Neospora in Adult Dogs

Neospora has become increasingly common in veterinary neurology, especially in the last few years. Neospora is an obligate intracellular parasite that causes notable complications in cattle but is not commonly diagnosed in dogs. Dogs are a definitive host, which means upon infection, they will not pass this infection along to other hosts (unless that new host consumes their meat). In other words, do not eat a dog infected with Neospora (!!).

How do dogs  get infected?

The most common transmission is transplacental or juvenile onset neosporosis. Dogs that develop clinical signs at greater than 12 months of age probably have adult onset or the newly acquired form. This form has fecal/oral transmission.

What are the clinical signs of Neosporosis in adult dogs?

There are two forms of disease, which may occur separately or concurrently. First, we can see neuromuscular disease. Signs may include a strict myopathy (difficulty opening the jaw, tetraparesis with normal reflexes), neuromyopathy (myopathy signs plus patchy reduced reflexes) to a full neuropathy (reduced reflexes in multiple limbs along with clinical weakness). The other option is CNS signs, for which cerebellar signs and seizures predominate.

How is it diagnosed?

Adult onset, or acquired neosporosis, is diagnosed via IFA titer. Different papers have listed different “positive” IFA titers. A recent article from Sydney Australia by Kennedy et al(DOI: 10.1111/jvim.17219), listed the positive IFA titer as 1:800. Previous studies have listed anything from 1:200 to 1:800 as the positive titer rate. I typically recommend retesting if you get anything over 1:200. If it goes UP or remains above 1:400 it is likely clinically active and warrants treatment (if clinical signs are present). PCR inconsistently diagnosed Neospora in the recently published study.

How is it treated and do relapses occur?

The first line treatment for most studies is clindamycin (median dose 15 mg/kg PO q12h) x 12-17 weeks. Sulfa antibiotics are the second line of treatment, and several dogs received both drugs in the recently published study. Prednisone is important during active CNS disease to minimize the secondary inflammatory reaction during protozoal die-off. The dose and duration of prednisone is variable, but immunosuppression should be avoided. Relapses were common in the most recent study (9 relapses occurred in 4 dogs) highlighting the need for either longer treatment, or prompt treatment if signs recur. All signs were similar to the initial presenting signs except for one dog.

Take home message?

Remember to test for Neospora caninum when presented with a dog with CNS signs, myopathy, or neuromuscular signs. A simple titer using IFA is the best step, followed by consultation with your local neurologist.

Thanks for reading! I hope you have a wonderful start to November and look forward to working with you soon.

Tick Paralysis and Dogs

The ticks are still here but owners may have stopped applying topical treatments. So fall is the time to be on the look out for Tick Paralyses (okay, really anytime but now isn't a BAD time to be aware)!

What causes Tick Paralysis?

Salivary transfer from a Dermacentor (in America) and Ixodes (in Australia, for my Australian readers) will result in neuromuscular blockade. How it actually works is really pretty ingenious. (Skip this next part if you're in a hurry.) At the presynaptic terminal, acetylcholine packets must be released into the neuromuscular junction so they can then bind to the post synaptic (muscle) membrane receptors. The acetylcholine binds to the presynaptic membrane using specific proteins as well as calcium. The saliva from one of the aforementioned types of ticks will interfere with acetylcholine release at the presynaptic terminal by binding calcium. Amazing, really.  

What are the common clinical signs?

If you cannot release acetylcholine from the presynaptic membrane at the neuromuscular junction, what can you do?  Exactly...nothing. 

Therefore clinical signs are an ascending pelvic to thoracic limb flaccid paralysis. No reflexes, no motor, no paw replacement, nada. These signs begin 5-9 days after exposure to the tick saliva. Cranial nerves are RARELY affected. This is important because botulism more commonly affects cranial nerves and this can be one way to try to differentiate between these two diseases. 

How do you make the diagnosis?

1. Find the tick.
2. Remove the tick.
2.5 (Apply Frontline/Bravecto/other)
3. Clinical improvement should begin 24-48 hours after tick removal.
No specific testing is available to confirm the diagnosis. 

I once had to find a tick on an Old English Sheepdog waaaay back in the year 2000. Topical tick treatment wasn't as prevalent then as it is now, so our solution was to shave the dog. We found the tick between the dog's toes. (Insert eye rolling here!!) In 2023, I suggest applying Frontline/Bravecto (your choice of topical flea treatment) first then perform a non-invasive tick hunt and monitoring for clinical improvement. If ineffective after 48 hours you can either commence a thorough tick hunt, or search for other causes of flaccid paralysis. (Or, call me for a neurology consultation!)

How do you manage patients flaccid paralysis?

Flaccid paralysis means that the animal does not have reflexes, or voluntary motor. As such, these animals may be at risk of respiratory failure due to loss of intercostal muscle function. Frequent CO2 monitoring, respiratory watch and ventilatory support if needed can be very important in the early stages of disease. Due to the rapid recovery common with tick paralysis, most patients do not need long-term intensive nursing care or physical therapy. 

Thank you for reading!  I appreciate you, and all that you do for your patients. Please note that I'm currently in Australia and will have delays in email response and NO telephone service. You can message me through FB if you want to but otherwise email is best. Thanks!!

The Weak Lab

Here is the scene: You're evaluating a 10 year old MC Labrador retriever for a 6 month history of progressive difficulty walking. Signs were first noted in the pelvic limbs but have recently been noted in the thoracic limns. As an astute vet, you also discover that the dog has become hoarse, too. (Nice job!)

Physical examination: Unremarkable other that OA in the stifles from prior CCL injury and surgery .

Neurologic examination:
Mentation: BAR
Cranial nerves: Hoarse voice and harsh breathing consistent with laryngeal paralysis. Remaining cranial nerve examination normal.
Gait: ambulatory, slapping limb gait when walking, especially in the pelvic limbs. The dog appears to walk like he is wearing clown shoes.
Postural reactions: Absent paw replacement testing all four limbs

Reflexes: Absent femoral reflex (bilateral), reduced gastroc reflexes (bilateral), reduced distal withdrawal of all four limbs but most notable distal to the hock bilaterally, unable to obtain bicep reflexes (bilateral). Intact perineal, and reduced (but present) C. trunci throughout the entire TL region.
Palpation: Non painful spinal palpation, normal cervical ROM

Holy cow! What is this? (You might be wondering) This neurologic exam is all over the place!! I need help. (It's okay to stop here and call me or setup a consult.) However, since we're on a learning track today let's talk though this one together. I am willing to bet you can get this.

How to lesion localize this case if you lived inside of my brain:

1. First, we don't see any evidence of forebrain or brainstem disease, correct? (No CN deficits, no seizures, no mentation changes.) Okay, cross that off.

2. Secondly, all four limbs are involved. This cannot be T3-L3, or L4-S3 because ONLY the pelvic limbs would be affected. (See, we're getting somewhere!) Cross those off.

3. This leaves us C1-C5 or C6-T2 myelopathy, if this is spinal in origin. You might be tempted to say C6-T2 myelopathy because of the reflex deficits in the thoracic limbs but remember that we have reflex deficits in all four limbs and that just isn't possible with a C6-T2 myelopathy. You must have a lesion in the spinal cord plexus (C6-T2, L4-S3), or the nerve, or the neuromuscular junction to have a reflex deficit. Cross off C1-C5, and C6-T2.
   

4. Okay, big breath. This is NOT spinal cord in origin. It cannot be. It doesn't line up! We have ourselves a neuromuscular disease

What to do next, if you suspect neuromuscular disease

1. Neuropathy – reduced reflexes in multiple limbs, and/or limbs and head. Postural reactions may be reduced or absent. Pain is not noted on palpation. NO ataxia!

2. Junctionopathy – absent reflexes, non-ambulatory paresis or exercise induced non-ambulatory paresis. Depending on the severity, these animals may have a range reduced to absent postural reactions. (Myasthenia gravis is the exception. It is a junctionopathy but acts like a myopathy.)

3. Myopathy – Classically, these animals have a normal neurologic examination. (Think muscle disease, not neurologic disease) They are paretic (ranging from poorly ambulatory to ambulatory with fatigue) without any postural deficits or reflex deficits. Muscle pain, stiffness and pain on palpation may fool you into thinking they have spinal pain.

This case fits with a neuropathy, doesn't it? In fact, this is an example of a neuropathy. This dog has a neurodegenerative neuropathy common in Labrador retrievers. It is suspected to be genetic. The diagnosis is confirmed with muscle and nerve biopsy. (Yes, I can do these for you.)

Sadly, we do not have treatment available to reverse or slow down progression therefore treatment is supportive. Slings when needed, good solid footing such as rugs/carpet or yoga mats, and physical therapy are the mainstay of treatment. Supportive care with acupuncture has also been beneficial for some dogs.

Thanks for reading! Have a wonderful week and stay warm! I will be closed on January 28-29th. I appreciate your patience and look forward to connecting with you on Monday January 31st with any cases or questions you may have.

Tick Paralysis and Dogs

Tick Paralysis and Dogs

The ticks are still here but owners may have stopped applying topical treatments. So fall is the time to be on the look out for Tick Paralyses (okay, really anytime but now isn't a BAD time to be aware)!

What causes Tick Paralysis?

Salivary transfer from a Dermacentor (in America) and Ixodes (in Australia, for my Australian readers) will result in neuromuscular blockade. How it actually works is really pretty ingenious. (Skip this next part if you're in a hurry.) At the presynaptic terminal, acetylcholine packets must be released into the neuromuscular junction so they can then bind to the post synaptic (muscle) membrane receptors. The acetylcholine binds to the presynaptic membrane using specific proteins as well as calcium. The saliva from one of the aforementioned types of ticks will interfere with acetylcholine release at the presynaptic terminal by binding calcium. Amazing, really.  

What are the common clinical signs?

If you cannot release acetylcholine from the presynaptic membrane at the neuromuscular junction, what can you do? 

Exactly, nothing. 

Therefore clinical signs are an ascending pelvic to thoracic limb flaccid paralysis. No reflexes, no motor, no paw replacement, nada. These signs begin 5-9 days after exposure to the tick saliva. Cranial nerves are RARELY affected. This is important because botulism more commonly affects cranial nerves and this can be one way to try to differentiate between these two diseases. 

How do you make the diagnosis?

1. Find the tick.
2. Remove the tick.
2.5 (Apply Frontline/Bravecto/other)
3. Clinical improvement should begin 24-48 hours after tick removal.
No specific testing is available to confirm the diagnosis. 

I once had to find a tick on an Old English Sheepdog waaaay back in the year 2000. Topical tick treatment wasn't as prevalent then as it is now, so our solution was to shave the dog. We found the tick between the dog's toes. (Insert eye rolling here!!) In 2020, I suggest applying Frontline/Bravecto (your choice of topical flea treatment) first then perform a non-invasive tick hunt and monitoring for clinical improvement. If ineffective after 48 hours you can either commence a thorough tick hunt, or search for other causes of flaccid paralysis. (Or, call me for a neurology consultation!)

How do you manage patients flaccid paralysis?

Flaccid paralysis means that the animal does not have reflexes, or voluntary motor. As such, these animals may be at risk of respiratory failure due to loss of intercostal muscle function. Therefore CO2 monitoring, respiratory watch and ventilatory support if needed can be very important in the early stages of disease. Due to the rapid recovery, most patients do not need long-term intensive nursing care or physical therapy. 

I hope you are doing well and staying safe. I appreciate what you do to help clients and their pets. Let me know how I can help you manage your patients with neurologic disease.

On site consultation is available Monday through Saturday at variable times throughout the week. Email consults are completed in evenings. 

Have a good week!