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IXODES HOLOCYCLUS, A UNIQUE AUSTRALIAN PARASITE |
National Tick Paralysis Forum* |
BULLETIN No. 2, July 2000
Please Note: This is an online version of a printed newsletter.
INTRODUCTION
NATIONAL TICK PARALYSIS SURVEY
RESULTS OF NEW RESEARCH
RECOMMENDATIONS FOR MANAGEMENT OF TICK TOXICITY
MEDICAL APPROACH TO A TICK TOXICITY CASE
NURSING CARE
CONCLUSION
REFERENCES
This Bulletin, the second in a series from the National Tick Paralysis Forum (NTPF), follows a meeting of the Forum held in Sydney, February 23rd to 24th, 2000, supported by Merial Australia. The Bulletin reports the findings of a National Tick Paralysis Survey completed in late 1998 (Atwell, Campbell & Evans, 2000a). It also outlines some exciting new research on the cardiopulmonary effects of tick toxicity and provides the Forum's recommendations for the management of tick toxicity in dogs in the hope that the mortality associated with this disease may be reduced. These recommendations are based on the survey, the experience of clinicians contributing to the Forum and recent research findings.
NATIONAL TICK PARALYSIS SURVEY
Forty-two veterinary practices in coastal regions of New South Wales and Queensland participated in this survey. A prospective questionnaire was used to collect data on up to 15 cases of tick toxicity in dogs presented to each practice during September and October 1998. A total of 577 cases were reported. Data recorded included breed, age, weight, sex, coat type, the number, size and location of ticks, severity of toxicity, types of treatment and outcome. Significant findings from the survey are reported here.
Host Factors
Host gender, breed and bodyweight had no bearing on the prevalence of infestation or on clinical outcome. Similarly, there was no significant relationship between coat length or density and outcome, except that longer haired dogs tended to have more ticks than those with shorter hair. Thick or densely coated dogs had no increased chance of infestation or of a poorer outcome.
Older dogs were more likely to die. This could be a consequence any pre-existing age-related cardiopulmonary problem, as it is now established that cardiovascular depression occurs in paralysed dogs (Campbell, 2000).
Tick Attachment
Tick attachment sites were very similar to those seen in experimentally infected animals. The majority of ticks (78%) were found forward of the front legs, with the neck, ears and lips being common sites. Ticks are attracted to carbon dioxide and it may be that they preferentially move towards the source of expired carbon dioxide, irrespective of where they first contact the dog (Atwell, Campbell & Evans, 2000b).
Tick Removal
Similar mortality rates in dogs occurred irrespective of whether ticks were removed alive by a direct "pull" technique or were killed in situ. However, the average time in hospital was significantly lower in cases where live ticks were physically removed (43.4 versus 49.8 hours).
Scoring Assessment
The degree of gait and respiratory compromise was classified using the scoring system described in National Tick Paralysis Forum Bulletin No. 1. This scoring system was based on the gait classification system of Ilkiw and Turner (1988), together with 4 levels of respiratory compromise.
Gait and respiratory scores were closely correlated in the survey, such that most dogs with a high gait score also had a high respiratory score and vice versa. Mortality was also closely linked to score severity. Approximately 5% of dogs in this survey died, and the majority of dogs that died (82%) had progressive pulmonary dysfunction with no visible progression of paralysis.
Increasing gait and respiratory scores were associated with increasing tick numbers but were not related to tick size, suggesting that tick size alone does not determine the extent of host toxicity. Presumably other factors such as toxin secretion rate and host immune status have a bearing on outcome.
Tick Antisera
The average intravenous dose of tick antisera (TAS) was 1mL/kg, with a range of 0.1-8.0 mL/kg. There was no significant dose difference between surviving and non-surviving dogs (1.02 mL/kg versus 0.99 mL/kg). Similarly, there was no statistical relationship between mortality and TAS dose. This may indicate that there is a minimum dose of TAS required, with doses above this level providing no additional clinical benefit. Dogs that received a second intravenous dose of TAS had a significantly lower survival rate than dogs that did not. A second dose is usually only given to severe cases that are not responding to treatment. If these progressive signs are due to other problems, eg cardiac depression with progressive pulmonary oedema, such cases would be better treated by employing therapy to increase oxygen availability, reduce pulmonary oedema, and increase alveolar ventilation. As stated earlier, 82% of dogs that died did so with progressive respiratory distress (ie congestion and oedema) and not with the hypopnoeic or apnoeic patterns seen in progressive toxicity or fatigue of respiratory muscles.
The use of subcutaneous TAS at the site of tick attachment had no bearing on clinical outcome. Once in circulation, TAS may "mop up" existing toxin and neutralise any new toxin released from the tick attachment site, negating the need for any subcutaneous TAS depot. This also supports the need for a minimum TAS dose.
Other Medications
Acepromazine (ACP) was given to 85% of dogs, at an average dose rate of O.1 mg/kg and corticosteroids (especially dexamethasone) were used in 60% of cases. The mortality rate of dogs that received ACP and/or dexamethasone was not significantly different from those dogs that did not, nor was there any significant difference in dose rates between surviving and non-surviving dogs.
Cardiopulmonary Dysfunction
Pulmonary oedema occurs due to the cardiotoxic effects of I. holocyclus (Atwell & FitzGerald, 1994; Campbell, 2000), where reversible myocardial depression occurs during toxicity. In severe cases this is associated with raised PCV values and a fluid shift into the lung. Data from bronchoalveolar lavage (BAL) also supports the cardiogenic origin of this pulmonary oedema, helping to explain why the majority of dogs that die, do so with signs consistent with pulmonary oedema. In-vitro studies in rats and mice and assessment of case radiographs in dogs have confirmed these clinical data (Campbell, 2000).
Oesophageal Dysfunction
The majority of dogs with tick toxicity have oesophageal muscle weakness or paralysis (Fitzgerald, 2000). The combination of a poor gag reflex, saliva pooling and a dilated and filling oesophagus has the potential to cause severe upper respiratory tract distress (Atwell, 2000). Regurgitation induces a harsh groan as dogs attempt pharyngeal clearing with upper airway paresis or paralysis. This sound is often described by concerned owners and may persist after the dog is ambulatory.
Atropine and Hypertension
The use of atropine has been controversial since the experimental tick infestation work of Ilkiw (1979) when systemic arterial hypertension was thought to be the major cause of severe clinical signs and poor response to treatment. Routine atropine use was not advocated because it was considered that the associated increase in sympathetic drive may have led to increased systemic blood pressure. However high systolic blood pressure does not seem to be a common finding in natural cases of tick toxicity (FitzGerald, 2000; Campbell, 2000), and some dogs may actually become hypotensive. Atropine is therefore not contraindicated and its use may be beneficial in several ways, including the reduction of saliva secretion and subsequent pooling.
Atropine and TAS Reactions
A recent survey (Atwell & Campbell, 2000) shows that most TAS reactions (>75%) are probably preventable. These preventable reactions are associated with the Bezold-Jarisch reflex (Zucker & Cornish, 1981) due to receptors in the left ventricle that can induce the profound bradycardia and hypotension seen after some TAS injections. Atropine administered prior to TAS will prevent or reduce the chance of this reflex being activated.
RECOMMENDATIONS FOR MANAGEMENT OF TICK TOXICITY
Scoring Assessment
A clinical scoring system is a valuable aid in case assessment and for determining prognosis. The following scoring system has been recommended by the second Forum. This is based on the original scoring system proposed by NTPF 1, but has been modified for greater simplicity and ease of use.
Gait Score*
1: Mild ataxia or paresis
2: Able to stand unaided but cannot walk
3: Unable to stand, can right
4: Unable to right
*Previous gait scoring system had 5 categories
Respiratory Score
A: No clinical respiratory compromise
B: Mild compromise - increased respiratory and heart rates
C: Moderate compromise – restrictive breathing, gagging, retching
D: Severe compromise - expiratory grunt, dyspnoea cyanosis
Oesophageal and Airway Management
Regular suction of the pharynx, larynx and proximal oesophagus will minimise the severe upper respiratory tract distress caused by a combination of poor gag reflex, saliva pooling, and a weak or paralysed oesophagus. Alternatively, an oesophageal tube can be used to allow direct drainage and the avoidance of inhalation of oesophageal contents. The tube can be introduced directly into the oesophagus because the gag reflex is absent. Make sure there is no obstruction to the upper airway and consider endotracheal intubation or tracheostomy if necessary. Positioning the dog in sternal recumbency, or with the shoulder as the highest point if laterally recumbent, is also very important. Be mindful of the possible sequelae of megaoesophagus such as aspiration pneumonia and oesophagitis.
Thoracic Radiography
A single left lateral screening thoracic radiograph should be a cost-effective exercise, provided it is performed with minimal stress. It will reveal the presence of megaoesophagus and show any severe pulmonary oedema (usually seen first as peri-bronchial cuffing). It could also establish if inhalation pneumonia has developed and assess the degree of pulmonary vein engorgement an indicator of pulmonary venous hypertension due to early left-sided congestive heart failure.
Cardiopulmonary Dysfunction
A high PCV indicates that a fluid shift into the lungs has occurred (pulmonary oedema of cardiogenic origin) especially in a case that is neither hypothermic nor dehydrated. The use of diuretics and arteriodilating drugs is beneficial in these animals. Drugs that have been proven to have a pulmonary venodilating effect in the dog (such as intravenous furosemide) could also be of use, as would anti-anxiety therapy (such as opiates) to relieve the distress associated with severe oedema and associated dyspnoea.
Acepromazine, used at the higher cardiovascular dose rates (>0.4mg/kg) to reduce cardiac afterload and so relieve pulmonary oedema, would seem to be indicated, but there is no supportive data. Most ACP doses used in the Tick Paralysis Survey were well below the level required for any cardiovascular effect.
A general anaesthetic is indicated for profoundly dyspnoeic dogs, to allow intubation, oxygen therapy, pulmonary drainage, oesophageal suction and cardiopulmonary support.
Atropine Treatment
Atropine reduces saliva pooling and should therefore reduce the level of oesophageal maintenance required. It could also induce bronchodilation which may overcome the bronchoconstriction and obstructive breathing described by Ilkiw (1979).
Atropine used prior to TAS will also prevent or reduce TAS reactions induced via the Bezold-Jarisch reflex. It would be unwise to use it however, if the animal was showing signs of profound sympathetic drive.
Dexamethasone Treatment
Dexamethasone is routinely used in an attempt to prevent or minimise anaphylactic reactions to TAS, but probably has little benefit for the dog with tick toxicity. It will not prevent a systemic Type I anaphylactic reaction and will suppress the adrenal axis (Campbell, 2000). As most TAS reactions are of the Bezold-Jarisch type and anaphylaxis is unlikely with "same-species" antisera, it would seem that the benefit of dexamethasone is less than most users would expect. If necessary, protection from Type I anaphylactic reactions may be better prevented by subcutaneous adrenaline as used in the cat Malik 1998) and in human medicine with equine-derived antisera.
MEDICAL APPROACH TO A TICK TOXICITY CASE
- Avoid all forms of stress or anxiety. Provide a degree of anti-anxiety therapy without reducing respiratory drive e.g. acepromazine, benzodiazepines, opiates*
- Collect relevant history details, including time of onset of current toxicity, previous tick toxicity and TAS use etc
- Assess gait and respiratory scores and establish prognosis
- If respiratory score is high give pulmonary oedema therapy (oxygen, intravenous diuretic, vasodilator, sternal positioning)
- If profoundly dyspnoeic, induce non-cardiodepressive general anaesthesia to allow intubation, oxygenation, ventilation, pulmonary drainage, suction etc. Consider referral for 24 hour management and mechanical ventilation
- Give parenteral atropine (0.1-0.2mg/kg)
- Give pre-warmed TAS by slow intravenous injection
- Perform tick search and remove any ticks found by direct pull methods
- Collect blood for PCV
- Take lateral thoracic radiograph to assess presence and degree of pulmonary oedema, megaoesophagus or inhalation pneumonia, and reassess prognosis
- Initiate oesophageal management (earlier if there is obvious upper respiratory tract saliva pooling and obstruction)
- Consider cardiac ultrasound to assess fractional shortening. Dogs with significantly reduced fractional shortening have pulmonary oedema which may not be evident on x-rays.**
- Consider expired air or blood gas analysis to determine the need for ventilatory support
- Repeat a thorough tick search and apply a topical acaracide
- Repeat assessments and therapy as case progresses
- If PCV is very high (>50), consider the use of colloid or heta/penta starch fluids. However most dogs do not become dehydrated during hospitalisation, so intravenous fluid use should be considered carefully due to the risk of contributing to the development of pulmonary oedema if cardiac depression is present
*The benefits of the anti-anxiety effects of opiates are believed to outweigh any respiratory depression. Take care with dose rates.
** Consider available facilities, costs, case severity etc
- Avoid all forms of stress or anxiety
- Place in cool, darkened environment, monitor temperature and avoid clinical hypothermia
- Nil per os until paralysis and/or megaoesophagus have resolved
- If laterally recumbent, position dog with shoulder as highest point
- Use eye protectants to guard against corneal ulcers, dry eye and bedding rub
- Catheterise or express bladder manually, once or twice daily
- Continue oesophageal management
- If intravenous fluids are used, careful monitoring is essential
This Bulletin has summarised the results of the National Tick Paralysis Survey and outlined new research data on tick toxicity. Based on this information, the Forum has introduced a revised classification system for grading the gait and respiratory signs of tick toxicity and has made recommendations for management of cases of tick toxicity.
*Attendees to the second meeting of the National Tick Paralysis Forum were:
Chairman Dr Rick Atwell, Dr Fiona Campbell; The University of Queensland: Dr Norbert Fischer, Wollongong: Dr Mike Fitzgerald, Alstonville: Dr Chris Jensen, Brisbane: Dr David Johnson, Coffs Harbour: Dr David Jones, Lismore: Dr Bryn Lvnar, Pittwater: Dr Paul Matthews, Cairns: Dr Wayne Mizon, Bega: Dr Janine Aldred, Dr Elizabeth Evans, Dr Greg Little, Dr Maurice Webster, Merial.
Atwell RB (2000); Aust. Vet. Practit. In Press
Atwell RB & Campbell FE (2000); Aust. Vet. J. Submitted 5/00
Atwell RB, Campbell FE & Evans EA (2000a); Aust. Vet. ]. Submitted 5/00
Atwell RB, Campbell FE & Evans EA (2000b); Aust. Vet. Practit. In Press
Atwell RB & FitzGerald M (1994) Aust. Vet. Practit. 24, 156-161
Campbell FE (2000); Ph.D. Thesis, Univ. of Queensland, In Preparation
FitzGerald M (2000); M.VSc. Thesis, Univ. of Queensland, In Preparation
Ilkiw JE (1979); Ph.D. Thesis, Univ. of Sydney
Ilkiw JE & Turner DM (1988); Aust. Vet. J. 65, 236-238
Malik R (1998); Post Graduate Foundation in Veterinary Science, Univ. of Sydney, Proc. 318, 147-148
Zucker IH & Cornish KG (1981); Circ. Res. 49, 940-948
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