severely affected. At this age their maternal antibody protection has faded and they are often exposed to stress induced viral shedding from their mothers. For this reason we see outbreaks most often in the spring and summer. Although Feline Calicivirus tends to be less severe, pathogenicity varies with the strain of virus; some being nonpathogenic, others tending to cause oral ulcers, and still others that tend to cause pneumonia, with up to 30% mortality in young kittens. Chlamydia is an intra- cellular bacterium that causes chronic conjunctivitis and occasional mild rhinitis (nasal infection). There is no direct evidence that feline strains cause infection in humans, but at least minimal precautions would seem prudent in cases where the Chlamydial agent has been identified. HOW DO THEY GET IT? Direct contact with oculonasal secretions is the most likley mode of transmission and aerosolized droplet nuclei from sneezing episodes during acute infections greatly amplifies the spread. As mentioned, the chronic carrier state is very important in the spread of Feline URD. Shedding of FHV-I tends to occur following stress to the carrier and symptoms may or may not be apparent. Cats infected with FCV tend to shed continuously for a variable period that ends abruptly. The number of carriers, after an outbreak, diminishes logarithmically with time, and a few can continue as carriers for life. In one study, 80% of the cats with chronic stomatitis (infection of the mouth) had positive swabs for FCV, while none of the healthy cats did. Cats with untreated Chlamydia tend to remain carriers for months after being infected by direct contact with eye or nasal secretions from carriers or those with active infection. HOW DO YOU TREAT IT? In many cases no treatment is warranted as symptoms are mild and transient. Others may need prolonged nursing and vigorous inter- vention to treat dehydration, malnourishment, and opportunistic bacterial infections. Ulcerations of the mouth and tongue are common with FCV and ulcer- ations and bone lesions of the nasal turbinates are often seen with FHV-I. In either case, weeks of convalescence and ongoing nursing care may be needed. Kittens 8-10 weeks old may sometimes die acutely from interstitial pneumonia or overwhelming sepsis from immune suppression. Tetracycline or chloramphenicol ointments are generally prescribed for Chlamydia infections. Refractory cases may require 4-6 weeks of oral antibiotics as well. IS THERE ANYTHING ELSE I SHOULD KNOW? Early vaccination is important in pre- venting the more severe symptoms of URD in cats. There is now evidence that the use of the intranasal vaccine can prevent the development of chronic carriers with FHV-I, if administered at least 5-7 days prior to exposure, and will reduce the severity of symptoms if given only 24 hours before viral contact. In fact, it is generally conceded that vaccines, whether parenteral (injected) or intranasal, only reduce the symptoms of URD, but do not prevent acute infection. CANINE DISTEMPER Dr. Max Rust WHAT IS IT? Canine Distemper is a disease of wild and domestic canines, as well as some other species (e.g., ferrets & raccoons). In domestic dogs there are three forms: (1) The ACUTE form is characterized by coughing, vomiting, diarrhea, and loss of appetite. Mucopurulent oculonasal discharge usually progresses to pneumonia. This stage is often fatal, especially without treatment. Some dogs under treatment appear to recover only to develop subacute or chronic forms of the disease later. (2) There are two SUBACUTE forms: the Neurotropic form, characterized by variable nervous system signs such as blindness, anosmia (loss of smell), "chewing gum fits" and myoclonus (rhythmic involuntary muscle contractions), occuring weeks to months after the acute phase. The Viscerotropic form affects the digestive system, causing chronic debilitation. It is often fatal but rarely causes nervous symptoms. (3) CHRONIC distemper is also recognized in two forms: Multifocal Encephalitis, a slowly progressing paralysis with intermittent plateaus and varying other symptoms such as blindness and facial paralysis. Diffuse, Sclerosing Encephalitis or "Old Dog Encephalitis," characterized by seizures, circling, head pressing, and changes in cognitive and personality traits. HOW DO THEY GET IT? The agent that causes canine distemper is a Morbillivirus, closely related to bovine Rhinderpest and human Measles viruses. In fact, a form of human measles is used, in modified form, to vaccinate puppies for distemper. After replicating in local lymphoid tissues, the virus is spread via droplet nuclei that can carry it in the air for considerable distances from a cough or sneeze, whence it can contact the mucous membranes of susceptible animals. Because of this, distemper virus is highly contagious amoung susceptible populations. Studies have shown that epizootics (animal epidemics) continue to spread even when 95% of a population is immune; with most other viruses, e.g., canine parvovirus, epizootic spread ceases when 70% or more of the population becomes immune. Control of outbreaks is particularly difficult in animal shelters taking in large numbers of stray dogs and housing them in enclosed kennel areas. Symptoms of Acute CDV are seen at 10-14 days, post exposure. The virus has a preference for lymphoid and epithelial tissues. Virtually all of the symptoms are caused either by immunosuppression or immunostimulation. The respiratory and intestinal symptoms are a result of immunosuppression, allowing opportunist bacteria to overgrow, damaging the epithelial lining of the GI and respiratory tracts. The nervous symptoms are the result of immunostimulation by viral replication in nerve cells. The action of macrophages (a type of white blood cell) then damages nerve cells in the process of eliminating the virus. HOW DO YOU TREAT IT? There is no treatment regimen that is recognized as routinely effective. Antibiotics and immune stimulant measures are often helpful in eliminating respiratory symptoms, but have little or no effect on the subacute or chronic phases. Here, immunosuppressive drugs that might spare neuronal damage also spare the replicating virus. There is speculation that oxygen free radicals released by the immune system are largely responsible for nerve damage. This may be a rationale for the use of antioxidants such as vitamins C & E, superoxide dismutase, and other free radical scavenging antioxidants, which some practitioners use as an adjunctive treatment. No convincing proof exists that any of these measures have an effect. The late onset and refractory symptoms of subacute and chronic CDV and the high degree of transmissability make for much angst and frustration amoung practitioners, especially in treating young dogs coming from shelters or as strays. Dogs and puppies under treatment may appear to make a complete recovery only to develop neurologic symptoms weeks later. IS THERE ANYTHING ELSE I SHOULD KNOW? Only immunoprophylaxis (vaccination) has a proven, beneficial effect in combating the ravages of this virus in dogs. Puppies should be started on proper vaccine programs by 8 weeks of age. A combination of measles and canine distemper is most effective between the ages of 6 to 12 weeks. Thereafter, polyvalent adult vaccine may be given; the adult booster coming at 20-22 weeks of age. Adult immunity from vaccination is thought to last at least one year, and some studies have indicated that 75% of healthy vaccinates are still protected after three years without challenge. Since one in four loose their immunity in as little time as one year, it is still recommended that most dogs receive annual booster vaccinations.