Canine Distemper: infectious Etiology, Diagnosis and intervention
Rachna Poonia1, Durga Devi2
Email: rachnapoonia247@gmail.com
Introduction
Canine distemper also known Hard pad disease, Carre’s disease.Canine distemper is a highly contagious virus caused by the paramyxovirus. It is seen in dogs around the world, but it can also affect ferrets, racoons, skunks, grey foxes, and many other animals.
Etiology
Genus- Morbillivirus, Paramyxoviridae family, Non-segmented,single-stranded ,RNA genome
Lipoprotein-enveloped virus, Pantropic in nature 8 different genotypes Snyder Hill, A75/17, and R252 and strains are highly virulent and neurotropic.
Geographically distinct lineages of the canine distemper virus are genetically diverse. This diversity arises from mutation, and when two genetically distinct viruses infect the same cell, from homologous recombination.
Hosts
Dogs are the principal host for CDV, and they likely act as reservoirs of infection for wildlife. Eight of the 11 families of carnivores have been reported to be susceptible to canine distemper.
Zoonoses
Inapparent, self-limiting infections, occur in humans by parenteral inoculation of virulent CDV. Paget’s disease, an inflammatory bone disorder in humans, might be related to CDV acquired from exposure to dogs.
Epidemiology
The prevalence of canine distemper in the community has decreased dramatically due to the availability of vaccinations. However, the disease continues to spread among unvaccinated populations, such as those in animal shelters and pet stores. This provides a great threat to both the rural and urban communities throughout the United States, affecting both shelter and domestic canines. Outbreaks of canine distemper continue to occur throughout the United States and elsewhere and are caused by many factors, including proximity to wild animals and lack of vaccinated animals. This problem is even greater within areas such as Arizona, owing to the vast amount of rural land. An unaccountable number of strays that lack vaccinations reside in these areas, so they are more susceptible to diseases such as canine distemper. A mortality rate is up to 77% in dogs. (Weilley et al.,2016).
Transmission
Transmitted by aerosol or droplet exposure originating from respiratory exudates. Urine and other secretions also contain infectious virus. Viral shedding may follow infection for 60–90 days. Transplacental infection can occur in domestic dog.Virus is short-lived in the environment, but it can survive at lower temperatures e.g., 48 hr at 250 C and 14 days at 5 0 C (shen et al., 1980).
Clinical signs
It is estimated that 25 to 75% of the infections occur as subclinical infections.
Incubation period – 3-6 days. Initial transient fever after few days of infection followed by second stage of fever 8-9 days after infection with subsequent respiratory,GIT , CNS and cutaneous involvement. Lethargy, anorexia,Initially serous oculonasal discharge, conjuctivitis, non productive cough. Secondary bacterial infections resulting bacterial bronchopneumonia, dyspnea, mucopurulent discharge. Severe fatal pneumonia, without other signs, has been reported in neonatal infected pups.
Viral destruction of gastrointestinal tract can result in inappetance, vomiting, diarrhea, electrolyte imbalance, and dehydration. In nervous form signs are hyperesthesia, vocalization, seizures :chewing gum seizures is the classic sign.but tonic clonic seizures and status epilepticus can also occur vestibular signs like head tilt, nystagmus,strabismus,circling paraparesis or tetraparesis with ataxia.
Myoclonus : most commonly of masticator and temporal muscles, although limbs and other muscle group can be affected. Myoclonus often continues with activity, rest, sleep, or with light anesthesia. During rest and sleep, the frequency and severity of the myoclonus lessens.
Occular signs
Optic neuritis: sudden onset of blindness, dilated unresponsive pupils. Retinal detachment, chorioretinitis, uveitis.
Cutaneous lesions
Vesicular and pustular dermatitis in puppies. Rarely associated with neurologic complications, this is usually a favorable prognostic sign. Nasal and digital hyperkeratosis. It appears in late stages of clinical disease.Usually assosiated with various neurologic complications. Naso-digital keratosis is reported to occur in about 8% of cases with neurological disease.
Post-mortem findings
Thymic atrophy in infected pups. Hyperkeratosis of the nose and footpads, bronchopneumonia, enteritis, and skin pustules, Intracytoplasmic and intranuclear viral inclusions in epithelial cells of the skin, gastrointestinal tract, lung, renal pelvis, urinary bladder, central nervous system (CNS), and eye, depending on the stage and severity of infection.
Diagnosis
Virus isolation, serological tests, PCR, cytological demonstration of CDV inclusion bodies, Immunochromatographic assay, Immunohistochemistry, Immunocytology
Differential diagnosis
Leptospirosis
Canine infectious hepatitis
Canine infectious respiratory disease complex
(Kennel Cough)
Intoxicants such as lead or organophosphates can
cause simultaneous GI and neurologic signs
Rocky Mountain spotted
Treatment
There is no cure for canine distemper, but your vet can recommend supportive care and symptom treatment.
Some treatments for canine distemper may include:
- Broad-spectrum antibiotics
- Pain relievers
- Seizure medications
- Electrolytes
- IV nutrition
- Ascorbic acid I.V. have immunomodulator and antioxidant
- Vita A also play an important role for the treatment of canine distemper in ferrets but mechanism is still unknown.
- Survival rates are higher in dogs treated with anti canine distemper antibodies (0.4 ml/kgIV,IM,SC)
- Few antiviral drugs have been tested invitro for CD like Ribavarin,5-ethynyl-1-beta-d ribofuranosylimidazole-4-carboxamide and proanthocyanidin
- Seizures control require diazepam, phenobarbital, or potassium bromide.
- Variable or temporary success in halting neurologic signs can result from a single anti-CNS edema dose (2.2 mg/kg, given intravenously [IV]) of dexamethasone
Prevention
Modified live vaccines have proved very effective. Recombinant vaccine-eg canary pox vectored recombinant vaccine that expresses H and F protiens, rabies virus recombinant vaccine . Primary vaccination should be done at age of 6 to 8weeks,with repeat vaccination at every 3-4 week until 16 week of age. Revaccination (booster) at either 6 months or 1 year of age, then every 3 years.
Vaccine strains –Onderstepoort, Lederle, Rockbor
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