Paralysis Tick

[Shivani]

Hi Dr Jeff, Here in the tropics we have the paralysis tick. Max is currently on Bravecto (which also covers fleas and other ticks) but I would like to not have to give him this product. Alas by the time symptoms of having a paralysis tick show, things can progress rather quickly and the dog can suffer irreversable damage if not addressed asap. I have had a look on the forum for discussion on this particular tick but dont see any. Could you give me some advice on if there is a natural solution to this issue.

 

[Dr. Jeff]

Hi again Shivani.

As documented in this article, it looks like your daily ticks will prevent the paralysis. It can take up to 3-5 days of feeding for toxicosis from these ticks:

Tick paralysis in Australia caused by Ixodes holocyclus Neumann - PMC

Ticks are obligate haematophagous ectoparasites of various animals, including humans, and are abundant in temperate and tropical zones around the world. They are the most important vectors for the pathogens causing disease in livestock and second ...

www.ncbi.nlm.nih.gov

Regarding symptoms, they're a great clue to use the find helpful homeopathic medicines, like Lachesis, to slow or even stop progression of dis-ease.

Here's some excerpts from the above article:

CLINICAL PRESENTATION
Although tick paralysis in humans is most commonly reported in children aged 1–5 years, the problem does also occur in older children and adults (Grattan-Smith et al., 1997; Inokuma et al., 2003). The clinical presentation usually involves a combination of lethargy, weakness and unsteadiness of gait, often with ataxia, loss of appetite, dilated pupils, ascending symmetrical paralysis, slurred speech and depressed deep-tendon and gag reflexes (Grattan-Smith et al., 1997; Edlow and McGillicuddy, 2008). Laboured breathing, bradycardia, decreased oxygen saturation and asystole have also been reported (Grattan-Smith et al., 1997). In addition to neuromuscular paralysis, the toxin from Ix. holocyclus can produce myocarditis in children (Pearn, 1966). In older children or adults, double or blurred vision and photophobia may develop (Grattan-Smith et al., 1997; Edlow and McGillicuddy, 2008). Facial weakness or paralysis may be present and ascending flaccid paralysis can also occur if the tick is not removed quickly (Pearn, 1977). It is also worth noting that the removal of Ix. holocyclus from a patient can worsen the patient’s condition. In one case described by Miller (2002), for example, facial-nerve paralysis occurred hours after the removal of Ix. holocyclus ticks from around the patient’s face. Similarly, tick removal apparently led to deterioration in four of the six cases described by Grattan-Smith et al. (1997). Stone et al. (1989) hypothesised that such delayed toxicity was caused by the disruption of the feeding lesion during the removal of the tick, which caused the release of toxin that had been bound to cells or tissues. Surprisingly, despite the continued deterioration and then slow recovery seen in many Australian patients following the removal of Ix. holocyclus, removal of De. andersoni and De. variabilis from North American patients results in recovery within a day (Garrettson, 1984).

And regarding the toxicity of the ticks:

TOXICITY OF TICKS
An interesting clinical phenomenon is the fact that Ix. holocyclus need several days of engorgement on their host before signs of paralysis manifest. Ross (1935) and Goodrich and Murray (1978) observed that the SG from Ix. holocyclus only produced marked toxicity, when injected into mice, if they came from ticks that had previously fed on dogs for 5 days. The SG collected from ticks that had fed for only 3 or 4 days on dogs produced much less toxicity when injected into mice (Kaire, 1966; Goodrich and Murray, 1978). Binnington and Stone (1981) subsequently confirmed that the toxicity of homogenates of Ix. holocyclus SG depended on the duration of tick feeding. Thus, although SG collected 1 or 2 days after the onset of feeding showed very little toxicity, the toxicity of SG increased with progressive feeding, peaking 4–5 days post-infestation and then decreasing until complete repletion. In both Ix. holocyclus (Binnington and Stone, 1981) and Rhipicep. evertsi (Neitz and Gothe, 1986), the timing of the peak production of toxin in the SG was found to coincide with the rapid engorgement phase of feeding (on days 4–5 post-infestation). The paralysis caused by Ix. rubicundus or De. andersoni is easily reversed, at least in its early stages, by removing the attached tick(s) (Stone, 1988). Paralysis in chickens induced by larvae of the genus Argas disappears when the replete larvae drop off the host (Mans et al., 2004). Paralysis caused by Ix. holocyclus, however, cannot be easily reversed and affected animals may still die despite removal of the ticks.

SG=salivary glands (of the ticks)