Parvoviruses are a large group; almost every mammal species (including humans) seems to have its own parvovirus. Fortunately, each virus is pretty specific about what animals it can infect (i.e. the pig parvovirus will not infect people, the canine parvovirus will not infect cats etc.) The canine parvovirus will affect most members of the dog family (wolves, coyotes, foxes etc.), with a new mutation that can affect domestic cats.
Parvoviruses are smaller than most viruses and consist of a protein coat (a "capsid") and a single strand of DNA inside. It is hard to believe that such a simply constructed organism could be so deadly; however, this virus has proven to be especially effective at infecting rapidly dividing host cells such as intestinal cells, bone marrow cells, cells of the lymph system, and fetal cells. Parvoviruses are not enveloped in fat the way many other viruses are which makes parvoviruses especially hardy in the environment and very difficult to disinfect away.
While the parvoviruses of other species have been well known for decades, the canine parvovirus is a relative newcomer. The original canine parvovirus, discovered in 1967 and called "CPV-1" or "the minute virus of canines," did not represent much of a medical threat except to newborn puppies. However, by 1978, a new variant, "CPV-2" appeared in the United States. This newer version seemed to represent a mutation from the feline parvovirus (which is more commonly known as the "feline distemper virus"), although there is some controversy regarding what the parent parvovirus actually was. Because this virus was (and is) shed in gigantic numbers by infected animals and because this virus is especially hardy in the environment, worldwide distribution of the virus rapidly occurred. At this time, the virus is considered to be "ubiquitous," meaning that it is present in EVERY ENVIRONMENT unless regular disinfection is applied.
In 1978, no dog had any sort of immunity against this virus. There was no resistance and the epidemic that resulted was disastrous. To make matters worse, a second mutation creating CPV-2a occurred by 1979, which seemed to be an even more aggressive virus. Vaccine was at a premium and many veterinarians had to make do with feline distemper vaccine since it was the closest related vaccine available while the manufacturers struggled to supply the nation with true parvo vaccines.
Over thirty years have passed since then. The most common form of the virus is called CPV-2b. Virtually all dogs can be considered to have been exposed to it at least to some extent which means that most adult dogs, even those inadequately vaccinated, can be considered to have at least some immunity. It is also worth mentioning that the newest, more severe strain of parvovirus: CPV-2c, which is rapidly becoming the second most common form of canine parvovirus discovered in 2000 is also able to infect cats. Cats vaccinated against feline distemper can be considered protected. Currently available vaccines cover all variants of canine including CPV-2c as do all the commercially available diagnostic test kits.
The biggest problem in protecting a puppy against this infection ironically stems from the natural mechanism of protection that has evolved. Puppies obtain their immunity from their mother’s first milk, the colostrum, on the first day of life. This special milk contains the mother’s antibodies against parvovirus and until these antibodies wane to ineffective levels, they will protect the puppy. The problem is that they will also inactivate vaccine.
Vaccine is a solution of inactivated virus, either live and weakened (“attenuated” or “modified”) or killed. This virus is injected into the puppy. If there is still adequate maternal antibody present, this vaccine virus will be destroyed just as if it were a real infection. There will be a period of about a week when there is not enough maternal antibody to protect the puppy but too much to allow a vaccine to work (This period is called the “window of vulnerability”). After this period has passed, vaccine can be effective.
The next problem is the age at which vaccine can be effective, because it is different for each individual puppy. We vaccinate puppies in a series, giving a vaccine every 2-4 weeks until age 16 weeks. By age 16 weeks, we can be certain that maternal antibodies have waned and vaccine should be able to “take.” It is important to note that some individuals, especially those of well-vaccinated mothers, must be vaccinated to 20 weeks (unless a “high titer” vaccine is used), to insure complete protection.
Killed vaccine is the least effective at penetrating maternal antibody. It is also associated with more vaccine reactions (since more stabilizing chemicals are used in a killed vaccine). Veterinarians often recommend using live parvo vaccine unless there is any question about the immunologic competence of the dog to be vaccinated and the dog is an adult. Killed vaccine should probably not be relied upon for puppies.
In the mid-1990’s a new innovation in parvo vaccination was developed known as the “high titer” vaccine. The term “high titer” refers to the amount of virus in the dose of the vaccine and means that there is a great deal more virus present than in the standard vaccines. When a puppy is vaccinated, maternal antibody binds the virus present. If a high titer vaccine is used, there is still virus left over after all the maternal antibody has been used up. This extra virus can then stimulate the puppy’s own immune system. High titer vaccines commonly produce full protection by age 12 weeks (although we recommend carrying vaccination to age 16 weeks to be certain - this is an especially good idea for breeds predisposed to infection such as the Rottweiler, Doberman pinscher, and American pit bull terrier).
Parvoviral infection must be considered as a possible diagnosis in any young dog with vomiting and/or diarrhea. With proper hospitalization, survival rates approach 80%.
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