This year’s Longitude Prize is focused on the growing problem of antibiotic resistant bacteria. They’ve put together a nice image, shown here, which showcases what they term ‘the ten most dangerous antibiotic resistant bacteria’. You can read more detail on each of them here:

The prize offers a £10 million prize fund for the development of a cheap, accurate, and easy to use bacterial infection test kit, which will allow doctors to prescribe the correct antibiotics at the correct time for patients, to try to help minimise the development of antibiotic resistance.


Also, REMEMBER!!!!

* Sulfonamides compete for albumin with:

  • Bilirrubin: given in 2°,3°T, high risk or indirect hyperBb and kernicterus in premies
  • Warfarin: increases toxicity: bleeding

Beta-lactamase (penicinillase) Suceptible:

  • Natural Penicillins (G, V, F, K)
  • Aminopenicillins (Amoxicillin, Ampicillin)
  • Antipseudomonal Penicillins (Ticarcillin, Piperacillin)

Beta-lactamase (penicinillase) Resistant:

  • Oxacillin, Nafcillin, Dicloxacillin
  • 3°G, 4°G Cephalosporins
  • Carbapenems 
  • Monobactams
  • Beta-lactamase inhibitors

* Penicillins enhanced with:

  • Clavulanic acid & Sulbactam (both are suicide inhibitors, they inhibit beta-lactamase)
  • Aminoglycosides (against enterococcus and psedomonas)

Aminoglycosides enhanced with Aztreonam

* Penicillins: renal clearance EXCEPT Oxacillin & Nafcillin (bile)

* Cephalosporines: renal clearance EXCEPT Cefoperazone & Cefrtriaxone (bile)

* Both inhibited by Probenecid during tubular secretion.

* 2°G Cephalosporines: none cross BBB except Cefuroxime

* 3°G Cephalosporines: all cross BBB except Cefoperazone bc is highly highly lipid soluble, so is protein bound in plasma, therefore it doesn’t cross BBB.

* Cephalosporines are ”LAME" bc they  do not cover this organisms 

  • L  isteria monocytogenes
  • A  typicals (Mycoplasma, Chlamydia)
  • RSA (except Ceftaroline, 5°G)
  •  nterococci

* Disulfiram-like effect: Cefotetan Cefoperazone (mnemonic)

* Cefoperanzone: all the exceptions!!!

  • All 3°G cephalosporins cross the BBB except Cefoperazone.
  • All cephalosporins are renal cleared, except Cefoperazone.
  • Disulfiram-like effect

* Against Pseudomonas:

  • 3°G Cef taz idime (taz taz taz taz)
  • 4°G Cefepime, Cefpirome (not available in the USA)
  • Antipseudomonal penicillins
  • Aminoglycosides (synergy with beta-lactams)
  • Aztreonam (pseudomonal sepsis)

* Covers MRSA: Ceftaroline (rhymes w/ Caroline, Caroline the 5°G Ceph), Vancomycin, Daptomycin, Linezolid, Tigecycline.

Covers VRSA: Linezolid, Dalfopristin/Quinupristin

* Aminoglycosides: decrease release of ACh in synapse and act as a Neuromuscular blocker, this is why it enhances effects of muscle relaxants.

* DEMECLOCYCLINE: tetracycline that’s not used as an AB, it is used as tx of SIADH to cause Nephrogenic Diabetes Insipidus (inhibits the V2 receptor in collecting ducts)

* Phototoxicity: Q ue S T  ion?

  • uinolones
  • Sulfonamides
  • T etracyclines

* p450 inhibitors: Cloramphenicol, Macrolides (except Azithromycin), Sulfonamides

* Macrolides SE: Motilin stimulation, QT prolongation, reversible deafness, eosinophilia, cholestatic hepatitis

Bactericidal: beta-lactams (penicillins, cephalosporins, monobactams, carbapenems), aminoglycosides, fluorquinolones, metronidazole.

* Baceriostatic: tetracyclins, streptogramins, chloramphenicol, lincosamides, oxazolidonones, macrolides, sulfonamides, DHFR inhibitors.

Pseudomembranous colitis: Ampicillin, Amoxicillin, Clindamycin, Lincomycin.

QT prolongation: macrolides, sometimes fluoroquinolones

First new antibiotic in 30 years discovered in major breakthrough

The first new antibiotic to be discovered in nearly 30 years has been hailed as a ‘paradigm shift’ in the fight against the growing resistance to drugs.

Teixobactin has been found to treat many common bacterial infections such as tuberculosis, septicaemia and C. diff, and could be available within five years.

But more importantly it could pave the way for a new generation of antibiotics because of the way it was discovered.

Scientists have always believed that the soil was teeming with new and potent antibiotics because bacteria have developed novel ways to fight off other microbes.

But 99 per cent of microbes will not grow in laboratory conditions leaving researchers frustrated that they could not get to the life-saving natural drugs.

Now a team from Northeastern University in Boston, Massachusetts, have discovered a way of using an electronic chip to grow the microbes in the soil and then isolate their antibiotic chemical compounds.

They discovered that one compound, Teixobactin, is highly effective against common bacterial infections Clostridium difficile, Mycobacterium tuberculous and Staphylococcus aureus.

Professor Kim Lewis, Director of the Antimicrobial Discovery Centre said: “Apart from the immediate implementation, there is also I think a paradigm shift in our minds because we have been operating on the basis that resistance development is inevitable and that we have to focus on introducing drugs faster than resistance

“Teixobactin shows how we can adopt an alternative strategy and develop compounds to which bacteria are not resistant.”


We Kill Germs at Our Peril (NY Times Review)

You never get something for nothing, especially not in health care. Every test, every incision, every little pill brings benefits and risks.

Nowhere is that balance tilting more ominously in the wrong direction than in the once halcyon realm of infectious diseases, that big success story of the 20th century. We have had antibiotics since the mid-1940s — just about as long as we have had the atomic bomb, as Dr. Martin J. Blaser points out — and our big mistake was failing long ago to appreciate the parallels between the two.


Antibiotic hunters

Bacteria known as Streptomyces (see images above) are the source of the majority of important antibiotics used in medicine today. These drugs have revolutionised the treatment of infectious disease since their introduction into clinical practice in the 1940s.

Recently, the World Health Organisation has warned of a “post-antibiotic era”, where people could die from simple infections that have been treatable for decades. This is because some disease-causing bacteria have evolved to become resistant to most currently used antibiotics, for example MRSA.

BBSRC investment in Streptomyces research since the 1960s has had a huge impact on our understanding and development of antibiotics, and scientists at the BBSRC-funded John Innes Centre are among those now using this knowledge to help discover and develop the new antibiotics needed to counter the threat of antibiotic resistance.

If you want to find out more about this area of research make sure you get yourself along to the Great British Bioscience Festival exhibit showing at the Science in Norwich Day on the 1 of June.

Read more:

Top image and middle image copyright: David Hopwood and Andrew Davis

Bottom image of copyright:Tobias Kieser


This GIF shows the scary rise in antibiotic resistance.   

We’ve been popping Z-Paks like sugar pills, and now we’re paying the price: bacteria are the hunters, we are the hunted. Bacteria evolve just like we do, and overprescribing antibiotics (especially for minor bugs like the seasonal flu) can make them less effective. Recently, there’s been a huge rise in antibiotic resistance, and unless we take some serious steps to change the way we use antibiotics, we could have a serious problem.

Learn how we can prevent the coming antibiotic crisis»

Fatal Superbugs: Antibiotics Losing Effectiveness, WHO Says

"Genetics is working against us, almost like a science-fiction story.

Susan Brink

for National Geographic


The spread of superbugs—bacteria that have changed in ways that render antibiotics ineffective against them—is a serious and growing threat around the world, according to the World Health Organization’s first global report on antibiotic resistance.

Once-common treatments for everyday intestinal and urinary tract infections, for pneumonia, for infections in newborns, and for diseases like gonorrhea are no longer working in many people.

The new report on the global threat adds to a Centers for Disease Control and Prevention report last year showing that two million people in the United States are infected annually with antibiotic-resistant bacteria, and 23,000 of them die each year as a result.

To understand the dangers posed by superbugs, National Geographic spoke with Stuart Levy, chair of the board of the Alliance for the Prudent Use of Antibiotics at Tufts University School of Medicine in Boston.

What exactly are superbugs?

They are bacteria resistant to one or more antibiotics, and they make it difficult to treat or cure infections that once were easily treated. The antibiotic has lost its ability to control or kill bacterial growth. The bacteria can grow even in a sea of antibiotics because the antibiotic doesn’t touch them.

How are the bacteria able to circumvent the power of antibiotics?

The bacteria have acquired the ability to destroy the antibiotic in order to protect themselves. They’ve developed a gene for resistance to, say, penicillin, and that gene protects them. A genetic mutation might enable a bacteria to produce enzymes that inactivate antibiotics. Or [a mutation] might eliminate the target that the antibiotic is supposed to attack.

A bacteria may have developed resistance to five or six antibiotics, so in treatment, you don’t know which one to choose. And the bacteria accumulate resistance by developing new genes. Genetics is working against us, almost like a science-fiction story.

Why are these superbugs spreading and the threat growing?

We’re continuing to use antibiotics in a bad way. They’re supposed to be used to combat bacteria, not viruses. The common cold is a virus. Any time you use an antibiotic when it’s not needed, you’re pushing antibiotic resistance ahead. People are misusing them in their homes. They may have a stockpile they’ve saved, and think taking [an antibiotic] will help them with a cold. They’re not helping their cold, and they’re propagating resistance.

What about other uses, such as using antibiotics in animal feed by the meat industry?

This is a big issue. About 80 percent of antibiotics manufactured are given to beef cattle, chickens, and hogs to help them grow better and put on more weight. They excrete them, and the antibiotics largely are not broken down. They enter the environment—the ground and the water—and retain their ability to affect bacteria and promote antibiotic resistance.

The Food and Drug Administration has come out with a voluntary plan for industry to phase out antibiotic use. I’ve been championing this for 30 years.

How can we combat the further growth and spread of superbugs?

By using antibiotics only when we need them. And by eliminating their use in animals. There’s a paucity of new antibiotics to take care of these multiresistant superbugs, so we’re at the mercy of the bacteria.

Are there new antibiotics in development?

The journal Microbe did a report this month on wakening to the need for new antibiotics. There are a number of new antibiotics being studied. They’re not there yet, but at least they’re in the pipeline.

text and photo from Nat Geo

Fungus discovered that wipes out antibiotic-resistant superbugs

If you get sick with an infection, you usually take antibiotics, which (if they do what they’re supposed to do) make you better by killing bacteria. This medical treatment seems simple, but many nasty types of bacterial are growing increasingly resistant to antibiotics. A team of scientists at McMaster University in Canada have found a molecule in some soil-dwelling fungus that is capable of disarming some antibiotic resisting properties, making even stubborn bacterial infections treatable with standard antibiotics.

Antibiotic resistance has been a source of concern for doctors, particularly since we haven’t discovered any new antibiotics since the 1980s. Finding this new molecule, called AMA, in a certain fungus that grows in soil is way easier than trying to create new treatments for superbugs from scratch. The superbugs in question contain New Delhi Metallo-beta-Lactamase-1, or NDM-1, and are considered a global threat by the World Health Organization. AMA effectively wipes out NDM-1, which then allows antibiotics to do their work.

In their experiments, the researchers combined the NDM-1 gene with harmless E. coli bacteria, and then infected mice with this engineered superbug. One group of mice were given both AMA and an antibiotic, the second group were given just AMA, and the third were given just an antibiotic. Of the three groups, only the mice receiving the AMA plus the antibiotic survived.

The implications for this research are that we may soon have a new weapon in our fight against one of the most challenging health care problems of this decade. Antibiotic-resistant superbugs are spreading rapidly across the globe, killing indiscriminately, and we need to stop them before it’s too late. Or as soon as we get around to it, anyway.

Via McMaster University

There are several aspects to the problem of antibiotic resistance. It’s very important to have highly specific targets, which kill the particular bacterium that’s causing the disease rather than using a spectrum of antibiotics that should only be used as a last resort when you don’t know what the disease is caused by and you don’t have time.
But there’s a larger problem—the problem of resistance is also due to an abuse of antibiotics.
Many people will go to a doctor and demand an antibiotic when they have a cold or a flu, for which these antibacterial compounds are useless. In many countries it is possible to buy antibiotics over the counter. Often, if people are poor, they will not take the full dose. In addition to also prescribing antibiotics for the flu the West uses antibiotics in feed to fatten up the cattle. That’s an abuse of antibiotics. This leads to the spread of resistant strains, rendering current antibiotics useless if resistance spreads too much.
In countries like India people will give you antibiotics prophylactically, as a way to prevent infection. This should only be done in very extreme cases because it’s again spreading resistance.
People now move all over the world, so if resistance emerges in one place it can very quickly spread to other places. So it needs a concerted attack… It is a broad social problem.