As far as the prescription pad is concerned, antibiotics are by and large the first and only line of defense against bacterial infections.

"They are more effective once an infection has started," Barbara Murray, director of the division of infectious diseases at the University of Texas Medical School in Houston, told BioWorld Today. Antibiotics "can pretty much stop bacterial growth immediately," while antibodies take extra time.

But, she added, "some studies suggest that antibodies can help or augment the immune response" when given in combination with antibiotics, particularly when the goal is prophylaxis. And with multidrug resistance an ever increasing problem - more than 20 percent of enterococci now are vancomycin-resistant - chemical antibiotics will need all the help they can get.

In the October 2006 issue of the Journal of Clinical Investigation, senior author Murray and her colleagues at Texas A&M, also in Houston, and the University of Minnesota Medical School in Minneapolis, reported on a potential target of prophylactic antibodies for the bacterium Enterococcus faecalis.

Like Escherichia coli, Enterococcus faecalis is a generally good-natured gut bacterium that goes bad when it goes astray - though there won't be any recalls of E. faecalis-tainted spinach: Unlike E. coli, which can be dangerous when ingested, E. faecalis does its damage when it gets into the bloodstream and lodges on the heart valves, where it can cause endocarditis.

Prophylactic treatment against endocarditis is recommended for some types of surgeries, and such prophylaxis is where antibodies can shine. "Antibodies are great for preventive things," Murray said.

In previous work, Murray and her colleagues found that patients infected with E. faecalis made antibodies to a number of bacterial proteins that are involved in anchoring the bacteria to each other, as well as other surfaces, enabling them to form so-called biofilms.

When bacteria band together in biofilms, they become the bane of antibiotics; banded together they are much more difficult to treat than individually. Murray said that while antibiotics can penetrate the biofilm, somehow the bacteria undergo a change in metabolic state when they are part of a biofilm that makes them less susceptible to antibiotics. Preventing biofilms from forming is thus an attractive strategy for fighting the often chronic infections they cause.

In the paper, the scientists focused on four of those proteins. Three were chosen because patients with endocarditis have a strong antibody response to them; the fourth was added because initial genetic analysis showed that it is located next to the other three and transcribed off of the same promoter.

Murray and her colleagues first puzzled over each protein individually, with little success. "We predicted they would stick to collagen and fibrinogen, but they didn't," she said. "So we were a bit perplexed."

The solution to the puzzle came when Murray and her group noticed that the proteins had some similarities to pili - fibers that some bacteria use to cling to host surfaces - and began to investigate them as a group, rather than individually. It wasn't the individual proteins, but "how they assembled" that was the problem, Murray explained.

The scientists found that the four proteins were part of a single operon; that is, they are transcribed off a single promoter and separated later in processing. The fourth of the proteins, sortase C (which has its own promoter in addition to being co-transcribed), assembles the first three, which the scientists renamed ebp A through C (for endocarditis and biofilm-associated pili), into a pilus-like structure that helps the bacteria form a biofilm.

The investigators created different mutant bacterial strains lacking a functional copy of one of the four proteins. In each case, lack of a protein led to reduced attachment of the bacteria to host surfaces, which is the first stage of biofilm formation.

Murray and her colleagues plan animal studies to test whether immunizing against the pili can help prevent them from developing endocarditis; such protection recently has been demonstrated for another bacterium, streptococcus.