drugs for the cure for distemper
21 Oct 2010
Until recently, canine distemper has been associated with a long history of pessimism with respect to treatment of infected animals and the disease was usually assumed to have a poor prognosis. Most care offered was only palliative, geared toward easing the suffering. Several factors had an important role in maintaining the status quo.
Misdiagnosis, miseducation, a lack of treatment, inadequate, or inappropriate treatment has historically created barriers and slowed the development of effective solutions to the disease. Even today the needs of affected animals often go unrecognized until the disease reaches the nervous stage and the distressed behavior and/or impaired functional state of the animal is more obvious and less responsive to treatment.
Research and funding for the most part have focused on preventative vaccination rather than on finding a cure for distemper.
Another factor is the outdated theory that the injuries that occurred were the result of a strictly autoimmune reaction, the thought being that initially the canine distemper virus was introduced, then subsequently eliminated, but that cytokines continued to attack and damage healthy tissue in the absence of a current pathogen. Based on that faulty assumption, anti-inflammatory and immunosuppressive drugs have been prescribed by some veterinarians in an attempt to bring the effects of the condition under control.
It was later considered that the action of macrophages on nerve cells is targeted on infected cells, indicating that the autoimmune reaction is likely a direct consequence of the presence of the virus. Often, owners seek expert help only when the disease is in its advanced stages (nervous phase) and prescription anti-inflammatory drugs (which are usually corticosteroids) undermine the immune system of the animal, allow the proliferation of the virus, and the autoimmune reaction increases as a means of containment of infected cells.
The most successful treatments for canine distemper are adaptations of established treatments used for other diseases caused by similar viruses, such as Ribavirin and vitamin A, which are used to treat measles, which is in the same viral genus (morbillivirus), and Interferon Alpha, also used for the treatment of measles and a vaccine used to immunize birds against Newcastle disease, which is in the same viral family, but a different genus (Paramyxoviridae - AVULAVIRUS).
The first references that suggested effective treatments for similar viruses could be effective for canine distemper arose when studies found that canine distemper was a disease comparable to measles and infected animals could be used to develop new technologies for treatment of measles. The question of whether the reciprocal would be true was resolved when studies assessed the efficacy of traditional treatments for measles, which were then successfully applied to animals with distemper.
Initially, induction of high levels of Vitamin A, used to treat measles including being recommended by the World Health Organization), produced a 100% cure in animals experimentally infected. The inected group given no Vitamin A supplementation all died. Currently, it is known that the direct inhibitor effect of retinoids (Vitamin A and subproducts) on the replication of the measles virus is what confirms the choice of Vitamin A as a treatment for canine distemper.
The confirmation of the effectiveness of Vitamin A in the treatment of canines, especially dogs, is its ability to convert the Vitamin A into nontoxic esters. This characteristic of carnivores is well known, which removes the risk of hypervitaminosis possible due to the maintenance of high doses.
For dogs, there is a benchmark to measure the risk of hypervitaminosis: a national research found that it takes a dose of 300,000 IU / kg daily for thirty days before the first signs of hypervitaminosis appear, and sixty days of ingestion at this dosage to kill the animal. This dosage, 300,000 IU / kg, is sixty times greater than the toxic limit established for humans.
The mechanisms of action that explain its effectiveness in the treatment of distemper remain unexplained, and this issue also exists with respect to measles. Some evidence points to an indirect action, such as checking that there is a reduction in the amounts of Vitamin A during infection, pointing to the hypothesis that Vitamin A is raw material for some mechanism of resistance to infection. The very characteristic antiinfective not specific Vitamin A is a mystery, however there was any doubt about its effectiveness, action mechanisms elucidated or not.
The adoption of Ribavirin as a treatment for canine distemper followed the same steps of Vitamin A, it was the principle used in cases of subacute sclerosing panencephalitis under measles. The first verification of the effectiveness occurred in vitro.It was observed that the distemper virus is very susceptible to Ribavirin and its mechanism of induction error catastrophe are needed from 0.02 to 0.05 micro mols to create an inhibitory effect on virus replication by 50%.
The main concern in the use of Ribavirin was the result of its interaction with the blood-brain barrier. The brain being an immunologically privileged area, the concern was the capacity of Ribavirin to overcome this barrier. In a study using mice with encephalitis due to measles it was found that once the virus has become established in phase nervosa, the blood-brain barrier in a way fails, reducing the restriction to the action of the Ribavirin in these areas. The verification of all these results in vivo resulted in an effectiveness of 80% in animals that had already reached the nervous phase of viral infection. The application of Ribavirin demands a close monitoring of the animal due the risk of leukopenia and the ingestion of long-chain tryglicerides (in other words, fats) in order to better absorb the drug and for preservation of gastric tissues, which are quite susceptible to Ribavirin.
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