My original hypothesis for the individually collected throat culture on Blood Agar Plates, that it would show a mixture of alpha, beta, and gamma hemolysis, was based on the results of the class control samples of S. pneumonia, S. aureas and S. epidermis. In these controls S. pneumonia shows alpha and beta hemolysis while S. aureas and S. epidermis showed beta and gamma hemolysis respectively. This hypothesis was based on the thought that the upper airway of most people would have at least a small mixture of all three of these bacteria as well as others.
This hypothesis was supported by research showing that up to sixty percent of healthy people are carriers of S. aureas (Schmidlin et al. 1291), while another study showed that S. epidermis is one of the most commonly found bacterial species on the human body (Otto, 2009, p556). Based on this data, and supported by the control plates, I expected to find all three types of hemolysis on the throat sample collected from a classmate. As expected the throat swab sample did indeed show alpha, beta, and gamma hemolysis which would indicate a mixture of different bacteria in the upper airway.
The second experiment with MSA plates did not turn out as expected. The class control MSA plate for S. pneumonia showed no growth at all and no color change. The lack of growth could be partially explained by the fact that MSA is a selective medium, selecting for staphylococci because of the high salt content, and the lack of color change could be due to the fact that pathogenic species preferentially ferment mannitol and produce acid changing the media color from red to yellow.
Another explanation is the possibility of the class control sample showing no growth or color change could be as simple as it being a bad culture. The MSA plates for S. aureas showed both growth and extreme fermentation while the S. epidermis sample showed growth but no fermentation, with its color change being easily explained by over active S. aureas. These results are supported by studies that would indicate that S. epidermis is generally non-pathogenic, maintaining a benign relationship with its host (Otto, 2009, p556). The MSA plate from the nose swab did show the expected results.
I expected the MSA plates to show mixed results similar to the Blood Agar plates, due to a combination of expected bacterial species, so growth and color change was expected if based only on the colonization of S. aureas explained in the previous study. The nose swab MSA plate did indeed show growth, but did not change color from red to yellow. Instead, the nose swab sample turned the MSA plate from red to pink. This may be explained by the bacterial sample making the plate more basic instead of producing an acid while the growth would indicate a nonpathogenic staphylococci colony, which would rule out the S. ureas found in the throat culture.
The results of both experiments would seem to support previous studies which indicate that a level of colonization by certain pathogenic species of bacteria is normal. This could also explain the prevalence of opportunistic infections found in persons with immune deficiencies. How can we maintain the normal level of enteric bacteria, while at the same time avoiding the dangers of an opportunistic infection? What are the benefits provided by this normal flora, and what are the risks of such co-habitants? These questions are and will be the subject of continuous tests and experiments for years to come.
Courtney from Study Moose
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