Carbohydrate Dynamics and the Crustacean Hyperglycemic Hormone (CHH): Effects of Parasitic Infection in Norway Lobsters (Nephrops norvegicus)

Abstract

The effects of a dinoflagellate parasite (Hematodinium sp.) on carbohydrate metabolism were examined in the Norway lobster, Nephrops norvegicus. Five stages of infection were observed. These included uninfected (Stage 0), subpatently infected (SP), and patently infected (Stage 1–4) lobsters. During patent infection, the concentration of glucose in the hemolymph was reduced significantly from its value of 180 μg ml−1 in uninfected (Stage 0) lobsters to 25.3 μg ml−1 in Stage 3–4. These changes were accompanied by significantly lower levels of hepatopancreatic glycogen in lobsters at Stage 2 (2.01 mg g−1) and Stage 3–4 (0.84 mg g−1) of infection than in those at Stage 0 (16.19 mg g−1) and Stage 1 (14.71 mg g−1). Due to disruption of the normal feedback loops which control the release of crustacean hyperglycemic hormone (CHH), plasma concentrations increased with the severity of infection from 32.2 fmol ml−1 in Stage 0 to 106.6 fmol ml−1 in Stage 3–4. The increased CHH concentrations occurred concomitantly with reduced concentrations of plasma glucose and tissue glycogen. A significantly increased hemolymph CHH titer (107.7 fmol ml−1) was also observed during SP infection. It is concluded that the parasite places a heavy metabolic load on the host lobster.