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Canine Distemper Virus
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Clinical Signs

The clinical findings vary depending on the virulence of the virus, on host immune system factors, and possible secondary bacterial infections.  Most infected animals remain sub-clinical but some become listless, have decreased appetite, fever, upper respiratory tract infections, nasal discharge, cough, vomiting, diarrhea, tenesmus, skin-pustules, hyperkeratosis of foot pads and/or planum nasale, and conjunctivitis (Greene, 2006).  Young puppies infected can have enamel hypoplasia with pits and possible exposure of the dentin (Greene, 2006).  Some strains cause optic neuritis and resultant sudden onset blindness (Greene, 2006). Neuropathy is also a finding in some CDV infections (Murphy et al., 1999).  Individual infections can have any multitude of the above listed signs.

Skin Lesions
Rarely in puppies there is vesicular and pustular dermatitis (Greene, 2006).

Hyperkeratosis 

Hyperkeratosis of the nasal plate and the footpads is often associated with neurological strains of the virus (Greene, 2006).  During the period of immunosuppression CDV spreads to keratinocytes, and by an unknown mechanism, stimulates epidermal proliferation.  This form of the disease is often referred to as “hard pad disease” due to the hard, thickened skin of the footpads (Engelhardt et al., 2005).

minkhardpad
(Picture courtesy of Dr. Wobeser, WCVM, Pathology)

CNS

Neurological signs
-localized involuntary twitching
-paresis or paralysis – most noted in the hind limbs
-ataxia
-convulsions “chewing-gum fits” characterized by salivation and chewing movements.  May have more sever symptoms such as paddling, involuntary urination and defication to grand mal seizures (Merck, 2005)

-postmortem-may see meningeal congestion, ventricular dilation, brain edema and possible necrosis with cavitation in the white matter(Greene, 2006).

Neuropathogenesis
 As the disease progresses the virus can infect the central nervous system.  CNS infection occurs during a viral induced immunosuppression when lymphoid tissues are being destroyed (Vandevelde and Zurbriggen, 1995).  At approximately ten days post infection the virus spreads to epithelial cells and/or the CNS.  Presumably, viral entry to the CNS is via viral infected immune cells (Vandeveld and Zurbriggen, 1995).  Demyelinating strains of CDV lead to grey matter and white matter lesions.  There is progressive neuronal demyelination, necrosis, and potentially polioencephalomalacia (Vandeveld and Zurbriggen, 1995).  CNS disease occurs by two mechanisms, acute disease and chronic demyelination.   There are many forms of this virus and thus varying pathogenesis.

 Acute infection occurs approximately three weeks post exposure and results in non-inflammatory disease.  CDV replicates in the glial cells, most commonly in the astrocytes and least commonly in the oligodendrocytes.  It is believed that demyelination is the result of CDV’s effect directly on oligodendrocyte metabolism or results because of viral induced changes in surrounding cells (Vandelvelde and Zurbriggen, 1995).  By three weeks post infection, acutely infected dogs have either fully recovered or have succumbed to the disease (Appel and Summers, 1999).

 Dogs infected with the chronic form suffer progressive demyelination and damaging immunopathologic reactions.  Damage to the CNS is largely attributed to the effects of the activated macrophages.  The activated macrophages release free radicals that damage tissue, vessels, and are procoagulative (Vandeveld and Zurbriggen, 1995).  Oligodendrocytes are rich in iron and are thus at increased risk of free radical damage.  There is perivascular cuffing around brain lesions and a progressive inflammatory response.  In chronically infected cases terminal disease may be delayed up to three months (Appel and Summers, 1999).

Another rare form of CDV associated neurologic disease is "Old Dog Encephalitis".  With this form of the desease seemingly recovered dogs have a reoccurance of disease and clinical neurological sings.  Signs way occure months or years after initial infection.  The pathophysiology of this form of the disease is not well understood (Murphy, et al., 1999).

Gastrointestinal Signs
Catarral enteritis is common in infected puppies.  Anorexia is followed by vomiting and diarrhea often develops.  The diarrhea may be fluid or may contain blood and mucus.  Severe dehydration from not drinking and from diarrhea and vomiting can result.  Rarely intussussception can occur from excessive straining to defecate (Greene, 2006).

Respiratory
Upper respiratory tract lisions include rhinitis, and bronchitis.  Initially there may be an interstitial pneumonia but there could be a bronchoalveolar pattern if there is secondary bacterial infection (Greene, 2006).

pneumonia
Radiograph of an interstitial pneumonia pattern.
Picture source: click here

Enamal Hypoplasia
Young puppies infected before eruption of permanent dentition may have pitted areas of enamal hypoplasia.  The presense of enamal hypoplasia in adult animals is almost pathognomonic for previous CDV infection (Greene, 2006).  Animals infected with CDV after eruption of their permanent dentition will not have enamal hypoplasia.

enamelhypoplasia
Picture source: click here

Ocular Signs
The virus can cause conjunctivitis and can effect the optic nerve and cause an optic neuritis and sudden onset blindness (Greene, 2006).  The pupils will be dialated and unresponsive if there is necrosis of the retina there will be gray-to-pink irregularities on the fundus of the eye (Greene, 2006).  Chronic leasions are associated with retinal atropy and scarring.

eyes
Bilateral conjunctivitis and ocular discharge in a raccoon.
(Picture courtesy of Dr. Wobeser, WCVM, Pathology)

Other Species Affected
(click on the images below)

felidae
hyaenidae mustelidae Procyonidae ursidae viverridae
FELIDAE
HYAENIDAE
MUSTELIDAE
PROCYONIDAE
URSIDAE
VIVERRIDAE