Kunzite:

Medical history

Medical History/Background for Kunzite

 

Kunzite is from a litter of nine puppies born to a mother dog who had been at the Cedar City Utah animal shelter and then in a foster home for two months before coming to Best Friends. The mother, a beautiful heeler named Amber broke with a bloody diarrhea two days after giving birth to her nine puppies. Although parvo can strike dogs of any age, it’s by far a disease of puppies. I can’t remember the last adult animal that I treated who was diagnosed with parvo, but all of Amber’s clinical signs screamed parvo and the SNAP test doesn’t lie.

 

When Amber presented to the Best Friends clinic she was dehydrated, vomiting, depressed and seriously sick. We placed an IV catheter in her cephalic vein and administered fluids to combat her losses, antibiotics to kill the bacteria that were translocating from her GI tract to her bloodstream and traveling around her body to various organs. This secondary bacterial invasion is one of the major reasons why parvo dogs and puppies die. We also gave her powerful IV drugs to control her nausea and vomiting. With aggressive treatment we knew the chance of her surviving was good, but there was no way she could nurse her puppies and beat the parvovirus, not to mention the risk to the puppies from being exposed to millions of viral particles. They had to be raised as orphans in foster care, and that the odds of all of them pulling through weren’t good. But we had to give it a shot.

 

At first the pups did well, thrived even. But then, tragically at ten days of life they began to die, almost without warning. There was no bloody diarrhea, just a short period of labored breathing, and then, sadly, death. We had to look at why these puppies died in order to help the living. The first necropsy I performed on the runt of the litter didn’t show much, no evidence of any kind of intestinal or other disease, though I thought the heart muscle looked a little "flabby". I attributed its death to "runt of the litter" syndrome and didn’t send any samples to the lab. The second showed more active inflammation of the heart and lungs, and some white streaks in the heart muscle. Vitamin and/or mineral deficiencies can cause that in other animals, but I had never seen this type of lesion in a puppy. Although the streaky heart muscle would have triggered an immediate image of large flashing PARVO sign in my brain if we were in Asia, it didn’t. It took my colleague Dr. Tara Timpson to break me out of my quest for another explanation of the cause of death. "It’s that myocardial form of Parvo!" she said. Dr. Tara hit the proverbial nail on the head and recognized it for what it was. Knowing earlier wouldn’t have stopped any of the deaths from happening; we would have simply had an answer sooner.

 

Most people who are familiar with parvo know it in its enteric (GI tract) form. The parvo virus infects dogs via the fecal oral route, i.e. a dog gets poop or dirt that once had poop in it and licks it off the virus off their feet. Parvo likes rapidly dividing cells to infect and replicate in, and finds those in the bone marrow and in small intestinal epithelial stem cells. The entire lining of the GI tract is shed and replaced on average every five days, so the stem cells that reline the small intestine are prolific replicators. Once they are infected they no longer make new copies of themselves, rather they are hijacked to replicate the virus. Since there is only one cell layer between the blood supply to the intestine and the lumen of the intestine the unfortunate puppy loses large amounts of fluid and blood, producing a characteristic malodorous diarrhea. That is not the only way the parvovirus can strike a young animal, however.

 

The canine parvovirus first jumped the species barrier from cats (feline distemper, which is also called panleukopenia, is caused by the feline parvo virus) to dogs some time in the early 1970’s in Eastern Europe. By the late 1970’s the virus had crossed the Atlantic and an epizootic (epidemics in animals are actually called epizootics) raged in puppies and dogs across the USA. I can distinctly recall going to the vet with our animals as a kid in the early 1980’s and hearing about this new and deadly disease called parvo for which there was at that point no vaccine. The canine parvovirus, which scientists labeled CPV-2, quickly mutated into two distinct forms, a type a and type b.

 

Type a attacked the heart muscle and lungs primarily and in a population of completely naïve and unvaccinated dogs the results were devastating. Puppies who were exposed to the parvovirus in-utero developed the myocardial form of the disease, and would often die shortly after birth. Over time as the population of dogs in the US developed immunity to CPV-2a that form became less and less common, and the type 2b, the bloody diarrhea form became more common. In vet school I learned about the type 2a, but we also learned that it was common in Asia still, but rarely ever seen in the US anymore. The rare exception was the isolated and unvaccinated dog who was exposed late in gestation. That dog was Amber.

 

Kunzite and one other littermate continue to thrive, but even if they survive puppy hood there is a chance they could develop congestive heart failure at 6 months or so because of the damage the virus did to their developing hearts in utero. There is also a chance they will live normal lives, which of course is what we are hoping for. It will likely take a visit to a board certified veterinary cardiologist and specialized echocardiography to determine if their hearts withstood the assault from the canine parvovirus and that can’t be done for some time. For now, we listen to their hearts frequently and we’ll plan some follow up diagnostics when the pups get a bit older. Kunzie’s remaining littermate already has a home and even with her possible future health problems, for now Kunzie is a sweet and "normal" puppy who we hope will find a special home of her own.