When injected, the mice contracted pneumonia and later died. He then injected mice with the nonpathogenic rough strain. The mice, as predicted, did not get sick at all. This first experiment led Griffith to first believe in the possibility that the polysaccharide coating on the smooth strain was the cause of the strain’s pathogenic nature. To test this hypothesis, he used heat to kill the smooth strain and injected it into mice. Since polysaccharides are not affected by heat, his hypothesis determined that heating the strain should not affect its nature. However, after he heated the strain and injected mice with it, he noticed that the strain had died and had lost its virulence and pathogenic nature. This proved that the polysaccharide coating on the smooth strain was not the cause of the mice contracting pneumonia. From the results of this experiment, Griffith next hypothesized that the disease was caused by some protein, which would have been denatured by the heat. He then injected the mice with a mixture of both the dead smooth strain and the live rough strain. Oddly, the mice died. When Griffith performed a necropsy, he noted the presence of live smooth
When injected, the mice contracted pneumonia and later died. He then injected mice with the nonpathogenic rough strain. The mice, as predicted, did not get sick at all. This first experiment led Griffith to first believe in the possibility that the polysaccharide coating on the smooth strain was the cause of the strain’s pathogenic nature. To test this hypothesis, he used heat to kill the smooth strain and injected it into mice. Since polysaccharides are not affected by heat, his hypothesis determined that heating the strain should not affect its nature. However, after he heated the strain and injected mice with it, he noticed that the strain had died and had lost its virulence and pathogenic nature. This proved that the polysaccharide coating on the smooth strain was not the cause of the mice contracting pneumonia. From the results of this experiment, Griffith next hypothesized that the disease was caused by some protein, which would have been denatured by the heat. He then injected the mice with a mixture of both the dead smooth strain and the live rough strain. Oddly, the mice died. When Griffith performed a necropsy, he noted the presence of live smooth