[6] It is the main suspect as the cause of scarlet fever, an infectious disease that affects small children.

In addition, none of the colonies containing the T12 genome was negative for speA, and therefore, the conclusion was drawn that all lysogens produced the toxin.

[10] However, McKane and Ferretti reported in 1981 that a spontaneous mutant of phage T12 induced speA production virulently.

[9] The very next year, Johnson and Schlievert and Weeks and Ferreti also found, independently, that the bacteriophage T12 carries the structural gene for speA.

[8][12] In 1986, Johnson, Tomai and Schlievert mapped the attachment site (attP) for T12 adjacent to the speA gene, and established that all bacterial strains producing the toxin carry either phage T12 itself, or a closely related bacteriophage.

[5] And finally, in 1997, McShan and Ferretti published that they had found the second attachment site (attR) for T12, while also revealing in another publication, which was also credited to Tang, that bacteriophage T12 inserts into a gene that encodes a serine tRNA in the host.

The bacteriophage T12 integrates into S. pyogenes chromosome by site-specific recombination into the anticodon loop of a gene that codes for serine tRNA.

The bacterial attachment site (attB) has a 96 base pair sequence homologous to the phage attachment site and is located at the 3’ end of the tRNA gene such that the coding sequence of the tRNA gene remains intact after integration of the prophage.

These cytokines(TNFα, TNFβ) seem to mediate the fever, shock and organ failure characteristic of the disease.

[13][17][18] Strep TSS is an acute, febrile illness that begins with a mild viral-like syndrome characterized by fever, chills, myalgia, diarrhea, vomiting and nausea and involves minor soft-tissue infection that may progress to shock, multi-organ failure, and death.

If the phage is present, indicator strains will become infected and go through the normal lysogenic cycle while the plates incubate, and then undergo lysis.

This was done in research by Johnson, Tomai and Schlievert in 1985 by isolating the DNA of Streptococcal strains and running a restriction digest using BglII.

UV light stresses lysogenic bacteria, leading the phages to propagate and burst the host bacterial cells.