\section{Passage 1}"Pathogens are acquiring resistance faster than we can introduce new antibiotics, and this is causing a human health crisis," says biochemist Kim Lewis of  Northeastern University.Lewis is part of a team that recently unveiled a promising antibiotic, born from a new way to tap the powers of soil microorganisms. In animal tests, teixobactin proved effective at killing off a wide variety of disease-causing bacteria-even those thathave developed immunity to other drugs. The scientists' best efforts to create mutant bacteria with resistance to the drug failed, meaning teixobactin could function effectively for decades before pathogens naturally evolve resistance to it.Natural microbial substances from soil bacteria and fungi have been at the root of most antibiotic drug development during the past century. But only about one percent of these organisms can be grown in a lab. The rest, in staggering numbers, haveremained uncultured and of limited use to medical science, until now. "Instead of trying to figure out the ideal conditions for each and every one of the millions of organisms out there in the environment, to allow them to grow in the lab, we simply growthem in their natural environment where they already have the conditions they need for growth," Lewis says.To do this, the team designed a gadget that sandwiches a soil sample between two membranes,each perforated with pores that allow molecules like nutrients to diffuse through but don't allow the passage of cells. "We just use it to trick the bacteria into thinking that they are in their natural environment," Lewis says.The team isolated 10,000 strains of uncultured soil bacteria and prepared extracts from them that could be tested against nasty pathogenic bacteria.Teixobactin emerged as the most promising drug.Mice infected with bacteria that cause upper  respiratory tract infections (including Staphylococcus aureus and Streptococcus pneumoniae) were treated with teixobactin, and the drug knocked out the infections with no noticeable toxic effects.It's likely that teixobactin is effective because of  the way it targets disease: The drug breaks down bacterial cell walls by attacking the lipid molecules that the cell creates organically. Many other antibiotics target the bacteria's proteins, and the genes that encode those proteins can mutate to 50 produce different structures.\section{Passage 2}Many good antibiotic families-penicillin, streptomycin, tetracycline-come from soil fungi and bacteria and it has long been suspected that, if we could grow more types of bacteria from soil-or55 from exotic environments, such as deep oceans-then we might find new natural antibiotics. In a recent study, researchers [Kim Lewis and others] found that they could isolate and grow individual soil bacteria-including types that can't normally be60 grown in the laboratory-in soil itself, which supplied critical nutrients and minerals. Once the bacteria reached a critical mass they could be transferred to the lab and their cultivation continued. This simple and elegant methodology is their most 65 important finding to my mind, for it opens a gateway to cultivating a wealth of potentially antibioticproducing bacteria that have never been grown before.The first new antibiotic that they've found by this 70 approach, teixobactin, from a bacterium called Eleftheria terrae, is less exciting to my mind, though it doesn't look bad. Teixobactin killed Gram-positive bacteria, such as S. aureus, in the laboratory, and cured experimental infection in mice. It also killed 75 the tuberculosis bacterium, which is important because there is a real problem with resistant tuberculosis in the developing world. It was also difficult to select teixobactin resistance.So, what are my caveats? Well, I see three. First, 80 teixobactin isn't a potential panacea. It doesn't kill the Gram-negative opportunists as it is too big to cross their complex cell wall. Secondly, scaling to commercial manufacture will be challenging, since the bacteria making the antibiotic are so difficult to85 grow. And, thirdly, it's early days yet. As with any antibiotic, teixobactin now faces the long haul of clinical trials: Phase I to see what dose you can safely give the patient, Phase II to see if it cures infections, and Phase III to compare its efficacy to that of 90 "standard of care treatment." That's going to take five years and $\pounds 500$ million and these are numbers we must find ways to reduce (while not compromising safety) if we're to keep ahead of bacteria, which can evolve far more swiftly and cheaply.Q: Information in Passage 2 best supports which conclusion about the mice in the experiment described in Passage 1? Answer Choices: (A)Exposure to teixobactin made them less susceptible to subsequent upper respiratory tract infections. (B)Gram-positive bacteria enhanced the effectiveness of teixobactin against their upper respiratory tract infections. (C)Their upper respiratory tract infections were likely not caused by gram-negative bacteria. (D)Teixobactin attacked the proteins of the bacteria that caused their upper respiratory tract infections.
A: Among A through D, the answer is
(A)Exposure to teixobactin made them less susceptible to subsequent upper respiratory tract infections.
(B)Gram-positive bacteria enhanced the effectiveness of teixobactin against their upper respiratory tract infections.
(C)Their upper respiratory tract infections were likely not caused by gram-negative bacteria.
(D)Teixobactin attacked the proteins of the bacteria that caused their upper respiratory tract infections.
Answer: 2