Mechanism

Some Basic Anatomical and Physiological Facts

The lancet liver fluke is around 5-15mm in length. At the mouth there is a stylet, a small slender pointed appendage. The acetabulum is the second sucker and is not located at the mouth. There are also two blind-ending intestinal caeca. The lancet liver fluke is digenetic, meaning that it is capable of reproducing both sexually and asexually. The cirrus is the intromittent organ (male sex organ) and there is an egg filled uterus that takes up a large portion on the body. The genital pore is the common external opening of both the male and female reproductive systems. The vitellaria are glands that produce yolk-filled cells, which are then carried to the ootype (the site where eggs are fertilized) and deposited around the fertilized ovum. There is no anus, so waste material must be egested through the mouth. The body is made of a tough syncitial tegument that protects the lancet liver fluke against the digestive enzymes of the third definitive host. The surface of the body is also used for gas exchange, as there are no respiratory organs. There is a lack of any specialized sensory organs and the "brain" is simply a pair of ganglia in the anterior region of the body, from which two or three pairs of nerve cords extend down the length of the body. [9]

Lancet Liver Fluke Anatomy/Physiology[8]

Mechanisms of Host Manipulation and the Brainworm

The lancet liver fluke employs one of the most intriguing methods of transmission, host manipulation. Host manipulation is the process by which parasites alter any phenotype (such as behavior, morphology, physiology) of their host by varying degrees in order to enhance their fitness benefits [10], which in many cases include the chance of successful transmission from one host to another.

Once the cercariae have penetrated through the crop of the ant and into the gaster they go through a stage of inactivity lasting anywhere from 16 to 25 hours, depending on the temperature. When this inactive stage is complete certain environmental triggers, such as an attraction to the subesophageal ganglion, cause all of the cercariae to begin migrating through the thorax to the head of the ant. Once there one cercaria immediately encysts itself in the subesophageal ganglion of the ant, forming what is known as the brainworm. By the time this occurs about 30% of the cercariae have left the gaster. The formation of the brainworm causes all the cercariae to return to the gaster in 1.5-2 days; if the cercariae are experimentally prevented from encysting in the subesophageal ganglion they will not return. Once back in the gaster the rest of the cercariae encyst, but this occurs much later than the formation of the brainworm. [6]

The specific mechanisms used by the cercariae to control the ant are not yet known. So far what has been discovered is that the modified behavior of climbing a blade of grass and grabbing it with the mandibles at the top is a sleep behavior observed in some phylogenetically older genera of ant (e.g. Ammophila). This behavior was most likely suppressed because of the development of new nesting patterns in some phylogenetically newer genera of ant (e.g. Formica). Therefore, it is quite possible that the neurons of the ants still retain the information/capacity for this old behavior, it is just being supplanted by the new behavior. These facts could lead to the conclusion that the cercariae, in particular the brainworm, may have found a way to reinstate the old behavior in order to use it to their advantage. [6]

When examining host manipulation with a broader scope, numerous studies have found that parasites may directly change host behavior by secreting neuroactive substances or indirectly change host behavior when their presence alone influences or interferes with biochemical pathways [10]. It can be very hard to distinguish between direct and indirect; secretions that cause manipulations could actually be intended for purposes such as host immune suppression. Following infection, parasites can alter the phenotype of their host directly or indirectly by altering concentrations of hormones or neurotransmitters. The host already synthesizes many of these substances, so it is advantageous for the parasites to use these existing biochemical pathways that have downstream effects on behavior. These pathways can be up- or downregulated to change the concentrations of their products, such as active neurochemicals [7]. The more indirect the method of changing the host phenotype is, the smaller the fitness cost will be. Applying the concept of extended phenotype (as discussed in Phylogeny), host manipulation in which a biochemical cascade is triggered to manipulate host phenotype may have the smallest fitness cost when a parasite can suppress the expression of one or more host genes by influencing them with its own [7]. It should be noted that even if the biochemical and physiological processes of the host are what are altered to produce the changes in phenotype, the real source of the host manipulation will still come from the parasite.

Adult Lancet Liver Fluke[3]