Vibrio cholerae question - Please help...

[Phloston]

---

Members don't see this ad.

In USMLE Rx, a vignette gave an obvious description of a woman with cholera. Then it asked for the mechanism of action of cholera toxin. Easy enough, right?

I knocked it down to two answers:

A) An A-B heat-labile toxin that permanently activates adenylyl cyclase to increase cAMP

and

C) An A-B toxin that activates adenylyl cyclase by ADP-ribosylation to increase cAMP


Now, when I saw this, I'm like, "seriously, both are correct." I chose A. The answer was C. 18% got it right. 60% chose A. Of course I could also count on USMLE Rx to not give a thorough explanation as to why A was wrong.

Cholera toxin is most certainly analogous to the ETEC heat-labile toxin, and it does act permanently.

Does anyone have any thoughts here?

I'd appreciate it,

 

[deano5709]

I remember coming across this one studying for pharm/micro and what turned me off to A was that I couldn't recall anyone ever saying that cholera toxin "was" a heat-labile toxin, just that it was in the same family. I knew C wasn't wrong and I couldn't say for 100% that it was heat-labile, so I had to go with C.

 

[MrBeauregard]

Answer C absolutely is correct: it is an A-B toxin, it works through ADP-ribosylation of G protein, and it increases cAMP activity.

Answer A is dicey. It is a heat-labile toxin, as all heat-labile toxins activate adenylyl cyclase (it's heat-stabile that activate guanylyl cyclase), and you are correct that it is analogous to ETEC heat-labile toxin. It just seems like the answer isn't completely correct. It does activate AC, but how. There is also something about the word 'permanently' that doesn't sit well with me (and I don't know why).

I personally would have gone with C, mainly because it mentions A-B toxin as well as ADP-ribosylation.

 

[hoodfigga1]

omg i had this question a few days ago and picked the wrong answer apparantly and it irked me as well. so i am taking a guess that the heat-lability has to be the underlying distinction (FA does not mention VC toxin being heat labile...) however it does PERMANENTLY activate Gs and thus AC. i have seen other questions where they did not have as many characteristics of VC toxin so jumbled around amongst the answer choices so the correct answer usually had to do with VC toxin being most similar to ETEC's heat labile toxin...

on another note (since im now ranting about RX), does any1 else notice how the FA pages they have pasted in the answer dont always correspond to the question topic but may be like a page or 2 off???

 

[Phloston]

50+ = the number of times I've heard/read:

ETEC heat-labile is analogous to cholera toxin
ETEC heat-stable toxin is analogous to Yersinia entercolitica Yst toxin


The only conclusion I can draw is that quite a few gallant textbook writers like to jump to simplicity and say the above solely because of the cAMP and cGMP relationship, respectively. Vibrio toxin is not analogous to ETEC heat-labile toxin in that it isn't even heat-labile! (per PubMed)

Similarly, Yst toxin isn't analogous to ETEC heat-stable toxin in the sense that the former invades and destroys host cells, leading to dysentery, whereas the latter just causes a secretory diarrhea.

 

[Phloston]

does any1 else notice how the FA pages they have pasted in the answer dont always correspond to the question topic but may be like a page or 2 off???

Yeah, of course. I've learned to put up with Rx's idiosyncrasies the same way I'd put up with my girlfriend's. Both are undeniably a benefit, but also very annoying at times. 👍

 

[MrBeauregard]

Actually, after reading over a couple of texts, I can see the mistake I have personally made: reading the word 'similar' as 'analogous'. I just read something that said "the heat-labile toxin of ETEC is similar to cholera toxin in that it activates AC..." This is not the same as being analogous to cholera toxin. Cholera toxin specifically acts via ADP-ribosylation, whereas ETEC heat-labile toxin activates AC, but I have never read exactly how it does so. Also, after perusing First Aid a bit, I haven't come across anything that states they are analogous; it only states that they are both AB toxins that activate adenylyl cyclase and increase cAMP activity.