Canine parainfluenza virus (CPIV) is a member of the family Paramyxoviridae, which includes canine distemper virus, simian virus 5 (SV-5), and human measles and mumps viruses. Human, simian, and canine type 2 parainfluenza viruses have all been called SV-5-like viruses because of their close antigenic relationship. Monoclonal antibody studies have shown minor antigenic differences between SV-5 isolates.21 Whether different SV-5 isolates are transmitted among humans, nonhuman primates, and dogs has been questioned. Genome sequence analysis has confirmed such close similarity that a proposal has been made to rename the virus simply parainfluenza virus-5.9 This virus has been associated with central nervous system (CNS) infections in dogs (see Clinical Findings). The virus associated with respiratory disease in dogs is CPIV,7 which causes an acute, self-limiting cough in the syndrome or complex of canine infectious respiratory disease (infectious tracheobronchitis; see Chapter 6) and is recognized worldwide as an important cause of respiratory disease in dogs.2,18 Serologic studies indicate that the overall prevalence of CPIV in the canine population is high but variable. Limited evidence exists that CPIV can produce infection outside the respiratory tract. Experimental inoculation of CPIV in newborn pups can cause viral spread to internal tissues. However, evidence shows that related but distinct paramyxoviruses can cause systemic or nonrespiratory infections in older dogs.11 In addition, parainfluenza virus was consistently isolated from the prostatic fluid of a dog.27 A parainfluenza virus-5 variant was isolated from the cerebrospinal fluid (CSF) of a 7-month-old dog with ataxia and paraparesis lasting 3 to 4 days.12 The dog had been vaccinated against canine distemper at 7.5 weeks of age. Gnotobiotic puppies inoculated intracerebrally with this virus isolate developed two forms of clinical illness.5,6 Some developed acute encephalitis characterized by seizures, myoclonus (involuntary rhythmic muscle contractions), and progressive neurologic signs within a few days after inoculation. Five of six inoculated dogs observed for 6 months after inoculation developed internal hydrocephalus, although clinical signs were not noted at the time. The hydrocephalus was thought to result from ependymitis with decreased absorption of CSF, with or without aqueductal obstruction (see Chapter 82 for additional discussion of this type of hydrocephalus from suspected infectious causes). Seven-week-old seronegative ferrets intracerebrally inoculated with this parainfluenza virus-5 isolate have also been found to develop a self-limiting nonsuppurative ependymitis and choroiditis.4 Subsequent studies3 with this virus isolate identified it as an SV-5 type strain, CPI+, and following inoculation of this strain into a gnotobiotic dog, a second parainfluenza virus, CPI−, was isolated. The latter virus appears to be a mutant strain that evolved in vivo with properties allowing it to persist in the host.3,10 A 6-week-old puppy was found in extremis as a result of acute hemorrhagic enteritis.16 Although a paramyxovirus variant was isolated, it has not been confirmed that it was responsible for the clinical illness. It is uncertain whether the CNS or gastrointestinal forms of disease caused by paramyxovirus variants occur with any frequency under natural circumstances. Neurologic illness has been more commonly recognized as a complication of other paramyxovirus infections, such as with canine distemper in dogs (see Chapter 3) and in humans with measles and mumps viruses (see later). In laboratory rodents, other paramyxoviruses have been shown to produce encephalitis and hydrocephalus that are very similar to those that result when the paramyxoviral variant is injected into dogs. A similar obstructive hydrocephalus and associated periventricular encephalitis was reported in a young fox; however, no infectious cause could be determined.17 Naturally occurring encephalitis, periventriculitis, and hydrocephalus of a suspected bacterial origin have been described in young dogs (see Periventricular Encephalitis, Chapter 82). Paramyxovirus-induced encephalitis or hydrocephalus can be confirmed serologically by the hemagglutination inhibition assay; however, because of the high prevalence of antibody in canine populations and the routine use of a vaccine for CPIV, confirmation requires demonstration of a rising serum antibody titer. CSF antibody titer to the parainfluenza virus 5 variant virus was shown to remain persistently high in dogs after experimental infection.12 Viral isolation can be performed using CSF or brain tissue of infected dogs. In addition, direct fluorescent antibody methods can be used to detect viruses in nervous tissue. For cases of enteritis, virus isolation and electron microcopy of feces would be most valuable. Serologic techniques such as virus neutralization or hemagglutination inhibition must be used to distinguish these variant paramyxoviral strains from CPIV.
Nonrespiratory Paramyxovirus Infections of Dogs
Parainfluenza Virus-5 Infection
Etiology
Clinical Findings
Diagnosis
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