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CLINICAL DIAGNOSIS OF TICK POISONING forI. holocyclus poisoning in dogs and cats

Presenting signs
Differential Diagnosis
Definitive Diagnosis
Notes

Presenting signs

The clinical signs in early cases of tick paralysis are non-specific and can sometimes be extremely difficult to distinguish from other disorders, particularly if there is no evidence of tick attachment. Additionally, whilst typical cases develop quickly (usually after 3-6 days) and deteriorate rapidly (within 1-2 days), there may be considerable variation to this. Some cases have been known to progress from stage 2 to stage 3 over as long as fourteen days (Fitzgerald, 1998). Sporadic cases present "out of season" - for example they are ocasionally seen in the middle of winter in the Illawarra. Ticks may also be acquired by pets taken to holiday areas and returning home to a location where local veterinarians do not expect to find tick paralysis (they might expect snake bite, for example, to be more likely). Another problem is that it is not unusual for an animal to show signs and deteriorate even when a tick has not been found- this is probably because some ticks may drop off or be scratched off by the animal and yet the toxin may still be causing increasing signs of poisoning for up to 48 hours later. Therefore when an animal presents with any of the signs below and is known to have been in a paralysis tick area in the previous 4 weeks, an open mind would consider the possibility of ticks being responsible.

• Change in voice or bark (usually muted)
• Coughing
• Hacking (throaty cough)
• Retching (straining as if to vomit)
• Licking repeatdedly (Maskiell, 2000)
• Gagging
• Loss of appetite
• Lethargy
• Groaning sound when lifted
• Vomiting
• Regurgitation
• Salivation (drooling)
• Noisy panting respiration (early)
• Slow grunting respiration (later)
• Wobbliness
• "Swimming" weakness- splayed frantic "paddling" in sternal recumbency on slippery surfaces
• Weakness in hind limbs
• Asymmetry of the muzzle
• Pupil dilation (especially in cats)
• Ocular discharge, pin-point pupil
• Faecal incontinence or diarrhoea
• Pain and lameness
• Focal Dermatitis
• Anxiety, hypersensitivty, distress
• Paralysis

Differential diagnosis

• Change in voice or bark- may be confused with laryngitis, laryngeal collapse, everted laryngeal saccules, laryngeal paralysis, laryngeal neoplasia/stricture, hoarseness from excessive barking
• Coughing- many other possible causes also
• Retching (straining as if to vomit)- many other possible causes also
• Gagging- many other possible causes also
• Loss of appetite- many other possible causes also
• Lethargy- many other possible causes also. In the early stages dogs may only show tiring after walking a relatively short distance (say 40-50 m), or they may walk normally but fatigue when climbing stairs, or they may be able to walk and even run, but not jump. [Smaller dogs seem to mask their weakness better than larger dogs]. It is useful to test the strength of cats by dropping them from 35-40 cm and seeing whether they land normally or collapse (Fitzgerald, 1998).
• Groaning sound when lifted under the sternum- may be confused with abdominal pain and spinal pain (with spinal pain there is usually arching of the back, straightening of a lowered neck and, there may be a sharp yelp when the dog is touched or approached if there is "nerve pinching"- these additional signs therefore suggest that the cause of groaning is NOT tick paralysis). Fitzgerald (1998) finds this to be one of the more useful signs in diagnosis. He suggests that it may be due to loss of strength in "splinting" muscles of the abdominals and rib cage leading to an involuntary exhalation through weakened and narrowed vocal cords.
• Vomiting- many other possible causes also
• Regurgitation- oesophageal disorders, other causes of megaoesophagus such as myasthenia gravis
• Salivation (drooling)-many other possible causes also (eg oral, oesophageal, gastrointestinal, neurological, toxic)
• Noisy respiration (rapid)- many nasopharyngeal and laryngeal causes also
• Grunting respiration (slow)- may be confused with many pulmonary conditions- eg contusions, allergic airway diseases, oedema, diaphragmatic hernia, etc. With the possible exception of allergic airway diseases and "obstructive" diseases most pulmonary conditions cause a "restrictive" breathing pattern that is rapid, in tick paralysis breathing rate is characteristically slow, despite being classically restrictive- the tick's paralysing toxin may be preventing the rapid breathing and may be somehow causing an obstructive component.
  Exceptions to this slow breathing pattern occur in the very early stages of tick paralysis when an animal may be hot and distressed, or when the complication of aspiration pneumonia is present. In aspiration pneumonia the breathing pattern may be rapid with increased effort in both inspiration and expiration, and typically moist crackles (rales) can be auscultated.
• Wobbliness- apparent ataxia or drunken stumbling gait. NB initially patellar reflexes may be normal or hyperreflexic. [I have even seen a case of appaent chronic low grade intoxication in a weak but ambulatory dog which had a slight clonus of a moderately strong patellar reflex]. Many possible toxic, spinal and cerebral causes. Full neurological assessment and possibly spinal radiography may be required to exclude these other causes. Fibrocartilaginous thromboembolism of the spinal cord can be particularly difficult to distinguish in some cases as there is usually no hyperpathia and a posterior paresis/ataxia may appear very similar- however finding some lateralisation, having a very sudden onset and lack of progression and a lack of dyspnoea often help to differentiate this condition.
• "Swimming"- splayed frantic "paddling" in sternal recumbency on slippery surfaces- also seen in very young puppies as a "swimmer syndrome"- a musculoskeletal growth deformity- may have dorsoventral compression of thorax and secondary joint deformities
• Weakness in hind limbs- this is also seen with myasthenia gravis (where front legs are equally affected); in some cases of tick paralysis animals may take several steps and then sit; after a minute or so they are able to repeat this action
• Asymmetry of the muzzle- also idiopathic and traumatic facial nerve neuropathy; occurs when a tick is on the muzzle.
• Pupil dilation- this is usually symmetrical and most prominent in cats. Pupils can dilate for many other reasons, including fear and anxiety, pain and shock, iridal/retinal/oculomotor and brain conditions and drugs/toxins.
• Ocular discharge, pin-point pupil- also many other causes of corneal injury and uveitis; occurs when a tick is near the eye. The small pupil may be associated with uveitis resulting from secondary corneal injury when the blink reflex is not protecting the globe.
• Faecal incontinence or diarrhoea- also many other causes; occurs when a tick is on or near the anus.
• Pain and lameness. Many other possible causes. This sign is very much the exception to the rule. Fitzgerald (1998) has seen this in 2 Maltese terriers (a breed well known for its low pain threshhold). The only lesion that could be found on both dogs was a recently attached Ixodes adult. No paresis was evident. People often report pain and inflammation from tick attachment.
• Focal Dermatitis. Many other possible causes also. [I have seen one dog presented for slight lethargy and a localised acute moist superficial pyotraumatic dermatitis or "hot spot", in this case initiated somehow by a tick found locally attached]. Again this is a very rare reason for presentation but goes to demonstrate the difficulty of diagnosing a condition which may begin with a relatively minor clinical sign but progress to be a fatal problem.
• Anxiety, hypersensitivty, distress. Small breeds of dogs may mask their ataxia and paralysis better owing to their relatively greater biomechanical strength. These dogs may nevertheless "feel" incapacitated and become distressed by this. Some small dogs (eg Maltese terriers) are also sensitive to any pain and inflammation which may make them hypersensitive to any kind of handling.
• Paralysis- again many other causes of "flaccid tetraplegia" such as:

• neuropathies- idiopathic polyradiculoneuritis, acute idiopathic polyneuropathy, distal denervating disease

• motor end plate synaptic transmission blockers- tick paralysis, botulism, snake envenomation, fenthion and aminoglycoside overdose. Myasthenia gravis.

• muscle diseases- polymyositis, hypokalaemic myopathy

• motoneuron diseases (affecting cell body)- spinal muscular atrophy - usually more insidious

Definitive diagnosis

• Possible access to ticks within an appropriate time interval.

• Clinical signs. Especially the incoprdoination/paralysis and the slow grunting respiratory pattern (note however that early cases may have a noisy/laboured panting). Vomiting, coughing and gagging are additional strong clues when combined with the above.

• Presence of tick(s) or tick crater(s).

• Response to treatment with antiserum .

• Electrodiagnostic testing. This may be helpful in a minority of patients on which a tick can not be found and respiratory distress associated with pulmonary oedema is not present. Neurophysiologic studies reveal no change in the size or latency of compound nerve action potential (CNAP), but there is a significant reduction in the amplitude of the compund muscle action potential (CMAP), suggesting transmission failure at the motor end plate. The reduction in CMAP amplitude is greater in the hindlimbs than in the forelimbs, which agrees with the physical findings. Conduction velocity and the CMAP response after reptetitive nerve stimulation are normal in tick paralysis, whereas denervation potentials are not detected during electromyogaphy. [cf American paralysis ticks Dermacentor andersoni (Rocky Moutain Wood Tick) and Dermacentor variabilis (American Dog Tick) where there may be some slowing of motor and sensory conduction and reduction in CNAP].

• Exclusion of snake bite toxins. In Australia for example, presynaptic toxin in the Brown snake (P. textilis) and even myotoxic snakes such as Eastern small-eyed snake (Cryptophis nigrescens) or tiger snake (Oxyuranus scutellatus) (Fitzgerald, 1998).

References:

Malik R, Farrow, BRH: Tick Paralysis in North America and Australia, in The Veterinary Clinics of North America, Small Animal Practice, Vol 21:1 Tick Transmitted Diseases, 1991.

Notes:

Snake envenomation

Australian tiger and brown snakes also result in a rapidly ascending flaccid paralysis associated with salivation, vomiting and pupillary dilation. However, systemic signs relating to coagulopathy, intravascular haemolysis or myonecrosis are often present in animals that have been bitten by snakes and the respiratory rate is usually increased (in tick paralysis it is slow because of prolonged expiration, and usually ends with a grunt when it is severe). Animals affected with snake bite may have haemoglobinuria (pink urine) or myoglobinuria (brown urine). The clotting time is invariably prolonged in dogs, and serum creatine kinase (CK) activity is elevated. In cats the neuromuscular signs predominate and a venom identification kit or favourable response to antivenom offers clues, because bite wounds are not easily found.

Time intervals

Typically, most cases of paralysis present 3-6 days after being in a tick environment. Then why should one be considering an interval of up to 4 weeks?The reason is that it has been found in experimental colonies that an adult female paralysis tick may engorge for up to 4 weeks. In actual fact this period of suspicion could theoretically be much longer if one was to assume that a dog brought home larval or nymphal stages of the paralysis tick. In such a situation the ticks could mature over the various moults on the dog and off it in its home environment over several months. It is apparently also possible for an attached female to reattach to another dog- in which case a dog could bring a tick home and have it infest another dog- see life cycle -in this situation the symptoms could theoretically develop earlier than the third or fourth day. I have not heard of any such instances however. In most cases the time taken for an adult female to fully engorge while on the host varies from 6 to 21 days (with the earliest signs starting on the 4th day), the period being longest in cool weather. Thus a dog may carry a tick up to three weeks without the tick being significantly engorged or causing paralysis. It may even be possible to have a low grade form of intoxication for a week or so. However in warm weather the female engorges rapidly, which means she also injects her toxin more rapidly, thus causing paralysis if the host is not immune.

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