Wall

 My backyard is quite steep, the soil is poor, thin, and rocky, and there are lots of mature oak and walnut trees. Erosion is a problem and I’ve been experimenting with different ways to manage it. I don’t want to put down sod because I don’t want to waste water on it or deal with the tons of chemicals it would need to remain alive on the aforementioned shitty soil. Clover does okay in some spots. It dies back in the summer but the roots remain and they help hold things in place. Throwing clover seed around isn’t going to solve the erosion issue however.

The biggest drainage problems are in the two farthest corners of my yard. After watching dirt pile up against the fence in those corners, I needed to get serious about fixing the problem this year.

I decided to build a retaining wall using those 22 lb paver blocks. Going into the project, I wasn’t sure I could do it. Conceptually, building a retaining wall with pavers isn’t hard. But there were complicating factors for this particular wall.

This was my first attempt at such a project, and of course I chose an area where I had to step up the bottom course FIVE TIMES to accommodate the natural change in elevation. It also took more blocks and paver base than I expected. 

 

 

 

Since I wasn’t ready to commit to an entire pallet of blocks, I got 18 blocks at a time from Home Depot. Because they are heavy, I could only move 4 at a time in the wheelbarrow. And because my yard is so steep and there are other barriers in place, I had to navigate half a dozen switchbacks for each trip. It took me an hour to move 18 blocks from driveway to the job site.

I teach dog classes on Sundays, so I could only work on the wall on Saturdays. Like most normal people, I have other stuff I also need to do on the weekends so I really could only work on the wall for a few hours each Saturday morning. It took 5 weeks to build it, including 6 hours to dig the initial trench. 

 

Is it perfect? Of course not. It’s not even all the same color because Home Depot ran out of grey blocks and I had to finish the wall with tan ones. But it’s reasonably level. I managed to work out the step-up process after a couple of false starts. And I did it all myself. 

 

 

There Are Always Surprises

In the lab, we conduct necropsies on all species, including companion animals (dogs, cats, small exotic mammals, reptiles); horses (racehorses, horses used for trail riding, barrel racing or other sports); wild animals; food and production animals (lots of poultry); animals used for research; animals kept in zoos or raised for display or exhibition; animals submitted by rescue organizations, animal shelters, or law enforcement that are involved in cruelty or abuse cases…the list goes on!

In the past couple of months, this is a cross section of cases I’ve worked up.

Chukar (a type of partridge) and quail raised for commercial hunting operations. One of each was submitted for necropsy. The birds were wasting and dying. I noted that the mucosal layer of the crop of both birds had thick rumpled folds. Histopathology identified crop worms (Capillaria spp.). That was the second time I’ve seen that pathology in quail.

A five-year-old blue and gold Macaw. Three weeks of listlessness, anorexia. Found dead in the cage. I noted that the proventriculus was dilated and flabby. Approximately 50% of the mucosal layer had been eroded off and the tissue was so thin it was transparent. Proventricular dilatational disease is a viral disease that affects psittacine birds. The virus causes neuropathy, most often in the nerves of the digestive system. It’s so common in macaws that it is informally called “macaw wasting disease.”

A dog that was found dead in the neighbor’s backyard. It was submitted by animal law enforcement officers from a nearby city. They suspected that the neighbor’s dog had killed it. I documented extensive lesions and trauma consistent with an attack by a larger animal. While we photograph nearly every necropsy case, legal cases like this one result in more extensive photo documentation.

A piglet that was part of a heart valve transplant research program. The piglet developed a persistent infection along the line of the surgical incision in the chest and body wall that was made when its main pulmonary valve was replaced with a valve from another piglet. Because it was on so many immunosuppressive drugs as part of the transplant protocol, antibiotic treatments could not effectively clear the infection. While not a legal case, the purpose of this necropsy was to document everything so these results could be factored into the research project.

A dozen, 15-day-old commercial broiler breeder pullets. Histomonas meleagridis is an amoeba that lives in the guts of cecal worms, a type of round worm with the formal name of Heterakis gallinarum. The worms are specialized to only live in that part of the chicken’s intestinal tract. Most chickens have a few cecal worms, and usually the amoeba isn’t a problem. But if the cecal worm burden gets too heavy, the amoebas can migrate out of the cecae and into tissues such as the liver where they cause severe systemic disease. The amoebas can also be shed in feces and can persist in the environment for quite a while. Fifteen days is too short for these birds to have developed a heavy burden of cecal worms (the worm life cycle is longer than that). Instead, the birds had to have picked up the amoebas directly from the litter. Where did the amoebas come from? From worms in the guts of previous flocks of birds run through that poultry house. In the US, litter is not cleaned out of poultry houses between every flock. As many as five or six flocks may be run through one house before all the litter is removed, the house is disinfected, and new litter put in.

Raccoons with distemper. Dogs with heartworm disease. Cats with feline hypertrophic cardiomyopathy. Rabbits with respiratory disease caused by Pasteurella. Cows with pneumonia and emphysema caused by eating perilla mint.

Veterinarians are expected to have knowledge of anatomy, physiology, and pathologies of many species, and how those vary with age, sex, and reproductive status. We also need to have some idea of husbandry and how the animals are used. The differentials for a 3 week old calf are quite different from those for a 5 year old cow who had her third calf earlier in the summer. And those differentials are a universe away from what I need to consider for a backyard laying hen or a kitten from a shelter.

Nothing is routine about being a veterinary pathologist. You have to pay attention because there are always surprises. It takes a lot of work to build and maintain a solid foundation of knowledge and expertise. And it’s not accomplished by one person working alone. I’m lucky to have reasonably sane colleagues and hard-working technicians. 

I like this job a lot. It opens a fascinating window into the pathology of so many different types of disease. It can sometimes be emotionally stressful for us, but it can be very satisfying to work up a case and get a definitive answer that can help a pet owner find some closure or help a farmer be more successful going forward.  

Afternoon Sun

 Frankie is a very busy dog. She will not settle as long as a person is around who could be cajoled into throwing a ball or toy for her. When I am in the kitchen, she will forcefully push a toy into the back of my legs or repeatedly drop it on my feet. Oh, you think that just ignoring her will cause her to stop? She interprets that as you not liking that particular toy and will bring you another one in short order. She is relentless, confident that she will wear you down eventually.

She is quite good in pens and crates, however, and will settle quickly. Many calm evenings are spent with Frankie in her playpen in the living room and Archie stretched out next to me on the couch while I read or watch TV. At trials and during class, she waits calmly in her crate. 

With the arrival of cooler weather, I've been putting her in an expen in the backyard when I come home for lunch. This has several advantages: Archie gets to hang out with me, I am not constantly harassed to play, and she gets to sunbathe. 

 

I know the picture is blurry. There is a double-paned window, screen, deck railings, and expen between the camera and Frankie. But she's calm and relaxed, soaking up the afternoon sun.

 

Up Close And Personal With The Anaerobes

Earlier this week we had a cow on the necropsy table. Various factors, including the fact that we have to incinerate during the day and the long holiday weekend, resulted in this cow being in our walk-in cooler for 6 days before we could get to her. The owner had dropped her off with another cow. I tried to talk him out of bringing two but he insisted. So now I had to do a necropsy on a rotten cow that was going to have zero diagnostic utility. 

A few minutes into it, I stabbed my arm with a very sharp, very contaminated knife. The wound was not large, and we quickly cleaned it with alcohol and slapped some antibiotic ointment and a bandaid on it. But as the day progressed, things began to head south. The area around the wound became firm, hot, had a faint purple tinge, and was welting up. It hurt to move my arm. Even brushing my arm against my shirt was quite painful. By early evening, with this progression of clinical signs, I realized that this was not a routine nick.

Off to urgent care I went. Once I went through the progression of clinical signs and emphasized "clostridium," the staff jumped into action. 

Because of a high risk of exposure to tetanus as a veterinarian in general and as a pathologist in the specific, I get boosters every 5 years. The last one was in 2020, so I was due anyway. Yes, tetanus booster please. 

Then they came in with the antibiotics, a broad spectrum cephalosporin. This one goes IM in the bum and it stings like crazy. I'm writing this more than 2 days after I got this shot and it still stings. 

It took two good nights of sleep and patience, but the miracle of pharmaceuticals knocked that nasty infection down. I have a healing nick in my skin and some bruising (that kind of acute inflammation causes a fair bit of collateral tissue damage), and a sore bum. But I will be fine.

In hindsight, I should have headed to urgent care much sooner, and I will chalk that up to a lesson learned. 

I am grateful that I have a job that provides decent insurance. I am grateful that I have access to health care for acute, emergent problems like this. I am grateful to the NPs at the urgent care who responded quickly and professionally even though it was the end of a long day for them. I am grateful that tetanus vaccines still exist (since I expect vaccines to become unavailable/hard to find/not covered by insurance in the coming months to years, I got measles and shingles vaccinations earlier this year). I mention these things because they are now in jeopardy for many citizens of this country. I'm worried. 

 

More Than You Ever Wanted To Know About Intestinal Parasites in Small Ruminants

 Whenever we have a small ruminant (sheep or goat) necropsy, the rule of thumb is that it is intestinal parasitism until proven otherwise. 

Cows get intestinal parasites too, but for the most part, due to differences in management and physiology, weaned animals and adults rarely develop such a heavy parasite load that it leads to death. There are always exception, especially for calves that are still nursing.

Sheep and goats have a particular problem with the roundworm Haemonchus contortus. The adult worms are small, around 1 cm long tops, and very thin. In small numbers, they are easy to miss. Haemonchus prefer to take up residence in the abomasum, the glandular part of the forestomach between the rumen and the duodenum. The adult worms and late-stage larvae burrow into the mucosa of the abomasum and feed on the blood of the animals. Heavy or even moderate but chronic loads of Haemonchus cause the animals to become anemic. When the animals begin to show clinical signs of the anemia, the owners deworm them but it's usually too late. Severe anemia secondary to Haemonchus parasitism is the cause of death of most of the sheep and goats that we see. 

 Coccidiosis is the other player in this small ruminant gut roulette. Coccidia are protozoal parasites, not worms. Infections have to be treated with entirely different products. For most of their lifecycle, coccidia are tucked deep into the intestinal mucosa. The result is erosion of the structure of the mucosal layer. The animals can't digest food anymore and often develop diarrhea, which is not usually observed in cases where only Haemonchus is present. But severe coccidiosis can also cause anemia! 

Many sheep and goat owners are small flock hobby farmers. They don't have a lot of space and can't rotate pastures. The animals shed ova and oocytes in their feces and repeatedly re-infect each other. Some of the owners decide the solution is to treat their animals constantly with dewormers and coccidiostats. The result is a short-term drop in adult parasites. But the treatments do nothing about ova and oocysts in the pastures. They are highly resistant to heat, cold, UV, etc. and sporulate into larvae to start the cycle anew. And overtreatment can result in the creation of drug-resistant populations of parasites. 

 One of the tests we try to run on every small ruminant necropsy is a fecal egg count. The result of this test is a count of ova or oocytes per gram of feces. Here is a graph showing the results of 47 fecal egg count tests during a two-year period. The left hand scale is a log scale, so each horizontal line increases by a factor of 10. Coccidia are Eimeria spp. and strongyles (strongyloids) are for the most part Haemonchus. Some animals only had Haemonchus, some only Eimeria. Some had both (the paired lines). Most of the animals represented here were severely anemic. 

 

 

 

The winner is the lamb necropsied by my colleague that had more than one million Eimeria oocytes per gram of feces. Truly astonishing. 

 Today I necropsied a lamb that wasn't anemic. No adult Haemonchus were in its abomasum. The general presentation of the lamb was consistent with sepsis, and while that was the cause of death, that's not a proximal diagnosis. What caused the sepsis? I kept looking. The animal had severe diarrhea and there was no digesta in its intestinal tract or feces in its colon. Nothing but gas. I started looking into the large bowel and found many adult roundworms. They weren't delicate, hair-thin Haemonchus but they were definitely strongyloids. The mucosa of the large bowel sections was eroded and irregular. Then I moved up to the small intestine. Surprise! Tapeworms. Adult tapeworms that were many, many inches long. 

Since we don't see intestinal worms very often in sheep and goats, I did a little research and decided that the worms were probably Trichostrongylus spp. They can also cause anemia like their cousin Haemonchus but they live in the intestines instead of the abomasum. Since I didn't see evidence of anemia, I thought that the tapeworms were probably the more significant problem. 

And the cause of the sepsis? Well, it's a cascade of unfortunate events. The intestinal mucosa is damaged by worms and larvae cavorting about. The tapeworms consume digesta (competing with the lamb for nutrients). The intestines stop functioning and no longer send proper signals to the rumen, which stops trying to send stuff into the intestines. Eventually, the intestinal environment becomes so compromised that gut bacteria decamp into the bloodstream. 

What had me scratching my head with the case was the fact that tapeworms are extremely easy to treat. We usually only see them in small animal cases associated with neglect and rarely in production animals. That problem was resolved when I called the owner and she told me that they hadn't dewormed ... in years. 

It's not a problem until it is, I suppose. She's now lost 6 lambs due to that decision. 

 

Frankie and JWW--Out of Novice At Last

Frankie and I have been struggling to advance in AKC JWW (Jumpers With Weaves). She's been stuck in Novice since I started trialing with her. At first she knocked bars, oh so many bars. That problem fixed itself as she started to understand the game better and learned to balance her speed with better take offs.

At the Novice level, the dogs are allowed a couple of errors but knocked bars are always an elimination. Bars down lost us a lot of Qs. But in JWW, the dog also can't take any wrong obstacles. Frankie has a tendency to curl into me so even when I want her to take 4 jumps in a straight line, she usually turns towards me and takes an off course. 

That's what happened in the video I've attached here. The third jump she takes is not the correct one even though I was doing my best to keep her from turning into me. I stopped and chose to use the Fix-N-Go option where you can go back and correct that mistake. The run is no longer scored or timed. I turned her around and wrapped her around the first jump (backwards, but it didn't matter anymore) and on the second attempt, she ran the course correctly. She bobbled the weave entrance but that's allowed in Novice. She rarely misses weaves in practice on grass but on this fast turf, she comes into the weaves very hot and sometimes misses the entry. I lifted her up like Simba at the end because she stayed with me all the way to the leash. 

 

 I only needed one more Q to get her (and me) out of Novice. And we pulled it off the next day! She almost breaks at the start line--that scooting forward is a problem and I'm working on it. Notice how she curls into me as she comes out of the tunnel. That's partly because that's what she does and partly because I wasn't in the right position to get her over the next jump. She never took any obstacles and she never crossed the plane of the next jump so the judge didn't call any faults while I was fumbling around getting her lined back up. It was just time on the clock, not errors. She hit the weaves super hot but managed the entry this time for a nice clean finish back to the tunnel. 

 

 I've learned a few things while trialing with Frankie this summer. She is true to herself. She becomes extraordinarily overstimulated in a flash of a second but is still predictable and trainable. Frankie is not Archie--she isn't looking to please me. She is willing to go along with my rules, more or less, so she can get what she wants. And what she wants to do is move. I may never have clean start lines with her. She crouches down like a sprinter in the starting block (good). Her focus forward training means she doesn't look at me but at the course in front of her (good). She drools (eh). She creeps forward (not good). Clearly I can shape some of that but I can't change her fundamental nature. 

I'm making peace with that because she's starting to get good at this agility thing. People stay late to watch her run, and although smooth fox terriers are in general crowd pleasers, they are staying late to watch because she's doing great things in the ring. I lost count of how many people told me at the trial how much progress she has made this summer. And I agree.   

Invite to the Agility Invitational

Archie got his third invite to the AKC Agility Invitational! He is the second-ranked Smooth Fox Terrier in the Preferred class. That's pretty good for my old man--he will be 10 years old in September. He's had a decent run of successes in the past few months and the invite is evidence of that.

 This is my fourth invite to the Invitational. My first was with Iz back in 2006, at the very first Agility Invitational event. 

Big events are not my thing. I don't like the crowds. I really don't like the Orlando venue. That's a lot of money and leave time to set aside for an event I don't want to attend. And Archie of course doesn't care. So I'm going to decline, opening up a spot for the next Preferred SFT in the rankings.