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IMMUNOLOGY OF TICK PARALYSIS
Reducing toxin toxicity (humoral immunity)
Reducing tick attachment (cutaneous immunity)
Reducing toxin secretion
Other kinds of immunity or resistance?
All-or-Nothing Immunity?
Chickens Immune?
Reducing toxin toxicity (humoral immunity)
Animals acquire humoral immunity after exposure to the toxin(s) of Ixodes holocyclus. Even natural hosts of the tick, such as the bandicoot, probably survive heavy infestations as a result of acquired immunity rather than intrinsic species resistance. This acquired immunity is apparently short lived, because bandicoots carrying heavy Ixodes burdens when captured may succumb to a single adult female tick after being free of ticks in captivity for several months.
The high incidence and severity of tick paralysis in dogs and cats in late winter and early spring may be related to loss of the immunity that was acquired during the previous season. It would ofcourse also be due to increased numbers of adult ticks at these times.
In the "laboratory" context dogs can develop immunity to tick paralysis if a number of Ixodes ticks are allowed to engorge for short periods of time. After 2 to 3 months of gradually increasing exposure, dogs can tolerate enormous numbers of ticks to full engorgement. The serum harvested from dogs prepared in this manner is commercially available for the treatment of tick paralysis. Inducing immunity experimentally takes approximately 20 weeks of repeated single tick exposures (see Note1). This can be accelerated using 7-8 ticks and peaks at 11-15 ticks (National Tick Paralysis Forum, bulletin No. 1). Once ticks are detached, the antibody levels decline quickly over 8-9 weeks. It can be reactivated to highly protective levels once a burden of approximately 5 ticks can be tolerated (Stone and Wright, 1980).
In the "natural" context, dogs in endemic areas, which are regularly exposed to I. holocyclus develop a strong immunity by 2-3 years of age. However, not all dogs will have their immunity sufficiently boosted for adequate protection (Dunsmore and Shaw, 1990). It is common for previously unexposed dogs to enter tick areas and be at risk.
Reducing tick attachment (cutaneous immunity)
Cutaneous immunity influences the occurence of tick paralysis in cattle, in which the disease is restricted to young calves that have not yet developed sufficient resistance to tick attachment.
In the artifical propagation of Ixodes ticks, guinea pigs cannot be used because some two weeks after the first larval challenge, subsequent larvae will not attach. Forty percent of larvae placed on tick-naive guinea pigs will successfully feed. Only one percent of larvae survive past day two in tick-exposed guinea pigs (Bagnall, 1975). This has been shown to be due to a localised skin immunity (associated with a marked basophil infiltration). When the same animals are challenged with intraperitonerally injected tick extract, they develop paralysis.
Similarly, rats can be used to feed I. holocyclus larvae but apparently they will not subsequently allow nymph stages to attach. This also suggests a cutaneous immunity. The best host for feeding nymphs would be a colony of bandicoots but the costs involved in this mean that it is more feasible to harvest adult female ticks from the environment (David Jones, AVSL, Lismore, pers com).
When a dog is challenged with 30 ticks, 28 will engorge in 6-8 days and two may remain attached but half engorged for 2 weeks. Again this suggests a weak cutaneous immunity is suppressing tick engorgement in dogs.
Reducing toxin secretion
There is a decrease in toxin content of salivary glands in ticks that have been placed on previously exposed bandicoots, when compared to toxin production by ticks that had been placed on tick-naive bandicoots. In ticks fed on previously tick-exposed hosts, toxin secretion was not detected in comparable quantities, even at 7 days (Goodrich and Murray, 1978).
Other kinds of immunity or resistance?
Stone et al (1983) showed that once hyperimmunity was reached in Beagles through cyclical exposure to ticks, that serum antitoxin antibodies consistently fell, depite being subsequently exposed to increasing numbers of ticks. Even when the serum anti-toxin antibodies were considered at a level not to confer immunity on the host dog, the dogs did not succumb to tick paralysis when challenged. The length of protection varied between dogs, from 33 to 102+ weeks.
The same progressive decline in detectable antibody titre is recognized in dogs kept continually infested for the prodcution of tick antiserum (Warne, 2002). Presumably there are other factors (eg. cellular immunity) that are either decreasing toxin secretion or some other way protecting dogs from later challenge. (Atwell R, 2002)
"An All-or-Nothing" Immunity?
[NF: Does one often encounter true cases of mild paralysis? No doubt in the wider veterinary context there will be some cases where immunity is seen in a partial stage of development, and one might therefore expect to see an occasional true "mild" case. But in the time frame of most sudden, natural exposures of tick poisoning this may be a rarity. In Ilkiw's experiments paralysis seemed to be an all-or-nothing event. In their first experiment (Ilkiw et al,1987) one dog (of 8) showed no clinical signs at all despite being infested with 3 adult female paralysis ticks, whereas the other 7 all died. In a further experiment (Ilkiw, 1987b) only 7 of 14 dogs infested with 3+ ticks showed signs of tick poisoning, and of these 7 at least 6 reached the moribund stage (the data does not clearly account for the 7th dog). These observations suggest that "mild" cases may be a rarity. Therefore what may seem to be a mild case may simply be an early case, and so still justify receiving a full dose of tick antiserum. Furthermore, the fact that so many dogs showed no signs at all in this second study raises the question of whether some dogs may even have an immunity unrelated to previous exposure (this is because it seems improbable that this random group of dogs had had so many pre-exposed dogs). Variability in ticks producing toxin is also possible but in these studies, the fact that each dog was infested with 6 ticks makes this seem less likely.]
Chickens Immune?
The possibility that chickens are immune to Ixodes holocyclus toxin has apparently been raised recently by researchers at University of Technology Sydney (see UTS- tick vaccine) and may help in the development of a vaccine against the tick toxin.
Note 1. As an example of how tick antiserum dogs are loaded with ticks, an adult female paralysis tick is applied for 3 days (72 hours) and then removed. Another is applied 4-7 (?)days later. Eventually multiple ticks are applied. When a dog is able to tolerate 100 engorging adult female ticks (perhaps a year later), then it will be producing protective tick antiserum. Occasionally a dog will show signs of poisoning on the 2nd day in which case it is removed earlier. (David Jones, A.V.S.L. pers com, 2000)
It is worth noting that the methods of inducing immunity may vary widely from this protocol. Some serum manufacturers only permit 15 ticks to be carried (Warne, 2002).
Bibliography
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.
Jones DK: Tick Paralysis; in JD Stewart Memorial Course for Veterinarians: Proceedings 149: Emergency Medicine and Critical care, The Post Graduate Committee in Veterinary Science, University of Sydney, 1991.
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