1860s
THE ENGLISH SURGEON JOSEPH LISTER, influenced by Louis Pasteur’s work on infectious agents, uses carbolic acid directly on wounds and surgical dressings, preventing most post-operative infections.

 

 

1881
STAPHYLOCOCCUS IS IDENTIFIED AS A CAUSE of wound infection by the Scottish surgeon Sir Alexander Ogston, who named it for the grape-like clusters (in Greek, staphyle) he observed under the microscope.

 

 

1884
STAPHYLOCOCCUS AUREUS IS ISOLATED BY German scientist Anton Rosenbach, who grows the two strains, S. aureus (“golden staph,” for the golden colonies it grows on bacterial media) and S. albus (white colonies), in pure culture.

 

 

1930s
A “COAGULASE” TEST ENABLES SCIENTISTS TO detect a plasma-coagulating enzyme secreted by S. aureus, still the most common cause of wound infections in hospitals. Coagulase-positive staph is the most virulent strain.

 

 

1941
THE MORTALITY RATE OF S. AUREUS bacteremia is reported as 81% in a Boston hospital. The same year, a British policeman seriously ill with S. aureus is cured by penicillin.

 

 

1940s
WIDESPREAD USE OF BENZYLPENICILLIN cures many staph infections. But having a “cure” leads to lapses in antiseptic and aseptic protocols. By the late 1940s, penicillin-resistant staph outbreaks begin to occur.

 

 

1959
WHEN PENICILLIN PROVES NO LONGER able to control staph infections, a new drug, methicillin, is developed. Introduced in Europe, it has a short-lived usefulness as the bacterium evolves to resist it.

 

 

1961
ETHICILLIN-RESISTANT S. AUREUS, NOW known as MRSA, is detected in a British hospital; during the next 10 years, multidrug-resistant staph becomes widespread in Europe, Australia and the United States.

 

 

1970s
DENMARK, THE NETHERLANDS, AND OTHER European countries establish stringent infection-control regulations; MRSA rates begin to drop there while holding steady or climbing in the United States and Britain.