Archive | Microbiology RSS feed for this section

Why Science Nerds Wear Glasses.

24 Oct

Ever wonder why science nerds wear glasses?
Recently, a contact lens wearing lass was infected by an amoeba which was infected by a virus which was infected by a virophage which was infected by a parasitic piece of DNA called a transpoviron. It’s like a microbial inception. (This article originally appeared on io9.com)

Woman with eye infection had an entire microbial ecosystem in her contact lens solution


by George Dvorsky

There’s a reason why optometrists say you should regularly replenish your contact lens solution and throw out your lenses after the expiry date. Last year, a young woman contracted an eye infection after using tap water to dilute her cleaning solution, and while wearing contact lenses that were two months past their expiry date. Subsequent analysis of her lens solution revealed an entire cornucopia of microorganisms that were spawned from a single amoeba, including a giant virus that was also infected with a virus — and a piece of DNA that was capable of infecting both of them.

Thankfully, the woman’s condition, keratitis, was not serious and was easily treatable — but the subsequent analysis of her contaminated lens solution was quite revealing, if not disturbing.

The research, which was conducted by Bernard La Scola and Christelle Desnues, was initially concerned with an amoeba they found in the fluid. But after looking at the amoeba more carefully, the researchers discovered that it hosted two different microorganisms, including a giant virus that had never been seen before (what is now called the Lentille virus).

This Lentille virus, after infecting the amoeba, created a kind of “virus factory” where its genetic material was copied, thus spawning new viruses that were architected from its genetic script.

Now, if this wasn’t surprising enough, the researchers also discovered that the Lentille virus was also infected with a virus, what’s called a virophage. This virus-within-a-virus, named Sputnik 2, is only capable of reproducing in cells infected by other viruses (in this case, the infected amoeba). Amoebas that are infected with this virus continue to release virophage particles, which means the virus can continue to infect other amoebas on their own.

But there’s still more: Both the giant Lentille virus and Sputnik 2 virophage contained even smaller parasites called transpovirons — highly mobile chunks of DNA that can relocate themselves into the genomes of viruses and tuck themselves away inside of virophages.

So, in summary, the researchers discovered that a transmissible DNA sequence managed to find its way into a virophage (and potentially the giant virus itself), which in turn latched onto a giant virus, which then infected an amoeba — an amoeba that eventually found its way into the eye of a 17-year old girl.
You can read the entire study at PNAS.

Microbe Painting

20 Apr

While in college, I spent a few years working at an art gallery. I absolutely loved it. It was an excuse to get out of the lab and meet people, and many artists appreciated my insatiable passion and constant pursuit of what I loved, even if they didn’t know what the hell a Gram’s stain was. Either they appreciated it, or lovingly put up with it. Either way, it rocked.
Right before one of my coworkers left to pursue greener pastures in another state, he painted me this incredibly adorable microbe painting.

I want to hug it forever!
^_^

Flesh-Eating Bacteria

10 Apr

I was gearing up to write a super-awesome article on flesh eating bacteria! It’s something everyone has heard about, though I can guarantee you that it’s not as scary as flesh-eating mould. (Flesh eating mould is one of the few things that truly grosses me out. I can handle flesh eating bacteria any day of the week, but the flesh eating mould is far more insidious. But that’s a tale for another day.)

However, Keith Veronese of I09 beat me to it, and did a far better job that I would have done. I added a few pictures, because there is no such thing as too many bacteria photos. Enjoy!

Does flesh-eating bacteria really make a meal out of you?

You first notice a bump — a tender, cherry red bruise. Over the next 12 hours, the center of this painful spot on your leg becomes dark violet in color. A day later this raised red bump ruptures and fluid oozes forth. I hope you are on the way to the hospital at this point, because flesh-eating bacteria might be running amok in your body.

These microbes have appeared in such films as the late-night scifi flick Cube Zero, in which a prisoner is sprayed with flesh-eating bacteria and melts before the audience’s eyes. But does this horrifying bacteria act as quickly as depicted in movies? And more importantly, do the bacteria actually dine on your flesh?

Does flesh-eating bacteria really make a meal out of you?

Flesh-eating bacteria formally goes by the mildly less frighting name necrotizing fasciitis in medical circles. Necrotizing fasciitis occurs through a cascading series of events, with the bacteria Clostridium perfringens and Streptococcus pyogenes commonly initiating the infection. The bacteria often enter through an open wound, particularly when the wound is left exposed in a foreign environment like seawater or sewage.

These bacteria lurk in benign places — a 14-year-old in South Carolina contracted the illness in2009 after removing rocks from the bottom of a local lake. He lost half of his palate, a portion of his nose, and several teeth as surgeons extracted flesh to prevent spreading of the bacteria. In another incident, the guitarist of the venerable thrash metal band Slayer contracted the diseasefrom a spider bite in 2011.

In necrotizing fasciitis, the bacteria doesn’t actually eat the flesh of your body. The bacteria sneaking their way into your body spur on the release of proteins, which have a toxic effect in increased quantities. Phospholipase A2 and antigens released by the bacteria enter the cells of your skin, fat, and the connective tissue covering your muscles and begin wreaking havoc. (Here’s an image of a necrotizing fasciitis infection, but be forewarned that it’s very graphic. Like, Krokodil graphic.)

Phospholipase A2 is often found in snake venom and bee stings. When excess Phospholipase A2 appears in the body, your cells respond by releasing arachidonic acid. The presence of additional arachidonic acid disrupts cells, causing inflammation and pain. Fortunately, the effects of Phospholipase A2 can act as a warning sign for those with necrotizing fasciitis, hopefully leading an individual to seek out treatment.

The antigens released are commonly a type of superantigen that causes non-specific activation of T-cells, or those cells that are the primary line of defense in your body’s immune system. The over-activation of T-cells leads to the release of enormous quantities of cytokines (a small protein) at the infection site. The cytokines start a cell signalling cascade that begins the destruction of tissue cells in the region. The foreign bacteria causing necrotizing fasciitis do not eat your flesh, but they do something a little more sinister — these bacteria turn your flesh against you.

What happens should you contract necrotizing fasciitis? Patients must receive intravenous antibiotics immediately and a series of surgical operations to remove dead tissue. If the operations are unsuccessful and the necrotizing fasciitis is contained to an appendage, amputation of an infected arm or leg is the safest course. Patients with necrotizing fasciitis often undergo hyperbaric oxygen treatment, with the hope that the increased oxygen levels help the body heal.

Several hundred individuals contract necrotizing fasciitis in North America each year. Even with treatment, 25% of patients that contract necrotizing fasciitis die from complications of the disease. Years of skin grafts and pain management follow those who are lucky enough to survive.

Also, an even scarier type of necrotizing fasciitis, Fournier gangrene, targets the perineum, and more specifically, the groin and genitals. Modern cases are not common, but the historical autopsies suggest that the Roman emperor Galerius and Herod the Great died of this malady. A 69-year-old Herod suffered from a combination of kidney failure and Fournier gangrene, degrading his flesh to the point that worms and maggots moved in and out of the affected areas freely. Fournier gangrene, when it appears in modern society, carries a 40% mortality rate.

The top image is a promotional photo for AMC’s The Walking Dead. Images linked from the article: Late diagnosed necrotizing fasciitis as a cause of multiorgan dysfunction syndrome: A case report and the CDC.

Microscopy Monday {No.5}

9 Apr

Potentially toxic filamentous cyanobacterium Anabaenopsis

Dr. Petr Znachor
Institute of Hydrobiology
Ceske Budejovice, Czech Republic

Technique: Differential interference contrast

You Will Never See Mold The Same Way Again

5 Apr


This video is mind-blowing in it’s quality and dedication. Many of these molds take days or even weeks to grow, and all such organisms, due to their spore-forming nature, must be handled in a designated Class III lab. This wasn’t some bored dude in his kitchen, this was a person with access to a designated space and a great talent for videography.

Microbiology Science Quickies: Coral Herpes, Dangerous Grilling, & Bacterial Communications

2 Apr

Ahhhh! So much science and health stuff to share! My poor web browser is drowning again!

You may have heard that the world’s coral reefs are collapsing, and while there are many theories, we have yet to fully explain why. It’s often assumed that climate change and pollution are the main culprits, and there is probably truth to that.
But now scientists are examining another culprit: a virus.
Particularly, a herpes virus.
From microbiologist Rebecca Vega-Thurber: “We were shocked to find that so many coral viruses were in the herpes family. But corals are one of the oldest animal life forms, evolving around 500 million years ago, and herpes is a very old family of viruses that can infect almost every kind of animal. Herpes and corals may have evolved together.”


That being said, I do not recommend you try to pick up chicks by telling them your penis can vanquish marine ecosystems.

As the days get longer and summer approaches, many people are firing up their grills to participate in the American tradition of consuming charred meat. However, grilling is not without it’s health risks. Along with E.coli and carcinogen formation, the traditional wire grill brush may also make you sick, NPR reports. SOme good news though: the use of antioxidant spices may reduce the negative effects of those delicious fatty meats, especially rosemary.  Additionally, proper grilling technique will typically kill the deadly E.coli o157:H7 strain.

Bacteria are pretty interesting critters that can not only talk to each other, they play prisoner’s dilemma to decide their fate.
“When faced with life-or-death situations, bacteria use an extremely sophisticated version of “game theory” to consider their options and decide upon the best course of action.” Of all the microbiology-related articles I’ve read lately, this is one of the most interesting.

According to Yale University, just the mere presence of a person in the room can cause bacterial levels to spike. When a person enters the room, they stir up bacteria. Says the article: “Many previous studies have surveyed the variety of germs present in everyday spaces. But this is the first study that quantifies how much a lone human presence affects the level of indoor biological aerosols.”

In biochemical news, researchers have captured the first images of vitamin B12 in action. In 3D, no less! Scientists from the University of Michigan Health System and the Massachusetts Institute of Technology report they have created the first full 3-D images of B12 and its partner molecules twisting and contorting as part of a crucial reaction called “methyltransfer.” This reaction is vital both human cells and in bacteria that consume carbon dioxide and carbon monoxide. Such bacteria live in the guts of humans, cows, and other animals, and aid with digestion.

Crochet Bactierophage

29 Mar

Made by  Rachael Penzo, and seen on Geek Crafts and Craftster, this adorable bacteriophage amigurumi is a million kinds of awesome. I love it so much. I’m tempted to try it, but I will just stab myself with crochet hooks again.

Glass E.coli

26 Mar

Glass E.coli sculpture makes me swoon with delight.

Etsy Find: NBDesigns

26 Mar

I love finging science-themed artists on Etsy! NBDesigns features designs that perfectly balance talent, adorableness, and delight.
Their products include:
Bacterium earrings, complete with adorable monotrichous flagella and organelles.

Bacteriophage earrings

DNA Electrophoresis Ladder earrings

Erlenmeyer Flask of Love, complete with a itty bitty heart.

Petri Dish earrings


A microbiology charm necklace, featuring a bacterium, a heart flask, and a petri dish.

A necklace of a macrophage eating an itty bitty heart

And, because I am a complete coffee addict, I have to include these awesome golden coffee bean earrings.
 If I brewed them, would they taste like art?

World Tuberculosis Day

24 Mar

Today is World Tuberculosis Day, a day dedicated to raising awareness to one of the world’s deadliest diseases, because no holiday is complete if it doesn’t involve celebrating the misery of millions of people.
That’s why Christmas is so popular.

Tuberculosis is a disease caused by the bacteria Mycobacterium tuberculosis, which is one of those bacteria that is really awesome to talk about and really annoying to work with.
Really, really, really annoying.
Seriously, you have no idea.
It sucks.

The Disease

Despite how charming Doc Holiday made tuberculosis look, the disease is just as annoying as the bacterium. If you catch tuberculosis, treatment can take anywhere from 6 months to 2 or 3 years, depending on it’s drug resistance. Oh yeah, it’s highly drug resistant. And we only really have 8 types of drugs to treat it with (2 first line and 6 second line drugs) . Mutli-drug resistant TB (MDR-TB) is resistant to rifampicin and isoniazid, the first line of drug defense doctors use. Extensively drug-resistant TB (XDR-TB) is also resistant to three or more of the six classes of second-line drugs. Totally resistant TB was first reported in 2003, and was pretty rare. At first. Now it’s a bit more widespread.
Because it’s an annoying bastard.

Also, if the drug resistance and multi-year treatment isn’t bad enough, in the United States, you have no choice on whether or not you get treated. You HAVE to get treated, because the disease is such a danger to public health. Part of the drug resistance is due to people no continuing their treatment, which can be rigorous. And while there is a vaccine, it’s has varying degrees of effectiveness against pulmonary tuberculosis.

On top of everything else, many cultures have a huge social stigma against those who have it, even after they’ve been cured. During the treatment, they may be completely ostracized from their village and even their families who fear the disease. You can’t blame the people for wanting to protect themselves, but it also leaves the patient , leaving them with no emotional support structure and facing the shame of disease. They will often find themselves alone, and become very depressed and stop taking their treatment. It’s a problem Doctor’s Without Borders has to face every day, and has done their best to bring public attention to the multiple issues surrounding the disease with their adorably named project “TB And Me”.

Most people think that TB is a “third world problem.” But in reality, it’s everywhere. There are parts of London which have rates nearly as high as Chinese provinces. Alaska is facing a tuberculosis epidemic among their homeless and do random sweeps every few weeks. Even my father caught tuberculosis as a boy living in Colorado. It is highly contagious: a person with active TB can infect 10 to 15 people a year. It killed 1.7 million people in 2009. Over 2 billion people are infected, though not all of these cased are active. Of these 2 billion, 10% will develop an active infection during their lifetime.

The Bitchy Diva

It’s a Class III organism, which means you have to use a bunch of annoying precautions when working with it. Not only do you have to process the specimens under a biohood, you have to do it in a special room completely dedicated to working with tuberculosis, and only tuberculosis. This room separated from the rest of the lab by a series of doors and negative air pressure. You also have to wear a special mask so you don’t accidentally inhale it, since the infective dose of M. tuberculosis is fewer than 10 bacterium. And before you work with it, you have to spread bleach-soaked paper towels everywhere, so that if by chance even one bacterium falls onto the counter, it will immediately die a horrible, bleachy death.

We don’t mess around with tuberculosis. It’s not a fun and cute bacteria like E.coli. It’s a high maintenance bitchy little diva that will slowly and violently murder your lungs if it gets a chance.

Science Stuffs

Mycobacterium are a genus of Actinobacteria. There are over 70 species of Mycobacteria, but most people are familiar with M. tuberculosis and M. leprae, the causative agent of leprosy. While most clinically significant bacteria grow within 18-48 hours, Mycobacteria takes it’s time. Some species will form colonies within 7 days (termed “rapid growers,” because microbiologists have a skewed perception of time), while other may take 6 weeks or longer to grow. Maybe they like to take their time growing because they don’t want to come across as desperate. Or maybe they’re just stubborn and will grow when they’re damn well good and ready.
Either way, it’s really annoying.

One of the most significant characteristics of Mycobacterium is their cell wall, which is thicker than most other bacteria and completely stuffed with mycolic acids that give it a waxy appearance. The cell wall consists of the hydrophobic mycolate layer and a peptidoglycan layer held together by the polysaccharide arabinogalactan, which is one of those words I love watching drunk people try to pronounce.

M. tuberculosis is a bacillus and may be considered Gram-positive, but this is actually a huge misnomer. Due to the high lipid content of their unique cell wall and general stubbornness, they do not retain any portion of the Gram stain, and thus are neither truly Gram positive  or Gram negative. While they don’t truly retain crystal violet, upon staining they can appear to be weakly Gram positive, because it likes to laugh in the face of logic. Or they won’t stain at all and be referred to as “ghosts.” Again, either way, it’s really really annoying.

If only they were this cute.

A much more useful stain for this species is the Ziehl–Neelsen stain, commonly referred to as the acid-fast stain.
M. tuberculosis is acid-fast, meaning they are resistant to decolorization by acids during staining.  This is due the the lack of an outer cell membrane. It decided somewhere along the way that outer cell membranes were too mainstream, and never bothered getting one.


 M. tuberculosis is nonphotochromogenic, meaning it won’t produce a pigment in the presence or absence of light. Their colonies are buff-colored, dry, rough, and honestly rather ugly. They look like demented warts.


If growth conditions are optimal in broth cultures, M. tuberculosis will actually grow in long, rope-like strands, which we called “cording,” which is actually pretty cool. M. tuberculosis is strictly aerobic, requiring high amounts of oxygen, which is why it loves to invade your lungs.. They are nonmotile, and lack spores and capsules. In terms of biochemical identification, they are negative for catalase, including the 68 degrees Celsius catalase test which is commonly performed on Mycobacteria species. They are positive for niacin and nitrate.

M. tuberculosis was first described on 24 March 1882 by Robert Koch, a guy every biologist should recognize, if not for all his grand achievements in the field of microbiology, then at least for his dapper style.

 Note the fine beard and bow tie, which can both be used to clean microscopes. He received a Nobel Prize in 1905 for his discovery. In 1998 we sequenced it’s annoying little genome.

Doctors Without Borders have made several awesome infographic posters to help educate about TB rates:
TB-infographic-treatment
TB-effects-infographic2-final

Stop TB - In My Lifetime, World TB Day, March 24. http://www.cdc.gov/tb/events/WorldTBDay/default.htm

Click here to learn more about World TB Day!
Click here to learn more about Tuberculosis and it’s growing drug resistance.

Tuberculosis Infographic

22 Mar

Antibiotic Resistance

22 Mar

Plastic-Eating Fungi

11 Mar

Plastic-Eating Fungi Found In The Amazon May Solve World’s Waste Problem

By Emma Hutchings

A group of students and professors from Yale University have found a fungi in the Amazon rainforest that can degrade and utilize the common plastic polyurethane (PUR). As part of the university’s Rainforest Expedition and Laboratory educational program, designed to engage undergraduate students in discovery-based research, the group searched for plants and cultured the micro-organisms within their tissue.

Several active organisms were identified, including two distinct isolates of Pestalotiopsis microspora with the ability to efficiently degrade and utilize PUR as the sole carbon source when grown anaerobically, a unique observation among reported PUR biodegradation activities.

Polyurethane is a big part of our mounting waste problem and this is a new possible solution for managing it. The fungi can survive on polyurethane alone and is uniquely able to do so in an oxygen-free environment. The Yale University team has published their findings in the article ‘Biodegradation of Polyester Polyurethane by Endophytic Fungi’ for the Applied and Environmental Microbiology journal.

 

Iditarod and Diphtheria

3 Mar

Today is the ceremonial start of the Iditarod! Which, if you live in Alaska, is kind of a big deal. And if you live elsewhere, it’s just another Friday.
Either way, today is a good day.

The Iditarod is a 1,000ish mile race (though this year it’s only 975 miles) commemorating the infamous diptheria epidemic and celebrated every year with a grand ceremonial start and Alaskans bickering which dog, Balto or Togo, deserves more credit for the original race.

The original run was actually a huge deal. Alaska is huge state with very few roads. Hell, even our capitol city cannot be reached by road. There weren’t, and still aren’t, any roads to Nome. So when the diphtheria epidemic hit Nome in 1925, people panicked. The nearest antitoxin supply was in Anchorage, about 1000 miles away. It was the middle of winter, and winter storms produced strong gales of -85 degrees F. Nearly every Alaskan can recite this story in their sleep.

So today, while most of Anchorage is crammed downtown to celebrate the ceremonial start of the Iditarod, I am curled up with  warm cup of coffee and celebrating the Iditarod in my own way: With good ol’ fashioned science.
(Plus it’s really, really snowy out today, and my poor little car still doesn’t have snow tires.)

Today’s topic: Corynebacterium diphtheriae!

(Yay!)

 C. diphtheriae is the adorable little bugger responsible for diphtheria, and has some odd little quirks that are fun to explore.
First, the basics: It’s a Gram-positive, highly pleomorphic bacilli, belonging to a peculiar group of bacterium called Actinobacteria. It is non-motile and aerobic. It often arranges itself in peculiar ways that microbiologists refer to as “Chinese letters.” (Unless you’re a Chinese microbiologist, in which case you would probably refer to them as Korean letters or something.) The less racist/more politically correct microbiologists refer to the morphology as a “picket fence” or “palisades” referring to how they lay next to one another. Its very distinct, instantly recognizable, and always makes me want to build kick-ass purple picket fence around my home.

(Because white picket fences are sooooo 6 decades ago.)

As for agars, C. diphtheriae is typically grown on Loeffler medium or tellurite agar. CTBA agar, which contains postassium tellurite, cystine, bovine serum, and sheep’s blood, is a common one found in labs due to the fact C. diphtheriae will form black colonies with characteristic brown halos, which differentiate it from most other Corynebacterium species.

(Be warned though, that C. ulcerans and C. pseudotuberculosis will also cause brown halos).

C. diphtheriae is also metachromatic, which means that a single stain will result in two or more different colors. This is due to the granules found at the polar ends of the bacterium, known as Babes Ernst Granules, which will stain a different color and are responsible for the notable club-shape of the bacterium. Ponder’s and Alberts’s stains can be used to demonstrate this phenomenon.

 Which looks pretty freaking groovy.

C. diptheriae produces a particularly nasty toxin which is responsible for Diptheria. Medical microbiologists must demonstrate the presence of the toxin, and they do so with the Elek’s Test. Developed in 1949, the Elek’s Test uses immunodiffusion to demonstrate the toxin. The patient’s isolate is placed on the agar in a straight line, alongside a known toxic and non toxic strains (which serve as positive and negative controls). Then a strip of paper containing antitoxin is laid across them in a perpendicular fashion. The antitoxin reacts with the toxin, forcing it to visibly precipitate out into the agar.


If the patient’s isolate contains the diptheria toxin, then peripitin lines will be formed. Iron will inhibit toxin production, so the Elek’s Test must be performed on a media with low iron content and an alkaline pH.

The toxin itself is pretty interesting. A bacteriophage with the Tox gene will infect a C.diptheriae bacterium, which will incorperate the Tox gene into its own genome and thus become a toxin producer. The toxin is secreted and actually nontoxic until it encounters trypsin, which will result and two fragments: A and B. Fragment B binds to receptors on eukaryotic cells and mediates the entry of Fragment A into the cell. Once in the cytoplasm, Fragment A disrupts protein synthesis. This disruption of protein synthesis is what contributes to the toxigenicity of the toxin.

Diptheria itself is characterized by a grey-white pseudomembrane formation on the throat, which honestly looks pretty nasty. And while I am usually all for disgusting photos of medical conditions, today I feel more like posting a photo of sled dogs, who hold the award for the most ridiculous tongues ever.

(All the better to lick your face with, my dear.)

So thank you, C. diphtheria, for giving Alaskans kickass piece of history that displays the extremes we will endure to help fellow Alaskans, a wonderful mid-winter celebration, and hilarious photos of sled dogs.

If you are interested in learning more, especially about the history of Diptheria epidemiology, Todar’s Online Textbook of Bacteriology is a wonderful resource.

Itty Bitty DNA Sequencer

2 Mar

A tiny DNA sequencer the size of a flash drive? For only $900? Yes please.

 

 The MiniON has been used successfully to read the genome of the lambda bacteriophage, which is about 48500 base pairs in length. Pretty impressive, little guy. I love the thought of having lab equipment I can carry around in my purse at all times. You never know when a science moment will occur, and you want to be ready! Like some super awesome superhero of science!

E.coli Is Pretty Damn Cute.

29 Feb

Not many people would consider Escherichia coli to be cute. Or any other bacteria, really.
But this little Gram-negative darling deserves some respect and appreciation. There are many strains, ranging from peacefully non-pathogenic to potentially fatal food poisoning, with an impressive range of genetic and phenotypic diversity. And don’t forget the menacing H0157:H7, a sneaky little punk who stole the notorious shiga toxin from Shigella.

E.coli 0157:H7 would totally have a mohawk.

Science owes a lot to E.coli.  It was one of the first organisms to have its genome sequenced. Since the initial sequencing in 1997, there have been 60 completely sequenced strains. So diverse is this organism that these 60 sequenced strains only share 20% of their DNA. The other 80% of each strain is wildly different!
In the 1940’s, Joshua Lederberg and Edward Tatum used E.coli to describe the phenomenon bacterial conjugation, where bacteria exchange and transfer genetic material via direct contact, much like a flash drive can transfer info between computers. In 1988, a long-term experiment involving 12 identical cultures of E.coli was set up.
In 2010, the cultures reached 50,000 generations, and display a wide variety of diversity, including one culture which can now utilize citrate. Citrate utilization is a common test used to differentiate Salmonella (positive) from E.coli (negative) in medical microbiology labs. While there has yet to be a known case of wild E.coli utilizing citrate, we now know that they can evolve to adapt that characteristic on their own.
You may have heard of Mutaflor, a probiotic used to treat gastrointestional disorders. That’s actually a specialized strain of E.coli! (I like to pretend that it wears those old-fashioned nurse uniforms).

E.coli has taught us so much about microbiology, genetics, and evolution. And if that isn’t adorable enough, E.coli is peritrichous, meaning that it has beautiful flagella everywhere!


Seriously, flagella everywhere! They probably give the best hugs! The flagella are like itty bitty rotary-powered protein tentacles. It’s basically the bacterial version of Cthulhu. Good thing they never bothered to evolve wings. (Yet.)

(First image from shardcore.com. They have wonderful art.)