I’ve already written a post about parasites that affect their hosts’ behaviour, but it’s such a cool subject that I don’t think anyone will mind another example of it :)
Species in the braconid genus Chelonus are egg-larval parasitoids. Parasitoids are parasitic in their larval stage and free-living as adults. Egg-larval parasitoids are those that, as adults, sting their hosts and inject their eggs when the host is in the egg or the larval stage. While it is not reserved for the parasitic Hymenoptera, it is true that most parasitoids are hymenopterans.
Systematically, Chelonus belongs to the Cheloninae subfamily which forms a monophyletic clade with the Adeliinae, and this clade is considered to be the basalmost microgastroid braconid taxon (Dowton & Austin, 1998).
Chelonus species only parasitise lepidopterans. The affected host larva (i.e. the caterpillar) begins pupating too early, at the pre-final larval stage instead of the final one. This is caused by the larval parasitoid releasing specific proteins (Hochuli et al., 1999) that reduce the caterpillar’s levels of juvenile hormone – the cue to starting metamorphosis. Physiologically, the first few steps of pupation start, including the production of storage proteins, but then all further development ceases at the prepupal stage. This developmental arrest is caused by a polydna virus injected during oviposition and activated by the parasite.
The origin of this virus is currently unknown, but it would be interesting to elucidate: other microgastroids also have polydna viruses, but the chelonine ones are different enough (Wyder et al., 2002) to be considered convergent. If that is the case, this would be a cool model system to study coevolution of viruses within the coevolution of hosts and parasites.
Eventually the larval parasite, which had been growing inside the host, breaks out (killing the host in the process, of course) and begins its own pupation, inside the pupation coccoon of its host – thereby being even safer than usual (in the wild, it may be that the pupa might have to overwinter instead of hatching within a week or two, hence why the protection is important). The already-mentioned increase in host storage proteins is beneficial for the nutritional value (Kunkel et al., 1990); it’s been shown by Kaeslin et al. (2005) that the parasite can very effectively take up nutrients from its prepupa host. Chelonus has obviously hit on a winning strategy.
There are rare cases of pseudoparasitism: a host is stung by the wasp, with the pupation being initiated too early – but in the pseudoparasitic cases, there is no actual parasite in the host. This is of interest when considering whether the parasite actually controls the host’s physiology, or whether the physiology is adversely affected by the parasite’s presence through no direct action of the parasite itself (see Lanzrein et al., 2001).
It could be, of course, that the parasite somehow died before maturing, but still released its “control” chemicals while alive – meaning that the parasite can control its host directly. Or it could be that the very action of getting the host eggs or larvae stung by the adult female wasp affected them mechanically or chemically (the oviposition fluid might be venomous, hence screwing with the pupation timing mechanism).
Note, however, that pseudoparasitism seems to be limited to a few Chelonus species; most of the time and in most species, the parasite actually needs to be there for the effects to be observed (Pfister-Wilhelm & Lanzrein, 1996).
Surprisingly (to me at least), Chelonus is not successful as a biocontrol agent, at least not when C. annulipes was tried against the pesky European corn borer; I’m not sure why.
In case anyone’s interested, Chelonus does have a fossil record in the form of three species from the 37 Ma Florissant Shale (Brues, 1910).
Brues CT. 1910. The parasitic Hymenoptera of the Tertiary of Florissant, Colorado. Bulletin of the Museum of Comparative Zoology 54, 1-126.
Dowton M & Austin AD. 1998. Phylogenetic Relationships among the Microgastroid Wasps (Hymenoptera: Braconidae): Combined Analysis of 16S and 28S rDNA Genes and Morphological Data. Molecular Phylogenetics and Evolution 10, 354-366.
Kunkel JG, Grossniklaus-Buergin C, Karpells ST & Lanzrein B. 1990. Arylphorin of Trichoplusia ni: Characterization and parasite-induced precocious increase in titer. Insect Biochemistry and Physiology 13, 117-125.
Hochuli A, Pfister-Wilhelm R & Lanzrein B. 1999. Analysis of endoparasitoid-released proteins and their effects on host development in the system Chelonus inanitus (Braconidae)–Spodoptera littoralis (Noctuidae). Journal of Insect Physiology 45, 823-833.
Kaeslin M, Pfister-Wilhelm R & Lanzrein B. 2005. Influence of the parasitoid Chelonus inanitus and its polydnavirus on host nutritional physiology and implications for parasitoid development. Journal of Insect Physiology 51, 1330-1339.
Lanzrein B, Pfister-Wilhelm R & von Niederhäusern F. 2001. Effects of an egg-larval parasitoid and its polydnavirus on development and the endocrine system of the host. In: Edwards JP & Weaver RJ (eds.). Endocrine Interactions of Insect Parasites and Pathogens.
Pfister-Wilhelm R & Lanzrein B. 1996. Precocious induction of metamorphosis in Spodoptera littoralis (Noctuidae) by the parasitic wasp Chelonus inanitus (Braconidae): Identification of the parasitoid larva as the key regulatory element and the host corpora allata as the main targets. Archives of Insect Biochemistry and Physiology 32, 511-525.
Wyder S, Tschannen A, Hochuli A, Gruber A, Saladin V, Zumbach S, Lanzrein B. 2002. Characterization of Chelonus inanitus polydnavirus segments: sequences and analysis, excision site and demonstration of clustering. Journal of General Virology 83, 247-256.
Research Blogging necessities :)
KAESLIN, M., PFISTERWILHELM, R., & LANZREIN, B. (2005). Influence of the parasitoid and its polydnavirus on host nutritional physiology and implications for parasitoid development Journal of Insect Physiology, 51 (12), 1330-1339 DOI: 10.1016/j.jinsphys.2005.08.003