Today’s column is about skin-colonizing bacteria.
The human body is teeming with life, much like a swamp or a sewer. It’s nice, I think, to regard yourself as a groundskeeper of something bigger, to see each meal not as mere fuel for your own cells, but for the trillions of bacteria that also call your meat sack home. Whenever I am feeling particularly alone in the universe, I like to learn about my corporeal friends: the mites that eat my eye boogers, the lactobacilli that keep my pussy fresh, how human feces is about 30 percent dead bacteria. Our microbes work to train our immune system, help us digest our food, and fight on our behalf. And when it comes to the body’s largest organ—our skin—their importance cannot be overstated.
The average human is walking around with 1.8 m2 of diverse ecological niches, all warm folds and wet invaginations and broad swaths of exposed skin. But skin is more than just waterproofing to keep the elements out; it’s also how we interface with the world at large and, as such, our skin is colonized by tons of shit. Bacteria, fungi, viruses, mites, all of which must be managed and, in turn, manage us. For example, your immune system works to modulate the microbiota of the skin, but the microbiota of the skin also work to teach the immune system how to do its job. It’s quite the quid pro quo.
Skin colonizers run the gamut from harmless to helpful, providing vital functions that we haven’t evolved to do without their help. Some micro-organisms may take on teacher roles, educating the body and priming it to recognize and respond to their pathogenic cousins. It’s all very sweet, of course, until it isn’t. Disruptions on either side of the functional truce can result in skin disorders, infections, and even death.
And on that note, I invite you to pull up a seat, my gross little friends. Today we are delving into the microbiology behind the abscess-filled world of the 2003 Saint Louis Rams.
From September through December of that year, the Rams saw eight significant infections in five of its 58 players. These infections sprang from turf burn on the elbows, forearms, or knees of offensive and defensive linemen and one linebacker, and rapidly progressed to large abscesses requiring surgical intervention; that is, the richly-satisfying and pus-filled world of incision and drainage. But these were no ordinary abscesses: the pus here was teeming with methicillin-resistant Staphylococcus aureus: MRSA, the difficult to treat infection and avatar of the modern era of antibiotic resistance.
Staphylococcus aureus is named for the golden hue of its grape-like clusters that appear when it is grown on sticky plates of blood agar. It’s a common colonist of the human body, and prefers to live inside the nose. Twenty percent of people are walking around with a persistent S. aureus infection in their anterior nares; 30 percent are intermittently colonized. This bacteria is also happy to set up shop at other sites too, such as the armpit, crotch, and GI tract. This is important because colonization provides the bacteria a path to infection if and when the body’s defenses are breached by things like shaving, surgery, or turf burn.
And once it gets in, S. aureus has a veritable armamentarium of ways to make itself right the fuck at home in your flesh prison. Here’s how it works—methicillin-resistant or otherwise.
There are two things that S. aureus can do very well: adhere to host cells and evade the immune system’s attempts to get rid of it. While the details of colonization are very complex and not completely understood, we know that the process they use involves stickiness and stealth, so that’s what I’m going to talk about today.
Well, that and redundancies. S. aureus makes a whole mess of virulence factors, molecules that help the bacteria establish infection. What is particularly noteworthy about our buddy golden staph is that they are a brick shithouse of virulence factors: over-built as fuck. Some of their virulence factors can do multiple jobs, and multiple virulence factors can do the same job. Safe to say, they have a lot to work with when it comes to getting cosy and setting up shop in your razor burn.
As I mentioned earlier, something that S. aureus does very well is stick to your cells. Specifically, S. aureus is covered in microbial surface components recognizing adhesive matrix molecules, known as MSCRAMMS. I like to pronounce this “M’Scramms” because it sounds like a saucy greeting and, since this is my column, that’s what we’re going to use today.
M’Scramms play a huge role in the initial attachment to the host, i.e. you. Seeing as step one to infection is “find a place to live,” these adhesins are very important. One of the major M’Scramms is known as FnBPA (fibronectic binding protein A) and it’s notable because it does two things very, very well.
First off, FnBPA (or fuckin’ BPA! as it rings in my head) is an adhesin, which does what it says on the label: helps stick the bacteria to its new host cell friend. It’s also, however, an invasin, which means it helps facilitate bacterial internalization into cells. FnBPA is so very good at getting mammalian cells to open up that when scientists coated tiny beads with the protein, absent all the other artillery S. aureus has in its arsenal, the cells still internalized the beads.
Sticky and invasive. And we’re just getting started!
Once adhered, here is some of the cool shit S. aureus can do to avoid your immune system. It can make it so that the immune cells tasked with gobbling them up cannot eat them. It can make zwitterionic capsules to promote abscess formation. It can disarm the body’s security system by blocking the call for help, making it so that the white blood cells floating around waiting for the call do not, in fact, get the call. It even makes something that kills certain white blood cells by causing them to become covered in tiny, fatal pores!
Truly, S. aureus does not fuck around.
Now, back to the St. Louis Rams. The strain of S. aureus that caused large abscesses in five of the team’s players wasn’t garden variety staph, but rather the dreaded MRSA. The antibiotic Methicillin was first introduced around 1960; within a year, methicillin-related isolates of S. aureus were reported. Suffice to say, it’s been squirrelly from the start. Today, MRSA is a big deal because it’s resistant to many antibiotics, making it difficult to treat, even in the healthiest of patients. Like football players.
The outbreak experienced by the Rams was a testament to how easily MRSA can spread and infect those unlucky enough to come into contact with it. While we usually discuss MRSA in the context of healthcare acquired infections, it’s a good reminder to be wary of the fact that MRSA can also persist in the community at large. And while the Rams who suffered its wrath were able to recover, not all athletes have been so lucky.
In 2016, former Giants tight end Daniel Fells was forced to retire after a months-long battle with MRSA that almost led to the amputation of his foot because the staph infection in his ankle was found to be resistant to antibiotics. MRSA is enough of a problem in locker rooms around the country that Colgate University has been fighting against outbreaks for over a decade. They haven’t made much progress, so you should keep washing your hands.