Gaffkemia, a bacterial disease of the lobster, Homarus americanus: effects of the pathogen, Gaffkya homari, on the physiology of the host

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Abstract
Gaffkya homari, the pathogen causing gaffkemia, was observed in vivo to reach its stationary growth phase (approximately 108 bacteria/ml of lobster hemolymph) in 4 days at 15 C. The bacterial totals at death ranged between 5 × 108 and 1 × 1010/ml of hemolymph. Among the main effects of the infection was the great increase in hemolymph clotting times followed by the essential elimination of clotting. The impaired clotting mechanism was a result of the drastic reduction in circulating hemocyte numbers rather than a reduction in hemolymph fibrinogen levels. Hepatopancreatic glycogen levels and hemolymph non-protein nitrogen concentrations dropped to minimal levels but hepatopancreatic lipid levels, hemolymph lactic acid, carbohydrate, and pH values were not significantly affected by the infection. An extreme hyperglycemic effect, attributed to stress, was observed in both control and infected lobsters. Death from gaffkemia, other than that stemming from a wounded animal bleeding to death because of the impaired clotting mechanism, was considered a result of an unsuccessful competition on the part of the lobster for its own readily available storage material. Gaffkemia appears to be a wasting type of disease produced by the bacterium, G. homari, which is resistant to the lobster's intrinsic defense mechanisms and finds lobster hemolymph an excellent medium for growth.

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