doc w/ Pen

journalist + medical student + artist

Tag: bacteria

Some little bug is gonna find you …

Bacteria are everywhere.

I’m reminded of this fact as I enter my last class-based unit of medical school, infectious disease. With this in mind, I’m also reminded of a song that my family listened to during my childhood. This was back in the day when people made “mixed tapes” with cassettes, not with an iTunes playlist. A friend of my dad’s made us this particular tape in the mid-1980s. It was a favorite on cross-country road trips to visit my grandparents in Colorado and Kansas. The tape was full of folksy songs about trains, whales, Star Trek, and … gut bugs.

“Some Little Bug” apparently dates back to the early 1900s. This particular version, which I’ve uploaded to YouTube and shared here, was digitized from that old cassette tape. You’ll find the lyrics below the YouTube link.

Enjoy. But not while eating.

“Some Little Bug”

In these days of indigestion it is oftentimes a question
As to what to eat and what to leave alone.
Every microbe and bacillus has a different way to kill us
And in time they all will claim us for their own.
There are germs of every kind in every food that you can find
In the market or upon the bill of fare.
Drinking water’s just as risky as the so-called “deadly” whiskey
And it’s often a mistake to breathe the air.

Some little bug is gonna to find you someday.
Some little bug will creep behind you someday.
Then he’ll send for his bug friends
And all your troubles they will end,
For some little bug is gonna find you someday.

The luscious green cucumber, it’s most everybody’s number
While sweetcorn has a system of its own.
And, that radish seems nutritious, but its behavior is quite vicious
And a doctor will be coming to your home.
Eating lobster, cooked or plain, is only flirting with ptomaine,
While an oyster often has a lot to say.
And those clams we eat in chowder make the angels sing the louder
For they know that they’ll be with us right away.

Some little bug is gonna to find you someday.
Some little bug will creep behind you someday.
Eat that juicy sliced pineapple,
And the sexton dusts the chapel
Oh, yes, some little bug is gonna find you someday.

When cold storage vaults I visit, I can only say, “What is it
Makes poor mortals fill their systems with such stuff?”
Now, at breakfast prunes are dandy if a stomach pump is handy
And a doctor can be called quite soon enough.
Eat a plate of fine pig’s knuckles and the headstone cutter chuckles
While the gravedigger makes a mark upon his cuff.
And eat that lovely red bologna and you’ll wear a wood kimona
As your relatives start packing up your stuff.

Those crazy foods they fix, they’ll float us ‘cross the River Styx
Or start us climbing up the Milky Way.
And those meals they serve in courses mean a hearse and two black horses
So before meals, some people always pray.
Luscious grapes breed appendicitis, while their juice leads to gastritis
So there’s only death to greet us either way.
Fried liver’s nice, but mind you, friends will follow close behind you
And the papers, they will have nice things to say.

Some little bug is gonna to find you someday.
Some little bug will creep behind you someday.
Eat that spicy bowl of chili and on your breast we’ll plant a lily
Oh yes some little bug is gonna find you someday.

The Kinky World of Bacterial “Sex” (and why we should care)

An image of Clostridium difficile, a potentially deadly bacteria.

An image of Clostridium difficile, a potentially deadly bacteria.

C. diff. It’s a name that may not mean much to the layperson, but to any health care worker, it causes shuddering and trembling.

Just ask my mom, who is a hospice nurse. She has a patient who has been afflicted with this nasty (and sometimes deadly) bacterial infection for weeks now. It can be resistant to most antibiotics, and is also quite resistant to destruction. Killing it requires bleach; soap and water or alcohol-based hand rub don’t do a thing. C. diff is also very infectious, so my mom’s patient has unfortunately had to be under isolation precautions this whole time. Which for anyone would be awful, but if you are in your last days of life, being isolated from the world – and having anyone who entered your world have to gown up and wear gloves – would be terrible. (At least I think so.)

So what exactly is C. diff, and what makes it so evil (to us at least)? Here is a bit about this robust bacteria, from the Mayo Clinic’s Web site:

Clostridium difficile (klos-TRID-e-uhm dif-uh-SEEL), often called C. difficile or C. diff, is a bacterium that can cause symptoms ranging from diarrhea to life-threatening inflammation of the colon. Illness from C. difficile most commonly affects older adults in hospitals or in long term care facilities and typically occurs after use of antibiotic medications.” (Source: Mayo Clinic)

Bacteria can be beautiful -  and also dangerous.

Bacteria can be beautiful –
and also dangerous.

That all said, bacteria are fascinating little buggers. (Not to mention beautiful under the microscope, as you can see from the picture at left.) And they are not all bad. There are bacteria in our bodies that are quite helpful to us, in fact. Bacteria can also be highly adaptive, which makes them all the more interesting – and potentially dangerous, when it comes to certain species.

One of the major issues facing health care today is MDROs – Multi-Drug Resistant Organisms. This includes several kinds of bacteria (such as Vancomycin-Resistant Enterococci, or VRE; and Methicillin-Resistant Staphylococcus aureus, or MRSA; as well as C. diff). As you can probably tell from the names, these organisms are resistant to specific drug treatments – the antibiotics vancomycin and methicillin, respectively, in the cases of VRE and MRSA.

But let’s step back for a moment. How do antibiotics work? Or rather, how are they supposed to work? Antibiotics are separated into different classes depending on how they affect bacteria. For example, antibiotics can target a bacteria’s:
1. Cell wall
2. Cell membrane
3. Essential enzymes

Antibiotics, when they work, cause destruction of the bacteria via one of these targeting mechanisms. Which is how they make us well again.

As I said, though, bacteria are highly adaptive. They can undergo “evolution” – favorable DNA changes – very rapidly, enabling them to resist an antibiotic’s targeting mechanism. Examples of these rapid adaptations include:

1. No longer relying on a glycoprotein cell wall
2. Enzymatic deactivation of antibiotics
3. Decreased cell wall permeability to antibiotics
4. Altered target sites of antibiotic
5. Efflux mechanisms to remove antibiotics
6. Increased mutation rate as a stress response

(Thank you, Wikipedia, for the very succinct list above.)

Anyone who has read much about evolution, though, knows that this process is usually a very slow one: favorable DNA mutations gradually accumulate over time via reproduction and the passage of these favorable mutations down to offspring.

But bacteria are a little, well, different in terms of their DNA-transferring and reproductive capabilities. And these differences are what enable them to rapidly exchange DNA mutations in an expedited manner. How does this work? Well, let me explain.

Bacteria have not one, not two, but THREE methods for sharing DNA. This is in addition to an extremely rapid method of asexual reproduction called binary fission. I will explore each of these in detail (with pictures, of course).

Enter the world of bacterial “sex” …

1. Conjugation. (See images, and explanation, below.)

Diagram of bacterial conjugation.

Diagram of bacterial conjugation.

Bacterial Conjugation: An image of the sex pilus

Bacterial Conjugation:
An image of the sex pilus.

Conjugation is the closest that bacteria get to mating (i.e., sex). What happens is that one bacterial cell, termed the “donor,” produces a cellular protrusion called a sex pilus. The sex pilus attaches to the “recipient” cell, and brings the two cells together. DNA is then replicated and transferred across the cell membranes, from the donor to the recipient. (Note: the donor possesses what is called an “F factor” – this is what enables it to transfer its DNA to the recipient. This F factor can also be transmitted, allowing both cells to then be donors.) This method of gene transfer can transmit antibiotic resistance from one bacterial cell to another.

2. Transformation. This is the process by which a bacterial cell basically absorbs DNA from the environment through its membrane, incorporates the exogenous (outside) DNA into its own, and then expresses those new genes. The new DNA can either be incorporated into the bacteria’s circular chromosome, or as a separate circular piece of DNA called a “plasmid.” (See the diagram below.)

Diagram of bacterial transformation.

Diagram of bacterial transformation.

An electron micrograph, and a diagram, of a bacteriophage. This is called a T4 bacteriophage.

An electron micrograph, and a diagram, of a bacteriophage.
This is called a T4 bacteriophage.

3. Transduction. This process is a bit more complicated to explain, as it involves not only bacteria, but bacteriophages (aka “phages”). Phages are little viruses that infect bacteria. (Yes, bacteria are subject to infection, too.) What happens is that these bacteriophages attach to the bacteria, inject their phage DNA, and the phage DNA takes over the cellular machinery of the bacterial cell. Rather than meet its own needs (i.e., produce bacterial proteins), the bacterial cell begins to express the phage genes, producing new bacteriophage components. These phage components are assembled, again with the help of the bacteria’s cellular machinery. Eventually, the bacteria lyses (breaks open), releasing the little viruses. Those new viruses can then go infect other bacterial cells. Sometimes, a piece of bacterial DNA gets “stuck” in a baby bacteriophage. So that when that bacteriophage goes on to infect another bacterial cell, the previous (and now lysed) bacteria’s DNA gets injected and incorporated into the new bacterial cell. To complicate matters, there are two different cycles of bacteriophage infection: lytic and lysogenic. In the lytic cycle, the bacterial cell is immediately destroyed (lysed) and the new baby phages are released. In the lysogenic cycle, the phage DNA is incorporated into the bacteria and remains dormant until activated by certain environmental or stress conditions. So in order for a bacterial cell to share its newly incorporated DNA (from the phage infection), it must be in the lysogenic cycle. (For a graphic explanation of transduction, see the diagram below. Note that in Step 5, this is a second bacterial cell which is being infected.)

Diagram of bacterial transduction.

Diagram of bacterial transduction.

E. coli cells, some of which are undergoing binary fission.

E. coli cells, some of which
are undergoing binary fission.

4. Binary Fission. So let’s assume a bacterial cell has gotten a piece of DNA that gives it antibiotic resistance. It could transmit that DNA via one of the mechanisms above, to one bacteria at a time. But bacteria also reproduce, albeit asexually. And they are quite efficient at it. In a very simplified explanation, a bacterial cell replicates its DNA (which is in the form of one circular chromosome), the two chromosomes move toward opposite “poles” of the cell, and then the cell splits in half, forming two new cells. These divisions are measured in “generation times,” which can be quite rapid. For example, under optimal conditions, E. coli’s generation time is about 17 minutes. For Staphylococcus aureus, it’s about 27-30 minutes. For S. aureus, that means that in 30 minutes, you go from 1 to 2 cells. After an hour, you have 4, then 8, 16, 32, and so on. It doesn’t take long, then, to develop a sizeable colony. (Source: Online Textbook of Bacteriology)

So what does this mean? In essence, once one bacteria (or a few) accumulate DNA mutations that confer antibiotic resistance, there are myriad ways – conjugation, transformation, and transduction – to spread that DNA around. And then those bacterial cells “reproduce” (asexually) via binary fission and a whole host of nasty, antibiotic-resistant bacteria results. So when someone is given an antibiotic, the bacteria that are NOT resistant will die, but those that ARE resistant will live, and continue to reproduce. Not good. (At least, not for us. Good for the bacteria, obviously!)
The misure and overuse of antibiotics contribute to this problem by helping antibiotic-resistant bacteria survive, proliferate, and then spread to other people. This is especially an issue in hospitals and other health care facilities, such as nursing homes, where people are in close contact with each other (or contaminated objects come into contact with people) and patients are often immune compromised to begin with.
Unfortunately, many of these so-called “superbugs” are resistant to multiple drugs, and are very virulent (infectious and harmful). And while there was a time several decades ago that saw wild discovery and development of new antibiotics, that has trailed off in recent years. In part because antibiotics are not seen as the “cash cows” that other drugs may be, and in part because the low fruit of antibiotic development has been plucked, it seems.
There is now an effort (at least of some sorts) to search for new sources of antibiotics, both natural and synthetic, as well as to curtail unnecessary use of antibiotics. But the “superbugs” are here to stay. For a good while, at least. And it’s all thanks to the kinky world of bacterial “sex.”

My First Research Symposium

One thing I have learned about “being” in science is that it involves poster presentations. Some people like them, some people hate them, but they are a part of the job. I saw my mentor and supervisor at UIC, Olga, make several posters (to present at various conferences) while I was working there. And for the Drosophila genetics conference, Dr. Kreher made one as well (which I wrote about earlier, and which included me as a secondary author!).

Today, I will present my first and very own poster at Dominican University’s “Undergraduate Research, Scholarship, and Creative Investigations Expo” (“URSCI” for short). This is an annual event at Dominican, where students from across different disciplines present their research work through both presentations and posters. For the poster portion, which is what I am doing, you have a designated time that you are supposed to stand by your poster and explain it / answer questions about it to anyone who is interested. While this might make some people nervous, I am really excited about the opportunity. I love talking about science (obviously), and I am also adept at explaining it in more basic language for people who might not be familiar with the concepts or procedures. That is one thing I learned well in journalism – you have to know your audience. So I know how to tailor my explanation, based on the people with whom I am talking.

The title of my poster is “Antibiotic Resistance of E. coli to Rifampicin and the Mutagenic Effects of Caffeine.” The work stems from a project I did in my Research Methods in Molecular Biology class, which I took last spring with Dr. Kreher. (I am currently working in his genetics lab with the fruit fly larvae.)


It was a fascinating project, and it had two components. As a class, we reproduced the experiments done in the late 1980s by two researches, Jin and Gross. They investigated how E. coli develop antibiotic resistance to a drug called rifampicin, which is used for tuberculosis. Based on their research, and previous work, they determined that rifampicin inhibits the bacteria’s RNA polymerase (which is what transcribes mRNA, which is later used to synthesize proteins). That’s bad for the bacteria, because without the necessary cellular proteins, the bacteria will die. But Jin and Gross also discovered that the bacteria can develop, at a particular rate, specific mutations in the gene (rpoB) encoding for a particular subunit of its RNA polymerase. These mutations allow the bacteria to survive treatment with rifampicin.

We repeated Jin and Gross’s experiments, growing E. coli on agar plates containing rifampicin (as well as another antibiotic, carbenicillin, to which our bacteria had been engineered with a resistance gene, so that only the bacteria we were studying would grow – no random bacteria from the environement would grow, because the carbenicillin would kill it). We were able to generate resistant bacterial colonies as well, and sequenced their DNA. In comparing the sequenced DNA to the wild-type rpoB (RNA polymerase) gene, we found some of the same nucleotide mutations as Jin and Gross, as well as a couple of mutations that were unique to our experiments.

The second part of the project was to choose a substance – any substance within reason, that could be procured at a store or from a chemical supply company – and see how that affected the mutation rate. Each student (there were eight of us in the class) had to choose something different. I chose to work with caffeine, which is a suspected mutagen, based on some scientific literature that I found. So my hypothesis was that treating the bacteria with caffeine would increase the rate of mutation, and hence the rate of antibiotic resistance. I tested two concentrations of caffeine, 1 mg/mL and 3 mg/mL. What I found was very interesting – not only did the caffeine fail to increase the mutation rate, it actually (especially at the higher concentration) killed much of the E. coli! So I did some more literature research, and found that caffeine has been shown to also have an antimicrobial effect on E. coli. Who would’ve thought?!

I absolutely love science. You don’t always get what you expect, in terms of results (I certainly didn’t), but you usually learn something. And that’s the point: discovery.