Take Care of that Lettuce!

I’m sure you’ve heard the iconic analogy between brains and Jell-O, or hesitantly reached a hand into a brown-paper bag containing “brains” only to find that it must have been mislabeled since it is just spaghetti! But the brain is a bit reminiscent of lettuce as well! The meninges, delicate layers of tissue that bear hug the brain, enfold the brain in much the same fashion as each leaf in a head of lettuce wraps around and looks out for those beneath it. When this tight-fitting, multi-piece lettuce suit gets rumpled or agitated, meningitis takes the stage!

 

Image of Jell-O brain by Angel Schatz.

And young adults between 16 and 25 (i.e. us!) happen to be one of the most affected groups! Just since we’re young and healthy, does not mean we can’t get meningitis. In fact, living in dorms and with roommates boosts our chances of being a not-so-lucky winner of this uber-contagious “vacation.”

Meningitis is just inflammation of the brain’s lettuce layers. This disease takes the “your greatest enemy is yourself” idea to heart, as the immediate antagonist is your own immune system! When the immune system, our own microbial Ghostbusters, replies to a call for help, it loosens up our capillaries and makes them ultra-leaky. This means that more blood can find the problem area quicker and more fluid gushes from capillaries into afflicted tissues. This slackening of TSA for our blood allows more white blood cells and other fighter cells to report to the battlefront asap! But this excess fluid and blood causes swelling, reddening, and heat and the immune system booby traps the area with pain signals to ensure that you baby that body part.

In other words, the immune system is the puppeteer behind inflammation! Now before you call mutiny, the immune system is on your side! Inflammation, although inconvenient, is a sign that your body is fighting back against an invader and is typically helpful. But in meningitis, it is a reckless move.

For one, the brain and its meninges room together in our one-bedroom skull, so when the meninges swell up, the brain gets squished, meaning it is under more pressure. This compression, although slight, of perhaps our single most important, and certainly irreplaceable (imagine a brain transplant!), organ is dangerous. Plus, since capillaries now lose fluid left and right and blood pressure has eased, less blood and consequently less oxygen is getting to the brain. A brain hungry for oxygen throws temper tantrums in the form of seizures and can also have nerve damage.

But as usual, the true culprit for meningitis is a microbe. Bacteria, viruses, fungi, parasites, and even amoebas (tiny, single-cell organisms that thrive in geothermal pools) can cause meningitis. But so long as you keep from dunking your head in hot springs (because we have so many in State College), I’d say you’re fairly safe from amoebas.

While viral meningitis is the most frequent, bacterial meningitis is direr, and on some occasions, even fatal. Bacteria such as Streptococcus pneumoniae (yep, the same big bad behind pneumonia!) and Neisseria meningitides tend to infect the respiratory tract before spreading via the blood to the brain.

Neisseria meningitides, in particular, causes meningococcal meningitis, the highly contagious form we face as college students. Scarily enough, some meningococcal cases cause severe, adverse side effects including brain damage, and 10-15% wind up being fatal. If that’s not incentive to always wash your hands, I’m not sure what is!

So how do we avoid getting our lettuce layers all rumpled?

Foremost, get the meningitis vaccine. Most of you likely have it already since Penn State requires it to live in undergraduate housing. But there is an additional vaccine for another type of meningococcal bacteria that is not required.

Plus, even if vaccinated, be sure keep an eye out for any symptoms that might peek out. And if you have any reason to believe that you might have meningitis, seek medical attention as soon as possible. Cases caught early tend to lack severe side effects and nerve damage.

Just look at Haemophilus meningitis, once the leading type, but today it is no more than a footnote in most meningitis articles. Why? Thank the Haemophilus Influenza B vaccine!

In other words, get vaccinated, be aware, and you’ll be a-okay!

Ancient Egyptians Know What's Up!

I assume everyone has had a scratch or even worse: the deadly papercut, before. Before Band-Aids and Neosporin, the ancient Egyptians’ go-to for healing the nefarious papyrus-cut was some good old mold. According to a publication in the Mycologist, Imhokep, a legendary Egyptian healer (later worshiped as a god of medicine), used mashed up moldy bread to treat skin wounds. While this might sound crazy, or at least counterintuitive when you consider ringworm and other fungal infections, it is actually way ahead of its time.

Named from the Latin word for paintbrush, Penicillium notatum (aka P. chrysogenum) is quite the artist. A fungus with the mycelium, hyphae, spores, and so on, it is particularly fond of decorating bread with some blue, green, and sometimes even yellow spores. And since Penicillium notatum is not prone to infecting us, although some can have allergic reactions to its spores, it is often used for student microbiology labs here at Penn State! In my Microbiology 203 lab class, our first experiment investigated ideal growing conditions for P. notatum. So, I speak from experience, when I say that this fungus is partial to room temperature and damp conditions!

 

Photo of Penicillium by AJC1.

But as you can guess from Penicillium’s spoiler of a genus name, we have this pesky, bread-poaching fungus to thank for one of the most important discoveries in microbiology. Ever.

What do you get when you cross a two-week vacation and a messy scientist? Apparently, the advent of antibiotics.

Alexander Fleming, a not-so-tidy lab technician, neglected to clean his lab bench before taking a two-week leave, and when he returned he noticed a bunch of white fuzz in one of his Staphylococcus cultures. Of course, this was our friendly neighborhood bread mold, Penicillium notatum! It was not P. notatum that made Fleming take another look; rather, it was how it seemed almost as if the fungus kept the Staph bacteria at arm’s length, not allowing it to come near! Plus, when Fleming took a closer look with a microscope, the bacteria seemed to be “lysing” or dying.

In the end, Fleming found that P. notatum secreted a substance able to kill Staph and a slew of other bacterial species. Upon isolating and examining the properties of this secretion, Fleming promptly passed it off to Howard Florey and Ernst Boris to tackle the impossible task of purifying it as a stable compound. And some 10-20 years later, we had Penicillin, the world’s first, and now the most widely used, antibiotic!

Ironically enough, in his initial publication about Penicillin, Fleming didn’t even mention using it for therapeutics! Instead, he focused on its ability to help identify bacteria since it could inhibit some bacteria but not others.

Speaking of inhibition, how precisely does Penicillin play bacteria’s kryptonite?

Penicillin’s claim to fame lies in its special “beta-lactam” ring of three carbons and one nitrogen atom. This ring is the lock pick to a bacterium’s ability to build cell wall. The beta-lactam ring grabs onto a specific type of transpeptidase (called Penicillin-binding proteins or PBPs), the enzyme that weaves strands of cell wall material together. Penicillin then becomes clingy and controlling, keeping a transpeptidase from binding to other molecules and doing its job, and allowing new cell wall to unravel.

But Penicillin is not only the granddaddy of antibiotics, but also a more select class known as Beta-lactam Antibiotics. The Beta-lactam club includes other antibiotic celebrities like methicillin, ampicillin, and amoxicillin!

And since our cells oh-so-conveniently missed the boat on getting a cell wall, Penicillin can keep who is the rival bacteria and who is the home team straight!

But why does bread mold even produce this medical wonder child?

Penicillium notatum evidently does not see anything wrong with playing dirty! When there is nutrients and space on the line, why not take out the competition? Penicillium notatum might be a friend to us, but not so much to the bacteria it is contending with!

It sounds like the ancient Egyptians were actually on the right track!

Mycelium, Hyphae, Spores, Oh My!

As hygienic, tidy college students, surely, we have never found our only slightly stale bread bedazzled with blue and green fuzz or our carpet (that hasn’t seen a vacuum since September) accented with a tasteful, mottled blemish. Right?

Photo by Helena Jacoba.

Enter fungi, the final member of microbiology’s big three! Both abundant and diverse, fungi range from the yeasts used in winemaking, to lichens that festoon trees, to mold on fossilized leftovers from the back of the fridge, and sometimes we even eat fungi on our Pizza!

And although we know upwards of 99,000 different fungal species, scientists find nearly 1200 new species each year! So, let’s touch on the criteria for a fungus.

Foremost, fungi is a eukaryote-exclusive club. To get in, you must show nucleus at the door. Accordingly, no one from the microbes we have been meeting and greeting with thus far even has a change! Viruses, for one, do not even have a cell, not to mention a nucleus, and as hinted by the designation “prokaryotic” or “before the kernel,” bacteria came before the nucleus. But since eukaryotic cells tend to be of larger volume and higher complexity, order is vital. To avoid losing enzymes within the vast cytoplasm or having a million and one different tasks going on simultaneously and interfering with one another (a metaphor for college life?), cells embraced a control freak approach. Each eukaryotic cell has everything for a specific process sorted and painstakingly packaged into tiny compartments or “organelles.”

Yet despite this additional nucleus and a handful of organelles, fungal cells tend to be fairly simple. Fungi have only 1% of the quantity of DNA we have and only 1.3 three times the largest known bacterial genome.

Fungi also value vintage and friends in high places! Not quite as ancient as bacteria, it is still estimated that fungi have been around for roughly 450 million years, about 25 million years before plants. Although an early species, fungi have actually been found to be more related to animals than to plants.  

And fungi have a few fun quirks and handy superpowers!

For one, a fungus does not digest its food within the cell, but rather, does so externally. The tiny molecules produced by this out-of-body digestion absorb into the cell via its walls.

So, how do fungi look?

Well, each genus and each species appears a bit different beneath a microscope, but the style that is simply all the rage among fungi is mycelium. Mycelium refers to the fungal body with branching thread-like protrusions. These ever-growing tentacles form from tube-like cells, known as hyphae.

But fungi also largely reproduce via spores. Spores, the survival kits of the microbial world, consist of only the necessities to whether a storm and pass on your genes: a cell or two carrying the genetic material of the fungus, some food, and any protective measures. Spores produced by fungi can withstand dry, hot environments before kickstarting growth upon reaching a favorable environment, but bacterial spores put them to shame with their incredible ability to withstand harsh environments. Yet, whereas these bacterial endospores serve merely as a survival mechanism, fungal spores predominately play a role in replication.

Photo by Nick Bramhall.

“Fruiting bodies” that produce these spores range from a variety of microscopic options to the shelf fungi and mushrooms we know so well! The diversity and unique nature of fungi (even when it has laid siege to your last slice of bread) is simply astounding!