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          Canine Distemper           

(Hardpad disease)

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Canine Distemper
Canine Distemper

Canine Distemper 

(Hardpad disease)

Roger Ross DVM
http://animalpetdoctor.homestead.com

Introduction:
Canine distemper is a highly contagious, systemic, viral disease of dogs seen worldwide. It is characterized by a diphasic fever, leukopenia, GI and respiratory catarrh, and frequently pneumonic and neurologic complications. The disease occurs in Canidae (dogs, foxes, wolves), Mustelidae (eg, ferret, mink, skunk), most Procyonidae (eg, raccoon, coati mundi), and some Viverridae (binturong).

Etiology and Pathogenesis: Canine distemper is caused by a paramyxovirus closely related to the viruses of measles and rinderpest. The enveloped virus is sensitive to lipid solvents and most disinfectants and is relatively unstable outside the host. The main route of infection is via aerosol droplet secretions from infected animals. Some infected dogs may shed virus for several months.

Virus replication initially occurs in the lymphatic tissue of the respiratory tract. A cell- associated viremia results in infection of all lymphatic tissues, which is followed by infection of respiratory, GI, and urogenital epithelium, as well as the CNS. Disease follows virus replication in these tissues. The degree of viremia and extent of spread of virus to various tissues is moderated by the level of specific humoral immunity in the host during the viremic period.

Clinical Findings: A transient fever usually occurs 3-6 days after infection and there may be a leukopenia (especially lymphopenia) at this time, but these signs may go unnoticed. The fever subsides for several days before a second fever occurs, which lasts <1 wk. This may be accompanied by serous nasal discharge, mucopurulent ocular discharge, and anorexia. GI and respiratory signs may follow and are usually complicated by secondary bacterial infections. An acute encephalomyelitis may occur in association with or immediately after the systemic disease, or in the absence of systemic manifestations. Hyperkeratosis of the footpads ("hardpad" disease) and epithelium of the nasal plane may be seen.

Neurologic signs are frequently seen in those dogs with hyperkeratosis. CNS signs include the following:
1) localized involuntary twitching of a muscle or group of muscles (myoclonus, chorea, flexor spasm, hyperkinesia), such as in the leg or facial muscles;

2) paresis or paralysis, often beginning in the hindlimbs evident as ataxia, followed by ascending paresis and paralysis; and

3) convulsions characterized by salivation and chewing movements of the jaw (petit mal, "chewing-gum fits").

The seizures become more frequent and severe, and the dog may then fall on its side and paddle its legs; involuntary urination and defecation (grand mal seizure, epileptiform convulsion) often occur. A dog may exhibit any or all of these neurologic signs in addition to others in the course of the disease. Infection may be mild and inapparent or lead to severe disease manifest by most of the above signs. The course of the systemic disease may be as short as 10 days, but the onset of neurologic signs may be delayed for several weeks or months.

Chronic distemper encephalitis (old dog encephalitis [ODE]), a condition often marked by ataxia, compulsive movements such as head pressing or continual pacing, and incoordinated hypermetria, may occur in adult dogs without a history of signs related to systemic canine distemper. Convulsions and neuromuscular twitching (chorea) do not seem to occur with ODE. Although canine distemper antigen has been detected in the brain of dogs with ODE by fluorescent antibody staining, dogs with ODE are not infectious and replication-competent virus has not been isolated. The disease is caused by an inflammatory reaction associated with persistent canine distemper virus infection in the CNS.

Lesions: Thymic atrophy is a consistent postmortem finding in young puppies. Hyperkeratosis of the nose and foot pads may be present. Depending on the degree of secondary bacterial infection, bronchopneumonia, enteritis, and skin pustules may also be present. Histologically, canine distemper virus produces necrosis of lymphatic tissues, interstitial pneumonia, and cytoplasmic and intranuclear inclusion bodies in respiratory, urinary, and GI epithelium. Lesions found in the brain of dogs with neurologic complications include neuronal degeneration, gliosis, demyelination, perivascular cuffing, nonsuppurative leptomeningitis, and intranuclear inclusion bodies predominantly within glial cells.

Treatment: Treatments are directed at limiting secondary bacterial invasion, supporting the fluid balance and overall well-being of the dog, and controlling nervous manifestations. Antibiotics, electrolyte solutions, protein hydrolysates, dietary supplements, antipyretics, nasal preparations, analgesics, and anticonvulsants are used. No one treatment is specific or uniformly successful. Dogs may recover completely from systemic manifestations, but good nursing care is essential. Despite intensive care, some dogs do not make a satisfactory recovery. Unfortunately, treatment for neurologic manifestations of distemper are unsuccessful. If the neurologic signs are progressive or severe, the owner should be appropriately advised.

Prevention: Successful immunization of pups with canine distemper modified live virus (MLV) vaccines depends on the lack of interference by maternal antibody. To overcome this barrier, pups are vaccinated with MLV vaccine when 6 wk old and at 2-to 4-wk intervals until 16 wk old. Measles virus induces immunity to canine distemper virus in the presence of relatively greater levels of maternal distemper antibody. An MLV measles vaccine and a combination of MLV measles and MLV canine distemper vaccine are available. These vaccines must be administered IM. Pups 6-7 wk old should receive the measles or combination vaccine and at least two more doses of MLV distemper vaccine when 12-16 wk old. Many varieties of attenuated distemper vaccine are available and should be used according to manufacturers' directions. Annual revaccination is suggested because of the breaks in neurologic distemper that can occur in stressed, diseased, or immunosuppressed dogs.
reprinted with kind permission from Roger Ross
http://animalpetdoctor.homestead.com

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Canine Distemper

AnimalPetDoctor.com

Before the 1970's it was common place for vets to have to euthanize dogs on a weekly basis because of distemper virus.  Those pets and stray dogs that weren't lucky enough to be euthanized by a humane veterinarian were either shot or died a slow, miserable death. 

In those countries where vaccination has been common place for the last 50 years, this terrible disease is now rare. 

But the disease is till present in our wild dog population, coyotes, wolves, and the stray dog populations.

And in other parts of the world, the disease is still out of control.

Vaccination is the most important thing you can do to protect your pet. Being thankful that you live in a country with a vigilant animal border control and disease control center is also important.

The following information is from the client information series collection of veterinary information from the
TEXTBOOK OF VETERINARY INTERNAL MEDICINE
by Alfred M. Legendre

Canine distemper is a disease that primarily affects the lungs, intestinal tract, and nervous system of dogs. Among the virus-induced diseases in dogs, the mortality rate of distemper is second only to that of rabies. The virus is highly contagious and is passed directly from dog to dog by close contact. The virus is easily killed by detergents and heat. The virus dies within minutes in a warm environment but can persist for weeks at near-freezing temperatures.

Young, unvaccinated dogs 3 to 6 months of age are most often infected with distemper. Nasal discharges containing virus are aerosolized by sneezing, thereby spreading the virus. The virus establishes itself in the nasal passages of a susceptible dog, multiplies, and spreads through the body. Dogs develop a fever a week after infection but this fever may not be noticed. Two weeks after infection, the virus produces severe damage to the cells of the nasal passages, eyes, lungs, and intestinal tract. These damaged tissues com-monly become secondarily infected with bacteria. This combined infection with virus and bacteria produces loss of appetite, fever, snotty nose, thick discharge from the eyes, pneumonia, and diarrhea. The virus infects the pads of the feet, producing a hard, scaly thickening referred to as "hard pad" disease. The virus also damages the immune system, thereby interfering with the body's ability to fight off the infection.

If the bacterial component of the infection can be con-trolled with antibiotics, the dogs will appear normal for 2 to 3 weeks until signs of brain and spinal cord disease occur. Half of the dogs with distemper develop neurologic disease. The canine distemper virus is attracted to and grows well in nervous tissue. The damage done to the brain and spinal cord results in epileptic seizures and localized seizures of the head often called "chewing gum fits." Damage to the spinal cord can produce weakness and paralysis. Nerve damage may also produce involuntary twitching of the legs. Most dogs with neurologic disease die or are euthanized.

Making a definite diagnosis of distemper can be difficult if the dog does not develop the typical snotty nose-pneumonia syndrome. After the initial 14 days of the infection, the virus is difficult to identify in swabs of infected tissues. Increasing antibody titers against distemper in dogs that have not been vaccinated strengthen the suspicion of distemper. It is especially difficult to diagnose distemper in dogs with nervous system signs that have not had the other typical signs of distemper.

Currently, no drugs are available to treat the distemper virus, so treatment with antibiotics is aimed at controlling the secondary bacterial infection. The antibiotic treatment relieves many of the signs of disease but does not prevent the virus from entering and damaging the brain and spinal cord. Nursing care; good-quality, palatable food; and a stress-free environment are helpful in improving appetite and general well-being. Because the treatment options are limited, prevention by vaccination is the prime strategy.

Vaccines against distemper should be started when puppies are weaned. If the mother has been vaccinated or recovered from an exposure to distemper, she will pass protection (antibodies) against distemper to her puppies in her milk. These maternal antibodies protect the pups for a few weeks after birth. The amount of antibodies passed from the mother to her pups depends mainly on the level of the mother's antibodies. The antibodies not only protect the pups from distemper but also interfere with the pups' response to vaccination.  As long as the pups have maternal antibodies, they cannot be successfully vaccinated.

By 6 weeks of age, half of the litters of pups no longer have enough antibodies to interfere with vaccination. As the pups grow, the antibodies obtained from the dam are gradually broken down, and by 13 weeks of age more than 95 per cent of the pups are susceptible to distemper and can be protected by vaccination. It is not economically feasible to measure antibodies in the pups, so a vaccine schedule has been developed to protect pups optimally against distemper.

Vaccines should be started  soon after weaning, at 6 to 7 weeks of age, and given every 2 to 3 weeks until the puppies are 14 weeks of age. The pups should be kept away from other dogs until the vaccination schedule is complete. This scheme of vaccination has proved effective in preventing this lethal disease.
reprinted with kind permission from Roger Ross
http://animalpetdoctor.homestead.com

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chloebutton  talabutton  

The above information is simply informational. It's intent is not to replace the advice of a veterinarian nor to assist you in making a diagnosis of your pet. Please consult with your own veterinarian for confirmation of any diagnosis. Your pets life may depend on it.