Wednesday, November 28, 2012

The more we know, the more complex the web

In light of our recent post on helminth infection and its possible protective effects, Dan Parker, our resident infectious disease expert, alerted us to a new paper (Nov 15, open access) in Malaria Journal from a group in French Guyana about the effects of helminth infection on malaria infection and transmission. Titled "Helminth-infected patients with malaria: a low profile transmission hub?," the authors propose that concomitant malaria and helminth infection are a special problem.
Studies in humans have shown increased malaria incidence and prevalence, and a trend for a reduction of symptoms in patients with malaria. This suggests that such patients could possibly be less likely to seek treatment thus carrying malaria parasites and their gametocytes for longer durations, therefore, being a greater potential source of transmission. In addition, in humans, a study showed increased gametocyte carriage, and in an animal model of helminth-malaria co-infection, there was increased malaria transmission. These elements converge towards the hypothesis that patients co-infected with worms and malaria may represent a hub of malaria transmission.  

If this is true, because helminth infection and malaria overlap in much of the world, helminth control could be an important aspect of malarial control (though, does that then set people up for the chronic autoimmune diseases that seem to be associated with helminth control in the industrialized world?). The question of co-infection has not been ignored in the last decade or so, the authors write, but the results have been somewhat confusing. Infection with hookworm, for example, has been associated with increased malarial infection while infection with Ascaris is associated with lower incidence of malaria and decreased severity. Mechanisms have been proposed, such as that anemia increases susceptibility, or that helminth infection modulates immune responses, and differing study designs may account for some of the discrepancy.

But, if co-infection really is a factor in increased transmission and higher prevalence of malaria, this shows yet again the insidious complexity of malarial control. The new 'longform' digital magazine, Aeon, recently posted an essay by David Barash, evolutionary biologist "and aspiring Buddhist" that, among other things, described a project to understand why some years trees were more infested with gypsy moths than others. Gypsy moths cause great damage to North Eastern forests of the US, but only periodically.

 The suspicion was that gypsy moth periodicity was somehow connected with acorn crops, which vary greatly from year to year. High crop years were associated with low gypsy moth infestations, and vice versa. High crop years, as it turns out, are also associated with high white-footed deer mouse populations, too, as they love acorns. And they also love gypsy moth larvae, and feast on both.

But, white-tailed deer also love acorns, and they carry deer ticks, often infested with Lyme disease.
What are the practical implications? Foresters might be tempted to try to distribute additional acorns, inhibiting gypsy moth outbreaks in order to improve lumber yields. But this might bring about Lyme disease epidemics: more mice mean fewer gypsy moths, but also more ticks. Alternatively, public health officials who want to reduce Lyme disease might look into various ways of chemically suppressing mast production, which might in turn bring about gypsy moth infestations. Finally, it’s possible that Lyme disease outbreaks might be correlated, oddly enough, with how many acorns are produced that year by the forest.
The interconnected, ecological nature of life is, in part, what makes controlling deadly diseases like malaria, or debilitating helminth infections, so difficult. Each tweak has potential unintended consequences, to some degree because we don't really understand the whole web in the first place. Which only means we need to get better at seeing the whole.


Marnie said...

Great posts on malaria. I've been distantly followin the work to try to develop a vaccine for malaria. I very much appreciate your last article on the beta globin complex and this one on complexity/helminths/malaria.

Anne Buchanan said...

Thanks, Marnie. As I'm sure you know, many people in the field believe a vaccine just isn't possible. In part, as I understand it, this is because acquired immunity (acquired the hard way -- from having malaria) is so short-lived. But Dan would have a lot more to say about this than I do.

Unknown said...

There are some malariologists who at least appear to be very optimistic about developing a vaccine, and they tend to be the ones who are actually working on that end. I, and most people I know working with malaria, are pretty pessimistic about that. A large part of the reason is as Anne mentioned: if the vaccine is based off of boosting natural immunity, it’s going to have to get around the problem of losing that natural immunity (quite quickly). Another really basic reason is that malaria parasites are quite adept at avoiding road blocks to their survival.