Depletion of glycogen and adenosine triphosphate as major factors in the death of lobsters (Homarus americanus) infected with Gaffkya homari

Abstract

Development of high numbers of Gaffkya homari, the pathogen causing gaffkemia in lobsters, occurs first in the hepatopancreas, followed immediately by development in the heart, and considerably later in the hemolymph. Significantly lower bacterial numbers develop in the muscle only after an appreciable lag period. Glycogen declines drastically in the tail muscle, heart, and hepatopancreas reaching nominal levels in the hepatopancreas by the 9th day of about a 2-week overall infection period recorded at 15C.A slight reduction of tail muscle ATP and about a 50% reduction in heart ATP were observed over the course of the infection; non-bacterial ATP in the hepatopancreas was virtually absent from the 9th day of the infection onward. The main conclusion based upon the foregoing suggests death was the result of hepatopancreatic dysfunction caused by G. homari disrupting or bringing to a halt the central metabolic processes of the lobsters. Trials to determine whether a bacterial toxin was produced in vivo and had acted as a contributory factor in the deaths were uniformly negative.