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Western Newts

 

California Newt, Taricha torosa
Photo by Fred & Diana Adams of California

http://www.backyardnature.net/pix/newt-cal.jpg

 

A Toxic Salamander

Western Newt is the vernacular name for the genus Taricha of which there are three species: torosa, granulosa, and rivularus.  These are toxic salamanders found exclusively in particular regions of California, the western halves of Oregon and Washington, and western costal Canada up through parts of Alaska (3).  Being newts, they are salamanders that spend the majority of their time on land (2).  Ideal places to find them are rock crevices and logs though when breeding they prefer slow moving pools along costal streams.  While they resemble the rough skinned newt they can be distinguished in a few ways.  The clearest way is to note that California Newts have lighter colored lower eyelids that match the color of their bellies.  They also have lighter color backs and larger eyes that protrude outside the width of the head when looking from above.  California Newts prefer more humid areas as well.  Their bodies are not slimy, though they may appear so when in and out of breeding pools.  Rather, they are usually warty and may approach eight inches long, the larger end for a newt (1).  Most notably however, is the toxicity of California Newts--the most toxic of poisonous newts (3). image source: http://www.npwrc.usgs.gov/narcam/idguide/range58.gif

 

Not for Human Consumption

The toxin exhibited by Taricha torosa is known as tarichatoxin or tetrodotoxin (TTX), the same neurotoxin found in pufferfish (3,5).  While researchers were not sure if these were the same, research has been confirmed that they are, biochemically speaking.  Tarichatoxin has 1% of the potency of TTX, the more potent, water soluble variant. The pure active ingredient's chemical structure is shown here.  All poisonous newts have a form of TTX that varies in potency with species (Taricha is the most potent, Triturus is the least potent) and age (juveniles are several times more potent than adults) (3). 

image source: http://upload.wikimedia.org/wikipedia/en/2/2f/Tetrodotoxin.png

 

In addition to curling its tail away from its head when feeling threatened, California newts will secrete this toxin through their granular skin glands (3).  Therefore it is recommended that they not be touched with bare hands or at least that hands be washed in the event of contact.  Oral ingestion is the more common route of toxicity. One newt is enough to cause serious problems in humans if ingested.  While this may sound silly, there is a chance of human ingestion as at least one case has been documented .  A toddler once fatally consumed a portion of the tail of an Oregon Rough Skinned Newt--a species somewhat less toxic than the California Newt but still harmful (7).  Thus it is not inconceivable that similarly curious dogs, raccoons, or other mammals might try a bite...

 

http://www.californiaherps.com/salamanders/images/tttorosaym052.jpg

 

Toxic Effects

Within 20 minutes to three hours of ingestion symptoms of TTX may appear as hypertension, respiratory paralysis, and nerve unresponsiveness at high dosages.  Less extreme effects may be felt as numbness and tingling.  Though paralyzed, a victim of TTX poisoning will still be conscious.  This is caused by site specific binding of TTX to voltage gated sodium ion channels in the nervous tissues.  Any binding to the extracellular pore opening of this ion channel inactivates it, blocking sodium ion flow (4).  There are two types of these ion channels--those with high affinity for TTX and those with low affinity for TTX.  Those with low affinity are primarily in cardiac tissue while ion channels with high affinity for TTX are distributed throughout the rest of the body.  Based on this information it can be expected that cardiac arrhythmia would result from higher doses.  A secondary effect of this toxicity is the inability of brain cells to receive oxygen properly resulting in a lightheaded feeling and overall weakness (3).  A mouse bioassay has been developed to monitor TTX in pufferfish though the only recommendation for treatment is assisted respiration (5).

http://www.treelink.com/flippart/hypertension.jpg

above image by Danny Filippone

 

Snakes Get Hungry Too

It is suspected that the newts acquire their toxicity by ingesting or otherwise acquiring bacteria such as Vibrio spp (3).  Likewise, some common garter snakes, Thamnophis sirtalis, may become poisonous by ingesting Taricha granulosaThey are able to prey on the rough-skinned newt for the same reason the newts are able to tolerate their own toxin.  A point mutation in the gene that codes for the sodium ion channel of concern has rendered certain snakes' ion channel functional and completely resistant to TTX.  This does not make the garter snake venomous, only poisonous.  A poisonous garter snake will do no more harm when biting since it still does not possess venom producing glands.  It becomes harmful, however, when eaten by its predators such as birds and mammals.  This evolution in snakes then can be used to observe toxicokinetics of TTX.  For example, three weeks after ingesting one newt it was observed that an average of 42 micrograms of TTX remained in a snake's liver (6). http://www.mikeredmer.com/Thamnophis_sirtalis_H3578_preview.jpg

 

 

Sources used for this section:

 

(1) http://www.npwrc.usgs.gov/narcam/idguide/ttorosa.htm

 

(2) http://www.sandiegozoo.org/animalbytes/t-salamander.html

 

(3) http://www.livingunderworld.org/caudata/database/salamandridae/taricha/

 

(4) http://intl.jgp.org/cgi/reprint/49/5/977.pdf

 

(5) http://vm.cfsan.fda.gov/~mow/chap39.html

 

(6) Williams, Becky L, Edmund D. Brodie Jr, and Edmund D. Brodie. "A Resistant Predator and Its Toxic Prey:
          Persistence of Newt Toxin Leads to Poisonous (Not Venomous) Snakes." Journal of Chemical Ecology.
          30(10) 1901-1919
Science+Business Media B.V., Formerly Kluwer Academic Publishers B.V. 2004.

 

(7) King, Brent R. MD, Richard J. Hamilton, and Zach Kassutto MD. "Tail of newt: An unusual ingestion." Pediatric
          Emergency Care. 16(4):268-269
Lippincott Williams & Wilkins, Inc. August 2000.