[paul cotter (OP)]

At the moment there is a flurry of concern about group a streptococcal infection, especially among young children. I seem to remember a suggestion that phage activity modulates pathogenicity in streptococci, similar to the situation with diphtheria where toxin generation requires a particular phage.

[evan_au]

Bacteriophages actively set about destroying their bacterial targets.
- Your microbiome contains many types of bacteria, balanced by many types of phages which reduce the chance that one kind of bacteria will produce a monoculture in your gut.

A prophage differs from a "normal" phage in that it  is a retrovirus held latent within the bacterial DNA (just like HIV hides within the human genome). When triggered, the prophage starts multiplying in the host cell, bursting it open to spread more phage particles.
https://en.wikipedia.org/wiki/Prophage

In Diptheria, the toxin is encoded on the prophage genome. This toxin affects the human host.
https://en.wikipedia.org/wiki/Diphtheria_toxin

Overall, I expect it is more typical that a phage attack would reduce the quantity of a bacterial pathogen (and thus reduce the severity of a bacterial infection). Diptheria appears to be an exception...

[paul cotter (OP)]

I remember now where I heard of possible phage modulation of strep pathogenicity( gettin' old, you know ). It was when there was another scare story, namely that of necrotising fasciitis. Overall there has been an apparent reduction in strep pathogenicity, one rarely hears of post strep glomerulonephritis or rheumatic heart disease. I don't know if this is due to improved living conditions or an inherent reduction in pathogenicity.