The Scientist recently published a long look at the development of a vaccine for staph infection — a vaccine that as recently as the 1960s was considered impossible to develop by most reputable authorities.
Without going into too much detail about the chemistry of it all, for a variety of reasons researchers in the 1960s concluded that the outer layer of the staph bacteria lacked polysaccharides.
In fact, the staph bacteria do contain polysaccharides. Researcher Walter Karakawa demonstrated this and then went on to develop a vaccine for staph that takes advantage of this. The vaccine has proven relatively successful in initial human tests on people with compromised immune systems, and should prove to be a boon in the routine protection of surgical patients against staph infection (patients are currently given antibiotics, but the staph bacteria has increasingly developed resistances to many antibiotics).
From that discovery Ali Fattom of Nabi Biopharmaceuticals worked to develop a vaccine for staph, which again many researchers said was impossible even if staph did contain polysaccharides. The major factor in Fattom\’s proving that a vaccine would work was his development of an animal model of staph in mice. When Fattom looked back at previous efforts to locate polysaccharides he found that researchers had never created an animal model for the disease. According to The Scientist,
This brush with termination [when his vaccine project was almost cancelled] marked a turning point, for it convinced Fattom that he needed to demonstrate with an animal model that antibodies against polysaccharides protected against infection. This had not been done earlier because the NIH and Univax [who had both done polysaccharide vaccine development] researchers did not develop an animal model. [NIH vaccinologist John] Robbins\’ goal had been to get the vaccine into the clinic quickly and safety, not to research the molecular basis of virulence. So animal model development had been deferred.
. . .
In 1996 Fattom finally developed a mouse model in which a reasonable innoculum caused infection. With this model he was the first to demonstrate that conjugate vaccines protected against lethal injections of Staphylococcus aureus. Knowing he would need corroboration, he then invited Jean C. Lee of Harvard to test his vaccines in her endocarditis model with rats. A year later the results were just as predicted — the vaccines protected Lee\’s rats. Now, at last, skeptics started to come around. Maybe the vaccine would work.
And work it apparently does. A clinical trial of the vaccine in dialysis patients found the vaccine cut the rate of staph infections by 57 percent. The vaccine should perform even better in routine pre-surgical administration since the patients in that clinical trial had characteristics such as diabetes and high uric acid levels that inhibit production of white blood cells.
The vaccine is still undergoing further clinical trials, but barring any unforseen events should reach market within a few years. Not bad for a few people armed just with a hypothesis and some mice.
Source:
Impossible vaccine tames Staphylococcus aureus. Tom Hollon, The Scientist, 16[14]:24, July 8, 2002.
