New plague research has just been published with particular importance for the discussion of the early-phase transmission and transmission by proventricular blockage. B.J. Hinnebusch, Senior Investigator at the Laboratory of Zoonotic Pathogens, NIH, NIAID, Rocky Mountain Laboratories, has long been one of the sharpest critics of the early-phase theory of transmission, see, for instance, his article “Biofilm-Dependent and Bio-Film-Independent Mechanisms of using Transmission of Yersinia pestis by Fleas”, Advances in Experimental Medicine and Biology, 954; 2012: 237‒243. In these days, he publishes with co-authors an evidently crucial article on this topic: Hinnebusch, B.J. Bland, D.M., Bosio, C.F., Jarrett, C.O., “Comparative Ability of Oropsylla montana and Xenopylla cheopis Fleas to transmitt Yersinia pestis by two Different Mechanisms” PLOS Neglected Tropical Diseases | DOI: 10…1371/journal.pntd.0005276 January 12, 2017: 1-15.
They used fleas of Oropsylla montana provided by two of the central advocates of the early-phase theory, which excludes that different strains of this flea could affect the outcome. The conventional vector of plague ‘par excellence’, Xenopsylla cheopis, was used for comparison. Contrary to earlier assertions by the advocates of the early-phase theory that Oropsylla montana rarely develop proventricular blockage, it was shown to block earlier and surviving longer after becoming blocked than X. Cheopis, and that transmission by blockage was as good as or better than observed for X. cheopis. This (re)confirmed earlier research on the vector capacity of this species of flea (see, e.g., the fully referenced comments in my monograph The Black Death and Later Plague Epidemic in the Scandinavian Countries, 2016: 377, 403, 630, 658).
In this article, the early-phase theory is dismantled as an important or significant means or mechanism of transmission of plague. In a personal communication by email of 01.03.17, Hinnebusch states that “In fact, I think early-phase transmission only has a role in very special circumstances, such as during an epizootic of plague in a dense [rodent] population that is both highly susceptible (LD50< 10) and that routinely develops very high bacteremia levels (>108 to 109 Y. pestis/ml) before death. High flea density is also a likely precondition, as intermittent challenges from just a few fleas at a time would frequently lead to resistance rather than productive, transmissible disease (bacteremia).”
This also means that early-phase transmission is of no significance in plague epidemics, except perhaps, at the individual level, the occasional transmission of immunity-inducing tiny doses of plague bacteria (that will be easily dealt with by the human immune apparatus). It will also become clear that Hinnebusch et al. corroborate and deepen earlier plague research: it is pointed out that this type of early-phase transmission was identified by the Indian Plague Research Commission (IPRC) in 1907 and that the pioneering studies of Bacot of the IPRC on blockage in fleas IPRC 1914 and 1915, are still tenable and relevant. The bibliography contains studies from the entire 1900s, not least 1940s, which have kept their value as fine research.
Finally, I will point out that my recently published monograph contains a long study of early-phase transmission in Chapter 12: 625-655 (with bibliographic references included in the General Bibliography). Its conclusions and basic analysis agree with this recent study by Hinnebusch et al.
Ole J. Benedictow,