Neurologic Problems in Camelids

Pamela G. Walker, DVM, MS, DACVIM  

There are many causes of neurologic problems in neonatal and mature camelids, some more common than others. As owners it is very important to know what is “normal” for each of your animals, keeping in mind that some animals may have some odd things that are “normal” for them! It is also easy to confuse weakness from illness with neurologic signs. I will present the information based on age, then in more detail for the problems that are not age related.

 Newborn Crias:  do not be alarmed if many of them appear to have a head tilt for a few days, some may be quite dramatic and give the cria a quizzical appearance. This head tilt may be present even in crias born unassisted. It is probably due to in – utero positioning of the neck that will relax in a few days and the head will be straight.

 Seizures/depression:

1. Serious problems can occur in newborn crias; hyper or hypoglycemia can result in severe depression or seizure activity and must be diagnosed and treated immediately and aggressively to save the cria. Both conditions can present in a similar fashion, using a hand – held glucometer determine the glucose concentration of the cria, if it is low immediately squirt 2 to 3 mL of 50% Dextrose into the crias mouth and call your veterinarian. If the glucose concentration is high (> 400 mg/dL), see if the cria will nurse plain warm waterfrom a bottle, it you feel comfortable tubing the cria, tube 4 to 6 oz of plain warm water and call your veterinarian.
   
   
2. Meningitis or septicemia from possible failure of passive transfer may present as seizures. Keep in mind that even though it appears as if a cria nurses very well, there are many things that can interfere with absorption of colostrum (see cria care lecture). In the case of meningitis or septicemia, the cria should be treated aggressively with intravenous antibiotics, fluids and plasma (call your veterinarian).
   
   
3. (Depression, but still able to walk around can indicate some degree of oxygen lack during delivery (neonatal hypoxia). These crias can frequently be taught to be a normal cria, if they do not respond by the end of day 1 of birth, then treatment with DMSO may help (yes, call your veterinarian).

 OlderCrias:

1. Trauma can be a “not uncommon” cause of neurologic signs in crias as they tend to not pay attention to where they run or what is in front of them! If you find a cria down, be aware of what it could have run into and when you move the cria, keep it in the same position as it was found. If the cria is able to move/stand, but has an abnormal neck/head position put the cria in a small area until examined by your veterinarian and radiographs taken. Depending on the force of the impact, the cria may have subluxation of vertebra causing forelimb and/or rear limb signs based on where the injury is located. On occasion the injury can be severe enough to sever the spinal cord. These animals will be unable to stand, even with assistance and will have no feeling in their legs. Some injuries may be conservatively treated with stall rest with or without a neck cast. In a few cases surgical management may be attempted by an experienced surgeon, but camelids are prone to many complications.
   
   
2. Meningitis can also occur in older crias, the cause or source may never be determined, however I have had one case of Listeriosis meningitis (see below) in a three month old cria that presented as sudden onset as if it was trauma. Crias with meningitis may just be very depressed or may be unable to right themselves, or found circling. Treat as directed above.
   
    
3. Another cause of more progressive neurologic signs in crias usually under 12 months is a condition called hemivertebra. This is where one or more vertebra does not develop properly causing a wedged shaped with subsequent misalignment of adjacent vertebra (subluxation) and pressure on the spinal cord. When this abnormality occurs in the cervical, thoracic or lumbar part of the spinal cord, it is a fatal condition, diagnosed by radiographs. Clinical signs are usually an uncoordinated gait, possibly falling down when attempted to restrain, especially if the head and neck are manipulated. I have had an unusual presentation in one male alpaca that was approaching 2 years of age that had been shown the previous fall, but now had a somewhat “sideways” gait and would stumble when walking on uneven ground. Radiographs showed an abnormal vertebra and necropsy confirmed the diagnosis of hemivertebra. On occasion, this is the cause of crooked tails but does not usually cause any significant problem (with the gait). With the exception of crooked tails, these animals do not live, we have no idea if it is a heritable condition, but it is recommended that this match not be repeated.
   
    
4. Vertebral body abscess and brain abscess will present as paresis or paralysis, usually in the rear limbs, but the clinical signs will vary based on where the abscess is located. It is not always possible to determine the initial cause, but it is usually secondary to bacteremia (bacteria in the blood) which may be transient and the cria may not show any definite signs. The onset will usually progress over several days, with vague signs and maybe a fever. Diagnosis is difficult and will require advanced testing such as CSF tap, contrast radiographs and possibly a CAT scan. If your veterinarian is suspicious of a brain abscess based on clinical signs and advanced diagnostics are not possible then attempting treatment with anti-inflammatories and high doses of antibiotics (Naxcel or Nuflor or Baytril) is one option and see how the cria responds.
   
   
5. Rickets, although a metabolic condition, will present initially as a possible neurologic problem. Rickets is a lack of Vitamin D in growing animals. Milk does not contain Vitamin D, so if a nursing cria does not get exposure to sunlight because of weather, fiber cover or wearing a coat, they will be at risk for rickets. Clinical signs usually show up between 4 and 7 months of age. Early signs are lameness, not wanting to play with herdmates and painful walking as if on “egg shells” progressing to a posture with a hunched back and a reluctance to rise. There is also swelling of legs joints (carpi, tarsi and fetlock joints) and the bone-cartilage junction of the ribs. Angulation of the front and/or back legs may also be seen in some animals. Diagnosis can be made by presence of classic clinical signs and lack of Vitamin D supplementation with definitive diagnosis done by using radiographs and measuring serum Vitamin D concentration. It is also important to measure serum Calcium and Phosphorous concentration as sometimes supplementation is needed (can use Fleet enema orally for Phosphorous). Treatment is Vitamin D by injection at 1000 IU/lb, SC (subcutaneous) every 2 months. Prevention is easily done by giving Vitamin D 1000 IU/lb, SC, every 2 months OR 33,000 IU, PO, every 2 weeks during times of minimal sunlight. Most of the signs will be reversed with treatment, however I have had one adult female that had rickets as a cria that developed a deformed pelvis as a result and was unable to deliver a cria through the pelvic canal.

 
ANY AGE

Inner or middle ear infection: can be a complication of upper respiratory disease or pneumonia that moves into the lower ear canals, but does not show up as drainage from the outer ear. It can also be caused by Spinous ear ticks (Texas, Colorado) that enter the ear and present with an ear droop progressing to a head tilt. Inner/middle ear infections may initially present with only a head tilt, and may progress to a drooped ear and facial never paralysis. On occasion there may be circling or problems walking (ataxia). Diagnosis can be as simple as examining the ear with an otoscope, and starting on long term antibiotics (10 to 14 days). But frequently more advanced diagnostics are needed such as radiographs and/or CAT scans to determine the location and extent of the problem. In some cases, surgery is needed to drain the infection. Depending on the extent of the problem, with or without surgery there may be temporary to permanent complications such as paralysis of the nerves of the face. Some of the things that may occur as part of disease or complication of surgery is an inability to close the eye, pack feed/cud in the cheek and a drooped ear.

 Meningeal Worm infection: is a disease in the mid-west and eastern part of the United States caused by the parasite Parelaphostrongylus tenuis. The definitive host is the white tail deer and the intermediate hosts are snails & slugs. Camelids eat the snails and slugs – these are soft shelled snails and small slugs. Clinical signs can be seen in 45 to 53 days after ingestion. Clinical signs are due to tissue destruction and inflammation and vary as there is random migration of the larvae in the spinal cord and/or brain. The most classic presentation is rear limb weakness progressing to paralysis. These signs progress to the front legs. Other signs can include:  an exaggerated gait, stumbling, stiffness, overall weakness, circling, blindness, head tilt, seizures and death. The signs can start suddenly or be a more gradual onset over months.

There is no definitive test that can be done to diagnosis this disease. CSF taps may show increased eosinophils and will rule out other possible causes (Listeria, Meningitis). Frequently a diagnosis is made based on response to treatment. Prevention is trying to put up a deer proof fence and using a deep gravel barrier on the outside of the fence to prevent the migration of snail and slugs across into the pasture. Also important is to remove any dead fall of leaves, etc to eliminate a favorable environment for snails and slugs to live. You can use molluscicide, but must be careful to not contaminate the local water source. Some farms use guinea hens in the pastures to keep down the snails and slugs. Prophylactic use of Avermectins (Ivermectin, Dectomax) is the most common means of prevention, but is not always 100% so must be used in connection with the above listed management practices. They should always be given SC, as they are not effective as Meningeal worm prevention if given orally or topically.

Current dose recommendations are Ivermectin 1.5 mL/100 lbs, SC, every 30–45 days. Dectomax 2.0 mL/100 lbs, SC, every 45–60 days.Treatment is most successful if done early in the course of the disease before too much tissue destruction occurs and is directed at killing the larvae and controlling the tissue damage. The main drug used in treatment is Fenbendazole (Panacur/Safeguard) at 23 mg/lb (23 mL/100 lbs), orally for 5 to 10 days. To reduce inflammation use Banamine 1 mL/100 lbs, SC once to twice a day. If there seems to be no response (still unable to stand), then Prednisolone 0.5 to 1 mg/lb, IM, SC or IV can be used daily for two to three days. More aggressive anti-inflammatory such as DMSO (0.5 gram/lb, IV, daily) can be attempted. One dose of an Avermectin should also be given to kill any migrating larvae while still in the muscles.

The Avermectins do not readily cross into the brain, so are not effective as treatment, in fact if a high dose is used in an attempt to get into the brain, the animal may die (side affect of drug). In addition to medical therapy, it is very important to initiate physical therapy including massages, passive range of motion and using a sling to aid in standing, If possible, use of a float tank can also be beneficial for recovery. Be aware that the water temperature must be maintained at body temperature to prevent muscular shock.

Heat stress: can occur throughout most of the United States as camelids cannot tolerate heat especially heat with humidity very well. The reason why heat stress is included in a talk concerning neurologic problems is that the first clinical signs frequently observed is being “down”. Early signs are open mouth breathing, increased respiratory rate and weakness progressing to being unable to stand. When there is a down camelid in hot weather and in a region with Meningeal worm, treatment needs to be included for both heat stress and Meningeal worm.

Treatment for heat stress  involves moving to a cool place, hosing down belly and “armpits” with cool water, pouring alcohol down back and placing frozen water bottles (wrapped with towel) under the belly and in “armpits”. If an air-conditioned room is not available, then placing a fan will help with the cooling process. If they are not sheared, then they must be sheared!! Giving Banamine will help with inflammation, but will not directly lower the temperature, in fact the rectal temperature (initially 104 – 105 F) may not drop for many days, even though there are improvement in clinical signs.

Prevention of heat stress is very important and shearing yearly will be adequate in most camelids. This is a common practice in the alpaca community, but llamas are either not sheared yearly, or just have a barrel or lion cut, leaving all the heavy neck wool in place and are more prone to heat stress. In addition to shearing, there should always be shade shelters present plus fresh water – preferably in the shade. Routine activities such as toe and teeth trimming, halter training and transportation should be done only in the early morning or late evening when it is cooler.

One important thing to be aware of with your full fleeced show males is that they are prone to testicular heat stress (edema) and possibly permanent damage. A way to reduce the heat accumulation is to wrap their tail fiber so there is a “breeze way” under the tail and over the testicles. Be sure to not wrap the tail too tight, check it every few days, especially if it rains, plus use light color wrap as the color may “bleed” onto the fiber.

Polioencephalomalacia: is a lack of Vitamin B₁ (thiamine) in the first compartment. This results in interference to the glucose pathway to the brain and subsequent softening. The cause of polio is generally undetermined, but is usually associated with something that interferes with the normal balance in the first compartment such as change of fee or stress (birth). On occasion polio will occur with over dosage of Amprolium (Corid) because the drug will replace thiamine in the glucose pathway to the brain. Polio can also occur in some animals given Sulfa drugs; the reason for this is unknown and is usually fatal as it does not respond to thiamine. The first clinical sign is usually depression, but the one noticed first is blindness.

Usually they are found wandering aimlessly or found walking into barn walls or feeders. In some cases the signs progress to circling and seizuring. The blindness is due to the visual center in the brain being affected and not due to direct damage to the eyes. Treatment is Thiamine at 9 – 18 mg/lb, SC every 4 to 6 hours initially continuing for several days after the clinical signs have improved. Thiamine concentrations vary with different products, so calculate amount to be administered carefully. Must be used with extreme caution if given IV as it can cause seizures. Start with lower dose, increase only if the animal is not responding (still depressed, blind).

Anti-inflammatories (Banamine, Prednisolone, DMSO) are also beneficial as there is considerable inflammation. I have had a few cases that remain blind even though all other signs improve (appetite, no longer depressed). These same animals seem to regain some peripheral vision over months to years, but cannot see things close up. They do very well in a group and can still raise a cria. I have also had several animals that seemed to initially respond, but then start to seizure and have to be euthanized, necropsy confirmed the diagnosis of Polio.

 Listeriosis: caused by the bacteria Listeria monocytogenes and causes micro-abscess in the brain. The bacteria enter the body from wounds in the mouth or from newly erupted teeth and is usually seen in younger, growing animals (< 4 yrs). Clinical signs typically are on one side and include circling to only one side, head tilt, drooping lip, nose deviated with a collapsed nostril and unable to close an eye – all on the same side. This is not a very common disease in camelids, but unless treated early and aggressively, it is usually fatal. I prefer IV antibiotics, but an attempt can be made with Procaine Penicillin G 20,000 IU/lb, SC, twice a day and Banamine 1 mL/100 lbs for two days. If during that time, there is no improvement or the worsening of clinical signs, the treatment should be switched to IV. I prefer Ampicillin at 5 mg/lb, IV, QID but Oxytetracycline at 9 mg/lb, IV, SID can also be tried. Anti-inflammatories (Banamine, Prednisolone, DMSO) are also beneficial as there is considerable inflammation. In some cases, the clinical signs may improve to a point, but some residual signs may remain, most of the time they can still be a functional part of the herd.
 Ryegrass Staggers: is caused by grazing pastures with endophyte infected ryegrass, the toxins are increased in dry weather. The clinical signs are head tremors and the treatment is removal from the affected pasture. On occasion, the tremor may be permanent with long term exposure.

Viral causes of Neurologic signs:

Eastern Equine Encephalitis (EEE) – seen mainly in the eastern United States, in late summer and fall and spread through mosquito vectors from avian hosts. A recent report (2007) of 8 alpacas, 1 llama, aged 3.5 weeks to 12 years were diagnosed with EEE, 6 were euthanized, 2 died naturally, 1 survived – the 3.5 week old cria. Clinical signs are non-specific and include depression, fever, uncoordinated gait, seizures, balance problems, unable to rise and curling head/neck over the back. Testing of suspicious animals can be done using a serologic test (plaque reduction neutralization titer PRNT) and postmortem diagnosis by Reverse-transcriptase PCR and Immunohistochemistry of CNS tissues (brainstem). Mammals are considered dead-end host due to low virus load in the blood. Although there is some evidence that the equine vaccine can be used safely in camelids, it is only advised in areas of high risk and where there have been reported cases.

 West Nile Virus (WNV) – seen across the United States, in late summer and fall, spread through the Culex mosquito. Clinical signs usually involve a twisting posture of the neck, uncoordinated gait, sensitivity to touch, inability to rise, severe depression. Overall, camelids are at low risk for developing the disease; however even with aggressive supportive care and treatment, there is a high fatality rate. Similar testing can be done for WNV as in EEE. The equine WNV vaccine can be used in camelids and does seem to be protective based on clinical response and research trials. It is recommended to give three vaccines 3 weeks apart in areas considered to be high risk.
 

Rabies – has been reported in camelids in the United States. Clinical signs early in the course of the disease include lameness, uncoordinated gait and paralysis in rear legs (similar to Meningeal worm). This will progress to either an aggressive form or a paralytic form. In the aggressive form there may be aimless running around, self-destruction, excessive biting or chewing and attacking herdmates and people. They also may bloat, vocalize more than normal and scratch at themselves. The paralytic form will have continued depression, salivation, rectal straining, circling, paralysis of the face and larynx, and unable to rise. As with any mammal, this is a fatal disease. Convulsions and coma then death occur 1 to 4 days after the onset of clinical signs. Because of human exposure, any camelid with an unexplained neurologic condition should have a necropsy to determine the cause. There is no approved vaccine for camelids; however killed rabies vaccines are routinely used in endemic areas.
 
In conclusion, there are many causes of neurologic problems, many of which can be treated successfully if found early in the course of the disease. However many of the problems look similar initially so treatment is frequently targeted for more than one problem. Depending on where the animal is located (keep in mind where it was two months ago also) the main ones to be aware of are: Meningeal worm infection, Polioencephalomalacia, Listeriosis, and West Nile Virus.