tentaculate, predator?
In most studies of feeding in medusae, hydromedusae are grouped together with scyphomedusae, siphonophores, and sometimes even ctenophores. Clearly, though differing in complexity and size, many elements of hunting will be highly similar between the hydromedusae, scyphomedusae, and cubomedusae because of their similar body shape. The section on foraging strategies will regard the medusae as a whole, though crossing taxonomic boundaries, as will the discussion of locomotion and energetics.
Figure 3.14 Cubomedusae. (a) Cross section through the bell of Carybdea; (b) longitudinal section through Tripedalia; (c) the Chirodropid medusa Carybdea. (d) The Chirodropid medusa Chiropsalmus.
Sources: (a–c) Conant (1898); (d) Redrawn from Mayer (1910), plate 47.
General Considerations
Perspective is important when evaluating the foraging behavior of medusae. Equipped with rudimentary sensory systems and limited locomotory capabilities, they forage in a profoundly three‐dimensional environment. Prey are captured on tentacles deployed in a stationary ambush or a slowly moving array as the animal swims forward. Stinging cells (nematocysts) on the tentacles paralyze the prey, which are then conveyed to the mouth and digested. Since both locomotion and the sensory field are quite limited, feeding success of a medusa will be determined by the number of its physical encounters with prey and the effectiveness of its tentacles in subduing the prey item.
In their mathematical model of predator–prey interactions in zooplankton, Gerritsen and Strickler (1977) assumed that the “encounter radius” of a predator was determined by its sensory system. In the case of medusae, it is determined by the volume enclosed within their tentacle array and the likelihood that a prey item once within the “kill zone” will contact a tentacle and be trapped (Madin 1988).
The Cnidae
The stinging organelles, or cnidae, that give the phylum Cnidaria its name are highly complex intracellular structures unique to the phylum. They are formed inside cells called cnidoblasts (Brusca and Brusca 2003), which are formed from interstitial cells in the epidermis and gastrodermis. The mature cnida in its cell is a cnidocyte. The majority of cnidocytes are located on the tentacles in small, blister‐like groups called “batteries” or in the epidermis of the oral region.
The cnida in its discharged state consists of a cup‐shaped basal capsule, a basal “shaft” or “butt” (Hyman 1940; Arai 1997), and ends in a long hair‐like tubule that is often invested with a spiny armor (Figure 3.15). The venom used to subdue prey is either “injected” from a pore at the end of the tubule, much like a syringe works, or is introduced as a coating on the tubule, much like a poisoned dart. The trick to understanding the process of eversion or discharge is to understand how the cnida is coiled in its resting state. If you can imagine poking your finger into that of an empty rubber glove from the wrong side so that it turns “outside in”. you will have a good idea of how the cnida is coiled. In its resting state, it is literally turned outside in. When discharged, the pressure from within the cnida’s basal capsule causes it to evert, just as the finger on the rubber glove would pop back out to normal if you blew into the bottom of the glove. Cnidae can only be discharged once.
Their older name, nematocysts, is still very much in use, and the term cnidocyte then becomes nematocyte. In the newer terminology, only the stinging cnidae are termed nematocysts, to distinguish them from other types of cnidae that, for example, stick to prey (spirocysts) instead of envenomating them (Brusca and Brusca 2003).
Nematocysts, or cnidae, are considered to be “independent effectors”: their discharge is not governed by the nervous system of the medusa but will discharge when stimulated directly by prey contact. The nematocyst has a “lid” or operculum (Figure 3.15) that covers the capsule and acts as a trapdoor. When the cnidocyte discharges, the operculum is flung open. The cnidocil, a bristle located next to the operculum, is believed to be the mechanoreceptor or “trigger” responsible for nematocyst discharge. Though the cnidocytes are considered independent effectors, their sensitivity threshold can be modified by the nutritional state of the medusa. A starved medusa will have a lower threshold for discharge than a well‐fed one.
What causes the cnidocyte to discharge? At least three theories purport to explain how a discharge is achieved. The first is the osmotic hypothesis, wherein a high osmotic pressure (high ion concentration) is maintained inside the nematocyst capsule by active ion transport and perhaps by sequestration of small organic osmolytes. Discharge of the cnidae is effected by a change in permeability of the capsule, causing water to rush down its concentration gradient, swell the capsule, and evert the nematocyst tubule. The second explanation is that the cnida formed within the cnidocyte is already in a state of tension owing to the coiling of its collagen‐like structure, much like a jack‐in‐the‐box with the lid closed. The third is that contractile proteins in the cnidocyte squeeze the basal capsule and pop out the tubule. All three explanations are feasible, but the process happens so quickly that it has not been possible to pin one down as the most likely.
Figure 3.15 Nematocyst structure. (a) Before discharge; (b) after discharge.
Source: Schultze (1922).
Venoms
Venoms are injected when nematocysts discharge. The virulence of the injected toxins varies considerably from species to species, depending partly on the venom itself but also on how much is delivered. For example, the number of tentacles contacted by an unfortunate swimmer brushing up against a Portuguese Man O’War (Physalia physalis) will likely be much larger than that in a similar encounter with Chrysaora, the sea nettle. The cubomedusae are rightfully most famous for the potency of their venom, particularly the sea wasp, Chyronex fleckeri, which can kill a grown man. Within the hydrozoa, the siphonophores are the most potent stingers, with the widely distributed Portuguese Man O’War the best known. It deserves every bit of its nasty reputation as a world‐class stinger.
All venoms have a few properties in common, and cnidarian venoms are no exception (Hessinger 1988). First, most venoms act on cell membranes. Membranes are the most accessible part of any cell, always play an important role in cell integrity and function, and can be disrupted in a variety of ways. Second, most venoms are proteinaceous. Of the three major types of biomolecules (proteins, lipids, and carbohydrates), proteins are the most plastic in structure and function. They range from enzymes, which can literally change shape, to blood pigments, to inert structural molecules such as the keratins. They are the most amenable to biological design. Also, most proteins are readily digested, so the predator is not poisoned by its own venom! Third, venoms act rapidly. To be effective, toxins must kill, stun, or paralyze the prey quickly to prevent escape.
When considered on a dose‐specific basis (μg kg−1 body mass), cnidarian venoms are among the most deadly known to science, on a par with those of the kraits and the mambas. Purified venoms of the sea wasp and Man O’War show a median lethal dose in mice of less than 50 μg kg−1 body mass. Symptoms in mice of poisoning with purified cnidarian venom include severe respiratory
