13.3.2. Host manipulation and development of parasitoids

Parasitization may kill or paralyze the host, and the developing parasitoid, called an idiobiont, develops rapidly, in a situation that differs only slightly from predation. Of greater interest and much more complexity is the konobiont parasitoid that lays its egg(s) in a young host, which continues to grow, thereby providing an increasing food resource. Parasitoid development can be delayed until the host has attained a sufficient size to sustain it. Host regulation is a feature of konobionts, with certain parasitoids able to manipulate host physiology, including suppression of its pupation to produce a “super host”.

Many konobionts respond to hormones of the host, as demonstrated by (i) the frequent molting or emergence of parasitoids in synchrony with the host’s molting or metamorphosis, and/or (ii) synchronization of diapause of host and parasitoid. It is uncertain whether, for example, host ecdysteroids act directly on the parasitoid’s epidermis to cause molting, or act indirectly on the parasitoid’s own endocrine system to elicit synchronous molting. Although the specific mechanisms remain unclear, some parasitoids undoubtedly disrupt the host endocrine system, causing developmental arrest, accelerated or retarded metamorphosis, or inhibition of reproduction in an adult host. This may arise through production of hormones (including mimetic ones) by the parasitoid, or through regulation of the host’s endocrine system, or both. In cases of delayed parasitism, such as is seen in certain platygastrine and braconid hymenopterans, development of an egg laid in the host egg is delayed for up to a year, until the host is a late-stage larva. Host hormonal changes approaching metamorphosis are implicated in the stimulation of parasitoid development. Specific interactions between the endocrine systems of endo-parasitoids and their hosts can limit the range of hosts utilized. Parasitoid-introduced viruses or virus-like particles (Box 13.1) may also modify host physiology and determine host range.

The host is not a passive vessel for parasitoids — as we have seen, the immune system can attack all but the adapted parasitoids. Furthermore, host quality (size and age) can induce variation in size, fecundity, and even the sex ratio of emergent solitary parasitoids. Generally, more females are produced from high-quality (larger) hosts, whereas males are produced from poorer quality ones, including smaller and superparasitized hosts. Host aphids reared experimentally on deficient diets (lacking sucrose or iron) produced Aphelinus (Hymenoptera: Aphelinidae) parasitoids that developed more slowly, produced more males, and showed lowered fecundity and longevity. The young stages of an endophagous konobiont parasitoid compete with the host tissues for nutrients from the hemolymph. Under laboratory conditions, if a parasitoid can be induced to oviposit into an “incorrect” host (by the use of appropriate kairomones), complete larval development often occurs, showing that hemolymph is adequate nutritionally for development of more than just the adapted parasitoid. Accessory gland secretions (which may include paralyzing venoms) are injected by the ovipositing female parasitoid with the eggs, and appear to play a role in regulation of the host’s hemolymph nutrient supply to the larva. The specificity of these substances may relate to the creation of a suitable host.

In superparasitism and multiparasitism, if the host cannot support all parasitoid larvae to maturity, larval competition often takes place. Depending on the nature of the multiple ovipositions, competition may involve aggression between siblings, other conspecifics, or interspecific individuals. Fighting between larvae, especially in mandibulate larval hymenopterans, can result in death and encapsulation of excess individuals. Physiological suppression with venoms, anoxia, or food deprivation also may occur. Unresolved larval overcrowding in the host can result in a few weak and small individuals emerging, or no parasitoids at all if the host dies prematurely or resources are depleted before pupation. Gregariousness may have evolved from solitary parasitism in circumstances in which multiple larval development is permitted by greater host size. Evolution of gregariousness may be facilitated when the potential competitors for resources within a single host are relatives. This is particularly so in polyembryony, which produces clonal, genetically identical larvae (section 5.10.3).

Chapter 13