Commercial Fisheries News - February 2003
By Kari Lavalli (firstname.lastname@example.org)
While scientists don't know for sure what causes shell disease, one or more of three types of bacteriaVibrio, Pseudomonas, and Aeromonasare always found in the lesions.
These bacteria have a chitinase enzyme that can break down the chitin portion of the shell. They are also capable of initiating infection in otherwise healthy lobsters.
Besides being present in lesions, the bacteria are found in the pores and setal pits. Setal structures detect water currents and chemicals, performing functions equivalent to smelling and tasting in humans.
These hair-like structures are found on antennules, legs, mouthparts, tail fans, swimmerets, and carapace surfaces. Since setal structures are less calcified, they may be more vulnerable to bacterial infection. The setae also often break during the course of normal feeding activities, exposing yet another avenue for infection.
The lobster responds to shell disease by depositing melanized, wound-reaction tissue, usually in the form of brownish nodules or membranous material, and by increasing chitin formation in the lesion area.
If the animal is unable to stop or contain the invading microorganisms, the shell in the lesion area becomes pliable, and secondary pathogens may invade other body tissues.
Some studies have detected additional bacterial agentsAerococcus viridans within the lesions or near the diseased area of the shell.
Aerococcus viridans causes gaffkemia, also known as red tail. It enters through lesions, proliferates in the hemolymph (blood) and tissues, and eventually kills the lobster.
Once infected by gaffkemia, temperature determines the lobster's lifespan. At colder temperatures, the animal may live weeks to months, but at warrner temperatures, the lobster may die within two weeks.
Other disease agents, including protozoa and fungi, although rarely observed on the surface of shell disease lesions, can cause secondary infections.
Physiologically, shell disease-infected lobsters show a reduction in hepatopancreas lipid and hemolymph protein and a significant increase in ash content in both. These differences suggest problems with the transport and deposition of minerals to the exoskeleton and/or withdrawal of such nutrients from the shell.
We've been aware of shell disease for many decades, but we still do not understand why some lobsters are able to survive after being infected, while others die.
However, the higher occurrence in recent years of this disease in commercially important species like lobsters, crabs, and shrimp has spurred interest in the disease and federal agencies such as Sea Grant are now funding more research to better understand it.