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TWiM 70 Letters

Jim writes:

Just heard TWIM 67 -- excellent of course -- and recalled, like Elio, being in basic training in the 60's when meningitis cases occurred on the base and we had to sleep with all the barracks windows open. I think we were double-bunked but can't recall if we slept head-to-foot, or if adjacent bunks were reversed. It was a cold time of year and open windows didn't improve the experience, but it seems like they were closed after a couple weeks.

Smithfield, VA

Richard writes:

Good morning, day, evening (depending on your time of day). Esteemed

Firstly my weather report, for Weston super Mare, uk.

It is currently 3 centigrade (feels like 2C), dew point 4C, humidity
78%, there has been 1mm of rain/sleet, with a 50% chance of further
precipitation, and the wind is 16 km/h from the WNW. It is currently
dark so no visibility, but this is estimated as 2 miles, as it is
cloudy with light rain.

The predicted high for the day (2PM) 9C, with humidity of 68%, and dew
point of 4C, with predicted wind of 21km/h, a 40% chance of
precipitation (rain or sleet), to is expected to be partly sunny, with
good visibility >10 miles predicted.

I hope the weather report meets your increasingly exacting requirements :)

My question is actually fairly simple; Giardia lamblia and a number of
other eukaryotes lack mitochondria. Most of them appear to be
anaerobic, and I can see the point that the mitochondria and electron
transport mechanism might well be selected against.

However, no where can I find if it is clear that mitochondria where
selected against, and lost. Or if these bugs are a branch, that where
started before eukaryotes adopted mitochondria.

I'm not scientist, but simply an interested party. I actually work as
an engineer, on sewage treatment plants. So I do get to see a lot of
bacteria, since they do all the work, treating the sewage. Given
plenty of oxygen, and the correct nutrients, they do a fine job of
this, and then happily settle out, leaving clean enough water that it
can be returned to the environment (or with minimal treatment, and
filtration, to the drinking water supply, as is becoming more

However it is my personal theory, that apoptosis in eukaryotic cells
derives from the incorporation of a once parasitic bacterium. Such a
parasite requiring a method to kill the host cell, in order to
proliferate into the medium, to infect other cells. I hypothesise that
this was co-opted by eukaryotes, in order to allow for apoptosis (or
programmed cell death).

Knowing if apoptosis occurs in eukaryotes that lack mitochondria, and
if they are a pre mitochondria branch, would answer my question.
However I have been unable to find the required information.

I wonder if you can point me in the right direction, and also thought
the subject might lead to an interesting conversation on the podcast.

Many thanks for your ongoing series of podcasts.

I have emailed this to both TWIP, and TWIM. I suspect it is better
suited to TWIM, but my research has been on parasites, since these
seem better studied, so have included TWIP.

Thanks in advance for any insights you may be able to provide, or
simply interesting conversation.


John writes:
Dear TWIMmers,

I just saw this article about the rise of drug resistance:


It seemed a bit sensationalized to me, but as far as I could tell was pretty good on the facts, and I thought it might make an interesting listener pick of the week. I'd love to hear what you all think of it.

Reading the article, I wondered what we could do to keep resistance from arising in new antibiotics. For example:

a. Could a drug company refuse to license a new antibiotic for veterinary use or for agricultural use somehow? (Ideally we would just ban mass agricultural use of antibiotics, but who knows whether that will ever happen.)

b. Could someone develop two new antibiotics with different mechanisms of action, but only sell them in a combined form? That would probably slow down development of resistance, sort of like the use of multiple anti-retrovirals in treating HIV patients.

c. Would it be possible to develop a new antibiotic, and then evolve resistant microbes and try to redesign the antibiotic to overcome the resistance? If you went through a couple of these cycles of changing the antibiotic and then evolving resistance to the new antibiotic, is it likely that would yield a final product that was hard to evolve resistance to? Or would the microbes just find a different way to become resistant?

Thanks for your wonderful podcast, and for answering my amateur questions,




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