Links, news, and paper highlights: January 2016

I’m trying to do a better job of keeping up with parasite ecology and epidemiology related news this year. Here’s some recent work that might be of interest:

Links:

Tasmanian devils have TWO types of infectious cancer!

Romans were wormy, despite relatively good hygienic practices.

The West African Ebola outbreak is over.

It looks like the mosquito-borne Zika virus is the likely culprit of the rapid increase in microcephaly in infants born in Brazil.

Paper highlights:

Pertussis, also known as whooping cough, kills tens of thousands of children per year, despite high global vaccination coverage. Additionally, developed countries with high pertussis vaccine coverage – like the United States – have experienced bigger outbreaks in recent years. Many hypotheses have been suggested to explain the “resurgence” of pertussis: (1) there is waning immunity to the vaccines and adults act as bacterial reservoirs; (2) the new acellular vaccine isn’t as good as the previous whole-cell vaccine; (3) the vaccines protect against infection but not transmission; and (4) there isn’t really a resurgence; we’re just better at detecting pertussis now than we used to be. A recent paper argues that all of those commonly held views are wrong and proposes some new hypotheses. Cool stuff!

Antibiotic resistance is a huge challenge facing global medicine. We usually assume that when bacteria evolve resistance to a given antiobiotic, the mutation that provides resistance is costly. Because we assume that those resistance mutations are costly, we also assume that if we stop using an antibiotic, the bacteria populations will evolve back to their susceptible state by acquiring compensatory mutations that restore the function(s) lost by resistance mutations. But resistance mutations vary in how costly they are. Some aren’t costly at all. And there are only so many compensatory mutations that can restore a given function. So, we can’t necessarily expect a resistant population to revert to susceptibility, whether a compensatory mutation pops up in the population or not. Furthermore, there are many other possible mutations that can reduce or eliminate any cost of resistance just by increasing overall bacterial fitness, without actually returning lost functions. We might be overlooking the importance of those “generally beneficial mutations” in the evolution and subsequent loss of antibiotic resistance in bacterial populations. Check it out.

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