THE POSSIBILITIES FOR RHUMB – After the initial neuro-exam, these were the possibilities that we were told she could have.
DEFINITION – The upper motor neurons originate in the brain and travel downward to connect with the lower motor neurons. The latter localize both in the brainstem and the spinal cord and are the mediators between the brainstem and the spinal cord and their peripheral targets, the muscles.
ENCHEPHALITIS / MENENGITIS – (catch all) Inflammation of the brain, however, it also may be accompanied by the inflammation of spinal cord (myelitis), and/or the inflammation of the meninges (meningitis), membranes which cover the brain and spinal cord.
Symptoms appear suddenly and rapidly progress – fever, seizures, behavioral changes, decreased responsiveness, head tilt to either side, paralysis of face, uncoordinated movements or circling, unequal size of pupils (anisocoria), smaller sized pinpoint pupils, decreased consciousness
Causes can be – idiopathic, Immune-mediated disorders, postvaccinal complications (adverse vaccine reaction), viral infections (canine distemper, rabies, parvovirus), bacterial infections (anaerobic and aerobic), fungal infections (aspergillosis, histoplasmosis, blastomycosis), parasitic infections (Rocky Mountain spotted fever, ehrlichiosis), foreign bodies
TICK BITE – Tick paralysis is an acute, ascending motor paralysis that occurs in dogs and cats. The cause is a neurotoxin in the saliva of certain species of adult ticks. Dermacentor species predominate as a cause in North America. The onset of symptoms is 5 to 9 days after tick attachment, and include loss of coordination progressing to paralysis, changed voice, and difficulty eating. Death can occur secondary to paralysis of the respiratory muscles, but in North America, a good prognosis results once the ticks are removed
MORTALITY RATE 10%
RABIES – This would be based on a known bite or altercation with a suspected infected animal, and a bite/wound is almost always present – Early symptoms can be seen 2-10 days after infection and include – Muscle pain, restlessness, irritability, chills, fever, malaise, a general feeling of sickness and discomfort, photophobia, a fear of bright lights, anorexia, or disinterest in food, vomiting, diarrhea, inability or unwillingness to swallow, cough, paralysis of the throat and jaw muscles may follow.
The disease progresses to severe behavioral changes, hyper-salivation, bark, tone changes, paralysis, and death.
MORTALITY RATE 100%
MYASTHENIA GRAVIS – Acquired myasthenia gravis (MG) is a disorder of neuromuscular transmission resulting from autoantibody mediated destruction of the nicotinic acetylcholine receptors at the neuromuscular junction. Acquired MG is the most common neuromuscular disorder that can be diagnosed in dogs.
The symptoms are unpredictable and can be gradual or sudden – exercise intolerance or weakness when exercising, gradually worsening weakness, sudden collapse or falling over, sleeping with eyes open, drooping of eyelids, excessive drooling, wretching/regurgitating, change to the sound of bark and/or whine, trouble swallowing, coughing (may indicate aspiration pneumonia), difficulty breathing
MORTALITY RATE 50 – 60%
BOTULISM – C. botulinum and its spores are widely distributed in soils, sediments in fresh and coastal waters, the intestinal tracts of fish and mammals, and the gills and viscera of shellfish. The bacteria can only grow under anaerobic conditions. Botulism occurs when animals ingest preformed toxins in food or C. botulinum spores germinate in anaerobic tissues and produce toxins as they grow.
Types A, B, E and F cause illness in humans (poorly canned foods, raw honey…) Type C affects animals, and it is extremely rare in dogs and usually follows feeding on carrion. Compared to other species, dogs and cats are relatively resistant to botulism. Antitoxin can only be used before signs of paralysis.
Symptoms – Typically, symptoms occur within a few hours to six days after eating spoiled animal meat that is infected with the Clostridium botulinum type C preformed neurotoxin. At onset, ascending paralysis, difficulty swallowing, visual issues FULL ARTICLE
MORTALITY RATE – 5-10%
IDIOPATHIC POLYRADICULONEURITIS / COONHOUND PARALYSIS – is inflammation of the nerve roots. Clinical signs often develop 7–14 days after a raccoon bite or scratch (Coonhound Paralysis); however, other affected animals have not been exposed to raccoons.
A similar syndrome can develop in dogs and cats 1–2 weeks post-vaccination. An immune-mediated reaction to raccoon saliva or other antigen is suspected.
Initially, there is a short-strided gait in the pelvic limbs that progresses within 1–2 days to flaccid tetraparesis or tetraplegia and, in some cases, to facial and laryngeal weakness. Occasionally, the thoracic limbs are initially affected. Death from respiratory paralysis can occur in severe cases. Spinal cord reflexes are weak to absent, and severe muscle atrophy is evident within 10–14 days. Pain perception is intact, and some dogs may appear hyperesthetic, showing signs of discomfort on palpation of the trunk or limbs. Mentation and appetite are not affected. Urination, defecation, and tail movement usually remain normal.
MORTALITY RATE – unknown to 5-15%
GUILLAIN BARRE SYNDROME – (ghee-yan-bar) is a classic lower motor neuron disorder. It is a reactive self limited auto immune disease in which the body’s immune system attacks part of the peripheral nervous system and which presents as acute generalized weakness, paralysis, and can include complications with the respiratory system. FULL ARTICLE
MORTALITY RATE – unknown
TOXOPLASMOSIS – Toxoplasmosis is caused by Toxoplasma gondii, a protozoan parasite that infects humans and other warmblooded animals. It is found worldwide. Felines are the only definitive hosts of the parasite. Adult animals with vigorous immune systems control the spread of the parasite efficiently; therefore, toxoplasmosis usually causes no signs in healthy dogs.
MORTALITY RATE – unknown
ACCIDENTAL / MALICIOUS POISONING – Any class of neurotoxin, neurotoxic drug, or organophosphates.
FULL ARTICLE on why people poison animals
MORTALITY RATE – high (that is the intent of poison)
GENETICS – Multidrug Resistance 1 is inherited as an autosomal incomplete dominant disease. Dogs only need to inherit one copy of the MDR1 mutation to be at risk for sensitivity of certain drugs. Dogs with 2 copies of MDR1 can have more severe reactions.
P-glycoprotein is a pump that removes certain drugs and toxins from the body. A mutation in the ABCB1 gene associated with MDR1 prohibits P-glycoprotein’s ability to limit absorption, distribution, and excretion of drugs. Dogs with one copy of the MDR1 mutation can have some drug sensitivity. Dogs with two copies of this mutation can experience more serious neurologic symptoms like excess salivation, tremors, anorexia, blindness and possibly death.
The following is a list of drugs known to cause reactions – Acepromazine (tranquilizer), butorphanol (pain control), doramectin, doxorubicin, emodepside, erythromycin, ivermectin (found in heartworm medications), loperamide (anti-diarrheal agent), milbemycin, moxidectin, paclitaxel, rifampin, selamectin, vinblastine (anti-cancer agent), vincristine and vinorelbine
MORTALITY RATE – unknown
RHUMBS PRECLINICAL HISTORY – Rhumb was MDR1 normal/clear (genetic panel completed in 2017). She was an intact female, and had whelped her litter of five puppies in February of 2018. No traumas, no wounds, no wildlife altercations. Rhumb was not a scavenger, she didn’t pick up objects, trash, dead animals, or rotting vegetation from the ground. She was raw fed and vibrantly healthy.
RHUMBS PRECLINICAL SYMPTOMS – Rhumb was coming into her proestrus cycle (4-5 days in), both behaviorally and physically, but her vulva was not swollen yet. Rhumb had thrown up part of her dinner the night before, no reason for concern. While it was not normal for her, there was no behavior or mobility change or cause for us to panic. That night she was out doing chores with us and playing with her puppies in the yard past 10pm. She hopped up on the bed at midnight, we snuggled for a bit, and we all tucked in for the night. Normal day normal evening.
RHUMBS SYMPTOMS – From the time we woke up (to what was a seemingly normal day), to when I was told she would not be coming off of a ventilator, and then my request to euthanize her, was 6 hours.
ONSET OF SYMPTOMS – rapidly ascending symmetrical paralysis, consuming her limbs, diaphragm, lungs, and larynx, and lastly her heart failing. Hyper-salivation, gagging, eyes tearing profusely. No rectal tone.
NOTED IN CLINIC – No behavioral changes, No Fever, Normal Blood Work, Good Distal Pulses
NECROPSY – After 3 weeks the report came back –
REASON FOR SUBMISSION – “tetraparesis, hypersalivation, dyspnea. Patient rapidly declined and was euthanized”
PATHOLOGIST COMMENTS – It is three paragraphs, but this part will suffice “A definitive cause for clinical signs has not been found. Necropsy of the dog was fairly unremarkable”. Further testing at another university was recommended and we declined, or rather have declined for now.