Tick Alert Group Support Incorporated

Tick Poisoning in Animals - In Depth

By Norbert Fischer B.VSc. (Syd)

• Tick Poisoning
• Ticks causing Poisoning
• Historical Perspectives (> separate page)
• Time to Onset
• Presentation
• Early Effects 
• Advanced Effects
• Staging Severity
• Diagnosis
• Prognosis
• Tick Removal
• Nursing Care
• Antiserum
• Supportive Treatments
• Cats
• Toxinology (separate page)
• Immunology (separate page)
• Prevention (separate page)
• Natural Remedies (separate page)
• Native Australian Fauna (separate page)
• Research (separate page)

Tick Poisoning

Since paralysis of skeletal muscles is just one of the many effects a paralysis tick's toxin the term tick poisoning more accurately reflects the wide ranging signs of the toxicity syndrome.

Ticks that cause Poisoning

A number of ticks world-wide have been associated with a paralysis syndrome.

Paralysis can be rated according to its duration (transient to long lasting), its extent (localised to generalised paralysis) and its severity (mild paresis to paralysis and other poisonous effects). These vary according to genus, species, the life cycle stage, and the gender (sex) of the tick and possibly with seasonal factors.

Tick Species

There are seven genera of ticks worldwide which have been associated with paralysis in animals- they are- Ixodes, Dermacentor, Amblyomma, Rhipicephalus, Haemaphysalis, Otobius and Argas. Human cases of tick paralysis have been reported from Australia, North America, Europe and South Africa and have been caused by only the first three of these, namely Ixodes, Dermacentor and Amblyomma.

 In all, the potential for producing paralysis has been demonstrated, described or suspected in 64 species of ticks belonging to 7 Ixodid and 3 Argasid genera (Merck Veterinary Manual, 8th ed 1988). Another reference (Gothe, 1979) states that up to 43 tick species in 10 genera have been incriminated in tick paralysis in humans, other mammals, and birds (cited in Goddard, 1998). Only three or four have a venom which can be fatal (UTS, 1998). The most deadly species is concentrated in eastern Australia.

Tick Species		Common Name	Host Species paralysed	Distribution	Features
I. holocyclus		Australian Paralysis Tick	Mammals, birds, reptiles	Australia	The most severe form of paralysis of all ticks worldwide
I. cornuatus		Australian Indigenous Tick		Australia	Implicated in paralysis. Differentiation from I. holocyclus not always clear.
I. hirsti		Marsupial or Cat Tick		Australia	Possibly implicated in paralysis
Rhipicephalus sanguineus		Brown Dog Tick		USA	Has been associated with paralysis in the USA
Dermacentor variabilis		American Dog Tick		N America
D. occidentalis		Pacific Coast Tick		N America
D. andersoni		Rocky Mountain Wood Tick		N America
Dermacentor albipictus		Winter Tick		N America
Ixodes scapularis		Western Black-legged Tick, the Deer Tick		N America
Amblyomma americanum		Lone Star Tick		N America
Amblyomma maculatum		Gulf Coast Tick		N America
Otobius megnini		Spinous Ear Tick)
Argas radiatus			birds		Cupp EW, 1991
A. persicus			birds
Ixodes rubicundus		Karoo Paralysis Tick		S Africa	Merck Veterinary Manual 1988
Rhipicephalus punctatus				S Africa
Rhipicephalus evertsi evertsi				Africa (sub-Sahara)
Argas walkerae				Africa (sub-Sahara)

^ Diagram showing the occurrence of tick paralysis globally taken from a relatively old article (Gregson, 1973) produced by the Canadian Department of Agriculture. Probably in need of review. Interestingly Rhipicephalus sanguineus, a tick distributed worldwide, is only recorded in this diagram as producing paralysis in South America.

Tick gender

It is generally the female tick of all species that is responsible for causing paralysis. However, the gender neutral larval and nymphal stages of Ixodes holocyclus also elaborate small amounts of the paralysing toxin (Moorhouse, 1981). Adult males might produce toxin but as they do not engorge on a host (other than perhaps the female tick) any toxin is not of medical or veterinary consequence.

Tick stage

It is generally the adult stage of tick that causes paralysis. In the case of Ixodes holocyclus, large numbers of larvae (hundreds? possibly less) and nymphs (tens?, possibly less) have also been associated with tick paralysis.

Poisoning caused by The Australian Paralysis Tick

Most mammals such as calves, sheep, goats, foals, pigs, cats, cavies, rats, mice and man can be infested by the Australian Paralysis Tick. Fatalities resulting from a single engorged adult female tick are mostly reported in the young animals of the larger species and all ages and sizes of the pet species (dogs and cats).

Larvae and nymphs can also produce toxic reactions in the host. Fifty larvae or five nymphs will kill a 40 g rat, larger numbers of either can induce paralysis in dogs and cats.

One adult female can kill four different susceptible rats during engorgement. Although it is not typical, an engorging adult female apparently can reattach several times to different dogs (Jones, 1991).

Rating the paralysis

Paralysis caused by ticks can be rated according to duration, anatomical extent and severity:

Duration

1. A transient paralysis that generally resolves when the tick is removed- e.g. the North American Dermacentor spp.
2. A more prolonged paralysis which persists or even worsens after the tick is removed- e.g. the Australian Ixodes holocyclus

Extent

1. Localised to certain muscles in the vicinity of the tick. This is occasionally seen with the Australian paralysis tick. Most noticeably, eyelid paralysis occurs in dogs with ticks on the face and may result in a loss of the blink reflex and consequent irritation leading to ocular discharge and even corneal ulceration. Some other examples- a tick on the face may cause displacement of the muzzle's midline. Occasionally ther may be apparent limb weakness. A tick near the anus may cause faecal incontinence or apparent diarrhoea.
2. Generalised and involving the entire animal but often first noticeable as an ataxia (incoordination) and paresis (weakness) of the hind limbs in dogs, cats etc. This is the more usual presentation of paralysis caused by the Australian paralysis tick.

Severity

1. Lethragy to complete atonic paralysis of all striated/skeletal muscle tissue (which in dogs includes a major portion of the oesophagus).  Ixodes holocyclus also causes cardiotoxicity, seen as a reduced left ventricular fractional shortening (Atwell, Campbell and Evans, 2000)
2. Effects other than paralysis which may actually be more life threatening. See Effects of Ticks.
3. Later development of tick-transmitted diseases.

Time to Onset

Clinical signs of tick intoxication are usually observed 3-7 days after attachment of the tick. However the period preceding the onset of symptoms appears to depend on the rate of engorgement of the parasites rather than on a fixed time period. In some dogs, clinical signs may not be seen until all ticks have engorged and dropped off replete. 

From experience gained in deliberate loading of kennelled dogs for antivenom production, one tick can remain half engorged on a dog for 7-8 days before eventually engorging. A tick can also remain attached and partially engorged for up to three weeks before either completing its engorgement and dropping off or dropping off without repletion. Thus it is cited in some studies that for some susceptible dogs up to 4-8 ticks are required to induce paralysis.

But the interval may be even 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 - in this situation the symptoms could theoretically develop earlier than the third or fourth day.

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. In warm weather however the female engorges rapidly, which means she also injects her toxin more rapidly, thus causing onset of clinical signs in the typical 3-4 days (if the host is not immune).

Presentation

Some dogs may be presented for lethargy, inappetence, coughing, gagging, or grunting (as though in pain).

Some dogs may be presented for regurgitation or vomiting, which may persist throughout the course of the disease.

Most dogs are presented for weakness in the hind legs.

Similar signs are seen in cats with tick paralysis but affected animals are typically more distressed and agitated. Initially there is also often a change in voice, especially noticeable in Burmese and Siamese cats. This may be accompanied by retching. Pupillary dilation is prominent in cats but vomiting is rare in comparison to the dog.

A rapid onset of signs appears to be associated with more severe disease and a higher likelihood of fatality. A single engorged adult female tick can kill the largest dog.

Early Effects

The most difficult and frustrating situation arises when the early signs of tick paralysis occur at the same time as another illness which shares some of the symptoms. This may cause one to exclude tick poisoning in its early stages. Examples include concurrent gastrointestinal conditions and neurological conditions.

Advanced Effects

The advanced effects of tick poisoning have been organised according to body systems or regions.

Diagnosis

Differential diagnosis

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 occasionally 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 few weeks (occasionally longer) tick poisoning should be considered..

Definitive diagnosis

Diagnosis is based on clinical judgement using several criteria. It is not always straightforward in early cases. There are no blood tests for toxin detection yet available.

Staging Severity

Staging tick paralysis allows for a simplified communication about the status of a tick-poisoned animal. Staging is probably of less use in determining the dose of antiserum because dosage is pre-emptive of reaching a severe stage.

The staging method proposed by the Merial Tick Paralysis Forum (1998), based on the method of Dr Ross Sillar is as follows:

In this system greater importance is placed on respiratory compromise. A dog classed as a 2D may have a poorer prognosis and warrant more aggressive therapy and more careful observation than one classed as 3B.

Prognosis

"In dogs with tick paralysis caused by Ixodes holocyclus, the disease progresses in stages from weakness, inability to walk, inability to right, and loss of withdrawal reflexes, to a moribund state, with death following within 2 hours" (The Merck Manual, 1998).

Robert Wylie of Ulladulla Veterinary Hospital has provided the following statistics from his veterinary practice. See his homepage, and the frequently asked questions pages. "Some animals which are only mildly affected may recover without treatment by a veterinarian. However to leave an animal untreated is taking a risk with the life of the animal. If you are thinking of NOT treating, at least contact a veterinary clinic for advice and preferably have the animal examined by a veterinarian. Veterinary treatment will significantly improve the chances of survival of any affected animal. However some will die even with the best treatment. The ones which die usually have had a larger amount of toxin injected than normal (as occurs if more than one tick is present) or have been left too long and become severely ill before the owner presents the pet for treatment. Very young and very old animals also tend to be more severely affected, or animals suffering from any other disease or stress at the same time. In my early years of treating dogs and cats with tick paralysis I had 41 deaths out of 415 cases presented (10.1%) over a three year period. In later years I got this down to 36 deaths out of 691 treated (5.2%) over a six year period. In every case the more severely affected the animals were when presented for treatment, the higher the mortality rate. Treatment of animals showing only mild wobbliness of the legs was 100% successful, with no failures. The most seriously affected group (animals which were paralysed and unable to lift their head at time of presentation for treatment) had a 36% mortality rate despite treatment. However we still saved 64% of these severely affected animals, all of which would certainly have died without treatment".

With current (1999) treatment regimes around 5% of tick victims die despite treatment (The Veterinarian, Dec-Jan 2000, p1, article by Jonica Newby, quoting research by Dr Rick Atwell, University of Queensland). The figure of 5% was also presented at the National Tick Paralysis Forum No.2 (Feb 2000) based on a national survey (Atwell et al, 2000). Some practices report that the mortality rate seems to vary from year to year (David Johnson, Coffs Harbour, at NTPF No. 2, 2000) but it is unknown whether this variation is outside statistical deviations. More intensive management using artificial ventilators might further reduce the mortality rate but at a considerably increased labour and equipment cost (Mike Fitzgerald, Alstonville, pers com). Applying pharmacological methods of reducing cardiac, pulmonary and oesophageal dysfunction is a current the focus of interest in treatment strategies.

Tick Removal

Attachment Sites

This section based on: Atwell RB, Campbell FE and Court E (2000): The Attachment Sites of the Paralysis Tick (Ixodes holocyclus) on dogs, Aust Vet Practit, 30(2)

Bancroft, in 1884, observed that the Australian paralysis tick usually attached "about the head and ears" of dogs (Bancroft, 1884). A recent survey (Atwell et al, 2000) has confirmed that the head and neck account for 70% of attached ticks in both naturally acquired and experimental infestations. This was despite the fact that in the experimental infestations 50 ticks were evenly dispersed along the dorsum (head, neck and back) of each dog. Additionally it was found that significantly more ticks attached to the chest and belly than to the crown, back and flanks, suggesting a preference for attachment to ventral sites.

^ The darker blue areas indicate the higher chances of tick attachment.	^ Common attachment sites	^ Occasionally missed sites

When searching for ticks on dogs bear in mind that any accessible epithelial surface provides a possible point of attachment. Some of the more unusual sites include: within the mouth, under the tongue, the ear canal (even on the tympanic membrane), the nostril, the anus, the vulva and within the prepuce.

Natural infestation

In a prospective study involving 42 veterinary clinics on the eastern coast of Australia the attachment site of ticks was recorded for the first 13-15 dogs presented to each clinic with tick paralysis (Sept-Nov, 1998) (Atwell et al, 2000).

^ Location of 806 ticks following natural infestations in 577 dogs. Ref: Atwell RB, Campbell FE and Court E (2000): The Attachment Sites of the Paralysis Tick (Ixodes holocyclus) on dogs, Aust Vet Practit, 30(2)

Experimental Infestation

Eight hyperimmune Foxhounds of varying age, gender, size, colour and coat length were used. At infestation 50 unfed adult female ticks were evenly dispersed along the dorsum (head neck and back) of each dog. No artificial stimulationwas employed to induce tick attachment. One day later the location of all live ticks (attached and unattached) was recorded using the same body divisions as for natural infestations, and at 3 days all ticks were removed. At 7 days the dogs were again infested with 50 ticks and at days 8, 9 and 10 the location of the ticks recorded, and they were then removed. This procedure was repeated at 7 day intervals for another 5 cycles. Overall each dog was infested 7 times with 50 ticks and these ticks were removed and recorded on 19 occasions (Atwell et al, 2000).

^ Table 2: Means of the percentages of individual tick loads at each site from all 19 counts following seven experimental infestations on eight dogs. Ref: Atwell RB, Campbell FE and Court E (2000): The Attachment Sites of the Paralysis Tick (Ixodes holocyclus) on dogs, Aust Vet Practit, 30(2)

Tabulated Summary of Attachment Sites for both Natural and Experimental Infestations of Ixodes holocyclus in Dogs

^ Figure 1: Atwell RB, Campbell FE and Court E (2000): The Attachment Sites of the Paralysis Tick (Ixodes holocyclus) on dogs, Aust Vet Practit, 30(2)

Theories on distribution

The attachments of paralysis ticks are not random- some kind of attachment site specificity clearly occurs. The question is whether the specificity is related to the initial contact of tick and host, whether it is a result of tick migration after host contact, or whether it is a result of host removal after host contact. Some of the teleological theories, which may be mutually inclusive, are:

• Bandicoot factors. It is perhaps reasonable to assume that the greatest selection pressure for the evolution of preferred sites comes from factors determined by the natural host, the bandicoot. What these bandicoot-specific factors may be has yet to be shown.
• Tick mating. Tick localisation may provide improved intraspecific contact for a low-density population on the host (Rohde, 1979)
• Tick feeding. Skin may be more attractive to the tick at the preferred sites- more supple for hypostome penetration, or better blood supply for feeding.
• Tick protection. Preferred site may provide protection from host grooming, and/or from external abrasion as the dog moves.
• Tick interspecies competition. This is unlikely in the dog because of the small numbers of ticks present. (Could it be a factor in the bandicoot?- what is the significance of other tick species in bandicoots?) (Holmes, 1973)
• Expired respiratory gases may be attractive to the tick. (Garcia, 1962)
• Host removal. The attachment pattern may to some extent reflect the act of the host detecting and removing or displacing the ticks through normal grooming habits. This could particularly apply to cats for example, where ticks are much more rarely found in groomed areas of the coat. The attachment process thus could still be random but the removal process not. This theory probably offers only a partial explanation of the distribution pattern. One would expect variations according to host species.

Searching

It has been claimed that more than 90% of ticks are found from the shoulders forward but they can be found anywhere on the integument- occasionally inside the mouth (even under the tongue!), nostril, ears, vulva and anus. The predilection for the head and forequarter sites is also seen when ticks are artificially placed on the backs of dogs (National Tick Paralysis Forum, Bulletin No. 1, 1999). In a national survey (Atwell RB et al, 2000) the dogs with longer coats had greater numbers of ticks but clipping dogs to search for ticks did not improve survival rate. Nevertheless clipping the coat may be useful in animals with a dense or matted coat.

Searching the animal for ticks is done with minimal stress. Some veterinarians use acaricidal sprays or rinses to guard against ticks missed by seaerches.

Searching is best performed using two hands and running the fingers through the coat symmetrically, starting from the muzzle and working back over the head and ears, down around the neck , then chest and front legs. Pay attention to the lips folds, the face around the eyes and inside the earflaps.

Also check carefully around the carpal pads and digits.

The neck area may require repeated searches because of the loose skin folds here.

Then search the remainder of the torso and hind legs, and around the anus or vulva/prepuce.

On the abdomen nipples can often be confused with ticks- one should be able to part the hair and check. Clipping away hair or matting it down with water may help to identify suspicious nodules. If multiple skin tumours are present they can also make searching difficult and full body clipping may be required.

Multiple searches by different people are most successful, though rather time-consuming.

Removal

Based on a recent survey (Atwell RB et al, 2000) neither the chemical pre-killing of ticks nor the injecting of antiserum under the tick lesion improved mortality or recovery time. The severe anaphylactic reactions that occur when ticks are removed from humans have not been reported in dogs (NTPF Bulletin No.1). That squeezing the body of the tick as it is being removed might cause the injection of more toxin is so far a theoretical concern in dogs. Similarly whether it might increase the chance of injecting tick-borne microbial disease organisms in dogs in Australia also unknown. Nevertheless, it may still be a reasonable precaution to grasp as close to the skin as possible when attempting removal.

If the animal has not yet shown signs of tick paralysis, removal of the tick may prevent development of the disease. However, if the animal is showing any signs then removal of the tick is not sufficient, because the disease is very likely to progress for up to 48 hours in the absence of specific therapy.

Animals in anxious respiratory distress are best sedated before attempting tick removal. This is particularly the case with cats which can develop a state of frenzied gagging and struggling with handling. Atropine has also been recommended for cats in this state. The salivary and respiratory secretions may precipitate laryngospasm or aspiration of plugs of mucus.

Nursing Care

Animals must be kept in a comfortable, quiet, stress-free environment. This can mean the difference between life and death. Animals are often in respiratory distress and may have little compensatory reserve to cope with further oxygen demands brought about by anxiety.

The sternal position is probably best for easing respiration and reducing hypostatic congestion. If the animal is in lateral recumbency it should be turned at least every 4 hours to prevent development of hypostatic pneumonia (Ilkiw, 1980). This has however been questioned because some practitioners (Fitzgerald, 1998) report that patients often rapidly deteriorate and even die after turning. They advocate never turning recumbent patients, however, it may be preferable to turn more frequently whilst paying careful attention to any decline in oxygenation (using pulse oximetry) and providing oxygen support where necessary.

Food and water are initially withheld whilst the animal is paralysed because pharyngeal dysfunction, megaoesophagus, laryngeal paresis and a weak cough all predispose aspiration pneumonia.

There are theoretical grounds for preventing tick patients from becoming overheated. Paralysed animals are unable to thermo regulate normally because they cannot readily shiver nor seek warmer or cooler places nor adopt heat conserving/releasing postures. Therefore core temperature needs to be monitored and controlled artificially. Both hyperthermia and hypothermia are possible problems depending on the ambient temperatures and other factors (eg brachycephalic dogs are prone to hyperthermia). In most cases hospital ambient temperature should be normal room temperature. However, the animal should not be trying to shiver. A slightly cool and de-humidified air-conditioned environment is usually ideal. Sedation and anaesthesia also promote hypothermia and this needs to be anticipated if these treatments are used. Numerous complications are possible with hypothermia and these may be just as life threatening as the tick paralysis itself. Using electronic thermometers (which don't require shaking down) will more reliably detect hypothermia in clinical settings.

Good comfortable bedding which drains away urine and helps prevent pressure sores is recommended. Towels and sandbags may be useful to stabilise an animal in the sternal position but should not cause crowding and anxiety. The pharynx should be swabbed clean after episodes of vomiting or regurgitation to minimise the risk of aspiration. Calm reassurance may benefit some dogs and cats too.

Food and water should be withheld until the patient is mobile and has not vomited for 24 hours. Water can then be given in small amounts, and food can be offered thereafter if there is no vomiting.

After recovery, a period of convalescence should be imposed. Exercise should be restricted and high ambient temperatures avoided. Violent exercise within a day of complete recovery from tick paralysis has resulted in collapse and sudden death, and extremes of heat may cause recovered animals to relapse into paralysis.

Antiserum

Some veterinarians will permit a dog which is being repeatedly infected with paralysis ticks throughout the year (and thus may have some degree of immunity) to be carefully observed and not treated with antiserum, despite the presence of early signs. Not treating a dog with antiserum when it is showing clinical signs is risking the life of that animal is a decision usually made because of economic circumstances or because of some other concern with repeated dosing with antiserum. It is important to note that immunity is short-lived and may not last more than a few months. There is always a risk in trying this as there is no established means of assessing the immune status. Perhaps a test for immune status will become available in the future. 

Hyperimmune serum is derived from dogs deliberately but carefully infected with paralysis ticks. It is available for injection to neutralise circulating toxins. It is much more effective if given early in the course of paralysis whilst toxin is still either circulating or in the tick lesion, that is, before it has bound to its site of action at the neuromuscular junction (and possibly other) receptors. This becomes all the more important when one realises that there is a delay of 8-12 hours before signs of reversal of paralysis are seen. Placement of an indwelling intravenous catheter facilitates slow intravenous injection of the antiserum and any fluids and adjunctive drugs.

Dosage

Tick antiserum acts to neutralise the toxin at the neuromuscular junction of skeletal muscle. Cardiac muscle receptors, however, are different. It is thought that cardiac toxicity is thus independent of skeletal muscle toxicity and moreover that tick antiserum does not protect against this cardiac toxicity (Gower, 2004).

The efficacy of hyperimmune serum has in the past varied between manufacturers and between batches and so precise doses were difficult to recommend. The traditional rule was to give 0.5 mL/kg body weight to dogs but this dosing method has been questioned (Atwell and Fitzgerald, 1994). Tick antisera are now standardised to contain at least 500 CSIRO neutralising units per mL. In one retrospective survey it was found that giving dogs doses greater than 0.1 mL/kg did not enhance survival rates (Gower, 2004). This needs to be interpreted with caution and further research is required in this area.

In practice, higher doses (1.0 mL/kg) are given to severely affected animals and in these animals many veterinarians give as much anti-tick serum as an owner can afford- even 2mL/kg. Perhaps the only limitation here is the potential for vascular overload if it is given too quickly. Smaller animals may benefit from relatively larger doses as it is reasoned that it is a given amount toxin that requires neutralizing, rather than a given weight of animal. On the other hand larger dogs have the antiserum diluted in a larger volume of body mass and so the reaction of antibody and toxin may be lessened, necessitating higher doses for larger animals. A combination of dosing strategies is probably required. In general dosage should match or exceed the  recommendations of serum manufacturers.

Should early or "mild" cases receive any less antiserum? It may be prudent to assume that most such cases are being seen early rather than being mild and still give a standard 'full dose' (whatever that may be).  The initial additional cost of antiserum is perhaps countered by shorter hospitalisation and secondary support costs.

Premedication for serum reactions

Reactions to administration of antiserum may be divided into two broad categories: physico-chemical and immunological. Physico-chemical reactions include the Bezold-Jarisch reflex (mediated via receptors in the left ventricular outflow tract), anaphylactoid reactions (mediated via non-Ab-dependent mast cell degranulation), and nausea reactions (mediated via the chemoreceptor trigger zone (CTZ) in the brain). True immunological reactions are usually anaphylactic (mediated via Ab-dependent mast cell degranulation). The distinction between anaphylactic and anaphylactoid reactions is esoteric in the emergency context- the clinical signs are identical and they are managed similarly. Concurrent B-J and anaphylactic reactions are also possible.

Pretreatment with antihistamines and/or corticosteroids does not prevent anaphylactic reactions but will blunt the physiological response (Cohen RD, 1995). It will also help prevent the "late phase" or "biphasic" anaphylactic response.

In dogs the trend is towards not using corticosteroids routinely because they may cause secondary problems and worsen the outcome if there is aspiration pneumonia (Malik et al, 1991).

Anaphylactic/oid serum reactions appear to be quite rare in dogs (even with second treatments).

In cats, Malik et al (1991) have recommended the routine administration of intravenous hydrocortisone (at 30 mg/kg) prior to the slow intravenous injection of antiserum (5-10 mL). Adrenaline (1.0 mL of 1:10,000 solution) is kept ready in case of an anaphylactic reaction. Other veterinarians give antiserum to cats intravenously after premedicating with acepromazine or antihistamine. Others again give antiserum to cats intraperitoneally. Intravenous administration would be expected to give quicker results but possibly at the cost of increased stress of handling and serum reactions. A so-called "despecified" tick antiserum which is more purified may be better suited for treating cats.

Fitzgerald (1998) suggests that antiserum is given to dogs intravenously and without premedication. He suggests that it should also be given intravenously to cats but in this species with premedication to reduce the chances of anaphylaxis. Cats that are only very mildly affected may be given antiserum intraperitoneally, though the recovery period may be slightly longer.

Pre-warming of the antiserum may be important in reducing reactions in cats and small dogs. Cold antiserum is more likely to induce a Bezold-Jarisch reflex.

Jones (1991) recommends diluting antiserum in an equal volume of 0.9% NaCl when it is used intravenously for cats and small dogs. Care should be taken with the additional load on circulating blood volume, particularly in very small dogs and in cats as crystalline fluids can be expected to redistribute quickly into pulmonary interstitial tissue.

Antiemetics. Administering tick antiserum slowly, ie over 15-30 minutes, helps to minimise nausea associated with bolus infusions. This reaction is probably due to the cresol preservative that is found in the antiserum (R. Sillar pers com, quoted by Fitzgerald, 1998). Premedication with the antiemetic prochlorperazine (Stemetil®) may help to reduce this.

Route of injection

In dogs the intravenous route has the most acceptance.

In cats both intravenous and intraperitoneal routes are often satisfactory. The intravenous route is probably more effective but is more stressful to administer and perhaps more of a risk for anaphylaxis. Adequate sedation, premedication with adrenaline and hydrocortisone and slow administration of diluted serum might overcome these risks in cats. Intraperitoneal injections are not entirely without risk however. In a struggling patient the antiserum may enter liver, spleen, gravid uterus, bladder and intestine. If the tissue is vascular (eg liver, spleen) the rapid injection may cause an acute reaction similar to an IV reaction. Injection into a hollow viscus (bladder and intestine) may risk causing poor absorption and peritonitis.

Antiserum injection in sheep, goats, calves and foals should be by the intravenous (IV) route, whereas in the lamb, kid and small pigs the intra-peritoneal (IP) route is satisfactory, although it gives a slower response. In koalas and other marsupials, the rabbit and guinea pig the IP or intra-muscular (IM) routes should be used. Because it may take up to 12 hours to be absorbed from the IM route a doubled dose should be used, particularly in severe cases.

In mildly affected animals with a straightforward ascending paralysis, removal of ticks and administration of hyperimmune serum usually results in obvious clinical improvement within 24-48 hours, although there is often little change within the first 12 hours. Failure to respond to hyperimmune serum after an appropriate interval may suggest the presence of undetected ticks.

Supportive Treatments

 Cats

Treatment of cats presents some differences to dogs:

• Cats can be more 'highly strung'
• Cats have a more sensitive larynx
• Cats are more predisposed to antiserum reactions, both Bezold-Jarisch and anaphylactoid/anaphylactic type (Atwell and Campbell, 2001).

Initial stabilisation

Cats showing clinical signs of partial upper respiratory tract obstruction can be observed for a short period of time in a quiet, oxygen rich environment. Observation should be from a distance that does not stimulate anxiety. The early initial application of ‘benign neglect’ can resolve acute respiratory signs without the need for physical or pharmacologic intervention in many cases (Musca F and Gunew M, 2004).

Intravenous of Intraperitoneal antiserum?

In one relatively small retrospective survey it was found that, whilst the recovery rates were similar, the clinically recognisable antiserum reactions of any kind were only associated with cats given antiserum by the intravenous route (Musca F and Gunew M, 2004).

A treatment protocol for cats (based on Musca F and Gunew M, 2004)

Assess stage.

Possibly tranquilise based on degree of respiratory distress - Consider:

• Diazepam 0.2 mg/kg IM
• Methadone 0.1 mg/kg IM
• ACP 0.03 mg/kg IM
• Consider General Anaesthesia?

Possibly give adjunctive oxygen:

• Oxygen box if distressed
• Nasal oxygen if compliant

Place IV catheter

Collect blood (jugular venapuncture if compliant) and urine samples

• Routine PCV/TP, UA;
• FBC/MBA UA if older cat ;

Remove tick(s) by direct pull method

Pre-medications

• Atropine 0.04-0.06mg/kg (0.06-0.1mL/kg) 5 min prior to TAS if IV, 20-30 min prior to TAS if SC
• Prednisolone sodium succinate (Solu-Delta Cortef^®) 5-10mg/kg IV 5 min prior to TAS
• Adrenalin 0.1 ml / cat* of 1:1000 SC 5 min prior to TAS. Draw up identical amount in syringe to have ready in case of anaphylaxis

Give Tick Antiserum 1 mL/kg at room temp

• IP bolus
• IV diluted in 25mL saline infused over an hour Severely affected cats may need this delivery

Nursing and monitoring - continuous

• Maintain normal body temperature
• Clear upper respiratory tract
• Suction (Tomcat catheter on end of syringe)
• Consider a tracheostomy in severe URT obstruction
• Nil by mouth
• Positioning Sternal if able to be maintained - Head down, shoulders as highest point, if lateral recumbency
• Eye lubrication as required

Repeat tick search

• 2-3 independent (different people)
• Finger walking and/or combing searches
• Consider cat clip
• Frontline spray (note: wet coat may predispose to hypothermia. Flammable.)
• Consider Proban PR (off label use)

Consider chest radiograph

• if pulmonary oedema: furosemide 1-2 mg IV q6h