By Patrick Yang ’20

The hospital is considered a place of treatment, but hospitalization also runs the risk of bacterial sepsis – an often fatal immune response to bacterial infection. Bacterial sepsis frequents patients who are connected to medical devices like needles and catheters, which can easily launch the bacteria into the bloodstream. That infection, compounded with an already compromised immune system, can prove to be fatal. Despite the efforts of hospitals to maintain a pristine and hygienic environment, bacterial sepsis remains a concern because bacterial species have developed antibiotic resistance. Specifically, the leading cause of sepsis, Staphylococcus epidermidis, is resistant to three commonly used antibiotics: penicillin, amoxicillin, and methicillin. It is widely assumed that the virulence of sepsis bacteria is caused by their extracellular structures, which cause an overreaction when detected by our immune system. However, a recent discovery by Dr. Michael Otto and co-researchers at the National Institute of Health shows that toxins released by bacteria may actually mediate sepsis.

The team investigated the effects of the toxin, psm-mec, by injecting 6-10 week old female mice with four strains of S. epidermidis. Two strains were normal bacteria strains, but the other two were genetically modified through DNA splicing to lack the psm-mec DNA locus. Without the psm-mec DNA locus, the modified strains lacked genetic instructions and could not produce the toxin. Researchers injected the strains into the tail vein and the mice were constant monitored for 120 hours. Within 40 hours, all of the mice that were injected with the normal strains had died. In contrast, mice injected with the strains that could not produce psm-mec survived with a 50%-100% rate after the 120 hours. Bacteria content in the blood (measured in CFU/mL) was also measured after 12 hours. Mice injected with the normal strains had an average of 0.6 x 107 or 1.9 x 104 CFU/mL, depending on the strain, yet mice injected with strains without psm-mec had approximately zero bacteria in their blood. This significant difference in survival rate and bacteria content in the blood reveals psm-mec’s role in S. epidermidis’s survival in the body.

These results are only found in murine models, but the discovery of a potential target to reduce the survival of antibiotic-resistant bacteria is very promising. As a result of this research, future antibiotics may begin targeting the toxins during bacteria sepsis, rather than the bacteria themselves.

References:

1. M. Qin, et al., Toxin mediates sepsis caused by methicillin-resistant staphylococcus epidermidis. Public Library of Science 13, (2017). doi: 10.1371/journal.ppat.1006153.
2. Image retrieved from: https://www.pexels.com/photo/view-of-operating-room-247786/