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canine core vaccines
• Canine Rabies Virus
• Canine Distemper (CDV)
• Canine Parvovirus (CPV)
• Canine Adenovirus-2 (CAV-2)
• Canine Parainfluenza # (CPiV)
• Leptospira #
→ *protection from CAV-1 (Viral Hepatitis) is provided by parenterally administered CAV-2 vaccine (Tracheobronchitis)
→ # Risk evaluation
puppy vaccinations (<16 wks)
one dose of vaccine containing modified live virus (attenuated) CPV, CDV, and CAV-2 is recommended every 3-4 wks from 6-8 wks of age, with the final booster being given no sooner than 16 wks of age
vaccines in dogs older than 16 wks of age
• two doses of vaccine containing modified live virus (attenuated) CPV, CDV, and CAV-2 given 3-4 wks apart are recommended.
• After a booster at 6 months to 1 year, revaccination is recommended every 3 years thereafter, ideally using a product approved for 3-year administration, unless special circumstances that warrant more frequent revaccination
canine parvovirus (CPV)
• Highly contagious virus: acute, infectious GI illness, young dogs; Rottweilers, Doberman Pinschers, American Pit Bull Terriers, English Springer Spaniels, German Shepherds: increased risk of disease
• Assuming sufficient colostrum ingestion, puppies born to a dam with CPV-ABs are protected from infection for the first few weeks of life; susceptibility to infection increases as MDA wanes. Stress (weaning), concurrent intestinal parasitism, or enteric pathogen infection (Giardia spp): more severe clinical illness
canine parvovirus spread
• Virus is shed in feces of infected dogs within 4–5 days of exposure (often before clinical signs develop), throughout the period of illness, and for ~10 days after clinical recovery.
• The virus affects GI tracts: spread by direct dog-to-dog contact, contaminated stool, environment (fomites/surfaces), people (clothes, shoes).
• Resistant to heat, cold, humidity, drying; it can survive in the environment for long periods of time.
• Due to the highly contagious nature infected dogs must be isolated in order to prevent the spread of the infection
canine parvovirus replication
• Viral replication initially: oropharynx lymphoid tissue → hematogenous dissemination.
• Target: rapidly dividing cells small-intestinal crypt epithelium, lymphopoietic tissue, bone marrow → epithelial necrosis, villous atrophy, impaired absorptive capacity → disrupted gut barrier function (bacterial translocation and bacteremia).
• Lymphopenia and neutropenia: WHY?
parvovirus signs
• Signs: lethargy, loss of appetite, fever, vomiting, severe, often bloody, smelling, diarrhea (enteritis).
• Vomiting and diarrhea: rapid dehydration, and most deaths from parvovirus occur within 48 to 72 hours following the onset of signs
parvo in utero
Infection in utero or in pups <8 weeks old or born to unvaccinated dams without naturally occurring antibodies can result in myocardial infection, necrosis, and myocarditis (pale streaks in the myocardium): heart failure
parvo testing
• Commercial kits for detection of AG in feces are available; good to excellent sensitivity and specificity.
• All animals with relevant clinical signs should be immediately tested: appropriate isolation.
• False-negative results: early in the course of the disease (before peak viral shedding), because of the dilutional effect of large volume diarrhea, or after the rapid decline in viral shedding (within 10-12 days of infection)
parvo disinfection
• All parvoviruses (dogs and cats) remain infectious for at least a year in contaminated cages, kennels, rugs, towels, grass, soil, etc.
• Thorough disinfection (e.g., sodium hypochlorite [bleach] solution) is necessary before new animals are admitted to the locations. When soil, grass, rugs, are contaminated, disinfectant is often not effective or cannot be used
canine distemper (CDV)
• Highly contagious; genus Morbillivirus (measles), family Paramyxoviridae.
• Virus sensitive to lipid solvents (e.g., ether), most disinfectants (phenols, quaternary ammonium compounds); relatively unstable outside the host.
• Virus is shed in all body secretions acutely infected animals: direct contact, aerosol, respiratory droplet exposure.
• Some infected dogs may shed virus for several months
• Hyperkeratosis of the nose and footpads in dogs with neurologic manifestations: “hard pad disease”
• The distemper virus attacks “epithelial cells.” In puppyhood the buds of the permanent teeth are still developing (from epithelial cells); the adult teeth stained and pitted enamel: “enamel hypoplasia”
distemper replication
• Virus initially replicates: lymphatic tissue respiratory tract → viremia → infection of all lymphatic tissues → respiratory, GI, urogenital epithelium, CNS, optic nerves; disease follows virus replication in these tissues. The degree of viremia/extent of viral spread to various tissues is moderated by the level of specific humoral immunity in the host (ABs)
• Diphasic fever, leukopenia, GI and respiratory catarrh, frequently pneumonic and neurologic complications.
• Large number of species susceptible to infection: Canidae, Mustelidae (ferret, skunk, otter), raccoon, red panda, bear, Asian elephant, Japanese monkey, large Felidae
distemper signs
• Most commonly: signs of clear of green nasal and ocular discharge, loss of appetite, depression
• Typical pathological features include:
– interstitial pneumonia
– encephalitis with demyelination
• CNS signs: muscle twitching (“distemper myoclonus”), seizures (salivation, jaw movements) “chewing gum fits”. The clinical signs of neurological disease may not appear until several wks (acute encephalitis), months (subacute encephalitis) or even years later (“old dog encephalitis”)
canine infectious hepatitis (CAV-1)
• A worldwide, contagious disease; adenovirus
• Signs vary: slight fever, congestion mucous membranes to severe depression, marked leukopenia, coagulation disorders, jaundice (yellowish tinge to skin).
• Resistant to lipid solvents (e.g., ether), acid, formalin. It survives outside the host for weeks or mo, but a 1-3% solution of sodium hypochlorite (household bleach) is an effective disinfectant.
• Ingestion of urine, feces, or saliva of infected dogs: main route of infection. Recovered dogs shed virus in their urine for ≥6 months
• Initial infection occurs in the tonsillar crypts and Peyer patches → viremia → disseminated infection.
• Vascular endothelial cells: primary target, then hepatic and renal parenchyma, spleen, and lungs.
• Chronic kidney lesions and corneal clouding (“blue eye”): immune-complex reactions after recovery from acute or subclinical disease
CAV-1 symptoms/side effects
• Clotting time is directly correlated with the severity of illness: result of disseminated intravascular coagulation (vascular endothelial compromise), and failure of the liver (replace consumed clotting factors)
• Coagulopathy (prolonged prothrombin time -clotting time of plasma-: more than 9.5 sec, thrombocytopenia, increased fibrin degradation products).
• Hemorrhage: bleeding around deciduous teeth, spontaneous hematomas.
• CNS involvement is unusual, vascular injury (convulsions from forebrain damage)
Canine Hepatitis (CAV-1) & Canine Adenovirus 2 (CAV-2) vaccine
• Vaccination against a closely related virus, canine adenovirus type 2 (CAV-2, one of the causes of infectious canine tracheobronchitis or “Kennel Cough” or Canine Respiratory Disease Complex) protects against both infectious canine hepatitis (CAV-1) and respiratory illness caused by CAV-2.
• CAV-2 vaccines: most commonly used to protect against CAV-1 and CAV-2, due to the potential for side effects from the CAV-1 vaccine (bluing of the eye, shedding of virus).
• CAV-1 vaccines are no longer available in the United States
canine Rabies Virus (Zoonosis)
• Genus Lyssavirus, family Rhabdoviridae; neurotropic.
• A severe, often fatal, polioencephalitis specifically affecting the gray matter (cellular bodies) of the dog's brain (CNS).
• Virus transmitted to dogs in US: a bite (saliva) from a diseased carrier/vector (foxes, raccoons, skunks, bats).
• During 2000-2004: more cats than dogs rabid in the US; spillover infection from raccoons in the eastern US; fewer cat vaccination laws, roaming habits of cats.
• Rabies: throughout the world; few countries rabies-free: successful elimination programs or island status and enforcement of rigorous quarantine regulations
rabies spread
• Usually: saliva infectious at the time clinical signs occur; dogs, cats, ferrets may shed virus for several days before onset of clinical signs (skunks: 8 days before onset).
• The incubation period: prolonged and variable. Typically: virus at the inoculation site for a considerable time: effective action of local infiltration of rabies immune globulin during human post-exposure prophylaxis.
• Most rabies cases in dogs: 21–80 days after exposure.
• Once the symptoms have begun, the virus progresses rapidly.
• Rare natural aerosol transmission in a cave inhabited by millions of bats: virus to olfactory nerve endings
rabies prodromal stage
only mild signs of CNS abnormalities (1-3 days). Most dogs will then progress to either the furious stage, the paralytic stage, or a combination of the two, while others succumb to the infection without displaying any major symptoms
furious rabies “made dog syndrome”
extreme behavioral changes, overt aggression, attack behavior; lose caution and fear of people and other animals hydrophobia; death from progressive paralysis
paralytic rabies “dumb rabies”
weakness, loss of coordination (ataxia), followed by paralysis; paralysis of the throat and masseter muscles, profuse salivation, inability to swallow, dropping of the lower jaw
rabies diagnostic
• The only acceptable method for confirming suspected rabies infection: keep the dog quarantined (locked cage for 10 days).
• Diagnostic test requires that the animal be euthanized: detection of rabies virus from any part of the affected brain, tissue from at least 2 locations in the brain (brain stem -hippocampus in carnivores-, cerebellum).
• Diagnosis in the US: using a post-mortem direct fluorescence ABs test performed by a state-approved laboratory for rabies diagnosis