For the last decade or so, bacteria that are immune to the effects of antibiotics have been a persistent and growing threat in medicine. Ultimately, the problem goes back to the antibiotic not being administered long enough to kill off the entire colony. The few survivors that managed to make it through the increasing toxicity of their environment because they either had a gene which rendered them immune (and the toxins released when the other bacteria died weren't enough to poison them) or assembled one and survived long enough to breed and pass the gene along to other bacteria. This means that the pharmaceutical industry has been scrambling to find new antibiotics that won't harm the patient any more than they absolutely have to... except that now we're seeing antibiotic resistant yeasts in the wild, also. A strain of the yeast candida auris was discovered in 2009.ev in Japan that is resistent to every commonly used drug used to treat fungal infections, including caspofungin, amphotericin B, and fluconazole. Since that time, the dangerous strain of c.auris has spread to the United States, India, South Africa, Pakistan, Kuwait, South Korea, Colombia, the UK, and Venezuela. The fungus is known to invade the body through open wounds in an opportunistic fashion and take up residence in the bloodstream, where it subsequently causes organ failure. It is also known to infect the lungs to some degree, as evidenced by having been extracted and cultured from same. The US Center for Disease Control published a bulletin on 24 June 2016 describes the outbreak in more detail, including the risk factors for contracting the infection (diabetes, recent surgery and antibiotic use (both of which impact the integrity of the body overall), and the presence of large venous catheters). Unfortunately, c.auris is difficult to differentiate from several other less-critical fungal species without extensive testing so it can be misdiagnosed until it is too late; the CDC advises the use of MALDI-TOF mass spectrometry or DNA sequencing (analyzing the D1-D2 region of the 28s rDNA) to confirm infection.