Max Delbruck, Emory Ellis, and Salvador Luria asserted that the plaque-forming unit (PFU) is a spot where a single bacterium has been infected by at least one phage. The phages liberated by the infected bacteria create a halo around the host producing the plaque. They used Poisson distribution to corroborate their assertion.
Before them, Felix d'Herelle demonstrated that the PFUs are proportional to the number of phages rather than bacteria, indicating that the plaques are related to the former.
Yet, Jules Bordet continued to claim that the PFUs were due to the bacteria: when plating the bacteria, some will undergo spontaneous lysis. Once activated, the lytic factor will diffuse around (just like the phages in the model above), generating a plaque.
This model completely disregards d'Herelle's proof and seems to apply to lysogeny. In theory, it should be easy to assess that if one started with bacteria only, it is possible to recover phages after the induction has occurred.
It is more complicated to demonstrate, once and for all, that lytic phages cause the plaques and not the bacteria. In fact, let us assume that we add phages to a bacterial population and that only those bacteria that are metabolically (to use Bordet's words) predisposed to lysis will actually lyse, resulting in a plaque.
How can one discriminate this case from the one given by d'Herelle and followers that the plaque is due to one or more phages infecting a host?
What has been the historical demonstration of this model?
How was Bordet's model dismissed once and for all?
Thank you
I can't really answer your question about who demonstrated it first, but I would like to add that it is actually complicated to demonstrate lysogen and not so easy. If you recover phages from an uninduced lysogen, they will not form plaques on that strain. You can only observe plaques if you have a different strain that is itself not a lysogen.
To further complicate things, if you have a lysogen and a nonlysogen strain they need to be very similar and share the same restriction modification system in order to see plaques, otherwise the phage will be restricted. So for example seeing lambda plaques from E. coli K12 strains can be observed on a few other E. coli strains but on many strains it is restricted so you would never really see them. So you can see lambda plaques on E. coli C but not on E. coli B. And at the time there were no non-lysogenic K12 strains because they did not know K12 was a lysogen.
This is why the early literature on lysogens is often very confusing. In hind sight it all makes sense but at the time there were many different complications that were not understood or appreciated.
I am not really sure of the problem: you can make a dilution series of a (lytic) phage suspension as well as recently infected cells - cell washing and the use of chloroform to kill cells, etc, will allow you to prepare these without the complexity of phage with infected cells, and infected cells with page. When you plate these out onto a sensitive host, there should be a direct correspondence between the number of phage / infected cells and the number of plaques.
You can also determine the number of progeny released by each infected cell (the burst size) which will give an idea of how many viable phage initiate the development of a plague on a plate - though the relative density and growth rate of the host cells and the diffusivity of the phage are also important factors to remember.
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