Between Scylla and Charybdis: how helminth control in wild animals affects their susceptibility to pathogenic microbes

When I read scientific articles I focus on how results fit into their conclusions. Especially I am very skeptical to research data or their interpretation which become headlines news all over the web.

In my opinion, when one writes about science news it would help if before publishing anything on open forum to read and analyse it in order to understand what novelty research brings and/or its limitation.

As an example, lets analyse research article recently published in journal Science. In this study, the authors has treated free roaming wild African buffalos with anti-helminth drugs to reduce acquisition or shedding of worms (reduce TH2 immunity) and increase their TH1 immunity to pathogenic microbe, mycobacterium bovis, a bovine tuberculosis (a deadly disease in buffalos).

All buffalos (total of 216), both in control (108) or treated (108) groups were mycobacterium bovis-free at the beginning of experiment. The authors claim that while anti-helminth treated group shed fewer worms or worm eggs during the course of observation, there was no much different in infection with mycobacterium bovis between treated (33 out of 100 = 33%) or control (36 out of 101 = 36%) groups. However the graph itself shows that by the end of observation period (~4 years), ~80% of analysed buffalos in control group acquired mycobacterium bovis infection compared to ~45% in treated group.

Next, the authors showed that anti-helminth treatment had a major impact on survival of infected buffalos: while ~36% of mycobacterium bovis-infected buffalos died in control group, mortality rate of mycobacterium bovis-infected buffalos in treated group was ~7%.

Using mathematical model for disease transmission, the authors estimated that due to increase in survival of mycobacterium bovis-infected buffalos, mycobacterium bovis would spread more in buffalo population.   

In summary, the authors claim that anti-helminth treatment reduces the mortality from mycobacterium bovis in buffalos, but at the same time has no effect on rate of acquisition of mycobacterium bovis infection (???), but rather it increases spread of mycobacterium bovis in buffalo population. 

Here is what do not understand: (1) aren't the rate of acquisition of infection and its spread the same? How can be one different from another? (2) Fig. 2b shows that control buffalos were infected in higher rates compared to treated buffalos. What about that?

David Usharauli