The emerald cockroach wasp is a mother on a mission. This parasitic insect lays its eggs on cockroaches, but to minimize the risk of the host’s many microbes and pathogens to her eggs, the wasp does what many human mothers today would do. The wasp arms her babies with sanitizer before dropping them off.
Antibiotic resistance is a well-known menace: Witness the dangers of hospital-acquired MRSA infections, or the totally drug-resistant tuberculosis found in India earlier this year. FDA statistics show that over 80 percent of antibiotics used in the US are given to livestock, and heavy animal use is thought to be one of the drivers of resistance among human pathogens. So it behooves veterinarians and public health officials alike to stamp out antibiotic resistance in animals.
In the hunt for how this resistance develops, though, scientists have been mostly looking at bacteria inside the digestive system. But it turns out they might have, er, the wrong end of things—a new study finds that drugs excreted in pee and feces may be even more worrisome than those circulating in the bloodstream.
Bacteria invisible to the naked eye find their way to many of the external surfaces of our bodies, including the naked eye. But the eye isn’t defenseless against this onslaught of microbes—researchers have found that it has special weapons for fighting back.
This fight happens at the surface of the cornea, the eye’s clear outer layer. New research published in the Journal of Clinical Investigation has found that keratin—a type of protein that gives structure to the cornea and other tissues like skin, teeth, hair, and mucous membranes—protects against bacteria. If the eye is like a fishbowl, it’s made of shards used for self-defense. Researchers say the new finding may lead to the creation of new kinds of antibiotics.
Most of us assume that by the time food arrives at the grocery store, it’s been checked for any chemicals that might harm us. That’s not necessarily the case: food manufacturers and federal employees test for some known culprits in some foods, but the search isn’t exhaustive, especially when it comes to imported items. Recently, scientists working with ABC News checked to see whether imported farmed shrimp bought from grocery stores had any potentially dangerous antibiotic residue, left over from the antibiotic-filled ponds in which they are raised. It turns out, a few of them did.
Out of 30 samples taken from grocery stores around the US, 3 turned up positive on tests for antibiotics that are banned from food for health reasons. Two of the samples, one imported from Thailand and one from India, had levels of carcinogenic antibiotic nitrofuranzone that were nearly 30 times higher than the amount allowed by the FDA. The other antibiotics the team discovered were enroflaxin, part of a class of compounds that can cause severe reactions in people and promote the growth of drug-resistant bacteria, and chloramphenicol, an antibiotic that is also a suspected carcinogen.
Thanks to antibiotics, we tend to think of urinary tract infections as no big deal. Pop some cipro, and you’re done. A good thing, too—if the E. coli that usually cause UTIs crawl up the urinary tract, they can cause kidney failure and fatal blood poisoning.
But antibiotics may not be saving us from UTIs for very much longer. Scientists tracking UTIs from 2000 to 2010 found a dramatic uptick in cases caused by E. coli that do not respond to the drugs that are our first line of defense. In examining more than 12 million urine analyses from that period, they found that cases caused by E. coli resistant to ciprofloxacin grew five-fold, from 3% to 17.1% of cases. And E. coli resistant to the drug trimethoprim-sulfame-thoxazole jumped from 17.9% to 24.2%. These are two of the most commonly prescribed antibiotics used to treat UTIs. When they are not effective, doctors must turn to more toxic drugs, and the more those drugs are used, the less effective they in turn become. When those drugs stop working, doctors will be left with a drastically reduced toolkit with which to fight infection.
For frequent readers of this blog and Carl Zimmer’s The Loom, the bacterium Clostridium difficile may ring a bell. It’s a germ that can cause devastating, intractable gut infections, and is one of the reasons behind the recent development of fecal transplants to try to give the patient healthy gut bacteria to fight back with. C. difficile is on more people’s radar these days, and with good reason. A new Centers for Disease Control report shows that infections from C. difficile and another gut pathogen, norovirus, have grown more common and much more lethal in the last fifteen years. In 2007, they killed more than double the people they’d killed ten years before, jumping from 7,000 to 17,000. Most of those who died were elderly.
Bacteria that have evolved defenses against antibiotics are something of a disaster waiting to happen. Whenever a new drug-resistant strain, or a gene that confers resistance, crops up in a new place—as when the NDM-1 gene, which confers resistant to up to 14 drugs, showed up in drinking water in New Delhi—it’s another nail in coffin of a world in which we can heal nearly everything. Scientists are looking into how to get around that resistance, though, and there are some hopeful headlines now and then, including a recent study from researchers at North Carolina State University in which they identified a molecule that can boost the efficacy of two antibiotics against bacteria 16-fold.
The molecule, which the researchers found by testing about 50 candidates to see if they could reduce the number of NDM-1-carrying K. pneumoniae by a significant amount, doesn’t have any antimicrobial properties of its own. It’s an adjuvant, which means it has to be applied in tandem with another drug to have any effect—in this case, the antibiotics carbapenem and cephalosporin. The researchers checked a couple of different ways that it could be working, and found that it was making bacterial membranes easier for the drug to get through, but not enough to account for all of its surprising strength: it lowered by 16 times the amount of antibiotic required to knock the bacteria on their behinds. That’s handy, because taking massive amounts of antibiotics—enough to overwhelm the defenses of resistant bacteria—can be hazardous to your health, and if adding in this adjuvant tips the scales so that safe amounts can knock out infections, that’s pretty neat.
As an antibiotic sidekick, it’s definitely still on the mysterious side. But the team writes that they are looking further into its mechanism, so stay tuned.
Image courtesy of Muriel Gottrop / Wikimedia Commons
Takin’ one for the team.
What’s the News: Clearly, as anyone suffering through a cold right now can tell you, our immune systems aren’t all they could be when it comes to keeping us disease-free. And what’s worse, the same viruses that have some people hawking up phlegm for weeks can give their roommates or spouses no more than a brief sniffle, hammering home the fact that the immune system wealth isn’t distributed evenly. Why hasn’t evolution dealt with this problem already and given us all impenetrable defenses?
As it turns out, it’s not just that evolution takes its own sweet time. It’s also that a species benefits from having individuals be immune to some things and vulnerable to others, a new study shows.
Shiga toxin is nasty stuff. If you are infected with a Shiga-producing bacterium, like Shigella dysenteriae or some E. coli strains, there is no clear treatment: if you are given antibiotics, your infected cells will explode, spraying the toxin all over neighboring cells and exacerbating your symptoms. Each year, 150 million people are infected with Shiga-producing bacteria, which cause dysentery and food poisoning, and a million of those die. The lack of effective treatment for such Shiga toxicosis infections is one of the main reasons this year’s outbreak of E. coli poisoning in Europe was so deadly, with more than 3,700 people infected and 45 dead. But now scientists studying how the toxin makes its way around the cell have discovered that treating mice with the metal element manganese makes them resistant to Shiga poisoning. Since manganese’s chemistry is already well understood and it’s readily available, the possibility of using it as a treatment is exciting.
Here’s how manganese blocks Shiga’s spread, according to the group’s experiments in cultured human cells:
For the better part of a century, antibiotics have given doctors great powers to cure all sorts of bacterial infections. But due to bacteria’s nasty habit of evolving, along with widespread overuse of these drugs, disease-causing bacteria are evolving antibiotic resistance at an alarming rate, making it much harder, and at times impossible, to wipe them out. DARPA, the military’s research agency, is eyeing an innovative solution to the problem: Rather than struggling to make better antibiotics, ditch them altogether. It may be time to start killing bacteria a whole new way.