Strain-based immunity?

Strain-based immunity?

This news article highlights results from a study exploring whether people exposed to a particular strain of Lyme disease are immune to that strain for any length of time. The news article gives a nice layman’s summary of the research article. The main result is that it seems statistically more likely that the participants were immune to the strain they were re-infected with for some time, since the strains present in their subsequent infections tended to be different than the strain present in their initial infection. The participants in this study only included people who had multiple culture-confirmed erythema migrans rashes. Blood and skin were cultured to identify Bb strains could be extracted. In addition, the participants were treated ‘with standard courses of antibiotics’ after each rash (I read this as ~3 weeks oral doxy), at which point the rash resolved. Participants had evidence of disseminated infection before treatment, meaning the results cannot be attributed to only involving people who were just infected and quickly and decisively treated. Most participants were infected at least a year after their initial infection. 

There is no arguing with the fact that participants in the study had been infected with multiple strains, likely at different times. However, the authors do not address the question of whether the original strain could still be present and even symptom causing, just not implicated in the rash. The authors do state that ‘our findings do not support the hypothesis that relapses in antibiotic-treated patients would be more likely to be culture-negative’ and then go on to say that 63% of participants had a culture positive second episode. However, since the inclusion criteria for the study was to have a rash, which indicates some sort of presence of Bb on the skin, it is not surprising to me that culturing was relatively successful (I do not have a reference handy to back up the idea that rashes would be easier to culture, does anyone know of one?). In addition, if rashes are associated with early stage infection the inclusion criteria may even have biased the study toward people who are likely to have been re-infected. So one possible explanation for the results is that people developed immunity. But I think another possible explanation is that when people were re-infected with new strains, they developed new erythema migrans rashes. However, when people are re-infected with or relapsing from strains with which they were previously infected, they are harder to culture and their symptoms express in other ways. The authors do not address this possibility in their article.

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