I’ve somehow made it through 5 stories without talking about one of the most famous pathological agents… bacteria. It’s time.
There are plenty of good bacteria – they make yogurt or break down our trash– but the most famous are the bad ones. They have names like E. coli, Staph, and Strep, and we don’t particularly enjoy their presence. Generally, when bacteria invade, the invaded part gets warm, swollen, and tender (though there are many exceptions). Let’s learn more by looking at one particular kind of invasion: a urinary tract infection (UTI).
Jill, sadly, has a UTI. It’s not terribly surprising – one half of women will have a UTI in their lifetimes (though men are susceptible, too), and UTIs are one of the most frequent infections in the US (up there with the common cold). To get one, E. coli bacteria must find their way into Jill’s urethra and start migrating up into her bladder.
Usually, that’s a fairly difficult task for the E. coli. A trip to the restroom rinses most bacteria out like the proverbial spider out of a waterspout.
A few things can give the invading E. coli an advantage: injuries to the cells lining the urethra let the bacteria gain a foothold, genetics can make Jill more susceptible2, and some bacteria use hooks like ice climbers to hang on tight to the walls instead of being rinsed off. Poor Jill. These bacteria survive, start to multiply, and continue to trek upwards.
Cells hanging out in Jill’s urethra and bladder realize they’re in trouble and call for HELP. Jill’s body responds by making the blood vessels bigger and leakier in the area, drawing more white blood cells to the bladder and helping them get out of the blood vessels and into the fight. (Meanwhile, the leakiness also lets out plasma and causes swelling in the area.)
Our favorite heroes – the neutrophils – are really here to save the day this time. They essentially smell their way to the bacteria in a process called chemotaxis. Bacteria and the cells sounding the alarm release various chemicals. The neutrophils sense these chemicals and move toward areas where the chemicals are more and more concentrated, which helps them pinpoint the bacterium3.
The neutrophils then swallow the bacterium whole in a process known as phagocytosis (literally, “cell eating”).
Granules inside the neutrophil then attack the bacterium with various chemicals (including reactive oxygen and lysozyme).
The bacterium dies.
These neutrophils sacrifice their lives to attack the bacteria – once they exit the blood stream, they’ll never return. In a UTI, the dead neutrophils will be rinsed out with the urine. When bacteria invade other locations, the dead neutrophils can pile up to form pus. *Taps plays.* Thank you for your service, White-Hatted Warriors.
Meanwhile, Jill is feeling the urinary urgency, frequency, and pain associated with a urinary tract infection.
Partly, the bacteria are to blame. Their little hooks and attempts to invade the bladder wall irritate the tissue and make it painful to urinate. As urine flows past, the nerve endings feel the need to alert Jill’s brain to the fact that something is injured there.
Party, Jill’s own defense mechanisms are to blame. The swelling associated with bringing the neutrophils to the rescue also pulls on the stretch receptor in her bladder. Normally, a signal from the stretch receptor means that the bladder is getting too full, and so Jill’s brain tells her, “FIND RESTROOM – NOW!” This time, however, the stretch receptor is getting tricked because of the pressure from the swelling and passes the false message on to Jill’s brain, even though she really doesn’t need to go4.
So, Jill’s feeling miserable, and the neutrophils are sending wave after wave of defenders after the invading bacteria. Often, they are able to take care of the infection on their own – but that means that Jill has to endure discomfort for a week or so, and the bacteria have the chance to move upwards into Jill’s kidneys and cause even more damage. So, Jill’s lovely doctor prescribes her antibiotics to give the neutrophils some much-appreciated reinforcement.
Oral antibiotics are absorbed into Jill’s blood stream and eventually make their way down to the warzone. Antibiotics have a lot of options for how to kill a bacterium:
1) Keep the bacterium from making a cell wall. Bacteria have really high pressure inside them and use a cell wall kind of like Spanx – to hold everything in. The antibiotic can keep a bacterium from making or repairing its cell wall, and so the bacterium bursts from its own pressure. Dead.
2) Keep the bacterium from controlling what goes in and out. All cells have really smart membranes that let in good things and let out bad things. An antibiotic can keep a bacterium’s membrane from working properly, so that it either lets in poison or dies in its own waste. Dead.
3) Keep the bacterium from making new DNA (instructions) or protein (useful stuff – membrane components, toxins, enzymes, cell skeletons, etc.). Eventually, lacking either of these things is fatal. Dead.
4) (My favorite) Trick the bacterium into eating non-nutritious food. Some antibiotics look like bacteria food, but have a small structural difference that keeps the bacterium from using it properly. It’s like painting a beautiful feast onto a piece of cardboard. The bacterium starves. Dead.
Success! This bacterial invasion has been repelled by the combined forces of our neutrophil heroes and the antibiotic reinforcements. Jill’s symptoms will go away about 36 hours after starting her antibiotics, and the fight will end a few days later.
Look out for a post on viruses coming soon! Anything else you’re curious about? Let me know in the comments!
Sources & Further Reading
In case you needed a reason to re-watch Potter Puppet Pals.
E. coli without the pain:
Good general info for patients: Urinary Tract Infections in Adults. National Kidney and Urologic Diseases Information Clearinghouse.
My source for explaining pain and frequency: Wrenn, Keith. Chapter 181: Dysuria, Frequency, and Urgency. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd ed.
Neutrophils attack: The Phagocytic Response of the Host from University of Wisconsin – Madison.
Kunin, Calvin. Urinary Tract Infections in Females. Clinical Infectious Diseases. 1994; 18: 1-12.
Mulvey, Matthew. Adhesion and entry of uropathogenic Escherichia coli. Cellular Microbiology. 2002; 4(5): 257-271.
An Introduction to Human Disease by Leonard Crowley (7th ed, 2007).
- Bacteria is plural, bacterium is singular (because it’s a Latin neuter noun). Now you can sound like a nerd. [↩]
- Susceptibility for recurrent UTIs tends to run in families, though it’s not exactly clear what the genetic changes are. Some theories are that susceptible people have stickier epithelial cells that help the bacteria hang on, they have shorter urethras that let bacteria get to the bladder quicker, or the shape of their urethras allows urine to pool instead of completely rinsing out. [↩]
- Check out this awesome video (with sound effects) of a neutrophil chasing a Staph bacterium. [↩]
- This is the best explanation I can find in the literature, though it leaves me somewhat unsatisfied. If you have a better reference/explanation, please let me know in the comments. [↩]