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Effects of a nonsteroidal ecdysone agonist tebufenozide on hostparasitoid interactions.

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Archives of Insect Biochemistry and Physiology 26:235-248 (1994)
Effects of a Nonsteroidal Ecdysone Agonist,
Tebufenozide, on Host/Parasitoid
Interactions
JohnJ. Brown
Department of Entomology, WashingtonState University,Pullman
Tebufenozide (RH-5992), a nonsteroidal ecdysone agonist, stimulated significant
( P 2 0.05) growth in both testes of post-diapausing codling moth larvae and a
dormant Ascogaster larva in its overwintering host's hemocoel. Tebufenozide
elicited the same responses in post-diapausingtestes and Ascogaster larvae as were
reported earlier in insects treated with 20-hydroxyecdysone (20-OHE) [Friedlander, J Insect Physiol 35:29 (1989); Brown et al., Endocrinological Frontiers in
Physiological Insect Ecology. Wroclaw: Wroclaw Technical University Press, pp
443-447 (1988)]. Only a trace (I1%) of ''C-tebufenozide was recovered from
gonads and exuviae of healthy larvae, or from Ascogaster larvae removed from
parasitized hosts; however, the renewed growth of testes and Ascogaster larvae
and apolysis of codling moth integument were an obvious response to the hormone
agonist. Most of the injected 14C-tebufenozidewas recovered from host fat body,
while the alimentary canal retained approximately 40% of the 14C-tebufenozide
fed in an artificial diet.
Host exposure to tebufenozide did not cause apolysis in endo- or ectoparasitic
hymenopteransfeeding on treated codling moth larvae; however, the endoparasitoid trapped in the host's hemocoel died as its host's tissue deteriorated. Different
results were observed on ectoparasitoidsdeveloping on treated hosts. Ectoparasitic
Hyssopus sp. (Eulophidae) larvae feeding on tebufenozide treated hosts pupated
in the normal length of time. Hyssopus adults which developed from larvae fed
tebufenozide treated hosts were fertile and produced as many progeny as adults
reared from solvent fed controls. There was no evidence of secondary poisoning
to Hyssopus sp. and codling moth exposure to tebufenozide may actually benefit
the rearing of this eulophid by maintaining the host in the susceptible larval stage
and preventing the host larva from spinning a cocoon. Q 1994 WiIey-Liss, Inc.
Key words: Ascogaster quadridentata, Cydia pornonella, testes, tebufenozide, codling moth
Acknowledgments: The author appreciates the gift of ''C-tebufenozidefrom Drs.A.C.T. H5uandC.R.
Carlson of Rhom & Haas, Spring House, PA, and thetechnicalhelpof D. Reed Larsen.This research was
supported in part by a grant to J.J.B. from the Washington State Tree Fruit Research Commission 6405.
Received February 4, 1993; accepted March 5, 1993.
Address reprint requests to Dr. John J. Brown, Department of Entomology, Washington State University,
Pullman, WA 991644382,
0 1994 Wiley-Liss, Inc.
236
Brown
INTRODUCTION
The testes of diapausing codling moth, Cydia pornonella L. (Tortricidae)larvae
are diminutive, darkly melanized, kidney-shaped tissues, with arrested spermatogenesis. Dormancy is maintained by the absence of molting hormone ill.
Dormant testes apparently respond to hemolymph ecdysteroids occurring
during diapause termination, because the addition of ZO-OHE*to in vitro cultures
of dormant testes initiates growth and a renewal of spermatogenesis [21.
In parasitized codling moths, an Ascogaster quadridentata Wesmael (Braconidae) larva diapauses as a small (V = 10.150 mm3) first instar parasitoid in the
hemocoel of its overwinteringhost. Dormancy of both insects is assured because
the host’s endocrine system is inactive, and host ptg activity is necessary for
post-diapause development of the parasitoid larva [31. Some Li parasitoid
larvae may not have a functional ptg and they may rely upon ecdysteroids in
their h o d s hemolymph [4]. This would be a logical explanation for dormancy in
the Cydia/Ascogaster system. Ligation of the host, caudal to the ptg, isolates the
dormant parasitoid larva in the abdomen and prevents the renewal of the
parasitoid’s growth, even when the host is transferred from dormancy-maintaining (OP:24S, 4°C) to DTC (16P:8S, 25°C). However, previous experiments
have shown that an injection of 20-OHE into the ligated host abdomen will cause
renewed parasitoid growth [51.
In summary, both testes and A. quadridentata larvae respond to a postdiapausing pulse of hemolymph ecdysteroids by renewing their growth and
development. However, parasitized codling moth larvae generally do not have
developing testes 1161; therefore, the parasitoid larva is the recipient of ecdysteroids in the host hemocoel. In the absence of host testes, the parasitoid can
monitor and interpret the host’s endocrine message signalling the end of
dormancy. The parasitoid resumes growth in response to the host’s release of
a post-diapausing pulse of ecdysteroids [3,71.
Ecdysteroids play a major role in host/parasitoid interactions and until
recently researchers had to depend upon commercially available 20-OHE to
study these endocrine interactions [81. This strategy would be comparable to
using JH rather than methoprene to study endocrine interactions. Besides being
prohibitively expensive, the action of in vivo degradative enzymes requires the
researcher to use dosages higher than the physiological titer of the natural
hormone. Tebufenozide (ring substituted 1,2 dibenzoyl-1 tert-butyl hydrazide;
RH-59921, is an ecdysteroid agonist structurally similar to the initial hydrazide
compound (RH-5849) discovered by Hsu and Aller [91. Tebufenozide may be
used to further our understanding of the role of ecdysteroids in host/parasitoid
endocrine relationships, just as methoprene has aided our understanding of JH
involvement.
*Abbreviations used: DMSO = dimethyl sulioxide; DTC = diapause terminating conditions;
EC50 =effective concentration needed to cause head capsuleslippage in 50% of the treated population;
IGR= insectgrowth rcgu1ator;JH=juvenilehormone;JHA=juvenile hormoneanalog;LD= longday;
L, =defines the instar or an age-day within a stadium (i.e., L,, L2, L1);20-OHE=2O-hydroxyecdysone;
P = photophase; ptg = prothoracic gland/s; RH = Rohm and Haas; S = scotophase; SD = short day.
Host Specific Ecdysone Agonist
237
Here, I report the response of testes in healthy codling moth larvae, or an Li
Ascogaster larva in the abdomen of its host, to an injection of tebufenozide.
Presumably if tebufenozide is acting as an ecdysone agonist, both testes in the
healthy larva and the L1 parasitoid larva should initiate post-dormancy growth
and development in response to the hormone mimic, as these processes were
demonstrated earlier to be under the control of ecdysteroids [2,51. This manuscript also examines the possible indirect toxic effects of the growth regulator
on hymenopteran endo- and ectoparasitoids feeding on hosts fed or injected
with tebufenozide.
MATERIALS AND METHODS
Insects
Nonparasitized codling moth larvae and those parasitized by A. quadridentutu
were reared individually in 35 cc plastic cups containing an agar-wheat germ-casein diet [3]. Long-day (LD = 16P8S) conditions promoted continuous growth,
while exposure to short-day (SD = 8P:16S) photoregimes at 25°C induced dormancy. Dormancy of codling moth larvae was maintained in a walk-in cooler
(OP24S, 4°C) for 3 months. Dormancy was rapidly terminated in these larvae by
transferring healthy or parasitized codling moth larvae to DTC (LD, 25°C).
Tebufenozide was incorporated into artificial diet and presented to nondiapausing codling moth larvae or dissolved in acetone and topically applied to
nondiapausing codling moths or injected with DMSO directly into the hemocoel
of diapausing larvae, to observe the effect of the ecdysone agonist on host
testicular development or endoparasitic A. quadridentutu larval growth and
survival. Testes and A. quadridentutu larvae were measured by an ocular micrometer, 5 days following treatment of codling moth larvae with enough
tebufenozide to initiate integumental apolysis within a 24 h period following
treatment. Some hosts, which had previously been exposed to various concentrations of tebufenozide (four hosts/concentration/treatment, repeated three
times) by either interhemocoelic injection or via diet, were presented (one
host/one parasitoid adult) to Hyssops (Eluchertus) sp. (Eulophidae)adults after
the host’s head capsule had slipped forward, and ovipositional behavior and
reproductive success of these ectoparasitoids was noted.
Chemicals
Tebufenozide was weighed and dissolved in DMSO for addition to an artificial
diet or direct injection into the larva’s hemocoel. Rohm and Haas (Spring House,
PA) provided U 14C-A-ringlabeled tebufenozide (25.52mCi/mmol). Aliquots of
‘q-tebufenozide stored in methanol were evaporated to dryness under N2 and
redissolved in an equal volume of either DMSO, for incorporation into artificial
diet and injection into the host’s hemocoel, or acetone for topical application.
Recovery of 14C-Tebufenozide
Samples of whole insects, specific tissues, or artificial diet were homogenized
in 200 p1 saturated NaCl in 1%aqueous HC1 and extracted 3 times with 400 pl
of ethyl acetate:acetonitrile (2:1),with vigorous vortexing and centrifugation at
2,940g for 10 min between washes [lo]. The pooled organic layers were evapo-
238
Brown
rated to dryness, resolubilized in 100pl of ethyl acetate:acetonitrile(2:l). Recovery rates ranged from 50 to 70%. Eighty microliters were used for liquid
scintillation counting, while 10 pl of the remaining volume was spotted onto
250 pm normal-phase silica gel TLC plates. One lane on each TLC plate used to
analyze each sample was devoted to the parent U-*'k-A-ring labeled tebufenozide. Radioactivity was analyzed by scraping 1 cm portions of each lane into
separate scintillation vials, adding Scinti Verse I1 (Fisher Scientific, Fairlawn,
NJ), and counting in a liquid scintillation counter. When the TLC plates were
developed in dich1oromethane:acetonitrile:aceticacid (67:33:1), tebufenozide
had an Rf of 0.70. Recovery of 'k-tebufenozide from pooled samples of various
host tissue or the parasitoids body was reported as a percentage of cpm
detected in each fraction. This allowed comparisonsto be made between pooled
samples without regard to the actual wet weight of each tissue. The amount of
' k -tebufenozide recovered from the host, Hyssopus pupae, or cpm present in
frass voided by Hyssopus larvae prior to pupation, was reported as cpm/mg
wet weight of host or parasitoid frass.
Statistical Analysis
The size of testes were measured by an optic-micrometer and volume was
calculated for each testis [V = 7c/6(L x W)21or fused testes [V = 4/3n x radius3]
[111.Similar measurements were made of parasitoid larvae [V = 7c/4 x L x W2]
[121. Mean volumes of each group were analyzed by one-way analysis of
variance (Fisher's LSD, P < 0.05).
RESULTS
Effect of Tebufenozide on Post-Diapause Development of Ascogaster
Larvae or Host Testes
Since diapausing codling moth larvae do not feed, tebufenozide was injected
into their hemocoel with a 33 gauge needle. All larvae were ligated posterior to
the site of injection, so that testes in healthy larvae or Ascogaster larvae in
parasitized hosts were incubated in vivo with tebufenozide, but isolated in their
host's abdomen, without exchange of hemolymph that bathes the ptg of the
codling moth larvae. An injection of either 2 or 4 pg tebufenozide/pl DMSO
caused both nonparasitized and larvae parasitized by Ascogas ter to initiate
apolysis in the abdominal integument within 24 h following treatment. All
injected and ligated larvae were held individually in LD, 25"C, 70% RH for 5
days, then testes from healthy larvae or Ascogaster larvae from hosts were
measured and compared to those from codling moth larvae injected with the
solvent carrier DMSO.
Testes in healthy larvae responded to an injection of tebufenozide by initiating
rapid growth (Fig. 1).The testes exposed to 4 pg of tebufenozide were significantly
(P I0.05) larger than those excised from larvae injected with DMSO alone. The
injection of tebufenozide caused the abdominal integument to initiate apolysis in
all codling moth larvae and a large percentage of gonads fused in response to the
ecdysone agonist. Testes generally fuse in the pharate pupal stage.
Ascogaster larvae removed from hosts injected with either 2 or 4 pg tebufenozide were significantly (P I 0.05) larger than those excised from hosts injected
h
E
E
!
Host Specific Ecdysone Agonist
239
A
0.2
0.0
0.1
T
DMSO
Only
2119
4Kl
Tebufenozide
Fig. 1. Testicular volume 5 days after post-diapausing male codling moth larvae were treated with
either 2 or 4 pg tebufenozide in DMSO or DMSO alone. The percentage of testes fused during the
time of the experiment i s shown within the column representingthat population. Mean (* S.D.) lengths
of parasitoid larvae, followed by the same letter, are not significantly different at P S 0.5.
with only DMSO. All hosts injected with tebufenozide initiated integumental
apolysis and a significant (P I0.05) number of Ascogaster larvae excised from
treated hosts had molted to their second instar (Fig. 2). None of the hosts injected
with DMSO alone initiated apolysis and all Ascogaster larvae dissected from
these solvent treated hosts were in their first stadium.
Recovery of l4 C-Tebufenozide From Injected Larvae
Both healthy and parasitized diapausing codling moth larvae were injected
with 'k-tebufenozide and 5 days later various tissues were collected and
extracted to recover the radiochemical. Eighty percent of the 'k-tebufenozide
recovered from post-diapausing codling moth larvae was isolated from perivisceral fat body and peripheral fat body associated with the new integument
(Table 1).One percent or less of the 'k-tebufenozide was recovered from testes
of healthy larvae or from Ascogaster larvae in parasitized individuals. The head
capsule and alimentary canal of both healthy and parasitized insects contained
approximately 4 and 11% of the recovered 'k-tebufenozide, respectively.
Reasons for the consistent 3-fold increase in "k-tebufenozide recovered from
the new integument of parasitized individuals compared to that recovered from
healthy larvae is unclear, and histological studies are planned to interpret these
findings.
Recovery of 14C-TebufenozideFrom Orally Fed Larvae 24 H Post-Treatment
The alimentary canal of treated larvae stored tebufenozide. The gut always
contained approximately 40% of the recovered I4C labeled hormone agonist,
regardless of the concentration of tebufenozide in the artificial diet. Larvae fed
240
Brown
h
E
E
v
3.5
3.0
B
1
B
-
I
'c1
.-0
I
m
2.5
c
0
2.0
CI
v)
Q
5
m
~.
C
1.5
DMSO
4P9
Te buf e nozi de
2P9
Only
Fig. 2. Length of parasitoid's body 5 days after post-diapausing parasitized codling moth larvae were
treated with either 2 or 4 pg tebufenozide in DMSO or DMSO alone. The percentage of Ascogaster
larvae that molted into their second instar during the time of the experiment is shown within the
column representingthat population; none of the parasitoids removed from solvent treated control
hosts molted. Mean (kS.D.) lengths of parasitoid larvaefollowed by the same letter are not significantly
different at P 4 0.5.
a diet containing 25 ppm had a greater percentage of labeled tebufenozide in
the perivisceral fat body and carcass, and a lower percentage recovered from
the alimentary canal and hemolymph, when compared to the distribution of
IT-tebufenozide recovered from individuals fed a diet containing 6.25 ppm
(Table 2). Once excessive amounts of tebufenozide penetrate the hemocoel,
either by absorption across the gut wall or direct injection, then increasing
amounts of "k-tebufenozide will be recovered from the fat body. This partitioning of the compound, which is first taken up by the gut and then enters into
fat body tissue, should be kept in mind in the following discussion of secondary
poisoning and indirect effects of tebufenozide on developing endo- and ectoparasitoid Hymenoptera.
TABLE 1. Percent Recovery of Tebufenozide From Pooled Samples of Various Tissues From
Healthy Male or Ascogaster Parasitized Post-Diapausing Codling Moth Larvae (n = 15) 5
Days After Injection of 1 pg 'k-Tebufenozide in 1 pl DMSO
Healthy larvae
Tissue
Alimentary canal
Perivisceral fat body
Testes or Ascogusfu larva
Body wall (including fat body)
Exuvium
Head capsule
-
Ascogaster parasitized larvae
x% S.D.
X% S.D.
11.3 f 2.4
40.0 5.9
0.8 f 0.3
40.7 f 1.7
4.0 f 0.8
3.3 f 1.2
11.3k 4.5
38.0 f 11.4
1 . o i 0.2
31.0+ 9.4
14.7f 2.1
4.7f 1.2
+
Host Specific Ecdysone Agonist
241
TABLE 2. Percent Recovery of Tebufenozide From Pooled Samples of Various Tissues From
Healthy Nondiapausing Codling Moth Larvae, 24 H After Being Offered Diet Containing
'k-Tebuf enozide
Diet with 6.25 pprn tebufenozide
Tissue
Alimentary canal
Perivisceral fat body
Hemolymph
Remaining carcass
X%
Diet with 25 ppm tebufenozide
-
x% S.D.
S.D.
43.2i6.6
13.4 2.6
10.2 2.6
33.0 3.0
36.6 f 3.9
14.6 & 1.6
9.1 i3.7
40.0 f 1.8
*
*
*
Effect of Tebufenozide on Parasitoid Survival Reared on Orally or
Topically Treated Nondiapausing Hosts
Codling moth larvae parasitized by A. quadridenfafawere isolated from diet
and held as pharate individuals until each had ecdysed into their 4th stadium,
then they were offered diet containing various concentrations of tebufenozide
for 24 h. All A. quadridenfafalarvae are in their first stadium at this time 1131.
The EC50 was 2.19 ppm and all host larvae fed diet containing 5 or more ppm
tebufenozide initiated apolysis within 24 h. Other hosts that had exited the diet
and had initiated the wandering stage were isolated from the general colony
and topically treated with either 1 pg tebufenozide dissolved in acetone or
acetone alone. The occurrence of host apolysis, in response to tebufenozide in
the diet or after topical application, determined the fate of the Ascogaster endoparasitoid. Ectoparasitic L3 Ascogaster larvae egressed from hosts that did not
initiate apolysis, but no L3 parasitoid larvae emerged from hosts that had initiated
apolysis in response to the hormone agonist. First instar Ascogaster larvae, of various
lengths, were found in hosts dissected for destructive sampling. Generally, the
endoparasitoid (L1) larva remained alive within the host hemocoel, as long as the
host tissue did not become discolored and start to decompose.
Hyssopus sp. females stung and oviposited on tebufenozide fed hosts. The
number of Hyssopus larvae surviving on a tebufenozide treated host was not
significantly ( P 2 0.05) different from the number expected to develop on a
nontreated host. When Hyssopus females were given a choice of a treated or
healthy host, they attacked and oviposited freely on both. Tebufenozide treated
hosts did not cause acute secondary effects or head capsule slippage in ectoparasitoid larvae; however, endoparasitic Ascogasfev larvae eventually died
because of the onset of host tissue deterioration.
Post-diapausing codling moth larvae injected with 'k-tebufenozide directly
into the hemocoel also supported Hyssopus larval development, but adult
eclosion of the wasps was reduced. These Hyssopus pupae, after feeding as
larvae on hosts injected with 0.1,0.5, or 1 pg 'v-tebufenozide, accumulated and
tebufenozide recovered from
retained the hormone agonist in their bodies.
these Hyssopus pupae had the same relative mobility as the parent compound,
when separated on TLC plates. Nondiapausing codling moth larvae fed various
concentrations (up to 25 ppm) "k-tebufenozide in an artificial diet for 24 h were
removed from the diet and caged along with 3 Hyssopus females for 7 days.
Hyssopus pupae reared from larvae that had fed on these orally tebufenozide
'v-
242
Brown
treated hosts failed to accumulate or at least retain 'k-tebufenozide; however,
the frass collected from larvae voiding their gut prior to pupation contained
increasing amounts of tebufenozide proportionate to the concentration in the
diet fed to their hosts (Table3). The number of progeny/host produced by these
Hyssopus adults, reared from larvae fed tebufenozide treated hosts, did not
differ significantly (P 50.05) from the averagenumber expected from a Hyssopus
attack on a nontreated host.
DISCUSSION
Ecdysteroid Agonistic Effects of Tebufenozide
For two decades [141 researchers have used synthetic JHA as tools to understand physiological responses to JH. Hormone analogs are not as susceptible to
degradative enzymes, which rapidly metabolize exogenously applied natural
hormone, so synthetic analogs are persistent in vivo. Physiologists and endocrinologists studying host /parasitoid endocrine interactionshave often applied
a JHA, such as methoprene, to the host and recorded its effect on parasitoid
development 181. Now researchers have a family of ecdysteroid agonists, including RH-5849 [15-181 and tebufenozide (RH-5992),that mimics the action of
20-OHE. These ecdysteroid agonists are highly selective for lepidopterans and
coleopterans 1191 and are reported to have low acute toxicity to bees 1201.
Therefore, tebufenozide should be of particular importance to researchers
investigating the endocrine interactionsbetween a lepidopteran host, susceptible to the actions of this hormone mimic, and hymenopteran parasitoids, which
presumably would be predicted to tolerate the hormone agonist.
Nondiapausing hosts fed tebufenozide during the first day of their 4th
stadium initiated apolysis within 24 h; however, all endoparasitic Ascogaster
larvae, removed from these pharate hosts, were still in their first stadium. This
was an expected result, because an A. quadridentutu larva remains in the first
stadium while its host undergoes 3 larval-larval molts, and it is only after the
host ceases feeding, wanders, and spins a cocoon, that the parasitoid larva molts
into its second instar [131.
Grossniklaus-Burgin and Lanzrein [21] surveyed the JHand ecdysteroid
titers of Trichoplusia ni attacked by another chelonine species, Chefonus sp. The
life cycles of Ascogaster and Chelonus are nearly identical. The Chelonus species
molts to its second instar, when its host JH titer has declined to an undetectable
level [21].Lepidopteran larvae, including the codling moth [22],generally cease
feeding when the hemolymph titer of JH declines to an undetectable level [231.
Therefore, if tebufenozide is administered orally, the host JH titer should be
expected to be high, thus preventing an Ascogaster molt. The sudden exposure
to an ecdysteroid agonist along with a high endogenous hemolymph titer of JH
would not differ from conditions the endoparasitoid had experienced in earlier
host larval- larval molts. Wandering codling moth larvae would be expected to
have a low titer of hemolymph JH [22]. A topical application of 1 pg tebufenozide administered to these larvae still did not initiate a molt in Ascogaster larvae
in their host's hemocoel, but it did elicit an integumental apolysis in all hosts.
Diapause in both the codling moth larva and its endoparasiticAscogaster larva
is maintained by the inactivity of the host neuroendocrine system and dor-
0.1
0.5
1.0
Amount injected
into each host (kg)
Hyssopus pupae fed
injected host
2.8
37.4
165.3
Injected hosts
18.7
121.4
294.2
Amount (cpm/mg) recovered from:
1.25
6.25
25.00
Concentration in
diet (pg/g)
3.3
6.1
46.5
Tebufenozide
fed hosts
1.7
3.2
1.5
3.9
8.5
11.4
Hyssopus pupae Frass from Hyssopus
reared from hosts
larvae fed orally
fed tebufenozide
poisoned hosts
Amount (cpm/mg) recovered from:
TABLE 3. Comparison of the cpmlmg Wet Weight Recovered From Hosts, Ectoparasitoid, and Frass of Ectoparasitoid Larvae Fed a Coding
Moth Larva Either Fed or Injected With 14C-Tebufenozide
244
Brown
mancy is terminated in both by a pulse of 20-OHE in the absence of JH 13,241.
Diapausing larvae do not feed, so the tebufenozide was injected directly into
the hemocoel and the hosts were immediately ligated, isolating the dormant
endoparasitoid in the host’s abdomen away from the host’s prothoracic gland.
A significant ( P 20.05) number of these endoparasitoid larvae molted to their
second instar in hosts treated with either 2 or 4 pg of tebufenozide, compared
to hosts injected only with DMSO (Fig. 2). Apparently RH-5849, another ecdysteroid agonist, can terminate diapause in Ostrinia nubilalis after a topical
application of 1 pg dissolved in acetone 1161. A transdermal route would avoid
the insult of puncturing the hemocoel, although ligation should still be used to
block the influence of ecdysteroids produced by host ptg on testicular growth
in healthy larvae or parasitoid development in parasitized individuals.
Friedlander and Reynolds [251 have reviewed examples, including C. POrnonellu 1261,where testes in diapausing lepidopterans respond to 20-OHE with
resumption of spermatogenicevents. Loeb 1271 emphasized renewed testicular
growth in response to 20-OHE. Our studies show that testes in diapausing
codling moth larvae are an excellent bioassay tissue for an ecdysteroid agonist
such as tebufenozide. Indeed, testes excised from larvae injected 5 days earlier
with 4 pg tebufenozide were significantly (P I0.05) larger in volume and more
of these testes were fused, as compared to testes removed from solvent treated
larvae (Fig. 1).However, lepidopteran testes are themselves a source of ecdysteroids 1281and they may synthesize enough ecdysteroids to control their own
internal milieu 1291.In this case, tebufenozide, an ecdysteroid mimic, may serve
as a hemolymph message, the same signal represented by 20-OHE in untreated
hosts, and is interpeted by the Ascogaster larva in a castrated host to mean that
the host’s diapause is terminating.
Secondary Effects of Tebufenozide on Endo- and Ectoparasitoidsof the
Codling Moth
Beneficial parasitoids are extremely susceptible to conventional neurotoxic
insecticides because of their searching activities, and if they are not killed
outright, their exposure to these pesticides often has sublethal effects [301. Host
exposure to IGRs can sometimes benefit the parasitoid population [311, but
more often host exposure to any pesticide is detrimental to parasitoids, and
especially jeopardizes endoparasitoid survival in treated hosts. Stark et al. I311
lists several reviews of the effect of pesticides on nontarget invertebrates and
Beckage et al. [32] summarized the effects of IGRs on insect endoparasitoids as
being either direct or indirect. Tebufenozide action must be considered an
indirect effect that causes the host to stop feeding prematurely due to precocious
stimulation of molting. The anti-JH fluoromevalonolactone causes Munduca
sexta to cease feeding [33]and benzyl-l,3-benzodioxole apparently causes morphological deformities in the mandibles of the host, preventing feeding [34].
Tebufenozide causes the host’s head capsule to slip forward within 7 to 24 h; as
a result the host stops feeding. Tebufenozide also may cause apolysis in the
ectodermally derived fore- and hindgut of the host, although we have no
histological evidence for this action. Regardless of the mode of action of tebufenozide on the host, the endoparasitic Ascogaster larva dies in its first
stadium.
Host Specific Ecdysone Agonist
245
The ectoparasitic Hyssopus attacked and parasitized treated hosts, regardless
of the concentration or manner of delivery of tebufenozide to the hosts. However, tebufenozide injected hosts caused some mortality in eulophid larvae and
pupae, and few adult wasps eclosed. Injection directly into the host’s hemocoel
probably delivered more tebufenozide to the hemolymph than what would
enter across the midgut of a host fed tebufenozide in an artificial diet. The
hemolymph RH-5849 peak in treated larvae and the 20-OHE peak in solvent
treated larvae of M. sexta were measured by Wing et al. [lo] and both decayed
in an identical pattern. The fat body is the tar et tissue for both ecdysteroids
1351 and RH-5849 [361. Forty percent of the 9-tebufenozide injected into
codling moth larvae accumulated in the perivisceral fat body, while the bulk of
orally administered 14C-tebufenozideremained in the alimentary canal. If fat
body uptake was measured concurrent to hemolymph loss we might be able to
determine the fate of these IGRs in an insect. Fat body uptake of tebufenozide
might explain the deIayed growth regulatory effects observed several instars
after exposure to these IGRs 1371. Premetamorphic energy demands that utilize
fat body reserves may cause the accumulated IGR to reenter the hemolymph at
a crucial endocrine-dependent time just prior to pupation. The fate of ingested
tebufenozide includes retention in the alimentary canal, slow absorption into
the hemocoel and uptake by the fat body. Hosts fed 25 ppm tebufenozide in an
artificial diet, a 10-foldgreater concentration than the EC50, still supported an
average number of progeny, and adult Hyssops resulting from these larvae
reared on treated hosts were fertile. Lower concentrations of tebuenozide may
even be beneficial in parasitoid rearing programs in that host susceptibility is
prolonged. Hosts exposed to the hormone agonist can not spin a cocoon which can
be an effectivephysical barrier against Hyssopus attack; it also prevents complete
pupation, thus maintaining the host in a susceptible stage for Hyssopus attack.
Endoparasitoids are inherently more susceptible than an ectoparasitoid feeding on an IGR treated host because of their physiology and life cycle. An
endoparasitoid inhabiting the hemocoel of an IGR treated host is in constant
contact with the growth regulator and some of the ecydsone agonist may
penetrate the parasitoid’s integument. The tebufenozide penetrating an endoparasitoid larva and metabolic waste products are retained until a meconium
can be deposited prior to pupation. We did not observe symptoms indicative
of an ecdysone agonist in A . quadridentutu larvae excised from tebufenozide
hosts; however Ascogaster larvae always died in hosts which had slipped their
head capsules in response to the IGR. An earlier study of Myzus persicae (Sulz)
parasitized by Aphidius matricariae (Hal.)simply observed death of endoparasitoids encased in an unshed old and new (double) cuticle, where apolysis had
occurred in the host integument but ecdysis was incomplete [381.
Alternatively, an ectoparasitoid may regurgitate enzymes into the hemocoel of
their host and then the imbibed predigested body fluids containing tebufenozide
must still cross the midgut of the ectoparasitoid larva or the growth regulator will
be eliminated in the parasitoid’s frass (Table 3). Refuge from dermal contact,
preingestive enzymatic action on host tissues, selective absorption across the
midgut cells, and continuous discharge of frass pellets collectively give a measure
of protection to ectoparasitoids, not found in endoparasitoids.
!?
246
Brown
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