I debated writing about this now since it’s an ongoing situation with a very unclear outcome, but that’s medicine. We also don’t have a lot of camelid content on the blog, and there’s an infectious disease component to this case, so figured it was worthwhile.

Mickey (photo right) is an older male alpaca, part of my small group.

Why do I have alpacas? Here’s the short version:

  • I had a flock of rare breed sheep.
  • Coyotes starting picking off the sheep so I got a llama (Dolly) for predator control.
  • Dolly sucked at her job, so I was soon left with no sheep and a llama.
  • I then got some alpacas to keep the llama company.

This past Saturday, we found Mickey down on his side and couldn’t get up. I had thought that he looked a little weak in the hind legs earlier that week and this was presumably a progression of that problem. He was bright, alert and a pretty textbook spinal disease case. Specifically, his signs were consistent with a spinal lesion between the 3rd thoracic and 3rd lumbar vertebrae (T3-L3), given the severity of his hind limb abnormalities but pretty normal front limbs.

The two leading causes for this condition in an alpaca are:

  1. Parasite migration through the spinal cord due to infection with the deer meningeal worm Parelaphostrongylus tenuis (P. tenuis).
  2. Spinal trauma. Mickey and the boys chase each other around at times and it’s been icy. I didn’t appreciate anything in his back that would suggest a spinal fracture or other traumatic event, but sometimes it can be hard to tell.

While I couldn’t rule out trauma, parasitic migration made more sense, and P. tenuis is a major issue for camelids (like alpacas, llamas) and moose in some regions. Like many parasites, it has an unusual life cycle (see illustration below):

  • P. tenuis normally lives in white tailed deer, which are abundant around here. The adult parasites live in the subdural space and associated tissues in the central nervous system. Females lay eggs in blood vessels, and the eggs travel through the blood to the lungs where they develop into larvae (L1 stage). The larvae penetrate the small air sacs (alveoli) in the lungs and are coughed up and swallowed. They’re then passed in the feces, and subsequently infect slugs and snails, developing to their L3 larval stage.
  • If an animal ingests infected slugs or snails, the larvae move from the intestinal tract and somehow find their way to the central nervous system. In white tailed deer (the definitive host), they develop in gray matter of the spinal cord and then migrate to the subdural space, mature to adults and the life cycle starts again, usually without causing any problems for the deer. However, in other species like alpacas, the larvae don’t mature, and instead stay in the gray matter, causing inflammation and significant damage. Usually this damage predominantly affects control of the hind limbs, but depending on the location(s) to which the parasites migrate, damage to other parts of the spinal cord or brain can occur, so it’s on my list for any neurological disease in a camelid.

Back to Mickey. Given the odds of parasitic disease, the lack of any additional treatment I could possibly providefor trauma and the limitations of field imaging (e.g. x-rays), I’ve been treating him as a presumed P. tenuis larva migrans case with antiparasitics, anti-inflammatories and nursing care. I could have done a spinal tap to try to confirm my suspicion, but if it was unremarkable I still wouldn’t rule out P. tenuis, so I’d still treat him. Given the hassles of performing a spinal tap and the limited likelihood that I’d find a different cause, I didn’t bother. (If he was in hospital where it was easier and more convenient, I’d likely have done it, as it would be interesting to know the results.)

Drugs are part of the treatment for this disease, but nursing care is a huge component. Any down large animal is always a concern, as they can damage their muscles and nerves lying down for too long simply because of their weight. Fortunately, alpacas are much lower risk for complications from short term recumbency given their smaller size. However, I still need to keep him in a well bedded area and move him around so that he’s changing positions and not laying in wet (urine soaked) bedding. That also helps reduce the risk of pressure sores, another major concern in recumbent animals.

Over the past few days, he’s been up and down (figuratively and literally). Most days, I can get him up with some assistance and he’ll take a few steps with me supporting and steering him by holding his tail. Some days have been better than others.

With any neurological disease, the first thing I want to see is that the animal stops deteriorating. If the animal just keeps getting worse, the prognosis is really bad. Mickey plateaued pretty early, which was a good start.

Yesterday, I tried him in an ad hoc sling I made from a repurposed hammock. It wasn’t much of a success since he didn’t try to stand. A sling can be good to get an animal off their feet and let them use their limbs, with support. But Mickey didn’t use the sling like that, he just hung there, so there was a risk the sling would just cause more damage. It was a nice try, but I abandoned it, at least for now.

This morning, Mickey got up with assistance and took the most steps he’s made so far, walking from the barn to a run-in shed/barn. Movement is good, but walking on ice is bad. However, there was a pretty good path for him and the shed is well bedded, so I let him lead the way and that was his spot for a while.

The video below is from this afternoon – his strongest effort yet, but still with some pretty obvious major abnormalities.

What’s the prognosis for Mickey?

I keep waffling on that. Milestone #1 was when he stopped deteriorating. Now we need to see how he improves. Neurological damage is slow to improve, and the degree of improvement is hard to predict. As long as he keeps improving, there’s hope. Once that initial improvement plateaus, I don’t expect major improvement after that. Animals with neurological damage can still improve a bit at that stage, probably in part by learning how to compensate for their deficits, but we don’t expect to see a dramatic improvement later on.

I’d like to think he’s still in the improvement phase. It’s hit and miss; he’ll look good one time and then bad a little later… that’s life managing neurological disease. But he’s showing enough improvement and is otherwise stable enough that he’s worth treating. The video from today is by far the best he’s been so that’s encouraging.

He didn’t like me much before and he’s definitely not a fan now given all the poking, prodding and medicating, but that’s life with livestock. More updates to come (good or bad).

Life cycle figure from: