| Canine Distemper Virus Disease – A Review |
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| Written by Administrator | |
| Sunday, 04 February 2007 | |
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Introduction to this article At first my intention was just to add content to this site. The article has increased in scope when I reviewed some of the literature and realized that despite being a practicing veterinary surgeon for 35yrs things change, knowledge changes and we start taking our knowledge for granted. Distemper as a word derives archaically; prefix ‘Dis-’ = ‘un’ or ‘not’ or a ‘negator’ as in dysfunction as a loss or change of function and ‘Temper’ as a ‘state’ or state of being or ‘wellness’ . Also consider ‘Temper’ as a hardened state of metal ‘state of temper’ and ‘intemperate’ with connotations of change of state/drunk or less able to function. Therefore the chosen word suits the diversity of clinical signs with which Distemper can present particularly those related to neurological and joint changes. Or simply put the patient feels crap – fever, headache, joint pain, dehydrated – quite apart from the visible symptoms and then later the neurological damage. Whilst on the derivation of this term I take the opportunity to criticize it’s use for other illnesses just as a term for severe illness as in ‘Cat Distemper’ – usually referring to feline panleukopaenia – an entirely unrelated virus. The profession has a responsibility to avoid misleading the public and ourselves by sloppy or colloquial usage. The Canine Distemper Virus (CDV) This is an RNA virus, from Genus: Morbillivirus Family: Paramyxovirus Order: Mononegavirales in a Group: Group V ((-)ssRNA). The genus includes measles, distemper and rinderpest and so closely related that I recall being taught that Human Measles vaccines will protect dogs against CDV and indeed CDV can protect against Rinderpest but probably not in the reverse sequence. And so closely related that mixing nuclear material from one member of the genus with capsules of another will allow the virus to rebuild. It was demonstrated as early as the 1950’s that human blood contained neutralizing proteins for CDV and the immunological relationship between these three morbilliviruses was identified 1960 (link) Virus structure is described as a single strand RNA enveloped to pleomorphic, spherical and filamentous forms 150-300nm diameter. (link) and RNA viruses have a high mutability which explains the species variations that sub-types of CDV have affected. Quite large as viruses go hence the possibility of diagnosis by viral inclusion bodies The virus is unstable outside the host, susceptible to lipid solvents and most disinfectants – easy to kill, difficult to treat and no specific cure. Families affected by Distemper Virus include Canidae (dogs, foxes), Procyonidea (includes raccoons and pandas), Mustelidae (ferrets, weasels, polecats), Mephitidae, (skunks and stink badgers) , some Felidae but not domestic cats (tigers, lions, leopards), Viveridae (Binturong - civets), Cetacea (whales, dolphins) Phocidae (seals) Distribution and signs CDV is found worldwide. However the incidence and severity will depend on prevailing subtypes and vaccinal population. My own Practice’s catchment area rarely sees CDV. Indeed this is almost to the point where there is risk of missing disease in it’s early stages as being unexpected and is not helped by the variety of presentations of signs. CDV vaccination remains the mainstay of prevention and control but that reduces incidence (of course) and may lead to complacency and an assumption that CDV is eradicated within any limited area. Those cases I have seen personally have been limited to mucopurulent coryzas (coryza = discharge from eyes and nose) deteriorating to pneumonic states with associated neurological signs. I have never seen the presentation of hardpad distemper. We also recognize the association with old dog encephalitis (ODE) and those patients which present with limited neurological signs but nevertheless test positive for CDV. Classic CDV mostly affects young dogs, particularly pre-vaccination or immunosuppressed or stressed, unvaccinated older dogs and then the ODE syndrome. Clinical signs can be highly variable. Usually a 10-14 day incubation or latent period followed by fever (which often goes unnoticed) then loss of appetite and mild conjunctivitis. The virus is lymphotrophic and spreads to nearby lymph nodes after initial inhalation. Replication here is followed by rapid spread through lymphatics and affects all lymphatic tissue in 2-5 days. Then viraemic from days 6-9 with a predisposition for epithelial and nervous tissues. The immunosuppression from lymphatic invasion explains the profound secondary infections that take advantage so the early signs progress with mucopuruent nasal and ocular discharges, diarrhoeas, pneumonia, bronchopneumonia and vomiting . Demyelination of neurological tissues and progression in ocular signs from conjunctivitis to keratoconjunctivitis and chorioretinitis and optic neuritis. Encephalomyelitis with classic perivascular cuffing and demyelination with variable signs from depression, weakness, paresis or paralysis, hyperaesthesia, ataxia, myoclonus and the classic rhythmic choreic twitches (usually seen late in disease or persisting after recovery). Seizures. One site I visited mentioned in utero infection as rare but possible (URL lost) with reported abortion or persistent infection in normal looking pups. That seems unlikely to me given the nature of usual rapid progression and would imply (to me) that there was ‘almost but not quite enough’ maternal antibody to give some control. And delay signs. Importantly, (link) discusses parvovirus infection in puppies recovered from CDV. When I was student we were given the following statistics: That 50% of patients contracting CDV would recover without treatment that 50% of those that wouldn’t recover thus would recover with treatment but with residual neurological signs and that left a mortality rate overall of 25%. I can’t find current statistics but the implication of my reading is that mortality rate is higher. That may reflect outbreaks predominating in unvaccinated areas (which implies poverty) with little therapy or paradoxically may reflect outbreaks of more virulent strains or standard strains in areas where vaccination has reduced wild or street virus ‘boosting’ vaccinations that have now lapsed (complacency). It may also reflect the development of vaccines with less shedding – where in the past the patient would have vaccinated in-contacts. Old dog encephalitis(ODE) is usually meant to infer adult infection with CVD and a bypass of visceral immunity to predominantly neurological signs. It therefore may present as any of those changes from seizure disorders to chorea. The texts claim this as a progressive, poorly responsive, disorder usually culminating in euthanasia. Without classic and progressive signs this can be difficult to diagnose. Simultaneous serum and cerebrospinal fluid (CSF) samples may show a disparity in CSF titres but will only demonstrate CDV in some 50% of patients affected. This form is not infectious to other dogs and reflects a chronic inflammatory process. Patients that apparently recover from the systemic form of CDV after a progession from initial clinical signs of some 10-14 days may demonstrate neurological signs ..often weeks to months later. The ‘hard pad’ form of CDV or hyperkeratosis of footpads and nasal planum is a late stage progression in apparently recovered animals This reflects accumulation of CDV in the stratum spinosum (link) Texts also refer to ‘distemper teeth’ but my own view is that that should be shlved as terminology. The patchy decalcification seen on secondary dentition (as I understand it) is a reflection of any febrile disorder during tooth bud formation – not specifically CDV. Further complications include the potential for immune mediated joint disease in recovered dogs. And the potential for that form of immune response may be part of the concern for autoimmune disease triggers with CDV vaccination? Finally there is an age related cardiomyopathy potential for CDV (link) Diagnosis Diagnosis is problematic. The variety of early presentations, particularly with mucopurulent coryza being a common finding in very severe bordatella infections, means that clinicians may not justify the cost of intensive testing for CDV and choose to wait (particularly in areas of low incidence). That may mean that CDV is only diagnosed when the progression becomes virtually pathognomonic i.e. late stage. Diagnostic tests include demonstrating inclusion bodies, typically in conjunctival scrapings, or time consuming laboratory work – virus neutralization, ELISA, etc (link) Post mortem diagnosis is more likely to show classic histopathological lesions in target tissues (link) I recall one patient with recurrent neurological signs, depression, headache manifestations, ataxia that spontaneously resolved and recurred at two wek intervals over three cycles before the owner elected euthanasia. Brain tissue submitted for histopathology showed areas of perivsacular cuffing on th surface convolutions of the brain with three distinct ages of progression. To me that implied repetitive partially successful immune responses. Treatment Conventional treatment is supportive and antibiotic therapy for the secondary infections. As far as I am aware there is no hyperimmune serum available UK although this was around when I was a younger vet but usually used as an immediate protection for in-contact animals prior to vaccination. I did try using it as therapy in one dog and also tried treating another pup with plasma from its unaffected dam. Neither patient was cured although the pup did survive for a very protracted illness (coincidence?). I have lost the link but did find a Korean pharmaceutical firm offering both hyperimmune serum or whole plasma as agents. Presumably large amounts may be more beneficial and I equally assume there is a potential for separation of immune globulins to concentrate sera effectively. I found nothing specific to indicate response rates. Prevention Prevention is still based in vaccination and isolation. To my knowledge all UK vaccines are live modified vaccine and no UK recombinant vaccine (link). UK vaccines are either from the Onderspoort strain or Rockborne strains. Intervet’s datasheet claims that its vaccine can be used safely in pregnant bitches previously vaccinated with the Onderspoort strain (link). Their datasheet also claims that where there is no interference with maternally derived antibodies immunity is achieved 1 week after vaccination. However we know that maternal antibody is variable and whilst early vaccination from 6weeks is advised in risk situations a final dose is recommended from 10weeks. Historically there was an option to use Measles vaccine at a young age to bypass maternal antibodies with the paradox that pups vaccinated thus would then pass maternal antibody to Measles to their offspring. Adverse reactions to vaccination The Veterinary products Committee (VPC) UK (link) Page 65 reports an incidence of serious adverse reactions in dog vaccines at 0.5 per 10,000 but I couldn’t find a clear indication of which component(s) may be involved. There are now reports of Vaccine Associated Sarcomas (probably better called Injection Site Sarcomas) in dogs as well as cats but with a much lower incidence in dogs. In cats the incidence is reportedly higher with adjuvenated vaccines but while Merial’s Felv vaccine is adjuvenated their Recombinant distemper vaccine (Purevax) isn’t. (link). This is based on a canary pox virus with distemper antigens spliced and is targeted at the market for those species too susceptible to CDV for conventional live virus vaccine (ferrets, exotic carnivores). I found evidence of this vaccine being available in combination with the usual components for dog use. However the only datasheet I could find for Recombitek (link) clearly states it contains canine distemper virus and no comment about adjuvents. link1 http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=223010 No. 2 : in india it it is not affordable to treat dog in leter stage
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'>  Submitted by shailesh2402 • 2008-03-09 08:44:01 No. 1 : atleast in india we cannot think about treating with plasma |
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| Last Updated ( Sunday, 04 February 2007 ) |
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