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john janovy jjanovy at unlinfo.unl.edu
Fri Dec 30 10:02:00 EST 1994


     Thanks to all of you who have contributed to the recent 
discussions of virulence; this exchange of ideas is very refreshing 
and useful, and especially so because it builds on a major 
presentation at the national meetings.  I remember listening to a 
senior member of our society, back in the late 1960s, bemoaning the 
fact that the annual meetings always seemed like the end of 
something--research finally presented after so much labor, friends a 
year older, etc.--and for that reason it made him sad to come to the 
meetings.  But it's clear that in this one case, at least, the 
meetings were a beginning instead of an end.  

     As you might suspect, this virulence discussion has generated a 
reasonable amount of talk on the dirt roads of cyberspace, too, so I 
feel a little bit of an obligation to pass along these ideas from the 

     Back in the 1970s, when there were several people in the lab 
working on kinetoplastid flagellates, and we had a large number of 
species in culture, it became obvious that in order to talk to one 
another about the work we were doing we had to distinguish between 
"infectivity" and "virulence."   "Infectivity" became the ability to 
establish an infection; "virulence" became a measure of the speed with
which an infection progressed through its so-called natural course; 
and, both were relative (but virulence moreso).  That pathology 
accompanied relatively high virulence was a given, although the 
haemoflagellates were microparasites and it was thus impossible to 
separate pathology from parasite reproductive rates.  But it was also 
a given that one could manipulate virulence, e.g. by passing certain 
strains of __L. donovani__ through hamsters or cell cultures without 
intervening axenic culture at room temperature.  Infectivity, however,
was a more stable trait, in that a species' scientific name was more 
of a measure of its infectivity--which in fact was host specifity 
viewed from the parasite's perspective--than of its virulence.

     Since that time, we have been involved with parasites that are 
generally considered avirulent, i.e. non-pathogenic, but highly 
infective--the eugregarines (which behave biologically as 
macroparasites)--and that are rather extraordinarily diverse, mainly 
because they appear to be quite host specific and their hosts are 
extraordinarily diverse.  For example, IF the beetle __Tenebrio 
molitor__ is representative of coleopterans, with four species of 
__Gregarina__, then there may be nearly a million species of the genus
__Gregarina__ in beetles alone.  [We know that __Te. molitor__ is not 
representative, however, so that the number of __Gregarina__ species 
may be closer to 100,000, of which only 1% have been described. 
{Clopton believes the number of undescribed __Gregarina__ spp. is 
higher, possibly much higher, than 100,000}]   When one considers the 
rest of the eugregarines, one finds an equally remarkable diversity of
parasites, again with little evidence for virulence (pathogenesis).  

     By any commonly accepted definition of the term "success," these 
eugregarine parasites are very successful.  It remains to be seen 
whether colonization of a new host, by a gregarine, involves initial 
pathology followed by mutual resolution of the physiological conflict 
to the standoff status--a traditional expectation.  But the lack of 
reproduction in the life cycle stage of interest (re the virulence 
discussion), thus the macroparasitic behavior, requires that such 
theoretical pathology be separated from parasite multiplication.  So 
it seems we can distinguish between pathology arising primarily from 
parasite proliferation in the host, and pathology arising from other 
causes ("physiological [biochemical, immunological] conflict"), at 
least in theory, and a microparasite might produce one type, or the 
other, or both, but a macroparasite is "restricted" to the latter.  
(The adult schistosomes might well be a case of macroparasites 
producing propagules [eggs] that in turn behave, pathologically, as 
microparasites.)  We might expect, then, that the evolutionary events 
leading to a particular host/parasite relationship are a function 
first of the parasite life cycle events that produce, or do not 
produce, parasite multiplication in the host, and second of the 
physiological (biochemical, immunological, etc.) compatability of the 
host and parasite.

     Parasite multiplication in the host, or lack thereof, in 
virtually every case is a truly ancient and plesiomorphic character.  
Thus the proliferation of parasitic nematode species post-dates the 
evolutionary events that preclude production of new adult nematodes 
from invaders all within (and only within) the body of an individual 
host.  Conversely, the proliferation of coccidian species post-dates 
the evolutionary events that require production of new merozoites from
invaders all within, and only within, the body of an individual host. 
If pathology associated with virulence is a driving force in the 
evolution of parasitic life cycles, then evidence for such should be 
found within microparasites only, and a proper comparative study of 
these types of life cycles should produce some  testable hypotheses.  
If pathology is a byproduct of virulence, however, then the only thing
a parasite must accomplish is transition to the next life cycle stage 
prior to the host's death.  In this latter case, we might expect the 
transition time to be rather fixed, especially in the case of large, 
long lived, hosts.  

     Again, the very diverse coccidians might provide some interesting
clues to the relationship between pathology, virulence, and life 
cycles.  For example, we might ask: What is the range, among all 
coccidians,  in time and number of merozoite generations from 
infection to oocyst production?  If the range is small, and the time 
short, compared to the life expectancy of an infected host, then one 
must question whether virulence related pathology is (has been) a 
significant driving force in the evolution of the H/P relationships in
this system.  Conversely, when comparative study of a particular 
system reveals a wide range of transition times, and life expectancies
of infected hosts close to at least some of those times, then the 
hypothesis of virulence/pathology driven co-evolution seems plausible.
 A traditional view of virulence--life cycle--evolution interactions 
predicts one would find old H-P associations in which the parasite 
underwent many asexual generations, produced large numbers of oocysts,
and generated little or no pathology (accomodation joined with 
production of large numbers of propagules).  IF indeed we define 
success in terms of numbers, then evolutionary co-accomodation in 
coccidia should produce an inverse relationship between extent of 
pathology and numbers of parasite generations among a group of related
host species (some of which were colonized recently).  However, my 
cursory examination of the literature suggests exactly the opposite is
the case (pathology and number of asexual generations are directly 
related).  Is it conceivable that co-accomodation results in REDUCED 
virulence, in this case reduced oocyst production, i.e. reduced 
"success?"  If so, then perhaps we parasitologists might define 
success as persistence of a species, rather than as the production of 
large numbers of offspring (not a new idea).

     The other aspect of virulence that I've not seen discussed at 
length in the parasitological literature is the relative contribution 
of parasitism to a host species' fitness in nature.  Granted, much of 
the parasitological literature addresses problems of disease, with the
tacit assertion that disease reduces fitness.  And, granted, that 
there are some elegant studies demonstrating (at best), or suggesting 
(at least) a relationship between parasitism and mating success, and 
even mate choice.  However, there is not to be found a broad and 
comparative examination of the relative contribution of parasitism to 
overall fitness.  If one could determine, for example, all of the risk
factors for an American Robin egg from the time it's laid until its 
chick reaches adulthood and produces another egg, then list those risk
factors in order of their impact, where would the nearly hundred 
parasite species reported from __Turdus migratorius__ be placed?  And 
would they be lumped together, or ranked individually? 

     It seems to me that we need some models that take into account 
the ideas of plesiomorphic vs. apomorphic characters, applying those 
ideas to aspects of parasite biology that may not yet have been 
studied in such a way (transit time, numbers of asexual generations, 
nature of biochemical interaction between host and parasite, etc.), 
combined with host species' life expectancies and relative risk 
factors in nature.  The data sets to be examined might include ones 
necessary to answer the question: Do the life cycle features we feel 
intuitively should be variable actually vary among a group of related 
parasite species?

John Janovy, Jr.
Biol Sci; UN-L
Lincoln, NE 68588-0118
jjanovy at unLinfo.unL.edu

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