Discussion: virulence

Peter W Pappas ppappas at magnus.acs.ohio-state.edu
Wed Dec 14 13:56:59 EST 1994

In article <Pine.HPP.3.91.941214100411.8925A-100000 at ac852.wfunet.wfu.edu>,
eric jona wetzel <wetzelej at WFU.EDU> wrote:
>Fellow Parasitologists ---
>Motivated by the recent admonition of John Janovy, I would be interested
>to hear some discussion regarding the 'evolution of virulence' as it has
>recently been put forth by Dr. Paul Ewald.
>Many of you attended a talk by Ewald at the last ASP meetings, in which
>he presented many of his hypotheses (most of which are also in his
>recent book, Evolution of Infectious Disease) about the relationship (as
>he sees it) between "virulence" and transmission, or "dependence on host
>mobility" as he put it at the ASP meeting.  According to Ewald, part of
>his motivation for this is to challenge the "traditional" view that
>parasites always evolve to a less virulent (i.e., benign) state -- he
>states that this is the general view held by parasitologists.
>His main premise is that, sometimes, parasites should evolve to a highly
>virulent state when it favors transmission, e.g., a parasite can afford
>to be highly virulent in an intermediate host (presumably causing
> reduced fitness) if compromising that host results in greater
>transmission to the definitive host.  Again, he ties much of this to host
>mobility; e.g., according to Ewald, malaria can 'afford' to be much more
>virulent in a human, even if it knocks that host down, since transmission
>is dependent on a mobile mosquito, in which (Ewald predicts) the parasite
>should necessarily be relatively benign (because of the need of
>So, what do folks think about this?  How, or should, we define virulence
>(since Ewald seems to change his definition depending on the scenario)?
>It certainly has merit in generating hypotheses, but how does this fit
>with infections with protozoan parasites?  helminths?  etc?
>It would be interesting to hear from a wide range of folks (ie., parasite
>ecologists, immunologists, etc.) on this, as this cuts across many of
>these areas.  Have at it!
>Eric J. Wetzel
>Dept. of Biology
>Wake Forest Univ.
>PO Box 7325
>Winston-Salem, NC 27109
>phone: 910-759-5577
>fax: 910-759-6008
>wetzelej at wfu.edu

Being neither an ecologist nor a evolutionary biologist, but rather a
physiologist/cell biologist, the above is a little out of my primary research
interest.  I do, however, have a couple of comments that might be appropriate.
Eric asks about the question of whether evolution of host-parasite
relationships will ultimately lead to decreased virulence; that's certainly
one of the basic tenets I learned when I took my first introductory
parasitology course (nearly 30 years ago!). Of course, I now know that there
are many "exceptions" to the rule.  Eric seems to assume that increased 
virulence in a host will decrease the "fitness" of a parasite, and perhaps we 
need some clarification here.  When we speak of the fitness of a parasite we 
can not view fitness from the standpoint of the relationship between the 
parasite and a single host (unless it has a one-host life-cycle).  Rather, 
fitness in the strict evolutionary sense refers only to the parasite's ability 
to reproduce -- a parasite with a higher "basic reproductive rate" will be more
successful than a parasite with a lower rate --- and the basic reproductive 
rate includes ALL aspects of the parasite's life-cycle that are important in 
reproduction and transmission (not just virulence).  Granted, increases in 
virulence might be expected to decrease the basic reproductive rate, but I can 
think of scenarios in which this might not be true.  For example, consider a 
hypothetical example of a tapeworm whose life-cycle involves an intermediate 
and definitive host.  Suppose the virulence of the infection in the definitive 
host increases, thus resulting in a decrease in the total number of eggs 
produced by the adult tapeworm (because the host is killed or dies sooner).  
But, suppose this increase in virulence is somehow linked to the parasite's 
ability to cause a behavioral change in the intermediate host so the
intermediate host is more likely to be eaten by the definitive host.  (Note
that the change in the intermediate host would not be cosidered a change in
virulence.)  The decrease in egg production could be off-set by the increased 
probability of transmission to the definitive host, so the end result is an
increase in the basic reproductive rate (aka fitness).  Or suppose the adult 
parasite produces some chemical that attracts the intermediate host to its 
feces (assuming the eggs are passed in the feces), so the intermediate host is 
more likely to ingest the eggs.  Again, this could result in increased fitness.
 The possibilities are endless!  I guess the "take home message" is that we can
not think about a parasite's fitness by examining just one aspect of its 
life-cycle.  Rather, we have to consider all aspects of the parasite's life 
cycle.  Also, I think we need to remember that even the smallest change in a 
parasite's basic reproductive rate (a change that might be almost impossible to
observe, let alone quantify) might, over long periods of time, have quite 
dramatic effects on a parasite's success.

Perhaps the above will generate some discussion among those who are more 
knowledgeable that I.
Peter W. Pappas, Professor/Chairperson, Department of Zoology,
The Ohio State University, Columbus, OH  43210  USA
E-mail: pappas.3 at osu.edu; FAX (614)-292-2030,
PHONE (614)-292-8088

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