Friday, December 27, 2013

Canine Parvovirus

Nearly every mammal species, humans included, has its own special parvovirus. Dogs are no exception to this rule. The canine parvovirus (CPV type-2b specifically, but CPV for our purposes) first emerged among domesticated dogs in Europe during the mid-1970s. This initial appearance quickly evolved into a worldwide epidemic of myocarditis and gastroenteritis. The virus is now known to infect both wild and domesticated canine species. A close relationship between CPV and the already well-known feline panleukopenia virus (FPV) was quickly established. It is thought that CPV came about as a result of a small mutation, or change, in the viral structure of FPV.

 Canine small intestine dilatation, luminal hemorrhage
Two decades after its appearance, CPV strikes much less frequently due to the development of effective vaccines. Outbreaks do still occur however, and it is widely acknowledged that the hard-to-kill viral particles are present most everywhere. Because of this, vaccinating your dog is of the utmost importance. Puppies and adolescent dogs are considered especially susceptible to exposure, and it is recommended that you avoid bringing your puppy to public places until after his vaccinations are complete.
Despite the fact that CPV particles are present in nearly every environment, not every dog becomes infected. This is because several factors influence the effectiveness of the virus. Host vitality (overall health of the dog, immune experience, vaccination status), virulence of the virus (the number of viral particles in a given area), and other environmental factors (stress, dry weather, cold weather) all interact and together ultimately determine whether or not an individual dog will become infected. The most influential factors seem to be the immune level of the individual dog and the number of viral particles the dog is exposed to, but if each factor is “just right,” a dog will become infected. When this occurs, a specific sequence of events is initiated as the virus attacks the body.

There is typically an incubation period of 3 to 7 days between initial infection and onset of first symptoms. CPV needs the help of rapidly dividing cells in order to successfully infect the host animal, and the first cells to be encroached upon are in the lymph nodes of the throat. The virus incubates here for a few days, replicating repeatedly until a vast number of viral particles have been produced. At this point, the virus has entered the bloodstream and is seeking out other organs containing rapidly dividing cells. The two areas typically hit hardest by CPV are the bone marrow and intestinal walls.
Within the bone marrow CPV destroys young immune cells. This causes a detectable drop in white blood cell count, which makes it significantly easier for the viral particles to invade the gastrointestinal (GI) tract. Damage to the lymph nodes and bone marrow, while significant, is minor when compared to the havoc CPV wreaks on the intestines. The lining of this organ is covered by miniscule, finger-like protrusions called villi. In turn, the villi bear microscopic projections called microvilli. Together, the villi and microvilli serve to increase the surface area of the intestine and allow it to better absorb nutrients. The cells that cover this surface are short-lived and are replaced continually by new cells that originate in the rapidly-dividing areas known as the Crypts of Lieberk├╝hn. It is here, where the cells are dividing most rapidly, that CPV stages its invasion and does the most damage.
By disabling the source of new cells, the virus prevents dead and dying cells on the villi and microvilli from being replaced. Consequently, the intestines can no longer adequately absorb nutrients. Severe diarrhea and nausea are the initial result, but eventually the villi and microvilli become so damaged that they begin to break down, and the bacteria that are normally confined to the GI tract embark on a deadly journey out of the intestine and into the bloodstream. This is the cause of both significant blood loss through diarrhea and widespread infection inside the body. To make matters worse, the body’s immune system is not quite up to par, as its ability to produce new white blood cells to combat infection has been hampered by the invasion of CPV into the bone marrow. CPV is not always fatal, but when it does kill, death is as a result of either extreme dehydration and shock, or of septic toxins produced by the intestinal bacteria roaming throughout the bloodstream.
Symptoms often associated with CPV include lethargy, depression, and loss or lack of appetite, followed by a sudden onset of high fever, vomiting, and diarrhea. If your dog is experiencing bouts of bloody diarrhea and/or vomiting, CPV is only one of several potential culprits. There are several tests that can be run by your veterinarian to help determine whether what is affecting your dog is CPV or some other problem.
By far the most common and most convenient method of testing for the presence of CPV is the fecal ELISA test. ELISA is an acronym for enzyme-linked immunosorbent assay. The test sounds daunting but can actually be completed by your veterinarian in less than 15 minutes and uses technology similar to that found in home pregnancy tests. A small stool sample is necessary for the completion of the ELISA test. Though the ELISA test is quite accurate, there are some cases in which a false positive or false negative result may be obtained. In this case, further measures may have to be taken to establish a diagnosis of CPV.
A simple measure of white blood cell count is often the clincher for a CPV diagnosis. Because one of the first things the parvovirus infects is the bone marrow, a low white blood cell count can be indicative of CPV infection. If the ELISA test was positive, but the dog has a normal white blood cell count, it is unlikely the animal is infected with CPV. If however the dog has both a positive ELISA reading and a low white cell count, a fairly confident diagnosis of CPV may be made.

Treatment procedures for dogs suffering from CPV are limited to a supportive capacity. A hospital stay is usually necessary, as fluids and nutrients are often given intravenously. Treatments may vary between individuals, but certain aspects are considered vital for all patients.
Fluid therapy is crucial in order to replace the vast quantities of liquid lost via vomiting and diarrhea. Because the digestive tract is in such distress, the most effective method of fluid replacement is the use of an IV drip. Antibiotics may be given, either intravenously or as injections, to help fight the effects of intestinal bacteria that may have entered the bloodstream. In addition, medications to control nausea are sometimes added to the IV fluid bag. Overall, care of dogs with CPV centers around fluid replacement and constant monitoring of bodily functions. There is unfortunately no magic formula that will lead to a complete cure in every case.

Veterinarians usually administer the CPV vaccine as part of a combination shot which includes, among others, the distemper and coronavirus vaccines. These shots are given every 3 to 4 weeks from the time a puppy is 6 weeks old until he is at least 16 weeks of age.

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