Every necropsy case is a puzzle. To find the solutions, my colleague and I have considerable agency to select the tests that we want to apply. At one end of the spectrum is the shotgun approach: collect every type of sample (tissues, swabs, fluids) and run every test available. But where's the fun in that? Not only does this approach lack elegance and waste resources, it isn't intellectually pleasing. It's lazy diagnostics. It's more challenging by far to build a list of differentials based on signalment and history, modify that list based on gross findings from the necropsy, then thoughtfully select specific tests that will rule in or rule out your top differentials for the cause of death.
Sometimes the necropsy itself is the only test we need. That is informally referred to as "grossing out" a case, meaning we are able to determine a definitive cause of death of an animal during the gross examination conducted during the necropsy, and the case is closed out with no further testing. Necropsies are meticulous and require a lot of careful examination, and the word "gross" in this context means we aren't using any special diagnostic tools beyond our eyes and fingers. For example, when we find heartworms in a dog who died suddenly or who had clinical signs like fainting, low energy, or coughing, and there are no other major findings such as pneumonia or masses in other organs, we gross that case out.
While it can be satisfying to close a case based only on the necropsy, it is even more satisfying to identify a pathology during necropsy and verify it with just a handful of carefully chosen tests. Those cases give us a lot of validation. We've had several cases like this recently.
A beef cow-calf operator brought in a yearling cow. The cow was petite, quite pretty. She'd been sick for a couple of days and had not responded to his treatments. He'd lost several from his herd in the past few days, all with similar clinical signs. All of the sick or dead cows were yearlings or older--he hadn't lost any nursing calves. That was interesting. Based on my initial conversation with him, it sounded like a toxicity event and not infectious disease that was killing his cows, and he agreed. We went through the list of the usual suspects--paint cans, old batteries, sheds with old bags of fertilizer, rusting 50-gallon drums containing mystery liquids--cows are both curious and relatively indiscriminate eaters. Nothing really fit though. So into necropsy I went.
Even if you think you know the answer, which I did not in this case, you still approach every necropsy systematically to make sure that you don't miss anything important. Heart, lungs, and spleen looked good. But the liver was moderately autolyzed. Autolysis refers to post-mortem changes that occur in tissues due to cell death and bacterial activity. The state of the liver didn't match the other tissues. I couldn't find anything wrong with the liver that would explain this, such as liver flukes or evidence of a bacterial infection in the liver. This was a symptom of something else, not the primary problem.
Next, I examined her gastrointestinal system. The rumen was filled with 20-30 L of a thin liquid slurry of finely shopped feed. Her abomasum, her glandular stomach, was red-black inside and contained a couple of liters of cloudy red-brown liquid. The rest of her intestinal tract was empty. All three of these observations were a surprise. Her rumen should have contained layers of material--a mat of feed at the bottom, a slurry on top, and a gas cap on top of that. Sure, this stratification gets a bit mixed up when animals are moved and transported after death, but the basic components can be identified at necropsy. I only saw slurry, and far too much of it. Her abomasum should have normally contained feed. It shouldn't be bloody. And she should have had digesta scattered all along her gut and feces in her colon. All of this added up to an animal that had stopped eating and had developed ileus, or a cessation of the normal peristalsis of her gut. She had continued to drink water, thus the rumen was distended with liquid. Cows can develop ileus as a result of torsion or displacement of the abomasum, heavy parasite load, blockage of the rumen by a foreign object (baling twine and plastic bags in cow rumens are common incidental findings, but they can sometimes cause problems), chronic diarrheal disease, or something called vagal indigestion related to dysfunction of the vagal nerve and rumen function. There was no evidence of any of this, so the ileus was a symptom, not the primary problem.
Next, I examined her kidneys. Kidneys are often the first tissues in a cow to autolyze, which refers to the post-mortem changes in tissues due to bacterial activity and cell death. This cow was very fresh so I didn't expect to see autolyzed kidneys. Normal cow kidneys are not quite as dark as our own but they fall well into the range of what we might call "kidney colored." Her kidneys were golden brown and covered with bloody pinpoints. The same pinpoints were visible inside in the renal cortices. These distinctive lesions are textbook examples of oak toxicity. Leptospirosis, an infection caused by bacterial spirochetes, was definitely a differential. But my other observations fit oak toxicity better. Oak toxicity is caused by tannins in leaves and acorns. It can cause hemorrhage in the glandular stomach, which was likely the precipitating cause of the ileus (the cow didn't feel good so she stopped eating), and liver necrosis, which set the liver up to autolyze faster than surrounding tissues. And it causes pinpoint hemorrhages in the kidneys.
I called the owner back and surprised him by asking about oak trees that might be in or around the pasture. Turns out that during stormy weather a couple of weeks prior, wind had knocked down several branches from an oak tree in the middle of the field. The producer had observed several of his cows eating leaves from the fallen branches. He didn't think much of it because he thought oak toxicity was only caused by buds or acorns, and we are past the time for the first and not yet into the season for the second. He gave them new forage and cleaned up the branches. I told him that young leaves and their stems are toxic too, and that unfortunately the damage had already been done. Nursing calves didn't eat any leaves so they weren't affected. And the leaf-eating had occurred long enough ago that no leaf remnants were in the rumen of this cow. I told him to expect more mortalities in the handful of cows that were still sick.
There is no bench test for oak toxicity. Diagnosis is made by gross findings and distinctive microscopic changes to the kidneys. I had to wait a couple of days for the tissues to fix in formalin, another day for trimming, and another day to cut and stain the slides. But eventually, I had the slides in my hand. Textbook case.
My colleague recently had a similar puzzle that he quickly solved. A breeder had submitted two French bulldog puppies, only 7 days old. She had already lost most of the litter. When this kind of thing happens in pure-bred dogs or cats, breed-specific genetic or congenital abnormalities top the differential list. That list is of course rather long for French Bulldogs and other brachycephalic breeds, especially since breeders are selecting for ever more extreme deformation of the faces of these dogs. I recently did a necropsy of an adult female Bulldog whose nasal
openings were positioned so far back on her head that they were over her
molars, not in front of her incisors. Selecting for extreme body deformities often comes with unanticipated deformities in critical things like hearts, skeleton, and brains. Oops.
But back to the puppies. For high litter mortality, you also have to consider canine parvovirus, which can be transmitted through the placenta. Ideally, the dam should have been vaccinated for parvovirus and she would have passed antibodies to her puppies when they nursed the first time or two, but the number of people who refuse to give vaccines to their dogs is growing. She could have been infected during pregnancy, and infected her puppies in utero. Canine herpesvirus is a bit more insidious. There is no vaccine. It can also be passed to the puppies in utero and often results in abortion in those cases, but the more common route is post-natal infection. It can result in high mortality in young puppies. Dogs older than about 8-12 weeks usually only get mild disease from herpesvirus, but they shed virus in all of their body secretions. Keeping it out of a kennel is a matter of biosecurity--wash hands and shoes, quarantine new additions, segregate animals of different ages, clean surfaces.
My colleague approached the necropsy with his usual care. Nothing significant turned up until he looked at the kidneys. The kidneys of both puppies had many small hemorrhages inside and out. Textbook example of canine herpesvirus infection. He was so excited by this finding that he called me down to necropsy to take a look. Definitive diagnosis of canine herpesvirus is available with a PCR test. It of course came back positive, and he closed the case with no further testing. We made slides of the kidneys for our own learning because they were such good examples of this disease. You could see inclusions comprised of many viral particles (far too small to see individually) in the nuclei of the cells lining the renal tubules.
Two interesting puzzles: cases of multifocal renal hemorrhage and nephritis identified at necropsy of two different species. When we combined our gross observations with signalment and history, we were able to land on diagnoses quickly. Two puzzles that we got a lot of satisfaction from solving!
