Host nutrition determines blood nutrient composition and mediates parasite developmental success: Manduca sexta L. parasitized by Cotesia congregata (Say)
Department of Entomology, University of California, Riverside, California 92521, USA
* Author for correspondence (e-mail: nelsont{at}ucr.edu)
Accepted 24 November 2004
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Summary |
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Key words: insect, development, nutrition, diet, parasitism, Manduca sexta, Cotesia congregata
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Introduction |
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During the associations of many insect endoparasites, including gregarious
braconid wasps of the genus Cotesia, with their lepidopteran larval
hosts, the effects of parasitism are initially mediated by a variety of
parasite-derived factors. These include polydnaviruses and/or venom, injected
into the host by the adult female parasitoid during oviposition
(Beckage et al., 1994;
Nakamatsu et al., 2001
;
Nakamatsu and Tanaka, 2003
).
Also involved are teratocytes, specialized cells derived from the serosal
membrane of the parasite egg (Dahlman and
Vinson, 1993
; Zhang et al.,
1997
). A critical role of such components is early suppression of
host defense responses that would otherwise encapsulate and destroy the
parasite egg or early larval stages
(Schmidt et al., 2000
). An
adult female Cotesia spp. deposits between 50 and a few hundred eggs
into the body cavity or haemocoel of a single host larva. Host larvae,
however, are often superparasitized, where more than one adult parasitoid
oviposit eggs. The eggs hatch and parasite larvae develop, feeding principally
on the host's haemolymph or blood, but also on the fat body following
disintegration through the action of teratocyctes
(Nakamatsu et al., 2002
). In
the case of Manduca sexta parasitized by Cotesia congregata,
mature, second instar parasite larvae emerge from the host, moulting to the
third stadium as they penetrate the cuticle
(Fulton, 1940
). Upon moulting,
parasite larvae spin cocoons and pupate.
Parasitism also brings about long-term physiological effects, many of which
may influence the ultimate success of parasite development. Depressed host
growth and increased development time are common responses
(Vinson and Iwantsch, 1980;
Beckage and Riddiford, 1983
).
Delayed host development may be important for ensuring sufficient time for
parasite growth and development (Smith and
Smilowitz, 1976
; Slansky,
1978
; Lawrence and Lanzrein,
1993
). Numerous studies, including investigations of a variety of
lepidopteran insects parasitized by Cotesia spp. demonstrate that
decreased food consumption accompanies the above effects
(Tanaka et al., 1992
;
Alleyne and Beckage, 1997
).
Otherwise, little is understood of the potential effects of nutrition on
parasitized host insects or of the importance of host nutrition to parasite
success.
Recent studies establish that dietary nutrient balance influences growth
and development of Manduca sexta over the last two larval stadia
(Thompson et al., 2005).
Feeding and nutrient intake differ markedly between normal and parasitized
larvae and depend on the ratio of digestible protein and carbohydrate. Growth
of parasitized larvae is equivalent to that of normal unparasitized larvae
when insects are maintained on diets having a ratio of casein (C) to sucrose
(S) between 1.0C:1.0S and 1.5C:0.5S, although development time of parasitized
larvae is longer. On diets having nutrient ratios with greater or lesser
protein, growth of parasitized larvae is severely depressed when compared with
normal larvae even though development times of parasitized insects are greater
on the less suitable diets. These results suggest that parasitized larvae may
exhibit different long-term feeding preferences than normal larvae. That
conclusion is consistent with results of a previous investigation
demonstrating that parasitized larvae, offered a choice of diets having
variable nutrient content, select a different ratio of nutrients from that
preferred by normal larvae (Thompson et
al., 2001
).
Understanding how host responses to nutritional variation mediate parasite growth and development is important to assess whether nutritional factors play a critical role in successful parasitism. The present study addresses how dietary protein and carbohydrate balance influences the development of C. congregata in M. sexta. We establish how host dietary nutrient ratio affects the total levels of blood protein nitrogen and trehalose, and in turn, how these metabolites affect parasite burden, the numbers of parasite larvae developing in individual hosts and total parasite biomass. Furthermore, we examine the relationship between host dietary nutrient ratio, blood metabolites and the numbers of mature parasite larvae that emerge from the host to pupate and complete development and the numbers of larvae that fail to emerge. Based on the findings of studies cited above, we predicted that the nutritional status of host larvae as affected by dietary nutrient ratio would influence parasite burden and success through effects on host blood composition.
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Materials and methods |
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Experimental diet and feeding protocol
Newly moulted fourth instar M. sexta larvae were fed a chemically
defined artificial diet containing variable levels of casein and sucrose as
digestible protein and carbohydrate, respectively
(Ahmad et al., 1989). The diet
also contained B vitamins, linseed oil, ascorbic acid and Wesson's salt
mixture, obtained principally from Bioserve (Frenchtown, NJ, USA) and
Nutritional Biochemicals (Cleveland, OH, USA). Six diets were employed, each
having the same total amount of casein and sucrose, but with different casein
to sucrose ratios as follows: 0.125C:1.875S, 0.25C:1.75S, 0.5C:1.50S,
1.0C:1.0S, 1.5C:0.5S and 2.0C:0S. The nutrient levels are indicated relative
to the amount of casein and sucrose in the stock formulation, that is, 1C:1S
relative to 90 g l-1 casein and 90 g l-1 sucrose. Groups
of 10 randomly selected normal and parasitized larvae were maintained on each
experimental diet for the feeding studies described below. Insects were housed
in a Precision Scientific incubator at 28°C with a 16 h:8 h light:dark
non-diapausing, long-day photocycle.
Larvae were fed on the experimental diets from the start of the fourth stadium until the end of the fifth stadium. In the case of normal larvae, the experiments were discontinued after approximately 25% of the larvae had stopped feeding and entered the wandering phase in preparation for pupation. At this point all larvae had reached approximately 8-10 g with a total development time between 7 and 15 days, depending upon diet. For parasitized larvae, the experiment was stopped at the time larvae ceased feeding prior to parasitoid emergence. The time also varied with diet, between 12 and 15 days.
Estimation of parasite burden and biomass
The number of parasites that emerged from individual host larvae maintained
on the various diets was determined at the end of the experiments by counting
parasite larvae and cocoons. After dissection of the gut of parasitized
larvae, the parasites failing to emerge were counted using a Wild dissecting
microscope. To determine parasite biomass, the emerged and non-emerged
parasites were collected and dried in an oven at 100°C for 24 h. Biomass
was measured on a Sartorius microbalance.
Estimation of host blood metabolite levels
Previously, we reported the effects of dietary nutrient ratio and
parasitism on equilibrium blood concentrations (mg ml-1) of
protein, total free amino acids and trehalose in normal and parasitized M.
sexta larvae (Thompson et al.,
2005). Here, we use those data to estimate the total quantities or
levels of these metabolites in the blood of normal and parasitized larvae
based on their final mass and water content, assuming 50% extracellular water
(Chapman, 1998
). Data are
presented as total protein nitrogen level (protein plus free amino acids) and
total trehalose (mg per insect).
Determination of host final mass and nutrient consumption
Diet consumption was determined as the difference between the total amount
of diet offered to larvae and the amount remaining in the diet cups at the end
of the experiment together with undigested diet remaining in the gut. Dry mass
of the diet remaining in the cups was determined by drying the diet in an oven
as described above. Initial dry mass of the diet offered to the insects was
estimated from the known ratio of wet/dry mass. Protein and carbohydrate
consumption were estimated based on the composition of each diet. The guts of
normal and parasitized larvae were dissected at the end of the experiment and
the diet remaining in the gut was removed. This diet was added to that
remaining in the cups, for estimation of diet consumption. The individual
carcasses of host larvae were dried as above and final host mass measured by
weighing.
General statistical analyses
Data showing the effects of dietary nutrient ratio on parasite burden and
biomass were examined by two-way analysis of variance (ANOVA). Analysis of
covariance (ANCOVA) using various parameters as covariates, were applied in
specific cases described below. The Shapiro-Wilk `W' test and normal
probability plots evaluated normality and homogeneity of variance. Except in
the case of parasite burden, data met the assumptions for analysis of
variance. Non-normally distributed data for parasite burden were square root
transformed.
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Results |
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The relationship between blood protein nitrogen and trehalose levels
(mg/insect) relative to nutrient consumption by hosts on the various diets is
shown in Fig. 1. For normal
unparasitized larvae, total blood trehalose decreased as the dietary level of
sucrose decreased, with the exception of the 0.125C:1.875S diet. This diet was
previously judged `pathological'
(Raubenheimer and Simpson,
1999) based on earlier findings that normal host larvae fail to
adjust consumption in response to the poor nutrient balance of this diet
(Thompson et al., 2005
). In
contrast, with parasitized larvae total blood trehalose increased as dietary
level of sucrose decreased reaching a maximum on the 1.0C:1.0S diet,
thereafter decreasing with further decreases in dietary carbohydrate. Total
blood nitrogen for both parasitized and normal larvae increased as dietary
protein level increased and was maximal on the 1.5C:0.5S and 2.0C:0.5S
diets.
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Effect of host dietary nutrient ratio on parasite burden and biomass
Dietary nutrient ratio had a significant effect on parasite burden, the
numbers of parasites developing in individual host larvae and total biomass,
regardless of whether parasites emerged to complete development
(Table 2;
Fig. 2). The parasite burden
and biomass of non-emerged parasites were greatest on the 1.0C:1.0S and the
1.5C:0.5S diets (Fig. 2AB).
Non-emerged parasite burden and biomass were lower in host larvae on the other
diets, but there was no significant difference between these diets. The burden
and total biomass of emerged parasites was more uniform between diets and
highest from host larvae on the 0.5C:1.5S, 1.0C:1.0S and 1.5C:0.5S diets
(Fig. 2AB). No parasites
emerged from larvae on the 0.125C:1.875S diet. On this diet parasite burden
was very low and the individual parasites were very small (parasite parameters
were not determined).
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The mass of individual parasite larvae that emerged or that failed to
emerge was similar for host larvae at all dietary nutrient ratios, except for
those from hosts on the 0.25C:1.75S diet
(Fig. 2C), where both emerged
and non-emerged parasites weighed less. A large portion of non-emerged
parasites appear to be mature second instar larvae, an observation previously
reported by Alleyne and Beckage
(1997).
We compared the burden and the biomass of emerged and non-emerged parasites from hosts on the individual diets by conducting an ANOVA analysis on the arithmetic differences between the two parasite populations. The results (not shown) demonstrate a significant effect of dietary nutrient ratio on the mean difference scores for both burden and biomass. Only in the case of the 1.0C:1.0S diet, however, were the difference scores between non-emerged and emerged parasite burden and biomass significantly different from 0, with emerged parasites being fewer and having less total biomass.
Effect of host blood nutrient levels on parasite burden and biomass
We estimated the total levels of protein nitrogen and trehalose in the
insects for which parasite data were available based on the total metabolite
levels reported above. First, we established the relationships between
metabolite levels and host final mass by applying ANCOVA using blood protein
nitrogen and trehalose levels as dependent variables, dietary nutrient ratio
as a main-effect treatment and final mass as the covariate. Dietary nutrient
ratio had a significant effect on both metabolites and in each case, there was
a significant covariate effect of final mass
(Table 3). Using the metabolite
levels predicted from linear regression equations, we modeled the effect of
protein nitrogen and trehalose on emerged and non-emerged parasite burden and
biomass (PROC REG followed by PROC G3 GRID and PROC G3D. SAS version 8.02.
2001. SAS Institute Inc., Cary, NC, USA). Data for protein nitrogen and
trehalose levels were first standardized (mean of 0.0 and standard deviation
of 1.0) and then used as dependent model variables. Standard variable
selection techniques (Freund and Little,
2000) were used to generate a best-fit model that considered both
linear and quadratic terms as independent variables and parasite burden or
biomass as dependent variables. Four predictive models were constructed.
Additionally, contour maps were generated from these data (PROC GCONTOUR) from
a 22x103 point matrix by interpolating a simple linear
function for the relationship between blood metabolite levels and final mass
(PROC G3 GRID).
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A linear model provided the best fit for emerged parasite burden and biomass, and quadratic and interaction terms involving protein nitrogen and trehalose were not included in these models (Table 4). Blood protein nitrogen and trehalose levels both predicted emerged parasite biomass (Fig. 3A). The relationship for parasite burden is not shown. Both protein nitrogen and trehalose levels were positively associated with increased emerged parasite burden and biomass (Table 5). Based on the standard regression coefficient, trehalose was the more important predictor of parasite biomass, while protein nitrogen was the more important in the case of parasite burden. With non-emerged parasite burden and biomass (Fig. 3C), both trehalose and protein nitrogen levels were important, but the relationships were more complex than with emerged parasite parameters (Fig. 3A). Here, the quadratic terms for both protein nitrogen and trehalose significantly contributed to the precision of the models in predicting non-emerged parasite burden and biomass (Table 5). The model component describing the interaction between trehalose and nitrogen did not contribute to the ability of the models to predict non-emerged parasite burden and biomass. Trehalose level (both linear and quadratic estimates) was the most important predictor of non-emerged parasite parameters. However, the overall effect of trehalose was similar to that of nitrogen. At intermediate levels of both metabolites, fewer numbers of non-emerged parasites are produced. Low and high levels of metabolites lead to greater numbers and biomass (Fig. 3C) of parasites failing to emerge.
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The contour maps illustrate the optimal levels of protein nitrogen and trehalose supporting parasite growth and development. The relationships between blood metabolite levels and emerged and non-emerged parasite biomass are shown in Fig. 3C,D. Relationships for parasite burden were similar but are not shown. Nutrient levels for the 0.5C:1.5S, 1.0C:1.0S and 1.5C:0.5S diets supporting the greatest numbers and biomass of parasites appear to occupy a common region in two dimensional space. Within this space, the nutrient levels varied between approximately 60 and 110 mg per insect trehalose and between 60 and 200 mg per insect protein nitrogen.
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Discussion |
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The relationships between blood protein nitrogen and trehalose levels in
normal and parasitized M. sexta larvae on the various diets are
strikingly similar to the nutrient intake arrays demonstrating the
relationships between protein and carbohydrate consumption
(Thompson et al., 2005).
Alterations of nutrient intake as a result of parasitism, therefore, may be an
adaptive strategy by C. congregata, where resultant blood metabolite
levels are closest to optimal for supporting parasite growth and development
on specific diets. The host blood metabolite array, the relationship between
blood protein nitrogen and trehalose levels, may represent a rule of
compromise for the parasite, somewhat analogous to the rules of compromise
apparent from nutrient intake arrays. Rules of compromise define how animals
regulate diet consumption, post ingestive responses and development time to
accommodate imbalances in dietary nutrient composition
(Raubenheimer and Simpson,
1999
; Thompson et al.,
2005
). Here, the rule of compromise involves the manner in which
parasitism affects host feeding and physiology to influence blood metabolite
levels. Although the host blood metabolite array for parasitized larvae
reflects nutrient availability rather than nutrient uptake by parasites, it is
similar to the nutrient intake arrays typically observed during development of
specialist feeders. In these cases, insects will suffer a large shortfall of a
deficient nutrient to avoid consuming a small surplus of an excessive
nutrient, as the nutrient ratio shifts away from the most optimal ratio. C
congregata is relatively host specific, having been reported from several
host species, all restricted to the family Sphingidae
(Gilmore, 1938a
). Host
specificity is, in part, defined by the ability of C. congregata to
modify the feeding and physiology of its host, M. sexta, resulting in
the most suitable milieu for supporting successful development of the immature
parasitic stage. Other parasitoids may bring about different effects on the
feeding and physiology of M. sexta, or other host species, likewise
producing suitable nutritional environments but reflecting different
developmental strategies and host specificity.
Parasites developing in M. sexta larvae include those that
successfully emerge from hosts to pupate and complete development and those
that fail to emerge. Over a wide range of final host size there is a maximum
number and total biomass of parasites that emerge from individual host larvae.
In our study, these were approximately 100 parasites and 100 mg total biomass.
This burden of parasites is considerably lower than the approximate 200
maximum number reported by Alleyne and Beckage
(1997) for M. sexta
larvae similarly parasitized by C. congregata but maintained on the
wheat germ-based rearing diet. Larvae purportedly grow as well on the
chemically defined diet as on the rearing diet
(Ahmad et al., 1989
), but
specific differences in nutrition may account for the different results for
emerged parasites. Depending on diet, the number and total biomass of
non-emerged parasites may exceed those of parasites that successfully emerge.
This phenomenon, a large number of parasites failing to emerge, has been
described in both field collected (Fulton,
1940
; Thurston and Fox,
1972
) and laboratory reared M. sexta larvae
(Barbosa et al., 1991
;
Alleyne and Beckage, 1997
).
Hosts reared on three diets, 0.5C:1.5S, 1.0C:1.0S and 0.5C:1.5S, supported
maximal and similar numbers and biomass of emerged parasites. Hosts on the
1.0C:1.0S supported the largest parasite numbers and biomass of parasites,
including both those that emerged and those that failed to emerge. The same
diet supports the greatest mass gain by parasitized larvae
(Thompson et al., 2005), and
has the ratio of protein and carbohydrate selected by parasitized larvae when
offered a choice of a high protein and a high carbohydrate diet
(Thompson et al., 2001
).
The effects of dietary nutrient ratio on parasite burden and biomass are supported by data showing the influence of blood nutrient levels on parasite parameters. Different responses of emerged and non-emerged parasites to blood nutrient levels were readily apparent from the models and contour maps illustrating these relationships. However, the specific nutrient levels supporting the greatest parasite burden and biomass reflect protein:carbohydrate ratios varying between approximately 1 and 1.5, within the range of the dietary nutrient ratios supporting the greatest parasite burden and biomass, whether emerged or non-emerged. Future investigations will examine how host protein and carbohydrate intake are partitioned into host and parasite growth.
Our studies estimate nutrient concentrations and levels at approximately
half way through the fifth stadium only and may not be reflective of nutrient
availability throughout the entire period of parasite development. The
concentrations of various blood metabolites in parasitized larvae may change
over time (Vinson and Iwantch,
1980). Studies by others demonstrate that in M. sexta
larvae parasitized early in the fourth stadium, blood protein concentration
continuously increases during the fifth stadium, albeit at a lower rate than
in normal larvae, and reaches approximately 11 mg ml-1 when feeding
stops (Beckage et al., 1989
;
Beckage and Kanost, 1993
). The
protein concentration then declines to approximately 7 mg ml-1 when
parasites emerge. In those studies, the protein concentration at mid-fifth
stadium, approximately 9 mg ml-1, is similar to the concentration
we observed at the same point of development in parasitized larvae on the
0.5C:1.5S diet (Thompson et al.,
2005
), although the latter diet contains about 20% less protein
than the wheat germ diet on which larvae were fed in the above
investigation.
Some investigators have suggested that parasite emergence is limited
because M. sexta host larvae become exhausted of blood and fat body,
concluding that parasites failing to emerge simply have not consumed
sufficient nutrients (Bentz and Barbosa,
1990; Alleyne and Beckage,
1997
). Some of our results appear to support this conclusion. The
observation, for example, that the burden, biomass and proportion of
non-emerged parasites to total parasites are highest in the largest hosts fed
the 1.0C:1.0S diet, that also have the greatest proportion of total parasite
biomass to final host mass. Our earlier results demonstrating that parasitized
larvae feeding on this diet significantly increase diet consumption
(Thompson et al., 2005
) would
suggest that larvae accommodate any increased demand for nutrients. The
present finding that non-emerged parasite burden increases along with
increased protein consumption would also argue against this. If nutrition were
limiting, we would predict that hosts maintained the 1.0C:1.0S diet, but with
low parasite burden, would have fewer and a lower proportion of parasites
failing to emerge. To test this, we exposed M. sexta larvae
individually to C. congregata females and removed hosts following a
single oviposition encounter. After completing development, the numbers of
emerged and non-emerged parasites were determined. Parasite burdens generally
ranged from 50 to 200, much lower than the burdens for superparasitized hosts
maintained on the better experimental diets. The wide range of parasite burden
may in part be due to the amount of time females spend during a single
oviposition, which varies from one to several seconds. Regardless of the
parasite burden, however, in every case at least half of the parasites failed
to emerge. This is consistent with, although somewhat higher than, the 25%
average non-emerged parasites reported by Thurston and Fox
(1972
) for field collected
host larvae with parasite burdens of 50-100.
Persuasive evidence against the hypothesis that nutrition limits parasite
emergence is the observation that many non-emerged parasites are mature second
instar larvae and appear morphologically indistinguishable from larvae that do
emerge. The similar mass of emerged and non-emerged parasites found in the
present study strongly suggests they were similarly nourished. In contrast to
results of some others (Beckage and
Riddiford, 1982; Alleyne and
Beckage, 1997
), we did not observe any significant decrease in the
size of individual parasites with increased parasite burdens. In our studies,
however, differences in parasite burden were achieved by maintaining hosts on
different diets, while in the studies of Alleyne and Bekage
(1997
) were found highly
variable parasite burdens and individual parasite mass in hosts maintained on
the same diet.
Additional study is necessary to assess the potential role of nutrient depletion in parasite failure to emerge. Experiments, for example, involving administration of supplemental nutrients through injection into hosts after cessation of host feeding may prove useful for indicating the potential of nutrition to alter parasite success. Alternately, parasitized hosts might be manipulated in a manner that extends the feeding period and total nutrient consumption. At this time, however, we believe that other factors are probably involved in determining parasite emergence, or failure to emerge.
Host nutrition may mediate parasite development and success through effects
on host endocrinology, which parasitism disrupts. Abnormally elevated blood
concentration of juvenile hormone and lower than normal 20-hydroxyecdysone
concentration occur during parasitism of many insects, including M.
sexta (Beckage and Gelman,
2001; Cole et al.,
2002
). Elevated juvenile hormone explains the decreased growth and
delayed development of parasitized host larvae and ultimately their failure to
pupate. Furthermore, juvenile hormone probably influences parasite
development, as application of juvenile hormone or methoprene, a juvenile
hormone agonist, to the cuticle of intact parasitized larvae prevents parasite
emergence (Beckage and Riddiford,
1982
). Host larvae probably display varying patterns of
developmental hormone concentrations depending upon nutritional status, as
reflected by the effects of nutrition on host size
(Nijhout, 1994
) as well as
parasite burden. In normal larvae, such responses ensure that moulting and
metamophosis occur at appropriate times under specific nutritional conditions.
Under suboptimal nutritional conditions, juvenile hormone concentrations may
remain high for longer periods, delaying development while larvae grow to an
adequate size. M. sexta larvae fed only sucrose during the first 3
days of the fifth stadium display delayed development and metamorphosis in
response to a slower than normal decrease in juvenile hormone synthesis
(de la Garza et al., 1991
). In
parasitized insects, particularly in host larvae on suboptimal diets, altered
hormone concentrations may desynchronize the development of the parasite. In
the case of M. sexta parasitized by C. congregata juvenile
hormone concentration begins to decrease a few days before parasite emergence.
If juvenile hormone is too high at the time parasites are ready to begin
emergence and moulting, parasites may become unresponsive and their further
development permanently delayed. Thus, the distribution of emerged and
non-emerged parasites may in part reflect differential response among
parasites to hormone levels in hosts on the various diets.
A significant loss of parasite resources appears to characterize the nutritional and developmental interactions between C. congregata and M. sexta. First, a large number of parasite eggs, or larvae, probably early instars that are no longer apparent upon dissection, fail to develop. We assume because all host larvae were reared under the same nutritional conditions, and were of the same developmental stage and size at the time of oviposition, that all are of comparable nutritional quality. Furthermore, because all hosts were parasitized in like manner, we assume that similar numbers of parasite eggs are deposited in most host larvae. Although the initial number of eggs was not determined, the difference in total parasite burden between the best and poorest diets suggests that if the above assumptions are accurate a large portion of eggs fail to develop. Although ovicide, the destruction during superparasitization of one parasitoid's eggs by another parasitoid, usually through use of the ovipositor, might provide an explanation, ovicide is unknown in Cotesia spp. or other gregarious endoparasites. Second, of the eggs that develop into mature larvae, a large portion fail to emerge. All of this suggests that C. congregata exhibits a high degree of imprecision in determining an optimal number of eggs to deposit in host larvae. This may in part be because C. congregata oviposits eggs quickly, and may therefore be unable to allocate eggs precisely. Also, assessing the optimal egg number required to efficiently realize the greatest reproductive potential or rate of gain of fitness is often compromised by fitness penalties for depositing too few eggs (Godfrey, 1994).
Fitness penalties for ovipositing more eggs than successfully develop
relate to the parasite's egg number, or capacity to produce eggs, and the
scarcity of host individuals to parasitize
(Weisser and Houston, 1993).
C. congregata, a pro-ovigenic koinobiont (Godfrey, 1994;
Quickie, 1997
) eclosing to the
adult stage with very large numbers of eggs, so that the fitness penalties for
ovipositing too many eggs may be minimal if hosts are scarce. C.
congregata parasitizes a variety of Sphingid moth larvae
(Gilmore, 1938a
), which
generally display wide dispersal patterns. M. sexta deposit eggs in
patches, but patches can be widely distributed and individual gravid female
moths may fly continuously over an entire night
(Gilmore, 1938b
). In
cultivated cotton, moths lay one to five eggs on individual plants and females
have as many as 2000 eggs. In the case of wild host plants, principally
solanaceous species, patches would be even more widely distributed. Because
over a rather wide variation in nutritional conditions the number and biomass
of emerged parasites is nearly constant, deposition of excess eggs by C.
congregata may not be adaptive, but neither may it be detrimental. The
potential adaptiveness of superparasitism may differ depending on whether
superparasitism is due to multiple parasitization by an individual parasitoid,
self-superparasitism, or is due to conspecific superparasitism, parasitization
by more than one parasitoid (van Alphen
and Visser, 1990
). Our casual observation during the present study
is that superparasitism was principally conspecific. In either case, however,
superparasitism may be adaptive for an individual parasitoid competing for
scarce hosts.
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References |
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