Introduction

 

The number of non-human cells in and on the human body exceeds that of human cells.  How is this possible?  When a person dies, bacteria quickly cause decay and putrefaction. How does the body prevent bacterial overgrowth during life?  The answer is the human body makes an antibiotic to control bacterial protein synthesis.  I know what it is, and how to make it.  A short history of antibiotics may be helpful.

Antibiotics, as a class of medicinal compounds, were first discovered by Paul Ehrlich and Sakahiro Hata in 1910.  They synthesized the compound Arsphenamine to treat syphilis.

In 1928, Sir Alexander Fleming discovered a compound he named Penicillin. The compound was secreted by the Penicillium fungus and inhibited bacterial wall protein synthesis. Other drugs were later added to the list of fungal-derived products with antibiotic properties.

During and after 1943, Albert Schotz and Selman Waksmain isolated the antibiotic Streptomycin from the soil bacteria genus Streptomyces. Further research on other members of this genus resulted in the discovery of additional antibiotics.

Most bacterial products successful in humans target bacterial protein synthesis. This is because the protein synthetic apparatus of bacteria differs from that of humans. While both bacterial and human ribosomes are involved in protein synthesis, they differ in their size, composition, and structure. This allows for the development of antibiotics that specifically target bacterial ribosomes without affecting human cells.

 While many bacterial products have antibiotic properties, only a select few are appropriate for human use. The pharmaceutical industry generally demands a Therapeutic Index of 10 or more before exploring a new drug.  My drug, which inhibits MRSA while sparing yeast mitochondria, has a T.I. of 15.

Another facet contributing to the success of an antibiotic is the lack of mutagenicity.  If the compound works by causing mutations in bacterial DNA it will lead to cell death.  This will put pressure on the genome, forcing bacteria to evolve away from the inhibitor, leading to the antibiotic resistance now seen around the world.  The effectiveness of a human antibiotic cannot be attributed to a mutational mechanism, as evidenced by the existence of over 7 billion humans.  The human antibiotic must leave bacterial protein synthesis in stasis without causing bacterial death.  Simultaneously, it must not inhibit human protein synthesis or cause human cell death.  My compound exhibits all of these characteristics at appropriate doses.