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UNRESOLVED ISSUES IN TICK PARALYSIS caused by Ixodes holocyclus

The inspiration for this page is derived from an article by Drs Michael Fitzgerald and Richard Atwell (Atwell R and Fitzgerald M (1994) Unsolved issues in tick paralysis. Australian Veterinary Practitioner, 24(3) 156-161.)

Some of the issues

• pulmonary oedema
• the effects on the sympathetic nervous system
• the effects on the central nervous system
• the effects on the afferent nervous system
• the role of alpha receptors
• hypertension
• cardiac toxicity, cardiac workload, cardiac hypoxia
• respiratory compromise
• phlebotomy as a treatment for pulmonary oedema
• dose of antiserum
• tick variability in toxicity
• dog variability in susceptibity- various breeds (German Shepherds, Collies more susceptible??), low muscle to weight ratio?; innate immunity?
• whether paralysis tick-transmitted (viruses and rickettsia, Babesia/Ehrlichia and spirochaetes) occur in Australian dogs
• late sequelae- cardiac injury- reports that working dogs are not as fit after paralysis and of sudden collapse and death in ensuing weeks after paralysis associated with exertion; any effect from repeated intoxication?
• ancillary drug therapies:
  • alpha adrenergic antagonists (phenoxybenzamine)
  • alpha2 agonists (xylazine)
  • methylxanthines (theophylline)
  • diuretics (furosemide)
  • barbiturates (pentobarbitone)
  • glucocorticosteroids (dexamethasone etc)
  • propofol (for anxiety and maintaining oxygen devices)
  • benzodiazepenes (diazepam; for anxiety and maintaining Oxygen devices)
  • opiates (eg morphine, methadone for anxiety and dyspnoea- with caution only)
    antiemetics (eg metoclopramide; for vomiting and reflux oesophagitis)
  • antisialics (atropine)
    antacids (cimetidine, ranitidine etc, for reflux oesophagitis)
  • ACE inhibitors (enalapril etc)
  • Ca channel blockers (diltiazem etc)
  • venodilators (nitroglycerin ointment)

pulmonary oedema

One of the more certain findings of Ilkiw et al was that the arterial to alveolar oxygen difference rises with progression of tick paralysis in dogs. This can be due to either an intrapulmonary shunting of circulation away from ventilated alveoli (i.e. a V/Q mismatch) or it can be due to a failure of oxygen diffusion as occurs with widening of the alveolar-capillary interstitial space (for example pulmonary oedema or other infiltration). The former (V/Q mismatch) most commonly occurs with alveolar diseases such as localised pneumonias, neoplasms and hypostatic congestion. Whilst hypostatic congestion may be a contributing factor in prolonged recumbency, it seems unlikely to be the sole or even major cause of hypoxaemia.

(Hypoventilation is associated with hypercapnia and this only develops terminally, and so despite the expected effects of paralysis on respiratory musculature, ventilatory failure does not seem to be a primary problem in most cases until quite late in the course). Pulmonary oedema seems to be the mostly likely reason for the relatively early onset of the alveolar to arterial oxygen difference.

Systemic hypertension alone does not cause pulmonary oedema unless it is associated with other defects such as

• a cardiac insufficiency- The most recent findings of Fiona Campbell, University of Queensland, suggest that myocardial failure (left sided), does in fact occur and may be the primary source of the oedema. [NF: Subjectively this used to seem unlikely to me as the apex beat and femoral pulse pressure are usually quite strong until the very late stages, well beyond the stage obvious dyspnoea had already developed. Wedge pressures need to be determined to support this haemodynamic cause for the oedema. On the other hand it could be similar to a cardiomyopathy with bilateral cardiac failure. In typical heart failure such as dilated cardiomyopathy or mitral insufficiency, there is an elevation in left ventricular preload. How then does insufficient left ventricular contractility (systolic function) cause elevated preload? There is presumably no valvular insufficiency. Is there a problem with ventricular filling, reduced diastolic function (eg reduced ventricular compliance). Interestingly myocardial relaxation is an active energy-requiring process (Marks and Abbott, 1998) , and if this is impaired in tick poisoning, it might explain pulmonary oedema.
• a pulmonary capillary or venous defect (increased permeability, or neurogenic venous sphincter contraction, as in the rat)
• a vascular overload (eg excessive fluid administration)- not likely unless on IV fluids or there is hypernatraemia.
• high volume ventilation, using either positive or negative lung inflation pressures (see below)

Question [NF]: Is the breathing pattern the cause or effect of pulmonary oedema, or both? Some speculations-

• Could there be in tick poisoning an oedematogenic effect similar to a high volume lung expansion as seen in artificial ventilation? In mechanical ventilation it is well established that pulmonary oedema may be caused by high volume (ie high tidal volume) ventilation rather than high pressure ventilation. Strapping a chest wall to limit chest expansion helps to prevent oedema caused by high pressure ventilation. Even negative pressure ventilation (iron lung) will induce pulmonary oedema if it causes high volume expansion. It appears, therefore, that end-inspiratory volume is the main determinant of ventilation-induced pulmonary oedema. The mechanism of oedema appears to be mediated by increased microvascular permeability. This in turn could be caused by:
  
  1. abnormal surfactant effect causing increased surface tension, hence reduced pressure around alveolar microvessels, hence increased transmuiral pressure
  2. increased pressure of extra-alveolar vessels

  Interestingly PEEP ventilation causes less oedema than ZEEP ventilation using the same end-inspiratory pressure, probably (also) because of different haemodynamic effects. Normally, however, PEEP has an adverse effect on cardiac output. (Dreyussl D and Saumon G, 1998)
  

• Could an elevated mean intrapleural pressure (eg by closure of the glottis) be obstructing pulmonary lymphatics and so causing or at least exacerbating pulmonary oedema? Would positive pressure ventilation have a similar effect, but one where oxygenation was a counterbalancing benefit? Is there a practical means of negative pressure ventilation for dogs?- note it would have to limit chest expansion (see above)
• Could cardiac output be limited by the breathing pattern? Could this in turn be responsible for a cardiogenic oedema?
• Why is pulmonary oedema a not well-described feature of tick poisoning in children?- could it be that artificial ventilation, which is commenced relatively early in these cases, is somehow protective against pulmonary oedema?- or are these just species differences?

pentobarbitone

According to Atwell and Fitzgerald (1994), pentobarbitone given IM at a low, non-anaesthetic dose, does improve dogs, particularly those in a distressed state, as it acts to sedate, induce peripheral vasodilation, reduces anxiety, struggling movement and airway resistance and epinephrine levels. Jensen (pers com, cited by Atwell and Fitzgerald, 1994), has used such therapy in cats using the IP route with success (when also given tick antiserum). There have also been incidental reports of unexpected success using such an approach in severe cases in dogs (Atwell and Fitzgerald, 1994).

dexamethasone

Dexamethasone might be used for various reasons in tick paralysis. It is still not clear from the limited work so far undertaken whether there is an overall benefit justifying routine use in all cases. Some veterinary practitioners claim better survival rates in clinical cases (Ilkiw and Turner, 1988b). Because empirical evidence is largely anecdotal the debate rests on theoretical discussion at this stage [to my knowledge].

In Ilkiw and Turner's experimental studies (1988a) four dogs showing clinical signs of tick intoxication after being infected with 6 paralysis ticks were given dexamethasone sodium phosphate (Dexadreson, Intervet (Australia) Pty Ltd, Lane Cove NSW 2065) at a dose of 0.5 mg/kg bodyweight IV every 12 hours. This was in addition to being dosed with hyperimmune serum (Lismore Supreme Serums) at 0.5 mL per kg IV. This treatment was instituted once dogs had reached an advanced stage of paralysis when they were no longer able to right themselves. Three of these dogs survived compared with only 1 survivor in the treated control group (also four dogs) who were given antiserum alone. Because the numbers in this study were relatively small, it is difficult to draw firm conclusions. More statistical information is required.

Benefits might be suppression of serum reactions and augmentation of metabolic responses of the stress of tick toxaemia. Anti-inflammatory effects might also be beneficial. Higher doses, as sometimes used in cardiovascular and septic shock, might be useful in stabilising deleterious effects on cell and lysosomal membranes. Unlike hydrocortisone, dexamethasone does not augment the vasoconstrictor responses to adrenaline (Ilkiw and Turner, 1988a).

Adverse effects include the many known side-effects of glucocorticosteroids generally. In tick cases, of partciular concern would be lowering immunity against micro-organisms in the event of aspiration pneumonia. Additionally there might be concern of aggravating nausea and vomiting through lowering threshhold for gastric ulceration and pancreatitis.

xylazine

Xylazine is an alpha2 agonist. Its effects are sedative, anxiolytic and (centrally) hypotensive all of which, theoretically, may benefit tick paralysis cases. However bradycardia and reduced cardiac output, combined with a predisposition for cardiac arrhythmias may be detrimental by causing both cardiac and systemic hypoxia. It has been postulated that using alpha2 agonists will decrease secretion of neurotransmitter and so reduce alpha1 receptor stimulation. It might also increase uptake of free neurotransmitter, thus having an overall negative effect on blood pressure. (Atwell and Fitzgerald, 1994). Unfortunately it is not even clear as yet whether the alpha agonist (sympathetic) state of tick paralysis is primary or secondary, let alone whether alpha 1 or alpha 2 receptors are relatively more important.

References:

Atwell R and Fitzgerald M (1994) Unsolved issues in tick paralysis. Australian Veterinary Practitioner, 24(3) 156-161.

Dreyussl D and Saumon G, (1998) in Topics in Anaesthesia and Critical Care. Applied Physiology in respiratory Mechanics, J Milic (ed.), Chapter 12, , Springer-Verlag, Italia, Milano.

Ilkiw JE (1983) Tick Paralysis in Australia, in Current Veterinary Therapy IX, ed RW Kirk, Lea and Febiger.

Ilkiw JE and Turner DM and Howlett CR (1987) Infestation on the dog by the paralysis tick Ixodes holocyclus 1. Clinical and histological findings. Australian Veterinary Journal 64 (5) 137-139.

Ilkiw JE and Turner DM CR (1987a) Infestation on the dog by the paralysis tick Ixodes holocyclus 2 Blood gas and pH, haematological and biochemical findings. Australian Veterinary Journal 64 (5) 139-141.

Ilkiw JE and Turner DM CR (1987b) Infestation on the dog by the paralysis tick Ixodes holocyclus 3 Respiratory Effects. Australian Veterinary Journal 64 (5) 142-144

Ilkiw JE and Turner DM CR (1988) Infestation on the dog by the paralysis tick Ixodes holocyclus 4 Cardiovascular Effects. Australian Veterinary Journal 65 (8) 232-235.

Ilkiw JE and Turner DM CR (1988a) Infestation on the dog by the paralysis tick Ixodes holocyclus 5 Treatment. Australian Veterinary Journal 65 (8) 236-33

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